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1.

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?

72. myocardial O2 demand is by


what?
afterload (proportional
to arterial pressure)
contractility
heart rate
heart size (wall
tension)
73. preload = ? ventricular EDV
74. afterload=? MAP (proportional to
peripheral resistance)
75. agents that preload? vEnodilators
(nitroglycerin)
76. agents that afterload? vAsodilators
(hydrAlazine)
77. preload with what? 1. exercise (slightly)
2. blood volume
(overtransfusion)
3. excitement (
sympathetic activity)
78. on Starling curve, force of
contraction is proportional to
what?
end-diastolic length of
cardiac muscle fiber
(preload)
79. on Starling curve, what are the
factors that increase
contractility?
sympathetic stimulation
catecholamines
digoxin
80. on starling curve, which
factors contractility?
loss of myocardium (MI)
blockers
Ca++ channel blockers
81. equation for EF? EF= SV/EDV = (EDV-
ESV)/EDV
82. EF is an index of what? ventricular contractility
83. normal EF? >=55%
84. EF in what? systolic heart failure
85. P =? Q x R
86. equation for resistance? resistance = (driving
pressure P)/(Flow Q)=
(8l)/r^4
87. equation for total resistance of
vessels in series?
= R1 + R2 + R3
88. 1/Toral Resistance of vessels
in parallel?
= 1/R1 + 1/R2 + 1/R3...
89. viscosity in what? 1. polycythemia
2. hyperproteinemic
states (multiple myeloma)
3. hereditary
spherocytosis
90. viscosity in what? anemia
91. pressure gradient drives
blood flow where?
from high pressure to low
pressure
92. resistance is proportional to what? viscosity and
vessel length
93. viscosity is inversely proportional to
what?
the radius to
the 4th power
94. what accounts for most of total
peripheral resistance?
arterioles
95. what vessels regulate capillary flow? arterioles
96. where is the operating point of the
heart on the cardiac and vascular
function curve?
intersection
where cardiac
output and
venous return
are equal
97. what causes the operating point of the
heart on the cardiac and vascular
function curve to shift straight down?
TPR,
hemorrhage
before
compensation
can occur
98. what causes the operating point of the
heart on the cardiac an vascular
function curve to shift straight up?
TPR,
exercise, AV
shunt
99. what causes the operating point of the
heart to shift downward and rightward
along the venous return curve on the
cardiac and vascular function curve?
heart failure
narcotic
overdose
100. what causes an upward shift in the CO
curve?
+ inotropy
101. what causes a downward shift in the CO
curve?
- inotropy
102. what causes a rightward shift in the
venous return curve?
blood
volume
103. what causes a leftward shift in the
venous return curve?
blood
volume
104. what is the X intercept of the venous
return curve?
mean
systemic
filling
pressure
105. what are the 5 phases of the left
ventricle in the cardiac cycle?
1.
isovolumetric
contraction
2. systolic
ejection
3.
isovolumetric
relaxation
4. rapid filling
5. reduced
filling
106. what is isovolumetric contraction? period between
mitral valve
closure and aortic
valve opening
107. what is the period of highest O2
consumption during the cardiac
cycle?
isovolumetric
contraction
108. what is systolic ejection? period between
aortic valve
opening and
closing
109. what is isovolumetric relaxation? period between
aortic valve
closing and
mitral valve
opening
110. what is rapid filling? period just after
mitral valve
opening
111. what is reduced filling? period just before
mitral valve
closure
112. what causes a rightward EDV
expansion without an upward
pressure expansion in the LV
cardiac cycle P/V curve?
preload SV
113. what causes a leftward ESV
expansion with an upward pressure
expansion on a LV cardiac cycle P/V
curve?
contractility
SV
EF
ESV
114. what causes a leftward ESV
contraction with an upward
pressure expansion on a LV cardiac
cycle P/V curve?
afterload
aortic pressure
SV
ESV
115. what causes S1 sound? mitral and
tricuspid valve
closure
116. S1 is loudest where? at mitral area
117. what causes S2 sound? aortic and
pulmonary valve
closure
118. where is S2 loudest? at left sternal
border
119. when is S3 heard? in early diastole
during rapid
ventricular filling
phase
120. S3 is associated with what? filling
pressures (MR,
CHF)
121. S3 is more common in
which types of ventricles?
dilated ventricles, but normal
in children and pregnant
women
122. when do you hear S4? "atrial kick" in late diastole
123. what causes S4? high atrial pressure
LA must push against stiff LV
wall
124. S4 associated with what? ventricular hypertrophy
125. what does JVP a wave
correspond to?
atrial contraction
126. what does the JVP c wave
correspond to?
RV contraction (closed
tricuspid valve bulging into
atrium)
127. what does the JVP x
descent correspond to?
atrial relaxation and
downward displacement of
closed tricuspid valve during
ventricular contraction
128. what does the JVP v wave
correspond to?
right atrial pressure due to
filling against closed tricuspid
valve
129. what does the JVP y
descent correspond to?
blood flow from RA to RV
130. what happens in normal
splitting?
inspiration
drop in intrathoracic pressure

