Cardiac Anesthesia Part 2

Travis Slade MD

Cardiac Action PontentialPhase Name Event Cellular Ion

Movement0 Upstroke Activation

(opening) of Na Channels

NA in

1 Early Repolarization phase Inactivation of Na channel

Cl inK out

2 Plateau Activation of slow Ca channel

Ca in

3 Final repolarization Inactivation of Ca channels

K out

4 Resting potential Normal permeability restored

Na outK in

Mechanism of Cardiac Muscle Excitation, Contraction & Relaxation

Figure 14-11: Excitation-contraction coupling and relaxation in cardiac muscle

• Preload: diastolic filling volume of the left ventricle (EDV reflects stretch of the cardiac muscle cells)

• Afterload: resistance to ventricular emptying during systole (the amount of pressure the left ventricle must generate to squeeze blood into the aorta

• Frank Starling Law of the Heart - the heart will contract with greater force when preload (EDV) is increased

• Myocardial Contractility - the squeezing force that the heart can develop at a given preload• regulated by:

• sympathetic nerve activity (most influential)• catecholamines (epinephrine norepinephrine)• amount of contractile mass • drugs

Definitions

Left Ventricular Volumes - Definitions

End Diastolic Volume (EDV) Volume at the end of diastole (end of ventricular filling)

End Systolic Volume (ESV)Volume at the end of systole(end of ventricular contraction)

Stroke Volume (SV) = EDV - ESV

*Ejection Fraction (EF) = SV EDV

ventricular norm: 62%

Ejection Fraction is the best indicator of heart performance and disease prognosis

Left

↑ Contractility related to : beta-sympathetic adrenergic nervescatecholamines: epinephrine

norepinephrine

drugs: digitalissympathomimetics

↓ Contractility related to:loss of contractile mass - myocardial Infarction

myocardial muscle disease - cardiomyopathy

drugs: anesthetics, barbiturates

Influences on Myocardial Contractility

Starlings Law of the Heart and Contractility

SV

leftventricular

performance

preload (venous return)

↑ contractility

normal contractility

↓ contractility(heart failure)

Hemodynamic Parameters

General Information EF = SV / EDV normal 65% CO = SV x HR normal (5 – 6L) Ohm’s Law Voltage = current x resistance BP =CO x SVR SVR = MAP – CVP / CO x 80 CPP = DP – LVEDP Coronary blood flow

is almost entirely controlled locally. CBF = CPP/CVR

Cardiac OutputNormal 4 – 6 L/min

Increased CO – Sepsis, tachycardia, increased blood volume, hyperthyroidism, hyper flow states with hepatic or mesenteric shunting

Decreased CO – Bradycardia, dysrhythmias, decreased blood volume, shock, valvular stenosis, cardiac tamponade, decreases inotropy, hypothermia, increased afterload, restrictive cardiomyopathies

Cardiac Index– Normal 2.5 – 3.5 L/min

Pulmonary Artery Pressure

Normal pressure 25/15 mmHg

Pulmonary Artery Wedge Pressure

Correlates with left atrial pressureReflects pulmonary venocapillary

hydrostatic pressureApproximates the LVEDPNormal pressure 5 – 15 mmHg

Parameters

The pressure-volume loop

VIII. NORMAL CARDIAC CYCLE

Phase I: Ventricular diastolic filling; this phase extends from the opening until the closure of the mitral valve. The normal diastolic chamber compliance ( ▲ V/ ▼ P) is high so intraventricular pressure rise is minimal.Frank Starling Law applies.

Phase II: Ventricular isovolumic contraction; phase two extends from mitral valve closure to aortic valve opening.

Intracavity systolic pressure rises rapidly to aortic diastolic pressure. The ventricular volume remains the same.

Law of LA Place radius

Normal Cardiac Cycle

– Phase III: Left ventricular ejection; this phase begins when the aortic valve opens (LV systolic pressure exceeds aortic pressure) and extends until aortic valve closure (aortic pressure exceeds LV end systolic pressure).

– Phase IV: Isovolumic relaxation; this phase extends from the aortic valve closure until mitral valve opening.

EJECTION D C A=MVO 2 ISVOL ISVOL B=MVC RELAX CONTRAC

C=AVO D=AVC A 1 B

Figure 1

PRESSURE VOLUME LOOP

The normal pressure volume loop is shown in Figure 1.

