Review session Flashcards
(98 cards)
1
Q
Main difference between slow/fast AP
A
Fast - upstroke by Na
Slow - upstroke by Ca (no phase 1,2)
2
Q
Slow AP conduction at ____?
A
SA/AV nodes
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
4
Q
Phase 4 in slow AP driven by which current
A
funny current
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)
6
Q
Phase 0 in fast AP driven by:
A
INa in
7
Q
Phase 1 in fast AP driven by:
A
IKto (transient outward K current)
8
Q
Phase 2 in fast AP driven by
A
Plateau = Ca in = K out
9
Q
Phase 3 in fast AP driven by:
A
Ikr/Ikr pushing K out
10
Q
Group 1 = ___ blocker
Example
A
Na channel
Procainamide/lidocaine
11
Q
Group 2 = ___ blocker
Example
A
beta
esmolol
12
Q
Group 3 = ___ blocker
Example
A
Potassium channel
amiodarone
13
Q
Group 4 = ___ blocker
Example
A
Calcium channel
Verapamil
Diltiazem
14
Q
Group 5 = ___ blocker
Example
A
miscellaneous
Adenosine, K/Mg
15
Q
Ib difference from Ia/Ic drugs
A
Lidocaine - targets ONLY depolarized ventricles (target inactivated)
Ia/Ic = on atria-ventricles (target open)
16
Q
Class III effects
A
blocks repolarization (K) --> rhythm control increase QT - refractory
17
Q
Class I effects
A
delays upstroke (conduction) and decrease AP - rhythm control
18
Q
Class II effects
A
Decrease heart rate/AV conduction (block beta) - increase phase 4 time (decrease slope)
19
Q
Class IV effects
A
Decrease AV conduction/HR
Block Ca = slow phase 0 in node
20
Q
_____ have greater ratio of vascular dilation to cardiac effects
A
Dihydropryidines/nifedipine
21
Q
_____ mostly affects cardiac nodal tissue (phase _) and cardiac muscle (phase _)
A
class 4 - verapamil/diltiazem 0, 2
22
Q
Adenosine is an _____ nucleoside, acts as ___ on _____ receptor at ____
A
endogenous
Agoinst
A1/P1 purinergic receptors
AV node
23
Q
Adenosine causes ____
A
hyperpolarization (increase IK1) - reduce phase 0
Increase refractory period
24
Q
Digoxin, vagal maneuver, Ach, Adenosine on slow AP
A
phase 4 - hyperpolarized + decrease slope
25
Ach acts on __ receptor and adenosine acts on __ receptor - coupled to ___
M2
A1
Gi/o
26
Bradyarrhytmias due to 2 facotrs:
failure to initiate (sinus node dysf)
| Failure to conduct - AV block
27
Treatment of Sinus Node dysfunction (brady)
Pacemaker
| remove causative agent (Beta/ca blocker)
28
Treatment of AV block (brady)
Acute: Dopamine, epi, atropine, electrical stimulation/transvenous pacing
Chronic: permanent cardiac pacing
29
Rate control drugs
class II (beta) IV (CCB) - AV blocks
Digoxin - parasympathomimetic
Adenosin - membrane hyperpol
30
Rhythm control drugs
Class I, III
increase refractory period (block K) (Ia,III)
Decrease conduction velocity (block Na channels - I, III-amiodarone)
31
Causes of Tachy
```
triggered automaticity (afterdepol EAD/DAD)
Reentry
```
32
Sinus tachycardia treatment
