NCC Cardiac Content
♥ Cyanosis Central / Peripheral Cardiac / Pulmonary
♥ Arrhythmias
♥ Anomalies (Cyanotic / Acyanotic) AV Canal Coarctation of aorta HLHS Pulmonary stenosis/atresia TOF TGA TAPVR
Fetal Circulation
Embryonic Development
Cardiac septation: begins middle of the 4th week and complete by end of 5th week Defects arising from problems in
septation: VSD, ASD, endocardial cushion defect (AV canal), malformation of tricuspid and mitral valves
Great Vessel Development Happens simultaneously with septation Defects that occur with great vessel
development: Truncus Arteriosus TOF Pulmunary and Aortic valve
malformations Transposition DORV
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
♥ Saturations: Pre and post
♥ Normal sinus rhythm
Underlying causes ♥ Vagal response ♥ 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
♥ 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 180-220 Sympathetic stimulation Fever
SVT Supraventricular Tachycardia
associated with:
Structural CHD
- 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
End of atrial systole
S1 Accentuated, may mean: Increased CO PDA, VSD, TAPVR, TOF AVM Anemia Fever
Diminished, may mean: CHF Myocarditis
Heart Auscultation Second heart sound – S2
Closure of aortic and pulmonic valves End of ventricular systole Split S2 is a normal finding and just reflects the aortic
valve closing before the pulmonic valve.
S2 First 48 hours
Normal to hear single S2 in first two days of life because of increased PVR. If you hear a split S2 at birth, could indicate abnormalities of P or A valves or alterations in PVR and SVR.
• After 48 hours • S2 split elongated
• ASD, TAPVR, TOF, Ebstein’s anomaly • Absent split
• Aortic stenosis, PPHN, TGA, TA
S3 & S4 S3: Only heard in left to right shunts
and mitral valve insufficiency S4: Should not be heard in newborn.
If so, indicates decreased ventricular compliance
Ejection clicks: Abnormal after 24 HOL and heard after S1. Associated with dilation of great vessels or malformation of PV and AV
Heart Murmur
♥ Blood forced through narrowed areas
♥ Regurgitation through incompetent or abnormal valves
♥ Increased flow across normal structures
Heart Auscultation
Heart Murmur Intensity
Grade I - barely audible Grade II - soft but audible Grade III - moderately loud, no thrill Grade IV - loud, assoc. with thrill Grade V - audible with stethoscope barely
touching chest Grade VI - audible with stethoscope not
touching chest
Heart Murmur Timing
♥ Systolic Heard between S1 and S2 of same beat S1 (murmur) S2 S1 (murmur) S2
♥ Diastolic Heard between S2 and S1 of next beat S1, S2 (murmur) S1, S2 (murmur)
♥ Continuous Starts in systole and extends into diastole
Normal/Innocent Murmurs
♥ Early soft midsystolic ejection murmur aka Peripheral pulmonic stenosis (PPS) Grade I-II/VI (no thrill) upper left sternal border, radiates to axilla and back
♥ Systolic ejection murmur (turbulence of blood flow across pulmonary valve)
Grade I-II/VI may be heard 1st week of life as PVR decreases and PDA closes
Up to 50% of neonates can have a murmur in the first 48 hours of life
Pathologic Heart Murmur
SYSTOLIC • Pan systolic murmur
♥ > Grade 3 murmur within hours of birth
Pathologic Heart Murmur
Assessment - Obeservation
♥ Precordium: quiet, visible, heave, thrill PMI - LLSB 5th intercostal space
PMI shifted to the right: Dextrocardia Tension pneumothorax Diaphragmatic hernia
PMI shifted to the left Tension right pneumothorax
Assessment - Palpation
♥ Pulses: compare upper to lower extremities and side to side (if not equal, could mean LOTO)
R Brachial and femoral equal in strength (R brachial = R subclavian = pre-ductal)
Pedal pulses palpable Weak: LOTO, myocardial failure or shock Bounding (=“aortic runoff”): PDA, aortic
insufficiency, systemic to pulmonary shunt
♥ CFT: press for 5 seconds, release < 3 seconds normal
Assessment Auscultation
arteriovenous malformation
Cyanosis - Peripheral
membrane involvement
Rule out hypothermia
Results from sluggish movement of blood to the extremities and increased tissue oxygen extraction
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.
