Cards Flashcards
(190 cards)
1
Q
Mechanisms of hydrocortisone to increase BP
A
Vasoconstriction
* decreased NOS
* decreased prostaglandin
* decreases catecholamine metabolism
* upregulates angiotensin-II receptors
Contractility:
* Increases Ca++
* increase adrenergic receptors
2
Q
Factors that promote closure of the PDA
A
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)
3
Q
Types of SVT
A
Orthodromic MCC
Antidromic tachycardia
AV nodal re-entry tachycardia
4
Q
Antidromic tachycardia
A
- p wave axis superior, inverted in II/avF, wide QRS with WPW
- less common
- Pathway: down accessory/antidromic, returns back to atria backwards
5
Q
AV nodal re-entry tachycardia
A
- p wave not visible- atria/ventricle depolarize SAME TIME
- less common
- slow and fast pathways
6
Q
Antiarrhythmic drug classes and where they work on phases
A
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
7
Q
Orthodromic tachycardia pathway
A
down AV node, up accessory/orthodromic pathway
(p wave after QRS)
8
Q
MCC SVT
A
Orthodromic tachycardia
9
Q
Orthodromic tachycardia EKG
A
p wave AFTER QRS, narrow QRS, +/- WPW
10
Q
Antidromic tachycardia pathway
A
down accessory/antidromic, returns back to atria backwards
11
Q
Antidromic tachycardia EKG
A
- p wave axis superior
- inverted in II/avF
- wide QRS with WPW
12
Q
AV nodal re-entry tachycardia EKG
A
p wave not visible- atria/ventricle depolarize AT SAME TIME
13
Q
Pulmonary artery sling compresses?
A
As the left pulmonary artery courses to supply the left lung, it compresses the distal trachea and right mainstem bronchus.
14
Q
postnatal EKG timing of in utero first degree block
A
at 1 year of age if transient
15
Q
MC association with truncus?
A
right aortic arch
16
Q
what is the first system to function in utero?
A
CV system
17
Q
what trilaminar layer does heart arise from?
A
mesoderm
18
Q
what are the developmental stages of heart formation
A
- tube formation
- looping
- septation
19
Q
when is heart formation complete?
A
7-8 weeks
20
Q
steps in tube formation
A
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
21
Q
steps in looping
A
ED 21: linear tube bends towards right
ED 22: distinct chambers appear
ED28: further looping until ventricles side to side
22
Q
steps in septation
A
ED 34: atrial septation
ED 38-46: ventricle septation
23
Q
{__,__,__}
A
{atrial situs = S, I or A ,
looping = D or L
great arteries = S or I}
24
Q
{S, D, S}
A
normal
25
{S, D, D}
dTGA
26
{S, L, L}
l - TGA
27
{I, L, I)
situs inversus totalis
28
fetal improved tolerance for low pO2
1. HbF high O2 affinity
2. increased Hb concentration
3. decreased O2 consumption
4. increased anaerobic metabolism
29
fetal compensation for hypoxemia
1. blood flow preferentially to heart, brain adrenals
2. dilation of DV; better oxygenated blood shunted to LA
3. suppressed respiration, bradycardia, decreased CO
30
CO =
= HR * SV
= systemic BP/total peripheral vascular resistence
31
ventricular wall stress =
= ventricular P x ventricular radius / wall thickness
32
which impacts CO more? preload or afterload?
preload bc afterload does not effect until a critical BP level is reached
33
SV =
= EDV - ESV
EDV = volume in LV at end of filling
ESC = volume in LV at end of ejection
34
how to increase EDV
increase preload or increase ventricular compliance/stretch
35
how to decrease ESV
increase contractility
decrease afterload
36
stroke work =
= MAP x SV
37
how does RV and LV stroke work compare?
RV 1/6 of LV
38
Qp/Qs> 1; what kind of shunt?
L > R
large is > 2
39
Qp/Qs < 1; what kind of shunt?
