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Cardio Quiz 1d

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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)
memorize

 

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
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Arrhythmias
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
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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)
memorize

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
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****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
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****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
memorize

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)
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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)
memorize

 

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)
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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)
memorize
***Review all FLAGGEd pictures***