no arrhythmia - need to treat underlying condition
33
EAD vs DAD afterdepol mechanism
EAD: increase ICaL
DAD: Increase NCX (high Ca - stimulates Na to come in)
34
EAD/DAD after depol AP
EAD: phase2/3 repol
DAD: after repol (during phase 4)
35
EAD common when
slow HR, low K extracellular, drug that prolong APD (phase 2)
results in long QT --> Torsades de pointes
36
DAD is caused by
intracellular Ca overload (Ischmeia, adrenergic stress, digoxin toxicity)
37
Epinephrine is a _____, causes:
beta agonists
| Ca overload, PVC, Vtach, Vfib
38
Reentry is characterized by ___ and requires 2 things:
retrograde conduction
1. unidirectional conduction
2. Conduction slower than refractory
39
SVT caused by ___
reentry in AV node
| SA --> Atrium --> AV --> loop AV --> Atrium
40
SVT acute treatment
Acute: Adenosine (transient AV block - terminate arrhythmias) - AV nodal block (beta/CCB), vagal maneuvers - terminate arrhythmias
41
SVT chronic treatment
Vagal maneuvers
AV nodal blockers (II, IV)
Ablation
42
Afib caused by ___
multiple microrenetrant wavelets
43
Afib treatment
Rate: AV nodal blockers
Rhythm control: I, III, Cardioversion, Ablation
Anticoagulation
44
EKG for PVC, common causes
wide QRS, no P wave
- normal
- Acute MI
- HF
45
Treatment for PVC
none
| beta blockers
46
Ventricular tachy cuased by:
```
Reentrant arrhythmia (prior myocardial scar)
automatic/triggered focus
```
47
Ventricular tachy treament (acute)
```
amiodearone
Cardio version (no stable)
```
48
Ventricular Tachycardia chronic treatments
Ablation
| ICD (+ Amiodarone, sotalol)
49
Ventricular Fibrillation treatment
electrical defib + Epi/vasopressin + amiodarone
Correct electroylte: KCl, MgSO4
50
Causes of Vfib
Prolonged QT, slow HR, hypokalemia
51
sympathetic tone = ___ influx enhanced by beta adrenergic receptor activity --> cause __
```
Ca
Triggered afterdepolarization (high Ca)
```
52
arrhythmia triggered by ___, maintained by ___
afterdpolarization
| Reentry
53
reentry commonly causes ____(issues)
A flutter, A fib, Torsades de pointes, ventricular fibrillation
54
Use dependence
Na overactive channels blocked; conduct slower (fraction of Na blocked)
Increase refractory period (remove inactivation takes longer)
55
Drugs that prevent remodeling
ACEI/ARB, beta blocker, aldosterone antag
56
HF management drugs
A - ACE/ARB
B - +beta
C - + diuretics/ spiro, digoxin, hydralazine/nitrate + biventricular packing/ICD
57
Most common diuretics
Furosemide (loop)/torsemide/butanide
58
K wasting drugs
acetazolamide, mannitol, loop agents, thiazides
59
K sparing drugs
Collecting tube:
Aldosterone antagonists (spiro, eplerenone)
Diuretics (Trimaterene/amiloride)
60
Loop diuretic effects
excrete Na
excrete K, H
Excrete Ca, Mg
Increase urate (gout)
61
thiazide ion similar/difference from loop
Ca increase!!!
