cpb surgical&clinical orientation

CP Bypass: Surgical &Clinical orientation 1

Cardio Pulmonary Bypass:

Surgical & Clinical Orientation

for

Students

of

Perfusion Technology, Anesthesiology

& Cardiac surgery

By

Dr. Anil G. Tendolkar


TO

MY REVERED TEACHER

DR. GURUKUMAR B. PARULKAR

Sir,Sir,Sir,Sir,

more I practiced cardiac surmore I practiced cardiac surmore I practiced cardiac surmore I practiced cardiac surgerygerygerygery

more I realised the importance of your teachings.more I realised the importance of your teachings.more I realised the importance of your teachings.more I realised the importance of your teachings.

Sincerely,Sincerely,Sincerely,Sincerely,

AnilAnilAnilAnil


Introduction

The art of planning & conducting perfusion based on patient’s pre-operative condition, state of

the heart, surgical step and etcetera, is fast disappearing. Today, perfusionists are becoming more

‘monitor oriented’, may be, more technically smart but poorer in clinical orientation.

I was fortunate to work under Dr. G.B. Parulkar, the then head of the department of cardiac

surgery, KEM Hospital Mumbai, India, initially as a resident in cardiac surgery and later as a junior

colleague. Dr. Parulkar taught us (his students) planning of CPB based on patient’s clinical condition,

CPB implications of every surgical step, different surgical checks and counter checks as to ensure a safe

CPB. This book is an attempt to archive the knowledge I acquired from Dr. Parulkar through years.

To understand clinical implications of a disease, understanding of pathophysiology of heart

diseases is essential. Hence, I have described pathophysiology of every disease before describing the

relevant CPB management.

Today, anesthesiologists & perfusionists are integral part of a cardiac surgical team. The three

work differently but simultaneously and share the same space. This, many a times, produces conflicting

situations. Hence it has become imperative for all the members of the team to know implications and

pitfalls of every surgical step.

I sincerely hope this book helps perfusionists, anesthesiologists and surgeons in improving their

understanding of cardiopulmonary perfusion and help them in achieving a successful outcome.


Preface

Dear All,

It is my proud pleasure to offer this book to you.

This book is not a text book and it is not intended to replace detail reading of cardio-pulmonary perfusion,

cardiac physiology or cardiac pathology. This book is meant only for improving the understanding of

cardiopulmonary perfusion from a clinical & surgical point of view.

I sincerely hope that this book helps you in achieving this goal.

Sincerely,

agt


Contents

1. Preoperative Assessment…………………………………………… 06

2. Relevant Pictorial Anatomy………………………………………… 09

3. Surgical Aspect of CPB ……………………………………………... 19

4. Mitral Stenosis ……………………………………………………….. 33

5. Mitral Regurgitation …………………………………………………. 40

6. Aortic Stenosis ……………………………………………………… 44

7. Aortic Regurgitation ………………………………………………… 49

8. Tricuspid Valve Disease ……………………………………………… 53

9. Multivalvar Affections ……………………………………………….. 56

10. Artificial Valves …………………………………………………….. 57

11. Atrial Septal Defect …………………………………………………... 59

12. Ventricular Septal Defect ……………………………………………. 68

13. Tetralogy of Fallot………………………..…………………………..... 74

14. Functional Single Ventricle …………………………………………… 81

15. Total Anomalous Pulmonary Venous Connection …………………… 89

16. Transposition of Great Arteries ……………………………………… 93

17. Coronary Artery Disease ………………………………………… 101

18. Mechanical Complications of CAD ………………………………… 117

19. Rupture of Aneurysm of Sinus of Valsalva …………………………. 120

20. LA Myxoma ………………………………………………………… 123


1. Preoperative Assessment

The importance of noting the following points in a preoperative assessment is,

1. Age: At extremes of ages tolerance of patients to artificial circulation is poor. Hence, for neonates,

infants and elderly, all the pharmacological and hardware interventions to reduce the inflammatory

response should be attempted.

2. Weight and Height: for calculation of body surface area (BSA) and hence, the flows.

3. Body Volume assessment: A cardiac patient could be in congestive cardiac failure with excessive

volume in the intravascular compartment. Conversely, some cardiac patients are vasoconstricted and in

these patients going on CPB yields a very low venous return. Thus, instead of going by a fixed formula

for body volume calculation, knowing the actual body volume status will help a perfusionist in

appropriate priming.

Body volume can be assessed by:

a) Clinical: raised JVP, edema feet, enlarged liver are associated with higher body volumes.

b) Mean CVP (Normal = 5-6mm of Hg) Higher pressure values are associated with higher

intravascular volumes.

c) Chest X-ray: Cardio-Thoracic (CT) ratio: (Normal < 50%) Higher ratio is associated with more

blood in the heart and or in the pulmonary circulation. Details of volume distribution will be

discussed with individual cases.

Prominent right heart border is associated with increased volume in systemic venous circuit.

d) 2D Echocardiography: This can estimate actual cardiac chamber size .Normal chamber

dimensions ( approximately) are

LV Internal Diameter (LVID): 2.0 cm in systole and 3.0 cm in diastole

LA: < 2.0 cm

RVID: < 1.0 cm

Remember that the above figures are of diameter (d = 2 r) of the chambers and volume of the

chamber would be 4/3 π r3.

Other descriptive terms in an echo report which indicate volume overload are,

a) IVC not collapsing during inspiration, b) dilated coronary sinus (in the absence of LSVC)

c) Volume Overload (VO) as RVVO/RAVO/ LAVO

4. Hemoglobin/ PCV: Any patient with liver congestion (as in CCF), frequent episodes of lower

respiratory tract infection (LRTI) (as in VSD) has low hemoglobin.

All patients with cyanotic heart disease have higher hemoglobin (polycythemia) as a

compensation for the decreased oxygen carrying capacity. The hemoglobin increases proportionate to the

arterial saturation.

5. Plasma Volume: Plasma volume is in inverse proportion with the Hb/ PCV value. Patients with low

hemoglobin (i.e. anemia) or CCF though have a proportionately large plasma volume; the serum protein

values are low due to poor nutrition as a result of heart disease (cardiac cachexia)

6. Systemic Vascular Resistance (SVR): In patients with a stenotic disease (e.g. mitral stenosis) SVR is

increased as a body compensatory mechanism. The rise in SVR is usually in proportionate with the

severity of stenosis.


SVR is low in patients with regurgitant or incompetent lesions (e.g. mitral regurgitation)

Preoperative and intraoperative medication can change the SVR.

Patients with high SVR have collapsed veins (inspect saphenous vein at the ankle- anterior to medial

malleolus) low volume pulse and a high diastolic pressure.

Patients with low SVR have a dilated vein, good or high volume pulse, and normal or low diastolic

pressure.

7.Organ Function : inadequate perfusion due to acute or chronic heart failure , atherosclerotic arterial

disease causing narrowing or occlusion of the arteries, cardio-arterial embolism, chronic venous

congestion affect the function of various vital organs like brain, liver and kidneys.

8. Arterial Tree: Artery may be blocked or significantly narrowed due to atherosclerosis or embolism.

As a result, CPB however well conducted, will not benefit the organ with vascular obstruction.

9. Arterial Cannulation: For median sternotomy aorta is the site of choice for arterial cannulation.

Other sites are

Site For

Cannulation

( Skin incision site)

Advantage Disadvantage

Ascending Aorta

( Sternotomy)

1.Performed through surgical incision

2.Clean area

3.Size of cannula is not a limitation

4.complications related to cannulation

can be easily detected

1.cerebral embolism

Femoral Artery

( Groin)

1.used for quick cannulation

2.percutaneous cannulation possible

3. can be performed prior to surgical

incision

4.scar can be concealed

1. in a potentially infected area

2. lymph collection possible

3. retroperitoneal dissection

Iliac Artery

( Lumbar-

retroperitoneal incision)

1.can be performed prior to surgical

incision

2.size of the cannula could be larger than

in femoral cannulation

3. cannulation in a cleaner area

1.deeper dissection than femoral

cannulation required

2. possibility of injury to ureter

3. retroperitoneal dissection due to

cannulation

Axillary Artery

( Axilla)

1.For cerebral perfusion

2.Used in combination with the above

mentioned sites

Venous cannulation: Apart from commonly used sites like RA appendage, SVC & IVC other used sites

are right ventricular outflow (RVOT), and femoral veins.

These sites will be discussed as per different situations.

Cardioplegia Delivery: Antegrade: 1) root 2) coronary ostial 3) through grafts


Retrograde: 1) RA 2) coronary sinus

Left Heart return: Normally, approximately 1% of the cardiac output (i.e. 1% of 5000 ml = 50 ml per

minute) returns back to heart via bronchial veins which open into pulmonary veins (PV). This is called

‘left heart return’. From PV, the blood eventually enters LA & LV. In a cardioplegically arrested heart,

accumulation of this blood in LA/LV obstructs the operative field, distends the heart and rewarms the

heart. In certain conditions the amount of left heart return could be more.

To prevent the above mentioned problems, the LH return is sucked away through a LH vent. Various sites

for LH venting are shown below.

LH Venting

Site

Operation Vent type

RSPV AVR, Ascending aortic operation

corrections through RA/RV sump, curved multiperforated

LA body MV surgery , MV+ other valve surgery Sump

VSD corrections through RA/RV long stiff

IAS Only TV surgery, corrections through

RA/RV

Sump

PA TOF correction through RV, LA myxoma

excision

Sump

LA appendage Only TV surgery, corrections through

RA/RV

Sump

LV apex AVR, any operation on aorta curved multi-perforated

ASD Any operation involving ASD closure Long stiff, sump

Aortic Root CABG Root cardioplegia cannula

Preoperative Medications: Patient is on oral or intravenous medications prior to surgery. These

medications alter SVR, blood volume, electrolytes or clotting status.

Prior Treatment: Prior operation or intervention changes the plan for surgical approach, surgical steps,

cannulation, cooling status, cardioplegia delivery.

Special Considerations: like early cross clamping may be required in some cases


2. Relevant Pictorial anatomy

Figure 2.1: Parts of heart and blood vessels that can be seen through a median sternotomy incision

Parts shaded gray are covered by pericardial fold or thymus or mediastinal fat. Hence require

dissection to visualise them. The rest are seen after opening the pericardium. (Parts shown with dotted

lines are posterior to the heart but in the pericardium)

Right sided structures are anterior and left sided structures are posterior. Thus, RA, aorta and right

superior pulmonary vein (RSPV) are anterior structures and are easy to cannulate.

For operating on a part beyond or distal to the structures shown above; pleura or thoracic cavity has to

be opened.

Fig 2.2: Surfaces of heart

Heart is a conical structure and with the surfaces as shown below. Coronary arteries located on

anterior surface are the easily seen and those on the posterior surface are the most difficult to see.


.

Figure 2.3: .The space between the medial surfaces of the two lungs is called Mediastinum

Mediastinum is divided into anterior mediastinum (shaded bluish-green in fig 2.4), containing heart

and thymus; and posterior mediastinum, containing trachea, esophagus and descending thoracic aorta.

Fig 2.4: Approaches to mediastinum

The mediastinal structures can be approached through the following incisions:

1. Median sternotomy 2.Right anterior thoracotomy

3. Left anterior thoracotomy 4.Left posterior thoracotomy


Figure 2.5: Arrangement of Cardiac Chambers

The right side chambers are anterior also, while the left sided chambers are posterior.

The arrangement of various chambers in relation to each other is shown below.

Note: LA is the posterior most chamber.

Anterior

Posterior


Figure 2.6: Anatomy of Inter Atrial septum (IAS)

SVC: Superior vena cava IVC: Inferior vena cava FO: Fossa Ovalis CS: coronary sinus

TV: Tricuspid Valve

Shaded area: Septum Primum. Nonshaded area: Septum Secundum (the line separating the two areas

is an imaginary line passing through coronary sinus and parallel to SVC & IVC

Figure 2.7: Parts of IVS: (The boundaries are not accurately defined)

m: membranous septum inlet: under the leaflets of tricuspid valve

outlet: below the pulmonary valve body: The remaining part of RV


Figure 2.8: Atrio-Ventricular Valve. The Tricuspid Valve and the Mitral valve are called right and left

AV valve, respectively. The basic plan of an A-V valve remains the same.

Annulus, cusps, chordae, papillary muscle and LV wall constitute MV apparatus. Chordae and

papillary muscles together are called ‘subvalvar structure/ apparatus’.

Figure 2.9: Mitral Valve (Close position) as seen during surgery through LA

1: Anterior commissure 2: Annulus 3: Anterior Mitral Leaflet (AML)

4: Posterior Mitral Leaflet (PML) 5: Common Annulus 6: posterior commissure


Figure 2.10: Tricuspid Valve (Close position) as seen during surgery through RA

1. Anterior Tricuspid Leaflet (ATL) 2 Septal Tricuspid Leaflet (STL)

3. AV Node 4. Annulus 5. Posterior Tricuspid Leaflet (PTL) 6. Coronary Sinus


Figure 2.11: Aortic valve (Close position) as seen during surgery through Aorta

1. Left Coronary Cusp (LCC) 2.Left Coronary artery (LCA)

3. Right Coronary artery (RCA) 4. AV Node

5. Right Coronary Cusp (RCC) 6.Non Coronary cusp (NCC)

7. Common (with MV) Annulus

Figure 2.12: Aorta (Longitudinal section)

1. Ascending aorta 2. Sinu-Tubular Junction 3.Sinus of Valsalva

4.Cusps or Leaflets 5. Annulus 6. Coronary artery


Figure 2.13: Coronary Artery Anatomy: (Arteries which are not accessible for surgical anastomosis

are shaded black).

The reasons some coronary arteries are not accessible for surgery are,

Left main (LM) & proximal LAD: posterior to MPA

Left Circumflex (LCx): deep in the left (i.e. posterior) AV groove & covered with great cardinal vein

Septal: deep in the IVS

Middle third of RCA: deep in the right AV groove, covered by fat

Figure 2.14: Coronary arteries and their related surfaces

Anterior Territory (Red) LAD and Diagonals

Posterolateral Territory (Creamy red): Ramus and OM

Inferior Territory (Green): PD & PLV


Figure 2.15: Drainage of Right SVC

.

Fig 2.16: Most common anatomy when L SVC is also present


Left SVC: Can be found as an associated anomaly with a number of congenital heart diseases.

Normally left subclavian vein (LSCV) and left internal jugular vein (LIJV) join to form left

innominate vein (L Inn V). The two innominate veins join to form right sided SVC. Left SVC is

formed by joining of LSCV and LIJV. The L Inn V is either absent or small in caliber. In fact, size of

L Inn V is inversely proportional to the size of LSVC. As blood from superior half of the body is

carried by an additional SVC, the size of right SVC is small.

The LSVC runs posterior to the heart, in the AV groove and, most commonly, opens into coronary

sinus. Rarely, as a rule in a complex congenital heart disease, LSVC opens into the roof of LA.

Bilateral SVC share the superior venous drainage, hence, does not impose any volume overload on

the heart.

Left SVC is managed by

ligation : if L Inn V is of significant in size

Drainage : a) by cannulation: b) with a cardiotomy sucker:


3. Surgical Aspect of CPB

Need for CPB:

For operating on a part of the body, the part has to steady, dry (blood free) and relaxed. The part should

be steady, so surgeon can dissect & place incisions accurately; the part should be dry, to allow surgeon to

view the operating area well and the part should be relaxed so that, it can be retracted to provide access.

Due to these requirements, cardiac surgery, initially, was considered an impossibility. This was because

heart continuously pumps blood to provide oxygen and nutrition to the entire body and stoppage of its

function results in anoxia and fatal damage to the tissues. The damage is seen maximum in organs which

are vulnerable to anoxia. Brain is one such organ and is the first to suffer damage. Hence a machine to

substitute the function of heart was devised.

Soon it was realised that far more number of cannulae and a much more complex circuit are required

when only heart is bypassed, rather than, when heart and lungs are bypassed together. The large number

of cannulae reduced the visibility of the operating field and complex circuit made conduct of bypass

difficult.

Thus, the help of heart lung machine maintains the perfusion primarily of brain and other organs while

heart is stopped and is being operated upon.

Basic Steps of OHS:

1) Sternotomy or Thoracotomy

2) Pericardiotomy and pericardial retraction

3) Placement of aortic & venous purse strings

4) Systemic heparinisation

5) Aortic and venous cannulation

6) Commencement of CPB, appropriate core cooling

7) Aortic crossclamping and delivery of cardioplegia

8) Cardiotomy and completing intracardiac procedure

9) Closing the cardiotomies and deairing the heart

10) Declamping the aorta & regaining of cardiac activity & contractility

11) Weaning off CPB

12) Decannulation & Protamine administration

13) Sternotomy / thoracotomy Closure

1) Incisions for OHS: (ref fig 3.1)

1) Median Sternotomy

2) Left posterior thoracotomy

3) Left anterior thoracotomy (left sub-mammary incision)

4) Right anterior thoracotomy (right sub-mammary incision)


Fig 3.1: Various incisions for CV operations

Operations that could be performed through the various incisions are:

1) Median Sternotomy: Any operation on the heart, pericardium, ascending aorta, arch of the aorta and

SVC can be performed through this incision. Importantly, any complication arising out of operation on

the heart can be managed. Arterial as well as venous cannulations can be performed through the same

incision and thus, a separate incision for cannulation is not required. Any complication arising out of

cannulation can be easily detected and rectified immediately.

2) Left Posterior Thoracotomy( Left Periscapular Incision): Operations on the distal aortic arch and

descending thoracic aorta are performed through this incision .Closed mitral valvotomy, pericardectomy ,

closure of PDA , repair of coarctation of aorta can also be performed through this incision.

3) Left Anterior Thoracotomy (Left Sub-mammary Incision): CABG to LAD, Diagonal system can be

performed. Closed mitral valvotomy and MPA banding can also be performed through this incision.

4) Right Anterior Thoracotomy (Right Sub-mammary Incision): Allows approach to RA and LA and

there by surgeries like ASD closure, TV surgery, Perimembranous VSD closure and MV surgeries can be

performed. CABG to RCA or PD can be performed. A separate incision for arterial cannulation may be

required


Fig 3.2: Transverse Section through thorax showing various approaches for CV

operations

Complications of Sternotomy: A) Accidental tear of the underlying structure is a dreaded complication of

median sternotomy (ref fig 3.3). The incidence is likely to happen,

a) in a redo cases where pericardium was not closed at the time of previous surgery. Following the first

operation, adhesions develop between sternum and the underlying structures.

b) if an underlying structure is dilated. Neck arteries or ascending aorta can be dilated due hypertension,

aneurysm or AR. While the venous side structures like left innominate vein, RA or RV is likely to be

damaged in patients with gross CCF or TV disease. In case of a tear, a hurried institution of CPB may be

required.


Fig 3.3: structures that can be damaged during median sternotomy

(Shown with a black line)

B) Opening of pleura: The inferior end of the right pleura can get opened if during sternotomy the lungs

are not properly deflated or remain inflated due to underlying lung disease. During bypass blood from the

pericardial well can seep into right pleural opening, resulting in a significant (3-4 liters) 4th space blood

loss. The heart being to the left of the midline left pleura is protected from accidental opening during

sternotomy. However, the left pleura can get opened during harvesting of pericardial patch, excising left

lobe of thymus, dissecting vertical vein in a case of TAPVC and harvesting of LIMA.

2) Pericardial Retraction: helps in a) lifting heart anteriorly to improve surgical visibility b) rotating the heart to

expose various parts of heart easily 3) create a pericardial well which helps in sump suction.


3) Placement of Purse-String Sutures: For preventing dislodgement, a cannula is placed through purse string

sutures. For aortic cannulation, two concentric purse string sutures are placed as on the ascending aorta

(ref fig 3.4)

Fig 3.4: Aortic purse string suture

Purse-strings are placed as distally as possible in cases where aortotomy is required (AVR, CABG). The

two ends of purse-string thread are passed through a hollow plastic tube called snugger or snare (ref. fig

3.5) with the help of a hook. This helps in tightening the purse-string around the cannula.

