RNC cardiac reviewElizabeth Rex, MS, NNP-BC

NCC Cardiac Content

♥ Transition to extrauterine life

♥ PDA

♥ CV AssessmentBPCVPEKGMonitoring Lines

♥ Cyanosis Central / PeripheralCardiac / Pulmonary

♥ Arrhythmias

♥ Congestive Heart Failure

♥ Hypertension

♥ Shock

♥ Cardiac Tamponade

♥ Anomalies (Cyanotic / Acyanotic)AV CanalCoarctation of aortaHLHSPulmonary stenosis/atresiaTOFTGA TAPVR

Fetal Circulation

3 fetal shuntsDuctus venosus Foreman ovaleDuctus arteriosus

Cardiovascular Transition

♥ 10 min = PaO2 50 mm hg♥ 1 hr = PaO2 62 mm hg♥ 2 days PaO2 75-85 mm hg

24 hours after birth:♥ Oxygen consumption triples♥ Significant increase in cardiac output♥ Left ventricle must remodel and hypertrophy

Respiratory Assessment

♥ Normal Rate: 30-60, easy effort

♥ Increased WOB: tachypnea, GFR, gasping

♥ Saturations: Pre and post

Heart Rate Assessment

♥ Normal rate 120-160 (may range 80-200)

♥ Normal sinus rhythm

Bradycardia

Underlying causes♥ ↑ Vagal tone ♥ Apnea♥ Hypoxemia ♥ Asphyxia♥ Hypotension ♥ Acidosis♥ Digoxin toxicity ♥ Central line in right atrium

Evaluate for shock♥ HR < 70 is usually pathologic

♥ Differentiate Sinus bradycardia - QRS complex follows each p wave ♥ Complete heart block

Complete Heart Block

♥ Ventricular rate 45-89 beats/min

♥ P wave unrelated to QRS

♥ Increased incidence with maternal lupus erythematosus

♥ If hydroptic at birth, will be critically ill

Tachycardia

♥ Abnormal tachycardia sustained HR>180- Assess for shock, CHF- Evaluate resp status, perfusion, pulses, BP

♥ Most common:Sinus tachycardia sustained HR 180-220Sympathetic stimulationFever

SVT Supraventricular Tachycardia

Sustained HR > 220♥ Usually well tolerated initially unless

associated with:

Structural CHD

Hydrops

SVT

- 15 lead EKG- Run while doing tx

- Vagal maneuvers - Stimulate a gag- Suction nasopharynx- Ice to nose and forehead

- Adenosine- Initial dose 100 mcg/kg- Rapid IV push over 1-2 seconds followed by flush- No response in 2 minutes increase dose 50-100 mcg/kg

- Cardioversion- 0.5 joules/kg

Heart Auscultation

♥ First heart sound – S1Closure of mitral and tricuspid valvesEnd of atrial systoleHeard best 5th intercostal space @ left midclavicular line or LLSB

♥ Second heart sound – S2Closure of aortic and pulmonic valvesEnd of ventricular systoleHeard best ULSB, called pulmonic valve area

Heart Murmur

Sound caused by turbulent blood flow

♥ Blood forced through narrowed areas

♥ Regurgitation through incompetent or abnormal valves

♥ Increased flow across normal structures

Heart Auscultation

Murmurs� Location� Transmission� Intensity� Timing� Quality� Grading I - VI

Heart Murmur Intensity

Grade I - barely audibleGrade II - soft but audibleGrade III - moderately loud, no thrillGrade IV - loud, assoc. with thrillGrade V - audible with stethoscope barely

touching chestGrade VI - audible with stethoscope not

touching chest

Heart Murmur Timing

♥ Systolic� Heard between S1 and S2 of same beatS1 (murmur) S2 S1 (murmur) S2

♥ Diastolic� Heard between S2 and S1 of next beatS1, S2 (murmur) S1, S2 (murmur)

♥ Continuous� Starts in systole and extends into diastole

Normal Murmurs

♥ Peripheral pulmonic stenosis PPS Grade I-II/VI upper left sternal border, radiates to axilla and back

