Cards Flashcards
Mechanisms of hydrocortisone to increase BP
Vasoconstriction
* decreased NOS
* decreased prostaglandin
* decreases catecholamine metabolism
* upregulates angiotensin-II receptors
Contractility:
* Increases Ca++
* increase adrenergic receptors
Factors that promote closure of the PDA
Functional closure
1. increase PaO2
2. Decrease BP in ductus arteriosus (fall in PVR)
3. Decrease PGE2
4. Decreased PGE2 receptors
Structural closure:
1. oxygen-mediated constriction: tissue hypoxia ductal media
2. Hypoxia induced GF (VEGF, TGF-beta)
Types of SVT
Orthodromic MCC
Antidromic tachycardia
AV nodal re-entry tachycardia
Antidromic tachycardia
- p wave axis superior, inverted in II/avF, wide QRS with WPW
- less common
- Pathway: down accessory/antidromic, returns back to atria backwards
AV nodal re-entry tachycardia
- p wave not visible- atria/ventricle depolarize SAME TIME
- less common
- slow and fast pathways
Antiarrhythmic drug classes and where they work on phases
I: active depolarization (Na block)
II and III: sustained depolarization phase (beta- and K-block)
IV: repolarization (Ca-block)
*Do not use Ca-channel blockers (verapimil) in neonates
Orthodromic tachycardia pathway
down AV node, up accessory/orthodromic pathway
(p wave after QRS)
MCC SVT
Orthodromic tachycardia
Orthodromic tachycardia EKG
p wave AFTER QRS, narrow QRS, +/- WPW
Antidromic tachycardia pathway
down accessory/antidromic, returns back to atria backwards
Antidromic tachycardia EKG
- p wave axis superior
- inverted in II/avF
- wide QRS with WPW
AV nodal re-entry tachycardia EKG
p wave not visible- atria/ventricle depolarize AT SAME TIME
Pulmonary artery sling compresses?
As the left pulmonary artery courses to supply the left lung, it compresses the distal trachea and right mainstem bronchus.
postnatal EKG timing of in utero first degree block
at 1 year of age if transient
MC association with truncus?
right aortic arch
what is the first system to function in utero?
CV system
what trilaminar layer does heart arise from?
mesoderm
what are the developmental stages of heart formation
- tube formation
- looping
- septation
when is heart formation complete?
7-8 weeks
steps in tube formation
ED 15: two flat sheets mesodermal angiogenic cells
ED 17: upper sheet expands and forms tube encircling other sheet; straightens out
ED 20: beats start in upper tube
steps in looping
ED 21: linear tube bends towards right
ED 22: distinct chambers appear
ED28: further looping until ventricles side to side
steps in septation
ED 34: atrial septation
ED 38-46: ventricle septation
{__,__,__}
{atrial situs = S, I or A ,
looping = D or L
great arteries = S or I}
{S, D, S}
normal
{S, D, D}
dTGA
{S, L, L}
l - TGA
{I, L, I)
situs inversus totalis
fetal improved tolerance for low pO2
- HbF high O2 affinity
- increased Hb concentration
- decreased O2 consumption
- increased anaerobic metabolism
fetal compensation for hypoxemia
- blood flow preferentially to heart, brain adrenals
- dilation of DV; better oxygenated blood shunted to LA
- suppressed respiration, bradycardia, decreased CO
CO =
= HR * SV
= systemic BP/total peripheral vascular resistence
ventricular wall stress =
= ventricular P x ventricular radius / wall thickness
which impacts CO more? preload or afterload?
preload bc afterload does not effect until a critical BP level is reached
SV =
= EDV - ESV
EDV = volume in LV at end of filling
ESC = volume in LV at end of ejection
how to increase EDV
increase preload or increase ventricular compliance/stretch
how to decrease ESV
increase contractility
decrease afterload
stroke work =
= MAP x SV
how does RV and LV stroke work compare?
RV 1/6 of LV
Qp/Qs> 1; what kind of shunt?
L > R
large is > 2
Qp/Qs < 1; what kind of shunt?