Fig 3.5: Snugger assembly

Purse-string for Venous Cannulation Sites: (ref fig 3.6)

a) SVC Purse-string: SVC Cannulation: straight or Pacifico cannula

b) RA appendage Purse-string:

i) SVC cannulation: straight or curved cannula

ii) IVC cannulation: straight cannula

iii) RA cannulation: straight cannula

iv) Two stage Cannulation: Cavo –Atrial cannula

c) IVC Purse-string: IVC Cannulation: straight or Pacifico cannula


Fig 3.6 : Venous purse string sites

4) Systemic Heparinisation: Adequate systemic hearinisation is essential prior to all further steps. At some

centers , a period of 3 minutes is allowed to elapse after heparin administration before cannulation is

begun; while at others, ACT of > 300seconds is necessary for cannulation.

5a) Aortic cannulation: Aortic or arterial cannulation is always performed first. This helps in managing blood

loss during cannulation and, in case of hypotension, allows commencement of CPB with a single venous

cannula or start a ‘suction bypass’.

Prior to cannulation, some surgeons loop aorta with a tape (called ‘go around’ or ‘taping’).Looping the

aorta helps in manipulation of aorta for purse string, cannulation and clamping. For looping the aorta,

dissection is carried on the left side of the aorta, in the areolar tissue between aorta and pulmonary artery,

and on the right side, between RPA and aorta (ref fig 3.7).

In cases with dilated aortae (systemic hypertension, poststenotic dilatation of AS, AR, aneurysm of

ascending aorta), tense MPA (due to PH) or with a previous surgery this looping could be difficult and

may result in injury to MPA, RPA or posterior surface of aorta.

The steps of aortic cannulation are,

a) both the cardiotomy suctions are put on

b) the aorta is incised within the purse-string and cannula is inserted

c) simultaneously, both the snuggers are tightened.

d) cannula & snuggers are tied together

e) aortic cannula is clamped and cap or a blocker over the connecting end of the cannula is removed

f) under controlled partial unclamping, surgeon checks the speed of at which blood gushes out

through the cannula. (to ensures that the tip of the cannula is in the lumen of the aorta.)

g) cannula is attached to the arterial line, without accidentally introducing any air bubble in the arterial

line.

h) cannula is fixed to the skin ( particularly if it is a straight tip cannula)*.


i) cannula and the arterial line are arranged in a smooth curve*.

Fig 3.7: looping of aorta prior to cannulation

Fig: 3.8: Direction of tip of the cannula

The tip of the cannula should be directed towards the arch of the aorta (indicated by the left shoulder of

the patient) and bevel directed inferiorly as to direct particulate emboli, if any, towards descending aorta.

Perfusionist should ensure that the cannula tip is in proper position at steps marked with asterisk (*), by

checking line resistance. During these steps cannula can dislodge.

Complications of aortic cannulation: a) dissection of aorta: (ref. fig. 3.9) likely with a thick atherosclerotic

aorta, short tip straight cannula and if a ‘blind’ or ‘close’ technique of cannulation is practiced. (In the

blind or close technique of aortic cannulation, the aorta is stabbed or scoured within the purse string and

the cannula is inserted without partially clamping the aorta)


b) selective cannulation of neck vessels : seen when aortic purse-string is too distal, with use of straight

cannula without a guard or a butt .

c) cannula tip abutting against posterior aortic wall: seen with small aorta ( ASD, VSD, tight MS) or due

to excessive insertion of a straight cannula.

d) breaking of purse-string suture.

Fig 3.9: Position of aortic cannula tip

Right Aortic Arch: In some congenital heart diseases like tetralogy of Fallot and truncus arteriosus, the

aorta arches over the right bronchus i.e. the transverse arch is directed towards the right. The descending

thoracic aorta crosses thoracic vertebrae at various levels to reach the diaphragmatic hiatus in the

diaphragm on left of spine.

(This is how a right aortic arch differs from aorta in situs inversus where the aorta passes through the

diaphragm on the right of spine.)

In right aortic arch or situs inversus, the tip of the arterial cannula should be directed to towards the

patient’s right shoulder

5b) Venous cannulation: SVC cannulation is always done first as this involves less retraction of heart and

hence, less chance of hypotension during cannulation. The sump suction is placed in the posterior

pericardial cavity and the stiff or metallic sucker is placed in the recess between SVC & the aorta.

Surgeon and the assistant hold corresponding sides of SVC or RA appendage, as the situation be, and

incision is placed within the purse-string suture to perform cannulation.


With the venous cannula appropriately placed, blood should rise in the cannula and the height of the

blood column should be equal to the central venous pressure. The blood column should move with

respiration. A continuously rising blood column indicates the cannula is fitting tightly into SVC or

wedging of the tip of the cannula into one of the tributaries. An absence of blood column in the cannula

indicates the tip of the cannula in periadventitial tissue.

Management of L SVC: The algorithm for managing LSVC is as follows

6) Commencement of CPB: When a perfusionist informs a surgeon ‘full bypass’, surgeon checks the following

a) RA should be totally empty with CVP < 0 mm of Hg

b) MPA should be soft

Causes of RA remaining full even on full CPB are

a) IVC cannula wedged in the hepatic veins

b) presence of L SVC

c) IVC cannula displaced in to RA/RV: seen in patients in gross CCF with dilated RA/IVC

If MPA is full, surgeon vents the left heart through an appropriate route. In a case with CHD, MPA is

tense on ‘full CPB’, then PDA should be suspected.

Left Innominate vein

(Bridging Innominate)

Lt Inno. Vein size >

LSVC

Lt Inno. Vein

absent or very small

Ligate or snug during

CPB

Manage by

sump suction

in the coronary

Manage by

Cannulation

Direct LSVC

Pacifico cannula

(on partial CPB)

Through RA – CS

straight cannula

(prior to CPB)

Through CS

straight cannula

( after opening RA

on cross clamp)


Cooling: Target temperature for cooling is according to the intra cardiac procedure time, if surgeon

intends circulatory arrest (in CHD or arch aneurysm cases) and quality of myocardial preservation

required.

During cardioplegic arrest myocardium gets continuously rewarmed due to left heart return and through

the surrounding viscera (aorta, lungs, liver) which are at a higher temperature. If the CPB perfusate

temperature is low, then this rewarming is slowed down.

Some surgeons don’t cross-clamp the aorta unless a certain temperature is reached (e.g. 320C).

During cooling the LV distends in patients with AR and TOF with aorto-pulmonary collaterals. Though

cooling reduces the heart rate, distension of LV, actually, increases the myocardial oxygen consumption.

Hence surgeon keeps a watch on LV distension, MPA fullness, PA diastolic pressure (on the monitor) &

broadening of QRS complex of ECG to avoid myocardial damage.

Cooling on CPB is delayed and patient is kept actively warm,

a) during release of intrapericardial adhesion on CPB

b) in patient with AR (cooling is started only when surgeon is ready to cross clamp)

c) till a patent BT shunt, PDA or MAPCA is ligated

7) Aortic cross clamp and delivery of cardioplegia: Aortic cross clamping is a crucial event and the following

check list is observed prior to cross clamping

a) availability of all the sutures, valves, patches and special instruments, if any.

b) no resistance on arterial line, i.e. acceptable line pressure

c) venous reservoir level is adequate, RA is empty and MPA is soft.

d) cardioplegia is ready to be delivered. This is particularly important in cases where early crossclamping

is required.

Indications for early cross clamping: Early cross clamping is required when severe LV distension is likely

to occur when cooling begins. This is seen in patients with

a) significant AR

b) cyanotic heart disease with large number of collaterals

c) Aorto Pulmonary Window

d) Truncus Arteriosus

Complications of aortic clamping:

a) incomplete clamping of aorta: occurs mainly in a tense and or dilated aorta. Making the aorta soft by

reducing the flows during cross clamping helps to prevent this complication. Failure to arrest the

heart completely or early recovery of heart from cardioplegia results due to this complication.

b) accidental clamping of tip of the aortic cannula: seen with straight tip cannula or if the cannula tip is

wrongly directed towards the aortic valve . The complication will result in a sudden increase

in arterial line pressure.

c) accidental clamping of cardioplegia cannula: will result in sudden increase in cardioplegia delivery

pressure

d) partial clamping of MPA: occurs when aorta is cross-clamped without adequate dissection between

aorta and pulmonary artery.(described under ‘go around’ of aorta p.25, fig 3.2 ). Due to partial

clamping of MPA, deairing (described later) becomes difficult.

e) injury to RPA: tip of the clamp can puncture the RPA, particularly in redo cases


Cardioplegia delivery: Cardioplegia is just one aspect of myocardial protection. The other important

aspects of myocardial protection are – prevention of LV distension at all times, and prevention of

rewarming of heart.

During delivery of antegrade root cardioplegia, surgeon checks the following

a) aortic root should be distended and should not be too tense( coronary block) or too soft( AR)

b) absence of LV distension

c) distended , turgid coronaries on the anterior surface of the heart( RV branches of RCA branches

and distal LAD are visible without dislocating the heart )

d) veins should be distended and their colour should change from, initial, dark blue to, later, bright

red as the delivery of cardioplegia progresses.

e) quick diastolic arrest of heart.

Management of antegrade root cardioplegia in patients with grade I to II AR: This grade of AR does not

require aortic valve replacement hence the aorta is not opened and cardioplegia is delivered through root

injection. But due to AR, the cardioplegia leaks into LV. Hence to avoid leak-back into LV as well as to

provide sufficient pressure-head for cardioplegia delivery, surgeon compresses the subaortic region

externally, during the delivery of the cardioplegia.

Cardioplegia by ostial route is delivered in all cases where aorta is opened. These cases are

a) aortic valve replacement or repair

b) Aorto Pulmonary window closure

c) Repair of rupture of the aneurysm of sinus of Valsalva

d) Ascending aortic aneurysm repair

e) Arterial switch operation ( for second cardioplegia, if required)

f) Repair of truncus arteriosus

Cardioplegia can be delivered through one ostium at a time or through the two ostia simultaneously with

the help two cannulae attached to a Y connection. A perfusionist has to adjust the delivery of cardioplegia

accordingly.

Cardioplegia is delivered retrogradely when,

a) antegrade delivery is not feasible due to coronary ostial block, coronary artery disease, difficult to

visualise coronary ostium ( e.g. redo AVR)

b) surgeon does not want interruptions during a prolonged surgery

Insertion of retrograde coronary perfusion (RCP) cannula: This can be performed prior to starting the

CPB or on CPB.A purse string is placed on RA anterior and inferior to RA appendage purse-string.

Guided by the left index finger, which is placed on the coronary sinus, the RCP cannula is introduced and

placed in the coronary sinus. Retraction of heart during the placement of RCP cannula may result in

hypotension; hence, some surgeons place the cannula on CPB. While inserting the cannula on CPB, RA

should be kept slightly full as to avoid air locking of the venous cannula (when inserting RCP cannula)

and also, to keep the mouth of coronary sinus open. Keeping RA full results in distension of heart. Hence,

RCP cannula should be inserted before commencing cooling.

During retrograde cardioplegia delivery, the coronary veins are tense and red in colour and the blood

coming retrogradely through the coronary arteries or ostia is dark in colour. The Middle cardiac vein (the

vein accompanying PD) should be turgid during delivery of retrograde cardioplegia. The middle cardiac


vein opens just distal to coronary sinus and its ostium can get blocked easily by the balloon of a

malplaced RCP cannula.

Cardioplegia is repeated every 30 to 40 minutes, according to expected cross-clamp time and some times,

during AVR, prior to lowering of valve. After lowering of valve visualisation of ostia could be difficult.

While repeating cardioplegia

a) surgeon discards the initial 30-50 ml of cardioplegia which has warmed-up in the tubing

b) vents out air from the aortic root( air enters aortic root through cardiotomy)

c) prevents air embolism to RCA by initially clamping the RCA

d) loosens the IVC loop if RA is likely to distend

8) Cardiotomy: to minimise the interference with the pumping function of the heart, cardiotomies are

a) as small as possible

b) avoid opening of ventricles ( pumping chambers)

c) avoid damaging coronaries or conduction system

9) Deairing of the heart: After completing intra cardiac procedure, all the cardiotomies are closed and the heart

is deaired. The technique of deairing the heart varies from surgeon to surgeon but all the techniques are

based on the principle of,

a) passive filling followed by active filling of heart b) filling the chambers in a serial manner.

These principles are achieved by,

i) just prior to closing cardiotomy, surgeon stops all the intra cardiac vents except aortic root vent

( passive filling)

ii) perfusionist by partially clamping the venous line fills the right side of the heart ( passive filling)

iii) surgeon gently presses the RV as to push the blood across pulmonary circulation to the left side

(active filling)

iv) anesthetist start ventilating ( active filling).Distended alveoli compress the pulmonary capillaries

and squeeze the air to PV-LA

v) surgeon deairs LA through cardiotomy / vent purse string ( active filling)

vi) surgeon massages LV and deairs the heart through aortic root. Remember, aortic root is the

highest and the last chamber prior to cross clamp. (active filling).

Once the surgeon is satisfied about deairing of heart, aorta is declamped.

Variations of the above steps of deairing are: a) aortic root may be deaired without attaching suction to

the root cannula. Blood squeezed out of heart is allowed to pass freely into the pericardial well.

(perfusionist should increase cardiotomy sump suction).

b) following MVR , a balloon catheter may be passed across the MV into LV and catheter connected to a

suction for air removal. LV is not massaged (for the fear of LV rupture) in this technique.

c) root suction continued for a long time after declamping. Some partially clamp the aorta, just distal to

the root suction to provide resistance to the LV ejection and ensure a better air removal.

d) head is lowered during air removal so that air , if any, on ventricular ejection would enter descending

aorta. Head low position, falsely, increases CVP and decreases venous return.

10) Declamping: After complete deairing, aorta is declamped. During aortic clamping, the aortic root is empty

and the aortic cusps could be in an open position. Hence, it is possible that at the time of declamping a

sudden gush blood coming from aortic cannula can distend the LV. Hence, at the time of declamping,

perfusionist lowers the arterial flow, allowing the root to distend & enable the cusps to coapt.


After declamping, myocardium gets perfused by warm, low potassium blood which washes away the

cardioplegia. Depending upon the time since the last cardioplegia, quality of myocardial protection and

serum potassium levels, the myocardium recovers and starts beating. The initial contractions are not

powerful. Also, the rhythm may not be sinus. Hence it is essential to keep the heart, in general, and, LV in

particular, empty. To keep the heart empty, left heart vents may be started or LA may be openly vented by

keeping LA purse-string or the last stitches of left atriotomy loose. When the later technique is used blood

pools up in the pericardial cavity and may seep into pleural cavity, if pleura is open. It is important to note

that aortic root suction can never empty a heart.

When ever a < grade II AR is left alone, after declamping , surgeon checks for LV distension and if

required, massages the LV till myocardial contractility is regained. LV may be vented by a LV apical

vent.

11) Weaning off CPB: After declamping aorta, heart regains activity and contractility. With adequate

contractility, if patient has bicaval cannulation, surgeon may decide to remove one of the venous

cannulae. This increases venous filling of the heart and thereby helps in providing pulsatile flow. Usually,

SVC cannula (the smaller of the two venous cannulae) is removed first. SVC cannula is clamped

appropriately, prior to removal.

Perfusionist now increasingly fills the heart, guided by the CVP and PA diastolic pressures. While

weaning off CPB, surgeon keeps a close watch on cardiac contractility, RA and PA filling and on PA

diastolic pressure, if available. While filling the heart, a rise in blood pressure with little or no rise in CVP

indicates an excellent contractility of heart.

The usual prerequisites for going off CPB are,

a) rectal temperature > 350C or nasopharyngeal temperature >37.5

0C

b) sinus rhythm is most preferred. If patient is in nodal rhythm the rate should be > 100/ min. Patients

with chronic AF rarely get converted to sinus rhythm, however, the ventricular rate should be more >

100/min. Temporary external pacing may be required for heart blocks. ST segments on ECG should be as

far as possible, isoelectric.

c) cardiac contractility: If myocardium has recovered from anoxia, it should be red in colour . The heart

should start ejecting on providing slight volume load i.e., the monitor will show a pulse wave form and

systolic blood pressure will rise with minimal or no rise in the CVP.

d) anesthesiologists should be able to ventilate both the lungs, easily . Collected secretions due to

unventilated lungs, endotracheal tube displaced while turning the table to improve surgical visibility,

collected blood or trapped air in the pleural cavity prevent normal expansion of the lungs.

e) if blood products are likely to be required, they should be available readily .

f) serum potassium levels, pH of blood ( ‘blood chemistry’) should be normal

With heart full and beating vigorously, bleeding from cardiotomy sites is checked.

12) Decannulation & Protamine Administration: Once hemodynamic stability is established after going off

CPB, venous cannula is removed. In case of bicaval cannulation if SVC cannula was removed earlier,

IVC cannula is removed after going off CPB.

Through aortic cannula, the residual blood in the venous reservoir is returned back, depending upon the

CVP and or the PA diastolic pressures. Anesthesiologist at this stage may increase the dose of

vasodilators as to increase the venous capacitance. A five to ten degree head high position also helps in

accommodating volume. A rough guide to amount of volume to be returned is to keep CVP, atleast, at the

preop value.


Heparin is reversed with protamine injection. Heparin-Protamine complex produces hypotension &

vasodilatation, called protamine shock, through various mechanisms. This occurs, usually, within

5minutes of starting protamine administration. One of the methods of managing this hypotension is to

infuse patient quickly. Hence many surgeons don’t decannulate aorta till the possibility of protamine

shock is over. To avoid clot formation around the tip of the aortic cannula after protamine administration,

blood returning through cannula should not be stopped completely.

Check list prior to starting protamine administration is:

1) no significant ( requiring suturing, heart retraction) cardiotomy site bleeding

2) hemodynamic stability

3) ability to fill up the heart quickly, if required

4) cardiotomy suckers are put-off ( some put it off after delivering 50% dose of protamine)

5) drugs to treat protamine shock are available.

Aortic decannulation is the last step of CPB. Prerequisites for aortic decannulation are

1) surgeon is satisfied with the operative correction.

2) there is no need to go back on CPB for achieving hemodynamic stability

3) no surgical cause of bleeding, requiring CPB to control it

4) all the blood from the venous reservoir is returned back

For decannulation, all ties around the cannula are cut, snuggers are loosened, and while surgeon removes

the cannula, an assistant simultaneously tightens the snuggers. Keeping the purse string-suture strands

tight, the plastic snuggers are discarded and the purse-strings are tied.

Complication of decannulation: Bleeding can occur from the cannulation site due to break of the purse

string suture, cut-through of the purse-string or loose tying. Bleeding could be very severe and may

require re-cannulation through a separate site.

Pericardial Closure: After confirming hemostasis, pericardium is closed. The closure starts over the aorta

and proceeds inferiorly for varying lengths.

Drains are placed to drain out the collected blood. When pleura is not opened, two drains are placed - one

behind the sternum (retrosternal) and the other, inside the pericardium behind the LV (retrocardiac). If

pleura is opened, it may be drained separately.

Pericardial closure can lead to tamponading effect on the heart, resulting in hypotension. This occurs in

cases where the heart is already distended or has an external conduit. In such situations, keeping the

pericardium open corrects the hemodynamics.

Pericardium is not closed whenever pericardium is used as a patch, e.g. RVOT patching of TOF.

13) Sternal closure: Thoracic integrity is established by approximating the two halves of the sternum. This is

done by passing multiple wires or bands around or through sternum.

Sometimes, sternal closure can give rise to hypotension. This happens especially when an external

conduit is used or heart is distended. In such situation sternum is not approximated and skin also, may not

be closed. The wound is covered with antiseptic dressing (‘delayed sternal closure’)


4. Mitral Stenosis

Etiology: Rheumatic.

Congenital (This is a rare cause and is associated with hypoplastic LV, aorta, etc)

Pathology:

1. Fusion of AML and PML begins at commissures, near the annulus and extends to wards the center

of the orifice. The mitral valve area (MVA) becomes progressively narrowed.

Figure 4.1 Mitral Valve

A: Normal MV in close position B: Normal MV in open position

C: Stenotic MV in open position: 1.MV Orifice 2. Fused commissures

Severity of MS is classified according to the MVA.

Clinically undetectable MS: MVA > 2.5 cm2

Mild MS: MVA 1.5 cm2 to 2.5cm

2

Moderate MS: MVA 1.0 cm to 1.5 cm2

Severe MS: MVA < 1.0cm2

Critical MS: MVA ≤ 0.7 cm2

Cases coming up for surgical or interventional treatment of MS are with severe or critical MS.

2. Annulus, cusps thicken and may get calcified. Chordae thicken & fuse with each other.

Papillary muscles too fuse.