♥ Systolic ejection/ continuous Grade I-II/VI may be heard 1st week of life as PVR decreases and PDA closes

♥ Flow murmurGrade I-III/VI associated with anemia

Pathologic Heart Murmur♥ > Grade 3 murmur within hours of birth

♥ Pan systolic murmurMitral or tricuspid regurgitationSevere pulmonary diseaseAsphyxial injury of tricuspid valve

♥ Diastolic murmurAortic or pulmonic valve regurgitation

♥ Continuous murmurPDA, AVM, aortopulmonary window

Pathologic Heart Murmur

♥ Central cyanosis♥ Respiratory distress♥ Abnormal heart silhouette♥ ↑ or ↓ pulmonary vascularity on CXR ♥ Gallop

� CHF

Assessment - Palpation

♥ Skin: color, temperature, diaphoresis, edema

♥ Precordium: quiet, visible, heave, thrill PMI - LLSB 5th intercostal space

PMI shifted to the right:DextrocardiaTension pneumothoraxDiaphragmatic hernia

PMI shifted to the leftTension right pneumothorax

Assessment - Palpation

♥ Pulses: compare upper to lower extremities and side to side

� Brachial and femoral equal in strength� Pedal pulses palpable� Concern if weak, thready, bounding

♥ CFT: press for 5 seconds, release < 3 seconds normal

♥ Liver: below right costal margin < 2 cm preterm< 3 cm term

Assessment Auscultation

Bruits

♥ Liver

♥ Anterior fontanelle

♥ May indicate AVM arteriovenous malformation

Assessment Auscultation

♥ First heart sound – S1

� Closure of the tricuspid and mitral

� End of atrial systole

� Heard best at the 5th intercostal space at the left midclavicular line or LLSB

Assessment Auscultation

♥ Second heart sound – S2� Closure of aortic and pulmonic valves

� End of ventricular systole

� Heard best • ULSB• Pulmonic valve area

Assessment Auscultation

Single S2 - Normal in first few days of life with ↑ pulmonary vascular resistance

♥ Splitting of S2 difficult to hear with tachycardia

♥ Absence of either aortic or pulmonic S2:� Severe aortic stenosis or atresia� Severe pulmonary stenosis or atresia� Truncus arteriosus� PPHN� Transposition of the great arteries� Tetralogy of Fallot

Cyanosis - Peripheral

♥ Acrocyanosis� Bluish discoloration hands and feet� No mucous membrane involvement� Often resolves by 48 hours of age� Rule out hypothermia

Cyanosis - Peripheral

♥ Circumoral cyanosis� Bluish discoloration around the mouth� Often associated with feeding� R/O central cyanosis

Cyanosis - Central

♥ Bluish discoloration of tongue and mucous membranes

♥ Caused by desaturation of arterial blood Hemoglobin carrying no O2 appears purple = reduced hemoglobin

♥ Cyanosis may be visible with 3-5 grams of reduced hemoglobin

♥ Indicates cardiac or respiratory dysfunction

Cyanosis - Pulmonary / Cardiac

Pulmonary Cardiac

Cyanosis Yes Yes

Respiratory Rate Increased Increased – often tachypneic no GFR Infant looks comfortable if no CHF

Work of breathing Increased Easy effort unless CHF – then GFR

Acid/Base Balance Increased PCO2 Decreased PCO2 with tachypneaRespiratory acidosis Metabolic acidosis

Mixed resp/metabolic if pulmonarydisease

CXR Asymmetric pattern of Increased or decreasedinfiltrates or other pulmonary vasculature pulmonary disease

Heart silhouette normal abnormal Size/shape/location

O2 Challenge test PO2> 150 PO2 < 150 for cyanotic CHD

Blood pressure

Methods for measuring

Arterial:

♥ Umbilical artery

♥ PAL Radial

♥ PAL Posterior tibialis

Hypertension

♥ Systolic or mean arterial BP > 95th percentile for birth weight, gest age, and post-natal age

95th percentile for systolic BP = 65 mmHg at 24 wks.

95th percentile for systolic BP = 90 mmHg at 40 wks post conception.

