Cardio Flashcards

1
Q

Mechanisms of Arrhythmias

A
  1. Abnormal automaticity
  2. Triggered acitivity (EADs, DADs)
  3. Re-entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Abnormal automaticity

A

non-pacemaker cells take on pacemaker AP and fire faster than SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Early Afterdepolarizations (EADs)

A

Prolonged AP

Slow HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Delayed afterdepolarizations (DADs)

A

Ca overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Re-entry

A

Impulse persists to reactivate the myocardium instead of dying out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Classes of anti-arrhythmics

A

Class 1: Na channel blockers
Class 2: B-blockers
Class 3: K channel blockers
Class 4: Ca channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Class 1 Anti-arrhythmics

A

Block fast Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Class 1a anti-arrhythmics

A

quinidine

procainamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Class 1b anti-arrhythmics

A

lidocaine

mexiletine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Class 2 anti-arrhythmics

A

Propanolol
Atenolol
esmolol

(block b-receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How to class 2 anti-arrhythmics work?

A

Decrease HR and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why must class 2 anti-arrhythmics be titrated?

A

Up regulate B receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Propanolol

A

Non-selective B blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Atenolol

A

B1 cardioselective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Esmolol

A

B1 cardioselective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Class 3 anti-arrhythmics

A

K channel blockers

Sotalol, amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sotalol

A

non selective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Amiodarone

A

Class 1, 2, 3, 4, and a1 blocker
Long half life
Limited use
Side effects (turns people BLUE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Class 4 anti-arrhythmics

A

Ca channel blockers

Diltiazem, Amlodipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Furosemide

A

Loop diuretic
CHF and pulmonary edema
Always use with ACE inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Loop diuretics

A

Furosemide

Torsemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hydrochlorothiazide

A

Thiazide diuretic

Distal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Sprionolactone

A

K-sparing

Distal tubule and collecting duct

24
Q

Arteriodilators

A

Relax smooth muscle of arterioles

Reduce AFTERLOAD

25
Q

Venodilators

A

Relax vein smooth muscle

Reduce PRELOAD

26
Q

Balanced or mixed vasodilators

A

act at both arteries and veins

27
Q

Nitrates

A

Venodilators
NO formation and reduction of Ca
Nitrogylcerin
Nitroprusside

28
Q

Sodium nitroprusside

A

Balanced vasodilator (both arteries and veins)

29
Q

Side effects of nitrates

A

Hypotension
Rebound hypertension
Cyanide poisoning

30
Q

Arteriodilator drugs

A

Nitroprusside
Amlodipine
Hydralazine

31
Q

Hydralazine

A

decreases cGMP

32
Q

Sildenafil

A

treats pulmonary hypertension

33
Q

ACE inhibitors

A

Enalapril
Benazepril

Given to patients with CHF to blunt effects of RAAS

34
Q

Mechanism of positive inotropic drugs

A

Increase amount of Ca available to increase contractility

35
Q

“Cost” of positive inotropes

A

Myocardial ischemia and monocyte death (due to increase oxygen consumption)

36
Q

Classes of inotropes

A
  1. Cardiac glycosides
  2. B adrenergic agonists (synthetic catecholamines)
  3. phosphodiesterase inhibitors
  4. calcium sensitizing agents
37
Q

Cardiac glycosides

A
Plant extracts (purple foxglove)
Digoxin
38
Q

How do cardiac glycosides work?

A

Inhibit Na/K ATPase pump -> increase intracellular Na

Na exchanges for Ca

39
Q

When are cardiac glycosides used?

A

Systolic myocardial failure

Atrial fibrillation

40
Q

Synthetic catecholamines are used for ____ inotropic support

A

Acute (half life is minutes)

41
Q

Examples of synthetic catecholamines (b1 agonists)

A

Dopamine

Dobutamine

42
Q

Dopamine

A

Act on alpha, b1, and dopaminergic receptors

(Low doses: vasodilation, DA receptors
Higher doses: positive inotropy, B1
Very high doses: vasoconstriction, a)

43
Q

Dobutamine

A

B1 effects

44
Q

Mechanism of Phosphodiesterase inhibitors

A

inhibit breakdown of cAMP

45
Q

Examples of phosphodiesterase inhibitors

A

Amrinone

Milronone

46
Q

Mechanism of Calcium sensitizing agents

A

Increases AFFINITY of troponin C for calcium during systole and diastole
Enhances contractility without increasing O2 consumption

47
Q

Examples of calcium sensitizing agents

A

Pimobendan

Levosimendan

48
Q

Pimobendan

A

“Inodilator”: positive inotrope AND systemic pulmonary vasodilator

49
Q

Beta receptors found in cardiac muscle

A

B1

50
Q

Beta receptors found in bronchial and vascular smooth muscle

A

B2

51
Q

Effects of beta blockade

A

Decrease HR (decrease SA node firing)
Improved myocardial perfusion
Slows AV nodal conduction
Decrease myocardial contractility (less O2 consumption)

52
Q

Use of beta blockers

A

anti-arrhythmics
HCM
CHF

53
Q

First generation beta blockers

A

Propanolol
Sotalol
(nonselectively inhibit both B receptors)

54
Q

Second generation beta blockers

A

Atenolol
esmolol
(b1 receptors only)

55
Q

Third generation beta blockers

A

additional vasodilatory properties
B2 stimulatory properties
added alpha blockade