3. Clot forms in the LA, usually, with the advent of atrial fibrillation.

Pathophysiology: Stenotic MV obstructs the flow of blood from LA to LV resulting in

a) Back Pressure Effect

b) Decreased Forward Flow

a) Back Pressure Effect: The chain of events is

Stenotic MV → incomplete emptying of LA→ LAVO→ LA enlargement till limit of compliance

of LA is reached → ↑LA pressure → ↑ PV pressure → ↑ pulmonary capillary pressure → ↑ PA

pressure → ↑ RV pressure → RV failure→ ↑ RVEDP→ ↑ RA pressure → ↑ SVC & IVC

pressure.

Back pressure effect results in accumulation of blood in the pulmonary circulation, RA, SVC/IVC

and liver (in that order). Liver congestion is called ‘chronic passive congestion’.

Back pressure effect is responsible for clinical features of dyspnoea, edema feet & ascitis.

Development of atrial fibrillation worsens the back pressure effect as LA emptying is incomplete.


b) Decreased Forward Flow: Flow (F) through any orifice is proportional to square of area (A) of

the orifice (F∝ A2). Rheumatic mitral stenosis is a progressive disease. As the MV orifice area

decreases, the flow throw MV progressively reduces.

Blood flows through MV during diastole. As the flow of blood through the stenotic MV decreases

significantly, duration of diastole becomes relatively short to fill the LV adequately. Reduced LV

filling leads to reduced forward flow, i.e. reduced cardiac output (CO). Initially, the

manifestations of reduced cardiac output are after exertion but later, manifestations are even at

rest.

Body Compensation:

a) ↑↑↑↑SVR: Pressure = CO x SVR, hence as the CO reduces, the SVR increases to maintain

systemic pressure. Atrial systole is responsible for approximately 25% of ventricular filling.

With the development of AF, atrial systole is lost and the ventricular filling is further

compromised.

b) Slowing of HR: Slowing of heart rate prolongs the duration of cardiac cycle and thereby

increases duration of diastole. This improves the ventricular filling as longer period for

ventricular filling is now available.

Treatment:

Medical: is indicated when the mitral stenosis is mild and when there are no complications.

Medical treatment is mainly directed at

a) slowing the heart rate and there by improving the ventricular filling, forward flow & CO

b) reducing the venous congestion by diuresis .

c) prevent repeated attacks of rheumatic fever.

Drugs used are

1) Digoxin: to control heart rate, particularly if the patient is in AF. Improves RV

contractility if the patient is in CCF

2) β Blockers: (the main stay of current treatment) to reduce heart rate.

3) Diuretics: to reduce congestion.

4) Injection Benzathine penicillin G: this is a long acting Penicillin for preventing

recurrence of Rheumatic fever. It has no effects on hemodynamics.

Balloon Mitral Valvotomy (BMV): Performed when a) the cusps are pliant b) there are no LA

clot c) there is no MR. This is an interventional procedure performed in the cardiac

catheterisation laboratory under local anesthesia.


Fig: 4.2: Technique of BMV

Complications: 1. Iatrogenic MR: occurs due to tear of the cusp or chorda during dilatation.

Patient requires emergency surgery if MR causes hemodynamic disturbance. Approach is

through median sternotomy with conventional CPB. As the approach to MV for BMV is trans-

septal, an ASD (septal perforation) would exist and hence, SVC and IVC should be tape –

snugged, to avoid venous airlock on opening the LA.

2. Perforation of cardiac chamber producing cardiac tamponade. Managing this complication

rarely requires CPB.

Close Mitral Valvotomy (CMV):

Fig4.3: Technique of CMV


CMV is performed when the cusps are pliant, and there is no LA clot or MR. CMV is

performed under GA without CPB, through left anterolateral thoracotomy incision. A

Tubb’s dilator is passed through LV apex and index finger is passed through LA

appendage. With the help of the index finger, the Tubb’s dilator is guided across the MV.

Dilator is opened once the tip of the Tubb’s dilator is across the mitral valve. (ref fig. 4.3)

Complications of CMV

1. Iatrogenic MR: Significant MR requires surgical correction.

2. LV apical or LA appendage tear.

3. Accidentally finding LA clot

Emergency surgery can be performed through left chest or through median sternotomy,

depending upon patient condition and surgeon’s choice.

For CPB through left chest, arterial return is by left femoral arterial cannulation and

venous drainage is through MPA or RVOT cannulation. If RA is dilated, RA can be

reached even through left chest also. (ref fig 4.4)

Fig. 4.4: View of the heart chambers through left chest after opening the

pericardium

Open Mitral Valvotomy: Performed through median sternotomy but can be performed through right

thoracotomy. The mitral valve is approached through a longitudinal paraseptal incision on the LA

body (ref. fig 4.5).


Fig.4.5 Incision for Open MV surgery

Other approaches to MV are shown below in fig 4.6

Fig.4.6 Approaches to MV

(FO= fossa ovalis)


Opening of LA and sucking of blood through cardiotomy suction yields a significant amount of blood

stagnant in LA and pulmonary circulation.

If LA Clot is present, declotting of LA is done first. Declotting involves washing of LA with saline

hence; cardiotomy sump suction should be stopped during the use of washing of LA.

Mitral valve is opened surgically using knife and scissors. Valve is tested for competence using

saline. Perfusionist should observe the same precautions as observed while washing of LA.

Complications & Accidents: 1. Accidental opening of RA: this occurs during atriotomy and results in

venous air lock and a sudden decrease in venous reservoir level. This is treated by temporarily closing

the rent in the RA with a side biting clamp (like a Cooley clamp), looping & snugging SVC- IVC &

then, suturing the rent in the RA

2. Breaking of LA suture while tying knot: this results in unknotting and opening of the left

atriotomy. This complication achieves a serious proportion if a surgeon ties the LA suture only when

the heart has regained its activity. Due to breakage of suture before knotting, the LA suture line

unwinds, and the atriotomy opens up. Opening up of left atriotomy suture line on a beating heart

results in sucking in of air into LA. If the heart has already started ejecting, patient can suffer from

systemic air embolism.

Perfusionist helps treating the problem by filling the heart (to make LA pressure positive) and by

keeping the aortic pressure high (as to prevent opening of aortic valve). Anesthesiologist helps by

keeping the lungs in a semi inflated state, which also makes the LA pressure positive. Depending

upon the extent of opening up of LA suture line, surgeon resutures the LA on a beating or on a cross

clamped heart or cardioplegically arrested heart.

3. Iatrogenic MR: is treated surgically if it is severe and is producing hemodynamic compromise

Mitral Valve Replacement: Performed if the mitral leaflets are severely calcified or if open valvotomy is

not satisfactory due to severe subvalvar fusion or indistinct commissures.

Approach, precautions & accidents are as mentioned for OMV.

MVR is performed with or without excising the AML and PML. If a leaflet is excised, it is excised

with its chordae and papillary muscles.

Complications and Accidents: 1. Accidental opening of RA: (see above, in OMV)

2. Breaking of LA suture: (see above, in OMV)

3. LV rupture: This is an early and dreaded complication of MVR. The rupture can occur at any level

from the level of mitral annulus to the base of papillary muscle. The repair of rupture requires a quick

resumption of CPB. LV rupture results in a significant blood loss. Perfusionists should assess patient

blood volume & hemoglobin, a fresh, and plan priming accordingly.

4. Stuck Valve: A mechanical valve leaflet/s can get stuck in an open or closed position. This is

usually due to subvalvar structures affecting the hinge mechanism of a valve. Management of this

complication requires early reinstitution of CPB.

5. Cardiogenic shock due to injury to Left Circumflex Artery will require emergency coronary

bypass.


Clinical assessment chart for MS

Parameter Findings comment

Age Around 30yrs

Body weight

&

Height

Low weight and height

Body Volume First pulmonary circuit volume increases then

the systemic venous circuit volume

PH status

CVP, liver enlargement, effusions

Hemoglobin Low nails, blood investigation

Plasma Volume Increased , but protein concentration is low as in body volume

LFT report

SVR Increased high diastolic BP, cold limbs, lower

limb veins are constricted,

Organ Function Liver: chronic passive congestion

Brain : infarction in patients with embolic

episodes

LFT: raised bilirubin and SGPT

Transient ischemic episodes,

hemiplegia

Arterial Tree Embolus can block any artery Pulse is not palpable

Check vascular Doppler studies Arterial

cannulation

Aorta

Femoral : for reopen heart cases

Venous

cannulation

Bicaval but tapes are not required unless

1)trans septal approach

2)previous BMV

3)TV surgery

Cardioplegia Antegrade through root

For associated grade I / II AR,

root compression will be required

Check 2DE report for grade of AR

Arterial Pressure Could be high ( > 60) on bypass Expect in patients with high SVR

Venous return Good if CVP raised, liver palpable

Left Heart

Return

Sump-sucker in LA

Preop

medications

Digoxin, diuretics

Beta blockers Check for potassium levels

Previous

interventions

CMV

BMV

OMV

MVR

Left thoracotomy scar

Median sternotomy scar



5.Mitral Regurgitation

The term incompetence and regurgitation are interchangeably used. When regurgitation of blood is

present, a valve is considered incompetent.

Classification of MR: There are different ways of classifying MR.

Etiological Classification: A disease can affect, simultaneously, different anatomical components of MV

Rheumatic

Infective endocarditis

Endomyocardial Fibrosis

Marfan’s syndrome

Secondary to LV dilatation

Myocardial infarction

Post procedural or post operative

Anatomical Classification: A change in configuration of any component of mitral valve apparatus will

result in MR . A component of MV apparatus can be affected by a number of etiologies.

Annulus: dilatation

Cusps: shrunken, destroyed, torn

Chordae: ruptured, shortened, lengthened (ref fig 5.1, 5.2 & 5.3)

Papillary Muscle: dysfunction, ruptured

LV: aneurysm resulting in relocation of the papillary muscle

Classification according to compensation:

Acute: where body compensation for MR is absent as in myocardial infarction

Chronic: where body has compensated for MR as in rheumatic heart disease

Pathology & Pathophysiology: In MR, LV has two outlets- aortic valve & incompetent mitral valve (fig 5.2).

Blood flows in inverse proportion to the resistance offered at each outlet.

The resistance at the aortic outlet is the resistance offered by the aortic valve plus the systemic vascular

resistance (SVR). Normal aortic valve offers no resistance to the flow but presence of aortic stenosis

increases the resistance. The resistance at the mitral valve depends upon the size of regurgitant area and

LA compliance (dilated thin walled LA is well compliant, while thick walled small LA is poorly

compliant).

The final hemodynamic problems produced by MR are similar to those produced due to MS, i.e. back

pressure effect and decreased forward flow

Figure 5.1: Competent MV Figure 5.2: Incompetence due to chordal shortening


Figure 5.3: Chordal lengthening and MV prolapse

a) Back Pressure Effect: LA is subjected to high pressure, for a brief period, during LV systole. Also,

the LA gets volume overloaded (LAVO) as it receives pulmonary venous blood as well as the

regurgitant blood from LV.

The LA is much thinner , as a result, more compliant in chronic MR than it is in MS, and hence, the

back pressure effects are delayed. In a chronic severe MR, LA size could be 7 to 8 cm when measured

on 2D-Echocardiogram.

b) Decreased Forward Flow: Depending upon the resistance at the two outlets of the LV, the blood

flows forward into systemic circulation.

Body Compensation:

a) ↓↓↓↓SVR: In order to increase forward flow the SVR falls. Also, patient could be on drugs like, ACE

inhibitors, which reduce SVR.

b) LV function compensation: LAVO produced due to MR is passed on to LV results in LVVO. As

per Frank – Starling law, the increased in the myocardial fiber length results in better contractility and

the LV is able to handle the LVVO by pumping out the extra blood. In a compensated case the LV is

able to maintain adequate forward flow. When LVVO results in myocardial stretching beyond

physiological limits, the LV function deteriorates and the patient decompensates.

Fig 5.4: Relation between LVEF & severity of MR

Treatment:

Medical: is indicated so far as the LV function is maintained and the PH has not developed.


Medical treatment is mainly directed at a) improving forward flow by reducing SVR and b) reducing

the venous congestion by diuresis.

Drugs used are

1) Digoxin: to control heart rate, particularly if the patient is in CCF or AF

2) After Load reducing agents: ACE inhibitors and Angiotensin receptor blockers are the main stay

of current treatment.

3) Diuretics: to reduce pulmonary congestion

4) Injection Benzathine penicillin G: this long acting Penicillin is for preventing repeat attacks of

rheumatic fever

Surgical: A) Mitral Valve Repair: is the first treatment of choice. Repair is feasible if the AML is intact and is

mobile. Repair is performed according to the anatomical problem, as shown

MV component Pathology Surgery

Annulus: dilated Annuloplasty

Cusp: short Advancement

Chordae: short Lengthening

long Shortening

Pap Muscle: ischemic Revascularisation

The approach to mitral valve is as described for OMV. Due to associated LAVO and LVVO, opening

of LA yields large amount blood in the cardiotomy suction. Due to washing effect of MR jet, blood is

not stagnant in LA and hence LA clots are rare.

B) Mitral Valve Replacement: is performed when patient has severe MR and the valve is

irreparable.

MVR with leaflet preservation: MVR when performed without preservation of the leaflet results in

deterioration of LV function. Hence MVR is performed by preserving AML& PML or with atleast,

preserving PML. (‘preserving PML’ means preserving the annulus-PML-chordae-papillarymuscle-

LV link)

Clinical assessment chart for MR


Age Around 30yrs

Body weight

&

Height

low weight and height

Body

Volume

Volume of blood in the pulmonary circuit

increases initially, followed by a rise in

volume of blood in the systemic venous

circuit

PH status, LA size, LV size



Plasma

Volume

increased , but protein concentration is low as in body volume

LFT report

SVR Low : chronic, compensated cases

High: acute , uncompensated cases

Low diastolic BP, wide pulse pressure,

bounding pulse,

High diastolic pressure, narrow pulse

pressure, cold limbs, collapsed

peripheral veins



Brain : infarction in patients with embolic

episodes



hemiplegia

Arterial Tree Embolus can block any artery Pulse is not palpable

Check vascular Doppler studies

Arterial

cannulation

Aorta:

Femoral : for reopen heart cases

small sized aorta

Venous

cannulation

Bicaval but tapes are not required unless

1)trans septal approach

2)previous BMV

3)TV surgery


For associated grade I / II AR,

root compression will be required


Arterial Pressure Could be low ( <30) on bypass in chronic

cases

seen in patients with long acting

ACE inhibitors


Left Heart Return Sump-sucker in LA

Preop medications Digoxin, diuretics

ACE inhibitors, AR inhibitors

Check for potassium levels

Previous

interventions

CMV

BMV

OMV

MVR

Left thoracotomy scar




6.Aortic Stenosis

Etiology: Congenital: subvalvar / valvar / supra valvar

Acquired: Rheumatic Heart Disease

Degenerative

Pathology: Various configurations of aortic stenosis are shown in figure 6.1. All acquired AS are valvar but, a

valvar AS could be congenital or acquired. Narrowing at annular level (annular stenosis) could always be

a co-existing pathology.

Fig. 6.1: Types of aortic stenosis


Fig.6.2: Opening of normal and stenotic aortic valve

Pathophysiology: In AS the aortic valve area gets reduced to les than 1cm

2. Narrow orifice produces

resistance to ventricular emptying during systole. The LV now has to generate far greater pressure to

pump blood into aorta (pressure overload). This produces LV concentric hypertrophy as this hypertrophy

is towards cavity of the LV, making the LV cavity small.

Fig. 6.3: LV hypertrophy in AS


The heart is small in size and dilates only in the last stage. Cardiac Output is maintained in the

compensated phase. The LV is muscle bound, hence, is poorly compliant. A slight volume overload gives

rise to rise in LVEDP. Till the mitral valve is competent, back pressure effects producing pulmonary

congestion are absent.

Body Compensation: Slowing of HR: due to AS, LV requires a longer time to eject blood through the aortic valve. Hence

slower heart rate helps in ejection. Drugs which slow down the heart rate help in compensation.

↑↑↑↑SVR: to maintain blood pressure, the SVR rises to compensate for the decreased cardiac output

Myocardial Perfusion: is critical in patients with aortic stenosis.

Myocardial Perfusion Pressure = Coronary Artery Pressure – Intramyocardial Pressure

In aortic stenosis due to myocardial hypertrophy intramyocardial pressure is high. Hence a higher aortic

pressure (i.e. coronary artery pressure) will be required to maintain myocardial perfusion during off cross

clamp period or while delivering cardioplegia.

Treatment: (of congenital AS will be described along with treatment for other congenital heart diseases)

Medical: has limited value in patient with aortic stenosis. Drugs which slowdown the heart rate without

affecting myocardial contractility are useful. After load reducing drugs should not be used. Diuretics are

required when patient is in CCF.

Balloon Aortic Valvotomy: This interventional procedure is performed in cardiac catheterization

laboratory. It is performed mainly in pediatric age group when the leaflets are pliant and there is no AR.

The access is retrograde through femoral artery – aorta -- aortic valve.

Complication: 1. Iatrogenic AR: managed surgically if hemodynamically significant.

Surgery: A) Open Aortic Valvotomy: Prior to the balloon intervention era, this was the treatment of choice in a

patient with severe AS. The aortic valve was opened under vision using conventional CPB in a

cardioplegically arrested heart. The approach was through aorta.

B) Aortic Valve Replacement: is performed when the cusps are rigid, calcified and or there is an

associated AR. The aortic valve is approached through an oblique, J shaped incision on the ascending

aorta.

Fig.6.4: Aortotomy for Aortic Valve Replacement


Cardioplegia is delivered through coronary ostia. In the absence of AR, some surgeons deliver the first

cardioplegia through root injection. Retrograde cardioplegia is also used.

Aortic cusps are excised and an artificial valve is implanted.

C) Aortic Root Widening: In aortic stenosis the annulus does not dilate. Such an annulus would

accommodate a valve which is small as compared to the BSA of the patient. To accommodate an

appropriate sized valve (Effective Orifice Area of the valve, preferably = 1.3 x BSA), the undilated

annulus is widened by cutting across the annulus and inserting a patch. Valve replacement is then

performed in the widened annulus.

There are a number of operations / techniques to widen the narrow aortic root.

Fig 6.5: Sites for aortic root widening (marked with black circles) (For legends ref to fig 4.8)

D) Percutaneous AVR: This an emerging technique in which a valve mounted on a catheter is deployed

across the aortic valve, through a percutaneous approach. Obviously, no incision or CPB is required.

Complications and Accidents: 1.Bleeding from aortic suture line: this complication is seen when aortic

wall is thin. The seriousness of complication is sometimes appreciated after coming off bypass when the

aortic pressure rises. If a ‘cut-through’ or a ‘dog ear’ is noted as a cause of bleeding then a surgeon may

go on bypass and take an additional stitch under low flows ( required for short period of less than 15

seconds) as to soften aorta.

2. Stuck Valve: A mechanical valve leaflet/s can get stuck, immediately following implantation, in an

open or closed position. This is usually due to subannular calcium or hypertrophied IVS preventing

adequate disc movements. Management of this complication requires early reinstitution of CPB.

3. Cardiogenic shock: Post-operative cardiogenic shock results from depressed myocardial contractility.

The cause of cardiogenic shock specific to AVR with mechanical valve is of prosthesis occluding a

coronary ostium, resulting in acute ischemia. The complication is managed with reinsertion of prosthesis

or with bypass grafting.


Clinical assessment chart for AS

Parameter Findings Method of assessment/ comments

Age Around 30yrs if RHD

> 50yrs if of degenerative etiology

Body weight

&

Height

low weight and height for RHD

Normally built for degenerative etiology

Body Volume Normal. CCF only in terminal cases

Hemoglobin Normal

Plasma Volume Normal

SVR Normal to increased high diastolic BP, cold limbs, lower

limb veins are constricted,

Organ Function Brain : infarction in patients with embolic

episodes

Liver : chronic passive congestion


hemiplegia


Arterial Tree Atherosclerotic changes may be present in

patients with degenerative etiology who

present late

Check vessels patency clinically and

with vascular Doppler studies

Arterial

cannulation

Aorta

Venous

cannulation

Single venous, two stage

Cardioplegia

1) all ostial

2) first through root, subsequent ostial

3) retrograde for maintenance


Arterial Pressure Should be high ( > 60)

Venous return Normal to Low

Left Heart

Return

Through RSPV vent passed to LA// LV

Preop

medications

Digoxin, diuretics

Beta blockers


Previous

interventions

BAV


7. Aortic Regurgitation

Etiology: Rheumatic Heart Disease

Syphilitic Heart Disease

Marfan’s Syndrome

Ventricular Septal Defect

Infective Endocarditis (Gives rise to acute AR)

Dissection of aorta (Gives rise to acute AR)

Pathology: Aortic regurgitation is due incomplete coaptation of leaflets. The incomplete coaptation may be due

to dilated annulus (with normal leaflets) or due to defective leaflets failing to coapt. The leaflets could fail

to coapt due to thickening and shrinkage (RHD), destruction (IE), prolapse & deformity (VSD), detached

attachment (dissection). Due to large volume of blood passing through the aorta, the aortic annulus is

dilated.