R > L
large of < 0.7
O2 consumption =
= amount O2 delivered by heart - O2 returning to heart
= blood flow x O2 arterial - blood flow x O2 venous
- O2 content = O2 Hb + O2 dissolved *
Qp/Qs =
= PBF/SBF
= {aorta O2 sat - mixed venous O2 saturation} / {LA or pulm vein O2 sat - pulmonary artery O2 saturation}
PVR =
= {Mean PA pressure - Mean LAP} / PBF
SVR =
= {Mean aortic P - Mean RAP} / SBF
R ~
{8 x viscosity x L} / pi x r^4
what reduction in Hgb is needed to see cyanosis?
3-5 g or reduced Hb/dl of capillary blood
preductal 100mmHg; post ductal 45 mmHg
CoA with PDA + PVR
preductal 45 mmHg; postductal 80mmHg
TGA + intact septum + PDA
+ PPHN or iAoA or preductal CoA
preductal 75 mmHg; 50 mmHg postductal
PPHN + R>L across PDA
65 mmHg postductal; 95mmHg venous
infradiaphragmatic TAPVR (obstructive)
hyperoxia test
paO2< 100 without CO2 retention = CHD
paO2 100-200 mixing lesion
paO2 > 250; CHD unlikely
S1 and S2
S1 = MV or TV
S2 = AV or PV
widely split S1
RBBB or Ebstein
widely split, fixed S2
volume overload (ASD, PAPVR)
single S2
PPHN, one semilunar valve (PA, AA, HLHS, TA)
P2 not heard in TGA, ToF or severe PS
paradoxically split S2
AV follows PV if LV ejection delayed in severe AS
what size should BP cuff be?
width = 2/3 - 3/4 circumference of extremity
how does A line transducer position effect reading
too low - elevates BP
too high - lowers BP
Mean BP =
= DBP + 1/3 (SBP + DBP)
what structural causes of CHF present at birth
HLHS + restrictve AS
severe TR or PR
large AV fistula
what structural causes of CHF present at DOL1
obstructive TAPVR
TGA
severe Ebsteins
what structural causes of CHF present at week 1-4
critical AS or PS
preductal CoA
NO MoA
normally made by L-arginine by NOS in endothelial cells
- activates guanylyl cyclase
- converts GTP to cGMP
- vascular smooth muscle relaxation and decreased vascular tone
remaining goes to blood, binds Hb and becomes oxidized to NO2 or NO3 which are inactive (no systemic hypotension)
what percent of those with CHD have other anomalies?
25%
recurrence risk of CHD
1 child: 2-5%
2 children: 5-10%
mother: 6.7%
father: 1.5 -3%
MC cyanotic CHD beyond infancy
TOF
MC cyanotic CHD presenting in 1st week
- TGA
- HLHS
MCC of mortality in 1st week
HLHS
where is the aortic valve in L TGA
- anterior and left of PV
- in dTGA: anterior and right
EKG findings on dTGA and LTGA
dTGA = right QRS (90-160), RVH
LTGA = absence of Q waves in I, V5, V6, may have AV block
what percent of TOF have right AoA?
25%
the VSD in TOF is mostly what type?
perimembranous
during the Tet spell, what happens to the murmur?
decreases intensity because of decreased flow across PV and more across VSD
management of Tet spell
- knee to chest
- morphine: break agitation
- HCO3: correct acidosis and decrease respiratory drive
- vasoconstrictors: increase SVR
oxygen to decrease PVR
QRS in pulmonary atresia and tricuspid atresia
TA = superior
PA = normal
truncus types
I (50-70%) = MPA from truncus then splits
II (30-50%) = each PA comes off posteriorly from truncus
III (10%) = each PA comes off laterally from truncus
EKG in Ebsteins
RBBB, RAE
WPW in 20%
occasional 1st deg AV block
TAPVR types
supracardiac = PV to vertical vein to innominate, azygous or SVC
cardiac = PV to RA directly or indirectly via coronary sinus to RA
infracardiac = PV cross diaphragm and drain into portal vein or hepativ vein or IVC
mixed
heart size in chest XR in obstructed vs nonobstructed TAPVR
obstructed = small or normal bc decreased blood flow to heart
nonobstructed = increased, snowman
Most common cause of CHF after second week
VSD
distribution of types of VSD
70% perimembranous
25% muscular
5-7% supracristal, conal, subpulmonary
5-8% posterior and inferior to perimembranous
timing of functional and anatomic closure of PDA
functional 90% by 48 hours
anatomic 2-4 weeks
constrictors of PDA
PGFa
acetylcholine
bradykinin
oxygen
dilators of PDA
PGE1
PGI2 (prostacyclin)
hypoxemia
acidosis
PS vs AS which is more successfully treated with balloon?
