cvs summary

7/29/2019 CVS Summary

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Cardiology Review

Lyn Vargo, PhD, NNP-BCClinical Assistant Professor

Stony Brook University and NNP Program

University of Missouri, Kansas City

The speaker has signed a disclosure form and indicated she has no significant financial interest or relationship with companies

or the manufacturer(s) of any commercial product/service that will be discussed as part of this presentation.

Session Summary

This presentation will provide an overview of cyanotic, acyanotic, obstructive, and other congenital heart

defects. There will also be a brief discussion regarding tacharrhythmias, brady arrhythmias, and pulseless

arrests, as well as compensated, decompensated, and irreversible shock.

Session Objectives

Upon completion of this presentation, the participant will:

understand principles related to cardiac physiology, neonatal cardiac physiology, fetal circulation,transitional circulation and their relationship to congenital heart disease;

recognize characteristics of different acyanotic, cyanotic and obstructive cardiac lesions and theirtypical presentation;

be able to describe specific management strategies for different categories of cardiovascularproblems;

be able to discuss different rhythm disturbances seen in the neonate; recognize different types of shock and treatment strategies.

Test Questions

1. In fetal circulation:

a. Left ventricular output is higher than right ventricular output

b. About 30% of the combined ventricular output goes to the fetal lungs

c. Right ventricular output is higher than left ventricular output

2. In the neonatal autonomic nervous system:

a. The parasympathetic nervous system is more well developed than the sympathetic nervoussystem

b. The sympathetic nervous system is more well developed than the parasympathetic nervous

system

c. Autonomic control of the heart rate is better controlled by catecholamine stimulation than

by vagal stimulation

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FANNP 23RD NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW

B13: CARDIOLOGY REVIEW Page 1 of 15


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3. Infants with acyanotic lesions (left-to-right shunt lesions) typically present:

a. At 2-3 days of age when the PDA closes

b. When the pulmonary vascular resistance falls

c. At birth

4. Which of the following drugs should be used to treat Wolff-Parkinson-White (WPW) Syndrome in the

neonate?a. Digoxin

b. Verapamil

c. Propanolol

5. In tricuspid atresia treatment with PGE1 to maintain ductal patency would:

a. Increase pulmonary blood flow

b. Increase systemic blood flow

c. Should not be used

6. A Blalock-Taussig shunt is:

a. An intra-atrial shunt that allows shunting of blood from the left atrium to right atrium

b. A shunt between a subclavian artery & a pulmonary artery that increases pulmonary blood

flow

c. An anastomosis between the aorta & pulmonary artery that provides systemic blood flow

References

Blackburn (2007). Maternal, fetal & neonatal physiology: A clinical perspective. Philadelphia: WB Saunders.

Brodsky & Martin (2003). Neonatology review. Philadelphia: Hanley Belfus, Inc.

Cloherty, et al. (2007). Manual of neonatal care. Philiadelphia: Lippincott-Raven Publishers.

Gomella, et al. (2009). Neonatology: Management, procedures, on-call problems, diseases & drugs. New York: McGraw-Hill.

Kenner, et al. (2007). Comprehensive neonatal nursing. St. Louis: Elsevier Saunders.

Martin, et al. (2006). Neonatal-perinatal medicine: Diseases of the fetus & infant. St. Louis: Mosby Elsevier.

Merenstein & Gardner (2006). Handbook of neonatal intensive care. St. Louis: Mosby Elsevier.

Park M.K. (2008). Pediatric cardiology for practitioners. St. Louis: Mosby Elsevier.

Polin, et al. (2008). Hemodynamics and cardiology: Neonatology questions & controversies. Philadelphia: WB Saunders.

Session Outline

See handout on following pages.




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Neonatal CardiacReview

Lyn Vargo,PhD, RN, NNP-BC

General CV principles

Blood always goes in the pathway of leastresistance.

Resistance is inversely related to flow. Blood always flows from higher pressure to

lower pressure. After birth, once the foramen ovale & pda

have closed we have a series circulation. In order to understand what is happening you

must think of where the blood has come from& where it is going in the series to see howthe different congenital heart defects will affectthe infant.

Basic Cardiovascular Principles Fetal Circulation




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Key Points of Fetal Circulation

The placenta not the lung is the organ of gasexchange.

Umbilical vein paO2 is 30-35 mmHg or 80-90%saturated (Importance of fetal hemoglobin).

Fetuses do not have a series circulation they have apara e crcua on. e rg e venr ces eaceject differentamounts of blood & both oxygenatedifferent parts of the body.

The left ventricle provides the most oxygenated bloodto the heart, brain & upper extremities (preductal)(1/3 of CVO) (paO2 26-28 or saturation of 65%).

