Exam 2 - Wendt (Arrhythmia/CHF) Flashcards
(109 cards)
1
Q
_______ cells have automaticity
A
Pacemaker
2
Q
pacemaker cells have (what ion) dependent spikes
A
Ca2+
3
Q
Ventricular myocytes have (what ion) dependent spikes
A
Na+
4
Q
Pacemaker Cells or Ventricular Cells?
have a very fast/immediate/vertical depolarization
A
Ventricular cells
5
Q
Pacemaker Cells or Ventricular Cells?
have Ca2+ dependent spikes
A
Pacemaker
6
Q
Pacemaker Cells or Ventricular Cells?
have Na+ dependent spikes
A
Ventricular
7
Q
Pacemaker Cells or Ventricular Cells?
Have high automaticity
A
pacemakers
8
Q
Pacemaker Cells or Ventricular Cells?
have low automaticity
A
ventricular
9
Q
Pacemaker Cells or Ventricular Cells?
are specialized non-contractile cells
A
Pacemaker
10
Q
Pacemaker Cells or Ventricular Cells?
are contractile cells
A
ventricular
11
Q
what are the phases of a Pacemaker cells action potential?
A
In order: Phase 4,0,3,4
12
Q
what is phase 4 in pacemaker cell action potential
A
“funny” current makes diastolic pacemaker current
annnnd
K+ channels/current is activated by vagus
13
Q
what is phase 0 in pacemaker cell action potential
A
calcium channel carries AP upstroke
14
Q
what is phase 3 in pacemaker cell action potential
A
repolarizing K+ current
15
Q
Myocyte action potential phases? (in order)
A
IN ORDER: Phases 4,0,1,2,3,4
16
Q
what is phase 0 in myocyte cells action potential
A
Na+ channel carries AP upstroke
17
Q
what is phase 1 in myocyte cells action potential
A
repolarizing K+ current (“transient upward”???)
18
Q
what is phase 2 in myocyte cells action potential
A
plateau Ca2+ current critical for muscle contraction
19
Q
what is phase 3 in myocyte cells action potential
A
repolarizing K+ current
20
Q
what is phase 4 in myocyte cells action potential
A
pacemaker current (very minimal?)
21
Q
Acetylcholine decrease _____ and ____ currents
A
HCN; Ca2+
22
Q
ACH activates ______ which causes hyperpolarization
A
GIRK
23
Q
_____ activates GIRK which causes hyperpolarizaiton
A
ACH
24
Q
ACH stimulates the G_____ channel
A
G (alpha I)
25
ACH is a a part of the (sympathetic or parasympathetic) system
PARAsympathetic
26
what does the GIRK channel do when activated?
it causes hyperpolarization by kicking K+ out of the cell
27
how many classes of antiarrhythmic drugs are there (according to Vaughn-Williams-Singh Scale)
4
28
what are the 4 classes of antiarryhthmic drugs
| according to Vaughn-Williams-Singh Scale
1 - Na+ channel blockers
2- Beta adrenergic antagonists
3- K+ channel blockers aka drugs that prolong refractory period
4 - Ca2+ Channel blockers
29
If another signal happens when an area is still under its refractory period what happens?
nothin' --- if still in refractory period a new beat won't occur
30
what are the common arrhythymias
```
atrial sinus arrhythmia
re-entry arrhythmia
a.fib
wolf-parkinson white
monomorphic ventricular tachycardia
AV nodal re-entrant tachycardia
Premature ventricular complexes
```
31
what beta blockers dose wendt mention
Esmolol, Acebutolol, Propranolol
32
Beta Blockers:
| slow ______ and _____ currents in SA/AV Node
Pacemaker/Ca2+
33
Beta Blockers:
| (increase or decrease) refractoriness of SA/AV node
INCREASE
34
Beta Blockers:
| (increase or decrease) P-R interval
increase
35
Beta Blockers:
| are good when the arrhythmia involves ______
catecholamines...
36
Ca2+ Channel Blocker Options for arrhytmias?
