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M2 - Pharm > FA Cardio Drugs > Flashcards

FA Cardio Drugs Flashcards

1
Q

4 Treatment options for essential (primary) HTN

A

AACD:

  • ACE inhibitors
  • ATII receptor blockers (ARBs)
  • DHP Ca2+ channel blockers
  • Thiazide Diuretics
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2
Q

4 Treatment options for HTN w/Heart Failure

A

AAB:

  • ACE inhibitors/ARBsDiuretics
  • Aldosterone antagonists
  • β-blockers (compensated HF)
    • C/I in cardiogenic shock
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3
Q

when should β-blockers be used carefully?

A
  • Caution in decompensated HF
  • C/I in cardiogenic shock
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4
Q

4 Treatment options for HTN w/diabetes mellitus

A

ABCD:

  • ACE inhibitors/ARBs
  • β-blockers
  • Ca2+ channel blockers
  • Thiazide Diuretics
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5
Q

Treatment options for HTN in pregnancy

A

HLMN:

  • Hydralazine (increases cGMP)
  • Labetalol (adrenergic blocker)
  • Methyldopa (alpha-2 agonist)
  • Nifedipine (Ca2+ channel blocker)
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6
Q

Class of drug protective against diabetic nephropathy?

A

ACE inhibitors/ARBs

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7
Q

Dihydropyridine Calcium Channel Blocker Drugs

A
  • Amlodipine
  • Clevidipine
  • Nicardipine
  • Nifedipine
  • Nimodipine
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8
Q

DHP Calcium Channel Blocker location of action

A

Vascular smooth mm

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9
Q

Non-Dihydropyridine Calcium Channel Blocker Drugs

A
  • Diltiazem
  • Verapamil
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10
Q

Non-DHP Calcium Channel Blocker location of action

A

Heart: SA and AV nodes

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11
Q

DHP Calcium Channel Blocker MOA

A
  • Block voltage-dependent L-type Ca2+ channels in vasc smooth mm
  • Inhibit MLCK
  • Arteriodilation
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12
Q

DHP Calcium Channel Blocker Clinical Use

A
  • HTN
  • Angina (incl. Prinzmetal)
  • Raynaud phenom

Note: except nimopidine

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13
Q

Nimopidine Clinical Use

A

subarachnoid hemorrhage (prevents cerebral vasospasm)

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14
Q

Clevidipine Clinical Use

A

HTN urgency or emergency

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15
Q

Non-DHP Calcium Channel Blocker Clinical Use

A
  • HTN
  • Angina
  • Afib/Aflutter
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16
Q

Calcium Channel Blocker Toxicity

A
  • Cardiac depression
  • AV block (non-dihydropyridines)
  • peripheral edema
  • flushing
  • dizziness
  • hyperprolactinemia (verapamil)
  • constipation
  • gingival hyperplasia
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17
Q

Hydralazine MOA

A
  • Increases cGMP
  • Causes smooth muscle relaxation
  • Vasodilates arterioles > veins
  • Reduces afterload
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18
Q

Hydralazine Clinical Use

A
  • Severe HTN (particularly acute)
  • HF (w/organic nitrate)
  • Safe to use during pregnancy
  • Frequently coadministered w/β-blocker to prevent reflex tachycardia
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19
Q

Hydralazine Toxicity

A
  • Compensatory tachycardia (C/I in angina/CAD)
  • Fluid retention
  • headache
  • angina
  • Lupus-like syndrome.
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20
Q

Hydralazine C/I

A

angina/CAD → causes compensatory tachycardia

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21
Q

Treatment Options for HTN Emergency

A
  • clevidipine
  • fenoldopam
  • labetalol
  • nicardipine
  • nitroprusside
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22
Q

Nitroprusside Clinical Use

A

HTN emergency

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23
Q

Nitroprusside MOA

A
  • direct release of NO → increase cGMP
  • releases cyanide
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24
Q

Nitroprusside Toxicity

A

Cyanide toxicity:

