Review session Flashcards
Main difference between slow/fast AP
Fast - upstroke by Na
Slow - upstroke by Ca (no phase 1,2)
Slow AP conduction at ____?
SA/AV nodes
IN nodal pacemaker cells, how does beta1, M2, and alpha 1 affect AP
beta 1 - increase phase 4 slope = increase HR/inotropy/lusitropy
M2/Alpha 2 - decrease phase 4 slope = decrease HR
Phase 4 in slow AP driven by which current
funny current
Phase 4 in fast AP is driven by
Ik1, Ina, Ica
Na/K and Na/C
(Na out/K in) (Na in/Ca out)
Phase 0 in fast AP driven by:
INa in
Phase 1 in fast AP driven by:
IKto (transient outward K current)
Phase 2 in fast AP driven by
Plateau = Ca in = K out
Phase 3 in fast AP driven by:
Ikr/Ikr pushing K out
Group 1 = ___ blocker
Example
Na channel
Procainamide/lidocaine
Group 2 = ___ blocker
Example
beta
esmolol
Group 3 = ___ blocker
Example
Potassium channel
amiodarone
Group 4 = ___ blocker
Example
Calcium channel
Verapamil
Diltiazem
Group 5 = ___ blocker
Example
miscellaneous
Adenosine, K/Mg
Ib difference from Ia/Ic drugs
Lidocaine - targets ONLY depolarized ventricles (target inactivated)
Ia/Ic = on atria-ventricles (target open)
Class III effects
blocks repolarization (K) --> rhythm control increase QT - refractory
Class I effects
delays upstroke (conduction) and decrease AP - rhythm control
Class II effects
Decrease heart rate/AV conduction (block beta) - increase phase 4 time (decrease slope)
Class IV effects
Decrease AV conduction/HR
Block Ca = slow phase 0 in node
_____ have greater ratio of vascular dilation to cardiac effects
Dihydropryidines/nifedipine
_____ mostly affects cardiac nodal tissue (phase _) and cardiac muscle (phase _)
class 4 - verapamil/diltiazem 0, 2
Adenosine is an _____ nucleoside, acts as ___ on _____ receptor at ____
endogenous
Agoinst
A1/P1 purinergic receptors
AV node
Adenosine causes ____
hyperpolarization (increase IK1) - reduce phase 0
Increase refractory period
Digoxin, vagal maneuver, Ach, Adenosine on slow AP
phase 4 - hyperpolarized + decrease slope
Ach acts on __ receptor and adenosine acts on __ receptor - coupled to ___
M2
A1
Gi/o
Bradyarrhytmias due to 2 facotrs:
failure to initiate (sinus node dysf)
Failure to conduct - AV block
Treatment of Sinus Node dysfunction (brady)
Pacemaker
remove causative agent (Beta/ca blocker)
Treatment of AV block (brady)
Acute: Dopamine, epi, atropine, electrical stimulation/transvenous pacing
Chronic: permanent cardiac pacing
Rate control drugs
class II (beta) IV (CCB) - AV blocks
Digoxin - parasympathomimetic
Adenosin - membrane hyperpol
Rhythm control drugs
Class I, III
increase refractory period (block K) (Ia,III)
Decrease conduction velocity (block Na channels - I, III-amiodarone)
Causes of Tachy
triggered automaticity (afterdepol EAD/DAD) Reentry
Sinus tachycardia treatment
no arrhythmia - need to treat underlying condition
EAD vs DAD afterdepol mechanism
EAD: increase ICaL
DAD: Increase NCX (high Ca - stimulates Na to come in)
EAD/DAD after depol AP
EAD: phase2/3 repol
DAD: after repol (during phase 4)
EAD common when
slow HR, low K extracellular, drug that prolong APD (phase 2)
results in long QT –> Torsades de pointes
DAD is caused by
intracellular Ca overload (Ischmeia, adrenergic stress, digoxin toxicity)
Epinephrine is a _____, causes:
beta agonists
Ca overload, PVC, Vtach, Vfib
Reentry is characterized by ___ and requires 2 things:
retrograde conduction
- unidirectional conduction
- Conduction slower than refractory
SVT caused by ___
reentry in AV node
SA –> Atrium –> AV –> loop AV –> Atrium
SVT acute treatment
Acute: Adenosine (transient AV block - terminate arrhythmias) - AV nodal block (beta/CCB), vagal maneuvers - terminate arrhythmias
SVT chronic treatment
Vagal maneuvers
AV nodal blockers (II, IV)
Ablation
Afib caused by ___
multiple microrenetrant wavelets
Afib treatment
Rate: AV nodal blockers
Rhythm control: I, III, Cardioversion, Ablation
Anticoagulation
EKG for PVC, common causes
wide QRS, no P wave
- normal
- Acute MI
- HF
Treatment for PVC
none
beta blockers
Ventricular tachy cuased by:
Reentrant arrhythmia (prior myocardial scar) automatic/triggered focus
Ventricular tachy treament (acute)
amiodearone Cardio version (no stable)
Ventricular Tachycardia chronic treatments
Ablation
ICD (+ Amiodarone, sotalol)
Ventricular Fibrillation treatment
electrical defib + Epi/vasopressin + amiodarone
Correct electroylte: KCl, MgSO4
Causes of Vfib
Prolonged QT, slow HR, hypokalemia
sympathetic tone = ___ influx enhanced by beta adrenergic receptor activity –> cause __
Ca Triggered afterdepolarization (high Ca)
arrhythmia triggered by ___, maintained by ___
afterdpolarization
Reentry
reentry commonly causes ____(issues)
A flutter, A fib, Torsades de pointes, ventricular fibrillation
Use dependence
Na overactive channels blocked; conduct slower (fraction of Na blocked)
Increase refractory period (remove inactivation takes longer)
Drugs that prevent remodeling
ACEI/ARB, beta blocker, aldosterone antag
HF management drugs
A - ACE/ARB
B - +beta
C - + diuretics/ spiro, digoxin, hydralazine/nitrate + biventricular packing/ICD
Most common diuretics
Furosemide (loop)/torsemide/butanide
K wasting drugs
acetazolamide, mannitol, loop agents, thiazides
K sparing drugs
Collecting tube:
Aldosterone antagonists (spiro, eplerenone)
Diuretics (Trimaterene/amiloride)
Loop diuretic effects
excrete Na
excrete K, H
Excrete Ca, Mg
Increase urate (gout)
thiazide ion similar/difference from loop
Ca increase!!!