Diltiazem and Verapamil
37
Ca2+ Channel Blocker:
| have a __________ block
frequency dependent
38
Ca2+ Channel Blocker:
| (increase or decrease) refractoriness of AV node
INCREASE!
| not SA node like beta blockers
39
Ca2+ Channel Blocker:
| (increase or decrease) the P-R interval
increase
40
what are the 3 different classes of Na+ Channel blockers (aka Class 1 Na+ Channel blockers)
1A; 1B; 1C
41
what antiarrhythmic drug class is class 1
Na+ channel blockers
42
what antiarrhythmic drug class is class 2
beta adrenergic antagonists
43
what antiarrhythmic drug class is class 3
K+ channel blockers (agents that prolong refractory period)
44
what antiarrhythmic drug class is class 4
Ca2+ channel blockers
45
what antiarrhythmic drugs are a part of Class 1A
quinidine
procainamide
disopyramide
46
what antiarrhythmic drugs are a part of Class 1B
lidocaine
tocainide
Mexilitine
Phenytoin
47
what antiarrhythmic drugs are a part of Class 1C
Propafenone
Flecainide
Moricizine
48
what antiarrhythmic drugs are a part of Class 3
```
(the K+ channel blockers)
Amiodarone
Dronedarone
Sotalol
Ibutilide
```
49
what antiarrhythmic drugs are a part of Class 5
```
These are all the misc. Drugs
Digoxin
Magnesium Chloride
Potassium Chloride
Adenosine
```
50
When beta adrenergic receptors are stimulated cAMP increases which directly increases activity of _____ channels --> increased ______ currents
HCN channels; DEPOLARIZING currents
51
When beta adrenergic receptors are stimulated cAMP increases which increases phosphorylation of _______ channels which increases amount of current these channels can pass and allows them to open at more _____ membrane potentials
L-type voltage gated Ca2+ channels; negative
52
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
does pure sodium channel block
1B and 1C
53
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
both widens QRS complex AND prolongs Q-T interval
1A
54
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
can reduce QT interval (but not clinically significant)
1B
55
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
Widens QRS complex
1A & 1C
56
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
will block both the open and inactivated state
1B
57
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
preferentially blocks open state
1A & 1C
58
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
ONLY blocks open state
1C
59
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has VERY slow dissociation (> 10 secs)
1C
60
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has rapid dissociation (millisecond)
1B
61
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has moderate to slow dissociation (seconds)
1A
62
QT interval is known as the time from the beginning of _________ to the end of _________
beg. of ventricular depolarization; to end of ventricular repolarization
63
what are the 3 mechanisms that can cause arrhythmia
enhanced automaticity
triggered activity
re-entry
64
the ____ Node cells exhibit the highest rate of automaticity
SA
65
Arrhythmias can be caused by trigger activity --- what does trigger activity mean?
depolarizations that arise abnormally from a normally generated sinus action potential
66
what does EAD and DAD stand for
EAD - early afterdepolarizaiton
| DAD - delayed after depolarization
67
what are the different types of trigger activity that cause arrythmias
EAD or DAD
68
Triggered Activity - EAD
is caused by ________
Arises from a _________ Vm
Caused by (rapid or slow) HR, or _____kalemia, or ______ syndrome
caused by PROLONGED AP
from a DEPOLARIZED
SLOWED HR, HYPOkalemia, or LONG QT syndrome
69
```
Triggered Activity - DAD
caused by ________
(increase or decrease) NCX current
arises from a ______ Vm
often seen with: (rapid or slow) HR, MI, _______ stress, or _______ intoxication
```
caused by Ca2+ overload
INCREASE in NCX current
arise from NORMAL Vm
RAPID HR; adrenergic stress, digoxin intoxication
70
what two things make up cardiac output
Stroke Volume and HEART RATE
71
what are the consequences of decreased cardiac output
Cardiovascular:
Tachycardia, Cardiomelgia, Arrhythmias, Fatigue/exercise intolerance
```
Respiratory:
SOB
Pulmonary Edema
Cyanosis
Orthopnea
```
72
definition of stroke volume
amount of blood ejected from da ventricles during contraction
73
______ increase stroke volume
| what hemodynamic concept..
contractility
74
what are the axis on a FrankSterling Relationship
Y-axis: Stroke Volume
| X-axis: PreLoad (aka left ventricular diastolic volume)
75
Preload is also known as ......