Pathophysiology: Blood ejected by the LV (called stroke volume –SV) into aorta during systole has, as if, two

outlets.

Fig 7.1: Pathophysiology of AR

One is the forward flow, i.e. towards the body, and this flow is controlled by the SVR; and the other, is

the regurgitant flow and is controlled by the compliance of the LV (LVEDP) and duration of diastole.

Lower SVR helps in improving forward flow while a lower LVEDP & a longer diastole increases the

regurgitant flow. Thus, out of each LV stroke volume a part (a major part in the compensated stage)

moves forward and a (minor) part regurgitates back into LV (ref fig 7.1)

The regurgitant flow adds up to the volume of blood the LV receives from LA through MV, resulting in

LVVO. The compliant LV dilates to accommodate the LVVO. As per Frank – Starling law, the LV

ejection is also increased till a physiological limit of LV fiber stretching is reached. At this stage the

LVEF starts decreasing (ref fig 5.4). The failing LV dilates, which dilates the MV annulus also. Due to

dilated annulus the mitral leaflets don’t coapt. This type of MR where only the annulus is dilated and the

leaflets are normal, is called functional MR.


The problems are summarised as

a) Decreased Forward Flow: This occurs only in the late stage of chronic compensated

AR. Due LVVO, the LV is ejecting more and the cardiac output (CO) is adequate for the patient’s

activities so far as LVEF is normal

b) Back Pressure Effects: Mitral valve remains competent till late. This prevents any back pressure

effects But when the ejection fraction starts falling, LVEDP increases, LV dilates and patient develops

functional MR ( due to dilated MV annulus) and pulmonary congestion.

Body Compensation: (is absent in patients with acute AR)

↓↓↓↓SVR: helps in forward flow

Increase LVEF: helps in handling the LVVO and in maintaining adequate forward flow inspite of

regurgitation.

Tachycardia: as aortic regurgitation occurs during diastole, slowing of heart rate increases the diastolic

period and hence, the total regurgitant volume.

Treatment: Medical: With preserved LV function patients are treated with after load reducing drugs.

Diuretics are required only when the LVEF fails.

Surgical: A) Aortic valve repair: Usually performed in children with VSD and when the AR is less than severe.

Details of perfusion are as described for aortic valve replacement.

B) Aortic Valve Replacement: is performed for severe AR with deteriorating LV function.

The aortic valve is approached through an oblique, J shaped incision on the ascending aorta (ref fig 6.4)

Cardioplegia is delivered through coronary ostia. If retrograde cardioplegia is used, usually it is for

maintenance of arrest.

Aortic cusps are excised and an artificial valve is implanted by suturing the artificial valve to the aortic

annulus.

C) Aortic root Replacement (Bental’s Procedure): In patients with syphilis or in patients with Marfan’s

syndrome, the root is aneurysmal with gross AR. The root is replaced with a valved conduit with

implantation of the coronary buttons & replacement of the ascending aorta. Root can be replaced by

retaining the patient’s valve (valve saving operation)

Fig. 7.2: Diagrammatic presentation of Bental’s operation


The procedure is also required in patients with aortic dissection.

D) Ross Operation: This is Aortic valve replacement with autologous pulmonary artery and replacing

the pulmonary valve with a homograft (aorta or pulmonary artery).

This operation is performed for AS as well as for AR.

Fig. 7.3: Ross operation

Complications and Accidents: a) VF prior to aortic cross clamping:

Patients who have severely depressed LV function or dilated LV, when are connected to CPB, due to low

perfusate temperature or ‘faster’ cooling develop bradycardia leading to severe LV distension and VF.

The arterial return from the aortic cannula keeps flowing freely into LV and distends the LV. Hence, in

patients with severe AR, cardioplegia should be ready before instituting CPB; left heart vent should be

inserted before connecting to CPB & cooling should be done gradually. Surgeon should be ready for

massaging LV and early crossclamping.

b) bleeding from aortic suture line: seen in patients with a thin aortic wall. Reinstitution of CPB may be

required so as to control bleeding from a difficult spot (usually the inferior end of the incision)

c) Prosthetic valve complications: as mentioned before


Clinical assessment chart for AR

Parameter Findings comments

Age Around 30yrs if etiology is

RHD, Marfan’s Syndrome or syphilis

> 50yrs if AR is due to dissection

Body weight

&

Height

Well built.

Marfan Syndrome patients are tall but slim

External and bony features of

Marfan’s syndrome

Body Volume Normal . CCF only in terminal cases

Hemoglobin Normal


SVR Decreased

Increased ( acute AR)

High volume brisk pulse, low (

zero) diastolic BP,

easily visible carotid, brachial and

radial pulses

cold limbs, absent pedal pulses

Organ Function Preserved in compensated cases

Arterial Tree Normal

Arterial

cannulation

Aorta

Femoral : for dissection extending into arch

Venous

cannulation

Single venous, two stage

Bicaval cannulation if has associated VSD or

if Ross procedure is planned

Cardioplegia all ostial

retrograde cardioplegia could be delivered for

maintenance of arrest

Arterial Pressure remains low due to low SVR

Venous return N

Left Heart Return Through RSPV in LA / LV

Preop medications ACE inhibitors, AT receptor inhibitors

Previous

interventions

BAV


8.Tricuspid Valve Disease

Etiology : Rheumatic Heart Disease (TS as well as TR)

Infective endocarditis ( TR ) (common among drug addicts)

(Congenital anomalies of TV will be discussed along with other congenital heart diseases)

Functional TR: secondary to significant distal valvular lesions (like, MS &/or MR)

Development of functional TR: due to back pressure effects secondary to MV disease, PH

develops. Long standing severe PH results in RV failure and the RV dilates. RV dilatation

leads to dilatation of the RV annulus. Dilated annulus prevents TV leaflets from coapting,

resulting in TR. In functional TR, the leaflets are normal.

Pathology: Normally, RA is thin walled and hence is a compliant chamber. Due to volume and or pressure

overload of TS or TR, it distends. As there are no valves at the openings of SVC and IVC to prevent back

pressure effects, with rise in RA pressure, the systemic veins distend, liver gets congested and patient

develops edema of the feet, pleural effusion & ascitis ( usually in that order).

Treatment: 1.Leave alone: Functional TR subside as the distal lesion like, MS & or MR is relieved. Patients

with TV disease are on heavy diuretics like Frusemide, Torsemide and Spironolactones.

2. Balloon Tricuspid Valvotomy: performed in cardiac catheterization laboratory without CPB or

anesthesia, if patient has isolated TS.

3. DeVega’s annuloplasty: When the dilatation of the TV annulus is severe, or along with tricuspid

valvotomy, tricuspid annuloplasty is performed.

Fig.8.1: DeVega’s Annuloplasty

In DeVega’s annuloplasty, a 2-0 Ethibond suture is passed as shown above to purse string the annulus

corresponding to the ATL and the PTL. (ref. fig 8.1)

4. Tricuspid Valvotomy: Like open mitral valvotomy, the fused commissures are opened.

5. Tricuspid Valve Replacement: If significant TS and TR are present together, the TV valve is usually

replaced.

All tricuspid surgeries are performed through RA, on CPB.

Usually, tricuspid surgery is performed after completing mitral and aortic surgery& closing LA and aorta.

Some surgeons prefer to perform TV surgery before aortic valve replacement, as the open ‘unoccupied’

aorta offers a free access to delivery of ostial cardioplegia.

TV surgery can be performed by the following techniques


1) aorta cross-clamped & heart is cardioplegically arrested: this technique provides a dry , still field with

no cannula in the field. Left heart vent is through LA suture line (in multivalvular cases) or through IAS

(isolated TV cases). Disadvantage of this technique is that it prolongs the cross-clamp time.

2) declamped aorta with empty beating heart or fibrillating heart: after closing left atriotomy and

aortotomy, the heart is deaired and aortic cross clamp is released .Left heart vent is maintained according

to the beating status. Now the RA is opened and TV surgery is performed. For this technique cardiotomy

suction is required to suck away the blood coming through coronary sinus. By this technique, aortic cross-

clamp time is shortened and damaging stitch causing heart block can be immediately corrected.

For both the techniques the SVC and IVC should be looped and snugged

Clinical assessment chart for TV Disease


Age Around 30yrs

Body weight

&

Height


Body Volume increased volume in systemic venous circuit PH status

CVP, liver enlargement,

effusions


Plasma Volume increased , but protein concentration is low as in body volume

LFT report

SVR according to proximal valve disease


Associated Renal dysfunction


S. Creatinine


Arterial cannulation Aorta

Venous cannulation Bicaval & tapes are required

IVC purse string may have to be taken on

partial CPB

Large sized venous cannulae are required

Cardioplegia according to the proximal ( i.e. aortic/ mitral)

lesion

Arterial Pressure Could be high ( > 60) on bypass

Venous return Very good . venous reservoir could overflow CVP raised, liver palpable

Left Heart Return Sump-sucker in LA ( multivalvular cases)

trans septal ( isolated TV cases)

Pre op medications Digoxin , diuretics ( Frusemide as well as

Aldactone)


Previous

interventions

as per proximal lesion Check for perforated IAS


9.Multivalvular Diseases

In India and south Asia, rheumatic heart disease (RHD) is highly prevalent.RHD is the most common

cause of multivalvular disease. RHD is responsible for mixed valvular disease, too, i.e. a valve could be,

simultaneously, stenotic as well as incompetent. The common combinations of multi valvular affections

are,

1. MS with AR

2. MR with AR

3. MS with AS

Certain features of multivalvular and mixed valvular lesions are:

1. The clinical picture will be according to the dominant lesion. e.g., if the MS is long standing

and severe, in spite of gross AR the diastolic pressure will not be low and the SVR will be high.

2. CCF is common: multivalvular and mixed valvular diseases are associated with large hearts &

severe systemic venous congestion. One of the largest LA dimensions is seen inpatients with

mixed mitral valve disease!

3. Myocardial Preservation: multivalvular conditions are associated with compromised LV as well

as RV function. Hence, myocardial protection receives top priority during surgery.

4. Functional valvular lesions: When a ventricle fails, it dilates. Dilated ventricle is associated

with dilatation of mitral or tricuspid valve (also called a-v valves) annulus. The dilatation results

in failure of leaflet coaptation. This gives rise to a-v valve (i.e. tricuspid or mitral valve)

regurgitation. When the distal lesion is treated, the ventricular dilatation regresses and the

annulus is back to original size and the functional regurgitation disappears.

Other causes of multivalvular diseases: these are Marfan’s syndrome (AR with MR) and

infective endocarditis (usually aortic and mitral valve) , Endo-Myocardial Fibrosis ( mitral and

tricuspid valve)

Management: Each valvular affection is treated on individual basis. Some of the salient features of

management are

a) Mild to moderate AR with other valvular affections: Mild to moderate AR does not warrant

surgery for aortic valve disease and, usually, these patients are taken up for mitral valve disease

or CABG. The AR poses problems w.r.t.

1) LV distension during cooling on CPB: appropriate venting is required

2) Delivery of root cardioplegia: requires compression of subaortic region

3) LV distension at the time of release of cross clamp:

b) Significant mitral and aortic valve disease: the mitral valve disease is treated first as retraction

of LA & passing sutures for mitral valve replacement in the presence of a prosthetic aortic valve

is very difficult.

c) Associated significant TV disease : please refer to the chapter on TV disease (p. 54)for details

During multivalvular surgery, due to long cross clamp time, multiple cardioplegia doses are

required. Hence problems like hyperkalemia, hemodilution should be anticipated.


10.Artificial Valves

Types of artificial valves:

A) Biological Valves: These are made from animal or human tissue. Depending upon the source of the

tissue, a valve could be

a) Autografts: these are obtained from patients own tissue. Currently, pulmonary artery is the

most popular autologous tissue for valve replacement.

b) Homografts: when a valve is prepared from tissue obtained from the same specie donor, it is

called homograft. Currently, human aorta & pulmonary artery are the commonly used homografts.

c) Heterografts: these valves are manufactured from tissues obtained from other species. Valves

made from pig (porcine) aorta and calf (bovine) pericardium are commercially available.

Each of these tissues could be implanted directly (called free or stentless valves) or implanted after

mounting the valve in a frame

Fig.10. 1 Free valve: Homograft Aorta

The free aorta is cut into one of the three designs as shown in fig 10.1

A) crown B) semi cylinder C) cylinder

Fig 10.2: Mounted valve: porcine aorta sutured in a cloth covered frame

A free valve offers a better ID/OD ratio than a mounted valve. As compared to a mounted valve, a free

valve implantation requires more skill for suturing and demands availability of a valve bank.


Biological valves do not require long time anticoagulation but have a limited lifespan (10 to 20 years) as

the tissue undergoes slow degeneration.

B) Mechanical Valves: Mechanical valves could be of one of the following designs (ref fig. 10.3)

Fig 10.3 Basic Design of Mechanical Valves

Currently, all over the world, only bileaflet valves are commercially available. the only monoleaflet valve

still available is TTK-Chitra valve and is available only in India

In a mechanical valve the leaflets are situated in a ‘housing’ and their opening and closing is

controlled by a ‘hinge’ mechanism. Outside the housing is the ‘sewing ring’ through which

sutures are passed, during valve implantation.

Fig. 10.4: Parts of a Bileaflet Valve

Mechanical valves have unlimited lifespan but, require lifelong anticoagulation.

Complications of Valve Surgery: These are also called ‘valve related events’.

a) Structural Dysfunction: The modern mechanical valves do not undergo any structural damage

resulting in dysfunction. Biological valves, however, undergo a slow structural degeneration. This process

of degeneration takes from months to years and results in stenosis and or incompetence of the biological

valve.

The hemodynamics and management are similar to any natural valve dysfunction.

b) Non structural dysfunction:


i) Valve thrombosis & Choked valve: This complication is seen in mechanical valves where, a leaflet or

disc does not move freely due to clot at the hinge mechanism (commonly, due to inadequate

anticoagulation); sub valvar chorda, plicated cusp or calcium preventing a full opening or closing of the

disc.

Choked valve is an acute complication. Patient usually presents in pulmonary edema or low

output state. Thrombolytic therapy may be initially offered to the patient. This therapy disturbs the

clotting system. Emergency surgery may be required to declot or replace the valve. Valve can get choked

in the immediate postoperative period (‘on table’). Sudden fall in pressure or failure to wean patient off

CPB are some of the ways this complication can present itself. The added features are pulmonary edema,

elevated LA pressures, and failure to hear valve clicks. Diagnosis is confirmed on trans-esophageal echo

(TEE), showing valve dysfunction. A surgeon may act on high suspicion and correct the underlying

cause.

ii) Paravalvular leak: due to friable annulus or due to faulty suturing technique, sewing ring – tissue

continuity is lost and a gap develops. Through this gap blood passes mainly, during systole (mitral /

tricuspid valve) or diastole (aortic valve). This flow of blood is turbulent and results in hemolysis.

Chronically, patient will have hemolytic anemia.

This complication can be managed only by surgery. Patient is anemic with relative liver

dysfunction. An old small leak may be closed with a stitch but a large size leak requires a re-replacement

of valve.

iii) Anticoagulation related hemorrhage: This is the most common valve-related complication & can

occur in any patient who is on warfarin. This could be due to drug interaction (with aspirin/ anti-

inflammatory drugs) or liver dysfunction. This complication is managed medically, i.e. nonsurgically.

iv) Thromboembolism: This is the second most common valve related complication. If embolism is to a

peripheral artery, the complication is treated with embolectomy, which is carried under local anesthesia.


11. Atrial Septal Defect

Etiology: Congenital.

Post BMV

Pathology: The inter atrial septum (IAS) develops mainly from two sources- septum primum (developing

first) and septum secundum (developing later). On operation table, the IAS looks one single septum

and the two septae cannot be distinguished. An imaginary line parallel to the SVC /IVC and passing

through coronary sinus roughly demarcates the two septae (ref fig 2.6). The part of IAS anterior to

this line has developed from septum primum and the part of the IAS posterior to this line is from

septum secundum. Depending on its position on the inter-atrial septum, an ASD is classified as

1) Primum ASD 2) Secundum ASD (commoner of the two ASDs).

Fig11.1: Showing IAS with its anatomical landmarks and position of various ASDs

Primum ASD: is always large in size. The inferior margin of the ASD is formed by the common

annulus of tricuspid and mitral valves. This ASD is associated with cleft of anterior mitral leaflet

(ref. fig 11.2) and as a consequence, MR of varying grade is always present.


Fig11.2: Normal AML and a cleft AML

Secundum ASD: could be of any size from a small sized, stretched patent foramen ovale (PFO) to a

large sized (> 2.5 cm in diameter) ASD. In Sinus venosus ASD (developing from sinus part of fetal

heart) the margin of the ASD towards the cava is absent. In posterior ASD, posterior margin is absent

The term ‘single atrium’ is applied when IAS is absent (it is a combination of all the ASDs shown

above)

Fenestrated ASDs: some times there are multiple small (2-3 mm in diameter) ASDs. Collectively they

produce a significant hemodynamic load.

Associated anomalies: (not in the order of frequency)

1) Partial anomalous pulmonary venous connection (PAPVC): associated with superior sinus venosus

(SV) ASD (ref. fig 11.3). Commonly one or two right pulmonary veins drain anomalously

into RA or SVC.

Fig11.3: Pathoanatomy of right PAPVC


2) Mitral valve disease (called Leutembacher’s syndrome): secundum ASD is associated with mitral

stenosis or regurgitation. Primum ASD with MR due to cleft AML is not Leutembacher’s

syndrome

3) Multiple shunts: ASD is associated with additional VSD or PDA

4) Valvar pulmonary stenosis: in PS, the shunt through ASD is usually left to right, but when RV

fails, shunt decreases and later becomes right to left

5) Left SVC: an additional L SVC producing bilateral SVC is found in many cardiac anomalies. The

size of L SVC is inversely proportional to the size of the bridging left innominate vein

(ref. fig. 11.4 & page 18)

Fig. 11.4: Various patterns of left SVC

Pathophysiology: Shunts through ASD are of two types

Facultative shunt: This is observed in isolated ASDs. The shunt is not essential for sustaining life

of the patient and infact, is a burden on the patient. These shunts are basically, L to R shunts and

the quantity of shunt dependents on many factors.

Obligatory shunt: In this condition, ASD is part of a larger pathological complex. This shunt is

essential for sustaining life of the patient. This type of shunt could be in any direction.

(Pathophysiology of ASD with obligatory shunts will be discussed with cyanotic heart diseases.)

The following discussion pertains to facultative type shunts

Due to the defect in the IAS blood flows from LA to RA – called left to right shunt at atrial

level. Blood flows form left to right because,


1) LA pressure is higher than the RA pressure (RA is more compliant than LA)

2) TV area is larger than MV area- i.e. TV offers less resistance to blood flow.

3) most importantly, RV end diastolic pressure (RVEDP) is lower than the LVEDP . In other

wards, RV compliance is much more than the LV compliance. Hence, blood flows easily via

LA-- RA–RV rather than via RA-LA-LV. The quantity of shunt is described as QP: QS, i.e.

amount of blood (Q) passing through pulmonary circuit (QP) to the amount of blood passing

through systemic circuit (QS). The QP: QS in a normal person is 1.0:1.0. An ASD requiring

surgery or intervention has QP: QS of more than 1.5:1.0

RA receives shunted blood as well as blood draining normally from SVC, IVC& CS, resulting in

RA volume overload (RAVO). The RAVO is passed on to RV (RVVO) and pulmonary artery.