venous return to the RV


RV stroke volume
RV ejection time
delayed closure of the
pulmonic valve
131. what else contributes to
the delayed closure of the
pulmonic valve in normal
splitting?
pulmonary impedance (
capacity of the pulmonary
circulation)
132. what does normal
splitting sound like?
A2 and P2 are close during
expiration,
A2 and P2 are only slightly
more separated during
inspiration
133. wide splitting is seen in
which conditions?
those that delay RV emptying
(pulmonic stenosis, RBB
block)
134. what happens in wide
splitting?
delay in RV emptying causes
delayed pulmonic sound
(regardless of breath)
135. what does wide splitting
sound like?
an exaggeration of normal
splitting
Ex: A2 and P2 are split as
wide as normal inspiration
Ins: A2 and P2 are split much
wider than normal
136. fixed splitting is
seen in what?
ASD
137. what happens in
fixed splitting?
ASD left to right shunt RA and
RV volumes flow through pulmonic
valve such that, regardless of breath,
pulmonic closure is greatly delayed
138. paradoxical
splitting is seen
in what?
conditions that delay LV emptying
(aortic stenosis, LBB block)
139. what happens in
paradoxical
splitting?
normal order of valve closure is reversed
so that P2 sound occurs before A2.
140. what does
paradoxical
splitting sound
like?
on inspiration, P2 closes later and moves
closer to A2, thereby 'paradoxically'
eliminating the split
141. what can cause a
systolic murmur
in the aortic
area?
aortic stenosis
flow murmur
aortic valve sclerosis
142. where is the
aortic
auscultation
area?
2nd intercostal space RSB
143. what causes a
systolic ejection
murmur in the
pulmonic area?
pulmonic stenosis
flow murmur (ASD, PDA)
144. where is the
pulmonic area
for ausculation?
2nd interspace LSB
145. what causes a
pansystolic
murmur at the
tricuspid area?
tricuspid regurgitation
ventricular septal defect
146. what causes
diastolic
murmur at the
tricuspid area?
tricuspid stenosis
ASD
147. where is the
tricuspid area
for
auscultation?
5th interspace LSB
148. what causes a
systolic murmur
in the mitral
area?
mitral regurgitation
149. what causes a
diastolic
murmur in the
mitral area?
mitral stenosis
150. where is the mitral area for
auscultation?
5th interspace mid
clavicular line
151. what causes diastolic
murmur at the left sternal
border?
aortic regurgitation
pulmonic regurgitation
152. what causes systolic murmur
at left sternal border?
hypertrophic
cardiomyopathy
153. what are the auscultation
findings in ASD?
pulmonary flow murmur
diastolic rumble
(tricuspid)
blood flow across the ASD
doesn't cause a murmur
because there is no
pressure gradient
murmur louder
diastolic murmur of
pulmonic regurgitation
from dilation of
pulmonary artery
154. the continuous, machine-like
murmur of PDA is best
appreciated where?
left infraclavicular region
155. what is the effect of
inspiration on ausculation?
intensity of right heart
sounds
156. what is the effect of
expiration on auscultation?
intensity of left heart
sounds
157. what is the effect of hand grip
maneuver on auscultation (
systemic vascular
resistance)?
intensity of MR, AR,
VSD, MVP murmurs
intensity of AS,
hypertrophic
cardiomyopathy murmurs
158. what is the effect of the
vasalva maneuver ( venous
return) on auscultation?
intensity of most
murmurs
intensity of MVP,
hypertrophic
cardiomyopathy murmurs
159. what is the effect of rapid
squatting ( venous return,
preload, afterload with
prolonged squatting)?
intensity of MVP,
hypertrophic
cardiomyopathy murmurs
160. conditions associated with
systolic heart sounds include
what?
aortic/pulmonic stenosis
mitral/tricuspid
regurgitation
VSD
161. conditons associated with
diastolic heart sounds
include what?
aortic/pulmonic
regurgitation
mitral/tricuspid stenosis
162. what does mitral/tricuspid
regurgitation sound like?
holosystolic, high-pitched
"blowing murmur"
163. mitral regurgitation is
loudest where?
at apex and radiates to
toward axilla
164. mitral regurgitation sound
is enhanced by what?
maneuvers that TPR
(squatting, hand grip) or
LA return (expiration)
165. MR is often due to what? ischemic heart disease,
mitral valve prolapse, LV
dilation
166. where is tricuspid
regurgitation loudest?
loudest at tricuspid area
and radiates to right
sternal border
167. tricuspid regurgitation
sound enhanced by what?
maneuvers that RA
return (inspiration)
168. TR can be caused by what? RV dilation
169. rheumatic fever and
infective endocarditis can
cause which heart sounds?
MR or TR
170. what does Aortic stenosis
sound like?
crescendo-decrescendo
systolic ejection murmur
following ejection click
radiates to carotids/heart
base
171. what causes ejection click in
aortic stenosis?
EC due to abrupt halting of
valve leaflets
172. pressure gradient in aortic
stenosis?
LV>> aortic pressure
during systole
173. pulse findings in aortic
stenosis?
'pulsus parvus et tardus'
pulses are weak with a
delayed peak
174. aortic stenosis can lead to
what?
Syncope, Angina, Dyspnea
on exertion (SAD)
175. aortic stenosis is due to
what?
age related calcific aortic
stenosis or bicuspid aortic
valve
176. what does VSD sound like? holosystolic, harsh
sounding murmur
177. where is VSD loudest? tricuspid area
178. VSD sound can be
accentuated how?
hand grip maneuver due to
increased afterload
179. what does MVP sound like? late systolic crescendo
murmur with midsystolic
click
180. what causes MC? sudden tensing of the
chordae tendineae
181. what is the most frequent
valvular lesion?
MVP
182. MVP is best heard where? over apex
183. when is MVP loudest? S2
184. severity of MVP? usually benign
185. MVP can predispose to
what?
infective endocarditis
186. MVP can be caused
by what?
myxomatous degeneration
rheumatic fever
chordae rupture
187. MVP enhanced by
what?
maneuvers that Venous return
(standing or vasalva)
188. what does aortic
regurgitation
sound like?
immediate high pitched "blowing"
diastolic decrescendo murmur
189. pulses in AR? wide pulse pressure when chronic;
can present with bounding pulses
and head bobbing
190. AR is often due to
what?
aortic root dilation, bicuspid aortic
valve, endocarditis, rheumatic fever
191. what murmur in
AR?
hand grip
192. effect of
vasodilators on AR?
intensity of murmur
193. what does MS
sound like?
follows opening snap
delayed rumbling late diastolic
murmur
194. what causes OS in
MS?
abrupt halt in leaflet motion in
diastole, after rapid opening due to
fusion at leaflet tips
195. pressure gradient
in MS?
LA>>LV during diastole
196. MS often occurs
secondary to what?
rheumatic fever
197. chronic MS can
result in what?
LA dilation
198. MS sound is
enhanced by what?
maneuvers that LA return
(expiration)
199. what does PDA
sound like?
continuous machine like murmur
200. when is PDA
loudest?
S2
201. PDA is often due to
what?
congenital rubella or prematurity
202. where is PDA best
heard?
left infraclavicular area
203. ventricular action
potential also
occurs where?
in bundle of His and Purkinje fibers
204. what happens in
Phase 0 of
ventricular action
potential?
rapid upstroke- voltage gated Na+
channels open
205. what happens in
Phase 1 of
ventricular action
potential?
initial repolarization- inactivation of
voltage gated Na+ channels. Voltage
gated K+ channels begin to open
206. what happens in
Phase 2 of
ventricular action
potential?
plateau-Ca++ influx through voltage
gated Ca++ channels balances K+
efflux
Ca++ influx triggers Ca++ release from
sarcoplasmic reticulum and myocyte
contraction
207. what happens in
phase 3 of
ventricular action
potential?
rapid repolarization= massive K+
efflux due to opening of voltage-gated
slow K+ channels and closure of
voltage gated Ca++ channels
208. what happens in
phase 4 of the
ventricular action
potential?
resting potential- high K+ permeability
through K+ channels
209. difference between
cardiac muscle AP
and skeletal
muscle?
1. cardiac muscle AP has a plateau,
which is due to Ca++ influx and K+
efflux, myocyte contraction occurs due
to Ca++ induced Ca++ release from the
sarcoplasmic reticulum
2. cardiac nodal cells spontaneously
depolarize during diastole resulting in
automaticity due to If channels
3. Cardiac myocytes are electrically
coupled to eachother by gap junctions
210. what do If chanels
do?
funny current channels responsible for
a slow, mixed Na+/K+ inward current
211. what is the
direction of the
leak currents in
cardiac
ventricular
myocytes?
K+ out
Na+, Ca++ in
212. pacemaker action
potential occurs
where?
in the SA and AV nodes
213. what happens in
phase 0 of the
pacemaker action
potential?
upstroke- opening of VG Ca++
channels
fast VG Na channels are permanently
inactivated because of the less negative
resting voltage of these cells
214. permanent fast VG
Na channel
inactivation in the
pacemaker cells
results in what?
slow conduction velocity that is used
by the AV node to prolong
