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Truncus
arteriosus gives
rise to what?
ascending aorta and pulmonary trunk
2. bulbus cordis gives
rise to what?
smooth parts (outflow tract) of left and
right ventricles
3. primitive ventricle
gives rise to what?
trabeculated left and right ventricles
4. primitive atria
give rise to what?
trabeculated left and right atria
5. left horn of sinus
venosus gives rise
to what?
coronary sinus
6. right horn of SV
gives rise to what?
smooth part of right atrium
7. right common
cardinal vein and
right anterior
cardinal vein give
rise to what?
SVC
8. what happens in
the normal
development of the
truncus
arteriosus?
neural crest migration truncal and
bulbar ridges that spiral and fuse to
form the aorticopulmonary (AP)
septum ascending aorta and
pulmonary trunk
9. what are the
truncus arteriosus
pathologies?
1. TGA
2. ToF
3. TA
10. what is the defect
in transposition of
the great vessels?
failure to spiral
11. what is the TA
defect in tetralogy
of Fallot?
skewed AP septum development
12. what is the defect
in persistent TA?
partial AP septum development
13. 3 steps in
embryologic
formation of
interventricular
septum?
1. muscular ventricular septum forms-
opening= interventricular foramen
2. AP septum rotates and fuses with
muscular ventricular septum to form
membranous interventricular septum,
closing interventricular foramen
3. Growth of endocardial cushions
separates atria from ventricles and
contributes to both atrial separation
and membranous portion of the
interventricular septum
14. improper neural
crest migration
into the TA can
result in what?
transposition of the great arteries or a
persistent TA
15. in interventricular
septum development,
membranous septal
defect causes what?
an initial left to right shunt, which
later reverses to a right to left shunt
due to onset of pulmonary
hypertension (Eissenmenger's
syndrome)
16. 8 steps in interatrial
septum
development?
1. foramen primum narrows as
septum primum grows toward
endocardial cushions
2. perforations in septum primum
form foramen secundum (foramen
primum disappears
3. foramen scundum maintains
right to left shunt as septum
secundum begins to grow
4. septum secundum contains a
permanent opening (foramen ovale)
5. foramen secundum enlarges and
upper part of septum primum
degenerates
6. remaining portion of septum
primum forms the valve of the
foramen ovale
7. septum secundum and septum
primum fuse to form the atrial
septum
8. foramen ovale usually closes soon
after birth because of LA pressure
17. what happens in
pathology of
interatrial septal
development?
patent foramen ovale, caused by
failure of the septum primum and
septum secundum to fuse after birth
18. when is there fetal
erythropoiesis in the
yolk sac?
3-10wk
19. when is there fetal
erythropoiesis in the
liver?
6wk-birth
20. when is there fetal
erythropoiesis in the
spleen?
15-30wk
21. when is there fetal
erythropoiesis in the
bone marrow?
22wk-adult
22. mnemonic for fetal
erythropoiesis?
young liver synthesizes blood
23. structure of HbF? 22
24. structure of HbA? 22
25. O2 content of fetal
blood in the umbilical
vein?
PO2~30
80% saturated with O2
26. O2 sat of umbilican
arteries?
low
FA Cardiology
Study online at quizlet.com/_ohup5
27. sites of 3
important
shunts of fetal
circulation?
1. ductus venosus
2. foramen ovale
3. ductus arteriosus
28. action of shunt at
ductus venosus
in fetal
circulation?
blood entering the fetus through the
umbilical vein is coducted via the ductus
venosus into the IVC to bypass the
hepatic circulation
29. action of the
shunt at the
foramen ovale in
fetal circulation?
most oxygenated blood reaching the
heart via the IVC is diverted through the
foramen ovale and pumped out the aorta
to the head and body
30. action of the
shunt at the
ductus
arteriosus in
fetal circulation?
deoxygenated blood entering the RA from
the SVC enters the RV, is expelled into
the pulmonary artery, then passes
through the ductus arteriosus into the
descending aorta
31. what happens to
fetal circulation
at birth when the
infant takes a
breath?
resistance in pulmonary vasculature
causes LA pressure vs RA pressure
foramen ovale closes (now called fossa
ovalis)
in O2 leads to in prostaglandins,
causing closure of ductus arteriosus
32. what helps close
PDA?
indomethacin
33. what keeps PDA
open?
