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Cardio > Dr. French's Review > Flashcards

Dr. French's Review Flashcards

1
Q

Drugs dissociate from the Na+ channels at different rates (recovery). Drugs with a slow recovery have greater effect on _____ _____ ______

A

cardiac conduction velocity

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2
Q

Drugs dissociate from the Na+ channels at different rates (recovery). Drugs with a slow recovery have greater effect on cardiac conduction velocity. Class IA anti arrythmatics like quinidine dissociate ____

A

slowly

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3
Q

Drugs dissociate from the Na+ channels at different rates (recovery). Drugs with a slow recovery have greater effect on cardiac conduction velocity. Class IC anti arrythmatics like Flecainide dissociate ____

A

very slowly

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4
Q

Example of class IB Na+ channel blocker

A

lidocaine

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5
Q

Are class I anti-arrhytmics use dependent or not?

A

yes they are USE DEPENDENT

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6
Q

Class I Na+ channel blockers decrease re-entry in a twofold manner:

A

decrease conduction velocity

increase the refractory period

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7
Q

Class I Na+ channel blockers are used to control rate/rhythm

A

rhythm

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8
Q

Class III K+ channel blockers increase the _____. What is so risky about this?

A

K+ channel blockers increase the QT interval, increasing the risk of Torsades

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9
Q

An example of class III K+ channel blockers is _____

A

amioderone (also class I too)

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10
Q

An example of Class II Beta blockers is ____

A

metoprolol

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11
Q

Beta blockers primarily control rate/rhythm

A

rate

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12
Q

Beta blockers are rate controllers because they:

A

decrease AV conduction to decrease heart rate

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13
Q

How do class III K+ channel blockers control reentry

A

by decreasing conduction velocity and increasing refractory period

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14
Q

Class IV Ca2+ channel blockers control rate how?

A

by decreasing AV conduction and heart rate

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15
Q

Are class IV Ca2+ channel blockers use dependent?

A

YES

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16
Q

Class IV Ca2+ channel blockers slow the rise of the action potential and prolong repolarization at the __ ___

A

AV node

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17
Q

How does adenosine act?

A

Inhibits AV nodal conduction with  refractory period

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18
Q

Electrophysiologic Effects of Adenosine or ACh or Digoxin (indirect via vagal stimulation)

A

Addition of Adenosine, ACh, Digoxin, or application of vagal maneuver causes hyper polarization and a decreased slope of phase 4 depolarization

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19
Q

ACh acts via the ____ receptor

Adenosine via the ___ receptor and both are coupled to ___ proteins

A

M2
M1
Gi/o proteins

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20
Q

1st degree AV block:

Is it of clinical concern?

A

Increased PR interval, usually not clinical concern

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21
Q

Which Mobitz type AV block is more serious?

A

Mobitz II, the disease of the His-Purkinje system is more unpredictable, and urgent treatment is needed to prevent asystole

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22
Q

What happens in mobitz I?

A

there is a progressive increase in PR interval until a beat is finally blocked

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23
Q

In 3rd degree complete heart block, describe what is seen

A

no association between atrial and ventricular depolarizations. P waves are regular but occur much faster than QRSs, which are also proceeding with regular rhythm

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24
Q

Treatment for acute AV block

A

Chronotropic agents: atropine, dopamine, epinephrine

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25
Q

Chronic treatment for AV block

A

long term pharmacotherapy is not possible, permanent cardiac pacing is often required

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26
Q

Major Actions of Antitachyarrhythmic Rate Control

A

Block conduction at AV node (Class II and IV), parasympathetic action to slow AV conduction (digoxin), membrane hyperpolarization (adenosine)

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27
Q

Major Actions of Antitachyarrhythmic Rhythm Control

A

Interrupt reentry or produce bidirectional block: class I/class III (amioderone)

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28
Q

Triggered automaticity

A

Site of abnormal initiation is outside the SA node

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29
Q

Two types of triggered automaticity

A

EAD, DAD

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30
Q

EArly afterdepolarizations commonly occur when…

A

heart rate is SLOE, extracellular K+ is LOW, and with drugs that prolong QT interval.
(watch out for torsades)

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31
Q

Because of a lengthened QT interval in an early after depolarization, what complication could occur?

