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Pharmacology > Antianginals and Antiarrhythmics > Flashcards

Antianginals and Antiarrhythmics Flashcards

1
Q

What are the two nitrates which increase NO levels and can be used to relieve angina?

A
  1. Nitroglycerine

2. Isosorbide dinitrate

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2
Q

What is the mechanism of action of nitrates which is beneficial?

A

Increase in NO causes vasorelaxation, primarily affecting veins but secondarily arteries and arterials.

Decreased venous capacitance leads to a reduction in preload, which is beneficial for failing hearts with lots of pulmonary congestion / dilation

Decreased arterial tone leads to reduction in afterload as well, reducing cardiac work

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3
Q

What are the three types of angina? Are nitrates effective in treating these?

A
  1. Classic angina - atherosclerotic obstruction of coronary vessel
  2. Unstable angina - Non-occlusive platelet clots near athersclerotic plaques, which are transient
  3. Variant angina - transient spasm of coronary arteries

Nitrates successfully treat all three, plus MI / CHF recovery

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4
Q

Why does high preload tend to occlude coronary vessels?

A

Leads to high end-diastolic pressure in failing hearts, and shortens the length of diastole, allowing for less time for oxygen delivery to myocardium (which occurs during diastole)

This explains why nitrates allow for greater oxygen availability / reduce oxygen consumption

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5
Q

How do nitrates help in variant angina?

A

Dilate the coronary arteries, preventing spasm

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6
Q

Why are nitrates especially good in unstable angina?

A

Nitrates also decrease platelet aggregation, decreasing the chances of forming thrombi

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7
Q

What are the common side effects of nitrates?

A

Orthostatic hypotension, reflex tachycardia -> treat with beta blockers, and throbbing headache (meningeal artery pulsations)

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8
Q

How are patients given nitrates, and do they ever lose effectiveness?

A

Given sublingually for fastest delivery, and tachyphylaxis is known to happen by a mechanism not well understood

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9
Q

What is Viagra / mechanism and when is it not effective?

A

Sildenafil - a phosphodiesterase 5 (PDE5) inhibitor

Not effective after prostatectomy causing nerve damage, so M2 receptors cannot be stimulated in the first place (requires initial parasympathetic signal in corpus cavernosum)

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10
Q

What is sildenafil used to treat in the cardiovascular world?

A

Pulmonary hypertension due to pulmonary fibrosis. Causes relaxation of pulmonary artery (PDE5 is found here), which reduces the right-sided afterload

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11
Q

What are the untoward effects and metabolism of sildenafil?

A

Flushing, visual disturbances, and headache

Priapus (erection >4 hours) is rare

Can cause MI if used with nitrates due to extreme hypotension

Metabolized via CYP3A4

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12
Q

What is the mechanism of action of ranolazine and what condition is it used in?

A

Inhibits the late sodium current which tends to be very large in ischemic tissues (this is a constant leak during depolarization). This channel normally increases intracellular sodium, facilitating increased calcium and a reduction in diastole length. Ranolazine thus decreases calcium and increases diastole length, making it useful for treatment of angina (but contraindicated in heart failure)

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13
Q

What is ranolazine used with and for?

A

Used in conjunction with nitrates, beta-blockers, or calcium channel blockers for treatment of classic angina

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14
Q

What is the mechanism of action of digoxin (cardiac glycoside)? How does this relate to toxicity?

A

Inhibits the isoform of Na/K-ATPase present in cardiac muscle (second greatest action is in GI tract, which will explain first signs of digoxin toxicity is GI distress)

This increases intracellular sodium levels and thus exchange for sodium via Na/Ca exchanger, which increases intracellular calcium levels

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15
Q

Why is digoxin super juicy?

A

Improves the efficiency of contractions by accumulating calcium to be released by SER without increasing oxygen consumption significantly

  • > less sympathetic tone is needed to drive cardiac output
  • > heart rate and vascular tone are reduces, decreasing the filling pressure and thus reducing heart size / oxygen demand
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16
Q

What is the main issue with digoxin?