Beginning at point A, the mitral valve opens and rapid ventricular filling begins.

Filling continues to B where following atrial contraction, systole begins and the mitral valve closes.

PRESSURE VOLUME LOOP

The segment AB illustrates the diastolic pressure volume relationship of compliance of the ventricle.

At C, following a period of isovolumic contraction, the aortic valve opens and ejection begins.

Point D, depicts aortic valve closure and the end of systole.

Segment DA is the beginning of diastole – the period of isovolumic relaxation.

CONTRACTIVITY AFTERLOAD

Figure 2

SV

PRESSURE

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Normal loop

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Know : preload

when end-diastolic volume (preload) increases, the LV empties to the previous end diastolic volume. SV increases

when end-diastolic volume (preload)

decreases, the LV empties to the previous end diastolic volume. SV decreases

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Know: afterload

when afterload increases, the heart empties less completely (decreased SV). Both preload and end-systolic volume increase in this case. Ventricular chamber dilates

when afterload decreases, the heart empties more completely (increased SV). Both preload and end-diastolic volume decrease in this case. Ventricular chamber size decreases or “shrinks”.

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Know: contractility

when contractility increases, ventricle empties more completely (decreased end-systolic); and decreased end-diastolic, but not as much as end-systolic, so SV increases

when contractility decreases, end-systolic volume increases; end-diastolic increases, but not as much as end-systolic vol., so SV decreases

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CV formulas Formula SV = CO/HR SI = SV/BSA SVR=(MAP-CVP)80 CO PVR=(PAP-PCWP)80 CO

Normal Values 60-90 ml 40-60 ml/m2 900-1500 dynes/sec/cm 50-150 dynes/sec/cm

Figure 2 re-labels Figure 1: EDV = end diastolic volume,ESV = end systolic volume, SV = stroke volume. SV/EDV = ejection fraction, a global

representation of how well the heart ejects blood (forward and/or backwards!)

PRESSURE VOLUME LOOP

Cardiac Disease

Case Study

65 YOM in excellent physical conditionAcute onset of SOB and chest discomfortTaken to cath lab PA pressures 60-

80mmHGSystolic Pressure 90-110 mmHg

Cont.

Heart cath shows less than 50% lesion in RCA, and SEVERE MR.

What happened? Taken to OR emergently. PA cath pressures just prior to CPB were 80-90

(BAD = of pressures) mmHg and systemic systolic BP was 90-100 mmHg.

Pink frothy sputum in ETT. Difficult to ventilate.

Regurgitant Lesions

Volumn overload of LA or LV

Mitral Regurgitation

Left atrial volume overload secondary to blood flowing back into the LA.

Causes: MI, endocarditis, mitral valve stenosis, dilation of the mitral valve secondary to LV hypertrophy.

Clinical signs: pansystolic murmur at LL sternal border/apex, regurgitation factor >0.6, pulmonary edema, and ↑ PVR

Anesthetic goal: mild ↑ HR , mild decrease in SVR FAST, FULL, FORWARD

Acute vs Chronic MR

Acute MR: No LV/LA enlargement, LVED and LA pressures are higher. SR ususally present

Chronic MR LA and LV are usually enlarged. Pressures are above normal but not severe.

What is the usual rhythm? afib Why? Due to stretch.

AI

Leads to volume overload of the LV causing syncope, angina and dyspnea (CHF)

Decrescendo murmer (why- think of the pathophysiology)

Aortic runoff leads to decreased diastolic BP and hence?

Acutely is usually caused by subacute bacterial endocarditis

Aortic Regurgitation.

Case Study

78 YOM with ground level fall at home Open left femur fracture BP 109/56, HR 110, RR 18, Physical Exam: SEM SAB with hyperbaric tetracaine 4 minutes after block placed BP drops to 85/50,

complains of chest pain and becomes restless. patient then cardiac arrest. What will you give?

What was the lesion and what happened

Aortic Stenosis

Survival based on symptoms if untreated (angina = 5yrs, CHF = 3 yrs, Syncope =1yr)

Ischemia especially threatening in AS setting 2ndary to LVH- pump against force

Must maintain diastolic pressures (decreased SVR= decreased CPP)

Anesthesia Goals:– Avoid increased HR and decreased SVR– Atrial kick (30% kick) VERY important for CO hence

rapid HR and A Fib poorly tolerated.

