Cardiology Flashcards
Characteristics of aortic valve regurgitation
Volume overload of LV
Dilated aota due to high stroke volume
increased systolic BP/decreased diastolic BP = wide pulse pressure + bounding pulses
Murmur: early diastolic blowing, LSB
Characteristics of mitral valve regurgitation
Volume overload of LA/LV
Murmur: systolic blowing, apex; diastolic at apex
Characteristics of tricuspid valve regurgitation
Volume overload of RA/RV
Murmur: can be normal in newborn with elevated PVR; systolic blowing at LLSB, diastolic rumble at LSB
If severe, enlarged pulsatile liver and distended neck veins (blood backing up into IVC/SVC)
Hypertrophic cardiomyopathy
Pompe, Hurler, Noonan
Infant of a diabetic mother, postnatal steroids- transient
Variable ventricular hypertrophy with increased inotropic function
Diastolic dysfunction is a prominent feature
Digoxin contraindicated: increases contractility which may lead to increased obstruction
Dopamine acts of which receptors at which doses?
2-4: dopaminergic, renal vasodilation and splanchnic vessels
2-6: beta 1/2 chronotropy (HR) and contractility
6-10: alpha 1 vasoconstriction
10-20: alpha 1 increased PVR
Congestive or dilated cardiomyopathy
Increased risk of abnormal myocardium, abnormal coronary perfusion or following arrhythmia
Decreased ventricular inotropic function during systole associated wtih dilatation of left atria and left ventricle
Restrictive cardiomyopathy
Least common
Abnormal ventricular filling during diastole associated with stiff ventricles
Normal initial systolic function
Atrial dilatation out of proportion to ventricular dilatation (stiff walls of RV/LV)
Where does norepinephrine work?
Endogenous catecholamine
Increases SVR and CO by alpha 1, beta 1 & 2
Constricts systemic vascular»_space; pulmonary vascular
risk of hypocalcemia, hypoglycemia
Mechanism of action of dobutamine
Acts directly in alpha and beta receptors without release of norepi
NO CHANGE IN SVR
Hydrocortisone
Hyperglycemia
Osteopenia
Inhibits immune function and somatic growth
Associated with SIP if concurrnet indomethacin
Aid in hypotension by decreasing breakdown of catecholamines, increase calcium in myocardial cells and upregulating adrenergic receptors
Pericardial effusions
Etiology: pericarditis, severe anemia with CHF, post-cardiac surgery, leak from central venous catheter
pulses paradoxus
pericardial tamponade, tachycardia, hypotension
EKG finding in ALCAPA
deep Q waves in I, aVL, V4, V5, V6
Cardiac rhabdomyoma
MC primary cardiac tumor in neonates
usually multiple
EKG= delta wave (predisposed to SVT, WPW)
increased risk if tubeous sclerosis
HLHS
RV + tricuspid valve represent systemic ventricle + AV valve
Paliation with Norwood procedure
Mutations: HAND1, NOTCH1
Recurrence HLHS sibling 8%
Recurrence of any congenital 22%
Normal neonatal EKG findings
Normal QRS measured in V5: 20-80msec
Axis term: +55 to +200
Axis preterm: +65-+174
Predominant myocardial substrate prenatally and postnatally
Prenatally: glucose, lactate
Postnatally: fatty acids
Characteristics of asplenia
- Sequence of bilateral RIGHT-sidedness: 2 right lungs, midline liver, 2 gallbaldders
- Always severe cardiac malformations: aorta and IVC juxtaposed (100%), TAPVS (90%), TGA/bilateral SVD/PS/PA (75%)
- Howell-Jolly bodies, Heinz bodies
- Increased risk of infection: Strep pneumoniae
- Cyanosis
- Poor prognosis
Characteristics of polysplenia
- Sequence of bilateral LEFT-sidedness: 2 left lungs, midline liver, increased incidence of biliary atresia
- Less severe cardiac malformation: azygous return of IVC/TAPVR (70%), bilateral SVC (50%), AVC (40%)
- Cyanosis
- Poor prognosis: better than asplenia
Boot shaped heart
TOF
Snowman
TAPVR- supracardiac
Egg on a string
D-TGA
REVERSE DIFFERENTIAL
Extremely large heart
Ebstein’s anomaly
LITHIUM!!!