transmission from the atria to the
ventricles
215. what happens in
Phase 2 or
pacemaker
potential?
plateau is absent
216. what happens in
phase 3 of the
pacemaker
potential?
inactivation of the Ca++ channels and
activation of K+ channels K+
efflux
217. what happens
in phase 4 of
the pacemaker
potential?
slow diastolic depolarization- membrane
potential spontaneously depolarizes as
Na+ conductance (If different from Ina
in phase 0 of ventricular action potential)
218. phase 4 of the
pacemaker
potential
accounts for
what?
automaticity of SA and AV nodes
219. slope of phase
4 in the SA
node
determines
what?
HR
220. effect of
ACh/adenosine
on SA node?
the rate of diastolic depolarization and
HR
221. effect of
catecholamines
on SA node?
depolarization and heart rate
222. effect of
sympathetic
stimulation on
SA/AV node?
the chance that If channels are open
and thus HR
223. P wave
corresponds to
what?
atrial depolarization
224. atrial
repolarization
in ECG?
masked by QRS complex
225. PR interval
corresponds to
what?
conduction delay through AV node
226. normal PR
interval?
<200 ms
227. QRS complex
correspondes
to what?
ventricular depolarization
228. normal
duration of
QRS complex?
<120s
229. QT interval
corresponds to
what?
mechanical contraction of the ventricles
230. T wave
corresponds to
what?
ventricular repolarization
231. T wave
inversion may
indicate what?
recent MI
232. ST segment
corresponds to what?
isoelectric, ventricles
depolarized
233. U wave is caused by
what?
hypokalemia
bradycardia
234. relative speed of
conduction in the
heart?
purkinje > atria > ventricles >
AV nodes
235. relative speed of
conduction in the
pacemaker cells?
SA node> AV> Bundle of
his/purkinje/ventricles
236. what is the conduction
pathway in the heart?
SA node atria AV node
common bundle bundle
branches purkinje fibers
ventricles
237. dominant pacemaker in
heart?
SA node pacemaker inherent
dominance with slow phase of
the upstroke
238. what is the delay in the
AV node?
100ms delay- atrioventricular
delay; allows time for
ventricular filling
239. what happens in
torsades de pointes?
ventricular tachycardia,
characterized by shifting
sinusoidal waveforms on ECG,
can progress to ventricular
fibrillation
240. what predisposes to
torsades de pointes?
anything that prolongs the QT
interval
241. treatment for torsades
de pointes?
magnesium sulfate
242. congenital long QT
syndromes are most
often due to what?
defects in cardiac sodium or
potassium channels
243. what condition has long
QT syndrome that
presents with severe
sensorineural
deafness?
Jervell and Lange-Nielsen
syndrome
244. how does atrial
fibrillation look?
chaotic and erratic baseline
(irregularly irregular) with no
discrete P waves in between
irregularly spaced QRS
complexes
245. atrial fibrillation can
result in what?
atrial stasis and lead to stroke
246. tx for atrial fibrillation? rate control
anticoagulation
possible cardioversion
247. what does atrial flutter
look like?
a rapid succession of identical,
back-to-back atrial
depolarization waves
'saw tooth' appearance
248. pharmacologic
conversion to sinus
rhythm in atrial
flutter?
Class IA, IC, or III antiarrhythmics
249. rate control in atrial
flutter?
-blocker or calcium channel
blocker
250. what does ventricular
fibrillation look like?
a completely erratic rhythm with no
identifiable waves
251. severity of
ventricular
fibrillation?
fatal arrhythmia without
immediate CPR and defibrillation
252. features of 1st degree
AV block?
prolonged PR interval >200ms
asymptomatic
253. features of 2nd
degree AV block
Mobitz type I
(Wenckebach)?
progressive lenghtening of the PR
interval until a beat is dropped
usually asymptomatic
254. features of Mobitz
type II?
dropped beats that are not preceded
by a change in the length of the PR
interval
255. severity of Mobitz
type II?
these abrupt, nonconducted p
waves result in a pathologic
condition
256. mobitz type II is often
found as what?
2:1 block, where there are >=2 p
waves to 1 QRS
257. mobitz type II often
treated with what?
pacemaker
258. mobitz type II may
progress to what?
3rd degree block
259. what happens in 3rd
degree (complete)
heart block?
the atria and ventricles beat
independently of each other
both p waves and QRS complexes
are present, though P waves bear
no relation to the QRS complexes
260. which rate is faster in
3rd degree heart
block?
atrial rate is faster than ventricular
rate
261. 3rd degree heart
block is usually
treated with what?
a pacemaker
262. which disease can
result in 3rd degree
heart block?
Lyme disease
263. ANP is released from
where?
atrial myocytes
264. ANP is released in
response to what?
blood volume and pressure
265. ANP causes what? generalized vascular relaxation
and Na+ reabsorption at the
medullary collecting tubule
266. effect of ANP on
renal blood flow?
constricts efferent renal arterioles and
dilates afferent arterioles (cGMP
mediated), promoting diuresis and
contributing to the escape from
aldosterone mechanism
267. aortic arch
baroreceptors
transmit info
where?
via vagus nerve to solitary nucleus of
medulla (responds only to BP)
268. carotid sinus
baroreceptor
transmits info
where?
via glossopharyngeal nerve to solitary
nucleus of medulla (responds to and
in BP)
269. what happens at
baroreceptors in
response to
hypotension?
arterial pressure
stretch
afferent baroreceptor firing
efferent sympathetic firing and
efferent parasympathetic stimulation
vasoconstriction, HR, contractility,
BP
270. baroreceptors
are important in
the response to
what?
severe hemorrhage
271. effect of carotid
massage on
baroreceptors?
pressure on carotid artery stretch
afferent baroreceptor firing HR
272. baroreceptors
contribute to
which reaction?
Cushing reaction
273. what happens in
Cushing
reaction?
triad of hypertension, bradycardia, and
respiratory depression
274. mechanism of
Cushing
reaction?
ICP constricts arterioles cerebral
ischemia and reflex sympathetic
increase in perfusion pressure
(hypertension) stretch reflex
baroreceptor induced-bradycardia
275. what happens in
stimulation of
peripheral
chemoreceptors?
carotid and aortic bodies are stimulated
by PO2 (<60mmHg), PCO2, and
pH of blood
276. what happens in
stimulation of
central
chemoreceptors?
are stimulated by changes in pH and
PCO2 of brain interstitial fluid, which in
turn are influenced by arterial CO2
277. central
chemoreceptors
do not directly
respond to what?
PO2
278. what is the organ
with the largest
blood flow?
Lung (100% of CO)
279. what is the organ with
the largest share of
systemic cardiac output?
liver
280. which organ has the
highest blood flow per
gram of tissue?
kidney
281. which organ has the
largest arteriovenous O2
difference?
heart
282. why does heart have the
largest arteriovenous O2
difference?
becuase O2 extraction is 80%
283. how is O2 demand met in
heart?
O2 demand is met by
coronary blood flow, not by
extraction of O2
284. what is the normal
pressure in the RA?
<5
285. what is the normal
pressure in the RV?
25/5
286. what is the normal
pressure in the PA?
25/10
287. what is the normal
pressure in the LA?
<12
288. what is the normal
pressure in the LV?
130/10
289. what is the normal
pressure in the aorta?
130/90
290. PCWP is a good
approximation of what?
left atrial pressure
291. when is PCWP> LV
diastolic pressure?
mitral stenosis
292. how is PCWP measured? Swan Ganz catheter
293. what is autoregulation? how blood flow to an organ
remains constant over a wide
range of perfusion pressures
294. what are the factors
determining
autoregulation in the
heart?
Local metabolites
(vasodilatory)-CO2, adenosine,
NO
295. what are the factors
determining
autoregulation in the
brain?
Local metabolites
(vasodilatory)-CO2 (pH)
296. what are the factors
determining
autoregulation in the
kidneys?
myogenic and
tubuloglomerular feedback
297. what are the factors
determining
autoregulation in the
lungs?
hypoxia causes
vasoconstriction
298. what are the factors
determining
autoregulation in skeletal
muscle?
local metabolites- lactate,
adenosine, K+
299. what are the factors
determining
autoregulation in the skin?
sympathetic stimulation
most important mechanism-
temperature control
300. what determines fluid
movement through
capillary membranes?
starling forces
301. what are the 4 starling
forces?
Pc
Pi
c
i
302. what is Pc? capillary pressure- pushes
fluid out of capillary
303. what is Pi? interstitial fluid capillary-
pushes fluid into capillary
304. what is c? plasma colloid osmotic
pressure- pulls fluid into
capillary
305. what is i? interstitial fluid colloid
osmotic pressure-pulls fluid
out of capillary
306. equation for net filtration
pressure?
Pnet= [(Pc - Pi) - (c - i)]
307. what is Kf? filtration constant (capillary
permeability)
308. what is Jv? net fluid flow= Kf x Pnet
309. what is edema? excess fluid outflow into