R > L
large of < 0.7
40
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 *
41
Qp/Qs =
= PBF/SBF
= {aorta O2 sat - mixed venous O2 saturation} / {LA or pulm vein O2 sat - pulmonary artery O2 saturation}
42
PVR =
= {Mean PA pressure - Mean LAP} / PBF
43
SVR =
= {Mean aortic P - Mean RAP} / SBF
44
R ~
{8 x viscosity x L} / pi x r^4
45
what reduction in Hgb is needed to see cyanosis?
3-5 g or reduced Hb/dl of capillary blood
46
preductal 100mmHg; post ductal 45 mmHg
CoA with PDA + PVR
47
preductal 45 mmHg; postductal 80mmHg
TGA + intact septum + PDA
+ PPHN or iAoA or preductal CoA
48
preductal 75 mmHg; 50 mmHg postductal
PPHN + R>L across PDA
49
65 mmHg postductal; 95mmHg venous
infradiaphragmatic TAPVR (obstructive)
50
hyperoxia test
paO2< 100 without CO2 retention = CHD
paO2 100-200 mixing lesion
paO2 > 250; CHD unlikely
51
S1 and S2
S1 = MV or TV
S2 = AV or PV
52
widely split S1
RBBB or Ebstein
53
widely split, fixed S2
volume overload (ASD, PAPVR)
54
single S2
PPHN, one semilunar valve (PA, AA, HLHS, TA)
P2 not heard in TGA, ToF or severe PS
55
paradoxically split S2
AV follows PV if LV ejection delayed in severe AS
56
what size should BP cuff be?
width = 2/3 - 3/4 circumference of extremity
57
how does A line transducer position effect reading
too low - elevates BP
too high - lowers BP
58
Mean BP =
= DBP + 1/3 (SBP + DBP)
59
what structural causes of CHF present at birth
HLHS + restrictve AS
severe TR or PR
large AV fistula
60
what structural causes of CHF present at DOL1
obstructive TAPVR
TGA
severe Ebsteins
61
what structural causes of CHF present at week 1-4
critical AS or PS
preductal CoA
62
NO MoA
normally made by L-arginine by NOS in endothelial cells
1. activates guanylyl cyclase
2. converts GTP to cGMP
3. 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)
63
what percent of those with CHD have other anomalies?
25%
64
recurrence risk of CHD
1 child: 2-5%
2 children: 5-10%
mother: 6.7%
father: 1.5 -3%
65
MC cyanotic CHD beyond infancy
TOF
66
MC cyanotic CHD presenting in 1st week
1. TGA
2. HLHS
67
MCC of mortality in 1st week
HLHS
68
where is the aortic valve in L TGA
- anterior and left of PV
- in dTGA: anterior and right
69
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
70
what percent of TOF have right AoA?
25%
71
the VSD in TOF is mostly what type?
perimembranous
72
during the Tet spell, what happens to the murmur?
decreases intensity because of decreased flow across PV and more across VSD
73
management of Tet spell
* knee to chest
* morphine: break agitation
* HCO3: correct acidosis and decrease respiratory drive
* vasoconstrictors: increase SVR
oxygen to decrease PVR
74
QRS in pulmonary atresia and tricuspid atresia
TA = superior
PA = normal
75
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
76
EKG in Ebsteins
RBBB, RAE
WPW in 20%
occasional 1st deg AV block
77
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
78
heart size in chest XR in obstructed vs nonobstructed TAPVR
obstructed = small or normal bc decreased blood flow to heart
nonobstructed = increased, snowman
79
Most common cause of CHF after second week
VSD
80
distribution of types of VSD
70% perimembranous
25% muscular
5-7% supracristal, conal, subpulmonary
5-8% posterior and inferior to perimembranous
81
timing of functional and anatomic closure of PDA
functional 90% by 48 hours
anatomic 2-4 weeks
82
constrictors of PDA
PGFa
acetylcholine
bradykinin
oxygen
83
dilators of PDA
PGE1
PGI2 (prostacyclin)
hypoxemia
acidosis
84
PS vs AS which is more successfully treated with balloon?