Hypertension Treatment

♥ Varies with cause of hypertension

♥ Tx etiology if possible

♥ Anti-hypertensive only if hypertension immediately life threatening

CVP

♥ In most cases the trend in CVP is more helpful than absolute value

♥ CVP may be difficult to interpret because it is affected by several factors:� hypervolemia� myocardial failure� excessive ventilatory pressures� grunting respirations� tension pneumothorax� pleural effusion� UVC tip in portal system

Cardiac CycleSystole & Diastole

Systole is contraction of the ventricles

Diastole is the relaxation and filling of the ventricles followed by a small atrial contraction

Adult

Cardiac Cycle

average neonate’s cardiac cycle is≈ 0.4 secs, based on a HR of 150

Supraventricular tachycardiaHR 230 60 ÷ 230 = 0.26 secsHR 300 60 ÷ 300 = 0.2 secs

Cardiac Output The volume of blood pumped by the left ventricle in 1 min 120 -200 ml/kg/min

CO = stroke volume x HR

Cardiac Output

Influenced by changes in HR, pulmonary vascular resistance, and systemic vascular resistance to flow

Also influenced by the amount of blood returning to the heart

Stroke Volume Relatively fixed at 1.5 ml/kg

Factors that affect SV

♥ Preload

♥ Afterload

♥ Contractility

Preload

The volume of blood in the ventricle beforecontraction

Dependent upon venous return to the heart

An ↑↓ in preload can significantly affect CO in the neonate’s non compliant heart

Clinically, a measure of pressure rather than volume

Preload Changes

↓ ♥ Intrapartum blood loss

♥ Hypovolemia ♥ Peripheral pooling secondary to bacterial sepsis

↑ ♥ Fluid overload

♥ Left to right shunt thru PDA, VSD, PFO

Contractility

Speed of ventricular contraction -Intrinsic pumping ability

Neonate’s heart has a limitedcapacity to increase contractility

Cannot be clinically measured

Contractility

Decreased by:AcidosisHypoxiaHypocalcemiaHypoglycemiaHypercarbiaMyocarditis

Resistance to blood leaving the ventricles

Dependent on the systemic vascular resistance and pulmonary vascular resistance

After-load can be reduced by IV infusions of vasodilators

Cardiovascular function is modulated by the autonomic nervous system

Baroreceptors

Baroreceptors and chemoreceptors in the aorta and carotid sinuses provide feedback to the autonomic nervous system

The parasympathetic or sympathetic nervous systems are then stimulated

Sympathetic stimulation through the ganglionic chain releases norepinephrine and epinephrine which act on the SA node, the AV node, the atria and the ventricles.

Alpha- and beta-adrenergic receptor stimulation

alpha - ↑ contractility and ↑ ratebeta – vasodilatation, bronchodilation, and smooth muscle relaxation

Congestive Heart Failure

♥ Myocardial dysfunction in which the heart is unable to pump enough blood to meet its needs, to dispose of venous return adequately, or a combination of the two

♥ May result from CHD or acquired heart diseases with volume or pressure overload or from myocardial insufficiency

Potential Causes

♥ Structural cardiac defects♥ Cardiomyopathy♥ Cardiac arrhythmias♥ AV malformations♥ Multiple hemangiomas♥ Asphyxia♥ Bronchopulmonary dysplasia

♥ Hypoglycemia♥ Hypocalcemia♥ Severe anemia♥ Polycythemia♥ Fluid overload♥ Renal Failure♥ Adrenal insufficiency♥ Hyperthyroidism

CHF - fetal causes

♥ SVT♥ Severe bradycardia d/t complete heart block♥ Anemia♥ Ebstein’s anomaly♥ Myocarditis

Presentation:Hydrops

Treatment:Digoxin

CHF - occurring the first day of life

♥ Asphyxia

♥ Hypoglycemia

♥ Hypocalcemia

♥ Sepsis

CHF - occurring the first week of life

♥ PDA

♥ Adrenal Insufficiency

♥ Closure of PDA with ductal dependent lesion:

