Cardiovascular Flashcards
what does the bulbis cordis become
smooth parts (outflow tract) of both ventricles
what does the primitive pulmonary vein become
smooth part of left atrium
what does the left horn of the sinus venosus become
coronary sinus
what does the right horn of the sinus venosus become
smooth part of the right atrium (sinus venarum)
what do the right common cardinal vein and right anterior cardinal vein become
SVC
blood supply for SA and AV nodes
RCA
effect of aortic regurgitation on pulse pressure
increased
effect of tamponade on pulse pressure
decreased
effect of exercise on pulse pressure
increased
effect of obstructive sleep apnea on pulse pressure
increased (increased sympathetic tone)
effect of aortic stenosis on pulse pressure
decreased
MOA for catecholamines increasing contractility
inhibition of phosphobalamban –> more intracellular Ca++
MOA for beta blockade decreasing contractility
lowers cAMP
which calcium channels are for myocardium
nondihydropyridine
LaPlace’s Law
T = pr / 2t
effect of increased TPR on venous return given fixed MAP
decrease
JVP A: peak or descent? meaning?
peak. atrial contraction (absent in afib)
JVP C: peak or descent? meaning?
peak. RV contraction (while atrium is still contracted)
JVP X: peak or descent? meaning?
descent. atrial relaxation
JVP V: peak or descent? meaning?
peak. filling (“villing”) of right atrium against closed tricuspid
JVP Y: peak or descent? meaning?
descent. emptYing of right atrium into RV
fixed spliting caused by
ASD
paradoxical splitting caused by
something delaying aortic closure e.g. aortic stenosis, LBBB
effect of hand grip (increased afterload) on auscultation
increase MR, AR, VSD murmurs
Decreased HCM murmurs
later onset of MVP click/murmur
effect of valsalva or standing up (decreased preload) on auscultation
decreased intensity of most murmurs (including AS)
Increased intensity of HCM murmurs
Earlier onset of MVP click/murmur
effect of rapid squatting (decreased after load, increase preload) on auscultation
increased intensity of AS
decreased intensity of HCM murmur
Later onset of MVP click/murmur
AS murmur
systolic crescendo-decrescendo
MR/TR murmur
holosystolic, blowing murmurs
AR murmur
early diastolic decrescendo, blowing murmur
MVP murmur
mid-systolic click and late crescendo murmur
VSD murmur
holosystolic, harsh-sounding, loudest at tricuspid
MS murmur
diastolic opening snap and late rumbling murmur
PDA murmur
continuous machine-like murmur, loudest at S2
U wave present in
hypokalemia and bradycardia
causes of long QT
hypokalemia, low magnesium
congenital long QT syndromes
drug induced
Congenital long QT syndromes
Romano-Ward: AD, pure cardiac
Jervell and Lange-Nielson: AR, sensorineural deafness
Drug-induced long QT
anti-arrhythmic (IA, III), antibiotics (e.g. macrolides), anti-psychotics (e.g. haloperidol), anti-depressants (e.g. TCAs), anti-emetics (e.g. ondansetron)
Brugada syndrome ECG pattern
pseudo RBBB and ST elevations in V1-V3
AD, MC in Asian males. Increased risk of ventricular tachyarrhythmia and sudden cardiac death
AV block 2nd degree, mobitz type I
lengthening PR interval
AV block 2nd degree, Mobitz type II
random dropping
congenital defects causing early cyanosis
truncus arteriorsus, transposition, tricuspid atresia, tetralogy of fallot, TAPVR (total anamalous pulmonary venous return)
4 abnormalities in tetralogy of fallot
VSD, overriding aorta, pulmonic stenosis, RVH
fetal alcohol syndrome: cardiac congenital defect association
ASD, VSD, PDA, Fallot
rubella: cardiac congenital defect association
septal defects, PDA, pulmonic stenosis
Down: cardiac congenital defect association
AV septal defect, ASD, VSD
maternal diabetes: cardiac congenital defect association
transposition
prenatal lithium: cardiac congenital defect association
Ebstein abnormality
Turner syndrome: cardiac congenital defect association
bicuspid aortic valve, coarctation of aorta