PS
85
ALCAPA
left main coronary from PA
1. elevated PVR, adequate perfusion of ALCAPA
2. decreased PVR, not enough blood flow; rely on collaterals
3. asymptomatic reliance on collaterals
4. as PVR continues to drop, less into collaterals --> myocardial ischemia (anterolateral distribution)
86
egg on a string
d TGA
87
snowman
supracardiac TAPVR
88
extremely large heart with decreased PBF
ebsteins
89
small heart with increased PBF
obstructive TAPVR
90
peaked P wave
RAE (especially lead II)
91
increased P wave duration
LAE
92
absent Q wave in v5 and v6
L TGA, single ventricle, L BBB
93
deep Q wave in left leads
LVH, biventricular hypertrophy
myocarditis
restrictive cardiomyopathy
94
deep and wide Q wave
infarction
hypertrophic cardiomyopathy
95
deep Q waves in I, aVL, V4, V5 and v6
ALCAPA
96
R QRS deviation
neonates until 1 month
TOF
97
when do you see normal QRS in infants
after 1 month age
PA with intact septum
98
L superior QRS
TA
AVC
99
EKG leads corresponding to part of heart
100
EKG with corresponding locations
101
which presents later in pregnancy flutter or SVT?
atrial flutter
102
which is more likely associated with hydrops; flutter or SVT?
SVT
103
treatment of SVT in utero
1. digoxin
2. if sick amiodarone or if less ill flecainide
104
treatment of flutter in utero
1. digoxin
2. sotalol
NOT amiodarone
105
treatment of EAT
betablocker if severe and prolonged
does not response to cardioversion or adenosine
106
treatment of MAT
amiodarone
does not response to cardioversion or adenosine
107
treatment of JET
normalize electrolytes
minimize inotropes
atrial pacing
amio
procainamide
+/- cooling
108
**neonatal** treatment of atrial flutter
stable: block atrial (digoxin) and ventricular rates
unstable: DC synchronized cardioversion or esophageal pacing
109
**neonatal** treatment of atrial fibrillation
DC defibrillation
digoxin to slow rate
110
treatment of orthodromic tachycardia
vagal
adenosine
111
treatment of antidromic tachycardia
vagal
adenosine
112
treatment of AVnRT
vagal and adenosine
113
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
114
treatment of Vtach
stable - amiodarone, lidocaine or beta blocker
unstable - DC cardioversion
115
treatment of Vfib
DC defibrillation, lidocaine, amiodarone
116
MoA adenosine
blocks AV node
dc SVT
unmask atrial flutter
117
MoA amiodarone
K+ channel blocker
118
MoA digoxin
AV block
119
MoA flecainide
Na channel block
120
MoA propanalol
beta blocker
121
flecainide toxicity
renal, levels increase when NPO
milk affects absorption
122
which med should you not put in fridge because it precipitates
flecainide
123
MoA sotalol
K + channel blocker
less effective than amiodarone
some beta block
124
MoA verapamil
CCB - slows AV node conduction
125
which med causes sudden death if used < 12 months
verapamil
126
WPW aspects
1. prolonged QRS
2. shortened PR
3. slurring QRS = delta wave
127
WPW a.w
ebstein
ltga
but also in structurally normal hearts
128
what causes WPW
secondary to electrical pathway between atrium and ventricle bypassing AV node; SVT
129
first deg AV block
PR prolongation
130
treatment of first deg AV block
not needed
131
second deg AV block type 1
wenckebach
increasing PR until drop
132
treatment of second deg AV block type 1
not needed
133
second deg AV block type II
dropped beats; no change in PR interval
134
treatment of second deg AV block type II
pacemaker
135
third deg AV block
dissociation of A and V rates
136
third deg AV block a/w
LTGA, AVC
lupus
cardiac surgery
137
treatment of AV block
asymptomatic - no treatment
symptomatic or poor risk factors - pacemaker
138
RBBB on EKG
right axis deviation
rSR', prolonged QRS
slurring of S in I, v5 and V6
139
RBBB a/w
Ebstein
cardiac surgery
140
LBBB on EKG
left axis deviation
prolonged QRS
loss of Q waves in I, V5, V6
wide S in V1 and V2
141
QTc =
= QT / sqrt(RR interval)
142
causes of prolonged QT
hypocalcemia
myocarditis
long QT syndrome
143
what is first line treatment of prolonged QT
propanolol; then pacemaker
144
what is sick sinus syndrome
SA node injury after surgery
slow irregular sinus rate a/w a.flutter and a.fib
145
when should you use infant size pads in cardioversion/defibrillation?