PGE1, PGE2
34. post natal
derivative of the
umbilical vein?
ligamentum teres hepatis, contained in
falciform ligament
35. postnatal
derivatives of
umbilical
arteries?
medial umbilical ligaments
36. postnatal
derivatives of
ductus
arteriosus?
ligamentum arteriosum
37. postnatal
derivative of
ductus venosus?
ligamentum venosum
38. postnatal
derivative of
foramen ovale?
fossa ovalis
39. postnatal
derivative of
allantois?
urachus-median umbilical ligament
40. what is the
urachus part of?
the allantoic duct between the bladder
and the umbilicus
41. what finding is a
remnant of the
urachus?
urachal cyst, or sinus
42. postnatal derivative
of the notochord?
nucleus pulplosus of intervertebral
disc
43. LCX supplies what? lateral and posterior walls of left
ventricle
44. LAD supplies what? anterior 2/3 of interventricular
septum, anterior papillary muscle,
and anterior surface of left ventricle
45. PD supplies what? posterior 1/3 of interventricular
septum and posterior walls of
ventricles
46. acute marignal
artery supplies
what?
right ventricle
47. SA and AV nodes are
usually supplied by
what?
RCA
48. frequency and
features of right
dominant coronary
circulation?
85%
PD arises from RCA
49. frequency and
features of left-
dominant coronary
circulation?
8%
PD arises from LCX
50. frequency and
features of
codominant
circulation?
7%
PD arises from both LCX and RCA
51. coronary artery
occlusion most
commonly occurs
where?
in LAD
52. when do coronary
arteries fill?
during diastole
53. most posterior part
of the heart is what?
LA
54. enlargement of LA
can cause what?
dysphagia (due to compression of the
esophagus) or hoarseness (due to
compression of the left recurrent
laryngeal nerve)
55. transesophageal
echocardiography is
useful for
diagnosing what?
LA enlargement
aortic dissection
thoracic aortic aneurysm
56. equations for
cardiac output?
CO= SV x HR
Fick's:
CO= (rate of O2
consumption)/((arterial O2 content)-
(venous O2 content))
57. equation for MAP? MAP= CO x TPR
MAP= 2/3 diastolic pressure + 1/3
systolic
58. pulse pressure=? systolic pressure - diastolic pressure
59. pulse pressure is
proportional to
what?
stroke volume
60. equations for stroke
volume?
SV = CO/HR = EDV - ESV
61. during the early
stages of exercise CO
is maintained by
what?
HR and SV
62. during the late stages
of exercise, CO is
maintained by what?
HR only (SV plateaus)
63. what happens during
exercise if HR is too
high?
diastolic filling is incomplete and
CO
64. cardiac variables that
affect stroke volume?
SV CAP
Stroke Volume affected by
Contractility, Afterload, and Preload
65. SV when what? preload, afterload,
contractility
66. contractility (and SV)
with what?
1. catecholamines
2. intracellular Ca++
3. extracellular Na+
4. Digitalis
67. how do
catecholamines
contractility?
activity of Ca++ pump in
sarcoplasmic reticulum
68. how does a in
extracellular Na+
contractility?
activity of Na+/Ca++ exchanger
69. how does digitalis
contractility?
blocks Na+/K+ pump
intracellular Na+ Na+/Ca++
exchanger activity intracellular
Ca++
70. contractility and SV
with what?
1. blockade
2. heart failure (systolic
dysfunction)
3. acidosis
4. hypoxia/hypercapnia
(PO2/PCO2)
5. Non-dihydropyridine Ca++
channel blockers
71. effect of anxiety,
exercise, and
pregnancy on SV?
688. effect of
ezetimibe on
HDL ?
no effect
689. effect of
ezetimibe on
TG?
no effect
690. MOA of
ezetimibe?
prevent cholesterol reabsorption at small
intestinal brush border
691. AE of ezetimibe? rare in LFTs
diarrhea
692. effects of
fibrates on
LDL?