Stenotic Lesions

Cause pressure overload

Avoid increases in HR and decreases in SVR

Sevo/Iso ; not Des- tachy /Halothane- d/t sensization of catecholamine

Mitral Stenosis causes a fixed CO and increased PP leading to edema and RV failure

Mitral Stenosis

Normal valve 4-6 cm moderate to severe is <2 cm.

Physical Exam will show an rumbling diastolic murmer. Why? Think about the lesion and physiology

Mitral stenosis

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Intra-Aortic Balloon Pumping

The principle is to:1. reduce the afterload and 2. increase coronary perfusion by lowering the

systolic and raising the diastolic pressure. A plastic balloon is placed in the thoracic aorta

and alternately inflated and deflated in time with the heartbeat.

This procedure is a short term measure and is only used in specialized centers.

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Intra-Aortic Balloon Pumping

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Intra-Aortic Balloon Pumping

1. Medical use has been confined mainly to patients with cardiogenic shock following myocardial infarction and

2. In patients with unstable angina have been treated by counterpulsation before coronary arteriography.

3. Balloon counterpulsation has also been used preoperatively in patients going to surgery with high-risk coronary artery disease and poor left ventricular function.

4. It has also been used in patients with acute mitral regurgitation and 5. Rupture of the ventricular septum with myocardial infarction or

trauma.

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Intra-Aortic Balloon Pumping

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INTRODUCTION

13 million Americans (7%) of population have coronary artery disease.

Half of all deaths related to cardiovascular disease result from CAD.

Coronary Artery disease is the leading cause of death among American men and women

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Facts on Heart Disease 1 in 3 adults – both men and women - has some form of cardiovascular

disease. About every 26 seconds an American will suffer a coronary event and about

every minute someone will die from one. Each year about 1.5 million Americans will have a heart attack with absolutely

no warning signs. For about half of those, the heart attack will be fatal.

In 90% of adult victims of sudden cardiac death, two or more major coronary arteries are narrowed or blocked.

Brain death and permanent death start to occur in just 4-6 minutes after someone experiences cardiac arrest.

The cardiac 64 CT scan provides 3-D images of the heart so detailed heart disease can be detected even at the earliest stages. It is in the earliest stages that heart disease is the most treatable.

In the time it took to read this, two people had a coronary event and one of them died.

Source: American Heart Association-2006 Update

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4. Objectives-Pre-Assessment Testing

Discuss Assessment with emphasis on the following: H & P EKG CXR Stress Testing Exercise Stress Testing Myocardial Perfusion Scintigraphy Radiographic Angiography Echocardiography- Doppler Pet Scan / CT Scan / MRI / MRS Cardiac Cath- GOLD STANDARD BUT PRICEY!!!!

Case Study

64 YOM in OR for open AAAECG after induction shows NSR PA cath placed- can still show pressure with

clamping30 minutes into surgery, PA cath pressures

unchanged.ECG shows ST segment depression in V5

of greater than 3 mm.

Diagnosis?

What other tool can you use to assist in assessing this problem?

Myocardial Ischemia

Related to myocardial oxygen supply and demand Demand determined by:

– Wall tension (preload and afterload)– Contractility (max velocity of contraction)– Heart rate

Myocardial oxygen supply determined by:– Coronary blood flow X arterial O2 content

Coronary blood flow determined by CPP (Dys – LVED) and patency of coronary arteries

Diagnosis

For intraoperative ischemia the standard monitor is? What is the most sensitive? – ST segment changes are a sensitive indication

of perturbation in the O2 supply and demand relationship

– Other events must occur first Increased LVEDV-LVEDP Regional wall motion abnormalities Decreased EF

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Assessment Echocardiography

Gastroscope with transducer

Echocardiography is a non-invasive, painless diagnostic method in which pulses of high frequency sound are transmitted into the body.

The “echoes” of the ultrasound returning from the surfaces of the heart and other structures are electronically plotted and recorded.

One, two, or three-dimensional images can be created to demonstrate heart and vessel anatomy, abnormalities and disease states.

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Transesophageal Echocardiography

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Transesophageal Echocardiography

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Transesophageal Echocardiography*

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Transesophageal Echocardiogy

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Transthoracic/transesophageal ECHO

transducer to the front of the chest. The ultrasound beam travels through the chest wall (skin, muscle, bone, tissue) and lungs to reach the heart. Because it travels through the front of the chest or thorax a standard echocardiogram is also known as a TRANSTHORACIC echo.

