Cardiac Flashcards
Gastrulation
cardiac development - the arrangement of the 3 germ layers
Heartbeat begins & blood pumping
at 22-23 days of life and begins pumping blood during week 4
Complete cardiac development
occurs at 6 weeks - disorders of this embryological age include transposition, dextrocardia
Maternal Diabetes and CHD
Diabetes prior to conception increases risk by 2-4x; Elevated insulin levels result in hypertrophic cardiac tissue,
common CHD: transposition, VSD, cardiomyopathy
Rubella and CMV r/t CHD
PDA, ASD, VSD
SLE r/t CHD
fetal and neonatal complete congenital heart block and dilated cardiomyopathy
Maternal influenza r/t CHD
Right ventricular outflow tract obstruction
Male infants more likely CHD
COA, aortic stenosis, TGV, hypoplastic left heart
premature infants r/t CHD
PDA, ASD, VSD
weak pulses
shock, myocardial failure, or left outflow obstructions
bounding pulses
cardiac runoff (surplus), aortic insufficiency, systemic to pulmonary shunts (left to right)
continuous bruit murmur over fontanelle and liver
AV malformation
CHD associated with Trisomy 21
AV Canal, VSD, PDA, ASD-1 and -2, TF
CHD associated with Trisomy 18 (Edwards syndrome)
VSD, polyvalvular disease, ASD, PDA
Trisomy 13 (patau’s syndome)
PDA, VSD, ASD, Coarctation, AS, PS
3 physiological states of CHD
- low cardiac output
- Congestive Heart failure
- Cyanosis
Low Cardiac Output
defect that obstructs flow of blood out of heart or when heart is unable to pump effectively
Management of Low Cardiac Output
Correct heart rate (increase)
fluid administration
correct acid base imbalance
Meds to improve heart function
Signs of Low Cardiac Output (8)
pale, mottled skin
decreased LOS
Decrease UOP
Cap Refil >3 seconds
hypoglycemia
metabolic acidosis
increased serum lactate
Weak pulses
Signs of CHF (8)
flaring
tachypnea
retractions
tachycardia
pulmonary edema
cool, clammy skin
diaphoresis
fatigue
Management of CHF
Meds (diuretics)
Limit fluid administration
Resp. Support
Improve Nutrition
Temperature Control
Congestive Heart Failure
occurs when there is a defect that causes an increase in blood to the lungs
Cyanosis (in relation to CHD)
When the defect causes a decrease in blood flow to the lungs
Differentiating Cyanosis (Respiratory or Cardiac)
Respiratory - cyanosis decreases with crying, improves with O2 admin, signs of resp. distress present
Cardiac - cyanosis increases with crying, doesn’t improve with O2 admin, tachypnea but no signs of distress
Hyperoxia test
Take radial arterial Blood gas (pre ductal) on room air
Admin 100% FiO2 for 10 minutes
Repeat ABG
PaO2 <150mmHg - Cardiac
PaO2 >150mmHg - Respiratory
Interventions for cyanotic cardiac defects
Maintain high hematocrit (to maximize o2 carrying capacity)
Fluid administration
admin of supplemental o2
prostaglandins to keep PDA open
S1
closure of mitral and tricuspid valves during ventricular systole
heard at apex
Loud at birth decreases in intensity over 48 hours
s1 is louder with increased cardiac output
s2
sound of the semilunar ( aortic and pulmonary valves) closing
heard best at the base of the heart
s3
if heard, signified rapid or increased flow across the AV valves
commonly heard in premature infants with PDA
s4
always pathologic, heard in conditions characterized by decreased compliance or CHF
Ejection clicks
snappy, high frequency sounds, if present can be heard after the first heart sound, commonly heard during the first 24 hours of life and are normal at that time, but always considered abnormal after 24 hours
associated conditions : aortic or pulmonic stenosis, pulmonary artery, systemic or pulmonary hypertension, truncus arteriosus, TOF
Systole
the period when the heart contracts and the heart chambers eject blood
Diastole
heart relaxes, and the chambers fill with blood
Grade I murmur
barely audible, audible only after careful auscultation
Grade 2 murmur
soft, but immediately audible
grade III murmur
of moderate intensity, but not associated with a thrill
grade IV murmur
louder (may be associated with a thrill)
Grade V murmur
Very loud, can be heard with the stethoscope rim barely on the chest
Grade VI murmur
extremely loud; can be removed with the stethoscope just slightly removed from the chest
systolic ejection murmurs
the most common innocent murmur
usually grade I-II/VI
Best heard along the mid and upper left sternal border