interstitium
310. edema is commonly caused
by what?
capillary pressure (heart
failure)
plasma proteins
(nephrotic syndrome, liver
failure)
capillary permeability
(toxins, infections, burns)
interstitial colloid osmotic
pressure (lymphatic
blockage)
311. what is the most common
cause of early cyanosis?
Tetralogy of Fallot
312. which congenital heart
diseases make up the
right to left shunts
(early cyanosis)-blue
babies?
5T's
Tetralogy of Fallot
Transposition of the great vessels
persistent Truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary
venous return
313. features of Persistent
Truncus Arteriosus?
failure of truncus arteriosus to
divide into pulmonary trunk and
aorta
314. most patients with
persistent truncus
arteriosus have what?
accompanying VSD
315. tricuspid atresia is
characterized by what?
absence of tricuspid valve and
hypoplastic RV
316. tricuspid atresia
requires what for
viability?
both ASD and VSD
317. what happens in
TAPVR?
pulmonary veins drain into right
heart circulation (SVC, coronary
sinus, etc)
318. TAPVR is associated
with what?
ASD and sometimes PDA to
allow for right to left shunting to
maintain CO
319. which congenital heart
abnormalities make up
the left to right shunts
(late cyanosis)-blue
kids?
VSD
ASD
PDA
320. what is the most
common congenital
cardiac anomaly?
VSD
321. findings in ASD? loud S1, wide, fixed split S2
322. what do you use to
close PDA?
indomethacin
323. what is the frequency
of the congenital left to
right shunts?
VSD > ASD > PDA
324. what happens in
Eisenmenger's
syndrome?
uncorrected VSD, ASD, or PDA
causes compensatory pulmonary
vascular hypertrophy, which
results in progressive pulmonary
hypertension
325. what happens in
Eisenmenger's
syndrome as
pulmonary resistance
increases?
the shunt reverses from left to
right to right to left, which causes
late cyanosis, clubbing, and
polycythemia
326. tetralogy of fallot is
caused by what?
anterosuperior displacement of
the infundibular septum
327. what is the
mnemonic for the
components of ToF?
PROVe
1. Pulmonary infundibular stenosis
2. RVH
3. Overriding aorta (overrides the
VSD)
4. VSD
328. what is the most
important
determinant for
prognosis in ToF?
pulmonary infundibular stenosis
329. in ToF early cyanosis
(tet spells) caused by
what?
a right to left shunt across the VSD
330. difference between
isolated VSD and
VSD in ToF?
isolated VSDs usually flow left to
right (acyanotic)
in tetralogy, pulmonary stenosis
forces right to left (cyanotic) flow
and causes RVH
331. how does RVH in
ToF look?
boot shaped heart on CXR
332. patients with ToF
learn what
compensatory
mechanism?
squat to relieve cyanotic symptoms
333. why do patients with
ToF squat?
reduces blood flow to the legs,
PVR, and thus the cyanotic right
to left shunt across the VSD
334. what is the preferred
treatment for ToF?
early, primary surgical correction
335. what happens in
transposition of
great vessels?
aorta leaves RV (anterior) and
pulmonary trunk leaves LV
(posterior) separation of systemic
and pulmonary circulations
336. transposition of the
great vessels not
compatible with life
unless what?
a shunt is present to allow adequate
mixing of blood (VSD, PDA, or
patent foramen ovale)
337. transposition of
great vessels is due
to what?
failure of aorticopulmonary septum
to spiral
338. prognosis of
transposition of
great vessels?
without surgical correction, most
infants die within the first few
months of life
339. coarctation of the
aorta can result in
what?
AR
340. what is infantile type
of coarctation of the
aorta?
aortic stenosis proximal to insertion
of ductus arteriosus (preductal)
341. preductal coarctation
of the aorta is
associated with what?
Turner syndrome
342. what needs to be
checked in infantile
coarctation of the
aorta?
check femoral pulses on physical
exam
343. what is adult type
coarctation of the
aorta?
stenosis is distal to ligamentum
arteriosum (postductal)
344. postductal coarctation
of the aorta is
associated with what?
notching of the ribs (due to
collateral circulation),
hypertension in upper extremities,
weak pulses in lower extremities
345. postductal coarctation
of the aorta is most
commonly associated
with what?
bicuspid aortic valve
346. what is going on in
patent ductus
arteriosus in the fetal
period?
shunt is right to left (normal)
347. what happens to
patent ductus
arteriosus in the
neonatal period?
lung resistance and shunt
becomes left to right with
subsequent RVH and/or LVH and
failure (abnormal)
348. patent ductus
arteriosus is
associated with what
finding?
continuous machine like murmur
349. in PDA, patency is
maintained with
what?
PGE synthesis and low O2 tension
350. uncorrected PDA can
eventually result in
what?
late cyanosis in the lower
extremities (differential cyanosis)
351. when is PDA normal? PDA is normal in utero and only
closes after birth
352. which congenital
cardiac defect is
associated with 22q11
syndromes?
truncus arteriosus
ToF
353. which congenital
cardiac defects are
associated with Down
syndrome?
ASD
VSD
AV septal defect (endocardial
cushion defect)
354. which congenital
cardiac defects are
associated with
congential rubella?
septal defects
PDA
PA stenosis
355. which congenital cardiac
defects are associated with
turner syndrome?
coarctation of the aorta
(preductal)
356. which congenital cardiac
defects are assciated with
Mafan's syndrome?
aortic insufficiency and
dissection (late
complication)
357. which congenital cardiac
defects are associated with
infants of diabetic
mothers?
transposition of great
vessels
358. hypertension is defined as
what?
BP >= 140/90
359. what are the risk factors
for hypertension?
age
obesity
smoking
genetics
black>white>asian
360. 90% of hypertension is
what?
1 (essential) and related to
CO and TPR
361. 10 % of hypertension is
what?
mostly 2 to renal disease
362. features of malignant
hypertension?
severe
>180/120
rapidly progressing
363. hypertension predisposes
to what?
athersclerosis
LVH
stroke
CHF
renal failure
retinopathy
aortic dissection
364. what are the signs of
hyperlipidemia?
atheromas
xanthomas
tendinous xanthoma
corneal arcus
365. what are atheromas? plaques in blood vessel wall
366. what are xanthomas? plaques or nodules
composed of lipid-laden
histiocytes in the skin,
especially the eyelids
367. what do you call a
xanthoma of the eyelid?
xanthelasma
368. what is a tendinous
xanthoma?
lipid depost in the tendon,
especially the achilles
369. what is corneal arcus? lipid deposit in cornea,
nonspecific (arcus senilis)
370. what are the 3 classes of
arteriosclerosis?
Monckberg
arteriosclerosis
atherosclerosis
371. what is
Monckberg
arteriosclerosis?
calcification in the media of the arteries,
especially radial or ulnar
372. severity of
monckberg
arteriosclerosis?
usually benign
does not obstruct blood flow
intima not involved
373. typical
presentation of
monckberg
arteriosclerosis?
pipestem arteries
374. what are the two
subtypes of
arteriosclerosis?
hyaline
hyperplastic
375. what is hyaline
arteriosclerosis?
thickening of small arteries in essential
hypertension or DM
376. what is
hyperplastic
arteriosclerosis?
onion skinning in malignant
hypertension
377. what is
atherosclerosis?
fibrous plaques and atheromas form in
intima of arteries
378. what type of
disease is
atherosclerosis?
disease of elastic arteries and large and
medium sized muscular arteries
379. what are the
modifiable risk
factors for
atherosclerosis?
smoking
hypertension
hyperlipidemia
diabetes
380. what are the
non-modifiable
risk factors for
atherosclerosis?
age, gender ( in men and
postmenopausal women), and positive
family history
381. what is
important in the
pathogenesis of
atherosclerosis?
inflammation
382. what is the
progression of
atherosclerosis?
endothelial cell dysfunction
macrophage and LDL accumulation
foam cell formation fatty streaks
smooth muscle cell migration (involves
PDGF and FGF), proliferation and ECM
deposition fibrous plaque complex
atheromas
383. important
histological
finding in
atherosclerosis?
cholesterol crystals
384. what are the
complications of
atherosclerosis?
aneurysms
ischemia
infarcts
peripheral vascular disease
thrombus
emboli
385. what is the relative
frequency of
location of
atherosclerosis?
abdominal aorta > coronary artery >
popliteal artery > carotid artery
386. what are the
symptoms of
atherosclerosis?
angina
claudication
but can be asymptomatic
387. what is an aortic
aneurysm?
localized pathologic dilation of the
aorta
388. what are the 2 types
of aortic
aneurysm?
AAA
TAA
389. AAA is associated
with what?
atherosclerosis
390. AAA occurs more
frequently in who?
hypertensive male smokers> 50yo
391. TAA is associated
with what?
hypertension, cystic medial necrosis
(Marfan's) and historically 3
syphilis
392. what happens in
aortic dissection?
longitudinal intraluminal tear