At times, closely positioned ribs, obesity and emphysema may create technical difficulties by limiting the transmission of the ultrasound beams to and from the heart.

A transesophageal echo, the echo transducer is placed in the esophagus. Since the esophagus sits behind the heart, the echo beam does not have to travel through the front of the chest, avoiding many of the obstacles described above. It offers a much clearer image of the heart, particularly, the back structures, such as the left atrium, which may not be seen as well by a standard echo taken from the front of the heart.

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Echo

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DopplerIn Doppler-echocardiography, the “speed”

at which blood flows can be measured for estimating pressure changes in evaluating heart valve function. (Shows how fast it is flowing)

Doppler color flow mapping superimposes color to show the direction of blood flow across valves or through small defects in the heart.

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Doppler Ultrasound

Depicts blood flow. It is an adaptation of ultrasound testing.It is used to diagnose the location and

degree of valve blockages.Presence of heart muscle (pericardial)

disease.

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Doppler

Why V5/II?

95% of ischemic events can be detected by analysis of the the info from these two leads

Lead II axis parallels the atria showing P wave better than other leads which enhances diagnosis of dysrhythmias and detection of inferior wall ischemia.

Lead V5 lies over 5th intercostal space and ant axillary line. Good compromise position for detecting anterior and lateral wall ischemia. True V5 lead only possible with at least 5 lead wires.

ECG changes

ST segment depression 2mm is critical index

T wave abnormalitiesNew onset arrhythmiasNew conduction abnormalities

PA Cath

Poor tool neither sensitive nor specific for for myocardial ischemia

Intraoperative Signs

HypotensionECG changes

– ST and T changes– ST depression > 1mm shows transmural

ischemia– Q waves > .03 secs is diagnostic of myocardial

ischemia

Treatment

Increase O2 supply– Increase FiO2– Increase CPP (CPP= DP-LVEDP)– Increase subendocardial blood flow with NTG

Decrease Myocardial O2 Demand– Decrease preload increases with NTG– Avoid and treat tachycardia (start slowly and

temporarily –why? Hr 90’s try esmolol-just a little; beta blockers may not be tol as a big dose; just give a little and then give more if needed; don’t give metroprolol. )

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How much oxygen is in the blood

The amount of oxygen in the blood is calculated using the formula: [1.34 x Hgb x (SaO2/100)] + 0.003 x PO2 = 20.8ml Oxygen is carried in the blood in two forms:

a) dissolved b) bound to hemoglobin. Dissolved oxygen obeys Henry’s law – the amount of oxygen

dissolved is proportional to the partial pressure. For each mmHg of PO2 there is 0.003 ml O2/dl (100ml of blood). If this was the only source of oxygen, then with a normal cardiac output of 5L/min, oxygen delivery would only be 15 ml/min.

Tissue O2 requirements at rest are approximately 250ml/min, so this source, at normal atmospheric pressure, is inadequate.

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Hemoglobin is the main carrier of oxygen

Each gram of hemoglobin can carry 1.34ml of oxygen. This means that with a hemoglobin concentration of 15g/dl, the O2 content is approximately 20ml/100ml.

With a normal cardiac output of 5l/min, the delivery of oxygen to the tissues at rest is approximately 1000 ml/min: a huge physiologic reserve.

Hemoglobin has 4 binding sites for oxygen, and if all of these in each hemoglobin molecule were to be occupied, then the oxygen capacity would be filled or saturated. This is rarely the case: under normal conditions, the hemoglobin is 97% to 98% saturated. The amount of oxygen in the blood is therefore related to the oxygen saturation of hemoglobin.

Taking all of these factors into account, we can calculate the oxygen content of blood where the PO2 is 100mmHg, and the hemoglobin concentration is 15g/L:

[1.34 x Hb x (saturation/100)] + 0.003 x PO2 = 20.8ml

This figure changes mostly with the hemoglobin concentration: when the patient is anemic the oxygen content falls, when polycythemic, it rises.In either case the O2 saturation of hemoglobin may be 97 – 100%, but there may be a large discrepancy in content.