Small heart with increased pulmonary blood flow
Obstructive TAPVR (infradiaphragmatic)
Conduction pathway
- SA node –> contraction of both atria (P WAVE)
- Impulse hits AV node –> delay allows ventricles to fill (PR SEGMENT) (protects from atrial tachycardias)
- Impulse rapidly spreads down bundle of His to bundle branches and Purkinje fibers to myocardia cells–> ventricular contraction, atrial repolarization (QRS WAVE- Q= septal depolarization)
- Ventricles repolarize –> ventricular relaxation (ST SEGMENT, T WAVE)
Fetal SVT
- More common than atrial flutter
- HR 240-310, 1:1 AV association
- ~28-32 weeks gestation
- hydrops may develop- depends on duration, degree of immaturity
Treatment:
1st line –> Digoxin (inhibits Na/K/ATPase- slows conduction, prolong AV node refractory period)- IV to mom
2nd line if FETUS LESS ILL–> Flecainide- more effective but 7-15% mortality; Sotolol- mortality rate higher
2nd line if FETUS ILL –> amiodarone (K channel blocker- incr refractory period): give 1-2 days after dig started, give orally
Post-natal management:
Monitor for complications of meds:
1. hyperbilirubinemia
2. anemia from bone marrow suppression
3. greater risk of NEC
Fetal atrial flutter
- Less common
- HR 425-500, VARIABLE AV contraction
- Irregular
- Majority with underlying reentrant tachycardia
- Later in pregnancy than SVT
- Hydrops less common, if CHD, worse prognosis than SVT
Treatment:
1. Digoxin- IV to mom
2. Sotalol (K channel blocker with beta blocker effect): tx of choice for refractory atrial flutter
Amiodarone NOT EFFECTIVE
Post-natal management:
Monitor for complications of meds:
1. hyperbilirubinemia
2. anemia from bone marrow suppression
3. greater risk of NEC
Fetal ventricular tachycardia
Associated with:
1. complete heart block
2. long QT syndrome
3. myocarditis
Often combo of bradycardia or AV block and tachycardia
HR 210-260
Difficult to treat
Fetal sinus tachycardia
setting of maternal thyrotoxicosis
Fetal AV block
AV block and fetus with NORMAL cardiac anatomy and EXPOSURE to maternal SSA/SSB Abs
1. positive Abs = more likely to need pacing at birth, develop cardiomyopathy, more severe form of block
2. Majority pregnancy women are asymptomatic
3. Fetus presents with 2nd or 3rd degree AV block
AV block and fetus with ABNORMAL cardiac anatomy and WITHOUT maternal antibodies
1. poorer prognosis
2. higher risk for hydrops and severe congestive heart failure
3. congential heart defects: atrial isomerism with asplenia or polysplenia, L-TGA, AV septal defect
4. usually require pacing in neonatal period
Fetal ectopy- what is baby at risk for?