693. effects of
fibrates on
HDL?
694. effects of
fibrates on TG?
695. MOA of
fibrates?
upregulate LPLTG clearance
696. AE of fibrates? myositis
hepatotoxicity
cholesterol gallstones
697. PK of digoxin? 75% bioavailability
20-40% protein bound
t1/2=40h
urinary excretion
698. MOA of digoxin? direct inhibition of Na+/K+
ATPase leads to indirect
inhibition of Na+/Ca++
exchanger/antiport
[Ca++]i positive inotropy
stimulates vagus HR
699. clinical use of digoxin? CHF
atrial fibrillation
700. why use digoxin in
CHF?
contractility
701. why use digoxin in
atrial fibrillation?
conduction at AV node and
depression of SA node
702. what are the major
types of side effects seen
in digoxin toxicity?
cholinergic
ECG
hyperkalemia- poor prognostic
indicator
703. what are the cholinergic
side effects associated
with digoxin toxicity?
nausea
vomiting
diarrhea
blurry yellow vision (VanGogh)
704. ECG side effects seen in
digoxin toxicity?
PR
QT
ST scooping
T wave inversion
arrhythmia
AV block
705. factors predisposing to
digoxin toxicity?
renal failure
hypokalemia
quinidine
706. how does renal failure
predispose digoxin
toxicity?
excretion
707. how does hypokalemia
predispose digoxin
toxicity?
permissive for digoxin binding
at K+ binding site on Na/K
ATPase
708. how does quinidine
predispose digoxin
toxicity?
digoxin clearance; displaces
digoxin from tissue binding
sites
709. what is the antidote for
digoxin toxicity?
slowly normalize K+
lidocaine
cardiac pacer
anti-digoxin Fab fragments
Mg++
710. what type of drug are all
the type I Na channel
blocker
antiarrhythmics?
local anesthetics
711. MOA of class I
antiarrhythmics?
conduction (especially in
depolarized cells)
slope of phase 0 depolarization
and threshold for firing in
abnormal pacemaker cells
712. what does it mean
that class I
antiarrhythmics are
state dependent?
selectively depress tissue that is
frequently depolarized
(tachycardia)
713. what causes
toxicity for all class I
antiarrhythmic
drugs?
hyperkalemia
714. which drugs are the
Class IA
antiarrhythmics?
Quinidine
Procainamide
Disopyramide
The Queen Proclaims Diso's
Pyramid
715. MOA of Class IA
antiarrhythmics?
AP duration
ERP
QT interval
716. Class IA
antiarrhythmias
affect what kind of
arrhythmias?
atrial and ventricular arrhythmias,
especially reentrant and ectopic
supraventricular and ventricular
tachycardia
717. quinidine toxicity? cinchonism- headache, tinnitus
718. procainamide
toxicity?
reversible SLE-like syndrome
719. disopyramide
toxicity?
heart failure
720. toxicities common to
all Class IA
antiarrhythmics?
thrombocytopenia,
torsades de pointes due to QT
interval
721. which drugs are the
class IB
antiarrhythmics?
Lidocaine
Mexilitine
Tocainide
I'd Buy Lidy's Mexican Tacos
(phenytoin)
722. which type of
antiarrhythmic is
best post MI?
IB
723. MOA of class IB
antiarrhythmics?
AP duration
Preferentially affect ischemic or
depolarized Purkinje and
ventricular tissue
724. Class IB
antiarrhythmics are
useful in what?
acute ventricular arrhythmias
(especially post MI) and in digitalis
induced arrhythmias
725. toxicity of Class IB
antiarrhythmics?
local anesthetic
CNS stimulation/depression
cardiovascular depression
726. which drugs are class IC
antiarrhythmics?
flecainide
propafenone
727. mnemonic for IC
antiarrhythmics?
