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Cardiovascular > Review session > Flashcards

Review session Flashcards

1
Q

Main difference between slow/fast AP

A

Fast - upstroke by Na

Slow - upstroke by Ca (no phase 1,2)

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2
Q

Slow AP conduction at ____?

A

SA/AV nodes

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3
Q

IN nodal pacemaker cells, how does beta1, M2, and alpha 1 affect AP

A

beta 1 - increase phase 4 slope = increase HR/inotropy/lusitropy
M2/Alpha 2 - decrease phase 4 slope = decrease HR

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4
Q

Phase 4 in slow AP driven by which current

A

funny current

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5
Q

Phase 4 in fast AP is driven by

A

Ik1, Ina, Ica
Na/K and Na/C
(Na out/K in) (Na in/Ca out)

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6
Q

Phase 0 in fast AP driven by:

A

INa in

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7
Q

Phase 1 in fast AP driven by:

A

IKto (transient outward K current)

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8
Q

Phase 2 in fast AP driven by

A

Plateau = Ca in = K out

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9
Q

Phase 3 in fast AP driven by:

A

Ikr/Ikr pushing K out

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10
Q

Group 1 = ___ blocker

Example

A

Na channel

Procainamide/lidocaine

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11
Q

Group 2 = ___ blocker

Example

A

beta

esmolol

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12
Q

Group 3 = ___ blocker

Example

A

Potassium channel

amiodarone

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13
Q

Group 4 = ___ blocker

Example

A

Calcium channel
Verapamil
Diltiazem

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14
Q

Group 5 = ___ blocker

Example

A

miscellaneous

Adenosine, K/Mg

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15
Q

Ib difference from Ia/Ic drugs

A

Lidocaine - targets ONLY depolarized ventricles (target inactivated)
Ia/Ic = on atria-ventricles (target open)

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16
Q

Class III effects

A 
blocks repolarization (K) --> rhythm control
increase QT - refractory
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17
Q

Class I effects

A

delays upstroke (conduction) and decrease AP - rhythm control

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18
Q

Class II effects

A

Decrease heart rate/AV conduction (block beta) - increase phase 4 time (decrease slope)

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19
Q

Class IV effects

A

Decrease AV conduction/HR

Block Ca = slow phase 0 in node

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20
Q

_____ have greater ratio of vascular dilation to cardiac effects

A

Dihydropryidines/nifedipine

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21
Q

_____ mostly affects cardiac nodal tissue (phase _) and cardiac muscle (phase _)

A 
class 4 - verapamil/diltiazem
0, 2
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22
Q

Adenosine is an _____ nucleoside, acts as ___ on _____ receptor at ____

A

endogenous
Agoinst
A1/P1 purinergic receptors
AV node

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23
Q

Adenosine causes ____

A

hyperpolarization (increase IK1) - reduce phase 0

Increase refractory period

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24
Q

Digoxin, vagal maneuver, Ach, Adenosine on slow AP

A

phase 4 - hyperpolarized + decrease slope

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25
Q

Ach acts on __ receptor and adenosine acts on __ receptor - coupled to ___

A

M2
A1
Gi/o

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26
Q

Bradyarrhytmias due to 2 facotrs:

A

failure to initiate (sinus node dysf)

Failure to conduct - AV block

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27
Q

Treatment of Sinus Node dysfunction (brady)

A

Pacemaker

remove causative agent (Beta/ca blocker)

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28
Q

Treatment of AV block (brady)

A

Acute: Dopamine, epi, atropine, electrical stimulation/transvenous pacing
Chronic: permanent cardiac pacing

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29
Q

Rate control drugs

A

class II (beta) IV (CCB) - AV blocks
Digoxin - parasympathomimetic
Adenosin - membrane hyperpol

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30
Q

Rhythm control drugs

A

Class I, III
increase refractory period (block K) (Ia,III)
Decrease conduction velocity (block Na channels - I, III-amiodarone)

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31
Q

Causes of Tachy

A 
triggered automaticity (afterdepol EAD/DAD)
Reentry
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32
Q

Sinus tachycardia treatment

A

no arrhythmia - need to treat underlying condition

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33
Q

EAD vs DAD afterdepol mechanism

A

EAD: increase ICaL
DAD: Increase NCX (high Ca - stimulates Na to come in)

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34
Q

EAD/DAD after depol AP

A

EAD: phase2/3 repol
DAD: after repol (during phase 4)