forming a false lumen
393. aortic dissection
associated with
what?
hypertension
bicuspid aortic valve
cystic medial necrosis
inherited connective tissue disorders
(Marfans)
394. aortic dissection
presents how?
tearing chest pain radiating to the
back
395. in aortic
dissection, CXR
shows what?
mediastinal widening
396. possibilities for the
false lumen in
aortic dissection?
can be limited to the ascending aorta,
propagate from the ascending aorta,
or propagate from the descending
aorta
397. aortic dissection
can result in what?
pericardial tamponade
aortic rupture
death
398. what are the
ischemic heart
disease
manifestations?
angina
coronary steal syndrome
myocardial infarction
sudden cardiac death
chronic ischemic heart disease
399. pathology involved
in angina?
CAD narrowing >75%
no myocyte necrosis
400. stable angina is
mostly 2 to what?
atherosclerosis
401. presentation of
stable angina?
ST depression on ECG
retrosternal chest pain with exertion
402. Prinzmental angina
occurs when?
at rest 2 to coronary artery spasm
403. ECG finding in
prinzmental
angina?
ST elevation
404. pathology involved
in unstable angina?
thrombosis with incomplete coronary
artery occlusion
405. presentation of
unstable/crescendo
angina?
ST depression on ECG
worsening chest pain at rest or with
minimal exertion
406. what happens in
coronary steal
syndrome?
vasodilator may aggravate ischemia
by shunting blood from area of
critical stenosis to an area of higher
perfusion
407. myocardial is most
often due to what?
acute thrombosis due to coronary
artery atherosclerosis with complete
occlusion of coronary artery with
myocyte necrosis
408. ECG findings in
MI?
ECG initially shows ST depression
progressing to ST elevation with
continued ischemia and transmural
necrosis
409. what is sudden
cardiac death?
death from cardiac causes within 1
hour of onset of symptoms, most
commonly due to a lethal arrhythmia
(V-fib)
410. sudden cardiac
death is associated
with what?
CAD up to 70% of cases
411. what is chronic
ischemic heart
disease?
progressive onset of CHF over many
years due to chronic ischemic
myocardial damage
412. relative frequency
of coronary artery
occlusion in MI?
LAD >RCA > circumflex
413. what are the
symptoms of MI?
diaphoresis
nausea
vomiting
severe retrosternal pain
pain in left arm and or jaw
shortness of breath
fatigue
414. what are the gross
findings within 0-
4h of MI?
none
415. what are the LM
findings within 0-
4h of MI?
none
416. what are the risks
within 0-4h of MI?
arrhythmia
CHF
exacerbation
cardiogenic shock
417. what are
the gross
findings
within 4-
24h of MI?
infarct and dark mottling; pale with
tetrazolium stain distal to occluded artery
418. what are
the LM
findings
within 4-
12h of MI?
early coagulative necrosis
edema
hemorrhage
wavy fibers
419. what is the
risk within
4-12h of
MI?
arrhythmia
420. what are
the LM
findings
within 12-
24h of MI?
contraction bands from reperfusion injury
release of necrotic cell content into blood
beginning of neutrophil migration
421. what is the
risk within
12-24h of
MI?
arrhythmia
422. what are
the gross
findings
within 1-3
days of MI?
hyperemia
423. what are
the LM
findings
within 1-
3days of
MI?
extensive coagulative necrosis
tissue surrounding infarct shows acute
inflammation
neutrophil migration
424. what is the
risk within
1-3 days of
MI?
fibrinous pericarditis
425. what are
the gross
findings
within 3-
14days of
MI?
hyperemic border;
central yellow-brown softening
maximally yellow and soft by 10 days
426. LM
findings
within 3-
14days of
MI?
macrophage infiltration followed by
granulation tissue at the margins
427. what is the
risk within
3-14 days of
MI?
free wall rupture leading to tamponade,
papillary muscle rupture, ventricular
aneurysm, interventricular septal rupture due
to macrophages that have degraded important
structural components
428. what are the gross
findings 2weeks-
months post MI?
recanalized artery
gray white
429. LM findings 2 weeks-
months post MI?
contracted scar complete
430. risk 2weeks-months
post MI?
dressler's syndrome
431. what is the gold
standard for dx of MI
in first 6h?
ECG
432. use of cardiac troponin
I in diagnosis of MI?
rises after 4 hours and is elevated
for 7-10 days; more specific than
other protein markers
433. use of CK-MB in
diagnosis of MI?
useful in diagnosing reinfarction
following acute MI because levels
return to normal after 48 hours
434. CK-MB predominantly
found where?
in myocardium but can also be
released from skeletal muscle
435. ECG changes in MI? ST elevation (transmural infarct)
ST depression (subendocardial
infarct)
Q waves (transmural infarct)
436. necrosis in transmural
infarct?
necrosis
437. subendocardial
infarcts due to what?
ischemic necrosis of < 50% of
ventricle wall
438. transmural infarct
affects how much of
cardiac structure?
affects entire wall
439. subendocardial infarct
affect what structure?
subendocardium especially
vulnerable to ischemia
440. ECG in transmural
infarcts?
ST elevation
Q waves
441. ECG in subendocardial
infarct?
ST depression
442. Q waves in V1-V4,
where is the infarct?
Anterior wall (LAD)
443. Q waves in V1-V2,
where is the infarct?
Ateroseptal (LAD)
444. Q waves in V4-V6,
where is the infarct?
anterolateral (LCX)
445. Q waves in I, aVL,
where is the infarct?
lateral wall (LCX)
446. Q waves in II, III, aVF,
where is the infarct?
inferior wall (RCA)
447. in MI, what is an
important cause of
death before reaching
hospital?
cardiac arrhythmia
448. cardiac arrhythmia in
MI is common when?
in first few days
449. what are the
complications of MI?
cardiac arrhythmia
LV failure and pulmonary
edema
Cardiogenic shock
Ventricular free wall rupture
papillary muscle rupture
IVS rupture
ventricular aneurysm
formation
postinfarction fibrinous
pericarditis
450. what is Dressler's
syndrome?
autoimmune phenomenon
resulting in fibrinous
pericarditis (several weeks post
MI)
451. factors associated with
cardiogenic shock in MI?
large infarct- high risk of
mortality
452. in MI ventricular free
wall rupture ?
cardiac tamponade
453. in MI, papillary muscle
rupture?
severe mitral regurgitation
454. in MI, IVS rupture? VSD
455. factors associated with
ventricular aneurysm
formation in MI?
CO
risk of arrhythmia
embolus from mural thrombus
456. when is the greatest risk
for ventricular aneurysm
formation in MI?
1 week post MI
457. what is the most common
cardiomyopathy?
dilated (congestive)
cardiomyopathy 90%
458. dilated cardiomyopathy
is usually what origin?
often idiopathic, up to 50%
familial
459. specific etologies of
dilated cardiomyopathy
include what?
ABCCCD
Alcohol abuse
wet Beriberi
Coxsackie b virus myocarditis
chronic Cocaine use
Chaga's disease
Doxorubicin toxicity
hemochromatosis
peripartum cardiomyopathy
460. what are the findings in
dilated cardiomyopathy?
S3
dilated heart on U/S
balloon appearance on chest X
ray
461. what is the treatment for
dilated cardiomyopathy?
Na+ restriction
ACE inhibitors
diuretics
digoxin
heart transplant
462. what happens in
hypertrophic
cardiomyopathy?
hypertrophied interventricular
septum is too close to mitral valve
leaflet, leading to outflow tract
obstruction
463. 60-70% of
hypertrophic
cardiomyopathy are of
what origin?
familial
AD
myosin heavy chain mutation
464. hypertrophic
cardiomyopathy is
associated with what?
Friedreich's ataxia
465. morphologic findings
in hypertrophic
cardiomyopathy?
disoriented, tangled,
hypertrophied myocardial fibers
466. what is a cause of
sudden death in young
athletes?
hypertrophic cardiomyopathy
467. what are the findings
in hypertrophic
cardiomyopathy?
normal sized heart
S4
apical impulses
systolic murmur
468. what is the treatment
for hypertrophic
cardiomyopathy?
blocker or non-dihydropyridine
calcium channel blocker
(verapamil)
469. what ensues in
hypertrophic
cardiomyopathy?
diastolic dysfunction
470. gross appearance in
hypertrophic
cardiomyopathy?
asymmetric concentric
hypertrophy (sarcomeres added in
parallel)
471. pathogenesis of
hypertrophic
cardiomyopathy?
proximity of hypertrophied
interventricular septum to mitral
leaflet obstructs outflow tract,
resulting in systolic murmur and
syncopal episodes
472. major causes of
restrictive/obliterative
cardiomyopathy
include what?
sarcoidosis
amyloidosis
postradiation fibrosis
endocardial fibroelastosis
Lofflers syndrome
hemochromatosis
473. what is endocardial
fibroelastosis?
thick fibroelastic tissue in
endocardium of young children
474. what is Loffler's
syndrome?
endomyocardial fibrosis with a
prominent eosinophilic infiltrate
475. what ensues in
restrictive/obliterative
cardiomyopathy?
diastolic dysfunction
476. what is CHF? a clinical syndrome that occurs in patients
with an inherited or acquired abnormality
of cardiac structure or function, which is
characterized by a constellation of clinical
symptoms (dyspnea, fatigue) and signs