result of turbulent flow across pulmonary valve and associated with rapidly decreasing pulmonary resistance
Continuous systolic or crescendo systolic murmur
usually Grade I-II/VI
best heard at upper left sternal border
caused by transient left-to-right flow through the DA
Pathologic murmurs heard in the delivery room
usually a result of stenosis or regurgitation
continuous murmur
occurs in 1/3 of premature neonates with a PDA
Hepatomegaly
occurs with increased central venous pressure. A liver more than 3cm below the sternal border indicates right-sided heart failure in a term infant
Blood pressure changes after birth
BP decreases in the first 3-4 hours of life because of fluid shifts into and out of the vascular space; systolic pressure reaches a minimum at 3-4 hours and plateaus at 4-6 hours
Pulse Pressures
difference between systolic and diastolic pressures;
normal: term: 25-30
preterm: 15-25
widened pulse pressures indicate aortic runoff as in pDA
ASD begins as a ___ to ___ shunt
left to right
Eventually, in ASD, the ___ to ____ shunt causes _____ and eventually leads to ____
Eventually, in ASD the right to left shunt causes pressures to increase and eventually leads to pulmonary hypertension
ASD signs and symptoms
often asymptomatic; large ejection murmur
most common types: 1) secundum (assoc with Holt-Oram) 2) Primum (AV Canal assoc) 3) sinus venosus 4) coronary sinus
MOST CLOSE BY AGE 2
surgery indicated for sinus venosus, secundum ASD
Ventricular Septal Defects
most common congenital heart defect; shunting left to right in the ventricles
With large VSDs, there is overload in the ____ side of the heart resulting in:
right; pulmonary overcirculation, CHF, respiratory distress, and pulmonary edema; infants may also experience poor growth
VSD presentation
acyanotic with a grade II, holosystolic harsh murmur located at the lower sternal border which may not be audible until PVR decreases;
Larger VSDs may result in CHF symptoms;
CXR may show normal - large heart size and increased pulmonary vascular markings;
Arrthymias secondary to VSDs
PVCs, PACs, signs of RVH on EKG, tachycardia
Dextrocardia
heart is on the right side of the body
2 types of dextrocardia
- levocardia
- situs inversus
Levocardia
heart is formed on the right side of the body, but no change in rotation of the heart
Situs inversus
heart is formed on the right side of the body, heart is completely rotated to the right, aorta arches to the right
Ebstein’s anomaly
displaced tricuspid valve down into the right ventricle creates a small right ventricle
= a decrease in ventricular output,
= only allows an insignificant amount of blood into the pulmonary artery
creating a ductal dependent lesion
often accompanied by an ASD
ebsteins anomaly
ebstein’s anomaly presentation
cyanosis dependent on degree of right-to-left atrial shunting; holosystolic murmur varying from grade I-VI
low PaO2 on ABG (<20)
CXR abnormal for cardiomegaly and diminshed pulmonary vasculature
EKG positive for abnormal P waves, SVT, and Right Bundle branch block
May be associated with wolfe-parkinson-white syndrome, COA, ASD, and PA
Ebsteins anomaly management
- o2 administration
- prostaglandins to increase pulmonary blood flow and relieve hypoxemia
- sildenafil (vasodilator) to decrease right ventricular afterload
Tetralogy of Fallot
4 related disorders:
- pulmonary stenosis
- VSD
- overriding aorta
- Right ventricular hypertrophy
The most common cyanotic heart defect
TOF
TOF presentation
ABG shows normal pH, normal Co2, pO2 depends on degree of right-to-left shunting
a “boot shaped” heart on CXR
CBC will show information about possible coinciding anemia or sepsis
A large VSD lessens symptomatic CHF
TOF management
TOF maybe ductal dependent and require prostaglandins, surgical repair
TOF
Truncus Arteriosus
during embryology the outflow track fails to divide the pulmonary artery and aorta; So, there is one single trunk responsible for systemic and pulmonary circulation;
Truncus Arteriosus management
associated with extracardiac anomalies (PS, dysplastic valves, ect, aortic arch interruption), Associated with DiGeorge,
pansystolic lower left sternal border murmur
widened pulse pressures
based on acidosis, murmur, CHF symptoms may be present depending on amount of pulmonary blood flow
o2 may remain close to 85% until PVR decreases and pulmonary blood flow increases
