Cardio Quiz 1d

eem8u's version from 2016-12-05 01:28

Principles of arrhythmias

Action Potential Review
Question Answer
why are there different AP shapes in different parts of heartdifferent ion channel composition
ventricular action potential (AP) - resting voltage, mediated by?-85mV, resting potential = K + out vs. NCX in
ventricular action potential (AP) - phase 0upstroke (at electrical stimulus) = Na + influx
ventricular action potential (AP) - phase 1Notch = Na + in vs. K + out
ventricular action potential (AP) - phase 2 Plateau Ca2+ in vs. K + out
ventricular action potential (AP) - phase 3repolarization = K+ out
ventricular action potential (AP) - phase 0upstroke, Na+ in
general direction of ventricular depolarization /repolarizationendo >> epicardium then epi >> endocardium (for this reason tT wave upright)


Ion Channel Physiology Review
Question Answer
negative current defined ascation going IN cell
****3 states of voltage-dependent Na — % at -80 mV, infinity timeC (85%) > Inactivate (15%) / O (0)
****3 states of voltage-dependent Na — % at 0 mV, infinity timeinactivate (99.5) > Open (0.5%) > closed (0%) — (inactivated cells started as open)
Na+ channel state during diastole85% closed , but available
Na+ channel state during upstroke/ plateauopen >> inactivated
% Na+ channels (~85%) are in closed, but avaialbe state before upstroke depends on ________TIME spent in diastole (at -80mV)
drugs preferential bind to voltage dependent Na+ gates at what stateOPEN or Inactivated


Question Answer
sinus brady/tachcardia indicatesdysfx in SA node (see 9.19)
describe morphology of paroxysmal supra ventricular tachycardiaNarrow QRS / w/ tachycardia (see 9.20)
Narrow QRS / w/ tachycardia - cause(usually paroxysmal supra ventricular tachycardia) >> two pathways in the AV node (excitation must be occurring through conduction system b/c of efficiency) - see 9.20
describe atrial flutter vs fibrilliationP waves radom/indistinct w/ irregular R-R (it is flutter when you can still see P wave) (see 9.21)
atrial flutter/fib - why are R-R intervals irregularonly *some* atrial excitation propagate>> ventricles (see 9.21)
describe morphology of premature ventricular contraction (PVC)WIDE QRS complex, if they have different shapes —> multiple ectopic foci (normal QRS are fast> ~ 1 small box) (see 9.22)
describe morphology of ventricular tachycardiaWIDE QRS, no P waves, > 100 bpm (see 9.23) - can be monomorphic or polymorphic


Arrhythmia mechanisms
Question Answer
Early Afterdepolarizations (EAD) occur whenAP is TOO LONG / HR too slow!!
****EAD - channel involved (and voltage)reactivation of Ica (at -20)
Delayed Afterdepolarizations (DAD) result fromspontaneous release of intracellular Ca2+
****DAD occurs when (2)cell overload w/ Ca2+ >> 1- ***fast heart rate (cause accumulation) // 2- B-adrenergic stimulation (b/c of positive inotropy)
DAD - full AP occurs whenCa influx activates Na+ current
***DAD - mediated by what channel & MECHANISMIncrease in [Ca 2+ ] >>>> more likely Ca2+ release from SR >>> extrusion of Ca2+ via NCX >> Electrogenic, 1 ca2+ out for 3 Na+ into cell >> net +1 in >> depolarization >>> AP
explain reentry (see 9.30)**premature** stimulus encounters refractory tissue >> blocked on only one side >> propagates slowly on left >> returns to right, no no longer refractory >> crates a loop >>> EAD or DAD
2 possible cause of reentry1- damaged tissue 2- temporary difference in refractoriness
“second bump” of DAD caused byIna current (sodium channels)

Drugs used to treat arrhythmias

Drugs for AntiArrhythmias
Question Answer
strategy to prevent EADblock Ca2+ current
****strategy to prevent DAD (2)1- beta block (inhibit inotropic force that causes accumulation) 2- block Na+ channels — that can be trigged by depolarization
calculate AP wavelengthλ = CV * APD = conduction velocity x action potential duration
normal wavelength of AP50cm/s (6inches/s) ~ about the size of the heart
wavelength and preventing reentryIf wavelength > path length, reentry will spontaneously terminate
wavelength as strategy for treatmentIncrease APD >> increase wavelength >> terminate reentry
class I antiarrhythmics divided byHow quickly they unbind to closed state of I-na


****Vaughan-Williams Classification System
    (see 9.38)
Question Answer
Class I / target / strategyI-na >> Prevent spontaneous release (of Ca) & DADs from triggering action potentials
class II / target / strategyβ-ARs >> prevent positive inotropy/lower HR >> prevent Ca overload & DADs
class III / target / strategyI-kr >> Increase wavelength so that reentrant arrhythmias self-terminate (prolong repolariztation = prolong APDuration)
class IV / target / strategyI-ca >> Prevent EADs, reduce Ca2+ overload
describe B-activation in ventricular myocyteNE/epi bind B receptor > Gs beta-gamma subunit dissociation >> adenylate cyclase activated >> cAMP >> PKA >>> 1- activates L-type channel 2- activates PLB channel at SR >> positive inotropy
****Why are Ca-channel blockers antiarrhythmic?**AV-node** upstroke depends on Ca+ // block >> (1) slower upstrokes and (2) longer delays between AP’s (in PVST through AV node OR in a fib)
Ca-channel blockers can help to prevent (3)1- PVST w /conduction through AV node // 2- A Fib (fewer atrial impulses conveyed) // 3 - DAD's