Key Points of Fetal Circulation

The right ventricle is primarily responsible forsupplying less oxygenated blood to thedescending aorta, lower body & placenta(post ductal) (2/3 of CVO)(paO2 15-2555%saturated.)

A very small amount of the blood coming fromthe RV goes to the fetal lungs for growth &development of the fetal lungs ( PVR in lungs)(paO2 15-2555% saturated).

In the fetal heart right sided pressures arehigher than left sided pressures (by10-12%).

Transitional Circulation

Parallelcirculationmustchangetoseriescirculation

Immediateclosureofductus venosus &foramenovale.

ClosureofPDAat4896hoursofage

Decreaseinpulmonaryvascularresistancewhichoccurssuddenlyatbirth&thencontinuestodecreaseoverfirst68weeksof

life.

Cardiac Output

CO=HEART RATE (HR) X STROKEVOLUME (SV)

VOLUME:

1. preload

2. afterload

3. contractility




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4 Physiologic Components of SVin the Neonate

Heart ratemost important in determiningcardiac output in the neonate & fetus.

Neonates have a decreased ability to increasestroke volume because the fetal myocardiumhas relatively few contractile elements & ispoorly innervated by the sympathetic nervoussystem.

Parasympathetic System predominates in theneonate.

Most common signs of CardiacDisease

**Cyanosis5mg/dl reduced hemoglobin inthe peripheral capillary blood.

**Congestive Heart failure

Respiratory Distressoccurs due to.

***Most infants with cyanosis from cardiacdisease dont have respiratory distress.

If cyanosis is caused by fixed right-to leftshunt (cardiac lesion), increasing inspired O2will have little effect.

What about Murmurs?

Remember, the absence of a murmur doesnot rule out CHD. Up to 20% of infants whodie from CHD during the first month of lifedont have a murmur.

hours, usually Grade I-II, are usually systolic,and arent associated with other symptoms.

Pathologic murmursPersist beyond 48hours, may occur at birth, day 3, one week or

when PVR falls, may be louder than a GradeII. May be diastolic.

Defin ition of Congestive Heart

Failure

The blood supply to the body isinsufficient to meet the metabolic

.

CHF is a manifestation of an underlyingdisease or defect, rather than a diseaseitself.




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Cause of Congestive Heart Failure

1. Volume Overload

2. Pressure Overload

3. Cardiomyopathy

4. Dysrhythmias

5. Anemia

6. Asphyxia

Sympathetic Stimulation & CHF

Signs & Symptoms of CHF

Tachycardia*

Hepatomegaly*

Tachypnea*

Cardiac Enlargement

Gallo Rh thm

Decreased peripheral pulses & skin mottling

Decreased Urine output

Diaphoresis

Decreased activity

Failure to thrive/feeding problems

Diminished cardiac output

Neonatal Shock

Definition: Blood flow to tissues is inadequateto meet metabolic requirements leading totissue hypoxia, metabolic acidosis, irreversiblecellular changes & subsequent cellular death.

1. Early Compensatedusuallyvasoconstricted & BP maintained.

2. Decompensated infant becomeshypotensive.

3. Irreversibleend organ failure/death




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Types of shock

Hypovolemic shock: perinatal events(tight nuchal cord, cord avulsion, cordprolapse, placental abruption, feto-maternal transfusion, birth trauma).

Distributive shock: sepsis

Cardiogenic shock: Asphyxia, metabolicproblems, CHD, arrhythmias, bacterialor viral infection, obstruction to venousreturn (pneumos).

Acyanot ic Heart Defects

Typically present with Left-to-right shunting ofblood

Lesions include PDA, VSD, ASD, AV canal(ECD)

Signs & symptoms include signs of pulmonaryovercirculation & CHF

Most typically wont present until pulmonaryvascular resistance has fallen at 4-6 weeks ofage (exceptions are PDA in preterm infant &AV canal)

May present with some signs of respiratorydistress due to pulmonary over circulation

Left-to-right Shunt Lesion CXR

Typical Findings:

Cardiomegaly

Increased pulmonary

vascular markings

Patent Ductus Arteriosus

Presents with pulmonaryovercirculation

Bounding pulses

Widened pulse pressure

cl

ra e - con nuousor machinery murmur

Preemies may presentwith systolic murmur.

Cardiomegaly &

increased pulmonarycongestion on x-ray




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Ventricular Septal Defect

Most common cause ofCHF.

Harsh, Pansystolicmurmur best heard at

- th border

CXR shows cardiomegaly& PV markings.

Size of defect willdetermine presentation &management.