Transposition of great arteries
deoxygenated blood returns to the Right ventricle, and circulated by the aorta, an oxygenated blood returns to the left ventricle and returns to the lungs via pulmonary artery; resulting in a parallel circuit
ASD, PDA, and VSD provide opportunities for mixing blood
more common in males
PaO2 will be low if the septum is intact
PG-E1 indicated; ductal dependent
TAPVR (Total anomalous Pulmonary Venous Return) types
4 types
- Supracardiac (most common) - pulmonary blood returns oxygenated blood into the superior vena cava
- infracardiac - pulmonary vein routes through the diaphragm and into the IVC
- cardiac (routes pulmonary veins through coronary sinus or right atrium
- mixed
TAPVR signs
“snowman sign” on CXR; presentation varies because of the different types; an obstructive TAPVR the result is venous congestion and decreased pulmonary flow;
TAPVR may be asymptomatic
INFRACARDIAC PRESENTS IN THE NEONATAL PERIOD
Tricuspid atresia
the right atrium and right ventricle are not connected due to agenesis of the tricuspid valve; resulting:
right ventricular hypoplasia
Pulmonary artery hypoplasia
VSD
Blood shunts across the ASD, goes to the lungs via left-to-right shunting via the PDA or VSD
Relies on the presence of an ASD for survival
PGE required (ductal dependent)
Prostaglandin E1 (Alprostadil) Use and Side Effects
to maintain ductus patency;
larger ductus requires lower dose, small ductus requires higher dose;
Major side effect: apnea
other side effects: hypotension & tachycardia
Coarctation of the Aorta (interrupted aortic arch)
an obstruction or constriction of the aortic arch near the PDA; a ductal dependent lesion
generally develops postnatally
associated with Turners syndrome
twice as high in males as in females
more severe obstruction results in left sided heart failure or poor cardiac output
Signs of COA
diminshed femoral pulses; cardiomegaly on CXR and increased cardiac markings;
ABG reflective of shunting
COA management
ductal dependent = PG E1 for infants with poor perfusion and signs of CHF
continuous inotropes such as dopamine and dobutamine are suggested for cardiovascular support
metabolic acidosis should be corrected;
Hypoplastic Left Heart
characterized by coinciding spectrum disorders: aortic valve atresia, mitral valve atresia, severe left ventricular hypoplasia, aortic hypoplasia and COA
An ASD is required to mix blood and decrease pulmonary edema; Only available circulation is blood traveling from the PA through the DA to the aorta
critically ductally dependent to prevent systemic hypotension, acidosis, organ perfusion
associated with turner syndrome, trisomy 9, 13, 18, holt-oram, smith-lemli-ortiz, jacobsen
HLHS presentation
presents as cyanosis, tachynpea, with no murmur; perfusion and palpable pulses with diminish with ductal closure;
HLHS management
PG E1 to maintain patency, avoid oxygen with HLHS because it is a vasodilator
volume expansion and inotropes help balance pulmonary circulation with system circulation; eventual surgery
AV Canal Defects
The endocardial cushion fails to form the center of the heart;
AV Canal Association
Trisomy 21
AV Canal presentation
Presents as desaturation and cyanosis due to right-to-left shunting until PVR decreases and flow is reversed as in CHF;
AV Canal management
addressing cyanosis with supplemental O2, care of CHF which may involve lasix, digoxin, and an afterload reducer;
avoid oxygen in the presence of CHF as it is a vasodilator and may increase pulmonary blood flow
surgical correction at 2-6 months
Aortic Stenosis
a valvular disease resulting in left-sided outflow obstruction
if critical it results in decreased systemic output and cardiogenic shock
males affected x3 than females
Aortic Stenosis Associations
associated with Williams syndrome
Aortic stenosis presentation
harsh midsystolic murmur audible with systolic ejection click; a palpable thrill at the suprasternal notch should be evident;
pulse oximetry will show a gradient between the upper and lower extremities due to Right to left shunting
management is PG E1 - if CHF - surgical procedure
PDA associations
more common in females and associated with chromosome 12;
PDA presentation
results from left-to-right shunting which may also decrease cardiac output and increase the workload of the left side of the heart