  • ETC inhibition → block ATP synth
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25
Q

Fenoldopam MOA

A
  • Dopamine D1 receptor agonist → coronary, peripheral, renal, and splanchnic vasodilation
  • Decreases BP
  • Increases Natriuresis
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26
Q

Fenoldopam Clinical Use

A

HTN emergency

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27
Q

Nitrate Drugs

A
  • Nitroglycerin
  • isosorbide dinitrate
  • isosorbide mononitrate
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28
Q

Nitrates MOA

A
  • Increase NO in vascular smooth muscle → increase cGMP → smooth mm relaxation → vasodilation
  • Dilate veins >> arteries
  • Decrease preload
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29
Q

Nitrates Clinical Use

A
  • Angina
  • Acute coronary syndrome
  • Pulmonary edema
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30
Q

Nitrates Toxicity

A
  • Reflex tachycardia (treat with β-blockers)
  • HypOtension
  • Flushing
  • Headache
  • High doses: Methemoglobinemia
  • “Monday disease” in industrial exposure
    • develop tolerance for vasodilating action during the work week, loss of tolerance over weekend
    • Tachycardia, dizziness, headache upon reexposure
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31
Q

Treatment Goals for Angina

A

Reduction of myocardial O2 consumption (MVO2) by decreasing 1+ of determinants:

  • End-diastolic volume (preload)
  • BP
  • HR
  • Contractility
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32
Q

Treatment Options for Angina

A
  • Nitrates
  • Beta-blockers
  • Nitrates + Beta-blockers
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33
Q

Effect of Nitrates on:

  • EDV
  • BP
  • Contractility
  • HR
  • Ejection time
  • MVO2
A
  • EDV: decrease
  • BP: decrease
  • Contractility: no effect
  • HR: increase (reflex)
  • Ejection time: decrease
  • MVO2: decrease
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34
Q

Effect of Beta-blockers on:

  • EDV
  • BP
  • Contractility
  • HR
  • Ejection time
  • MVO2
A
  • EDV: no effect or decrease
  • BP: decrease
  • Contractility: decrease
  • HR: decrease
  • Ejection time: increase
  • MVO2: decrease
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35
Q

Effect of Nitrates + Beta-blockers on:

  • EDV
  • BP
  • Contractility
  • HR
  • Ejection time
  • MVO2
A
  • EDV: no effect or decrease
  • BP: decrease
  • Contractility: little/no effect
  • HR: no effect or decrease
  • Ejection time: little/no effect
  • MVO2: significantly decrease
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36
Q

Beta-blockers C/I in angina

A

Partial agonists:

  • Pindolol
  • Acebutolol
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37
Q

Cardiac Glycoside Drugs

A

Digoxin

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38
Q

Digoxin MOA

A
  • Direct inhibitor of Na+/K+ ATPase
    • binds to same site as K+
    • Indirect inhibitor of Na+/Ca2+ exchanger
    • Increase intracell [Ca2+] → positive inotropy
  • Stimulates Vagus nn → decreases HR
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39
Q

Digoxin Clinical Use

A
  • Heart failure (CHF)
    • increased contractility
  • Afib
    • decreased conduction at AV node
    • depression of SA node
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40
Q

Digoxin Toxicity

A
  • Cholinergic
    • blurred/yellow vision
    • arrhythmias
    • nausea/vomiting/diarrhea
  • EKG:
    • Increased PR
    • Decreased QT
    • T-wave inversion
    • ST scooping
    • AV block
  • Hyperkalemia
    • indicates poor prognosis
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41
Q

Factors predisposing to Digoxin toxicity

A
  • Renal failure → decreased excretion
  • HypOkalemia
    • permissive for digoxin binding at K+-binding site on Na+/K+ ATPase
  • CCBs (Verapamil, Amiodarone)
  • Quinidine → decreased clearance
    • displaces digoxin from tissue-binding sites
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42
Q

Treatment for Digoxin Toxicity

A

Most often caused by hypOkalemia!