| excrete Na, K, H, increase gout
62
ACEI (-pril)/ARB (-sartan) effects:
(Pril/sartan) vasodilation, decrease aldosterone activation, anti-remodeling effect
63
Angiotensin II effects:
arterial constriction
Increase CO, Na reabsorption, H2O retention, thirst
Increase arterial BP
64
ARB targets ___
AT-1 receptors
65
ACEI adverse effects
```
Hyperkalemia
Hypotension
Decrease RBF
cough
category D pregnancy
```
66
Beta blockers can _____ HF in the short run
exacerbate
| wait till pt stablized on ACEI
67
add aldosterone antagonist when _______ after ____ therapy
LVEF <30
| ACEI/ARB and beta
68
Vasodilators effects
decrease afterload (hydralazine)
Reduce cardiac work
Less mitral reguritation
Venous vasodilation (decrease preload - ISDN)
69
vasodilators include
hydralazine
| Isosorbide nitritate
70
Digoxin used for:
A fib (rate control anti-arrhy)
71
Digoxin works by
block Na/K pump - accumulate Na; NCX pumps Na out, Ca in
| - increase inotropy
72
digoxin overdose >1.2 ng/mL results:
high Ca --> afterdoplarization (risk with hypokalemia)
| High Ca > PVC> Vtach > Vfib
73
___kalemia predisposes to Digoxin toxicity
hypo
74
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)
75
diuretics functions and includes:
reduced fluid volume
Bumetanide
Furosemide
torsemide
76
Inotropes function/includes:
Increase contractiility
Dobutamine
Milrinone
Digoxin
77
Vasodilators fcn/includes:
```
Decrease pre/afterloads
Nitroglycerin
nitroprusside
Nesiritide
nitrates
```
78
Acute vs chronic drugs
beta agonism vs antagonism
NE/E, dopamine, dobutamine, digoxin/milrione
beta blocker
79
Dobutamine vs Milrinone uses and avoidance
Use: short term management for low CO + congestions
Dob avoid: with beta blocker
Milrionine avoid: with hypotension
80
Atropine is a _____lytic; propranolol is a ____ lytic
parasympatho (atropine = increase HR)
| sympatho (propranolol = decrease HR)
81
E, NE, Dobutamine, Dopamine are _____ , acts on:
Symapthomimetic drugs - adrenergic agonists
(a1, b1, b2) E
(a1, b1) NE
(b1) dob
82
Metoprolol, carvedilol are ___ and acts on:
adrenergic antagonist
Met (b1)
Carv (a1, b1, b2)
83
Muscarinic antagonists include
M2 --> decrease HR
| Atropine antag. M2
84
Cycle of adrenergic receptor from alpha 1 receptor
a1 -> Gq -> activate PLC -> release IP3/DAG --> (release stored Ca, activate PKC)
85
cycle of adrenergic receptor from b1/b2
b1/b2 -> Gs -> adenylyl cyclase - increase cAMP ->PKA -> increase Ca movement through LTCC
86
Cycle of adrenergic receptor from alpha 2 receptor
a2 --> Gi --> decrease cAMP -> Open K channels (hyperpolarize)
also Go --> decrease Ca movement
87
Cholinergic receptor M1 and M2/3/4
M1/3 - Gq - Increase PLC
| M2/3/4 - Gi - Decrease adenylyl cyclase
88
Nicotinic effect
alter ionic perm - increase Na/Ca conduction - depolarize
89
b1 receptor (agonist) effect on heart
SA node - HR up
AV: Conduct speed up
A/V muscle - inotropy up
90
NE to ___; Ach to __
b1 - Gs
M2 - Gi
Both affect adenylate cyclase
91
receptor subtype on Bp (a1, b1, b2)
a1 - vasoconstrict, reflex bradycardia/preload/afterload
b1 - HR up/inotropy up
b2 - vasodilation, reflex tachy
92
Hemorrhage - events from baroreceptor
less tresth, baroreceptor less fire - increase sympathetic fiure/decrease para - vasoconstrict, HR up, contractility up, BP up
93
Hemorrhage - events from kidney
decrease RBF - release renin - convert angiotensiongen to ATI - (ACE) - ATII - Increase Na reabsorption/water reabsorption = increase BV
94
Gq effect
PLC/PKC --> increase Ca (IP3R activation/SR Ca release)
95
PKA of 4 things and effect:
PLB - lusitropy, inotropy
RYR - sensitive - inotropy
LTCC - slow inact - inotropy
TnI - lusitropy
96
sympathetic sitmulation causes:
vasoconstriction
up HR
up inotropy
97
ADH/vasopressin made in the ___ released by ____; stimulated by ____
hypothalamus
Pituitary gland
hypovolemia, hypotension, high osmolarity, ATII, sympathetic stim
98
ADH effects
increase water reabsorption
| Vasoconstriction