PS
ALCAPA
left main coronary from PA
- elevated PVR, adequate perfusion of ALCAPA
- decreased PVR, not enough blood flow; rely on collaterals
- asymptomatic reliance on collaterals
- as PVR continues to drop, less into collaterals –> myocardial ischemia (anterolateral distribution)
egg on a string
d TGA
snowman
supracardiac TAPVR
extremely large heart with decreased PBF
ebsteins
small heart with increased PBF
obstructive TAPVR
peaked P wave
RAE (especially lead II)
increased P wave duration
LAE
absent Q wave in v5 and v6
L TGA, single ventricle, L BBB
deep Q wave in left leads
LVH, biventricular hypertrophy
myocarditis
restrictive cardiomyopathy
deep and wide Q wave
infarction
hypertrophic cardiomyopathy
deep Q waves in I, aVL, V4, V5 and v6
ALCAPA
R QRS deviation
neonates until 1 month
TOF
when do you see normal QRS in infants
after 1 month age
PA with intact septum
L superior QRS
TA
AVC
EKG leads corresponding to part of heart
EKG with corresponding locations
which presents later in pregnancy flutter or SVT?
atrial flutter
which is more likely associated with hydrops; flutter or SVT?
SVT
treatment of SVT in utero
- digoxin
- if sick amiodarone or if less ill flecainide
treatment of flutter in utero
- digoxin
- sotalol
NOT amiodarone
treatment of EAT
betablocker if severe and prolonged
does not response to cardioversion or adenosine
treatment of MAT
amiodarone
does not response to cardioversion or adenosine
treatment of JET
normalize electrolytes
minimize inotropes
atrial pacing
amio
procainamide
+/- cooling
neonatal treatment of atrial flutter
stable: block atrial (digoxin) and ventricular rates
unstable: DC synchronized cardioversion or esophageal pacing
neonatal treatment of atrial fibrillation
DC defibrillation
digoxin to slow rate
treatment of orthodromic tachycardia
vagal
adenosine
treatment of antidromic tachycardia
vagal
adenosine
treatment of AVnRT
vagal and adenosine
differences between orthodromic, antidromic and AVnRT
orthodromic - MC; down AV node up accessory; p wave retrograde
antidromic - down accessory and returns backwards to atria, may have delta wave
AVnRT - p wave may not be visible bc atria and ventricle depolarize same time; down slow path; up fast path
treatment of Vtach
stable - amiodarone, lidocaine or beta blocker
unstable - DC cardioversion
treatment of Vfib
DC defibrillation, lidocaine, amiodarone
MoA adenosine
blocks AV node
dc SVT
unmask atrial flutter
MoA amiodarone
K+ channel blocker
MoA digoxin
AV block
MoA flecainide
Na channel block
MoA propanalol
beta blocker
flecainide toxicity
renal, levels increase when NPO
milk affects absorption
which med should you not put in fridge because it precipitates
flecainide
MoA sotalol
K + channel blocker
less effective than amiodarone
some beta block
MoA verapamil
CCB - slows AV node conduction
which med causes sudden death if used < 12 months
verapamil
WPW aspects
- prolonged QRS
- shortened PR
- slurring QRS = delta wave
WPW a.w
ebstein
ltga
but also in structurally normal hearts
what causes WPW
secondary to electrical pathway between atrium and ventricle bypassing AV node; SVT
first deg AV block
PR prolongation
treatment of first deg AV block
not needed
second deg AV block type 1
wenckebach
increasing PR until drop
treatment of second deg AV block type 1
not needed
second deg AV block type II
dropped beats; no change in PR interval
treatment of second deg AV block type II
pacemaker
third deg AV block
dissociation of A and V rates
third deg AV block a/w
LTGA, AVC
lupus
cardiac surgery
treatment of AV block
asymptomatic - no treatment
symptomatic or poor risk factors - pacemaker
RBBB on EKG
right axis deviation
rSR’, prolonged QRS
slurring of S in I, v5 and V6
RBBB a/w
Ebstein
cardiac surgery
LBBB on EKG
left axis deviation
prolonged QRS
loss of Q waves in I, V5, V6
wide S in V1 and V2
QTc =
= QT / sqrt(RR interval)
causes of prolonged QT
hypocalcemia
myocarditis
long QT syndrome
what is first line treatment of prolonged QT
propanolol; then pacemaker
what is sick sinus syndrome
SA node injury after surgery
slow irregular sinus rate a/w a.flutter and a.fib
when should you use infant size pads in cardioversion/defibrillation?