LV (left ventricular) End diastolic volume
76
Afterload and ____ are inversely related
SV (stroke volume)
77
Frank-Starling Relationship
| a failing heart can't compensate and increase _____ when _____ increases
can't increase SV when preload increases
78
what are the axis in a force tension graph
Y-axis: Stroke Volume
| X-axis: Afterload
79
what are the two types of CHF
Systolic Failure
| or Diastolic Failure
80
Types of CHF:
Systolic Failure has....
deficit in _______
and a ______ heart
deficit in CONTRACTION
| THIN/DILATED heart
81
Types of CHF:
Diastolic Failure has....
deficit in _______
_______ walls that cannot relax
deficit in FILLING
| STIFF/THICK that cannot relax
82
what are the 3 types of cardiac remodeling (due to CHF is why we talked about them)
Cardiac Dilation
Pathological Hypertrophy
Physiological Hypertrophy
83
CHF - Cardiac Remodeling:
| which one does NOT have fibrosis
Physiological hypertrophy
84
CHF - Cardiac Remodeling:
| which one has thinning walls
cardiac dilation
85
CHF - Cardiac Remodeling:
| what can cause pathological hypertrophy
Chronic HTN
| Aortic valve stenosis
86
CHF - Cardiac Remodeling:
| what can cause physiological hypertrophy
Chronic Exercise
| Pregnancy
87
CHF - Cardiac Remodeling:
| what can cause cardiac dilation
MI or other insults (like HF)
88
Renin/Angiotensin System:
| ______ makes angiotensinogen
Liver
89
Renin/Angiotensin System:
| _____ makes Renin
kidney
90
Renin/Angiotensin System:
| ______ makes ACE
Lungs
91
Renin/Angiotensin System:
| Angiotensin II causes _____ and _____ secretion
Aldosterone/ADH
92
Renin/Angiotensin System:
overall leads to
increased ________ and increase _______ and increased __________
water retention; blood volume; sympathetic activity
93
2 Main CHF Tx Strategies
Manipulate Hemodynamics
Inhibit compensation
94
CHF Tx Strategies
Manipulate Hemodynamics and Inhibit Compensation -
which one improves mortality
inhibiting compensation
95
CHF Drugs
| what drugs are used to manipulate hemodynamics
vasodilators (organic nitrates, hydralazine)
diuretics
angiotensin inhibitors
inotropic agents (digoxin, PDE3 inhibitors, Bera-adrenergic agonists)
96
what are the 3 classes of inotropic agents used in CHF and are they used for chronic or for acute therapy only?
Cardiac glycosides - chronic
PDE (phosphodiesterase) inhibitors - acute only
Beta adrenergic agonists - acute only
97
what drugs are known as PDE inhibitors and used in CHF as inotropic agents
milrinone and inamrinone
98
what drugs are known as Beta adrenergic agonists and used in CHF as inotropic agents
dopamine; dobutamine
99
how does Na+/K+ ATPase blockade cause higher contractility
when the ATPase is inhibited it creates more Na+ inside - the NCX channel then compensates and kicks out Na+ and brings in Ca2+ which causes more contraction/greater contraction
100
what drug is a cardiac glycoside
digoxin
101
what are some common digoxin toxicities
psychiatric - delirium/fatigue/malaise/confusion
G.I - anorexia, N/V, abdominal pain
Respiratory - increased response to hypoxia
C.V - pro-arrhythmic (atrial tachy, AV block)
102
what drugs are Vasopressin receptor antagonists
tolvaptan
| conivaptan
103
Tolvaptan or Conivaptan:
| which one is V2 selective
Conivaptan
104
Tolvaptan or Conivaptan:
| which one is V1A/V2 receptors
Tolvaptan
105
Vasopressin Receptor Antagonists are used for treating ________ in HF and ______
hyponatremia; SIADH
106
ADEs of Vasopressin Receptor Antagonists
hypotension
| osmotic demyelination
107
why is neprilysin inhibition helpful in CHF
under normal circumstances, neprilysin breaks down natriuretic peptides. but natriuretic peptides cause VSMC relaxation
108
what drug is a neprilysin inhibitor
Sacubitril
109
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has mixed block for Na+ and K+
1A