Copyright 2002 All rights reserved

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Oxygen Transport Hemoglobin is a molecule composed of four subunits. Each subunit is a protein

chain attached to a porphyrin ring containing one iron atom. As each iron atom can bind one oxygen (O2) molecule, hemoglobin can carry one, two, three, or four oxygen molecules.

Normal blood contains about 15-16 grams hemoglobin per 100 ml. Each gram of hemoglobin can carry about 1.34 ml of gaseous oxygen. Fully saturated arterial blood will contain about 20 ml of oxygen per 100 cc. The volume of oxygen in the blood is referred to as the O2 content. Because O2 content is dependent on the hemoglobin concentration, it doesn’t provide a good measure of lung function. The partial pressure of oxygen (PaO2), as measured in arterial blood, does provide an accurate picture of gas exchange in the lung.

The relative amount of oxygen in the blood compared to the carrying capacity of the hemoglobin is called the oxygen saturation, and is expressed as a percentage. It’s directly proportional to the PaO2 — the partial pressure of oxygen.

The hemoglobin in arterial blood is only about 97% saturated with oxygen because of venous blood that passes directly through the lung (physiologic shunt). Venous blood is about 75% saturated.

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Total calculated oxygen in blood

SPO2 90 PO2 60 Hg 15 Calculate amt. of O2 bound to Hg 1.34ml O2 x 15gm Hg = 20.1gm O2 per Hg 20.1 x 0.9 PO2 = 18.09 O2/100ml blood bound

to Hg Calculate amt. Of dissolved O2 (PO2 = 60) For each mm Hg of PO2 there is 0.003 ml

O2/100ml blood 0.003 ml O2/100 x 60mm Hg = 0.18 O2/100ml

blood 18.09 O2/100 ml bld bound to Hg plus 0.18

O2/100ml bld = 18.17 total ml O2/100 blood Normal is 15 – 20 ml per 100gm/min 18.09 + 0.18 = 18.27

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FYI

the hemodynamic change that is most important to avoid in patient with CAD is tachycardia and hypotension

this increases O2 consumption and may decrease O2 supply

CABG

Indications– Unstable angina– Severe angina namely no response to medical

management– High grade LM dz or 3 Vessel dz-

3 Vessel CADz

RCA, LAD, LCx

The Pump

Usual circuit is from both VC’s or RA to pump oxygenator and back to the aorta

Blood flow via venous drainage is gravity syphon (airlock can occur on this side of the circuit)

Filters 40 microns or less. Filter can be bypassed if obstructed but not a good idea

Pump

Mean pressure no less than fifty. Newer guidelines adjust for age

Can be hand crankedFlow is 2.0 to 3.0 L/minPulsatile and non pulse available

WHY Hemodilution

Decreased O2 CCIncreased microcirculationIncreased urine outputReduced blood demands

Case Study

59 YOF for CABG with severe 3 vessel dzLIMA taken down25,0000 units of heparin given for Pump3 minutes after heparin dose ACT = 178secs

(pre heparin control was 122)What is going on? What should you do?

Anti Thrombin 3 Defficiency

Treatment: FFP 2 units usually

On Pump

Monitor MAP, Cerebral oxygenation, Temperature at two sites- periph and centrally- need to cool body; measure core and peripheral and see how warm you are, important for metab, clotting, infx

Coming off Pump

Treat for recall during rewarming VERSED Be ready with drips and bolus drugs

– Norepi– Epi– Milrinone– Ephedrine- lesion is fixed now. HR not a prob.– Neo– Vasopressin- careful d/t spasms and ischemia; small

dosing ; GREAT DRUG– Ca++

Risk Factors for Difficulty Coming off Pump

Small coronaries- DMAir in grafts- tombstones but will clearPoor presurgical function (CHF etc)Long X-clamp timePoor myocardial preservation during X-

clamp

Off Pump

In addition to usual monitors and meds:– Decadron- high dose stops inflammatory

response (high dose- 1mg/kg)– Vassopressin- GREAT DRUG…b/p can dump

fast…with a bolus of vasopressin, this will work. Pressure flx servere with lifting the heart. One or two units will do. Know whats going on in the field.