♥ At least 5g of desaturated hemoglobin/dl is necessary before you can observe cyanosis.
♥ Also influenced by presence of anemia or polycythemia
♥ Indicates cardiac or respiratory dysfunction
= deoxygenated blood leaving the
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 tachypnea Respiratory acidosis Metabolic acidosis
Mixed resp/metabolic if pulmonary disease
CXR Asymmetric pattern of Increased or decreased infiltrates 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
Coarctation of the aorta
PDA
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 BP = 90/60 mmHg at 40 wks post conception.
Renal abnormalities most common cause
Hypertension Treatment
♥ Tx etiology if possible
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 Cycle Systole & 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 tachycardia HR 230 60 ÷ 230 = 0.26 secs HR 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 before contraction (or at the end of diastole – aka end diastolic pressure)
Clinically, a measure of pressure rather than volume
Dependent upon venous return to the heart
An ↑↓ in preload can significantly affect CO in the neonate’s non compliant heart
Preload Changes
sepsis
↑ ♥ Fluid overload ♥ Left to right shunt thru PDA, VSD, PFO
Contractility
Intrinsic pumping ability
Neonate’s heart has a limited capacity to increase contractility
Cannot be clinically measured
Decreased by: Acidosis Hypoxia Hypocalcemia Hypoglycemia Hypercarbia Myocarditis
Dependent on the systemic vascular resistance and pulmonary vascular resistance (increase in SVR or PVR = afterload)
After-load can be reduced by IV infusions of vasodilators
Resistance to blood leaving the ventricles
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 ↑ rate beta – 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
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 ♥ HLHS ♥ Hypoglycemia ♥ Severe tricuspid or pulmonary regurgitation ♥ Hypocalcemia ♥ Sepsis ♥ Systemic AVM
CHF - occurring the first week of life ♥ PDA ♥ TGA ♥ Adrenal Insufficiency ♥ TAPVR ♥ Closure of PDA with ductal dependent
lesion: Coarctation of the aorta Hypoplastic left heart syndrome Interrupted aortic arch
CHF - occurring beyond the second week of life
♥ VSD most common reason
CHF –pulmonary presentation
♥ Poor weight gain *** ♥ Poor feeding of recent onset *** ♥ Feeding intolerance ♥ Tachypnea, dyspnea that worsens during
feeding *** ♥ Increased WOB:
♥ Rales, rhonchi, wheezing *** ♥ Irritability, lethargy ♥ Pulmonary infiltrates on CXR
Pulmonary venous engorgement (aka Pulmonary Edema)
Cause is blood backing up in the pulmonary system Leakage of fluid into the
pulmonary interstitium
• 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
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
↓ 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
Hypertrophy effective in early stages as muscle mass ↑ compliance ↓
↓ compliance requires ↑ filling pressure for CO
CHF – mechanical compensatory mechanisms
Ventricular dilation occurs to accommodate volume
Initially the heart tries an increased force of contraction but soon fails
CHF - management ♥ Prone position
CHF - management
Fluids and nutrition Fluid restriction limiting PO feeding increased calorie feedings
Medications for CHF
Diuretics: Furosemide (Lasix)
Hypochloremia and hypokalemia can lead to metabolic alkalosis. Can also cause
hypocalcemia . Spironolactone (Aldactone)
K+ and Ca sparing; not as powerful as a diuretic
Medications for CHF
hypokalemia
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
Evaluate history
Physical exam
♥ 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
(gastroschisis) • Pleural effusions
Cardiogenic Cardiomyopathy
Drugs
1. Maximize cardiac output 1. epinephrine 2. dopamine 3. dobutamine 4. Milrinone 5. Isoproterenol (increases HR and
contractility)
Central venous hypotension, although CVP may be elevated with cardiomyopathy
Tachycardia
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).