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35
Q

EAD common when

A

slow HR, low K extracellular, drug that prolong APD (phase 2)
results in long QT –> Torsades de pointes

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36
Q

DAD is caused by

A

intracellular Ca overload (Ischmeia, adrenergic stress, digoxin toxicity)

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37
Q

Epinephrine is a _____, causes:

A

beta agonists

Ca overload, PVC, Vtach, Vfib

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38
Q

Reentry is characterized by ___ and requires 2 things:

A

retrograde conduction

  1. unidirectional conduction
  2. Conduction slower than refractory
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39
Q

SVT caused by ___

A

reentry in AV node

SA –> Atrium –> AV –> loop AV –> Atrium

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40
Q

SVT acute treatment

A

Acute: Adenosine (transient AV block - terminate arrhythmias) - AV nodal block (beta/CCB), vagal maneuvers - terminate arrhythmias

41
Q

SVT chronic treatment

A

Vagal maneuvers
AV nodal blockers (II, IV)
Ablation

42
Q

Afib caused by ___

A

multiple microrenetrant wavelets

43
Q

Afib treatment

A

Rate: AV nodal blockers
Rhythm control: I, III, Cardioversion, Ablation
Anticoagulation

44
Q

EKG for PVC, common causes

A

wide QRS, no P wave

  • normal
  • Acute MI
  • HF
45
Q

Treatment for PVC

A

none

beta blockers

46
Q

Ventricular tachy cuased by:

A 
Reentrant arrhythmia (prior myocardial scar)
automatic/triggered focus
47
Q

Ventricular tachy treament (acute)

A 
amiodearone
Cardio version (no stable)
48
Q

Ventricular Tachycardia chronic treatments

A

Ablation

ICD (+ Amiodarone, sotalol)

49
Q

Ventricular Fibrillation treatment

A

electrical defib + Epi/vasopressin + amiodarone

Correct electroylte: KCl, MgSO4

50
Q

Causes of Vfib

A

Prolonged QT, slow HR, hypokalemia

51
Q

sympathetic tone = ___ influx enhanced by beta adrenergic receptor activity –> cause __

A 
Ca
Triggered afterdepolarization (high Ca)
52
Q

arrhythmia triggered by ___, maintained by ___

A

afterdpolarization

Reentry

53
Q

reentry commonly causes ____(issues)

A

A flutter, A fib, Torsades de pointes, ventricular fibrillation

54
Q

Use dependence

A

Na overactive channels blocked; conduct slower (fraction of Na blocked)
Increase refractory period (remove inactivation takes longer)

55
Q

Drugs that prevent remodeling

A

ACEI/ARB, beta blocker, aldosterone antag

56
Q

HF management drugs

A

A - ACE/ARB
B - +beta
C - + diuretics/ spiro, digoxin, hydralazine/nitrate + biventricular packing/ICD

57
Q

Most common diuretics

A

Furosemide (loop)/torsemide/butanide

58
Q

K wasting drugs

A

acetazolamide, mannitol, loop agents, thiazides

59
Q

K sparing drugs

A

Collecting tube:
Aldosterone antagonists (spiro, eplerenone)
Diuretics (Trimaterene/amiloride)

60
Q

Loop diuretic effects

A

excrete Na
excrete K, H
Excrete Ca, Mg
Increase urate (gout)

61
Q

thiazide ion similar/difference from loop

A

Ca increase!!!

excrete Na, K, H, increase gout

62
Q

ACEI (-pril)/ARB (-sartan) effects:

A

(Pril/sartan) vasodilation, decrease aldosterone activation, anti-remodeling effect

63
Q

Angiotensin II effects:

A

arterial constriction
Increase CO, Na reabsorption, H2O retention, thirst
Increase arterial BP

64
Q

ARB targets ___

A

AT-1 receptors

65
Q

ACEI adverse effects

A 
Hyperkalemia
Hypotension
Decrease RBF
cough
category D pregnancy
66
Q

Beta blockers can _____ HF in the short run

A

exacerbate

wait till pt stablized on ACEI

67
Q

add aldosterone antagonist when _______ after ____ therapy

A

LVEF <30

ACEI/ARB and beta

68
Q

Vasodilators effects

A

decrease afterload (hydralazine)
Reduce cardiac work
Less mitral reguritation
Venous vasodilation (decrease preload - ISDN)

69
Q

vasodilators include

A

hydralazine

Isosorbide nitritate

70
Q

Digoxin used for:

A

A fib (rate control anti-arrhy)