  • Slowly normalize K+
  • Cardiac pacer
  • Anti-digoxin Fab fragments
  • Mg2+
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43
Q

6 Antiarrhythmic Drug Types

A
  1. Sodium Channel Blockers
  2. Beta-blockers
  3. Potassium Channel Blockers
  4. Calcium Channel Blockers
  5. Adenosine
  6. Mg2+
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44
Q

Class I Antiarrhythmic Drugs

A
  • Fast Sodium Channel Blockers
  • Divided into classes IA, IB, & IC
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45
Q

Class IA Antiarrhythmic Drugs

A

Abba Performed Dancing Queen:

  • Procainamide
  • Disopyramide
  • Quinidine
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46
Q

Class IA Antiarrhythmics MOA

A
  • Increase AP duration
  • Increase effective refractory period (ERP) in ventricular action potential
  • Increase QT interval
  • Decrease slope of Phase 0
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47
Q

How does Cardiac AP change w/Class IA Antiarrhythmics?

A

Moderately decreased slope of Phase 0

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48
Q

Class I Antiarrhythmics MOA

A
  • Slow or block conduction (esp in depolarized cells)
  • Decrease slope of Phase 0 depolarization
  • Increase threshold for firing in abnormal pacemaker cells
  • State-dependent (selectively depress tissue that is frequently depolarized [e.g., tachycardia]).
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49
Q

Class IA Antiarrhythmics Clinical Use

A
  • Atrial & Ventricular Arrhythmias
    • esp re-entrant and ectopic SVT and VT
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50
Q

Class IA Antiarrhythmics Toxicity

A
  • Cinchonism (headache, tinnitus with quinidine)
  • Reversible SLE-like syndrome (procainamide)
  • Heart failure (disopyramide)
  • Thrombocytopenia
  • Torsades de pointes due to increased QT interval
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51
Q

Torsades de pointes

A
  • Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG
  • Can progress to ventricular fibrillation
  • Associated w/prolonged QT interval
  • Rx: Magnesium Sulfate
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52
Q

Class IB Antiarrhythmic Drugs

A

Backstreet Boys Pretty Much Lack Talent:

  • Phenytoin
  • Mexiletene
  • Lidocaine
  • Tocainide
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53
Q

Class IB Antiarrhythmics MOA

A
  • Decrease AP duration
  • Preferentially affect ischemic tissue:
    • Already-depolarized Purkinje fibers/ventricular tissue
    • Activated Na+ channels
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54
Q

Class IB Antiarrhythmics Clinical Use

A
  • Acute ventricular arrhythmias (esp post-MI)
    • IB is Best Post-MI
  • Digitalis-induced arrhythmias
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55
Q

How does cardiac AP change w/Class IB Antiarrhythmics?

A
  • Slightly decreased slope of Phase 0
  • Shorter AP duration
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56
Q

Class IB Antiarrhythmics Toxicity

A
  • CNS stimulation/depression
  • Cardiovascular depression
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57
Q

Phenytoin S/E

A
  • hirsutism
  • gingival hyperplasia
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58
Q

Mexiletine S/E

A

Think Mexican food:

  • Oral administration
  • Severe GI upset
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59
Q

Tocainide S/E

A

Pulmonary fibrosis (loud S2)

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60
Q

What happens to cardiac AP w/Class IC Antiarrhythmics?

A
  • Larger decrease in slope of Phase 0
  • No change in AP duration
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61
Q

Class IC Antiarrhythmic Drugs

A

Carly (Rae Jepsen) is Extremely Freaking Painful:

  • Encainide
  • Flecainide
  • Propafenone
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62
Q

Class IC Antiarrhythmics MOA

A
  • Zero-order kinetics
  • No effect on AP length
  • Significantly prolongs ERP in AV node and accessory bypass tracts
  • No effect on ERP in Purkinje and ventricular tissue
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63
Q

Class IC Antiarrhythmics Clinical Use

A
  • SVTs, including Afib
  • Only as a last resort in refractory VT
  • C/I post-MI
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64
Q

Class IC Antiarrhythmics C/I

A
  • post-MI
  • structural & ischemic heart disease
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65
Q

What makes Propafenone unique?