presents with:
upper Left quadrant loud machine like systolic murmur
bounding pulses
visible precordium
widened pulse pressures
worsening respiratory status due to pulmonary edema
CHF
r/t pressure overload (AS, COA), volume overload (L-R shunting in PDA, TA, TOF, VSD, AV canal, single ventricle, AVM), a combo of pressure and volume overload (IAA, COA with VSD, AS)
CHF presentation
tachypnea, sinus tach, hepatomegaly
worsening CHF may include grunting, retractions;
later symptoms include poor feeding and growth
CHF management
decrease o2 consumption (thermoneutral environment)
o2 admin, fluid restriction, increased calories without volume,
pharm: PG E1 if due to ductal dep., diuretics, inotropes, digoxin, afterload reducers
Dopamine
an endogenous catecholamine that produces a cardiovascular response to stimulate dopaminergic, alpha-adrenergic, beta-adrenergic and sertoninergic receptors to increase BP
dose: 2 to 20 micrograms/kg/minute
Dobutamine
a cardioselective sympathomimetic amine with signficant alpha-adrenoreceptor mediated and Beta-adrenoreceptor mediated inotrope which reduces peripheral vascular resistance;
works best for neonates with cardiac dysfuction and elevated pulmonary vascular resistance;
Dobutamine added to Dopamine for infants with RDS improves BP
Epinephrine
an alpha and beta adrenergic agonist and sympathomimetic agent that increases BP and increases cerebral vascular blood flow
Milrinone
a phosphodiesterase 3 inhibitor which reduces afterload in neonates with CHD or with low cardiac output;
shown to improve oxygenation of infants with PPHN
vasopressin
a synthetic antidiuretic hormone that impacts the cardiovascular system by vasoconstriction (works similar to dopamine)
Premature Atrial Contractions
early depolarization of the atria but are not from the sinus node; True PACs are followed by a QRS complex,
Bigeminy refers to PACS every other beat
generally asymptomatic
Atrial flutter
a type of reentry tachycardia via the atrial myocardium at the tricuspid valve;
rate usually 300 to 600 bpm,
Atrial Fibulation
A Fib rare in neonates; a continuous dysrhythmia; associated with Ebstein anomaly, and wolfe-parkinson-white syndrome
Premature Ventricular Contraction
an early beat due to a spontaneous ventricular depolarization of the ventricles;
if baby is asymptomatic, neg family history, and PVCs disapear with higher heart rates - considered benign
Ventricular Tachycardia
originates below the bundle of his; impacts hemodynamics and cardiac function may require intervention
complete AV heart block (3rd degree)
indicates a disfunctional AV node; making the atria and ventricles independent of one another
associated with maternal SLE
Average BP for term infant (systolic, diastolic, MAP)
56-77 systolic
33-50 diastolic
MAP 42-60
Fetal circulation: deoxygenated blood leaves the fetus and returns to the placenta via the ___________.
umbilical arteries
Fetal circulation: Freshly oxygenated blood returns from the placenta to the fetus via __________ going into through the fetal ________ and then to the _________.
the umbilical vein
fetal liver
right atrium of the heart
Fetal circulation: From the right atrium, the blood shunts through the _______ into the ___________ and then is pumped into the ___________ and out of the ___________ to the rest of the body (brain first).
PFO into the left atrium and then left ventricle and out to the aorta
Fetal Heart pressures are higher on the _______ because ________
Right because the lung is collapsed, so pulmonary vascular resistance is very high!
After birth, pressures on the _____ side of the heart is higher because PVR decreases when _________.
Pressures on the Left side of the heart is higher because PVR decreases when the lung inflates.
D-transposition vs L-transposition
D-transposition (most common) occurs when the right ventricle emptys into the aorta which takes deoxygenated blood to the body and the left ventricle sends already oxygenated blood back to the lungs. Only opportunity for mixing are PDA, ASD, VSD
L-transposition - not as common, but occurs when the the Left and right ventricles are swapped. It ends up being less symptomatic because the vessels empty to the right places but are side by side instead of the pulmonary artery looping through the aorta like normal.