(edema, rales)
477. in CHF RHF
most often
results from
what?
LHF
478. isolated RHF
is usually due
to what?
cor pulmonale
479. which drugs
reduce
mortality in
CHF?
ACE inhibitors
blockers
ARBs
spironolactone
480. when do you
not give
blockers in
CHF?
acute decompensated HF
481. which drugs
are used for
symptomatic
relief in CHF?
thiazides
loop diuretics
482. which drugs
improve
symptoms and
mortality in
select patients
with CHF?
hydralazine with nitrate therapy
483. what are the
abnormalities
seen in CHF?
cardiac dilation
dyspnea on exertion
LHF
RHF
484. what is the
cause of
cardiac
dilation in
CHF?
greater ventricular EDV
485. what is the
cause of DOE
in CHF?
failure of cardiac output to during
exercise
486. what are the
manifestations
of LHF in
CHF?
pulmonary edema/PND
orthopnea
487. what is the
cause of
pulmonary
edema/PND in
CHF?
pulmonary venous pressure pulmonary
venous distentions and transudation of
fluid
488. histological finding in
LHF in CHF?
presence of hemosiderin laden
macrophages (heart failure
cells) in the lungs
489. what is the cause of
orthopnea in CHF?
venous return in supine
position exacerbates
pulmonary vascular
congestion
490. what are the
manifestations of RHF in
CHF?
hepatomegaly (nutmeg liver)
peripheral edema
jugular venous distention
491. what is the cause of
hepatomegaly (nutmeg
liver) in CHF?
central venous pressure
resistance to portal flow
492. rarely, hepatomegaly in
RHF leads to what?
cardiac cirrhosis
493. what is the cause of
peripheral edema in
CHF?
venous pressure fluid
transudation
494. what is the cause of
jugular venous distention
in CHF?
venous pressure
495. what are the symptoms of
bacterial endocarditis?
Bacteria FROM JANE:
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli
496. what is the most common
symptom of bacterial
endocarditis?
fever
497. what are roth spots? round white spots on retina
surrounded by hemorrhage
498. what are osler's nodes? tender raised lesions on finger
or toe pads
499. what are janeway
lesions?
small, painless, erythematous
lesions on palm or sole
500. what is necessary for
diagnosis of bacterial
endocarditis?
multiple blood cultures
501. organism that causes
acute bacterial
endocarditis?
S aureus
502. virulence of organism
that causes acute
bacterial endocarditis?
S aureus (high virulence)
503. presentation in acute
bacterial endocarditis
caused by S aureus?
large vegetations on previously
normal valves
504. what is the onset of acute
bacterial endocarditis caused
by S aureus?
rapid onset
505. organism that causes
subacute bacterial
endocarditis?
viridans streptococcus
506. virulence of the organism
that causes subacute
bacterial endocarditis?
low virulence
507. presentation in subacute
bacterial endocarditis?
smaller vegetations on
congenitally abnormal or
diseased valves
508. subacute bacterial
endocarditis can be sequelae
of what?
dental procedures
509. what is the onset of subacute
bacterial endocarditis?
more insidious onset
510. endocarditis may be
nonbacterial secondary to
what?
malignancy
hypercoagulable state
lupus (marantic/
thrombotic endocarditis)
511. S bovis is present in which
cause of endocarditis?
colon cancer
512. S epidermidis is present in
which cause of endocarditis?
prosthetic valves
513. which valve is most
frequently involved in
bacterial endocarditis?
mitral
514. tricuspid valve endocarditis
is associated with what?
IV drug use (dont TRI
DRUGS)
515. tricuspid endocarditis is
associated with which
organisms?
S aureus
Pseudomonas
Candida
516. what are the complications of
bacterial endocarditis?
chordae rupture
glomerulonephritis
suppurative pericarditis
emboli
517. rheumatic fever is a
consequence of what?
pharyngeal infection with
group A hemolytic
streptococci
518. early deaths in rheumatic
fever due to what?
myocarditis
519. late sequelae of rheumatic
fever include what?
rheumatic heart disease
520. relative frequency of valves
affected by rheumatic heart
disease?
mitral > aortic >>
tricuspid (high pressure
vavles affected most)
521. early lesion in rheumatic
fever is what?
MR
522. what is the late lesion in
rheumatic fever?
MS
523. Rheumatic fever is
associated with what?
Aschoff bodies
Anitschkow's cells
elevated ASO titers
524. what are Aschoff bodies? granuloma with giant cells
525. what are anitschkow's
cells?
activated histiocytes
526. immunology of rheumatic
fever?
Type II HSR; not a direct
effect of bacteria
Ab to M protein
527. symptoms of Rheumatic
fever?
FEVERSS:
Fever
Erythema marginatum
Valvular damage
ESR
Red hot joints (migratory
polyarthritis)
Subcutaneous nodules
St. Vitus' dance (Sydenham's
chorea)
528. acute pericarditis
commonly presents with
what?
sharp pain, aggravated by
inspiration, and relieved by
sitting up and leaning
forward
friction rub
529. ECG findings in acute
pericarditis?
widespread ST-segment
elevation and/or PR
depression
530. acute fibrinous
pericarditis is caused by
what?
Dressler's syndrome,
uremia
radiation
531. fibrinous pericarditis
presents with what?
loud friction rub
532. what are the causes of
serous pericarditis?
viral
noninfectious inflammatory
diseases
533. course of viral serous
pericarditis?
often resolves spontaneously
534. non infectious
inflammatory diseases
that cause acute serous
pericarditis?
RA
SLE
535. what causes
suppurative/purulent
pericarditis?
bacterial infections with
pneumococcus or
streptococcus
536. frequency of purulent
pericarditis?
rare with antibiotics
537. what happens in cardiac
tamponade?
compression of heart by fluid
(blood effusions) in
pericardium leading to CO
538. what happens to
pressures in cardiac
tamponade?
equilibration of pressures in all 4
chambers
539. what are the findings
in cardiac
tamponade?
hypotension
venous pressure (JVD)
distant heart sounds
HR
pulsus paradoxus
540. what is pulsus
paradoxus?
in amplitude of systolic blood
pressure by >=10mHg during
inspiration
541. pulsus paradoxus
seen in what?
severe cardiac tamponade
asthma
OSA
pericarditis
croup
542. what happens in
syphilitic heart
disease?
3 syphilis disrupts the vasa
vasorum of the aorta with
consequent atrophy of the vessel
wall and valve ring
543. in syphilitic heart
disease you may see
what?
calcification of the aortic root and
ascending aortic arch
544. syphilitic heart
disease leads to what
appearance?
tree bark appearance of the aorta
545. syphilitic heart
disease can result in
what?
aneurysm of the ascending aorta or
aortic arch and aortic insufficiency
546. what are the most
common primary
cardiac tumors in
adults?
myxomas
547. 90% of cardiac
myxomas occur
where?
in the atria (mostly left atrium)
548. myxomas are usually
described as what?
ball valve obstruction in LA
associated with multiple syncopal
episodes
549. what is the most
frequent primary
cardiac tumor in
children?
rhabdomyomas
550. cardiac
rhabdomyomas are
associated with
what?
tuberous sclerosis
551. most common heart
tumor is what?
mets from melanoma or lymphoma
552. what is Kussmaul's
sign?
in JVP on inspiration instead of
normal
553. what happens
in Kussmaul's
sign?
inspiration negative intrathoracic
pressure not transmitted to the heart
impaired filling of RV blood backs up
into the venae cavae JVD
554. Kussmaul's sign
may be seen in
what?
constrictive pericarditis
restrictive cardiomyopathies
RA or RV tumors
cardiac tamponade
555. Raynaud's
phenomenon
affects what
type of vessels?
small vessels
556. what happens
in Raynaud's
phenomenon?
blood flow to the skin due to arteriolar
vasospasm in response to cold
temperature or emotional stress
557. Raynauds
phenomenon is
most often seen
where?
fingers
toes
558. when is it called
Raynaud's
disease?
when primary (idiopathic)
559. when is it called
Raynaud's
syndrome?
when secondary to a disease process such
as mixed connective tissue disease, SLE,
or CREST
560. temporal
arteritis
generally affects
who?
elderly females
561. symptoms in
temporal
arteritis?
unilateral headache (temporal artery)
jaw claudication
562. temporal
arteritis may
lead to what?
irreversible blindness die to ophthalmic
artery occlusion
563. temporal
arteritis is
associated with
what?
polymyalgia rheumatica
564. temporal
arteritis most
commonly
affects which
vessels?
branches of carotid artery
565. pathology/labs
seen in
temporal
arteritis?
focal granulomatous inflammation
ESR
566. what is the
treatment for
temporal
arteritis?
high dose corticosteroids
567. Takayasu arteritis
typically affects who?
asian females <40yo
568. symptoms of takayasu
arteritis?
pulselessness disease:
fever
night sweats
arthritis
myalgias
skin nodules
ocular disturbances
569. pathology/labs seen in
takayasu arteritis?
granulomatous thickening of
aortic arch, proximal great
vessels
ESR
570. what is the treatment for
takayasu arteritis?
corticosteroids
571. what are the large artery
vasculitis disorders?
temporal arteritis and takayasu
