VERSION A
How do positional maneuvers affect blood flow and murmurs?
a) Standing\/Valsalva
b) Squatting\/Lying down
c) Sustained handgrip – ANSWER- -standing\/valsalva – decreased
cardiac filling, decreases most murmurs except MVP and HOCM
-squatting\/ lying down – increase cardiac volume, increased
murmurs except MVP, HOCM
-sustained handgrip – increases systemic resistance, decreases
murmur in HOCM, AS
What are the stages of the Valsalva maneuver? – ANSWER- -Phase one
is the onset of straining with increased intrathoracic pressure. The heart
rate does not change but blood pressure rises.
-Phase two is marked by the decreased venous return and consequent
reduction of stroke volume and pulse pressure as straining continues.
The heart rate increases and blood pressure drops.
-Phase three is the release of straining with decreased intrathoracic
pressure and normalization of pulmonary blood flow.
-Phase four marks the blood pressure overshoot (in the normal heart)
with return of the heart rate to baseline.
What causes a physiologic split S2? – ANSWER- Increased blood
volume in the RV prolongs systole and delays pulmonary valve closure
What causes a fixed split S2? – ANSWER- Pulmonary stenosis, PE, LV
pacer, RBBB, MR (early AV closure), ASD, RV failue
What causes a paradoxic split S2 – ANSWER- LBBB, RV pacing,
HOCM
What causes an S3? – ANSWER- Rapid LV filling – acute ventricular
decompensation, severe AR or MR
What causes a S4? – ANSWER- Decreased ventricular compliance
during atrial contraction – ischemic heart dz, AS, MR, HOCM,
hypertrophic or diabetic cardiomyopathy, HTN heart dz, concentric
LVH
Can you have a S4 with atrial fibrillation? – ANSWER- No – no atrial
contraction
What are the parts of the venous waveform? – ANSWER- A wave –
atrial contraction
X descent – atria relax, RV fills rapidly; Bottom\/middle of x descent is
TC valve closure (c wave)
V wave – ventricle contacting against closed TC valve
Y descent – TC valve opens, passive emptying into ventricle
What gives elevated a and v waves – ANSWER- Pulmonary HTN, RV
infarction
What leads to Large r side v waves – ANSWER- Septal rupture
What diseases lead to Large v waves – ANSWER- TR (right), MR (left)
Rapid x and y descent – ANSWER- Constrictive pericarditis, restrictive
cardiomyopathy, tamponade (x descent only, loss of y descent)
Large a waves – ANSWER- TS, severe RVH (on right), MS
Cannon a waves – ANSWER- AV disassociation – complete heart block,
ventricular pacing
Slow Y descent – ANSWER- Delayed atrial emptying – TS
Most important prognostic factor with CAD – ANSWER- Degree of LV
dysfunction
Causes of resting ST elevation – ANSWER- MI, pericarditis, LV
aneurysm, LBBB, ventricular pacing, LVH, early repolarization
Giving nitrates causes severe decompensation in a IWMI pt. What
happened? – ANSWER- Pt had R side infarction as well, the preload
reduction from the nitrate now meant little flow getting to the L side of
the heart
MR due to papillary muscle rupture is most common with MI in this
region – ANSWER- Inferior; posteromedial papillary muscle has only
single vessel supply (RCA) while the anterolateral has two vessels
VSD is more likely with MIs here – ANSWER- Anterior, inferior
Contraindications for B-blockers – ANSWER- Bradycardia,
hypotension, 2nd or 3rd degree AVB, pulmonary edema, asthma. NOT
DM
When to use non-dihydropyridne CCBs in ACS – ANSWER\u0002Contraindications to B blockers, continued ischemia, but NO LV
dysfunction
What anticoagulant to use with ACS – ANSWER- Enoxaparin good, but
have to stop 12-24 hrs before CABG
Fondaparinux is increased risk of bleeding, do not use if going to do PCI<\/p>\n\n\n\n