A

torsades de pointes

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32
Q

Delayed afterdepolarization occur most likely due to what?

A

intracellular Ca2+ overload, likely from activation of Na+/Ca2+ exchanger depolarizing the cell

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33
Q

Most common mechanism of tachyarrythmias

A

reentry, where a single impulse excites an area of the heart more than once

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34
Q

most common location for reentry in a supraventrcular tachycardia situation

A

AV node is most common for SVTs

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35
Q

Acute treatment for supra ventricular tachycardia

A

adenosine

36
Q

Treatment for chronic supra ventricular tachycardia?

A

AV node blockers, slow conduction or catheter ablation (95%)

37
Q

What causes a fib?

A

chaotic electrical activity in atria with multiple microentrant wavelets existing simultaneously

38
Q

Treatment for afib

A
  1. rate control with AV nodal blockers
  2. Rhythm control: class I and III, cardioversion, ablation
  3. Anticoagulation
39
Q

Ventricular tachycardia relies entirely on what for impulse origin and propagation?

A

ventricular tissue

40
Q

Most common mechanism of Ventricular tachycardia

A

reentrant arrhythmia, but automatic or triggered focus occurs in 10% of cases

41
Q

Acute treatment for Vtach if patient is awake and not hypotensive

A

amioderone

42
Q

Chronic treatment of Vtach

A
  • some success w/ pharm agents
  • Ablation cures 90%
  • ICD + amiodarone or sotalol to decrease shocks
43
Q

If someone in Vtach receives electrical defibrillation, it is followed by

A

epinephrine (or vasopressin) and amiodarone. If not controlled, repeat defibrillation

44
Q

Predisposing factors to torsades de pointes

A

prolonged QT interval, slowed HR, hypokalemia

45
Q

Treatment for torsades de pointes

A

correction of electrolyte abnormalities (KCl for hypokalemia and MgSO4

46
Q

What is the first drug you put someone on after HF diagnosis IF they have pulmonary-systemic venous congestion?

A

diuretics. Loop diuretics preferred because of efficacy, but a thiazide diuretic can augment the effect

47
Q

Are diuretics used chronically or acutely?

A

BOTH

48
Q

What is the most common loop diuretic used in HF?

A

furosemide

49
Q

What is the problem with furosemide and what can be used in its place?

A

absorption can be tricky, can use torsemide or bumetanide instead

50
Q

Are loop diuretics like Furosemide K sparing or K wasting

A

loop diuretics are K+ WASTING

51
Q

Rank K+ sparing, low dose/low ceiling thiazides and loop diuretics in terms of how efficacious they are for HF

A

Loops> thiazides > K+ sparing

52
Q

Are thiazides K wasting or K sparking?

A

Thiazides are K+ wasting

53
Q

Aldosterone antagonist’s effect on K+

A

increased plasma K+

54
Q

When are ACEIs started in HF treatment?

A

during or after optimization of diuretic therapy

Initiated at low doses and titrated to goal

55
Q

ACEI effects

A

Vasodilation
decreased aldosterone
ANTIREMODELING
increased bradykinin

56
Q

ARBs work how?

A

By blocking the Angiotensin II receptor

57
Q

Can ACE inhibitors be bused in pregnancy?

A

NO, they are category D!!!

58
Q

The two important aldosterone inhibitors are:

A

spirolactone (gynocomastia), eplerenone

59
Q

ACEI potential side effects on kidney

A

Decreased GFR. Monitor K+ and renal function

60
Q

After a HF patient is on diuretics and ACEIs, it is time to add…

A

low doses of beta blockers. TItrate them to goal as tolerated.