Coarctation of the aorta

Hypoplastic left heart syndromeInterrupted aortic arch

CHF - occurring beyond the second week of life

♥ VSD most common reason

♥ Truncus arteriosus

CHF –pulmonary presentation

♥ Poor weight gain♥ Poor feeding of recent onset♥ Feeding intolerance♥ Tachypnea, dyspnea that worsens during

feeding♥ Increased WOB:

Grunting, flaring, and retractingHead bobbing

♥ Rales, rhonchi, wheezing♥ Irritability, lethargy♥ Pulmonary infiltrates on CXR

Pulmonary venous engorgement

Cause is blood backing up in the pulmonary system

Leakage of fluid into the pulmonary interstitium

• Interferes with gas exchange

• LV dysfunction &/or overload may increase LV end diastolic pressure

CHF – CV presentation♥ Cold sweat on forehead - diaphoresis♥ Puffy eyelids, dependent edema♥ Pallor, mottling, cyanosis♥ Increased precordial activity ♥ Peripheral pulses initially full but decrease in

end stage, prolonged CFT♥ Tachycardia, gallop rhythm, BP changes♥ Decrease in urine output (<0.5 ml/kg/hr),

increase in specific gravity♥ Sudden weight gain in end stages♥ Hepatomegaly ♥ Cardiomegaly on CXR

Systemic venous engorgement

Blood backing up in the systemic system

Leakage of fluid into the periphery interstitium and liver

Hepatomegaly

RV dysfunction &/or overload my increase RV end diastolic pressure

CHF – SNS compensatory mechanisms

↓ Systemic BP activates baroreceptors

↑ sympathetic stimulation

♥ ↑ HR

♥ ↑ cardiac contractility

♥ ↑ arterial BP

CHF – SNS compensatory mechanisms

Catecholamine release↑ venous tone ↑ blood return to the heart

↓ circulation to skin, kidneys, extremities, & splanchnic bed

↓ Renal blood flow stimulates release of renin angiotensin, and aldosterone

which triggers retention of Na and fluid, resulting in increased circulating blood volume

↑ Blood volume puts additional work load on the heart

CHF – mechanical compensatory mechanisms

Cardiac muscle thickens to ↑ myocardial pressure

Hypertrophy effective in early stages

as muscle mass ↑ compliance ↓

↓ compliance requires ↑ filling pressure for CO

CHF – mechanical compensatory mechanisms

Hypertrophied heart eventually becomes ischemic

Ventricular dilation occurs to accommodate volume

Initially the heart tries an increased force of contraction but soon fails

CHF - management♥ Elimination of underlying causes

♥ Elimination of precipitating causes

♥ Treatment:� fluid restriction� supportive care with supplemental FiO2� limiting PO feeding� increased calorie feedings� diuretics� inotropic/chronotropic agents� afterload-reducing agents

Medications for CHF

Diuretics:Furosemide (Lasix)

Spironolactone (Aldactone)

Digoxin:positive inotropic ↑ cardiac contractility

negative chronotropic ↓ HR

Shock

♥ An acute state in which circulatory function is inadequate to supply sufficient amounts of O2 and nutrients to meet metabolic demands

♥ In most cases, cardiac output is low

♥ In early shock, compensatory regional vasoconstriction may temporarily maintain normal BP

Hypotension

♥ Late sign - cardiac decompensation

♥ Treatment of shock based on more than BP:

Evaluate history

Physical exam

Labs

Shock

♥ As shock progresses, compensatory mechanisms fail and there is widespread cellular damage

♥ Insufficient delivery of O2 results in anaerobic metabolism and lactic acidosis.

Shock

♥ If shock persists, irreversible injury to vital organs occurs, death ensues despite vigorous treatment that may temporarily return cardiovascular measurements to normal

Shock Etiology

♥ Hypovolemia

♥ Asphyxia

♥ Cardiogenic causes

♥ Sepsis

♥ Drugs

Hypovolemia

Blood loss

Inadequate placenta transfusion

Feto-maternal transfusion

Severe dehydration

Asphyxia

Antepartum

Intrapartum

Respiratory failure

Impaired O2 transport due to severeanemia or hemoglobinopathy

Cardiogenic

Cardiomyopathy

Dysrhythmias

Congenital malformation

Hypocalcemia

Severe hypoglycemia

Sepsis

Especially early onset group B beta-hemolytic Streptococcal

Drugs

Hypovolemic infants whose BP has been maintained by vasoconstriction and are given vasodilators