A

Blocks Na+ channels AND beta-adrenergic receptors (decreases cAMP)

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66
Q

Class IC Antiarrhythmics Toxicity

A
  • Pro-arrhythmic
  • C/I post-MI, structural & ischemic heart disease
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67
Q

Class II Antiarrhythmic Drugs

A
  • Metoprolol
  • propranolol
  • esmolol
  • atenolol
  • timolol
  • carvedilol
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68
Q

Class II Antiarrhythmics MOA

A
  • Decreases cAMP, Ca2+ currents
    • → decreases SA and AV nodal activity
  • Decreases slope of nodal AP Phase 4
    • → suppresses abnormal pacemakers
  • Increases PR interval
    • b/c AV node particularly sensitive
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69
Q

Longest-acting beta-blocker

A

Propanolol

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70
Q

Shortest-acting beta-blocker

A

Esmolol

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71
Q

3 Beta-blockers safe to give to pts w/asthma, COPD, DM

A

Partial agonists:

  • Acebutolol
  • Atenolol
  • Pindolol
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72
Q

2 Beta-blockers used for HTN emergencies

A

Also have alpha-1 blocking activity:

  • Labetalol
  • Carvedilol
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73
Q

Beta-blocker than can decrease mortality post-MI or in CHF

A

Metoprolol

74
Q

Drug that blocks beta-adrenergic receptors and K+ channels

A

Sotalol

  • Messing w/K+ → prolonged QT interval → arrhythmia
  • Keep pt in hospital and monitor
75
Q

Class II Antiarrhythmics Clinical Use

A
  • SVT
  • Ventricular rate control for Afib & Aflutter
76
Q

What happens to cardiac AP w/Class II Antiarrhythmics?

A
  • Decreased slope of Phase 4
  • Prolonged repolarization
77
Q

Class II Antiarrhythmics Toxicity

A
  • Impotence
  • Exacerbation of COPD/asthma
  • CV effects (bradycardia, AV block, HF)
  • CNS effects (sedation, sleep alterations)
  • May mask signs of hypOglycemia
  • Metoprolol can cause dyslipidemia
  • Propranolol can exacerbate vasospasm in Prinzmetal angina
  • β-blockers cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity
78
Q

Treatment for β-blocker overdose

A
  • saline
  • atropine
  • glucagon
79
Q

Class II Antiarrhythmic Drug Type

A

Beta-blockers

80
Q

Class III Antiarrhythmic Drug Type

A

Potassium Channel Blockers

81
Q

Class III Antiarrhythmic Drugs

A

All I Do is Sing:

  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol
82
Q

Class III Antiarrhythmics MOA

A
  • Increase AP duration
  • Increase ERP
  • Prolong QT interval
83
Q

Class III Antiarrhythmics Clinical Use

A
  • Ventricular arrhythmias
  • Afib/Aflutter
  • VTach (Amiodarone, Sotalol)
84
Q

Class III Antiarrhythmics Toxicity

A
  • Sotalol: torsades de pointes, excessive β blockade.\
  • Ibutilide: TdP
  • Amiodarone:
    • pulmonary fibrosis
    • hepatotoxicity
    • hypothyroidism/ hyperthyroidism
    • acts as hapten
      • corneal deposits
      • blue/ gray skin deposits → photodermatitis
    • neurologic effects
    • constipation
    • CV effects (bradycardia, heart block, HF)
85
Q

Amiodarone S/E

A
  • Iodine effects
    • pulmonary fibrosis
    • hepatotoxicity
    • hypothyroidism/ hyperthyroidism
  • Hapten effects
    • corneal deposits
    • blue/ gray skin deposits
    • photodermatitis
  • Neurologic effects
  • Constipation
  • CV effects (bradycardia, heart block, HF)
  • Blocks P450 (increases serum levels of certain drugs)
86
Q

Monitor what 3 things with Amiodarone?