SVT in first month of age
PAC
- common in newborns
- originates in atrium, leads to contraction before sinus node
- early p wave- different axis/morphology
- typically benign
Associated with:
1. hypokalemia
2. hypoglycemia
3. hypercalcemia
4. drugs
5. hypoxemia
6. cental line irritation of right atrium
PVC
- Early beat with abnormal and prolonged QRS, ST slope away from QRS, no P wave
- originates below AV node and bundle of His
- Unifocal or multifocal
Asymptomatic with isolated PVCs, normal cardiac anatomy- no treatment
Causes:
1. digoxin toxicity
2. infection
3. Ca/K/Mg abnormalities
4. hypoxemia
5. acidosis
6. CHD
7. excess aminophylline/caffeine
8. myocarditis
Atrial flutter
SAWTOOTH PATTERN: II, III, avF, V1
rate 300-500 bpm
starts and ends suddenly
- difficult to distinguish from SVT- ice/adenosine can reveal flutter at slower rate
- Stable: block atrial (digoxin) and ventricular rate
- Unstable: synchronized cardioversion, pacing
Types of SVT
Orthodromic tachycardia
1. p wave AFTER QRS, narrow QRS, +/- WPW
2. MC form in neonate
3. Pathway: down AV node, up accessory/orthodromic pathway (why p wave after QRS)
4. responds to vagal/adenosine
Antidromic tachycardia
1. p wave axis superior, invereted in II/avF, wide QRS with WPW
2. less common
3. Pathway: down accessory/antidromic, returns back to atria backwards
4. respons to vagal/adenosine
AV nodal re-entry tachycardia
1. p wave not visible- atria/ventricle depolarize AT SAME TIME
2. less common
3. slow and fast pathways are both present
4. responds to vagal/adenosine
SVT
Increased risk
1. CHD: ebsteins, L-TGA
2. medications: caffeine, epi
3. cardiomyopathy
4. myocarditis
5. cardiac tumors
6. fever
7. hyperthyroidism
NARROW COMPLEX QRS, p waves difficult to identify
Rate: 220-330- litte variation, begins and ends abruptly
Management:
1. Unstable: synchronized cardioversion (0.5-2J/kg)
2. Stable: vagal maneuvers, adenosine IV (transiently blocks AV node)
3. after SVT resolved, repeat EKG and determine if underlying rhythm abnormal
WPW
a type of SVT
- Prolonged QRS
- Shortened PR interval
- Initial slurring of QRS= DELTA WAVE
Secondary to electrical pathway between A and V, bypassing AV node, associated with SVT
Ebsteins, L-TGA
How does milrinone work?
- phosphodiesterase 3 inhibitor (ihibits cAMP breakdown–> incr intracellular Ca–> incr contracility–> vascular smooth muscle relaxes–> vasodilation, dec afterload)
- inotrope: NOT dependent on neurotransmitter stores/receptors
- decreases SVR
- some pulmonary vasodilation
- R heart failure or weaning from bypass
may induce thrombocytopenia
Digoxin
- inhibits Na/K/ATPase pump in cardiac myocytes–> incr Ca influx –> incr contractility + decr afterload
- decreases SVR
- Use: CHF
- Anti-arrhythmic: decr AV conduction
- Toxicity: GI sx, decr HR, prolonged PR interval, AV block
monitor K+ and Ca levels
Dobutamine
B1»_space; B2, little alpha activity
- chronotrope and inotrope –> synthetic catecholamine (incr cAMP levels)
- may decr SVR
- Use: Cardiogenic shock, myocardial dysfunction (no incr afterload) –> improves coronary blood flow and myocardial oxygen delivery
no effect on renal blood flow
Dopamine
- endogenous catecholamine, precursor to epi and NE, alpha and beta - more peripherally
- inhibits Na/K/ATPase and Na/H+ pump
- effect: releases endogenous NE–> decr effectiveness with prolonged use
- ++chronotrope, + inotrope
- incr SVR –> effect is dose dependent
- septic shock!
low dose= dilates renal vasculature
inhibits thyrotropin release–> inaccurate thyroid screen results
if extravasation, use phentolamine (alpha agonist)
Epinephrine
- MOST POTENT vasopressor, endogenous catecholamine
- Beta 1 and 2 at lower doses (<0.3), alpha at higher doses
- ++chronotrope, +inotrope
- SVR effect is dose-dependent: dilation at lower doses, constriction at high doses
- side effects: hypokalemia, local tissue ischemia, renal vascular ischemia, severe hypertension
higher dose= incr diastolic pressure, better coronary artery perfusion due to increased afterload
Infections associated with myocarditis
Parvo B19 and Coxsackie
Rubella
What congentical heart issue can maternal aspirin use cause?
