Random Cardio Pathophys HY Flashcards
Which form of AV block may be physiologic?
mobitz I Wenckebach
a fib tx
- anti-coagulation to prevent stroke(CHADS)
- rate control: AV blockers, slow ventricular rate (BB, NDCCBS)
- rhythm control (IA, IC, III)
- Ablation
Vtachy/fib tx
acute: if hemodynamically stable –> III or IB
defibrillation/cardioversion
chronic: implantable cardioverter defibrillator (ICD)
anti-arrhythmia med therapy for reducing freq of ICD
comes from one pt of ventricle - likely prior scar
monomorphic VT
reentrant arrhythmia
_____ prevents conduction through bypass tract in WPW
procaniamide
IA: Na/K blockade, intermediate binding/dissociation properties
_______ is used to tx ventricular tachycardia
lidocaine
IB: rapid binding/dissociation
_______ used to tx Afib (w/ normal heart structure)
Flecanide
IC: slow binding and dissociation
Class III
reverse-use dependence, greater effects at slower HR
use: a fib/flutter w/ structure abnormal heart, vfib/tachy to reduce freq of ICD discharge
NDCCBs
block AV node, SVTs, - ionotrope
DCCBS
purely vasodilators, vascular smc
HTN/chronic stable angina
aspirin MOA
blocks COX1/2 to reduce prostaglandin metabolic –> reduced thromboxane-mediated platelet aggregation
P2Y12 receptor blockers
prevent ADP-mediated platelet aggregation
can be given w/ aspirin to prevent stent thrombosis
nitrates + _______ = extreme vasodilation/hypotension
nitrates (PROD cAMP) + PDE-5 (prevent degradation of cAMP) = extreme vasodilation/hypotension
CONTRAINDICATED
type I infarct
acute thrombotic occlusion of coronary a.
type II infarct
inadequate O2 supply bc of inc O2 demand in setting of “fixed coronary blockage”
____ blockers worsen bundle branch blocks
Na chan blockers
HMG-CoA reductase inhibitors
morbidity or mortality benefit in ASCVD?
both morbidity and mortality benefits in ASCVD
statins primary prevention when 10-yr ASVCD risk >
statins primary prevention when 10-yr ASVCD risk >7.5%
CHL drugs lowering LDL as much as possible in pts w/ established ASCVD
PCSK9 inhibitors
Ezetmibe
early afterdepolarization (EAD)
QT prolonging meds
class III anti-arrhythmics
delayed afterdepolarization (DAD)
digoxin toxicity
ST-elevation MI
EKG changes
acute: ST elevation
hrs: ST elevation, dec R wave, Q wave begins
days 1-2: T wave inversion, Q wave deeper
days later: ST normalizes, T wave inverted
weeks later: ST & T normal, Q wave persists
Inferior STEMI
GI sx
nitroglycerin induced hypOtension
AV node block if AV node ischemic
proximal RCA occlusion –> RV infarction
tx for possible VT/VF post-MI
defibrillator
tx for chronic claudication
smoking cessation m. training PDEi (Pletal) statin surgery
aortoiliac occlusion
rare
presentation: limb ischemia, acute abd pain
tx: revascularization
poor prognosis
infrainguinal occlusion
more common
often embolic (fib)
tx: remove emboli, bypass obstruction
good prognosis
aneurysm: __+% increase in diameter or vessel
50+%
repair aneurysm if
asymptomatic >5-5.5cm
or
triad of abd/back pain, hypOtension, pulsatile abd mass
type B aortic dissection tx
medical therapy
surgery only for critical tissue loss
type A aortic dissection tx
urgent surgical repair
high risk rupture/death in 48 hr
primary aortic root dilatation
Marfan’s, cystic medial necrosis, hypertension
–> aortic regurgitation
tx of which valvular disease includes afterload reduction and diuretics
mitral regurgitation
amyloid CM comm produces ___ HF bc compliant __ is affected more strongly
amyloid CM comm produces RIGHT HF bc compliant RV is affected more strongly than LV
gradient between PA diastolic P and wedge
obstructive shock (PE)
harsh systolic murmur and palpable thrill
VSD
ASD more commonly affect M or F?
F
VSD more commonly membranous or muscular?
membranous
PDA murmur
continuous during systole and diastole
maternal Li use
PDA
Ebstein’s Anomaly
maternal rubella
PDA
pulmonary a. stenosis
Eisenmenger’s syndrome
ASD/PDA/VSD –> inc pulm BF damaging vasculature –> arterial remodeling that inc resistance to flow
as pulm vascular R inc, Qp:Qs dec
Qp L)
cyanosis, high risk of death reactive polycythemia and hyperviscosity paradoxical embolus: brain abscess arrhythmia, HF hemoptysis Hypertrophic osteoarthropathy (clubbing)
TOF tx
Black-Taussing Shunt
full surgical correction
coarctation of aorta more common in M or F?
males
coarctation of aorta is associated w/
bicuspid aortic valve
PDA
Pericarditis CP
CP sharp/positional, improves w/ leaning fwd, worse w/ inspiration
pericarditis ECG
diffuse ST elevation not explained on basis of occluded coronary a.
PR depression
pericarditis tx
NSAIDS, colchicine
earliest stage of passive ventricular filling
y-descent
blunted y-descent
tamponade
prominent Y-descent
constrictive pericarditis
AA for normal heart struc
IA, IC
AA for abnormal heart struc
III
Ablation in AVNRT
ablate SLOW pathway
development of Q wave
infarct
NSTEMI ekg
ST depression or T wave inversion
proven clinical benefit for HF
ACEi
ARB
bblockers
mineral/aldo blockers
polymorphic VT
wide complex tachy
- likely from more widespread sources
- acute ischemia, meds that prolong QT interval
- TDP
type B aortic dissection most commonly occur
just beyond L subclavian origin
when to repair asymptomatic carotid blockage
when stenosis progresses >75%
HCM leads to which type of HF
HF w/ preserved EF
EF in amyloid induced restrictive CM
mildly dec contractility –> EF ~ 40-50%
VSD more commonly affect M or F?
1:1
PDA more commonly affect M or F?
F
equal diastolic filling pressures
tamponade