PGE1isoproterenolmagnesium

Shock Presentation

Cardiovascular

� Systemic arterial hypotension

� Narrow pulse pressure

� Central venous hypotension, althoughCVP may be elevated with cardiomyopathy

� Tachycardia

Shock Presentation

Respiratory

� Tachypnea� Retractions� Grunting� Apnea

Other signs

� Prolonged capillary fill time

� Oliguria� Hypothermia� Metabolic

acidemia

Cardiac Tamponade –a medical emergency

♥ The hemodynamic result of fluid accumulation in the potential space surrounding the heart or pericardium.

♥ Excessive fluid accumulation results in ↑ pericardial pressure, causing ↓ ventricular filling, ↓ cardiac output and hypotension.

♥ The rapidity of fluid accumulation influences the hemodynamic effect.

♥ Beck’s triad (jugular venous distension, hypotension, and muffled heart sounds).

PICC

cardiactamponade

Congenital Heart Disease

Increased Pulmonary Flow:PDA - Patent Ductus Arteriosus

VSD – Ventricular septal defectAV Canal – Endocardial Cushion

partial or complete30% are infant’s with trisomy 21

ASD – Atrial Septal Defect

Congenital Heart Disease

Ductal dependent lesions that decrease pulmonary blood flow:

TOF - Tetralogy of Fallot with severe PS or PA

PA - Pulmonary AtresiaPS - Pulmonary StenosisTA - Tricuspid Atresia

Congenital Heart Disease

Mixed lesions:TGA -Transposition of the great arteries

TAPVR - Total anomalous pulmonary venous return

HLHS - Hypoplastic left heart syndrome

TA -Truncus arteriosus

Ductal Dependent Defects

♥ Need to have PDA open for systemic or pulmonary circulation

♥ PGE1 continuous infusion to open and maintain ductal patency

EKGcardiac depolarization is the result of an electrical

discharge across the myocardial cell

cardiac depolarization is measured by the EKG

reflects abnormal hemodynamic burdens placed on the heart

right ventricular prominence normal after birth

major tool to evaluate arrhythmias and the impact of electrical imbalances

Echocardiogram

The Gold Standard

Provides rapid, non-invasive, and painless evaluation of the ♥ anatomy and flow by the use of ultrasonic waves

Cardiac Catheterization

♥ Invasive procedure to obtain data for a definitive diagnosis, intervene, or to prepare for surgery

♥ DiagnosticEvaluate hemodynamicsSelective angiography

♥ InterventionalBalloon atrial septostomy (Rashkind)Balloon valvuloplasty Balloon angioplasty

PDA

Shunts right to left flow in utero

Persistent PDA will shunt left to right as PVR decreases

Functional closure - constricted but can open again

Anatomic closure – permanently closed

PGE used to open PDA:If you need left to right flow for pulmonary perfusionIf you need right to left flow for systemic perfusion

erex

Self Study the following Congenital Heart Defects

AV Canal

♥ Endocardial Cushion Defect or Atrioventricular Septal Defect

♥ Partial involves the atria

♥ Complete involves atria and ventricles

AV canal Risk Factors

Trisomy 21Rubella or other viral illness during early pregnancyAlcohol consumptionPoorly controlled diabetesSmokingParent with a CHD

AV canal complications

♥ Cardiomegaly

♥ Pulmonary Hypertension

♥ Respiratory Tract Infections

♥ Congestive Heart Failure

Complications after correction of AV canal

♥ Regurgitant heart valves

♥ Stenosis of the heart valves

♥ Arrythmias

♥ PPHN

♥ Breathing difficulties associated with lung damage

COA – Coarctation of the aorta

♥ Juxtaductal narrowing of aorta

♥ Frequently associated bicuspid aortic valve

♥ Often associated with hypoplastic transverse arch

♥ Mild left heart hypoplasia

COA - Coarctation of the aorta

♥ As the ductus arteriosus closes the area of coarctation narrows

♥ The result is decreased systemic blood flow

♥ In severe cases, CHF results from decreased left ventricular function

With ducal closure shock and tissue hypoxia

HLHS – hypoplastic left heart syndrome

♥ Hypoplasia of left ventricle

♥ Severe mitral valve stenosis or atresia or severe aortic valve stenosis or atresia