Pulmonary hypertension
What congenital heart issue can maternal use of SSRI cause?
Pulmonary hypertension
How does maternal lupus increase risk for congenital heart block?
Maternal anti-Ro (SS-A)/La (SS-B) autoantibodies = IgG class = can cross placenta –> deposit on fetal myocardium–> disrupt calcium metabolism–> apoptosis of AV cells –> conduction abnormalities–> inflammation –> scar tissue and fibrosis, AV node calcification
risk indepedent of severity of maternal illness
- can be first sign of maternal Lupus
- once complete heart block established, it is permanent- AV node replaced by scar tissue
Narrow pulse pressure
pericardial tamponade
aortic stenosis
intravascular depletion
Widened pulse pressure
PDA (L to R)
Truncus arteriosus
Thyrotoxicosis
AV fistula
Aortic regurgitation
Vein of Galen aneurysm
- 40-60% present during neonatal period
- persistent embryologic prosencephalic vein of Markowski (anterior to vein of Galen)
- Neuro effects assoc with ischemic infarction, hemorrhage, and mass effect on brain structures
- Develops CHF: compensate for large CO that flows through aneurysm (95% present with CHF)
- Hydrocephalus and intracranial hemorrhage
Physical findings:
1. bounding carotid pulses –> bobbing of the head
2. cranial bruit
3. signs of CHF: hepatomegaly, murmur
4. thrombocytopenia, DIC: consumption within aneurysm
Causes for Neonatal Hypertension
H: Heart disease (coarct, PDA)
Y: yet undetermined
P: Pulmonary disease (BPD)
E: Endocrine disorder (CAH, adrenal hemorrhage, hyperaldosteronism, hyperthyroidism, Cushing)
R: Renal disease (thrombus, polycystic/dysplasitc/hypoplastic kidney, obstructive uropathy, ATN)
T: TPN (high calcium/salt)
E: ECMO
N: Neoplasm (Wilms, neuroblastoma, pheochromocytoma)
S: Surgery (abdominal wall defect repair)
I: Intoxication (dexamethasone, xanthines, adrenergic drugs, phenylephrine eye drops, cocaine)
O: Opioid withdrawal
N: Neurologic cause (seizures, pain, ICH, intracranial hypertension
Congenital cardiac condition most threatening to pregnant women and their fetuses
Eisenmenger syndrome- pulmonary hypertension
Factors that promote closure of the PDA
Functional closure
1. increase in PaO2
2. Decrease in blood pressure within the ductus arteriosus (postnatal fall in pulmonary vascular resistance)
3. Decreased concentration of PGE2 (decrease in placental PG production, increase in PG metabolism in lungs)
4. Decreased number of ductal arteriosus PGE2 receptors
Structural closure:
1. oxygen-mediated constriction of the PDA results in zone of tissue hypoxia in the ductal media–> signal for irreversible anatomic closure
2. Hypoxia induced growth factors (VEGF, TGF-beta) initiate ductal remodeling
with greater degrees of prematurity, ductal wall is more permeable to oxygen because it is thinner–> continued oxygen exposure doesnt allow for media hypoxia, cell death, remodeling which needs to occur for anatomic closure
iNO is contraindicated in which cardiac lesions:
HLHS
critical aortic stenosis
interupted aortic arch
lesions dependent on R to L shunting through PDA- need to keep pulmonary pressures high
Medication that has the most vasodilatory effect on PDA
Furosemide
stimulation of prostaglandin synthesis
Explain oliguria that occurs with indomethacin treatment for PDA
- Indomethacin blocks prostaglandin E production, prostaglandin E inhibits vasopressin/renin-angiotensin induced fluid retention -> without prostaglandin, fluid retention and oliguria occurs
- Indomethacin redistributes renal blood flow away from mature nephrons of inner cortex to immature nephrons of outer cortex
Effect of hemoglobin concentration and oxygen tension on oxygen content
Changes in afterload on the ventricular function curve
Changes in ventricular function with changes in inotropy
Pathogensis of meconium aspiration syndrome
Mainstays of therapy for meconium aspiration
oxygen
iNO
mechanical ventilation
insufficient evidence for steroid use, routine/prolonged Abx, amnioinfusion
What diagnosis has the highest mortality on ECMO?