arteritis
572. what are the medium
vessel vasculitis
disorders?
polyarteritis nodosa
kawasaki disease
Buerger's disease
(thromboangitis obliterans)
573. polyarteritis nodosa
affects who?
young adults
574. viral association with
polyarteritis nodosa?
HBV seropositivity in 30% of
patients
575. symptoms of
polyarteritis nodosa?
fever
weight loss
malaise
headache
abdominal pain
melena
HTN
neuro dysfunction
cutaneous eruptions
renal damage
576. polyarteritis nodosa
typically involves which
vessels?
renal and visceral vessels, not
pulmonary arteries
577. immunology of
polyarteritis nodosa?
IC mediated
578. pathology/labs seen in
polyarteritis nodosa?
transmural inflammation of the
arterial wall with fibrinoid
necrosis
lesions are of different stages
many aneurysms and
constrictions on arteriogram
579. treatment for
polyarteritis nodosa?
corticosteroids
cyclophosphamide
580. kawasaki disease affects
who?
asian children < 4yo
581. symptoms associated
with kawasaki
disease?
fever cervical lymphadenitis
conjunctival injection
changes in lips/oral mucosa
(strawberry tongue)
hand-foot erythema
desquamating rash
582. children with
kawasaki disease
may develop which
complications?
coronary aneurysms MI, rupture
583. treatment for
kawasaki disease?
IV immunoglobulin and aspirin
584. Buerger's disease
affects who?
heavy smokers, males <40yo
585. symptoms in
Buerger's disease?
intermittent claudication may lead
to gangrene, autoamputation of
digits, superficial nodular phlebitis
raynauds phenomenon
586. what is the pathology
seen in buerger's
disease?
segmental thrombosing vasculitis
587. what is the treatment
for buergers disease?
smoking cessation
588. what are the small
vessel vasculitis
disorders?
microscopic polyangitis
Wegener's granulomatosis
(granulomatosis with polyangitis)
Churg strauss syndrome
Henoch Schonlein purpura
589. what is microscopic
polyangitis?
necrotizing vasculitis commonly
involving lung, kidneys, and skin
with pauci immune
glomerulonephritis and palpable
purpura
590. pathology/labs seen
in microscopic
polyangitis?
no granulomas
p-ANCA
591. what is the treatment
for microscopic
polyangitis?
cyclophosphamide and
corticosteroids
592. what are the upper
respiratory tract
symptoms of
wegener's
granulomatosis?
perforation of nasal septum,
chronic sinusitis
otitis media
mastoiditis
593. what are the lower
respiratory
symptoms of
Wegener's
granulomatosis?
hemoptysis
cough
dyspnea
594. what are the renal
manifestations of wegener's
granulomatosis?
hematuria
red cell casts
595. what is the triad that
characterizes wegener's
granulomatosis?
focal necrotizing vasculitis
necrotizing granulomas in
the lung and upper airway
necrotizing
glomerulonephritis
596. what are the labs seen in
wegeners granulomatosis?
c-ANCA
CXR: large nodular
densities
597. what is the treatment for
wegeners granulomatosis?
cyclophosphamide
corticosteroids
598. what are the symptoms of
Churg-strauss syndrome?
asthma
sinusitis
palpable purpura
peripheral neuropathy
(wrist/foot drop)
can also involve heart, GI,
pauci-immune
glomerulonephritis
599. pathology/labs seen in Churg
strauss syndrome?
granulomatous,
necrotizing vasculitis with
eosinophilia
p-ANCA, elevated IgE level
600. what is the most common
childhood systemic
vasculitis?
henoch-schonlein purpura
601. henoch-schonlein purpura
often follows what?
URI
602. what is the classic triad of
henoch schonlein purpura?
skin: palpable purpura on
buttocks/legs
arthralgia
GI: abdominal pain,
melena, multiple lesions of
same age
603. pathology seen in henoch
schonlein purpura?
vasculitis secondary to IgA
complex deposition
associated with IgA
nephropathy
604. what is a strawberry
hemangioma?
benign hemangioma of
infancy
605. strawberry hemangioma
appears when?
first few weeks of life
(1/200 births)
606. course of strawberry
hemangioma?
grows rapidly and
regresses spontaneously at
5-8 years of age
607. what is a cherry
hemangioma?
benign capillary
hemangioma of the elderly
608. course of cherry
hemangioma?
does not regress
609. incidence of cherry
hemangioma?
frequency with age
610. what is a pyogenic
granuloma?
polypoid capillary hemangioma
that can ulcerate and bleed
611. pyogenic granuloma
is associated with
what?
trauma and pregnancy
612. what is a cystic
hygroma?
cavernous lymphangioma of the
neck
613. cystic hygroma is
associated with
what?
Turner syndrome
614. what is a glomus
tumor?
benign painful red-blue tumor
under fingernails
615. glomus tumor arises
from what?
modified smooth muscle cells of the
glomus body
616. what is bacillary
angiomatosis?
benign capillary skin papules found
in AIDS patients
617. bacillary
angiomatosis is
caused by what?
Bartonella henselae infections
618. bacillary
angiomatosis is
frequently mistaken
for what?
kaposi sarcoma
619. what is
angiosarcoma?
rare blood vessel malignancy
typically occuring in the head,
neck, and breast areas
620. angiosarcoma is
associated with
what?
patients receiving radiation
therapy, especially for BRCA and
hodgkins lymphoma
621. course of
angiosarcoma?
very aggressive and difficult to
resect due to delay in diagnosis
622. what
lymphangiosarcoma?
lymphatic malignancy associated
with persistent lymphedema (post
radical mastectomy)
623. what is kaposi
sarcoma?
endothelial malignancy most
commonly of the skin but also
mouth, GIT, and respiratory tract
624. kaposi sarcoma is
associated with
what?
HHV-8 and HIV
625. kasposi sarcoma is
frequently mistaken
for what?
bacillary angiomatosis
626. what is sturge-weber
disease?
congenital vascular disorder that
affects capillary sized blood vessels.
627. Sturge-weber
disease
manifests how?
with port wine stain (nevus flammeus) on
face
ispilateral leptomeningeal angiomatosis
(intracerebral AVM)
seizures
early onset glaucoma
628. what are the
antihypertensive
therapies for
essential
hypertension?
diuretics
ACEI
ARBs
Ca channel blockers
629. what are the
antihypertensive
therapies used
in CHF?
diuretics
ACEI/ARBs (compensated CHF)
K+ sparing diuretics
630. blockers must
be used
cautiously in
what?
decompensated CHF
631. blockers are
contraindicated
in what?
cardiogenic shock
632. what are the
antihypertensive
therapies used
in DM?
ACEI/ARBs
Ca channel blockers
diuretics
blockers
blockers
633. ACEIs are
protctive against
what in DM?
diabetic nephropathy
634. which drugs are
Ca channel
blockers?
nifedipine
verapamil
diltiazem
amlodipine
635. MOA of Ca
channel
blockers?
block voltage dependent L type calcium
channels of cardiac and smooth muscle and
thereby reduce muscle contractility
636. relative effect on
smooth muscle
of Ca channel
blockers?
Vascular smooth muscle-
amlodipine=nifedipine>diltiazem>verapamil
637. relative effect on
heart of Ca
channel
blockers?
heart-
verapamil>diltiazem>amlodipine=nifedipine
Verapamil-ventricle
638. clinical use of Ca
channel
blockers?
hypertension
angina
arrhythmias (not nifedipine)
prinzmental's angina
Raynauds
639. toxicity of Ca
channel
blockers?
cardiac depression
AV block
peripheral edema
flushing
dizziness
constipation
640. MOA of
hydralazine?
cGMPsmooth muscle relaxation
vasodilates arterioles > veins
afterload
641. clinical use of
hydralazine?
severe hypertension
CHF
first line tx for htn in pregnancy, with
methyldopa
frequently coadministered with blocker to
prevent reflex tachycardia
642. toxicity of
hydralazine?
compensatory tachycardia (CI in
angina/CAD), fluid retention, nausea, HA,
angina
Lupus like syndrome
643. commonly
used drugs for
malignant
hypertension
treatment?
nitroprusside
nicardipine
clevidipine
labetalol
fenoldopam
644. features of
nitroprusside
for malignant
hypertension?
short acting
cGMP via direct release of NO
645. toxicity of
nitroprusside?
can cause cyanide toxicity
646. MOA of
fenoldopam?
dopamine D1 receptor agonist coronary,
peripheral, renal, splanchnic
vasodilation BP and natriuresis
647. MOA of
nitroglycerine,
isosorbide
dinitrate?
vasodilate by releasing NO in smooth
muscle, causing cGMP in and smooth
muscle relaxation
dilates veins>>arteries
preload
648. clinical use of
GTN, ISDN?
angina
pulmonary edema
649. toxicity of
GTN, ISDN?
reflex tachycardia, hypotension, flushing,
HA, "monday disease" in industrial
exposure
650. what is
monday
disease in
industrial
GTN, ISDN
exposure?
development of tolerance for the
vasodilating action during the work week
and loss of tolerance over the weekend
results in tachycardia, dizziness, and HA
upon reexposure
651. what is the goal
of antianginal
therapy?
reduction of myocardial O2 consumption
(MVO2) by decreasing >=1 of the
determinants of MVO2: EDV, BP, HR,
contractility, ejection time
652. effect of nitrates on EDV?
653. effect of blockers on EDV?
654. effect of nitrates+ blockers on
EDV?
no effect or
655. effect of nitrates on BP?
656. effect of blockers on BP?
657. effects of nitrates + blockers
on BP?