71
Q

Digoxin works by

A

block Na/K pump - accumulate Na; NCX pumps Na out, Ca in

- increase inotropy

72
Q

digoxin overdose >1.2 ng/mL results:

A

high Ca –> afterdoplarization (risk with hypokalemia)

High Ca > PVC> Vtach > Vfib

73
Q

___kalemia predisposes to Digoxin toxicity

A

hypo

74
Q

digoxin drug interactions

A

diuretics, amphotericin B –> hypokalemia
Quinidine/verapmil/nifedipine - displacement = increase digoxin Cp
Epi - sensitizes heart to digoxin induced arrhythmias (increase Ca in cell)

75
Q

diuretics functions and includes:

A

reduced fluid volume
Bumetanide
Furosemide
torsemide

76
Q

Inotropes function/includes:

A

Increase contractiility
Dobutamine
Milrinone
Digoxin

77
Q

Vasodilators fcn/includes:

A 
Decrease pre/afterloads
Nitroglycerin
nitroprusside
Nesiritide
nitrates
78
Q

Acute vs chronic drugs

A

beta agonism vs antagonism
NE/E, dopamine, dobutamine, digoxin/milrione
beta blocker

79
Q

Dobutamine vs Milrinone uses and avoidance

A

Use: short term management for low CO + congestions
Dob avoid: with beta blocker
Milrionine avoid: with hypotension

80
Q

Atropine is a _____lytic; propranolol is a ____ lytic

A

parasympatho (atropine = increase HR)

sympatho (propranolol = decrease HR)

81
Q

E, NE, Dobutamine, Dopamine are _____ , acts on:

A

Symapthomimetic drugs - adrenergic agonists
(a1, b1, b2) E
(a1, b1) NE
(b1) dob

82
Q

Metoprolol, carvedilol are ___ and acts on:

A

adrenergic antagonist
Met (b1)
Carv (a1, b1, b2)

83
Q

Muscarinic antagonists include

A

M2 –> decrease HR

Atropine antag. M2

84
Q

Cycle of adrenergic receptor from alpha 1 receptor

A

a1 -> Gq -> activate PLC -> release IP3/DAG –> (release stored Ca, activate PKC)

85
Q

cycle of adrenergic receptor from b1/b2

A

b1/b2 -> Gs -> adenylyl cyclase - increase cAMP ->PKA -> increase Ca movement through LTCC

86
Q

Cycle of adrenergic receptor from alpha 2 receptor

A

a2 –> Gi –> decrease cAMP -> Open K channels (hyperpolarize)

also Go –> decrease Ca movement

87
Q

Cholinergic receptor M1 and M2/3/4

A

M1/3 - Gq - Increase PLC

M2/3/4 - Gi - Decrease adenylyl cyclase

88
Q

Nicotinic effect

A

alter ionic perm - increase Na/Ca conduction - depolarize

89
Q

b1 receptor (agonist) effect on heart

A

SA node - HR up
AV: Conduct speed up
A/V muscle - inotropy up

90
Q

NE to ___; Ach to __

A

b1 - Gs
M2 - Gi

Both affect adenylate cyclase

91
Q

receptor subtype on Bp (a1, b1, b2)

A

a1 - vasoconstrict, reflex bradycardia/preload/afterload
b1 - HR up/inotropy up
b2 - vasodilation, reflex tachy

92
Q

Hemorrhage - events from baroreceptor

A

less tresth, baroreceptor less fire - increase sympathetic fiure/decrease para - vasoconstrict, HR up, contractility up, BP up

93
Q

Hemorrhage - events from kidney

A

decrease RBF - release renin - convert angiotensiongen to ATI - (ACE) - ATII - Increase Na reabsorption/water reabsorption = increase BV

94
Q

Gq effect

A

PLC/PKC –> increase Ca (IP3R activation/SR Ca release)

95
Q

PKA of 4 things and effect:

A

PLB - lusitropy, inotropy
RYR - sensitive - inotropy
LTCC - slow inact - inotropy
TnI - lusitropy

96
Q

sympathetic sitmulation causes:

A

vasoconstriction
up HR
up inotropy

97
Q

ADH/vasopressin made in the ___ released by ____; stimulated by ____

A

hypothalamus
Pituitary gland
hypovolemia, hypotension, high osmolarity, ATII, sympathetic stim

98
Q

ADH effects

A

increase water reabsorption

Vasoconstriction

Cardiovascular (11 decks)

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