Cardiology Revie Cardiology Review.pdfMost common signs of Cardiac Disease Cyanosis—5mg/dl reduced hemoglobin in the peripheral capillary blood. Congestive Heart failure Respiratory

Cardiology Review Lyn Vargo, PhD, NNP-BC Clinical Assistant Professor Stony Brook University 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 the companies or the manufacturer(s) of any commercial product and/or 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 their

typical presentation; be able to describe specific management strategies for different categories of cardiovascular

problems;

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 nervous system

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

B11 FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW

B11: CARDIOLOGY REVIEW Page 1 of 14

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 presentation handout on the following pages.

FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW


Neonatal CardiacReview

Lyn Vargo, PhD, RN, NNP-BC

Basic Cardiovascular Principles

Fetal Circulation Key Points of Fetal Circulation

The placenta not the lung is the organ of gas exchange.

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

Fetuses do not have a series circulation they have a ll l i l ti Th i ht & l ft t i l hparallel circulation. The right & left ventricles each

eject different amounts of blood & both oxygenate different parts of the body.

The left ventricle provides the most oxygenated blood to 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 for supplying less oxygenated blood to the descending aorta, lower body & placenta (post ductal) (2/3 of CVO)(paO2 15-25—55% saturated.))

A very small amount of the blood coming from the RV goes to the fetal lungs for growth & development of the fetal lungs (^PVR in lungs) (paO2 15-25—55% saturated).

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

Transitional Circulation

• Parallel circulation must change to series circulation

• Immediate closure of ductus venosus & foramen ovale.

• Closure of PDA at 48-96 hours of age• Decrease in pulmonary vascular

resistance which occurs suddenly at birth & then continues to decrease over first 4-6 weeks of life.

Cardiac Output

CO=HEART RATE (HR) X STROKE VOLUME (SV) 3 COMPONENTS OF STROKE 3 COMPONENTS OF STROKE

VOLUME:1. preload2. afterload3. contractility

4 Physiologic Components of SV in the Neonate

Heart rate—most important in determining cardiac output in the neonate & fetus.

Neonates have a decreased ability to increase stroke volume because the fetal myocardium has relatively few contractile elements & is poorly innervated by the sympathetic nervous system.

Parasympathetic System predominates in the neonate.



Most common signs of Cardiac Disease

**Cyanosis—5mg/dl reduced hemoglobin in the peripheral capillary blood.

**Congestive Heart failure Respiratory Distress—occurs due to

increased pulmonary congestionincreased pulmonary congestion. Most infant’s with cyanosis from cardiac

disease don’t have respiratory distress. If cyanosis is caused by fixed right-to left

shunt (cardiac lesion), increasing inspired O2 will have little effect.

What about Murmurs?

Remember, the absence of a murmur does not rule out CHD. Up to 20% of infants who die from CHD during the first month of life don’t have a murmur.

Innocent murmurs—Occur during first 48Innocent murmurs Occur during first 48 hours, usually Grade I-II, are usually systolic, and aren’t associated with other symptoms.

Pathologic murmurs—Persist beyond 48 hours, may occur at birth, day 3, one week or when PVR falls, may be louder than a Grade II. May be diastolic.

Definition of Congestive Heart Failure

The blood supply to the body is insufficient to meet the metabolic demands of the organsdemands of the organs. CHF is a manifestation of an underlying

disease or defect, rather than a disease itself.

Cause of Congestive Heart Failure

1. Volume Overload2. Pressure Overload3. Cardiomyopathy4. Dysrhythmias5. Anemia6. Asphyxia



Sympathetic Stimulation & CHF

Signs & Symptoms of CHF

Tachycardia* Hepatomegaly* Tachypnea* Cardiac Enlargement Gallop RhythmGallop Rhythm 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 inadequate to meet metabolic requirements leading to tissue hypoxia, metabolic acidosis, irreversible cellular changes & subsequent cellular death.

3 types:3 types: 1. Compensated—usually vasoconstricted &

BP maintained. 2. Decompensated– infant becomes

hypotensive. 3. Irreversible—end organ failure/death

Types of shock

Hypovolemic shock: perinatal events (tight nuchal cord, cord avulsion, cord prolapse, placental abruption, feto-maternal transfusion, birth trauma). Distributive shock: sepsis Cardiogenic shock: Asphyxia, metabolic

problems, CHD, arrhythmias, bacterial or viral infection, obstruction to venous return (pneumos).