– Be ready for crash on pump- perfusionist on stand-by

Perioperative MI Risk of Reinfarction CHF Peak risk is 3-5 days after initial infarct Goldman Criteria (may be out of date) MI risked is probably increased in setting of:

– Prior MI within 6 months– CHF– Unstable angina– Prolonged thoracic or upper abd surgery– Preoperative hypertension– Intraop hypotension– Recent stinting

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CT SCAN

As with the heart, carotid vessels can be analyzed from any direction by digitally rotating the images. The vessels can be dramatically enlarged by as much as 10 to 20 times for a more thorough evaluation.

The technology is so superb that with the CT scan, a blood vessel that is only 1mm, or 1/50 of an inch can be viewed.

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Heart Scan Cost Cardiac 64 CT Scan Angiogram vs.

Cardiac Catheterization (Heart cath= $20,000)

CT: Covered by most insurance CT Cost about $2,000 Low Risk Procedure Outpatient Procedure Non-Invasive No Anesthesia Required 3-Dimensional Imaging of Heart and Vessels Visualization of Heart,

Heart Valves and Heart Muscle 4-Dimensional Imaging or Heart Pumping Action Pain Free Procedure 

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h. MRI/MRAMRI: Assess anatomy and heart muscle function Identify the presence of scar tissue in the muscle.

MRA: Specifically designed to detect CAD; and the degree

of narrowing. Highlights vulnerable plaque.

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Cardiac CT Scan

A cardiac CT scan can provide an image of the heart and its arteries so detailed that the presence of plaque, narrowing or stenosis of the arteries, calcium scoring and abnormal heart vessels can be determined with a degree of detail and accuracy previously only available through an invasive procedure such as cardiac catheterization or angiography.

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CT SCAN

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i. Cardiac Cath “Gold Standard” –

determines 3 V’ s

Vascularity Viability Ventriculography

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ELECTROCARDIOGRAPHIC SIGNS OF ISCHEMIA

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c. Assessment – Chest x ray

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d. Assessment Stress Testing

Dipyridamole-Potent vasodilator

Adenosine – Potent vasodilator/vascular smooth muscle relaxant via A2 receptor

Dobutamine – B1 receptor increases heart work via increase in heart rate. Useful in determining myocardial viability.

Regions that are hypokinetic, akinetic, dyskinetic at rest and improve with dobutamine probably contain areas of stunned myocardium. Perfusion to these areas increase with CABG or Angiography.

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e. Myocardial Perfusion Scintigraphy

Measure blood to myocardium and myocardial viability. Determines which regions of the myocardium are perfused normally/ischemic/stunned/Hibernating or infarcted.

Radio pharmaceuticals that accumulate in the myocardium are proportional to regional blood flow.

Thallium (similar to K in transport across cell membrane) & Technetium 99

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Stunned

Stunned - Acute ischemia (e.g., major coronary occlusion) can lead to stunning (segmental dysfunction) which is persistent for a variable period of time, up to two weeks, even after ischemia has been relieved. This a mismatched situation, in which MBF is normal, but function is depressed.

If ischemia lasts longer than 20 minutes, subendocardial necrosis usually begins. The clinical scenario is, e.g., acute myocardial infarction (AMI) and during percutaneous transluminal coronary angioplasty (PTCA) or cardiac surgery.

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stunned myocardium Stunned myocardium is a state when some section of the

myocardium (corresponding to area of a major coronary occlusion) shows a form of contractile abnormality. This is a segmental dysfunction which persists for a variable period of time, about two weeks, even after ischemia has been relieved (by for instance angioplasty or coronary artery bypass surgery).

In this situation, while myocardial blood flow (MBF) returns to normal, function is still depressed for a variable period of time.

Clinical situations of stunned myocardium are: acute myocardial infarction (AMI) after percutaneous transluminal coronary angioplasty (PTCA) after cardiac surgery

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hibernating myocardium Hibernating myocardium is a state when some segments of the

myocardium exhibit abnormalities of contractile function. These abnormalities can be visualized during echocardiography or ventriculography. The wall of the affected segments is ( hypokinetic, akinetic, or dyskinetic.