A
  • Liver fcn (hepatotoxicity)
  • Pulmonary fcn (pulm fibrosis)
  • Thyroid fcn (hyper/hypothyroid)
87
Q

What makes Amiodarone unique?

A

Amiodarone is lipophilic and has antiarrhythmic class I, II, III, and IV effects

88
Q

What happens to cardiac AP w/Class III Antiarrhythmics?

A
  • Markedly prolonged repolarization
  • Increased AP duration
89
Q

Class IV Antiarrhythmic Drug Type

A

Calcium Channel Blockers

90
Q

Class IV Antiarrhythmic Drugs

A

Cardioselective:

  • Verapimil
  • Diltiazem

Vasoselective:

  • Nimodipine
91
Q

Class IV Antiarrhythmics MOA

A
  • Decrease conduction velocity thru AV node
  • Increase ERP
  • Increase PR interval
92
Q

Class IV Antiarrhythmics Clinical Use

A
  • Prevention of nodal arrhythmias (e.g., SVT)
  • Rate control in Afib
93
Q

Class IV Antiarrhythmics Toxicity

A
  • Constipation
    • Gastrin uses Ca2+ as 2nd messenger for motility
  • flushing
  • edema
  • Gingival hyperplasia
  • CV effects (HF, AV block, sinus node depression
94
Q

What happens to cardiac AP w/Class IV Antiarrhythmics?

A
  • Slow rise
  • prolonged repol @ AV node
  • Increased depol threshold
95
Q

Nitrates C/I

A

Sildenafil (Viagra) – PDE-5 inhibitor

  • Giving concurrently can cause severe hypOtension → death
96
Q

Adenosine MOA

A
  • Increases K+ movement out of cell → hyperpolarization, decreased intracellular Ca2+
  • Slows SA and AV node activity
  • Prolongs AV node refractory period
97
Q

Adenosine Clinical Use

A
  • Drug of choice for Dx/Rx SVT
  • Very short acting
  • Effects blunted by theophylline and caffeine (adenosine receptor antagonists)
98
Q

Drug of choice for Dx/Rx SVT

99
Q

Adenosine S/E

A
  • flushing
  • hypOtension
  • chest pain
  • sense of impending doom
  • bronchospasm
100
Q

Adenosine blocked by?

A
  • Theophylline
  • Caffeine
101
Q

2 Other drugs that act on K+ channels?

A

Opiates:

  • Open K+ channels and close Ca2+ channels
  • Hyperpol → prevent signal transmission of pain

Sulfonylurea:

  • Closes K+ channels
  • Easier depol → increased insulin release
102
Q

Magnesium MOA

A
  • Gets in the way of Na+
  • Blocks depolarization
103
Q

Magnesium clinical use

A
  • torsades de pointes
  • digoxin toxicity (arrhythmia)
104
Q

9 Treatment options for CHF

A
  1. Diuretics: furosemide, torsemide
  2. Positive inotropes: digoxin, dobutamine, dopamine
  3. Vasodilators: nitrates, nitroprusside, nesiritide, hydralazine
  4. ACE Inhibitors: captopril, enalapril, ramipril
  5. ARBs: losartan, valsartan
  6. Aldosterone Antagonists: spironolactone
  7. Beta-blockers: metoprolol, carvedilol
  8. Calcium Channel Blockers: diltiazem, verapamil
  9. Morphine (for acute Rx of assoc pulm edema)
105
Q

Class I Antiarrhythmic Drug Type

A

Fast Sodium Channel Blockers

106
Q

4 Compensatory Mechanisms in CHF

A
  1. Frank-Starling: increase preload
  2. Sympathetic Stim: increase HR & contractility
  3. RAA System: sodium & H2O retention → increase blood volume → increase venous return (preload)
  4. Hypertrophy: increase ventricular mm mass
107
Q