Acyanotic Heart Defects

Typically present with Left-to-right shunting of blood

Lesions include PDA, VSD, ASD, AV canal (Endocardial cushion defect)

Signs & symptoms include signs of pulmonary g y p g p yovercirculation & CHF

Most typically won’t present until pulmonary vascular resistance has fallen at 4-6 weeks of age (exceptions are PDA in preterm infant & AV canal)

May present with some signs of respiratory distress due to pulmonary over circulation

Left-to-right Shunt Lesion CXR

Typical Findings:

Cardiomegaly

Increased pulmonary vascular markings

Patent Ductus Arteriosus

Presents with pulmonary overcirculation

Bounding pulses Widened pulse pressure

G d I IV/VI ti

cl

Grade I-IV/VI continuous or “machinery” murmur

Preemies may present with systolic murmur.

Cardiomegaly & increased pulmonary congestion on x-ray

Ventricular Septal Defect

Most common cause of CHF.

Harsh, Pansystolic murmur best heard at 3rd-4th left ICS at sternal3rd 4 left ICS at sternal border

CXR shows cardiomegaly & ^ PV markings.

Size of defect will determine presentation & management.



Atrial Septal Defect

3 types. Rarely develop failure. May have a Grade II/III/VI

systolic ejection murmurbest heard at upper leftbest heard at upper left sternal border.

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

AV Canal

30% occur in infants with Downs.

May be complete or partial.

Typically present with yp y pfailure early due to shunting at both atrial & ventricular level.

Grade III-IV/VI holosystolic regurgitant murmur at lower left sternal border.

Cyanotic Lesions

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

Tricuspid atresiaTetralogy of FallotTricuspid Insufficiency (perinatal asphyxia).Ebstein’s AnomalyEbstein s Anomaly

Typically blood is shunted from right side of heart to left side of heart

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

.

Right-to-Left Shunt Lesion CXR

Prostaglandin generally life saving with these cyanotic lesions by providing pulmonary blood flowfrom systemic circulation.



Cyanotic Lesions

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

TranspositionTruncus ArteriosusTAPVR

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

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

CXR will have normal or increased PV markings & ? Big heart.

Tetralogy of Fallot

1. Large VSD. 2. Pulmonary stenosis or

right ventricular outflow obstruction.

3. Overriding aortag 4. Hypertrophied Right

ventricle. Cyanotic. Pulmonary

blood flow may be duct dependent.

Grade III-V/VI systolic ejection murmur at middle & upper left sternal border.

Tricuspid Atresia

Right ventricle may be hypoplastic.

More than 90% of patients have a VSD

May be ductal dependent y p(especially if no VSD).

Management is geared to providing pulmonary blood flow.

A single S2 is often heard in infants with tricuspid atresia.

Management of Cyanotic Lesions with Decreased Flow

Prostaglandin—provides pulmonary blood flow. From aorta to pulmonary artery to lungs.

Palliative shunt—Blalock 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 (SVC to RPA) followed by a Fontan.



Cyanotic Lesions with Increased Flow MixingFlow---Mixing Lesions

TAPVR—Mixing Lesion

3 types. Pulmonary veins connect

to right atrium in one of three ways.

Complete cardiac mixing of arterial & venousof arterial & venous blood.

Blood flow to body is totally dependent on flow through right-to-left shunt through patent foramen or ASD.

Murmurs are rare.

Transposition

Parallel circuitry—separate circuits for pulmonary & systemic blood.

Only mixing of blood occurs through ASD, g ,VSD or PDA.

Cyanosis apparent in varying degrees.

CXR variable vascularity. Murmurs if present are

those of associated lesions.

Ebstein’s Anomaly

Low insertion of tricuspid valve which incorporates right ventricle making it very small.

Tricuspid insufficiency present in varying degrees.

Right-to-left shunting at foramen.

Pulmonary blood flow significantly decreased.

Huge heart on x-ray. Nonspecific systolic murmur,

diastolic murmurs, clicks & triple & quadruple rhythm heard.

Dysrhythmias frequent—WPW



Ebstein’s Anomaly CXR Truncus Arteriosus—3 Types.

One great vessel arises from both ventricles with overriding VSD.

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

Mixing of blood occurs in the common chamber.

Varying degrees of cyanosis. S2 is single. Loud pansystolic

murmur often heard at LLSB.