The phenomenon is highly significant clinically because it usually manifests itself in setting of chronic ischemia, which is potentially reversible by revascularization. The regions of myocardium are still viable and can restore its function. A new steady state develops between MBF and myocardial function, MBF is reduced and function is reduced. The clinical situations in which hibernating myocardium are:

chronic stable angina unstable angina silent ischemia after AMI

Case Study

83 YOM presents to OR for CABG.Report from ICU nurse states patient

condition deteriorated significantly overnight:– SPO2 down to < 92% on nonrebreather– Cough– Patient has severe SOB with supine position

Other Data

Patient is diabetic with insulin use for 20 plus years

Patient has mod to severe MR. (What are the numbers? )

Recent MIPA cath shows SVO2 50% CI = 1.2 to 0.8

Acute CHF

DyspneaDOEOrthopneaHx of MI, HTN, CHF

PE

S3 GallopRalesEdemaJVD

Labs BNP EKG ishemia/infarction Hypokinetic heart on echo Cardiac Cath:

– LVEDP >15 mmHg– EF less than .35– CI less than 2.o to 1.5 L/min/M2Know

BP determined by CO & SVR CO determined by HR & SV SV determined by preload, afterload, and

contractility. preload determined by volume & venous tone intravascular volume determined by amount of

Na+ in the body

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Ventricular hypertrophy

Concentric hypertrophy *chronic pressure overload (afterload); *size of LV chamber is not changed; *causes - chronic aortic stenosis *chronic hypertension.

Eccentric hypertrophy *chronic volume overload; *size of LV chamber is enlarged; *causes - chronic mitral insufficiency,*chronic aortic insufficiency

IHSS

Anesthesia considerations and treatments

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IHSS ( idiopathic hypertrophic subaortic stenosis)

HR - maintain Rhythm - keep sinus Preload - full, volume is first for hypotension Afterload - up, vasoconstrictor is 2nd Pathophysiology – hypertrophy intraventricular

septal muscle below aortic valve blocks outward flow during systole

Treatment - beta blockers, calcium channel blockers- avoid anything that changes ….

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IHSS (cont)

Anesthesia considerations:– Minimize sympathetic activation– avoid hypovolemia– No central nerve blocks, will decrease preload

and afterload– Phenylephrine is vasopressor of choice: no

increase in contractility, but increased SVR

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Arterial pressure waveforms

pulse pressure increases as arterial vessels become more peripheral.

pulse pressure is greatest in dorsalis pedis.

this phenomenon is attributable to an increase in systolic pressure and a decrease in diastolic pressure.

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Nonadrenergic CV drugsAntihypertensives

Direct-acting vasodilators - hydralazine, NTG, Nipride: arterial and veno- dilators.

Calcium channel blocker - Verapamil, Nifedipine: arterial dilators.- rapid acting can cause problems with cardiovasuc collapse

ACE inhibitors - Captopril, Enalapril: arterial dilators. Phosphodiesterase inhibitors - Inamrinone, milrinone:

block breakdown of cAMP, relaxes vascular smooth muscle- will increase ca.

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Adenosine (antidysrhythmic)

administered to– slow conduction through AV node– interrupt re-entry pathways through AV node– restore NSR in patients with SVT including

WPW syndrome.administer as rapid injection, 6-12 mgelimination 1/2 time is < 10 seconds

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REFERENCESBarash, P.G., Cullen, B.F., Stoelting, R.K. (1989). Clinical Anesthesia. Chapters 34, 35, 36.

Dinardo, J. (2006). Anesthesia for Cardiac Surgery, 3rd ed. Connecticut: Appleton & Lange.

Hensley, M. (2006). The Practice of Cardiac Anesthesia. Boston, MA:

Little Brown & Co.

Kaplan, J. A. (1991). Vascular Anesthesia. New York: Churchill Livingtone.

Mangano, D. T. (1991). Perioperative myocardial ischemia: New developments and controversies. ASA Refresher Courses in Anesthesiology.

Mangano, D.T., Silicianno, D., Hollenberg, M. et al. (1992).Postoperative myocardial ischemia. Anesthesiology. Morgan & McHale

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REFERENCES CONT’DMiller, R. D. (1990). Anesthesia. Churchill Livingstone. New York.

Rao, T. K., Jacobs, K. H. El-Etr A. A. (1983). Re-infarction following anesthesia in patients with myocardial infarction. Anesthesiology.59:499-505.

Reves, J. G., Hart, A. (1988). Anesthesia and myocardial ischemia. International Anesthesia Research Society, Review Course Lectures.

Stoelting, R. K., Dierdorf, S. F., McCammon, R. L. (2006.) Anesthesia and Co existing Disease, 2nd Ed.