Congenital Heart Defects
85% multifactorial 10% chromosomal 2% genetic 2% maternal or environmental
teratogens
Chromosomal abnormalities
You will often see cardiac defects with: Trisomies (esp. 18 and 13) Turner syndrome Noonan’s DiGeorge 22q11
Environmental Factors and Teratogens Thalidomide Anticonvulsants (Phenytoin,
Carbamazepine, Valporic Acid, Pentobarbital, Trimethadione)
Anticoagulants (Warfarin, Heparin) Lithium Alcohol Amphetamine
Maternal Disease and Viral Infections Diabetes: 5 x’s the risk of CHD (VSD,
DORV, TGA, TA and coarctation) Lupus (heart block) Rubella and CMV (PDA, PS, VSD,
ASD) Obesity
Increased Pulmonary Flow: PDA - Patent Ductus Arteriosus VSD – Ventricular septal defect AV Canal – Endocardial Cushion
partial or complete 30% are infant’s with trisomy 21
ASD – Atrial Septal Defect
Coarctation of the aorta
TOF - Tetralogy of Fallot with severe PS or PA
PA - Pulmonary Atresia PS - Pulmonary Stenosis TA - Tricuspid Atresia
Congenital Heart Disease
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
PDA
Persistent PDA will shunt left to right as PVR decreases
PGE used to open PDA: If you need left to right flow for pulmonary perfusion If you need right to left flow for systemic perfusion
Pathologic PDA
cardiomegaly on CXR Bounding peripheral pulses Active precordium Widened pulse pressure Low diastolic BP
Indomethacin
chance of ICH
Diagnostics: EKG cardiac 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
Diagnostics: EKG
Tall, peaked P waves are seen in RIGHT sided heart failure
Diagnostics: EKG
Wide, notched P waves seen in LEFT sided heart failure
Diagnostics: Blood Gas
Hyperoxygen Test 1. ABG @ RA 2. 100% FiO2 x 10 mins 3. @ 10 mins, draw ABG 4. If significant bump in PaO2, likely
respiratory. If not,
Diagnostics: X-ray
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
Diagnostic Evaluate hemodynamics Selective angiography
Interventional Balloon atrial septostomy (Rashkind) Balloon valvuloplasty Balloon angioplasty
Pressure Values from Cardiac Catheterization Systemic Arterial Pressure 60 – 90/20
– 60 mm Hg (birth to 5 days) R atrial pressure 3 mm Hg R vent. Pressure 30/3 mm Hg Pulmonary Wedge Pressure 6 – 10
mmHg L atrial pressure 8 mm Hg L ventricular pressure 100/6 mm Hg
erex
Congenital Heart Defects
Defects with INCREASED pulmonary blood flow PDA VSD ASD AV Canal
Obstructive defects with pulmonary venous congestion COA Aortic stenosis
Congenital Heart Defects Obstructive defects with DECREASED pulmonary blood flow TOF Pulmonary stenosis Pulmonary atresia Tricuspid atresia
Mixed Defects TGA TA TAPVR HLHS
Ventricular Septal Defect VSDs are most
common form of all CHDs
Presentation and management will vary according to size of VSD
50% - 75% of small defects will close spontaneously; 20% of large defects will close independently
VSD PVR
VSD
Moderate VSD • Fatigue with feeding • Recurrent respiratory
infections
murmur @ LLSB • CXR: increased
pulmonary vascular markings, cardiomegaly
Atrial Septal Defect
closure around 20%
Defect can be in ostium primum or secundum (most common)
PFO ASD
ASD
Symptoms present in 50% of patients IF ID’d in infancy (most go unrecognized)
Failure to thrive Recurrent respiratory infections Systolic murmur @ 2nd ICS LSB,
persistent split S2 if defect is large, diastolic murmur @ LLSB
AV Canal
♥ Partial involves the atria
♥ Left to right shunt
AV canal Risk Factors
Trisomy 21 Rubella or other viral illness during early pregnancy Alcohol consumption Poorly controlled diabetes Smoking Parent with a CHD
AV canal complications ♥ Cardiomegaly
♥ On auscultation, thrill at the LLSB. Loud pansystolic murmur at LLSB radiating to back
♥ Pulmonary Hypertension
♥ Regurgitant heart valves
♥ Arrythmias
♥ PPHN
COA – Coarctation of the aorta