Left Sided Obstructive Lesions

Will present with s/s of hypoperfusion & respiratory Occurs suddenly when the PDA closes. distress. Hypoperfusion (shock) is due to inadequate ejection

of blood by left ventricle into systemic circulation=hypotension & metabolic acidosiscirculation hypotension & metabolic acidosis.

May have some degree of arterial desaturation, but mostly lethargy, mottling, pallor, poor pulses, & respiratory distress.

CXR will show pulmonary congestion & cardiomegaly. Examples: HLHS, Coarctation of the aorta, & critical

aortic stenosis.

Left Sided Obstructive Lesion CXR



Coarctation of the Aorta

Constriction or discrete narrowing of aorta.

Most commonly occurs at junction of aorta & PDA (juxtaductal).

Blood flow to body occurs through PDA. Once PDA gcloses. Left ventricle must pump very hard to get through narrow area.

Bicuspid aortic valve is common (80%).

VSDs are common (40%) Prostaglandin life saving for

providing blood flow to bodywhen PDA closes.

BP differences.

Prostaglandin E1

Must be given by continuous infusion Side effects include: Apnea, peripheral

vasodilation (flush), hypotension, fever, seizures, bradycardia, irritability, muscle twitching or jitteriness lethargytwitching or jitteriness, lethargy, hypoglycemia, 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 4 Severe coarctation4. Severe coarctationCoronary artery flow is retrograde. Systemic circulation depends on

PDA & prostaglandin! Aren’t really cyanotic— shocky!Cardiomegaly with increased Pulmonary congestion.Nonspecific systolic murmur in 2/3of infants.

Hypoplastic Left Heart Syndrome Treatment

Surgery—Norwood initially. Glenn shunt & then Fontan. Transplantation Palliative Care Palliative Care



Aortic Stenosis Critical Aortic Stenosis

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

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

right sternal border. The intensity of the murmur is unrelated to the severity of the obstruction.

Infants have CHF due to pressure load of left ventricle.

Can appear shocky when PDA closes. Prostaglandin helpful.

Rhythm Disturbances

Tachyarrhythmias1. sinus tachycardia2 **supraventricular2. supraventricular

tachycardia Bradyarrhythmias Pulseless arrest

Dysrhythmias

Benign : sinus bradycardia, sinus tachycardia, sinus dysrhythmias. 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 , rapid conduction through an accessory bundle (Ex: WPW), g y ( ),or the existence of an ectopic atrial pacemaker. HR over 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 greater than 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. Atrial fibrillation very rare & is also almost alwaysAtrial fibrillation very rare & is also almost always

associated with serious heart disease. Difficult to treat. 3. Ventricular Tachycardia is also associated

with severe disease. Use DC cardioversion. Lidocaine also helpful.Maintenance treatment includes, inderal lidocaine, phenytoin, lidocaine, procainamide or amiodarone.

Bradyarrhythmias

4. In complete AV block the ventricular rate is slower 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 isn’t necessary unless HR slow & failure occurs. Will need pacemaker. Can try Isoproterenol may be tried to ^ rate until pacer in.

Electrolytes & Drugs Effects on Cardiac Rhythm Strips

Digoxin toxicity—May cause decreased Heart rate, prolonged PR interval, AV block.

Hypokalemia (<2.5)—depressed ST segment, biphasic T wave, Prominent U wave. May develop prolonged PR & blockdevelop prolonged PR & block

Hyperkalemia—Tall T wave (K >6.0) >7.5, long PR interval, wide QRS duration,

Tall T wave >9.0 absent P wave, sinusoidal QRS wave,

asystole and ventricular fibrillation can occur. Hypocalcemia—Prolonged QT interval Hypercalcemia—Shorter QT interval

HypertrophicCardiomyopathy Increased myocardial fiber size and # causes

hypertrophy of the ventricle with smaller than normal ventricular cavity.

The heart contracts better, but filling is impaired by relaxation abnormalities. Subaortic obstruction may occur.

Often seen in IDMs is thought to be due to hyperinsulinemia.

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-adrenergic blockers (propranolol). Do NOT use digoxin.



Cardiology Revie Cardiology Review.pdfMost common signs of Cardiac Disease **Cyanosis—5mg/dl reduced hemoglobin in the peripheral capillary blood. **Congestive Heart failure Respiratory

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Cardiology Revie Cardiology Review.pdfMost common signs of Cardiac Disease Cyanosis—5mg/dl reduced hemoglobin in the peripheral capillary blood. Congestive Heart failure Respiratory