super random Flashcards
(31 cards)
fatigue
represents a chronice mild impairment of CO in combination with a chronic moderate elevation of pulm cap pressure
shortness of breath on exertion
inappropriate increase in pulm cap pressure during physical exertion
chest tightness on exertion
development of myocardial ischemia during physical exertion
lightheadness on exertion
falling sytemic arterial pressure during exercise –> caused by inability to increase CO commensurately to the systemic vasodilation that accompanies exercise
why does patient have exertion angina if normal coronary arteries?
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.
Supraventricular tachycardia: treatment
ABCDE
Adenosine
Beta-blocker
Calcium channel antagonist
Digoxin
Excitation (vagal stimulation)
Ventricular tachycardia: treatment
LAMB:
Lidocaine
Amiodarone
Mexiltene/ Magnesium
Beta-blocker
ECG: contraindications
Recent MI
Aortic stenosis
MI in the last 7 days
Pulmonary hypertension
T wave inversion causes
INVERT:
Ischemia
Normality [esp. young, black]
Ventricular hypertrophy
Ectopic foci [eg calcified plaques]
RBBB, LBBB
Treatments [digoxin]
Atrial fibrillation: management
ABCD:
Anti-coagulate
Beta-block to control rate
Cardiovert
Digoxin
Anti-arrythmics: for AV nodes
Do Block AV”:
Digoxin
B-blockers
Adenosine
Verapamil
Murmurs: systolic
MR PV TRAPS:
Mitral
Regurgitation and
Prolaspe
VSD
Tricupsid
Regurgitation
Aortic and
Pulmonary
Stenosis
Summary of diet changes
reduce saturated/trans fat -> LDL; reduce calories/exercise/lose weight -> Glc, HDL TGs, wt; reduce ETOH ->TG
Features metabolic syndrome
abdominal obesity (waist circumference), impaired fasting glucose, low HDL, incr. TGs, and HTN
Acute CV events
perfect storm of impaired endothelial fxn, inflammation, impaired plaque stabilization, atherothrombosis, + thrombosis
features vulnerable plaque
a thin fibrous cap
large lipid-rich necrotic core
increased plaque inflammation
positive vascular remodeling
increased vasa-vasorum neovascularization
intra-plaque hemorrhage
glagov phenomenon
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
Lp PLA2
modified LDL by Lp PLA2 central to atherosclerosis, led to assay to measure levels and assess risk
murmurs due to MV problems
MVP with mid-late systolic MR -> mid- late systolic murmur, whereas MR due to flail produces holosystolic murmur
reasons for splitting sounds
RBBB WIDE split S2, LBBB PARADOXICAL split S2, WIDE FIXED split S2 due to ASD
S3 vs. S4
S3 = sound associated with volume overload LV, whereas S4 = sound associated with an atrium contracting against stiff ventricle
LDL target per silvestry
MOST cardiologists target an LDL < 70 in those with CAD or CAD risk equivalents (i.e. DM, PAD, etc)
what activates RAS
hypotension, hypovolemia, hyponatremia, and adrenergic activation
why is rapid drop in BP bad for people with CAD?
Rapid drop in BP is not good for pts w/ significant CAD where reflex tachycardia thru SNS could increase MVO2 and result in angina