A

It is great at therapeutic doses, but has a very narrow therapeutic window
-> GI disturbances, CNS effects like changes in color vision, then cardiac arrhythimas

  • it has many drug interactions which make this therapeutic window difficult to hit
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17
Q

What effect does digoxin have on conduction velocity and refractory period of AV node and how?

A

Reduces the conduction velocity and increases AV refractory period -> useful for treatment of atrial arrhythmias.

This is due to CNS modulation of vagal signalling, which is not well explained. It can be blocked via atropine.

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18
Q

What is the side effect of concern with Ranolazine?

A

Prolonged QT interval, and CYP3A4 interactions

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19
Q

What does digoxin do to action potential duration in the heart?

A

It shortens it -> probably due to increased potassium conductance due to higher levels of Ca+2 in cytoplasm

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20
Q

What is the primary type of arrhythmia caused by digoxin?

A

Delayed-after-depolarizations (DADs) due to excess calcium remaining in cytoplasm, causing another contraction

Progression of DADs can lead to a second, full extra contraction (bigeminy), which can initiate ventricular fibirillation

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21
Q

How is digoxin toxicity treated?

A

Reduction in level of digitalis via anti-digoxin Fab fragment

Previously, magnesium sulfate (which reduces hypomagnesia related arrhythmias as well as digoxin)

22
Q

Why might the early side effects of digoxin toxicity progress to way worse ones?

A

Early side effects = GI distress.

Vomiting can cause hypokalemia (due to compensatory K+ excretion for H+ absorption)

Hypokalemia increases cardiac pacemaker rate, action potential duration, and is arrhythmogenic, predisposing to DADs of digoxin

23
Q

What electrolyte inhibits digoxin binding?

A

Potassium. Hyperkalemia will reduce digoxin’s effectiveness, hypokalemia will increase it (also for reasons mentioned previously). Be careful when giving with furosemide (hypokalemia)

24
Q

What is the mechanism of action of dobutamine / its cardiac effects?

A

Primarily beta-1 agonist, which increases systolic pressure and cardiac output with only minor increases in cardiac oxygen demand. Diastolic blood pressure will not change since it has no effects on the peripheral resistance

25
Q

What is dobutamine used for?

A

Primarily for short-term management of acute cardiac decompensation when determining another regimen, or acute heart failure / MI.

Caution in MI due to slightly increased oxygen demands -> more ischemia

26
Q

What is the order of receptor agonism for dopamine?

A

D1 -> B1 -> A1

27
Q

What are the primary indications for dopamine?

A
  1. Short-term managment of congestive heart failure associated with renal dysfunction (increases blood flow to mesentery and kidneys via D1 receptors)
  2. Cardiogenic / septic shock at high doses
28
Q

What accounts for the plateau phase in cardiomyocytes?

A

Equilibrium potential met between outward conductance through potassium channels and inward calcium influx through L-type calcium channels

29
Q

What interval represents AV conduction time on the EKG?

A

PR interval

P wave is the atrial depolarization

30
Q

What does the QT interval represent?

A

Period from ventricular depolarization until its repolarization

31
Q

What are the four primary mechanisms of arrhythmogenesis?

A
  1. Altered automaticity
  2. Triggered activity
  3. Conduction defects - i.e. re-entry or block
  4. Accessory pathways
32
Q

What is altered automaticity?

A

When a latent pacemaker generates an escape rhythm due to pathologically low SA nodal firing rate (perhaps after MI)

Can also result from ectopic pacemakers which have faster rhythm than SA node

33
Q

What are the two types of triggered activity and how are they distinguished? What are their mechanisms?

A

Early after depolarizations - QT interval is prolonged and exceeds refractory period of sodium channels, triggering another action potential before the ventricle can fully repolarize (EADs arise during plateau phase)

Delayed after depolarizations - re-excitations occuring after ventricular repolarization (delayed as compared to early). Mechanism is unclear except for digitalis, which is due to intracellular calcium

34
Q

What can sustained EADs lead to?