RV and pulmonary artery dilate to accommodate extra blood till their compliance limits are

reached. The pulmonary pressure then starts rising (stage of development of PH). PH is initially

due to excessive flow (i.e. PVR is normal) but later on, PH is due to changes that develop in the

pulmonary vasculature. These changes in pulmonary vasculature are, initially, reversible (if the

ASD is closed) but, later on, become obliterative and hence, are irreversible (high and irreversible

PVR). Due to PH, RV has to generate more pressure to pump blood into pulmonary circuit. With

long standing PH, RV starts failing. When the RV fails, RVEDP rises. With a rise in RVEDP, the

L to R shunt decreases and finally, R to L shunt develops. This is called Eisenmenger complex.

L to R shunt in ASD fully develops, usually, by the age of two to four years. Hence it is very

unusual to find an infant with ASD, requiring surgery.

In ASD, LV out put is maintained till the last stage (hence SVR is normal).When a patient

presents prior to RV failure, JVP and volume in systemic venous compartment is normal.

Conditions which increase left to right shunt through ASD are: mitral stenosis or regurgitation,

additional shunts (VSD, PDA), PAPVC, development of systemic hypertension. In all these

conditions patient presents in failure.

Condition which decrease left to right shunt through ASD: pulmonary stenosis with RV failure

Conditions which have no effect on the left to right shunt through ASD: left SVC, IVC

interruption.

Natural History: An ASD present beyond neonatal period rarely closes.

1) remain asymptomatic for long time

2) RV failure

3) Supra Ventricular ( SV) Tachycardia

4) Eisenmenger Complex

Treatment: hemodynamically significant ASD (i.e. RVVO present) requires closure.

Medical: has no curative role. Drug therapy is mainly for symptomatic purposes.

Antibiotics: to control frequent lower respiratory infections (LRTI) which patients with ASD

have due to excessive pulmonary blood flow.

Diuretics: if patient has RV failure

Interventional: an ideal ASD for device closure is one which

1) is less than 2 cm in diameter

2) has well defined margins all around (hence not suitable for primum, SV and IVC defects)

3) has anomalies which can be treated by intervention (i.e. absence PAPVC & MR )


Fig. 11.5: Device closure of ASD

Complications: embolisation of device to LA or RV. This will require an emergency CPB to

retrieve the device and close the ASD.

Surgical Treatment:

A) Closure of secundum ASD: Secundum ASD is one of the few cardiac conditions that were treated

prior to CPB era. Salient features of management of a secundum ASD are

Incision: 1) Median sternotomy 2) Right anterior thoracotomy

Approach: irrespective of the skin incision, approach to ASD is through a right atriotomy.

Arterial cannulation is through aorta or through right femoral artery (for right thoracotomy).

Bicaval cannulation with snugging of SVC, IVC is mandatory.

Large venous return is found only in cases with Leutembacher’s syndrome or with multiple shunts.

Cardioplegia is delivered antegradely.

Being a short procedure (cross clamp time under 30 minutes) ‘drift cooling’ is allowed.

ASD is closed directly, if ASD is slit like; or with a patch, if ASD is large. Patch could be of autologous

pericardium, Dacron (a type of fiber) cloth or PTFE (poly tetra fluro ethylene- an inert material).

Some observe an additional step during deairing of the heart. After completing suturing of ASD patch, the

last few sutures are kept loose. Anesthesiologist inflates the lungs and holds the ventilation in mid

inspiration. This deairs the LA. The suture line is now tightened and tied while the lung is held in mid

inspiration. The rest of deairing is as per plan described earlier in ‘surgical aspect of CPB’. (Ch.3, p30)

Post op course and Complications: 1) Rhythm disturbance: Nodal rhythm is the most common rhythm

following secundum ASD closure. Heart blocks are common with primum ASD.

2) Pulmonary edema: seen in patients with direct closure of ASD, with MV disease. Edema can develop

immediate post CPB.

Management of associated anomalies

1) Right PAPVC: The proximal SVC appears dilated as it is draining PV blood, as well. This may

result in misjudging the size of the SVC cannula.


Fig11.6: site for SVC taping in a case with PAPVC

Techniques of SVC cannulation: 1) Through RA appendage with a straight wired cannula: this cannula

obstructs the surgical field and retraction of cannula is required while suturing the anterior margin of the

SV ASD. At the same time, presence of a cannula in SVC ensures SVC opening is not narrowed while

suturing the patch.

2) Direct high SVC Cannulation with a Pacifico cannula: This technique offers a clear operating field but

SVC opening can be narrowed while placing the ASD patch between SVC and PV.

Taping SVC: Irrespective of the cannulation technique, SVC has to be taped distal to the most superior

PV but proximal to the azygos vein. (ref. fig. 11.6)

ASD is closed in such a manner that the pulmonary veins drain under the patch through SVASD into LA

and the SVC drains over the patch into RA (ref. fig. 11.7)


Fig11.7: showing technique of closure of ASD with PAPVC

In case of narrowing of significant narrowing of SVC, the SVC is widened with a pericardial patch or by

using the RA appendage as a pedicle graft (atriocavopexy). For atriocavopexy a high direct SVC

cannulation or innominate artery cannulation is mandatory.

2) Mitral valve disease: mitral valve repair or replacement can be performed through ASD. For this ASD

may require enlargement

3) Multiple shunts: PDA requires midline closure any time prior to commencement of CPB & cooling.

VSD when present, is closed first as ASD is used for left heart vent

4) Valvar pulmonary stenosis: is dealt with in a variety of manner. Pulmonary valvotomy can be

performed prior or after the ASD closure. Some close the ASD, release the aortic cross clamp and then

perform valvotomy on an empty-beating or electively fibrillated heart

5) L SVC: please refer to the discussion in basics of OHS.

B) Closure of Primum ASD: Primum ASD is always large in size and due to associated MR, is

associated with a large L to R shunt and more than moderate PH. As a result, patient with primum ASD

always presents early for surgery.

Device closure is not feasible due to lack of margin inferiorly and associated MR.

Surgical steps are similar to those described for secundum ASD. Cleft of AML is closed with interrupted

sutures prior to ASD closure. Saline is used to test valve hence, perfusionist should be careful about saline

being sucked by the cardiotomy suctions. ASD is always closed with an autologous pericardial or PTFE

patch.

Clinical assessment chart for ASD


Age 5-8yrs.

in India adults can also present for surgery

Primum ASD would present early

( around 1year)

Body weight

&



Height

Body Volume Increased volume in pulmonary circuit.

High in patients with common atrium,

multiple shunts, Leutembacher’s syndrome,

primum ASD as they present with CCF.

heart size, calculated shunt



SVR Normal

Organ Function Normal


Arterial cannulation Aorta. aorta is small in size

Right Femoral Artery: may be required for

right thoracotomy approach

Venous cannulation Bicaval with tapes


Arterial Pressure Normal

Venous return Normal

Left Heart Return Sump-sucker in LA through ASD

Preop medications diuretics in adult ASD Check for potassium levels

Previous interventions Balloon closure


12. Ventricular Septal Defect

Etiology: Congenital

Acquired: following myocardial infarction

Classification: VSD is classified by various criteria

Fig12.1: Parts of Inter ventricular septum (IVS)

Criterion Nomenclature Importance

Relation with

membranous septum

Perimembranous

Muscular

close relation to conduction system

Position on IVS

( ref fig 12.1)

Inlet

Body

Outlet

approached through RA

approached through RA & or infundibulum

approached through infundibulum & or PA

Size Small

Medium

Large

conservative treatment

operate only if symptomatic

operate early

Relation to great vessel Subaortic

Subpulmonic

Noncommitted

Doubly committed

close relation to conduction system

develops PH early

complicated repair required

combination of above two

Ideally, every VSD should be described according to each of the above criterion.

Natural History:

Approximately 80% of all VSDs detected at birth close by 8years.Other outcomes are

1) some remain asymptomatic throughout life ( called maladie de Roger)

2) develop PH: high chance in large VSD

3) develop AR : high chance in sub pulmonic VSD

4) develop infective endocarditis: high chance with small VSD


5) develop PS: infundibular PS develops

Pathophysiology: In VSD, LV has two outlets and the flow through each outlet is in inverse proportion to the

resistance offered by each outlet and the distal circuit

Fig.12.2: showing resistance on pulmonary and systemic circuit

Resistance of systemic circuit: is contributed by aortic valve, aorta with all systemic arterial tree and SVR

Resistance of pulmonary circuit: is contributed by VSD size, infundibulum and pulmonary valve status,

and PVR.

As LV systolic pressure (120mm Hg) is much higher than the RV pressure (15 mmHg), presence of a

VSD results development of L to R shunt. Due to the shunt, RV is subjected to volume and pressure over

load since early intra uterine life. These overloads are carried to pulmonary circuit and the volume

overload is further is carried to LA & LV resulting in LAVO & LVVO. As described in chapter on ASD,

the pulmonary arteries initially dilate in response to volume-pressure overload. When limit of PA

dilatation is reached, pulmonary pressures start rising. Chronic and persistent rise in pressure, results in

development of obliterative changes in the pulmonary arteries and the PVR starts rising. Finally, RV &

LV pressures equal and shunt becomes R to L - called Eisenmenger Syndrome. Eisenmenger syndrome is

an inoperable state.

As per to Frank-Starling law, LVVO results in increased LV contraction. Gross LAVO or LVVO as seen

in a case with MR or AR, respectively, is never seen.

Associated Anomalies: (not in the order of frequency)

1) Multiple shunts

2) Coarctation of aorta

3) L SVC

Effect of associated anomalies and natural history on L to R shunt through VSD


AR: sagging aortic cusp closes the VSD partially & L to R shunt decreases.

PS: resistance to the pulmonary circuit increases and L to R shunt decreases.

Multiple shunts: increased L to R shunt

Coarctation of aorta: due to increased resistance on the systemic circuit L to R shunt increases

Treatment: 1) Conservative Treatment: No surgery is advised for a VSD with a diameter < 7 mm / M

2 BSA and without

PH, AR or infective endocarditis.

2) Medical treatment: is offered to babies who are awaiting surgery. It consists of afterload reducing agents

(ACE inhibitors, AR inhibitors), diuretics and iron replacement therapy. Afterload reducing agents

improve LV forward out put by reducing SVR.

3) Interventional treatment: device closure of VSD could be tried in some cases. As compared to the

success and popularity of device closure of ASD or PDA, success rate for VSD closure is much less.

Complications are similar to those for other device closures

4) Surgery: a)MPA banding: When a baby is too small by weight or age, for a center to handle and if the

CCF cannot be controlled with drugs , MPA banding is offered. This is also a treatment of choice if

patient has multiple (Swiss cheese type) VSDs.

Fig12.3: hemodynamic changes before & following MPA banding

Due to MPA banding RVOT obstruction is created which increases resistance to flow of blood from LV

to PA. This reduces the left to right shunt through the VSD & increases the forward flow through aorta.

MPA banding is performed as a closed heart operation through left thoracotomy or through a median

sternotomy. A tape is placed around MPA like a circular band. The length of the tape, i.e. circumference

of the band is according to the weight of the baby.


Due to increased forward flow the baby now thrives well and after few months to few years, is taken up

for VSD closure. At the time of intra cardiac repair the MPA should be debanded prior to coming off

CPB.

b) VSD closure: VSD closure is performed through median sternotomy, occasionally through right

thoracotomy. VSD is approached through RA, RV, PA or aorta depending upon the situation of VSD on

the IVS (ref fig 12.1) & associated procedure required.

Bicaval cannulation with snugging of SVC, IVC is mandatory, irrespective of approach.

VSD is closed directly, if small; or with a patch, if large. Patch could be of autologous pericardium,

Dacron or PTFE.

Post op course and Complications:

1) Rhythm disturbance: nodal rhythm, complete heart block (CHB). CHB is possible in perimembranous

and inlet VSDs. External, epicardial pacing will be required.

2) Residual VSD: significant VSD detected on a transesophageal echo (TEE), will require reinstitution of

CPB and cardioplegic arrest.

3) Inadequate correction: associated PS, AR may not be adequately corrected and will require

reinstitution of CPB and cardioplegic arrest.

Clinical assessment chart for VSD


Age 3-9 months.

in India patient can present in adulthood

Body weight

&

Height


Body Volume Increase in volume of the pulmonary circuit

heart size, calculated shunt



SVR low due to afterload reducing agents brisk pulse, check medications

Organ Function Normal

Arterial Tree coarctation could be present check lower limb pulses or

pressure

Arterial

cannulation

Aorta. aorta is small in size

on table visualisation

Venous

cannulation

Bicaval with tapes


root compression may be required if AR is

present

check 2Decho report

Arterial Pressure low due to after load reducing agents

anesthetists administering NTG or

vasodilators to reduce PH

check for medications and time of

administration

Venous return Low

Left Heart venting

/return

RA approach :through IAS/ VSD

RV approach : RSPV/ VSD/ PA

PDA if present will have to be

closed prior to CPB


Atrio–Ventricular ( AV) Canal Defects

Etiology: Congenital

Pathology: AV canal is the region where the two septae (IAS & IVS) and the two valves (MV, TV) meet.

Fig12.4: diagrammatic presentation showing situation of AV canal defect

PA approach : RSPV/ VSD/ PA

Preop medications ACE inhibitors, AT receptor inhibitors,

diuretics

check for K+

levels

Previous

interventions

MPA banding incision used. If sternotomy,

adhesions could be present


AV canal is the area which develops, embryologically, from A-V cushions. Hence these defects are also

called cushion defects. A patient with this defect has

1) ASD component as a Primum defect

2) VSD component as a large inlet VSD

3) MV component in the form of MV anomaly (cleft in the AML)

4) TV component as a TV anomaly (cleft in the STL)

Pathophysiology: it is a combination of ASD, VSD and MR resulting in a large L to R shunt with early

development of severe PH and biventricular failure (see Ch11, p.63)

Classification: AV canal defects are variously classified.

Complete AV Canal: This term is used when mitral valve and tricuspid valve have together one single

annulus, i.e. it is a common valve. Complete AV canal defects are further divided into A, B, C types

depending upon the valvular anatomy. Type A is the simplest variety.

Partial AV Canal: Any combination less than the four components of complete AV canal is loosely called

partial AV canal. Even Primum ASD with cleft in AML is called partial AVC

Treatment: Children present at a very early stage (1 to 4months)

1) Medical: consisting of diuretics and ACE inhibitors is useful only as preoperative treatment.

2) Surgery: Is the only possible treatment and consists of correcting the defects. MPA banding is not

useful. The AV node and the conduction system is in close proximity to the defect hence, there is a high

chance of development of complete heart block (CHB).

Perfusion management is as described for VSD. The chance of associated anomalies is higher than in a

case with VSD.

Gerbode Defect

Etiology: congenital

Pathology: Normally, the MV and the TV are not at the same level as a result a part of the interatrial

septum is actually an atrioventricular septum. A defect in this septum is called Gerbode Defect .

The defect is usually 3to 4mm in size and is closed surgically under CPB.

The clinical picture and the perfusion management is that like a VSD. The defect rarely gives rise to

severe PH. JVP / CVP is raised out of proportion to the PH status.

RA remains ‘full’ on CPB due to the shunt. The defect is close to conduction system and may require

temporary external pacing following surgery.


Fig 12.5: Diagrammatic presentation showing position of Gerbode Defect


13.Tetralogy Of Fallot

The condition is named after the French pathologist Fallot, who first described the pathological features of the

disease.

Pathology: The four (tetra) pathological features are (ref fig 13.1)

1. VSD

2. Right Ventricular Outflow Tract obstruction (RVOTO)

3. Right Ventricular Hypertrophy

4. Overriding of aorta

Out of the four elements, VSD & RVOT obstruction are responsible for the pathophysiological changes.

Fig. 13.1 Diagrammatic presentation of normal heart (left) and TOF heart (right)

1. VSD: is mostly single, perimembranous, subaortic and non restrictive. Non restrictive means as large

as the diameter of aorta.

2. RVOTO: The RVOT, i.e. RV infundibulum, pulmonary annulus, pulmonary valve, MPA, branch PA

are obstructed at various levels, in various combinations.

3. RV Hypertrophy: is as much as LV hypertrophy

4. Overriding of aorta: long axis drawn through the ascending aorta in a normal individual falls into LV

(no override). In TOF, the long axis falls on the inter-ventricular septum (IVS) or into RV cavity.

Accordingly the override is classified as no override to 100% override.

Pathophysiology; The VSD is nonrestrictive, i.e. the VSD is as large as the aorta and the blood flows from RV to LV

freely, without any gradient. Hence, the pressures in the RV & LV are equal during all phases of cardiac cycle.

Also, due to non restrictive VSD, RV ejects blood into aorta without any obstruction.


Fig13.2 Diagrammatic representation of RV with two outlets

Thus, RV has physiologically two outlets

1) RVOT: This is obstructed at various levels. An obstruction could be dynamic (infundibular stenosis) or

adynamic (annular and valvar stenosis, small pulmonary arteries). The resistance in this circuit is variable

from patient to patient depending upon the severity of obstruction at various levels. As compared to the

resistance offered by mechanical obstructions, resistance offered by the pulmonary vascular resistance

(PVR) is very negligible (PVR is of normal value).

2) Systemic circulation: This circuit consists of VSD, aortic annulus, aortic valve and systemic vascular

tree. There is no mechanical obstruction in this circuit and the resistance offered by this circuit is entirely

due to the systemic vascular resistance (SVR)

RV ejects blood, in inverse proportion to the resistance offered by the two circuits, into pulmonary and

systemic circulation resulting in a) decreased pulmonary flow b) systemic desaturation.

a) Decreased Pulmonary Blood Flow situation: due to right to left shunt, less than normal amount of

blood flows through pulmonary arteries and is available for oxygenation. It should be noted, however, the

blood leaving the lungs through pulmonary veins is fully saturated. In certain situations, called cyanotic

spells, blood flow to lung is severely reduced.

Body compensates for decreased pulmonary blood flow situation by the development of systemic artery

to pulmonary artery shunts called ‘systemico-pulmonary artery shunts’ or ‘broncho-pulmonary

collaterals’. These are small sized blood vessels arising from a systemic vessel like the descending aorta,

subclavian arteries, and bronchial arteries and reaching out to pulmonary artery anywhere from MPA

bifurcation to intrapulmonary arterioles. PDA in a patient with TOF is looked upon as one such collateral.

In patients with pulmonary atresia, a 3 to 4 mm diameter vessel can arise from, mostly, the descending

thoracic aorta and join pulmonary artery at various levels (intrapericardial PA, at the lung hilum, inside

the lung parenchyma). These are called Major Aorto Pulmonary Collateral Arteries (MAPCA).


Fig.13.3: MAPCA

MAPCA can be the sole supplier of blood to the lung or could be an additional supplier of blood along

with pulmonary arteries.

b) Decreased Systemic Saturation: This depends on the severity of right to left shunt and the amount of

compensatory systemic - pulmonary artery collateral blood flow. Persistent hypoxia is a stimulus for

erythopoiesis & results in increased hemoglobin. Oxygen carrying capacity of blood is equal to Hb x 1.34

x saturation. As saturation value, in a case with TOF, is less than 100% (i.e. 1), rise in hemoglobin helps

in improving the oxygen carrying capacity of blood.

Rise in hemoglobin increases pack cell volume (PCV) and thereby decrease the percentage of plasma in

blood. Increased PCV also increases the viscosity of blood. A rise in hematocrit of blood from 40% to

60% results in rise in relative viscosity from 4 to 8.

As a compensation to high viscosity, the coagulability of blood decreases. Platelet count is low and there

could be a disseminated intravascular coagulopathy (DIC) like picture.

‘Fallot Physiology’: Apart from TOF, there are a number of pathological conditions where, though the patho-

anatomy is different, the pathophysiology remains similar to that in TOF. Due to similarity in pathophysiology,

the CPB management too remains the same. These conditions are called- ‘Fallot physiology’. The cardinal

features of these conditions are ventricular septal defect, RVOT obstruction and right to left shunt across the

VSD, proportional to the severity of RVOT obstruction. The various pathological conditions usually included

under this terminology are,

1. VSD with PS

2. Severe PS with a small VSD

3. Double Outlet Right Ventricle ( DORV) with Pulmonary Stenosis

4. Pulmonary atresia with VSD


5. Corrected transposition with VSD PS

6. Tricuspid Atresia with PS

Cyanotic Spells: Patients with TOF, usually below the age of 5- 6yrs , suddenly or after a bout of crying become

intensely blue, tachypneic, and may even become unconscious. The mechanism of development of spell is as

shown below

Untreated cyanotic spell could result in cardiogenic shock and CNS events like, convulsions.