Cardiac remodeling

A
  • Occurs in chronic heart failure = unrelenting stimulation of heart tissue by NE, ATII, aldosterone + hypertrophy + sustained stress/pressure
    • Abnormal changes in gene expression
    • Increased cardiac myocyte apoptosis
    • Changes in heart shape and performance
108
Q

A failing heart does much worse very quickly when this happens

A

afterload increases → sharp decline in SV

109
Q

Treatment algorithm for systolic CHF

A
  • fluid retention should be treated before starting ACE inhibitor
  • Beta blockers should be started after fluid retention has been treated and/or dose of ACE inhibitor has been titrated
  • Pts that remain symptomatic can be given triple therapy: ARB + aldosterone antagonist (e.g. spironolactone) + digoxin
110
Q

Best diuretic for CHF

A

Loop diuretics (furosemide)

111
Q

3 drug types that reverse cardiac remodeling

A
  • ACE inhibitors or ARBs
  • Beta blockers
  • Aldosterone antagonists (e.g. spironolactone)
112
Q

Major sites of drug action in CHF

113
Q

This diuretic significantly reduces mortality in CHF

A

Spironolactone

114
Q

Diastolic vs. Systolic HF

115
Q

Goals for Treatment of Diastolic HF

A
  • Reduce HTN
  • Increase diastolic filling → rate control
  • Reduce edema
  • Reduce myocardial ischemia
  • Increase diastolic relaxation
116
Q

Best diuretic for HTN?

A

Hydrochlorothiazide

117
Q

Drugs C/I in Wolff-Parkinson-White Synd?

A
  • Calcium Channel Blockers (Class IV)
  • Digoxin

May cause Vfib

118
Q

Class of antiarrhythmics preferred for rate control in Afib?

A

Beta-blockers (Class II)

119
Q

preferred Na Channel blocker in Afib?

A

Flecainide (Class IC)

120
Q

Cardiac drugs that can cause lupus-like syndrome?

A
  • Procainamide
  • Hydralazine
121
Q

antiarrhythmic of choice in heart failure?

A

Amiodarone

122
Q

first-line agent for most cases of Afib requiring rhythm control?

A

Amiodarone

123
Q

drug of choice for acute paroxysmal SVT?

124
Q

beta-blocker adverse effects

A
  • fatigue
  • bronchospasm
  • bradycardia
  • peripheral vasospasm
  • decreased HDL, increased TG
  • mask signs of hypoglycemia in diabetics
  • insomnia, nightmares
  • ED
125
Q

Which drug is contraindicated in variant angina?

A

Beta-blockers

126
Q

Rx for CCB overdose?

A

IV calcium gluconate

127
Q

what effect does cimetidine have on CCBs?

A

increases bioavailability

128
Q

Ranolazine MOA

A
  • Not fully elucidated
  • Blocks late Na+ inward current in cardiomyocytes
    • Indirectly prevents intracellular Ca2+ overload due to ischemia
  • Partial fatty acid oxidation inhibitor
    • Shifts ATP production from fatty acid to carb oxidation
129
Q

Ranolazine Clinical Use

A

provide additional flexibility to existing medical therapies

130
Q

Ranolazine C/I

A

Preexisting QTc prolongation

131
Q

Ranolazine Interactions

A
  • Inhibitors of CYP3A increase plasma concentration of ranolazine
    • Ketoconazole, diltiazem, verapamil, macrolide antibiotics, protease inhibitors, grapefruit juice
  • Increases digoxin level 1.5x
132
Q

Class I antiarrhythmic subtype w/longest duration of action?

133
Q

Class I antiarrhythmic subtype w/shortest duration of action?

134
Q

Which antiarrhythmic is not indicated for SVT?

135
Q

Rx Torsades de Pointes

A

IV magnesium sulfate or isoproterenol

136
Q

Drugs Causing Prolonged QT Interval and/or TdP

A
  • Class Ia antiarrhythmics
  • Class III antiarrhythmics
  • Azole antifungals
  • Fluoroquinolone antibiotics
  • Macrolide antibiotics
  • Tricyclic antidepressants
  • Typical and atypical antipsychotics
  • Droperidol
  • Indapamide
  • Methadone
  • Ranolazine
  • Tamoxifen
  • TMP-SMX
137
Q

preferred drug for mild to moderate hypertension in the absence of comorbidity?