CDH
no evidence that surf or antenatal steroids improve outcomes
Dual hit hypothesis for CDH
- Bilateral lung hypoplasia during organogenesis
- Ipsilateral lung compression by abdominal herniation
overall CDH survival 70-90%
long term complications of CDH
CLD
PHTN
GE reflux
Feeding difficulties
scoliosis
developmental delay
hearing loss
Most common indication for neonatal ECMO
respiratory failure
sildenifil
phosphodiesterase 5
S looks like 5
Milrinone
phosphodiesterase 3
M looks like 3
Qp/Qs >1
L to R shunt
PDA
Qp/Qs<1
R to L shunt
PPHN
cardiac pressure volume loop
changes on pressure/volume loop due to changes in contractility/inotropy
changes on pressure/volume loop due to changes in afterload
changes on pressure/volume loop due to changes in preload
parts of EKG
sinus rhythm
PAC
atrial myocyte initiates a beat between impulses coming from the sinus node
Workup:
- ensure normal electrolytes
- remove PICC/UVC from atrium
- monitor
- consider echo if persists
look at the T wave immediately before unusual complex- altered= PAC
PVC
~20% premature, ~4% term
Reasuring features:
- single morphology
- isolated beats
- suppresses when HR increases
compensatory pause after the PVC beat
sinus bradycardia
may be benign- transient bradycardia and QTc prolongation < 470ms may occur after stressful delivery
channelopathies: congenital long QT syndrome
Neonatal long QT syndrome = cardiac channelopathy assoc with neonatal bradycartion
QTc up to 0.49 may be normal in less than 6 mo
Causes of prolonged QTc
- hypocalcemia
- hypokalemia
- hypomagnesemia
- CNS abnormalities
- myocarditis
- channelopathy
3 genes = 75%
1. KCNQ1=LQT1
2. KCNH2=LQT2
3. SCN5A=LQT3
prolonged QT and 2:1 AV heart block is a risk factor for what?
Torsades de pointes
First degree heart block
2nd degree- Mobitz 1/Wenckebach
BENIGN
- seen with medications or high vagal states
2nd degree/Mobitz II
PATHOLOGIC
- block is below AV node
- may progress to complete heart block
- may require pacemaker
- evaluate for: LQTS (when rhythm 2:1), myocarditis
Complete heart block
Maternal SLE- may be first sign of disease in mother
SSA/Ra, SSB/LA- cross placenta and deposit on AV node
Associated with L-TGA
Most likely type of tachyarrhythmia in term newborn
WPW
AV reentry tachycardia (AVRT)
atrial impulse enters through accessory pathway- dont see pause in electrical activity = DELTA WAVE
WPW
- can lead to a form of SVT
- fast: 220-300bmp, regular
- abrupt onset and termination
- 1:1 conduction
Treatment: break AV circuit
1. vagal maneuvers, adenosine- transiently block AV node
2. cardioversion, rapid atrial pacing- break the circuit
Congenital heart defect MC associated with accessory pathway
Ebstein’s
- displacement of TV disrupts normal barrier of conduction between A and V
Atrial flutter
CARDIOVERSION FIXES IT!