Treatment:

Medical: Medical treatment is mainly to relieve cyanotic spell, respiratory tract infection and anemia.

Inspite of increased hemoglobin these patients can have hypochromic microcytic anemia.

Some treat patients with restricted physical activity with tablet Propranolol (dose = 3mg/Kg/day in three

divided doses)

Surgical: a) Palliative surgery b) Corrective surgery

a) Palliative surgery: Decreased pulmonary blood flow is the root cause of patient’s problems. Palliative

surgery consists of procedures aimed at increasing the pulmonary blood flow. This was achieved,

historically, by a number of methods. Of these various methods, only the Blalock – Taussig (BT) shunt is

practiced today.

Indications for BT shunt are:


i) Patient ‘small’ by weight for a center: when a center is not geared to handle a baby with TOF

for a major operation - intracardiac repair (ICR), an operation of lesser gravity-BT shunt is

performed. (The criterion for ‘small’ will vary from center to center and from time to

time.)Following BT shunt baby thrives well and can be taken up for intracardiac repair when the

baby reaches appropriate age and weight.

ii) Small sized pulmonary arteries: The results of ICR depend upon the capacitance of pulmonary

arterial tree. Hence, when due to decrease pulmonary flow, the pulmonary arteries are small in

size BT shunt is performed to increase the pressure-head and dilate the pulmonary arteries.

iii) Uncontrolled cyanotic spells: When medical treatment fails to control spells.

iv) LAD coronary artery crossing the RVOT: This pathology may require an RV-PA conduit,

which may not be feasible for a variety of reasons.

BT shunt is a procedure performed without CPB. It can be performed through a right or a left

thoracotomy, and sometimes, through a median sternotomy. This operation consists of connecting

subclavian artery to ipsilateral pulmonary artery either directly (classical BT shunt) or through a

PTFE graft (modified BT shunt, ref fig 13.4).

Fig 13.4: Modified left BT shunt

Following BT shunt cyanosis improves, baby thrives well, and pulmonary arteries grow.

When the baby achieves institutional criteria for an ICR, the baby is operated for the final

operation. Following BT shunt, ICR repair could be performed after about 3months. Prior to ICR

the patency of BT shunt is checked. About 80% shunts are patent at the end of 1 year of surgery.

Changes in pathophysiology following BT shunt are

Feature Change following BT shunt

Pulmonary Blood Flow Increased but below normal

RVOT Obstruction Worsens to virtual atresia

Pulmonary annulus Enlarges

Pulmonary artery tree enlarge to normal size

LA Dilates to normal size

LV Develops, size normalises

Arterial Saturation Increases to about 85 to 90%

Hemoglobin Falls but still above normal


Feature Change following BT shunt

Blood viscosity Decreases

Platelet count Normalises

Subclinical DIC Absent

b) Corrective Surgery: This surgery has been variously called as ‘intracardiac repair’ (ICR) or ‘total

correction’. At the time of corrective surgery only those elements responsible for the pathophysiological

problem, namely RVOT obstruction and VSD, are corrected.

ICR is performed through median sternotomy with bicaval (tricaval, if L SVC is present) venous

cannulation.

Approach could be through RA &/or RV &/or PA.

Left heart is vented through RSPV (RV approach), IAS (RA approach), RVOT-PA (RV approach) and or

through VSD. Depending upon brochopulmonary collaterals, the left heart return could be excessive. An

excessive return occluding the operative field is managed by core cooling the patient and appropriately

reducing the pump flows.

A functioning BT shunt is dissected and looped prior to CPB and is ligated only on full CPB prior to core

cooling.

ICR consists of infundibular resection, closure of the VSD with a patch and widening the RVOT, if

required. The widening is performed with an autologous pericardium or with a PTFE patch. The RVOT

patch could be subannular (restricted only to the infundibulum) or transannular (extending into the MPA)

Accidents and complications: 1.Cardiogenic shock: One of the causes of postoperative cardiogenic shock

is inadequate relief of RVOT obstruction. This will require reinstitution of CPB and further widening of

the patch. If it is only an RVOT widening, then heart may not be cross-clamped

2. Rhythm disturbances similar to any VSD closure.

3. Bleeding: Cause of bleeding could be surgical and nonsurgical. Surgical cause is usually related to

bleeding from the RVOT patch. If bleeding requires a stitch, reinstitution of CPB may be required.

Nonsurgical cause is due to preoperative coagulation disturbances further compounded by CPB.

Clinical assessment chart for TOF

Parameter Findings comment/ Method of assessment

Age usually from 6 months to 2years.

in India adults can also present for surgery

Body weight

&

Height


Body Volume normal

Hemoglobin very high severity of cyanosis

May require blood letting

Plasma Volume Low

SVR normal or raised check medications

Organ Function Coagulopathy

CNS : cerebral abscess, cortical venous

thrombosis

Pulmonary tuberculosis.

Arterial Tree 25% have right aortic arch

Arterial Aorta.


Perfusion problems in patients with a preoperative high PCV

1) High viscosity. Baseline high viscosity increases out of proportion even at temperatures of 300C.

Hence hemodilution to 30% is required. On- table blood letting prior to institution of CPB is

required.

2) Low plasma volume: Due to higher PCV, the volume of plasma is low in the body. In such a patient,

if only crystalloids are used for priming it results in low oncotic pressure. Hence a colloidal

prime is required.

3) Low clotting factors: particularly low platelet count.

4) Low perfusion pressure: lower viscosity due to hemodilution, multiple aorto-pulmonary collaterals

result in low perfusion pressure. This is treated with vasoconstrictors. Vasoconstrictors which

do not cause renal vasoconstriction are preferred.

cannulation

Venous

cannulation

Bicaval with tapes Check for LSVC on 2Decho


root compression may be required for AR

check 2Decho report for AR in adults

Arterial

Pressure

low due to A-P collaterals and sudden

Hemodilution

Venous return Low

Left Heart

venting /return

RA approach :through IAS/ VSD

RV approach : RSPV/ VSD/ PA

PA approach : RSPV/ VSD/ PA

an extra suction line may be required

hemolysis due to excessive

suctioning should be checked.

Preop

medications β blockers

Previous

interventions

BT shunt incision used for BT shunt is

sternotomy, adhesions could be

present between sternum and the

heart


14. Functional Single ventricle

Definition: A group of conditions where for all practical purpose, there exists only one functioning ventricle, the

term – functional single ventricle (f SV) is used. Obviously, the pathological conditions included under

this terminology can not be repaired by incorporating the two ventricles as independent pumping

chambers.

Pathology: Conditions which are included in this group are

Anatomically single ventricle (of any type).

Tricuspid atresia (RV is rudimentary)

Mitral atresia (LV is rudimentary)

Double inlet ventricles (both the a-v valves open into one of the ventricles)

AV canal with mal-attachment or overriding of one of the two a-v valves (separation into two ventricles

is not possible)

Pathological features of tricuspid atresia are shown below to improve understanding

Fig 14.1: diagrammatic representation of intracardiac circulation in tricuspid atresia


For a case with tricuspid atresia (ref. fig 14.1), ASD is essential for survival. Hence the shunt across the

ASD is called ‘obligatory shunt’. Similarly, part of the mixed blood from LV got to go to pulmonary

circuit for oxygenation. Hence these patients must also have a VSD or PDA.

Associated Pathology: a. Pulmonary stenosis status: atretic, stenotic or no stenosis

b. Great vessels could be transposed or normal

Final surgical correction is possible only if patient has pulmonary stenosis resulting in normal PA

pressure and normal PVR.

Treatment : Stage I : The aim at this stage is to provide a balanced pulmonary flow so that patient thrives and

survives to the age of more than 5years , when the final ( Fontan ) operation can be performed.

a) Without PS (i.e. with increased pulmonary flow) these patients are operated for MPA banding to

reduce excessive blood flow through lungs and provide a controlled flow. (for further details on MPA

banding, please refer to chapter on VSD – Ch12. p 70)

b) With PS (i.e. with decreased pulmonary flow) if the systemic saturation is low (indicating severe PS)

& or patient has failure to thrive, then a systemico pulmonary artery shunt is performed. This could be a

BT shunt (ref to chapter on TOF-Ch13.p78) or a Glenn shunt.

Fig14.2: Glenn Shunt (original design)

Originally, the Glenn shunt was performed by anastomosing the distal right pulmonary artery to the side

of SVC through a right thoracotomy (ref. fig 14.1). The proximal SVC was, next, ligated.

This diverted the flow from SVC to the RPA only.


In the current version of the Glenn shunt, the distal end of the divided SVC is sutured to the side of RPA

(ref. fig .14.2). This allows blood from SVC to flow to both the right lung (through distal RPA) and the

left lung (through proximal RPA-LPA). Hence the current Glenn shunt is called bidirectional Glenn

shunt.

Fig.14.2: Bidirectional Glenn Shunt

Glenn shunt is usually performed through median sternotomy. Azygos vein is ligated. SVC is divided

and the distal SVC stump is anastomosed to the side of the RPA. While performing the Glenn

anastomosis, the SVC is cross clamped. Complete clamping of SVC results in steep rise in the distal SVC

pressure (to around 40 to 50 mm of Hg).Distal venous hypertension is managed by following ways.

1) no intervention: accept venous hypertension, offer only head high position

2) veno-venous bypass: blood from distal SVC is drained into a reservoir and is pumped back to RA.

3) temporary external shunt: the shunt is made up of two venous cannulae, joined through an appropriate

connection( p86, fig 14.6) . The shunt establishes an external venous pathway between distal SVC or

left innominate vein, on one hand and, the RA or PA, on the other. The drainage through this shunt is

by gravity and is facilitated by elevating the head-end of the patient (head-high). Head high may

result in arterial hypotension. Air removal should be carefully performed while joining the two

venous cannulae.

If there are bilateral SVC then a bilateral bidirectional Glenn shunt is performed.

The final treatment for a functional SV is ‘Fontan Operation’.


Fontan operation is based on the principle that RV is dispensable i.e. heart can function without RV.

Though the Fontan operation is not followed today in its original form (ref.fig. 14.3), the basic principle

remains the same, i.e., if PVR is normal, then pulmonary circulation could be maintained when the

systemic veins are connected to the pulmonary artery circuit, without obstruction.

Fig 14.3: Original version of Fontan Operation

In a modern day version of the Fontan operation , first a Glenn shunt is performed by anastomosing

SVC to RPA as an end to side anastomosis, ( hence called stage I Fontan) and then, IVC is connected to

the proximal RPA or to the disconnected MPA either through an intra atrial tunnel ( certainly requiring

CPB) or through a an extra cardiac conduit( may not require CPB)

Intra atrial tunnel: This is performed on cardioplegically arrested heart. CPB may be set in before or

after performing Glenn shunt.

Fig14.4: Fontan operation: Intra-Atrial Tunnel


Which ever may be the method used, a high SVC or left innominate vein cannulation is required. The

IVC is cannulated directly, as distally as possible. After cardioplegically arresting the heart, RA is opened

and with a patch (of pericardium / atrial wall/ PTFE) an intra atrial tunnel is created on the lateral RA wall

to drain IVC blood through the proximal SVC stump into pulmonary circuit.

This operation is also called total cavopulmonary connection (TCPC).

Extra cardiac tunnel: In an another modification, the IVC blood may be drained through an extra-

cardiac PTFE graft into pulmonary circuit. Anastomosis of the PTFE graft to IVC can be performed

without CPB (when graft is anastomosed to the side of the IVC), or by using venovenous bypass (when

graft is anastomosed to the end of the IVC).

Fig.14.5: Extra Cardiac Fontan Operation

This modification of Fontan operation is called Extra Cardiac Fontan operation (ECFO).

A Fontan operation functions well when the mean PA pressure is 15 mm of Hg or less. If following a

Fontan operation if the PA pressure is high or expected to be high, then a 3 to 4 mm fenestration is

created between the tunnel and the adjoining atrium. This is called fenestrated Fontan operation.

CPB Considerations:

1) Glenn Shunt:

a) On CPB: This is performed on a beating heart. (without crossclamping aorta and cardioplegically

arresting heart). Strict normothermia is required to be maintained. Only a single, but a high SVC or

innominate vein cannulation will be required. The beating heart drains the IVC. Bilateral SVC is common


in these complex heart diseases. In cases with bilateral SVCs, each SVC is cannulated during the

corresponding side (called ipsilateral) Glenn Shunt.

In Glenn shunt as well as in Fontan operation, disfiguration of major systemic veins is to be avoided.

Hence, to avoid narrowing of veins after tying the purse-string suture, surgeon usually places a small

sized purse string suture and prefers a small sized cannula.

b) Off CPB: This technique is more common. Glenn shunt requires cross clamping of SVC. This results

in rise of central venous pressure (CVP) to very high levels (40 to 60 mm of Hg) level. This could prove

dangerous for brain. To facilitate SVC drainage and reduce CVP while performing the Glenn shunt, an

external shunt may be inserted between SVC and RA or PA .Systemic heparinisation in the dose of

3mg / Kg is necessary. The circuit consists of (ref. Fig 14.6) a Pacifico metal tip venous cannula attached

to a straight venous cannula (if drained into RA) or to another Pacifico venous cannula (if drained into

PA)

Fig.14.6: External shunt during Glenn Shunt

The two cannulae are connected through a ¼” by ¼” connection with Luer –lock knob. The Luer – lock

knob helps in deairing the circuit. A head up tilt benefits venous drainage. Due to high PCV, blood

viscosity is high and may prevent adequate drainage.

2) Fontan Operation: General Considerations: i) A functioning Glenn shunt improves the arterial saturation only to 85 to

90%. Hence, with or without a previous Glenn shunt, a patient for Fontan surgery is, still, cyanosed and

with a high PCV. (ref. p.80 for problems associated with high PCV)

ii) With a previous midline shunt, sternotomy may result in an inadvertent injury to the underlying

structures and an emergency CPB may be required to be instituted.

iii) Following a Fontan operation, one of the factors determining the flow from systemic veins to LA is

the PVR. Hence prior to coming off CPB, the patient should be well dilated.


a) Fontan Correction on total CPB: When an intracardiac tunnel is planned bicaval cannulation, total

CPB with cardioplegic arrest will be required. Anastomosis of the proximal SVC stump to the PA is

performed last and, may be performed on a beating heart.

b) Fontan Correction on right heart bypass: This technique is used when ECFO is performed. After

performing Glenn shunt, IVC is drained through a femoral vein cannula or a distal IVC cannula, to a

reservoir. Blood is then pumped back to RA. This technique allows crossclamping of IVC without any

fall in the arterial blood pressure and permits an end to end IVC conduit anastomosis.

Fig. 14.7: Circuitry for right heart bypass during ECFO

c) Fontan Correction without CPB: An Extracardiac Fontan operation can be performed without using

any form of CPB. However, emergency setting up of CPB may be required, particularly, while

performing the IVC –conduit anastomosis. Glenn shunt and conduit- PA anastomosis are performed first.

IVC (with a small part of RA) is partially clamped and the conduit is sutured end to side. Head low and

raising the CVP by infusing patient helps in maintaining the hemodynamics during the partial clamping of

IVC. As the partial clamp on IVC is released, the IVC RA junction, proximal to the anastomosis, is

ligated.

Managing Fontan Physiology: The blood flow from systemic vein- pulmonary artery- pulmonary vein-

LA-LV is well maintained, provided,


1) there is no anatomical obstruction in the circuit: achieved by case selection , large sized anastomosis

2) PVR is low: achieved with NTG, sildenafil orally

3) systemic venous pressure is adequate: achieved by filling up the patient with colloids

4) intra- pleural pressure is negative: achieved by avoiding PEEP & ventilation adjustment.

5) LV diastolic pressure is negative: achieved by dobutamine support.

Renal failure sets in very early following Glenn shunt or Fontan surgery. Early and appropriate use of

DOPAmine, NTG and diuretics is of benefit. Postoperatively, spironolactones are more useful than

frusemides.


15. Total Anomalous Pulmonary Venous Connection ( TAPVC)

Definition: In TAPVC all the pulmonary veins drain into a systemic venous chamber, i.e. either a systemic vein

or RA.

Pathology: All the pulmonary veins initially open into a common chamber (CC). Depending upon where the CC

drains, a TAPVC is classified as,

a) Supracardiac: the common chamber drains through a vertical vein into left innominate vein (most

common) or into SVC. This variety forms 55% of all cases of TAPVC.

b) Intracardiac: the common chamber drains into coronary sinus or RA. This variety forms 30% of all

cases of TAPVC.

c) Intracardiac: The common chamber drains through a channel, which passes through the diaphragm,

and opens either into portal vein (most common), hepatic vein or IVC.

Fig.15.1: Diagrammatic presentation of Supra Cardiac TAPVC

Pathophysiology of TAPVC: typical features are


a) Cyanosis: TAPVC results in total mixing of all the pulmonary venous blood with systemic venous

blood. This mixing is irrespective of any factor, like RVOT obstruction or SVR and hence, the baby

is cyanosed since birth.

b) Volume overload: RA receives systemic as well as pulmonary venous drainage, hence, is volume

overloaded (RAVO). This over load passes on to RV (RVVO) and to pulmonary circuit. Similar to

the pathophysiology of an ASD (ref. Ch 11 p.63), RVVO gives rise to PH & RV failure.

c) Obligatory shunt across the ASD: For survival of the patient, a sufficient amount of blood from RA

has to cross over through the ASD and pass-on to LA for systemic circulation. Thus, the ASD in

TAPVC forms the obligatory shunt. The size of ASD decides the adequacy of the obligatory shunt. A

patient with a small, restricted ASD presents early to the physician (a neonate with a small PFO

presents at day one)

d) Early development of pulmonary hypertension: A combination of factors like, long course for the

pulmonary venous blood to open into a cardiac chamber, restricted ASD and volume overloaded

pulmonary circuit result in early development of pulmonary hypertension. Severe the PH, earlier the

patient presents.

Treatment:

Medical: helps in controlling failure, anemia and chest infection.

Balloon Atrial Septostomy (BAS): is an interventional procedure and is performed in neonates with

restricted ASD. It is performed within 3 days of birth. Following a BAS, obligatory shunt increases,

thereby increasing the systemic blood flow. Also, RVVO decreases and PH is relieved.

BAS is only a palliative procedure.

Surgical: Palliative surgery for TAPVC is of only historical interest.

Corrective Surgery: The principle of corrective surgery is establishing a direct communication

between the CC and LA, without any obstruction.

Through median sternotomy, the vertical vein is looped. CPB is established with bicaval cannulation.

On CPB, prior to opening of CC, the vertical vein acts like a left heart vent. After cardioplegically

arresting the heart, the vertical vein is snugged and the common chamber is opened (ref. fig. 15.2).

The common chamber is sutured to an opening made into the adjoining part of LA. The size of the

CC-LA anastomosis should be atleast, as large as the mitral valve annulus. ASD is now closed. The

vertical vein is ligated only after coming off CPB and after ensuring adequate hemodynamics. In case

of unstable hemodynamics, the vertical vein is left open and it acts as a vent for high pressured CC.


Fig.15.2: Supracardiac TAPVC correction, LATERAL VIEW

Clinical assessment chart for TAPVC

Parameter Findings comment/ Method of

assessment

Age usually 1- 6 months

Supracardiac and Intracardiac variety can

present late for surgery

Body weight

&

Height


Body Volume Increased as patients are in CCF

Hemoglobin Normal or low. Polycythemia is seen in

patients presenting after 2years

severity of cyanosis

Plasma Volume Normal or increased

SVR normal check medications

Organ Function nil


Arterial cannulation Aorta. Small aorta

Venous cannulation Bicaval with tapes .


Single cannulation for circulatory arrest

Cardioplegia Antegrade, through root

Arterial Pressure low due to vasodilators

Venous return Good

Left Heart venting

/return

Through CC / ASD

Preop medications Diuretics, ACE inhibitors

Previous interventions BAS


16.Transposition of Great Arteries ( TGA)

Definition: TGA is a condition where aorta arises from right ventricle and pulmonary artery arises from left

ventricle.