IC is CI in structural heart
disease and post MI
728. MOA of class IC
antiarrhythmics?
no effect on AP duration
729. clinical use of class IC
antiarrhytmics?
useful in ventricular
tachycardias that progress to
VF and in intractable SVT
usually used only as last resort
in refractory tachyarrhythmias
for patients without structural
abnormalities
730. toxicity of class IC
antiarrhythmics?
proarrhythmic, especially post
MI
significantly prolongs
refractory period in AV node
731. effects of class I
antiarrhythmics on
ventricular AP graph?
all class I- clockwise decrease
in slope of phase 0
IA- prolong AP- rightward
stretch of phase 3
IB- shorten AP- leftward
shrink of phase 3
IC- no effect- barely to the left
of normal AP
732. the class II
antiarrhythmics are
what type of drugs?
blockers
733. which drugs are used as
class II
antiarrhythmics?
metoprolol
propanolol
esmolol
atenolol
timolol
734. MOA of class II
antiarrhythmics drugs?
SA and AV nodal activity by
cAMP, Ca++ currents
suppress abnormal pacemakers
by slope of phase 4
735. which class II
antiarrhythmic is very
short acting?
esmolol
736. what part of the heart is
particularly sensitive to
class II
antiarrhythmics?
AV node
737. ECG changes seen with
class II
antiarrhythmics?
PR interval
738. clinical use of class II
antiarrhythmics?
ventricular tachycardia, SVT,
slowing ventricular rate during
atrial fibrillation and atrial
flutter
739. toxicity of class II
antiarrhythmics?
impotence
exacerbation of asthma
CV effects
CNS effects
may mask the signs of
hypoglycemia
740. CV AE of class II
antiarrhythmics?
bradycardia
AV block
CHF
741. CNS effects of class II
antiarrhythmics?
sedation
sleep alterations
742. AE specific to
metoprolol?
dyslipidemia
743. treat overdose of
metoprolol with what?
glucagon
744. cardiac AE specific to
propanolol?
can exacerbate vasospasm in
Prinzmental's angina
745. which are the class III
antiarrhythmics?
Amiodarone
Ibutilide
Dofetilide
Sotalol
AIDS
746. all class III
antiarrhythmics are
what type of drug?
K+ channel blockers
747. MOA of class III
antiarrhythmics?
AP duration, ERP
748. when are class III
antiarrhythmics used?
when others fail
749. ECG changes caused by
class III
antiarrhythmics?
QT interval
750. AE of sotalol? torsades de pointes
excessive block
751. AE of ibutilide? torsades de pointes
752. AE of amiodarone? pulmonary fibrosis
hepatotoxicity
thyroid dysfunction (40% I by
weight)
corneal deposits
skin deposits (blue/grey)
resulting in photodermatitis
neurologic effects
constipation
CV effects (bradycardia, heart
block, CHF)
753. what are the
antiarrhythmic effects
of amiodarone?
has class I , II, III, and IV
effects because it alters the lipid
membrane
754. what do you need to check
when using amiodarone?
PFTs
LFTs
TFTs
755. effect of all class III
antiarrhythmics on
ventricular AP curve?
wide rightward stretch in
phase 3 prolongs AP and
ERP
756. which drugs are class IV
antiarrhythmics?
verapamil
diltiazem
757. all class IV antiarrhythmics
are what type of drug?
Ca channel blockers
758. MOA of class IV
antiarrhythmics?
conduction velocity,
ERP, PR interval
759. clinical use of class IV
antiarrhythmics?
prevention of nodal
arrhythmias (SVT)
760. toxicity of class IV
antiarrhythmics?
constipation
flushing
edema
CV effects (CHF, heart
block, sinus node
depression)
761. MOA of adenosine as
antiarrhythmic?
K+ out of cells
hyperpolarizing the cell
+ Ica
762. adenosine is the drug of
choice for what?
diagnosing/abolishing
supraventricular
tachycardia
763. duration of action of
adenosine?
~15s
764. toxicity of adenosine? flushing
hypotension
chest pain
765. effects of adenosine blocked
by what?
theophylline and caffeine
766. clinical use of Mg++ as
antiarrhythmic?
effective in torsades de
pointes and digoxin
toxicity