Atrial Septal Defect

3 types.

Rarely develop failure.

May have a Grade II/III/VIsystolic ejection murmur

sternal border.

S2 may be widely split &fixed (older infants).

AV Canal

30% occur in infants withDowns.

May be complete orpartial.

Typically present withfailure early due toshunting at both atrial &ventricular level.

Grade III-IV/VIholosystolic regurgitant

murmur at lower leftsternal border.

Cyanotic Lesions

Cyanotic Lesions with decreased pulmonary blood flow(usually not in respiratory distress):

Tricuspid atresiaTetralogy of FallotEbsteins Anomaly

Tricuspid Insufficiency (perinatal asphyxia).Typically blood is shunted from right side of heart to left side

Cyanosis may initially only occur with cryingLevel of cyanosis dependent on amount of blood flow to the

lungs.CXR generally have decreased pulmonary markings.

Oligemic

.




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Cyanotic Lesions

Cyanotic Lesions with increased pulmonary blood flow(generally mixing lesions):

Transposition

Truncus Arteriosus

Mixing or separation of pulmonary venous return &systemic venous return.

Many of these infants will have CHF as well & somerespiratory distress.

CXR will have normal or increased PV markings & ? Bigheart.

Right-to-Left Shunt Lesion CXR

Prostaglandingenerally life savingwith these cyanoticlesions by providingpulmonary blood flowfrom systemiccirculation.

Tetralogy of Fallot

1. Large VSD.

2. Pulmonary stenosis orright ventricular outflowobstruction.

3. Overriding aorta

. yperrop e gventricle.

Cyanotic. Pulmonary bloodflow may be ductdependent.

Grade III-V/VI systolic

ejection murmur at middle &upper left sternal border.

Tricuspid Atresia

Right ventricle may behypoplastic.

More than 90% ofpatients have a VSD

May be ductal dependent(especially if no VSD).

Management is geared toproviding pulmonaryblood flow.

A single S2 is often heard

in infants with tricuspidatresia.




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Management of Cyanotic Lesionswith Decreased Flow

Prostaglandinprovides pulmonarybloodflow. From aorta to pulmonary artery to lungs.

Palliative shuntBlalock Taussig operation(systemic to pulmonary shunt using Gor-Tex ).

Definitive repair through a Fontan procedure(communication between right atrium &pulmonary artery) or a Glenn Procedure (SVCto RPA) followed by a Fontan.

Cyanotic Lesionswith Increased

---Lesions

TAPVRMixing Lesion

3 types. Pulmonary veins connect

to right atrium in one ofthree ways.

Complete cardiac mixing

blood. Blood flow to body is

totally dependent on flowthrough right-to-left shuntthrough patent foramenor ASD.

Murmurs are rare.

Transposition

Parallel circuitryseparate circuits forpulmonary & systemicblood.

Only mixing of bloodoccurs throu h ASD, VSDor PDA.

Cyanosis apparent invarying degrees.

CXR variable vascularity. Murmurs if present are

those of associatedlesions.




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Ebsteins Anomaly

Abnormally low insertion oftricuspid valve whichincorporates right ventriclemaking it very small.

Tricuspid insufficiency presentin varying degrees.

Right-to-left shunting atforamen.

Pulmonary blood flowsignificantly decreased.

Huge heart on x-ray. Nonspecific systolic murmur,

diastolic murmurs, clicks &triple & quadruple rhythmheard.

Dysrhythmias frequentWPW

Ebsteins Anomaly CXR

Truncus Arteriosus3 Types.

One great vessel arises fromboth ventricles with overridingVSD.

This artery has onevalve &gives rise to pulmonary,coronary & systemic arteries.

Mixing of blood occurs in thecommon chamber.

Varying degrees of cyanosis.

S2 is single. Loud pansystolicmurmur often heard at LLSB.

Rastellis procedure

Left Sided Obstruct ive Lesions

Will present with s/s of hypoperfusion & respiratorydistress.

Hypoperfusion (shock) is due to inadequate ejectionof blood by left ventricle into systemiccirculation=hypotension & metabolic acidosis.

ccurs su eny w en e c oses.

May have some degree of arterial desaturation, butmost striking is lethargy, mottling, pallor, poor pulses,& respiratory distress.

CXR will show pulmonary congestion & cardiomegaly.

Examples are: HLHS, Coarctation of the aorta, &critical aortic stenosis.




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Left Sided Obstruct ive Lesion CXR Coarctation of the Aorta

Constriction or discretenarrowing of aorta.

Most commonly occurs atjunction of aorta & PDA(juxtaductal).