Nomenclatures: Other names for the condition are

1) Complete TGA: Aorta takes origin exclusively from RV and MPA takes origin exclusively

from the LV

2) d TGA: ( d stands for dextro meaning right) as aorta is to the right of MPA

3) Simple Transposition: d TGA occurring in isolation

Pathology:

Fig. 16.1: diagrammatic presentation of pathoanatomy of d-TGA

Right ventricle : As the RV is the systemic pumping chamber, it is hypertrophied and dilated. The

thickness of RV increases with age. The RV function remains normal in the perinatal period.

Left ventricle: Normally LV is thicker than RV in the intrauterine life and after birth the LV thickness

goes on increasing. In TGA, as LV is a pulmonary pumping chamber, the LV thickness does not

increase after birth and by the age of 3months it is thinner than RV.

Aorta: is usually anterior and slightly to right


Coronary Arteries: A number of anomalies related to origin of coronary arteries are found.

Coronary anomaly determines the result of repair. Pulmonary vascular disease: There is an early development of severe pulmonary vascular disease. The

incidence is as high as 65% by the age of 1year. This incidence is even more in patients with

TGA –VSD.

Associated anomalies: VSD (in almost 50% of cases), pulmonary inflow stenosis (i.e. LVOT

obstruction, in almost 25% cases) are the common associated anomalies. Some sort of PDA is

seen in patients who come for surgery before the age of 1week.

Pathophysiology: In normal life, the pulmonary and systemic circulations are in series. In TGA the

pulmonary and systemic circulations run parallel. The RA receives deoxygenated blood from the

body which enters aorta through RV & gets further deoxygenated. The LA receives oxygenated

blood which enters MPA for further oxygenation. Unless there is a bilateral shunting between the

two circuits, the defect is incompatible with life. This bilateral shunting is called mixing. Mixing

occurs, most commonly, at atrial level through the PFO or ASD. Mixing occurs in a better

manner through VSD and or PDA. Infact patients with TGA-VSD present slightly late and have

a better natural history.

Symptomatology of patient depends upon: 1) Degree of mixing: High mixing allows adequate systemic

saturation and patient presents later. 2) Development of pulmonary hypertension: patient presents early

3) LVOT obstruction: controlled obstruction protects patient from development of PH. Severe LVOTO

leads to severe cyanosis.

If unoperated, survival is about 50% at 1 month and 15% at 6 months. The survival is better among

patients with TGA-VSD.

Management :

1) PGE1 infusion: is administered to newborns to keep the ductus arteriosus patent and thereby improve

systemic saturation. This is a temporary treatment.

2) Balloon Atrial Septostomy (BAS): this enlarges the existing PFO and thereby increases mixing of

blood & improves systemic saturation.

3) Arterial switch Operation (ASO): After ASO the LV becomes the systemic pumping chamber.

Hence the operation is performed before the LV wall thickness regresses, i.e. before 3months.

ASO consists of ( ref .fig 16.2 A –D ): 1) appropriately dividing both MPA & aorta, 2) transfer of

coronary arteries(as buttons) from proximal aortic stump to the proximal MPA stump, 3) anastomosing

distal aorta ( attached to the systemic arterial tree ) to the proximal MPA stump ( which is originating

from LV & now called neo aorta ) and 4) anastomosing reconstructed proximal aortic stump( originating

from RV & now called neo MPA ) to the distal MPA . (Pulmonary is brought anteriorly by a surgical

technique called Lecompte maneuver) 5) closure of ASD.

Of all these steps, transfer of coronary buttons from the original aorta to the neo aorta is the crucial step.


Fig.16.2A&B: Diagrammatic representation of surgery for d TGA


Fig.16.2C: Diagrammatic representation of surgery for d TGA


Fig.16.2D: Diagrammatic representation of surgery for d TGA

CPB can be conducted by one of the following methods:

i) Continuous CPB: with bicaval cannulation at temperature of 220C – 25

0C. This is the most preferred

method today

ii) Near continuous CPB: with single caval cannulation at temperature of 220C – 250C and circulatory

arrest for closure of ASD

iii) Total circulatory arrest: cooling and rewarming is with the help of CPB .The main operation is

performed during the circulatory arrest.

Aortic purse string is placed as distally as possible. Cave are directly cannulated. Ductus is always

ligated. RSPV is used to vent the left heart. Dissection is carried around aorta & MPA. The dissection

around right and left pulmonary arteries till their first branches is also required and may be performed on

CPB. Cardioplegia is delivered through aortic root. A surgeon may use cardioplegic arrest time only for

reconstructing aorta and for closing ASD and perform reconstruction of MPA on a perfused heart after

release of cross clamp.


4) Atrial Switch Operation: When a patient presents at an age of 3 months or more, regression of the

LV wall thickness is complete and the LV can no more be used as a systemic ventricle. The RV has to be

retained as a systemic ventricle. This is achieved by re-routing the blood in the atria. The rerouting is

performed using atrial tissue (Senning’s Operation; ref. fig. 16.3) or using autologous pericardium

(Mustard’s Operation)

Fig16.3 A: Diagrammatic representation of atrial switch operation (Senning’s operation)


Fig 16.3B: Diagrammatic representation of atrial switch operation (Senning)


Following an atrial switch operation (ref. fig. 13A &B) RA becomes a pulmonary venous atrium

(and the LA is the systemic venous atrium), hence, when CPB is used, the cave are cannulated

directly and as distally as possible. When hypothermic circulatory arrest is used for correction,

after the correction circulation is restarted by inserting the venous cannula into RA appendage

(which is now the pulmonary venous atrium) gently massaging the heart and ventilating the

lungs. Massage and ventilation pushes the systemic venous blood across the pulmonary circuit &

allows adequate venous return.

4) Rastelli Operation: When LVOT obstruction is present, it can be relieved by either resection

of muscle band or with a valved conduit placed between LVOT and MPA. Patients with LVOTO

can have a previously constructed BT shunt, and will require a take down prior to intracardiac

correction.

5) Rapid two stage correction: When a baby presents at an age of 3-4 months, the LV muscle

regression has already started. In such situation the LV regression is halted and the LV wall-

thickness is restored by performing MPA banding, initially. The Arterial switch operation is

performed 7 to 14days later. Banding is also performed if a neonate has multiorgan failure.


17.Coronary Artery Disease

Classification: Congenital: anomalies of coronary artery origin, course and distribution

Acquired: Atherosclerosis (atheroma = plaque, sclerosis = hardening) is the most common cause

Other names for atherosclerotic coronary artery disease are: Ischemic Heart Disease,

Atherosclerotic Heart Disease

Applied Physiology: The salient features are

1) Heart pumps (Cardiac Output- CO) in an adult, about 5 liters of blood per minute. This output changes

according to the needs of the body.

2) Heart consists of three layers – Epicardium, Myocardium, and Endocardium. Of these, myocardium

does the work (of pumping) requiring maximum amount of oxygen. Hence, the major blood supply is to

myocardium.

3) In lower animals like frog, heart’s requirements for oxygen and nutrients are met with by blood passing

directly from ventricular cavity to myocardium. But in humans, myocardium can obtain its nutritional

blood requirement only through coronary arteries. This coronary blood supply is about 250ml per minute.

4) The distribution of blood supply to various parts of the heart is according to work performed by a

cardiac chamber. Work Performed = Pressure generated by the chamber x Heart rate

As the rate of contraction of all the four chambers is the same, pressure generated by various chambers

decides the blood supply to the chamber. Hence, the major portion (almost 80%) of the coronary blood

supply is to LV myocardium (generating 120 mm Hg pressure).

5) Oxygen supply to an organ per minute = Oxygen extracted per ml x blood supply per minute.

Organs other than heart, at rest extract, on an average, only 35% oxygen from arterial blood. In these

organs, increase in demand for oxygen is met by increasing extraction as well as, by increasing the blood

supply.

But, in case of myocardium, maximum oxygen extraction (75-80%) takes place even at rest. Hence, an

increase in coronary blood supply is the only way of meeting the demand for extra oxygen.

Pathology: Ischemia means deficiency of blood supply. As blood is the sole carrier of oxygen, it also means

reduced oxygen supply. Myocardial ischemia is due to a discrepancy between demand and supply of

oxygen.

Increased Demand: hypertension, exertion (usually matched by supply)

Decreased Supply: (cause: result)

1) spasm or stenosis of coronary arteries or ostial stenosis: decreased flow

2) single coronary artery : reduced flow at the terminal branches

3) abnormal origin from PA: shunts off blood from myocardium to PA

4) coronary artery – venous fistula : coronary arterial blood is diverted into veins

Cause number 1 is an acquired cause, while number 2to 4 are congenital causes. Atherosclerotic heart

disease is the most common cause of coronary artery stenosis. Other causes are syphilitic heart disease

(ostial stenosis) calcific AS (ostial stenosis) and aortoarteritis.

Pathophysiology: Flow through a vessel is proportional to fourth power of its radius (F∝ R4)

Whenever a blood vessel gets blocked, collateral vessels develop (ref. fig. 17.1)


Fig. 17.1: Chronic arterial block

When the combined blood flow through the block and the collateral vessel is inadequate to meet the

oxygen demand of the tissue, ischemia is produced. Extreme ischemia results in infarction. Severity of

ischemia / infarction depends upon severity of block, acuteness of block (i.e. whether or not collaterals

have developed), site of the block on the coronary artery. (many use the words ‘block’, ‘stenosis’,

‘narrowing’ interchangeably).

Severity of block: Blocks are described on the basis of %age narrowing of diameter.

Fig. 17.2: Severity of block

Blocks are usually described in the multiples of 10 (i.e. 40%, 60%. not 47% or 63%). More than 90%

narrowings are described as 95%, 99% or 100%.

Certain commonly used terms w.r.t. blocks:


Significant Block: narrowing is 50% or more (i.e. lumen is < 50% of original diameter.)

Critical Block: narrowing is 70% or more (i.e. lumen is <30% of original diameter)

Subtotal Block: narrowing seems 100% on angiogram but still antegrade flow is observed.

Total Block : 100% narrowing with no antegrade flow.

Site of Block: (ref to fig 17.3, 2.13 &2.14)

Fig.17.3: schematic presentation of coronary artery anatomy

From surgical point of view, importance of a coronary artery is according to the area of myocardium

supplied by the artery. Obviously, Left Main artery (LM) is most important artery; and between S1 & Sn,

S1 will be more important as it supplies a larger area. The LM; LAD, D1&D2; left circumflex, OM1&

OM2; RCA, PD& PLV and Ramus Intermedius are considered as major vessels.

Terminologies used in CABG surgery:

Proximal Block: block is prior to the first branch of the artery. As the block is prior to even the first

branch, intra coronary collaterals do not develop.

LM Equivalent block: Block is in the proximal LAD & proximal LCx. A patient with these blocks has a

physiology & clinical picture like a LM block.

During a normal LV contraction all the myocardial segments move towards the center of the LV cavity

and this movement depends on the vascular status of the myocardium. LV contractility can be assessed

with 2Dechocardiography or with LV angiography.

LV contractility is classified according the speed and direction of the movement of the LV wall.

Normal kinesia: movement in a normal manner – normal myocardium

Hyperkinesia: movement at brisk speed – compensation, tachycardia

Hypokinesia: movement is less or slow – suggests an ischemic myocardium


Akinesia: no movement – suggests infarction

Dyskinesia: movement is away form the center of LV cavity i.e. in opposite direction to a normal

movement – suggests post infarct thin fibrous scar.

The various myocardial contractility patterns are expressed as Regional Wall Motion Anomalies

(RWMA).

Fig.17.4A: LV wall motion: normal & abnormalities


Fig.17.4B: LV wall motion : dyskinesia

Ischemia produces angina (i.e. pain) which can worsen slowly or suddenly and incapacitates the patient.

Due to infarction myocardial contractility decreases and ejection fraction falls. The LV is unable to

increase cardiac output in response to exertion. With fall in LVEF the compliance of the LV also falls and

the LVEDP rises. Back pressure effects now set in (see chapter 4 on MS). The patient now starts

complaining of dyspnoea.

Treatment: As ischemia is due to discrepancy between demand and supply, treatment is directed at

a) decreasing demand and or b) increasing supply

A) Medical: medical treatment is directed at

a) reducing the blood pressure and thereby reduce myocardial work.

b) increasing collateral blood flow

This is achieved by

reducing myocardial contractility & heart rate : β blockers, Carvedilol

reducing SVR : vasodilatation through calcium channel blockers or ACE inhibitors

treating coronary spasm: nitrates

Decreasing Demand Increasing Supply

Indirect

Methods

( non specific methods)

relief of stress

weight reduction

reducing activities

treatment of diabetes

treatment of anemia

yoga

( improve collateral flow)

regular exercise, stoppage of smoking

vasodilators : nitroglycerine, calcium channel

blockers

surgery: historical techniques

trans myocardial revascularisation

Direct

Methods

(decreases myocardium O2

requirement)

βBlockers

treatment of hypertension,

thyrotoxicosis and anemia

( action on the blocked coronary artery)

thrombolytic therapy

angioplasty

surgery : endarterectomy

CABG


While β blockers increase SVR, calcium channel blockers and ACE inhibitors reduce SVR. Patient’s

SVR will depend upon the sum total of drug effect plus patient’s vascular status.

Other components of medical treatment ( & their relevance to CPB) are

Antiplatelet drugs : Aspirin , Clopidogrel ( increased postoperative bleeding)

Cholesterol reducing drugs: Statins ( not relevant for CPB)

Antioxidants: reduce stress (not relevant for CPB)

B) Revascularisation: when coronary blocks are significant & multiple, they are in the major

vessels, and patient has evidence of ischemia, patient is advised revascularisation.

Revascularisation can be performed by

1.Angioplasty: it is performed with balloon and stent. Blocks which are discrete, few, and in proximal

vessels are ideal for angioplasty

Fig. 17.5: Balloon Angioplasty with stenting

Complications: a) Failed angioplasty: failure to pass across obstruction or dilate the blocking plaque

b) Dissection of the plaque: producing an acute, 100% obstruction of the lumen .This is an indication for

emergency CABG. Patient could be in cardiogenic shock and on heavy doses of antiplatelet drugs

2.Surgery : The surgical options for any arterial block are

Endarterectomy

Excision grafting

Bypass grafting

a)Endarterectomy: Removal ( i.e. ectomy) of the endothelial plaque is the most logical treatment. In the

early years of coronary artery surgery, this was the only treatment offered to the patient. Endarterectomy

as the sole treatment for CAD is not feasible as many arteries are not surgically targetable (e.g. LM, LCx)

and as atherosclerosis is a generalized disease, a plaque is rarely discrete for a surgical excision.


Fig 17.6: Technique of endarterectomy

A: arteriotomy B: dissection between plaque and the arterial wall

C: gentle traction on the plaque D: plaque removed proximally

E: plaque removed distally

Currently, coronary endarterectomy is performed only to facilitate performance of distal anastomosis

during bypass grafting operation. This is required when target vessel lumen is less than 1mm in diameter

or the plaque is too hard to suture. Patency of anastomosis falls when endarterectomy is performed. Distal

dissection of coronary artery can take place due to endarterectomy.

b) Excision grafting: consists of excising the blocked segment of the artery and replacing it with an

interposition graft. This treatment is not feasible for CAD as many arteries are not accessible & this

treatment results in sacrificing of branches.


Fig17.7 Excision Grafting

Blocked artery Excision grafting

c) Bypass grafting: In a bypass grafting operation the block in the artery is untouched and a parallel

channel (graft/ conduit) is created between a vessel proximal to the block to the vessel distal to the block.

Fig. 17.8: Bypass Grafting

Thus component of a bypass operation are,

a) Proximal vessel: should be large enough to provide required amount of flow and also, should be

healthy enough to perform anastomosis. Ascending aorta or its main branches are the common

proximal anastomotic sites.

b) Distal vessel: This is the coronary artery distal to the block. This also called target vessel. The artery

chosen should be large enough (> 1.5mm in diameter) for anastomosis and, as far as possible,

healthy & subepicardial (easily seen). Proximal part of a coronary artery is chosen for

anastomosis. The usually grafted vessels are mid LAD, D1& D2; Ramus intermedius;

OM1&OM2; PLV, Third part of RCA and PD.

c) Graft or Conduit: A conduit should be able to withstand arterial pressure, and should remain patent for

many years.

Conduits can be classified as


For coronary bypass surgery only autologous conduits are used. The conduits are classified as

a) Arterial Conduits: 1) Left Internal Mammary Artery –LIMA (currently renamed as Left Internal

Thoracic Artery – LITA)

2) Right Internal mammary Artery – RIMA (Currently renamed as Right Internal Mammary Artery –

RITA)

3) Radial Artery

4) Other arteries: like gastroepiploic artery, inferior epigastric artery are rarely used.

b) Venous Conduits: Great Saphenous Vein, Lesser Saphenous vein.

1) LIMA & RIMA: These are branches of respective subclavian arteries. Each IMA runs on the posterior

surface of chest wall, about 2.5 cm lateral to sternum and supplies blood to sternum and chest wall.

Distally, at the level of diaphragm IMA divides. LIMA and RIMA are dissected (‘harvested’) from chest

wall from subclavian vein superiorly to diaphragm inferiorly. From durability point of view, LIMA and

RIMA (in that order) are the grafts of choice for CABG. (ref fig 17.9)

2) Radial artery: Is the next popular arterial graft. As LIMA is almost always harvested, and it requires

surgeon positioned on the right side of the patient, left radial artery is usually harvested. (ref fig 17.10)

3) Great Saphenous vein: is the superficial vein of the lower limb and extends from medial malleolus to

the sapheno- femoral junction in the groin. Depending upon the number of grafts required, a variable

length of vein is harvested. (ref. fig. 17.11).


Fig 17.9: LIMA & RIMA: course

Fig 17.10: Radial artery harvested


Fig. 17.11: Great Saphenous vein in lower limb with important landmarks

Due to valves, a venous graft is sutured in such a manner that the distal end of the graft is sutured to aorta

(proximal anastomosis) and the proximal end of the graft is sutured to the coronary artery (distal

anastomosis). Because of change of proximal –distal ends of vein for anastomosis, the graft is called

‘reverse’ saphenous vein graft.

A conduit could be

Pedicled: attached to its parent artery or origin: such a graft lasts better but has a restricted reach.

Free: detached from its origin: such grafts can reach any part of the heart. Durability of a free graft is

inferior to a pedicled graft.

Radial artery and venous conduits are always a free graft


Fig17.12: various types of conduits

A conduit can also be classified as

a) skeletonised: conduit without surrounding fat fascia and venae commitantes. Skeletonised conduits are

longer in length

b) non-skeletonised (with Pedicle): conduit with surrounding fat fascia and venae commitantes

Procedure: CABG surgery can be performed by a variety of techniques as shown in the flow chart

below. A brief description of the various on-pump techniques is:

1) Intermittent Cross Clamp Technique: On CPB, patient temperature is maintained above 320 C to

avoid spontaneous fibrillation & to facilitate defibrillation, as and when required. Revascularisation of the

heart is performed in a cyclical manner. Each cycle consists of the following steps: on CPB, the aorta is

cross-clamped, and the heart is fibrillated with a fibrillator. Left heart is vented, usually, through aortic

root. A distal anastomosis is performed with in 15 minutes of cross clamp time. Cross clamp is released

and heart is defibrillated. While heart is beating empty on CPB, the proximal anastomosis of the

corresponding graft is performed. The cycle is repeated to complete myocardial revascularisation.

2) On–Pump Beating Heart Technique: This technique uses CPB as well as a stabilizer (Octopus).

Cardioplegia is avoided and heart is empty-beating. As the heart is kept beating, the patient temperature

has to be above 320 C

3) Cardioplegically Arrested Heart Technique (ONCAB): This is one of the oldest and most widely

used technique. Due to coronary artery block, cardioplegia may not be evenly distributed hence; various

cardioplegia delivery techniques are used. Some of them are:

a) antegrade followed by retrograde cardioplegia at each dose

b) antegrade to arrest the heart and repeat only retrograde cardioplegia


c) antegrade and retrograde cardioplegia together at each dose

d) any of the techniques described above plus cardioplegia is delivered through grafts after each distal

anastomosis

Insertion of retrograde cannula: This can be performed prior to starting the CPB or on CPB. A

purse string is placed on RA anterior and inferior to the venous purse string. The RCP cannula is inserted

guided by the left index finger, which is placed on the coronary sinus. Blood loss that occurs during

insertion is sucked through cardiotomy suction. As this technique involves retraction of heart (while

placing the guiding finger over CS), it may result in hypotension, hence some surgeons place the RCP

cannula on CPB. While inserting the cannula on CPB, RA should be kept slightly full as to avoid air

locking of the venous cannula and to keep the mouth of coronary sinus open.