****Class I drugs (Vaughan-Williams)
Question Answer
1a - rate of Na+ unblock & I kr blockmedium unlock / strong k block
1b - rate of Na+ unblock & I kr blockfast unblock / weak k block
1c - rate of Na+ unblock & I kr blockSlow unblock / weak k block
1a- effects (2)1- medium reduction in upstroke velocity (medium unblock rate) // 2- increase APD (strong K block)
1b- effects (2)1- small reduction in upstroke velocity (fast unblock) // 2- small APD **decrease**
1c- effects (2)1- LARGE reduction in upstroke (slow unblock) // 2- little change in APD
class I binding in pathologic cells? why ?more likely slightly depolarized >>> preferential binding of O and I >> effects are greater b/c more I state in depolarized
only administered IVlidocaine (1-2 hr half life)
which drug has non cardiac side effects- antibodies & lupusprocainimide
****which drug has anti-muscarinic activityALL class IA (procainamide, quinidine, etc.)
most dangerous class 1class IC (b/c they unbind so slowly)
****why do Class I cause pro arrhythmiaNa+ channel block >> slowed conduction velocity >> shorten wavelength >> promote reentry
why do class III cause pro arrhythmiaK channel block >> length depolarization >> APD prolonged >> EAD
define reverse rate dependence - relevant in which class?class III — prolong AP’s at more SLOW rates

Cardiomyopathy I

Overview I
Question Answer
diagnosis requires absence of (3)valvular dx, coronary dx, HTN dx
primary vs secondary myopathyintrinsic to heart vs 2nd to systemic disorder
possible causes of secondary myopathyinfection/drug/toxin/autoimmune dx/storage disorder
diastolic dysfx assc w/ _______ type(s)restrictive (stiff > less compliance) / hypertrophic (volume reduced)
systolic dysfx assc w/ _______ type(s) dilated (overstretch >> lost contractility)
most common typeDilated
seen peripartumDCM
caused by hemachromotosisDCM, RCM
100% familialHCM
asymmetrical + septal hypertrophyHCM
least commonRCM
fibroadipose replacement of myocardiumArhythmogenic Right Ventricular Cardiomyopathy (ARVC)
common cause of CM in childrenIsolated Left Ventricular Noncompaction (LVNC)


Overview II
Question Answer
LV enlargement and systolic dysfunction (Ejection fraction <50%)DCM
box car nucleidilated cardiomyopathy
endocardial fibrosisDCM
sarcoidosis can causeDCM, RCM
flabby heartDCM
risk of mural thrombiDCM (due to stasis)
myocyte necrosis & lymphocyte aggregate seen withDCM - VIRAL myocarditis
aspergillus infect. can causeDCM
Important cause of sudden cardiac death (SCD) in the young and in athletesHCM
path pattern - aberrant myofibers / disarrayHCM
possible obstruction of aortic valve/ coronary ostia HCM (septal hypertrophy)
ventricles normal sizedRCM
Loeffler’s endomyocarditis seen w/RCM
can be clinically silentArhythmogenic Right Ventricular Cardiomyopathy (ARVC)
sponge-like gross appearanceIsolated Left Ventricular Noncompaction (LVNC)


Dilated cardiomyopathy DCM
Question Answer
dilated most common amongmales 20-50
most common etiologyfamilial (25-35%) > idiopathic > infection
common infectious cause***COXsackie B virus, adeno virus, Chagas parasite, etc.
most common mutation / inheritance patternAutosomal dominate / TTN gene >> encores TITIN >> overstretch
fibrosis most commonly seenendocardium, over LV septum
DCM w/ eosinophilia- etiologyHypersensitivity myocarditis (Drugs)
***3 common drugs/toxins that causealcohol, cocain, anthracyclines
cytoplasmic vacuolization indicationsanthracycline toxicity in DCM
Brown cytoplasmic Iron pigment indicateshemochromatosis (can also use prussian blue)


Hypertrophic & restrictive Cardiomyopathy (HCM & RCM) & Other
Question Answer
HCM common protein defectbeta-myosin heavy chain
HCM inheritance patternAD
RCM most common infiltrate causeamyloid (AL)
temperate climate + male + hypereosinophiliaLoefflers endomyocarditis (RCM)
common protein mutation seen w/ Arhythmogenic Right Ventricular Cardiomyopathy (ARVC)desmosomal proteins
inheritance pattern w/ Arhythmogenic Right Ventricular Cardiomyopathy (ARVC)AD
etiology - Isolated Left Ventricular Noncompaction (LVNC)Arrest in endomyocardial morphogenesis in the embryonic development ( see photo)
***Review all FLAGGEd pictures***