until 1 year of age or 10 kg
146
cardioversion dose
0.25-0.5 J/kg
max 2 J/kg
147
defibrillation dose
1-2J/kg with max 4 J/kg
148
hypo and hypercalcemia on EKG
hypercalcemia = shortened QRS
hypocalcemia = prolonged
149
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
150
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
151
what is M mode on echo used for?
1. size of chambers, ventricular wall thickness
2. LV function
3. valve movement and septal wall motion
4. pericardial fluid
152
shortening fraction % =
{LV diastolic dimension - LV systolic dimension}/LV diastolic dimension x 100
normal = 28-40%
153
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
154
apical view good for:
AVC; all 4 chambers
155
subcostal view good for:
ASD
156
suprasternal view good for:
aortic arch
157
timing of fetal echo methods
transabdominal 18-32
transvaginal as early as 10 weeks
158
a1 location and effect
arterial and venous smooth muscles and cardiomyocytes
Vasoconstriction, increases contractility
gluconeogenesis decreases insulin release
159
a2 location and effect
sympathetic, CNS
blocks NE release, inhibits sympathetic output
vascular smooth muscle relaxation
160
b1
SA node, atrial and ventricular muscle
conduction cells
increase HR, conduction velocity, contractility, renin release
161
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
162
MoA milrinone
phosphodiesterase 3 inhibitor - inhibits cAMP breakdown
163
MoA digoxin
inhibits NaK ATPase leading to Ca influx
164
BT shunt
R subclavian to RPA
165
Fontan
SVC and IVC to PA
166
Glenn
SVC to PA
167
Norwood stage I
1. AS
2. divide MP; DKS proximal PA to ascending aorta
3. reconstruction of hypoplastic aorta
4. BT shunt or Sano
168
Norwood stage II
bidirectional Glenn; decrease volume overload on RV; remove shunt + SVC to PA
169
Norwood stage III
modified Fontan
both SVC and IVC to PAs
170
Rashkind
BAS
171
Rastelli
patch VSD + Sano
for dTGA with VSD + PS or DORV
172
primary myocardial substrate used by heart
fatty acids
173
mediator of normal pulmonary vascular transition at birth
NO
174
MC gene in long QT
KCNQ1
175
preferred treatment in hypertrophic cardiomyopathy
propanalol or other betablocker like esmolol
176
primary target of CCHD
HLHS
177
ALDH1A2
retinoic acid production enzyme
a/w TOF
178
major pathway of energy production in hypoxia-ischemia conditions
lactate dehydrogenase
179
WPW first line treatment
propanolol
180
the reaction involved in FaO by neonatal cardiomyocytes is catalyzed by
carnitine palmitoyl transferase
181
what causes widely split S2 in ASD
delayed RV depolarization with little change in venous return to RA with inspiration
182
when do endocardial cushions come together to form intracardiac septum?
week 8
183
MoA dobutamine
b1 agonist > B2, a1
184
MoA dopamine
inhibits NaK ATPase and Na/H pump
dopaminergic then beta some alpha at high dose
185
MoA epi
beta 1 and 2 > alpha
186
MoA isopreterenol
B1 and B2
187
MoA nitroprusside
decrease SVR
188
MoA NE
a1 > a2 > b1 > b2
189
MCC hypertrophic cardiomyopathy
Noonan
190
ductus comes from what arch?
L 6th aortic arch