On-Pump CABG is performed through median sternotomy.

4) Off Pump Coronary Artery Bypass Grafting (OPCAB): In this technique the entire operation is

performed without using heart lung machine. Gadgetry used are –tissue stabiliser (e.g. OCTOPUS) to

steady the tissue around the target coronary artery, tissue retractors (e.g. STARFISH and URCHIN), mist-

blowers (to drive away blood from the operating field) and intra coronary shunts (to maintain distal

myocardial perfusion).

As lifting and retraction of heart results in hypotension, the initial distal anastomoses are

performed to Diagonal and LAD which require the least lifting and retraction. Totally occluded vessels

are next grafted. OM anastomosis, which requires the maximum retraction, is performed the last.

The proximal anastomoses are performed by applying a single side biting clamp but aorta is punched for

holes one at a time.

Any hemodynamic instability during surgery may require establishment of CPB (conversion).

Amongst all the coronaries, the posteriorly situated target coronaries (OM) are most likely to require

establishment of emergency CPB.

Large heart (difficult to retract); unstable angina, lower EF or left main disease (hemodynamic

instability); deeply situated coronary artery or redo coronary (technically difficult) surgery are some of

the indications for conversion to ONCAB surgery.

Off-pump surgery can be performed through right (for RCA) and left (LAD & D) lateral

thoracotomies or through subcostal incisions and is called ‘MICAS’- minimally invasive coronary artery

surgery or MIDCAB – minimally invasive direct coronary artery surgery.

What ever may be the technique of surgery, a CABG operation consists of the following steps:

a) Conduit Harvesting: After sternotomy LIMA and, if required, RIMA is harvested. For harvesting

IMA many surgeons widely open the pleura. Simultaneously, other conduits are harvested as per

requirement. Great saphenous vein graft (RSVG) can be harvested from thigh (large caliber vein but

deeply situated in the fat) or leg (smaller caliber but superficial vein). LIMA is the most popular graft for

which surgeon has to be on the right side of the patient .Hence radial artery conduit, if required, is

harvested from left side.

To facilitate the dilatation of the conduits, anesthesiologists administer one or more of the following

vasodilators intravenously- NTG, diltiazem, nicorandil. Administration of vasodilators will change SVR

and thereby, the arterial pressure during CPB.

b) Distal Anastomosis: Once the conduits are harvested, conventional CPB is instituted (except in

OPCAB). In an atherosclerotic aorta, aortic cannulation may result in plaque embolisation. Hence femoral

artery may be chosen for cannulation. Patient is usually cooled to 280 C. conventionally, under

cardioplegically arrested heart; all distal anastomoses are performed first. As to avoid injury to LIMA,

anastomosis placed on the posterior surface of heart ( OM territory )are performed first, next are the

anastomosis placed on the inferior surface( PD, PLV territory ) and lastly, are the anastomosis on the


anterior surface( D&LAD). Cardioplegia can be repeated after each distal anastomosis or according to the

time elapsed after the last cardioplegia.

.

c) Proximal anastomosis: Proximal anastomosis can be performed prior to distal anastomosis,

particularly in OPCAB surgery.

Aorta is the preferred site for proximal anastomosis. After completing all the distal anastomoses, aortic

cross clamp is released. Deairing of the heart is not required as no cardiac chamber is opened. A partial

clamp is applied on the aorta and all the proximal anastomosis are performed, serially. For each proximal

anastomosis, the aorta is incised and a special punch is used to punch out a circular aortotomy. While the

proximal anastomoses are being completed, patient is rewarmed back to normal temperature.

Before starting the proximal anastomosis, the graft lengths require adjustment. During the distal

anastomosis stage, graft lengths are decided empirically. But prior to proximal anastomosis, graft length

should be adjusted in such a manner that after cessation of CPB, on a full beating heart, the graft is neither

redundant nor stretched. For achieving this goal, prior to refashioning a graft, the surgeon asks the

perfusionist to fill the heart and mimics the ‘lie’ of the graft on a ‘full’ heart.

The perfusionist should fill the heart carefully taking into consideration myocardial contractility &

reservoir level.

Complications: 1) Bleeding: control of bleeding from distal anastomosis on posterior surface may

require reinstitution of CPB.

2) Perioperative infarction: leading to cardiogenic shock. One of the causes of perioperative infarction is

graft blocked, kinked or stretched. CPB may have to be reinstituted to redo the anastomosis.

Following chart enlists various events during CABG and their CPB implication

Surgical step Event CPB implications

Sternotomy

right pleura open slow volume loss ( 4th space)

during CPB

IMA harvesting ipsilateral pleura open slow volume loss ( 4th space)

during CPB

vein harvesting harvested from thigh femoral artery not available for

arterial cannulation

conduit harvesting : NTG veno dilatation venous stasis: poor venous return

conduit harvesting :

Nicorandil, Diltiazem

arterial dilatation fall in SVR : low perfusion

pressure

OM anastomosis heart retracted to right sudden decrease in venous return

Lifting of heart Dislocation of RCP cannula

IVC kinking

Ineffective RCP

Decreased venous return if

2stage cannula is not used

OM anastomosis head low ↓ venous return

OM anastomosis Pericardial slitting or window resulting

in opening of right pleura

slow volume loss ( 4th space)

during CPB

PD, PLV anastomosis head low ↓ venous return

Partial clamping of aorta obstruction to the aortic cannula ↓ arterial pressure

↑arterial line resistance

Partial clamping of aorta remaining aortic lumen very small ↓pressure coronary perfusion


Clinical assessment chart for CAD

Parameter Findings Comment/Method of assessment

Age Above 50yrs.

Body weight

&

Height

Obesity is common.

Body Volume increased only in patients with

low (< 30%) EF , LV aneurysm

CVP

( liver enlargement, effusions are

uncommon)

Hemoglobin Normal

low in patients directly shifted from cathlab,

on preop IABP,

blood investigation

Plasma

Volume

Normal

SVR increased due to atherosclerosis,βblockers

decreased due to NTG, Cal Ch Blockers, ACE

inhibitors

diastolic BP, warmth of limbs, lower

limb venous filling

Organ

Function

Liver: cirrhosis due to associated

alcoholism

Brain : vascular insufficiency due to

atherosclerotic affection of cerebral blood

vessels

Kidney : renal artery stenosis, medical renal

disease due to chronic hypertension and

diabetes



hemiplegia

S. Creatinine

Arterial Tree Due to atherosclerosis all arteries are

1) rigid 2) can be significantly blocked

Check all pulses, vascular Doppler

studies

Additional

Diseases

Diabetes Mellitus

Chronic Obstructive Pulmonary Disease

Arterial

cannulation

Aorta :

Femoral : some use in all cases

check for TE Echo report for aortic

calcification or plaques

Venous

cannulation

Single, two-stage venous cannula. check for return during OM

anastomosis

Cardioplegia

see the flow chart

Arterial

Pressure

should be high ( > 60) on bypass to over

come the resistance offered by the rigid

arteries , blocks in the carotid artery system

during proximal anastomosis partial

clamping of aorta may not provide

adequate antegrade coronary perfusion

Venous return just adequate. check CVP before going on CPB

Left Heart Aortic root suction


Return

Preop

medications β blockers, CCB, ACE inhibitors, Nitrates,

Antiplatelets.

Heparin, IABP,

Thrombolytics

Heparin resistance

BT, CT, INR

Previous

interventions

PTCA

CABG


18.Mechanical Complications of CAD

Pathology: Myocardial infarction results in tissue necrosis. Depending upon the extensiveness of the necrosis,

adequacy of healing & quality of scar the following complications are seen.

1) Rupture of free LV wall

2) Rupture of IVS: post infarction VSD

3) Ischemic MR

4) LV aneurysm

Rupture of free LV wall: These patients rarely reach for surgery. Chronic ruptures behave as LV aneurysm

Post Infarction VSD: Results from severe necrosis of IVS. The common sites of VSD are

1) apical region 2) posterior inferior region of IVS

Pathophysiology: Acute development of VSD results in a sudden imposition of pressure and volume

overload on the RV and LV volume overload. Compromised LV function due to MI worsens the

hemodynamics (Ref Ch 12. P68 for details of hemodynamics of VSD). Patient is in severe cardiogenic

shock and pulmonary edema.

Timing of surgery is crucial. If patient is taken up immediately for operation, the surgical team has to deal

with a patient with severe cardiogenic shock and friable myocardium for suturing of VSD. Delay in

surgery is associated with kidney-liver-lung damage. Hence, patient is first, stabilised with ventilatory

support, IABP, after-load reducing agents, inotropes and taken up for surgery with in 15 days.

Conventional CPB is instituted with Bicaval cannulation. Approach to the VSD is through the LV infarct.

SVC & IVC are snugged just prior to opening of the LV. VSD is closed with patch. Simultaneous CABG

may also be performed. Due to extensive block and lack of viable myocardium, LAD rarely requires

grafting.

Clinical assessment chart for CAD with mechanical complications

Parameter Findings Comment/Method of assessment

Age Above 50yrs.

Weight &

Height

Obesity is common.

Body Volume increased in pulmonary and systemic circuit

as patient in Pulmonary edema & cardiogenic

shock

CVP, PA Diastolic pressure

(liver enlargement, effusions are

uncommon)

Hemoglobin Normal

low in patients on IABP

blood investigation

Plasma

Volume

increased

SVR increased due to atherosclerosis, cardiogenic

shock

decreased due to IABP, SNP.

diastolic BP, warmth of limbs,

lower limb venous filling

Organ

Function

Liver: cirrhosis due to associated

alcoholism

Brain :vascular insufficiency due to

atherosclerotic affection of cerebral blood



hemiplegia


Ischemic MR: Can be of mild to severe degree.

MR is mainly due to dysfunction of papillary muscle as a result of

1) Ischemia 2) Infarction 3) Rupture

Patient is in cardiogenic shock and pulmonary edema when MR is more than moderate in severity. Due to

acuteness of MR, compensatory mechanisms (Ref. Ch.5) are also absent.

Treatment of MR is as per the cause and severity of MR:

CABG only: when MR less than moderate and is due to ischemia of papillary muscle. Myocardial

revascularisation improves papillary muscle function and MR disappears. CPB management is as in any

CABG case.

CABG with MV Repair: when MR is more than moderate and is due to ischemia or infarction, MV is

repaired. Due to acute MR, LA is small and visualization of MV is difficult. Due to small LA, trans-septal

approach may be adopted.

CABG with MV Replacement: is performed when MR is severe and is due to papillary muscle infarction

or rupture.

Whenever MV surgery is performed bicaval cannulation is performed. Snugging of SVC & IVC will be

required if trans-septal approach is used. Coronary sinus lies just posterior to mitral annulus and

placement of retrograde cannula may affect the visibility of mitral valve and ease of placing sutures on

the posterior annulus. Hence retrograde cardioplegia may be avoided.

Distal anastomosis part of CABG (sometimes the entire CABG) is performed first. This ensures adequate

cardioplegia delivery through grafts. Also, when grafting to OM & or PD-PLV is required, lifting &

retraction of LV is safe .Lifting and retraction of LV could prove difficult, if not dangerous, in the

presence of a high profile prosthetic valve (e.g. any bioprosthesis), resulting in LV rupture.

Clinical assessment chart for Ischemic MR is as mentioned above for post infarct VSD

vessels

Kidney : renal artery stenosis, cardiogenic

shock

S. Creatinine

Arterial Tree Due to atherosclerosis all arteries are

1) rigid 2) can be significantly blocked

Check all pulses, vascular

Doppler studies

Additional

Diseases

Diabetes Mellitus

Chronic Obstructive Pulmonary Disease

Arterial

cannulation

Aorta :

Femoral : will be used for IABP

Venous

cannulation

Bicaval cannulation with snugging

Cardioplegia See the flow chart

Arterial

Pressure

should be high ( > 60) on bypass to over

come the resistance offered by the rigid

arteries , blocks in the carotid artery system

Conventional or Modified ultra

filtration will be required

in view of renal failure and CCF

Venous return Adequate. check CVP before going on CPB

Left Heart

Return

Through LV

Aortic root: after closing LV

Preop

medications

SNP, NTG, Heparin, IABP,

Thrombolytic

Heparin resistance

BT, CT, INR

Previous

interventions

PTCA

Device closure of VSD


LV Aneurysm: When myocardial infarction heals with a thin scar, the scar is unable to withstand the LV systolic

pressure and bulges outwards during systole. As a result of the dyskinetic expansion, LV aneurysm is

produced.

Due to the low resistance offered by the aneurysm, the LV empties part of its output into the aneurysm

rather than in the systemic circulation. Due to poor effective ejection patient develops a chronic

progressive low output state.

If a papillary muscle is also involved in the aneurysm then changed alignment of the papillary muscle

results in MR. The aneurysm can harbor clots and the aneurysm wall could be a source of ventricular

tachycardia.

Fig. 18.1: Development of LV aneurysm

Treatment of LV aneurysm is to close the opening of aneurysm with a patch (Dorr Procedure). Intra-

pericardial adhesions are encountered, especially around the aneurysm. Conventional bypass using two

stage venous cannula is instituted. Pericardial adhesions are released and through LV aneurysm the

opening into the LV cavity is closed with a patch. Additional CABG, MVR may be required.

Clinical assessment chart is as mentioned above for post infarct VSD


19.Aneurysm of Sinus of Valsalva

Etiology: 1. Congenital – involves either, right coronary sinus (75%) or non coronary sinus (25%). Left

coronary sinus is rarely involved. When aneurysm is of congenital etiology, aneurysm of sinus of

Valsalva (ASOV) is an isolated feature of the aorta, the rest of the aorta is normal.

2. Acquired - could be due to Marfan’s Syndrome, infective endocarditis, aortic dissection or

syphilis. In acquired ASOV any and all the three sinuses could be involved. The rest of the aorta

is also diseased.

Pathology & Pathophysiology: The description below mainly pertains to congenital ASOV. A congenital

ASOV develops due to defect in the aortic media. Though of a congenital variety, at birth no dilatation is

found. Due to persistent & long standing high aortic pressure, the weakened sinus dilates into an

aneurysm. An unruptured aneurysm compresses or dissects into adjoining structures to produce RVOT

obstruction, RCA compression and conduction blocks.

ASOV can rupture into adjoining structures (ref. fig 19.1) resulting in a high volume shunt. The aortic

annulus is inferior to pulmonary annulus and as ASOV grows inferiorly, ASOV never ruptures into PA.

ASOV is associated with VSD and or AR.

Fig19.1: Superior views of heart to show ASOV rupture sites


Rupture of ASOV results in a sudden, windsock like, fistulous communication between a high pressure

aorta (120/80 mm of Hg), and a low pressure RV (15/0 mm of Hg) or RA (mean 5mm of Hg). The

difference in the pressures between the two chambers is gross in systole as well as in diastole. This results

in a large left to right shunt, in systole and diastole. This large and sudden shunt results in a severe

volume and pressure over load on the RV, resulting in RV failure. Associated AR and or VSD worsen the

hemodynamics.

Fig: 19.2: Hemodynamics of RASOV

ASOV has been reported between 5 to 80 years of age with an average age of 30years. Unruptured ASOV

is rarely symptomatic and is detected accidentally. A ruptured ASOV quickly pushes a patient into gross

CCF and early death. Treatment: A) Medical treatment : is mainly for treating the gross failure. After-load reducing agents and

diuretics form the mainstay of the treatment.

B) Interventional treatment: isolated reports of closure of ruptured ASOV are available.

C) Surgical Treatment : Surgery is performed on semi-emergent basis. The windsock like fistulous

communication is closed through one of the chambers ( unicameral approach) or through both the

chambers ( bicameral approach). The fistulous tract can be closed by combination of following methods

a) ligating the sac b) transfixing the base of the sac c) patching the aortic opening of the sac.


Conventional bypass with bicaval cannulation and snaring of SVC & IVC is required. Early cross

clamping of aorta is required to avoid VF and LV distension on CPB. If patient has RASOV into RA, RA

will remain full even on total CPB, till aorta is cross-clamped. Cardioplegia is delivered through coronary

ostial or by retrograde route . Antegrade aortic route cardioplegia can be delivered only in a case with

RASOV into RA, after opening the RA and clamping the sac.

Associated VSD and AR are treated simultaneously.

Clinical assessment chart for RASOV

Parameter Findings Comments

Age Around 30yrs

Body weight

&

Height


Body Volume pulmonary circuit volume overloaded

with CCF, systemic venous circuit volume

overloaded

PH status


Hemoglobin Normal or Low nails, blood investigation

Plasma Volume increased

SVR low Low diastolic BP, high volume

brisk pulses


Kidney: dysfunction


Arterial Tree normal

Arterial

cannulation

Aorta

Venous

cannulation

Bicaval with tapes irrespective of the

approach


Retrograde

Arterial Pressure Could be low ( < 60) on bypass


Left Heart Return Sump-sucker in RSPV/IAS

Preop medications Digoxin, diuretics

Vasodilators


Previous nil


interventions

Special precaution On full bypass heart remains full

Early cross-clamping of aorta is required MPA, RA full

High PAD pressure


20.Left Atrial Myxoma

Introduction: This is a benign tumour of the heart, most commonly, arising from the left atrial side of fossa

ovalis.

Pathophysiology: The tumour has an external appearance of a bunch of small (1to3 mm) grapes. The tumour

could be pedunculated (i.e. with a stalk) or sessile (i.e. without a stalk). A tumour could be as large as the

LA cavity. Whatever be the type, the tumour occupies the LA cavity resulting in obstruction to

pulmonary venous flow into LA and or mitral- inflow. A pedunculated tumour can prolapse (i.e. leave its

natural anatomical position) during diastole into mitral valve or even LV, resulting in severe LV inflow

obstruction. A prolapsing tumour can prevent normal closure of MV leaflets, resulting in MR, in addition.

Fig. 20.1: Diagrammatic representation of LA myxoma.

The hemodynamic problems imposed by LA myxoma are similar to those of MS, namely, back pressure

effects giving rise to severe pulmonary venous congestion and decreased forward flow.

As the tumour is like a bunch of grapes, embolisation of the tumour is common and it could be the

presenting feature.

Treatment: Excision of tumour on CPB is the treatment of choice.

The most preferred approach to the myxoma is a trans RA-trans septal approach, though in the past,

left atrial approach was tried.


Fig.20.2: Approaches to LA

Bicaval cannulation with snugging of cave is required. RA is opened through a logitudinal right

atriotomy parallel to right a-v groove. Incision is placed at the posterior margin of fossa ovalis (FO)

and the myxoma is removed en mass with the septum at fossa ovalis.LA is thoroughly washed (check

for cardiotomy suctions). The approach offers inspection of all the four chambers of heart for any

additional myxoma. The defect at fossa ovalis is closed with a patch like in an ASD.

Clinical assessment chart for a case with LA myxoma


Age Around 30yrs

Body weight

&

Height

Normal

Body Volume Pulmonary circuit volume overloaded

with CCF, systemic venous circuit volume

overloaded

PH status

CVP, liver enlargement,


effusions


Plasma Volume Increased

SVR Normal, high in severe cases diastolic BP,

Organ Function Liver: chronic passive congestion LFT: raised bilirubin and SGPT

Arterial Tree normal

Arterial cannulation Aorta

Venous cannulation Bicaval with tapes irrespective of the

approach


Arterial Pressure Could be high( > 60) on bypass


Left Heart Return Sump-sucker in MPA

Preop medications Digoxin, diuretics Check for potassium levels

Previous

interventions

Recurrence of myxoma is known

Special precaution Heart distends if not vented

Avoid sucking saline washes into cardiotomy

suction


Concept, script and diagrams in this e book

by

Dr. Anil G Tendolkar

(agt)

• Formerly Professor of Cardio Thoracic Surgery

KEM Hospital, Mumbai, India.

• Formerly Professor & Head, Department of Cardio-Thoracic Surgery

LTMG Hospital, Sion, Mumbai, India

• National Coordinator for Post Graduate Diploma in Perfusion Technology

(run by IACTS) since 1995

• Currently,

Consultant CV Surgeon at Holy Family Hospital, Mumbai& Price Aly Khan Hospital Mumbai

Address of communication: [email protected]

cpb surgical&clinical orientation

Health & Medicine