excrete Na, K, H, increase gout
ACEI (-pril)/ARB (-sartan) effects:
(Pril/sartan) vasodilation, decrease aldosterone activation, anti-remodeling effect
Angiotensin II effects:
arterial constriction
Increase CO, Na reabsorption, H2O retention, thirst
Increase arterial BP
ARB targets ___
AT-1 receptors
ACEI adverse effects
Hyperkalemia Hypotension Decrease RBF cough category D pregnancy
Beta blockers can _____ HF in the short run
exacerbate
wait till pt stablized on ACEI
add aldosterone antagonist when _______ after ____ therapy
LVEF <30
ACEI/ARB and beta
Vasodilators effects
decrease afterload (hydralazine)
Reduce cardiac work
Less mitral reguritation
Venous vasodilation (decrease preload - ISDN)
vasodilators include
hydralazine
Isosorbide nitritate
Digoxin used for:
A fib (rate control anti-arrhy)
Digoxin works by
block Na/K pump - accumulate Na; NCX pumps Na out, Ca in
- increase inotropy
digoxin overdose >1.2 ng/mL results:
high Ca –> afterdoplarization (risk with hypokalemia)
High Ca > PVC> Vtach > Vfib
___kalemia predisposes to Digoxin toxicity
hypo
digoxin drug interactions
diuretics, amphotericin B –> hypokalemia
Quinidine/verapmil/nifedipine - displacement = increase digoxin Cp
Epi - sensitizes heart to digoxin induced arrhythmias (increase Ca in cell)
diuretics functions and includes:
reduced fluid volume
Bumetanide
Furosemide
torsemide
Inotropes function/includes:
Increase contractiility
Dobutamine
Milrinone
Digoxin
Vasodilators fcn/includes:
Decrease pre/afterloads Nitroglycerin nitroprusside Nesiritide nitrates
Acute vs chronic drugs
beta agonism vs antagonism
NE/E, dopamine, dobutamine, digoxin/milrione
beta blocker
Dobutamine vs Milrinone uses and avoidance
Use: short term management for low CO + congestions
Dob avoid: with beta blocker
Milrionine avoid: with hypotension
Atropine is a _____lytic; propranolol is a ____ lytic
parasympatho (atropine = increase HR)
sympatho (propranolol = decrease HR)
E, NE, Dobutamine, Dopamine are _____ , acts on:
Symapthomimetic drugs - adrenergic agonists
(a1, b1, b2) E
(a1, b1) NE
(b1) dob
Metoprolol, carvedilol are ___ and acts on:
adrenergic antagonist
Met (b1)
Carv (a1, b1, b2)
Muscarinic antagonists include
M2 –> decrease HR
Atropine antag. M2
Cycle of adrenergic receptor from alpha 1 receptor
a1 -> Gq -> activate PLC -> release IP3/DAG –> (release stored Ca, activate PKC)
cycle of adrenergic receptor from b1/b2
b1/b2 -> Gs -> adenylyl cyclase - increase cAMP ->PKA -> increase Ca movement through LTCC
Cycle of adrenergic receptor from alpha 2 receptor
a2 –> Gi –> decrease cAMP -> Open K channels (hyperpolarize)
also Go –> decrease Ca movement
Cholinergic receptor M1 and M2/3/4
M1/3 - Gq - Increase PLC
M2/3/4 - Gi - Decrease adenylyl cyclase
Nicotinic effect
alter ionic perm - increase Na/Ca conduction - depolarize
b1 receptor (agonist) effect on heart
SA node - HR up
AV: Conduct speed up
A/V muscle - inotropy up
NE to ___; Ach to __
b1 - Gs
M2 - Gi
Both affect adenylate cyclase
receptor subtype on Bp (a1, b1, b2)
a1 - vasoconstrict, reflex bradycardia/preload/afterload
b1 - HR up/inotropy up
b2 - vasodilation, reflex tachy
Hemorrhage - events from baroreceptor
less tresth, baroreceptor less fire - increase sympathetic fiure/decrease para - vasoconstrict, HR up, contractility up, BP up
Hemorrhage - events from kidney
decrease RBF - release renin - convert angiotensiongen to ATI - (ACE) - ATII - Increase Na reabsorption/water reabsorption = increase BV
Gq effect
PLC/PKC –> increase Ca (IP3R activation/SR Ca release)
PKA of 4 things and effect:
PLB - lusitropy, inotropy
RYR - sensitive - inotropy
LTCC - slow inact - inotropy
TnI - lusitropy
sympathetic sitmulation causes:
vasoconstriction
up HR
up inotropy
ADH/vasopressin made in the ___ released by ____; stimulated by ____
hypothalamus
Pituitary gland
hypovolemia, hypotension, high osmolarity, ATII, sympathetic stim
ADH effects
increase water reabsorption
Vasoconstriction