♥ Juxtaductal narrowing of aorta
♥ 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, pulmonary venous congestion
♥ In severe cases, CHF results from decreased left ventricular function
♥ If severe, with ductal closure, shock and tissue hypoxia
COA Male dominance 2:1
Associated with Turner Syndrome
Presentation: • Decreased or absent LE pulses • Higher blood pressure in UE; BPs may wax
and wane with bidirectional flow through PDA • “systolic thrill @ suprasternal notch” • Cardiomegaly + increased pulmonary vascular
markings on CXR
4 x’s more likely in males
3 types: Valvar is the most common
If AS is severe in utero, fetus will develop LV hypoplasia and L- sided syndrome
Aortic stenosis
LV is hypertrophied
Aortic Stenosis Presentation
If not diagnosed in utero and not severe, asymptomatic at birth , then progresses to CHF
Harsh systolic murmur in URSB that radiates
CXR: cardiomegaly but normal pulmonary vascular markings
Aortic Stenosis: Treatment
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
Boot shaped heart on CXR
TOF - Management
♥ 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 infant Increase systemic vascular resistance to decrease the right to left shunt at the VSD Knees to chest May need to be sedated FiO2 but will only improve oxygenation once right to left shunt is decreased May need intubation and correction of metabolic acidosis
Pulmonary stenosis ♥ Stenosis is a narrowing
♥ Varying degrees of narrowing; severity of symptoms depends on degree of narrowing
♥ Most common form is valvular
Mild Pulmonary Stenosis Loud systolic murmur at LUSB is the
only clinical finding
Severe Pulmonary Stenosis
♥ 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.
Pulmonary Atresia with VSD
PA Pulmonary Atresia with intact ventricular septum
♥ Atresia means not formed, so absence ♥ Atretic pulmonary valve ♥ Hypertrophied right ventricle ♥ Hypoplastic right ventricle ♥ Blood flow R to L across PFO ♥ Pulmonary blood flow is dependent on the PDA♥
Tricuspid Atresia
VSD often present
cases of tricuspid atresia
♥ 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: 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
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 VSD and a PFO/ASD that is not restrictive Use 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
- Treat hypotension, hypothermia
- Emergency corrective surgery is required to anastomose the pulmonary veins to the heart
CXR Cardiac or supracardiac
CXR Obstructed TAPVR CXR can be confused with RDS or PNA
Truncus Arteriosus One great vessel
arising from both ventricles, VSD
One vessel supplying systemic and pulmonary circulation
As PVR decreases, shunting occurs L to R across VSD overloading lungs and LV (unless PS)
Truncus Arteriosus
Bounding pulses, widened pulse pressure Severe cyanosis if TA with PS Harsh systolic murmur LLSB, systolic
ejection click, single S2 Management: Treat CHF (medications
include diuretics, digoxin and ACE inhibitors) Surgical repair
Sample Cardiac Questions
Normal values for pulmonary artery pressures in a term infant would be: A. RAP 7-10 mm Hg, LAP 5-7 mm Hg
and PAOP 4 mm Hg B. RAP 3 mm Hg, LAP 8 mm Hg and
PAOP 6-10 mm Hg C. RAP 10-20 mm Hg, LAP 12-14 mm
Hg and PAOP 10-14 mm Hg
The type of murmur commonly heard in patients with tricuspid atresia is: A. A diastolic murmur B. A systolic murmur C. A holosystolic murmur
An ASD results in: A. No damage to the septum B. A left-to-right shunt with volume
overload C. A diastolic murmur at the USB
Neonates with cyanotic heart defects are at particular risk for: A. Intrarenal kidney injury B. CHF C. Polycythemia
A mechanism by which a newborn can respond to increased volume is via: A. A baroreceptor stretch B. An increased heart rate C. A decreased PVR