A

Very dangerous arrhythmia called torsades de pointes

35
Q

What is conduction block versus re-entry?

A

Block -> ischemic area during to trauma, scarring, or ischemia which allows tissue past the block to generate escape rhythms (have their own pacemaker firing and subsequent arrhythmia)

Re-entry -> slowed conduction through ischemic area allows retrograde conduction slow enough to hit normal tissue after repolarization and trigger a depolarization loop

36
Q

What is an accessory pathway example?

A

A short circuit between atria and ventricles which can predispose to re-entry and tachyarrhythmias, as in Wolf-Parkinson-White syndrome

37
Q

What are the three states of a sodium channel?

A
  1. Resting / closed - ready to open
  2. Open - ion influx
  3. Inactive - refractory, not repolarized
38
Q

What type of channels do sodium channel blockers preferentially block?

A

Open / inactive channels -> dissociate from resting. Thus, they tend to preferentially block highly active tissues (more open / inactivated channels) as in anesthesia or ischemic tissue where depolarization lasts longer

39
Q

What is the mechanism of action of procainamide?

A

Blocks sodium channels and thus increases threshold and decreases conduction velocity in myocardium, but also blocks potassium channels (leads to longer depolarization and thus QRS duration)

40
Q

What is procainamide used for, and what are its untoward effects?

A

Secondary drug of choice for ventricular / atrial arrhythmias

Untoward effects -> possible torsades de pointe and can result in lupus-like disease in long-term use (like hydralazine)

41
Q

What are the two most commonly used anti-arrhythmic beta blockers, and what are they used against?

A
  1. Esmolol - short half life, atrial tachycardias
  2. Sotalol - some potassium channel blocking properies, useful against atrial + ventricular tachycardias

They both slow AV conduction and slow heart rate

42
Q

What is the primary side effect of beta blockers as anti-arrhythmics and when are they contraindicated?

A

Side effect: Torsades de pointes due to QT prolongation (especially sotalol)

Contraindicated in WPW syndrome

43
Q

For straight potassium channel blockers, what is their mechanism / possible complications?

A

Amiodarone

-> increases the refractory period of the heart, which can lead to EADs and possible torsades de pointes

44
Q

What are the general effects of amiodarone?

A

Inhibits inactive sodium channel, potassium channels, and calcium channels
-> prolongs refractory period

Inhibits alpha and beta receptors as well
-> increases AV conduction time, and causes bradycardia

45
Q

When is amiodarone used?

A

In atrial tachycardia as an oral med, can also treat recurrent ventricular tachycardias and fibrillation

46
Q

What are the cardiac side effects of amiodarone?

A

Bradycardia, decreased contraction, and heart block, though surprisingly no TdP

47
Q

What are the non-cardiac side effects of amiodarone?

A

Pneumonitis leading to pulmonary fibrosis

Hyper or hypothyroidism (it is an analog of thyroxin)

CNS symptoms

Also has many CYP3A4 and digoxin interactions

48
Q

What is verapamil / diltizem primarily used for / its mechanism of action?

A

Calcium channel blocker, binding primarily the open / inactivated form (favors active tissue) -> prolongs AV nodal conduction and refractoriness

Used for treatment of re-entrant supraventricular tachycardias / reduce risk of V-tach from atrial flutter or atrial fibrillation

49
Q

What is the only difference between verapimil / diltizem? What are they contraindicated in?

A

Verapimil has anti alpha-1 hypotensive abilities

Both contraindicated in WPW syndrome

50
Q

What is the mechanism of action of adenosine in anti-arrhythmia? Use?

A

Binds P1 purinergic receptors that open G-protein regulated potassium channels, inhibiting SA node, atrial and AV nodal conduction

-> immediate determination of supraventricular tachycardia (half-life of 6 seconds)

Pharmacology (54 decks)

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