Williams: cardiac congenital defect association
supravalvular aortic stenosis
22q11 syndromes: cardiac congenital defect association
truncus arteriosus, Fallot
term for eyelid xanthoma
xanthelasma. note corneal arcus is a corneal lipid deposit
most likely papillary muscle to rupture
posteromedial
cardiomyopathy associated with Friedreich ataxia
HCM
hypovolemic shock: skin, preload, CO, afterload
cold/clammy, very low preload, low CO, high SVR
cardiogenic shock: skin, preload, CO, afterload
cold/clammy, increased preload, very decreased CO, increased afterload
obstructive has same picture
distributive shock
two forms. both have low preload and low SVR
1) septic - warm skin, low preload, high CO, very low SVR
2) neurogenic - dry skin, low preload, low CO, very low SVR
microbes in tricuspid IV drug endocarditis
s aureaus, pseudomonas, candida
culture-negative endocarditis
coxiella, bartonella, HACEK (haemophilus, aggregatibacter [formerly actinobacillus], cardiobacterium, eikenella, kingella)
Beck triad (cardiac tamponade)
hypotension, distant heart sound, distended neck veins
kussmaul sign
paradoxical increase in JVP on inspiration
Note: seen in constrictive pericarditis, RCMs, tumors
pulsus paradoxus
decrease in amplitude of systolic BP by more than 10 during inspiration.
seen in tamponade, croup, severe asthma, sleep apnea, endocarditis
anti-HTN medications to use in pregnancy
hydralazine, labetalol, methyldopa, nifedipine
CCB to use for subarachnoid hemorrhages
nimodipine
CCB to use for hypertensive emergency
clevidipine
AE DHP CCBs
gingival hyperplasia and peripheral edema
drugs to use in HTN emergency
clevidipine, fenoldopam (D1), labetalol, nicardipine, nitroprusside (releases CN)
partial beta agonists that are contraindicated in angina
pindolol, acebutolol
ranolazine MOA
inhibits late phase of sodium current to reduce diastolic wall tension. does not affect HR or contractility, but can cause long QT
ezetimibe MOA
prevents cholesterol absorption
bile resin unwanted effect
increases TGs
fibrates MOA
upregulate LPL and induce HDL synthesis via PPAR-alpha
AE fibrates
myopathy
niacin MOA
inhibits hormone sensitive lipase in adipose tissue and reduces hepatic VLDL synthesis
AE niacin
flushing. hyperglycemia. hyperuricemia
Digoxin AE
hyperkalemia
class I anti-arr are
sodium channel blockers
name IA anti-arr
quinidine, procainamide, disopyramide
use IA anti-arr
atrial and ventricular arrhythmias, especially ectopic SVT and VT
use IB anti-arr
acute ventricular arrhythmias, especially post-MI, or digitalis-induce d arrhythmias
name IB anti-arr
lidocaine, mexiletine, (phenytoin)
name IC anti-arr
flecainide, propafenone
use IC anti-arr
atrial fibrilation and SVTs
class II anti-arr are
beta blockers
class III anti-arr are
potassium channel blockers
class IV anti-arr are
CCBs
beta blocker that causes dyslipidemia
metoprolol
beta blocker that can exacerbate vasospasm in prinzmetal angina
propranolol
name class III anti-arr
amiodarone, ibutilide, dofetilide, sotalol
“AIDS”
AE sotalol and ibutilide
torsades
adenosine MOA for anti-arr
increases K+ efflux from cells to hyperpolarize and decreaes calcium influx
use adenosine anti-arr
diagnosing/terminating certain forms of SVT
use Mg2+ anti-arr
effective in torsades and digoxin toxicity
uworld: class IA predominant actions
slows AP conduction velocity, prolongs APD
uworld: class IB predominant actions
no effect on AP conduction velocity, shortens APD
uworld: class IC predominant actions
slow AP conduction velocity, minimal effect on APD
uworld: class II predominant actions
slows sinus node discharge rate, slows AV node conduction and prolongs refractoriness
uworld: class III predominant actions
no effect on AP conduction velocity, prolongs APD
uworld: class IV predominant actions
slows sinus node discharge rate, slows AV nodal conduction and prolongs refractoriness
which anti-arrhythmic drugs prolong APD
classes IA and III
