super random

Question 1

fatigue

Answer 1

represents a chronice mild impairment of CO in combination with a chronic moderate elevation of pulm cap pressure

Question 2

shortness of breath on exertion

Answer 2

inappropriate increase in pulm cap pressure during physical exertion

Question 3

chest tightness on exertion

Answer 3

development of myocardial ischemia during physical exertion

Question 4

lightheadness on exertion

Answer 4

falling sytemic arterial pressure during exercise –> caused by inability to increase CO commensurately to the systemic vasodilation that accompanies exercise

Question 5

why does patient have exertion angina if normal coronary arteries?

Answer 5

Because of his left ventricular hypertrophy, he requires a greater than normal quantity of coronary flow. In addition, because of his aortic stenosis, his left ventricular systolic pressure increases more during exercise than does him aortic pressure. This causes a greater than normal
increase in his myocardial metabolic requirements in a setting where he does not have a commensurate increase in aortic (coronary perfusion) pressure. This combination of circumstances leads to a disparity between myocardial metabolic requirements and available coronary supply.

Question 6

Supraventricular tachycardia: treatment

Answer 6

ABCDE
Adenosine
Beta-blocker
Calcium channel antagonist
Digoxin
Excitation (vagal stimulation)

Question 7

Ventricular tachycardia: treatment

Answer 7

LAMB:
Lidocaine
Amiodarone
Mexiltene/ Magnesium
Beta-blocker

Question 8

ECG: contraindications

Answer 8

Recent MI
Aortic stenosis
MI in the last 7 days
Pulmonary hypertension

Question 9

T wave inversion causes

Answer 9

INVERT:
Ischemia
Normality [esp. young, black]
Ventricular hypertrophy
Ectopic foci [eg calcified plaques]
RBBB, LBBB
Treatments [digoxin]

Question 10

Atrial fibrillation: management

Answer 10

ABCD:
Anti-coagulate
Beta-block to control rate
Cardiovert
Digoxin

Question 11

Anti-arrythmics: for AV nodes

Answer 11

Do Block AV”:
Digoxin
B-blockers
Adenosine
Verapamil

Question 12

Murmurs: systolic

Answer 12

MR PV TRAPS:
Mitral
Regurgitation and
Prolaspe
VSD
Tricupsid
Regurgitation
Aortic and
Pulmonary
Stenosis

Question 13

Summary of diet changes

Answer 13

reduce saturated/trans fat -> LDL; reduce calories/exercise/lose weight -> Glc, HDL TGs, wt; reduce ETOH ->TG

Question 14

Features metabolic syndrome

Answer 14

abdominal obesity (waist circumference), impaired fasting glucose, low HDL, incr. TGs, and HTN

Question 15

Acute CV events

Answer 15

perfect storm of impaired endothelial fxn, inflammation, impaired plaque stabilization, atherothrombosis, + thrombosis

Question 16

features vulnerable plaque

Answer 16

a thin fibrous cap
large lipid-rich necrotic core
increased plaque inflammation
positive vascular remodeling
increased vasa-vasorum neovascularization
intra-plaque hemorrhage

Question 17

glagov phenomenon

Answer 17

arteries remodel to maintain constant flow despite increases in atherosclerotic lesion mass
Only after the blockage reached about 40 percent was the artery unable to keep pace and blood flow began to decrease

Question 18

Lp PLA2

Answer 18

modified LDL by Lp PLA2 central to atherosclerosis, led to assay to measure levels and assess risk

Question 19

murmurs due to MV problems

Answer 19

MVP with mid-late systolic MR -> mid- late systolic murmur, whereas MR due to flail produces holosystolic murmur

Question 20

reasons for splitting sounds

Answer 20

RBBB WIDE split S2, LBBB PARADOXICAL split S2, WIDE FIXED split S2 due to ASD

Question 21

S3 vs. S4

Answer 21

S3 = sound associated with volume overload LV, whereas S4 = sound associated with an atrium contracting against stiff ventricle

Question 22

LDL target per silvestry

Answer 22

MOST cardiologists target an LDL < 70 in those with CAD or CAD risk equivalents (i.e. DM, PAD, etc)

Question 23

what activates RAS

Answer 23

hypotension, hypovolemia, hyponatremia, and adrenergic activation

Question 24

why is rapid drop in BP bad for people with CAD?

Answer 24

Rapid drop in BP is not good for pts w/ significant CAD where reflex tachycardia thru SNS could increase MVO2 and result in angina

Question 25

note about Non-dihydropyridine CCAs

Answer 25

Non-dihydropyridine CCAs have effects on HR and AVN conduction, but also reduce IONOTROPY, therefore should AVOID THEM in HFrEF

Question 27

note about BB use in htn

Answer 27

remember w/ BB Tx of HF you are tempering the SNS maladaptive response to impaired cardiac function, not ness. tx underlying cause

Question 29

beta stimulation vascular smooth muscle

Answer 29

vasodilation, mech is Gprot and cAMP - deactivating MLCK, decreasing contraction

Question 30

beta adrenergic involvement in HF

Answer 30

Beta adrenergic mechanism of increased contractility - important in SHORT RUN to increase inotropy BUT
in long term - regulation of Beta receptor density important to responsiveness, remodeling, and prognosis in HF

Question 31

driving pressure for coronary flow

Answer 31

difference between LVEDP and Ao diastolic pressure as most flow occurs in diastole

Question 32

lowest oxygen saturation in venous blood at rest

Answer 32

oronary sinus blood at 40%

Question 33

PRELOAD

Answer 33

often clinically measured as LVEDP which is surrogate for LVEDVol which is surrogate for diastolic sarcomere length