Blood flow to body throughPDA, once this closes. Leftventricle must pump very hardto get through narrow area.

Bicuspid aortic valve iscommon (80%).

VSDs are common (40%) Prostaglandin life saving for

providing blood flow to body. BP differences.

Prostaglandin E1

Must be given by continuous infusion

Side effects include: Apnea, peripheralvasodilation (flush), hypotension, fever,seizures, bradycardia, irritability,muscle

, , ,hypocalcemia,hyperbilirubinemia, diarrhea,and

thrombocytopenia.

Dose: Initial 0.05-0.1micrograms/kg/minute.Use smallest dose possible

Maintenance 0.01-0.05micrograms/kg/min

Hypoplastic Left Heart Syndrome

Clinical spectrum of:1. Severe mitral stenosis or

atresia2. Severe aortic stenosis or

atresia3. Left ventricular hypoplasia. evere coarca on

Coronary artery flow is retrograde.Systemic circulation depends on

PDA & prostaglandin!Arent really cyanotic shocky!Cardiomegaly with increasedPulmonary congestion.

Nonspecific systolic murmur in 2/3of infants.




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Hypoplastic Left Heart SyndromeTreatment

SurgeryNorwood initially. Glenn shunt& then Fontan.

Transplantation

Aortic Stenosis

Critical Aortic Stenosis

Obstruction of the valve can occur above thevalve (supravalvular), at the aortic valve(valvular) or below the valve (subvalvular).

Valvular is most common. Grade II-IV/VI harsh systolic murmur in upper

right sternal border. The intensity of themurmur is unrelated to the severity of theobstruction.

Infants have CHF due to pressure load of leftventricle.

Can appear shocky when PDA closes.Prostaglandin helpful.

Rhythm Disturbances

Tachyarrhythmias

1. sinus tachycardia

.

tachycardia

Bradyarrhythmias

Pulseless arrest




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Dysrhythmias

Benign : sinus bradycardia, sinus tachycardia, sinusdysrhythmias. Generally require no treatment.

Pathologic: SVT (most common), Atrial flutter &fibrillation, V-tach & complete AV block.1. SVT is a result of dual AV nodal pathways , rapidconduction throu h an accessor bundle (Ex: WPW),or the existence of an ectopic atrial pacemaker. HRover 200. No change in HR with activity. Regular RR.

12-24 hours after occurs, infant will develop CHF. Treatment includes, vagal maneuvers, adenosine,

cardioversion (Use Synchronous mode always only!!). Medications used after conversion include Digoxin

(not with WPW though), propranolol IV (no CHF),esmolol, amiodarone, flecainide or procainamide.

Dysrhythmias

2.Atrial flutter is diagnosed when the atrial rate is greaterthan 220 minute. P waves are regular, characteristic saw-tooth pattern.

Often suggests serious organic heart disease.

Ventricular rate will depend on degree of AV block.

associated with serious heart disease.

Difficult to treat.

3. Ventricular Tachycardia is also associated

with severe disease. Use DC cardioversion. Lidocainealso helpful.Maintenance treatment includes, inderallidocaine, phenytoin, lidocaine, procainamideoramiodarone.

Dysrhythmias

4. In complete AV block the ventricular rate isslower than atrial rate

& there is no association b/w these rates.Bradycardia.

There is a strong association b/w this &maternal collagen disorders (Lupus).

Treatment isnt necessary unless HR slow &failure occurs. Will need pacemaker. Can try

Isoproterenol may be tried to rate until pacerin.

Electrolytes & Drugs Effects on

Cardiac Rhythm Strips

Digoxin toxicityMay cause decreased Heartrate, prolonged PR interval, AV block.

Hypokalemia (7.5, long PR interval, wide QRS duration, Tall Twave

>9.0 absent P wave, sinusoidal QRS wave,asystole and ventricular fibrillation can occur.

HypocalcemiaProlonged QT interval HypercalcemiaShorter QT interval




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HypertrophicCardiomyopathy

Increased myocardial fiber size and #causeshypertrophy of the ventricle with smaller than normalventricular cavity.

The heart contracts better, but filling is impaired byrelaxation abnormalities. Subaortic obstruction mayoccur.

Often seen in IDMs is thought to be due tohyperinsulinemia.

Ventricular septum wall is usually more hypertrophied. CHF can develop as well as gallops & systolic

murmur along LSB. Cardiomegaly evident. Generally resolves spontaneously, but treatment

includes general supportive care, B-adrenergicblockers (propranolol). Do NOT use digoxin.

Questions & Answers

Here are the answers to the questions:

1. c

2. a

.

4. c

5. a

6. b.

Any Questions?


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