61
Q

Important B-Blockers used for HF

A

carvedilol or metoprolol

62
Q

In HF, Beta-blocker are awesome because they….

A

-dampen the sympathetic tone and have ANTIREMODELING EFFECT

63
Q

What are the tough aspects of using Beta blockers for HF?

A

In the short term, they may may HF worse, but the long term improvements in LV function and survival are dose-dependent and are worth the long haul!

64
Q

When might aldosterone antagonists like spirolactone and eplerenone be added to the treatment plan for a HF patient?

A

aldosterone antagonists are added to therapy when the LVEF is <30% on ACEI/ARB and B-blocker therapy

65
Q

How do aldosterone antagonists work?

A

they block aldosterone’s effect on the kidney

66
Q

Which aldosterone antagonist is preferred and why might you have to switch?

A

spirolactone is preferred if tolerated, but if endocrine side effects are present, the patient might prefer eplerenone

67
Q

When might you consider adding Hydralazine plus isosorbide dinitrate to a HF patient’s therapy?

A

If ACEI and BB are ineffective or you have a HF patient who is intolerant to both ACEIs and ARBs.

68
Q

How does the combo of Hydralazine plus isosorbide denigrate work?

A

they produce vasodilation , therefore decreasing afterload and preload, reducing work, reducing mitral valve regurgitation

69
Q

Why might Digoxin be added to a treatment plan for HF?

A

added to help with:

  • systolic dysfunction symptom improvement (fatigue, dyspnea) for NYHA III and IV patients
  • atrial fibrillation to control the ventricular rate
70
Q

Can digoxin improve survival in HF patients?

A

yes, if the serum level is between 0.5 and 0.8ng/mL.

If it reaches 1.2ng/mL, symptoms will worsen

71
Q

Digoxin’s therapeutic action on myocardial cells

A

Inhibits the Na+/K+ pump, building up internal Na+ so that the Na+/Ca2+ exchanger reverses direction, therefore increasing Ca2+ in the cell. Increased Ca2+ taken up in SR, increasing isotropy/contractibility in future action potentials

72
Q

What happens during digoxin toxicity?

A

Ca2+ overload leads to PVCs, Vtach, and Vfib :(

73
Q

Describe Digoxin’s therapeutic window

A

NARROW

74
Q

Mechanisms of positive inotropic agents (B-AR agoinsts)

A

Drugs bind to AR transmit signal via guanine nucleotide regulatory protein to AC, which produces cAMP, which activates PKA. PKA targets a variety of intracellular targets with net effect of increased [Ca2+]

75
Q

of positive inotropic agents (B-AR agoinsts)

A

dobutamine, dopamine, epinephrine, isoproterenol, norepinephrine

76
Q

Mechanism of PDE inhibitors

A

prevent breakdown of cAMP to AMP by PDEs

77
Q

What kind of proteins are adrenergic receptors?

A

GPCRs

78
Q

Receptors that bins NE

A

a1, a2, B1

79
Q

Receptors that bind Epi

A

a1, a2, B1, B2

80
Q

a1 receptors work through ___ and cause what intracellular effects?

A

Gq protein–>activates PLC–>releases IP3 and DAG

IP3–>releases intracellular Ca2+stores
DAG activates PKC

81
Q

B1 and B2 receptors work through which G protein? intracellular mechanism

A

Gs–>stimulates AC–>increases cAMP–>PKA–>Intracellular Ca2+ movement through LTCCs

82
Q

A2 receptors receptors work through which G protein? intracellular mechanism

A

Gi inhibits adenylyl cyclase activity (decreases cAMP levels) - opens K+ channels (hyperpolarize membrane

83
Q

M1 and M3 –>G_ –>

A

Gq–> phospholipase C

84
Q

M2-M4 (heart lungs, CNS)–>G_–>

A

Gi–> decrease AC

85
Q

Receptor specificity of metoprolol

A

B1 only

86
Q

Receptor specificity of carvedilol

A

a1, B1, B2

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