until 1 year of age or 10 kg
cardioversion dose
0.25-0.5 J/kg
max 2 J/kg
defibrillation dose
1-2J/kg with max 4 J/kg
hypo and hypercalcemia on EKG
hypercalcemia = shortened QRS
hypocalcemia = prolonged
hyperkalemia by dose
> 6 tall peak T, short QT, depressed ST
> 7.5 prolonged PR, wide QRS, flat P
> 9 absent P, sinusoidal QRS, asystole and afibrillation
hypokalemia by dose
< 2.5 wide QRS, depressed ST, biphasic T + visible U wave
< 1 prominent U wave, flat T wave, prolonged PR and SA block
what is M mode on echo used for?
- size of chambers, ventricular wall thickness
- LV function
- valve movement and septal wall motion
- pericardial fluid
shortening fraction % =
{LV diastolic dimension - LV systolic dimension}/LV diastolic dimension x 100
normal = 28-40%
parasternal view good for:
long axis = left side (MV, AV, LV, LA, ascending aorta)l relationship to interventricular septum
short axis: PDA, semilunar valves, MV, papillary muscles, PA, RVOT, coronaries, LV
apical view good for:
AVC; all 4 chambers
subcostal view good for:
ASD
suprasternal view good for:
aortic arch
timing of fetal echo methods
transabdominal 18-32
transvaginal as early as 10 weeks
a1 location and effect
arterial and venous smooth muscles and cardiomyocytes
Vasoconstriction, increases contractility
gluconeogenesis decreases insulin release
a2 location and effect
sympathetic, CNS
blocks NE release, inhibits sympathetic output
vascular smooth muscle relaxation
b1
SA node, atrial and ventricular muscle
conduction cells
increase HR, conduction velocity, contractility, renin release
B2
arterial and venous smooth muscles, bronchial smooth muscles
smooth muscle relaxation
bronchial relaxation
increases HR and contractility
decreases intestinal motility and tone
induces glycogenolysis
increases insulin secretion
MoA milrinone
phosphodiesterase 3 inhibitor - inhibits cAMP breakdown
MoA digoxin
inhibits NaK ATPase leading to Ca influx
BT shunt
R subclavian to RPA
Fontan
SVC and IVC to PA
Glenn
SVC to PA
Norwood stage I
- AS
- divide MP; DKS proximal PA to ascending aorta
- reconstruction of hypoplastic aorta
- BT shunt or Sano
Norwood stage II
bidirectional Glenn; decrease volume overload on RV; remove shunt + SVC to PA
Norwood stage III
modified Fontan
both SVC and IVC to PAs
Rashkind
BAS
Rastelli
patch VSD + Sano
for dTGA with VSD + PS or DORV
primary myocardial substrate used by heart
fatty acids
mediator of normal pulmonary vascular transition at birth
NO
MC gene in long QT
KCNQ1
preferred treatment in hypertrophic cardiomyopathy
propanalol or other betablocker like esmolol
primary target of CCHD
HLHS
ALDH1A2
retinoic acid production enzyme
a/w TOF
major pathway of energy production in hypoxia-ischemia conditions
lactate dehydrogenase
WPW first line treatment
propanolol
the reaction involved in FaO by neonatal cardiomyocytes is catalyzed by
carnitine palmitoyl transferase
what causes widely split S2 in ASD
delayed RV depolarization with little change in venous return to RA with inspiration
when do endocardial cushions come together to form intracardiac septum?
week 8
MoA dobutamine
b1 agonist > B2, a1
MoA dopamine
inhibits NaK ATPase and Na/H pump
dopaminergic then beta some alpha at high dose
MoA epi
beta 1 and 2 > alpha
MoA isopreterenol
B1 and B2
MoA nitroprusside
decrease SVR
MoA NE
a1 > a2 > b1 > b2
MCC hypertrophic cardiomyopathy
Noonan
ductus comes from what arch?
L 6th aortic arch