Heart rate 250-350
Ventricular rate= 300 when 1:1
= 150 when 2:1
Mechanism of epinephrine for heart in a code
Increases dromotropy (increased conduction velocity)
Indomethacin for PDA closure
IV
NSAID, nonselective cyclooxygenase inhibitor that blocks prostaglandin synthesis
greater clearance with increasing postnatal age/weight
Successful closure of PDA in 60-80%, 25% relapse
Contraindications: PDA R to L, evolving IVH, NEC, poor renal function, SIP, severe thrombocytopenia
Complications: GI bleed, transient oliguria, incr Cr, hyponatremia (2nd to fluid retention), dec platelet aggregation, dec intestinal perfusion
Ibuprofen for PDA closure
IV or PO
NSAID, nonselective cyclooxygenase inhibitor that blocks prostaglandin synthesis
Similar efficacy as indomethasin (~70%), 25% relapse
Issues: similar to indomethacin
Acetaminophen for PDA closure
IV or PO
Decreases prostaglandin synthesis (thought to occur at the peroxidase site of cyclooxygenase)
Similar efficacy (70-80%) (lower if 3-day course)
When used as rescue after failed indomethacin–> ~45% with smaller or closed PDA
Improved efficacy if initiated within 1st week
Issues: less impact on renal function, incr LFTs (avoid if liver disease)
unknown long-term risks
Prostaglandin (PGE1)
Action: effect within 30 min, maintains PDA patency, most effective if initiated close to birth, vasodilator
Side effects; apnea (< 6 hrs of initiation, related to dose), fever, cutaneous flushing, bradycardia
Chronic effects: cortical bone proliferation
WORSEN clinical status:
1. TAPVR- obstructive
2. HLHS- restrictive/intact atrial septum
3. TGA- restrictive atrial septum
4. Mitral valve atresia with restricted PFO
Most common cause of a complete vascular ring
Double aortic arch
what embryonic week do the endocardial cushions come together to create the intracardiac septa?
8th week
cardiogenesis begins at the 5th week- formation of paired heart tubes
heart begins to beat during the 6th week
septation occurs between week 7-8
from what embryonic structure does the ductus arteriosus arise?
LEFT 6th aortic arch
embryonic structures of the heart
LEFT 6th aortic arch –> ductus arteriosus
proximal 6th aortic arches –> proximal branch pulmonary arteries
1st/2nd arches –> diseappear then portion of 1st arch –> maxillary artery
3rd arch –> carotid artery
RIGHT 4th arch –> RIGHT subclavian
LEFT 4th arch –> part of aortic arch
5th arch –> involutes
bulbus cordis = primitive heart = conotruncus
normal newborn EKG findings
right-sided forces
QRS axis initially deviated to the R
upright T waves in V1 –> RV strain
small QRS voltages i limg leads
T waves of low voltage
Abnormal P waves
right atrial enlargement on EKG
Tall peaked P waves
name highest to lowest O2 b/w umbilical and uterine vessels
UTERINE artery
UTERINE vein
UMBILICAL vein
UMBILICAL artery
QT interval
abnormal if > 0.44
can be normal up to 0.46 in females
QTc = QT/square root of R-R interval (sec)
repreasents duration of activation and recovery of the ventricular myocardium
can be caused by hypomagnesemia, hypocalcemia, hypokalemia
Syndromes:
Romano-Ward- AD
Lang-Nielsen- AR, assoc with deafness
Torsades de Pointes- tachycardia, vfib –> tx with magnesium
cardiac output
HR x SV
EKG changes with electrolytes
cerebral blood flow
alpha and beta receptors
sensitivity and specificity for CCHD
2003: sensitivity 60%, specificity 99%
low sensitivity for detection of interrupted aortic arch, DORV, Ebstein, coarct
how is cardiac output improved?
- inotropy- increase myocardial contraction with greater shortening fraction
- chronotropy- increase HR
- lusitropy: increase diastolic filling/increase myocardial relaxation during diastole (milrinone- UNIQUE)
- dromotropy: faster electrical conduction of cardiac contraction signals during systole (EPI)
benefit of lusitropy (milrinone)
negligible effect on myocardial oxygen consumption
decreases intracellular calcium to enhance lusitropy (diastolic relaxation)
Phosphodiesterase 3 inhibitor –> decreases cAMP
milrinone