658. effect of nitrates on
contractility?
(reflex response)
659. effects of blockers on
contractility?

660. effect of nitrates + blockers on
contractility?
little/no effect
661. effect of nitrates on HR? (reflex)
662. effect of blockers on HR?
663. effect of nitrates + blockers on
HR?

664. effect of nitrates on ejection
time?

665. effect of blockers on ejection
time?

666. effect of nitrates + blockers on
ejection time?
little/no effect
667. effect of nitrates on MVO2?
668. effect of blockers on MVO2?
669. effect of nitrates + blockers on
MVO2?

670. how do Ca channel blockers
compare to the effects of
nitrates and beta blockers on
MVO2?
nifedipine is similar to
nitrates
verapamil is similar to
beta blockers
671. which are the partial agonists
contraindicated in angina?
pindolol and acebutalol
672. effect of HMG-CoARI's on LDL?
673. effect of HMG-CoARIs on HDL?
674. effect of HMGCoARI's on TG?
675. MOA of HMGCoARIs? inhibit conversion of
HMG-CoA to
mevalonate, a
cholesterol precursor
676. AE of HMGCoARIs? hepatotoxicity (LFT)
rhabdomyolysis
677. effect of niacin on LDL?
678. effect of niacin on HDL?
679. effect of niacin
on TG ?

680. MOA of niacin? inhibits lipolysis in adipose tissue;
reduces hepatic VLDL secretion into
circulation
681. AE of niacin? red, flushed, face which is by aspirin or
long term use
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)
682. effect of bile
acid resins on
LDL?

683. effect of bile


acid resins on
HDL?
slightly
684. effect of bile
acid resins on
TG?
slightly
685. MOA of bile acid
resins?
prevent intestinal reabsorption of bile
acids; liver must use cholesterol to make
more
686. AE of bile acid
resins?
patients hate it-
tastes bad and causes GI discomfort
absorption of fat soluble vitamins
cholesterol gallstones
687. effect of
ezetimibe on
LDL?

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