♥ Hypoplastic ascending aorta and transverse arch

♥ Coarctation is a frequent finding

HLHS

Ductal dependent blood flow right to left to perfuse all regions of the body

Management: COA & HLHS

♥ To open PDA and to improve systemic perfusion

♥ Intubation and ventilation to reduce work of breathing and strain on the heart

♥ Avoid hyperoxia and hypocarbia (both will decrease PVR at the expense of systemic blood flow)

♥ Inotropic support may improve myocardial function

♥ Follow arm and leg BPs

TOF – Tetralogy of Fallot

♥ 4 anomalies� Large VSD� Right ventricular outflow tract obstruction� Overriding aorta� Right ventricular hypertrophy

♥ Symptom severity depends on the degree of right ventricular outflow tract obstruction

TOF

TOF - Management

♥ Supplemental FiO2 to treat cyanosis

♥ The majority are not ductal dependent

♥ If saturation still below 75% on oxygen may have significant pulmonary stenosis or atresia and need PGE

TET Spell Hypoxic Spell

♥ Cyanotic or hypercyanotic spell� Progressive hypoxia� Hyperpneic� Pale, flaccid� Immediate treatment needed� Organ damage if severe hypoxia and acidosis� Eventual loss of consciousness

TET Spell Management

Calm infantIncrease systemic vascular resistance to decrease the right to left shunt at the VSDKnees to chestMay need to be sedatedFiO2 but will only improve oxygenation once right to left shunt is decreasedMay need intubation and correction of metabolic acidosis

Pulmonary stenosis/atresia

♥ Stenosis is a narrowing

♥ Atresia means not formed, so absence

PS Pulmonary Stenosis

♥ Varying degrees of pulmonary valve narrowing

♥ If critical PS the right ventricle cannot eject sufficient blood flow to the pulmonary artery to maintain normal oxygen saturations.

♥ If critical PGE is required to allow blood to shunt left to right to perfuse the lungs

♥ A newborn with critical pulmonary stenosis and intact VSD presents an emergency situation that requires immediate treatment, either balloon dilation of the valve or surgery.

PS Presents with varying degrees of cyanosis after birth

PA Pulmonary Atresia with intact ventricular septum

♥ Atretic pulmonary valve ♥ Hypertrophied right ventricle♥ Hypoplastic right ventricle

♥ Pulmonary blood flow is dependent on the PDA

TGA – Transposition of the Great Arteries

Great arteries are transposed relative to the ventricles

TGA

♥ Circulation pattern is parallel

♥ The majority of the blood from each ventricle is circulated back to the same ventricle

♥ Mixing must occur:Best to have a VSDand a PFO/ASD that is not restrictiveUse PGE to open the PDA

♥ If no VSD and a restrictive PFO/ASD a Rashkind/Balloon septostomy may be needed

There needs to be adequate mixing at 2 sites!

TAPVR – Total Anomalous Pulmonary Venous Return

TAPVR Types

♥ Supracardiac emptying into the left vertical vein (most common type 80-90%) which then drains into the SVC

♥ Cardiac emptying into the coronary sinus or right atrium

♥ Infradiaphragmatic emptying into the vertical vein that descends through the diaphragm into the portal vein or IVC

Infracardiac Obstructed TAPVR

♥ Oxygenated pulmonary blood mixes with deoxygenated systemic blood and returns to the right atrium to shunt right to left across the PFO/ASD to get to the left atrium and eventually to the body

♥ Severe hypoxia and profoundly ill after birth

Management Infracardiac Obstructed TAPVR

- Intubation 100% FiO2

- Treat acid /base disturbance

- Treat hypotension, hypothermia

- Emergency corrective surgery is required to anastomose the pulmonary veins to the heart

CXR Cardiac or supracardiac

CXR Obstructed TAPVRCXR can be confused with RDS or PNA