A

Hydrochlorothiazide

138
Q

Which anti-HTN drug can cause immune hemolytic anemia with positive Coombs test?

A

Methyldopa

139
Q

sudden withdrawal of alpha-2 blockers can cause what?

A

rebound HTN

140
Q

Rx for rebound HTN from withdrawal of alpha-2 blockers?

A

alpha blockers (phentolamine)

141
Q

Venodilators

A
  • Nitrates
  • ACE inhibitors
  • Alpha-1 antagonists
  • Nitroprusside
142
Q

Arteriodilators

A
  • Calcium channel blockers
  • Hydralazine
  • Minoxidil
143
Q

Rx cyanide toxicity

A
  • sodium thiosulfate
  • hydroxocobalamine
144
Q

Which drug can be used to treat hypoglycemia in insulinoma?

A

Diazoxide (K+ channel activator)

145
Q

Which CCBs reduce heart rate and contractility and block conduction at AV node?

A

Verapamil and diltiazem

146
Q

Which CCBs cause vasodilation leading to activation of sympathetic reflexes and may lead to increase in heart rate?

A

Nifedipine

147
Q

Other names for ACE?

A
  • Kininase II
  • peptidyl dipeptidase
148
Q

Rx low-renin HTN?

A
  • Diuretic + CCB
  • ACE inhibitors and ß-blockers are less effective in pts w/low renin levels when used as single agents
149
Q

This substance may play a key role in resistant HTN

A

aldosterone

150
Q

Cardiac remodeling mediated by these 3 substances

A
  1. Aldosterone
  2. ATII
  3. NE (increased symp outflow)
151
Q

Drug that can increase survival in pt w/decompensated HF and edema?

A

Spironolactone

152
Q

2 drugs usually assoc w/reflex tachycardia

A
  1. Nitrates
  2. DHP-CCBs
153
Q

3 drugs usually assoc w/bradycardia and hypotension

A
  • non-DHP CCBs
  • alpha-blockers
  • beta-blockers
154
Q

Early sign of digoxin toxicity

A

Stomach upset / nausea / loss of appetite

155
Q

drug that can decrease mortality in MI and/or decrease arrhythmia after MI

A

Beta-blockers

156
Q

this drug is C/I in heart failure in certain patients (elderly; past MI) b/c of its potent negative inotropic effect

A

Verapamil (Non-DHP CCB)

157
Q

4 Rx goals for heart failure

A
  1. decrease preload
  2. decrease afterload
  3. increase contractility
  4. decrease remodeling
158
Q

4 Drugs that can decrease preload

A
  1. Diuretics (loop, thiazide)
  2. ACE inhibitors
  3. ARBs
  4. Nitrates (venodilators)
159
Q

3 Drugs that can decrease afterload

A
  1. ACE inhibitors
  2. ARBs
  3. Hydralazine (arteriodilators)
160
Q

2 Drugs that can increase contractility

A
  1. Digoxin
  2. Beta-blockers
161
Q

5 Drugs that can decrease cardiac remodeling

A
  1. ACE inhibitors
  2. ARBs
  3. Spironolactone
  4. Beta-blockers (metoprolol, carvedilol)
  5. Hydralazine + nitrates
162
Q

this drug can cause constriction of the afferent arteriole in the kidney

A

Acetazolamide: blocks carbonic anhydrase → increased NaCl to macula densa → increase in signal for afferent constriction, decrease in renin secretion → decreased GFR

163
Q

Which CCBs are used for arrhythmias?

164
Q

Which CCBs are used for HTN?

165
Q

Non-DHP Calcium Channel Blocker MOA

A
  • Block voltage-gated L-type Ca2+ channels in SA and AV nodes
  • Increase duration of Phase 0 (nodal depolarization)
  • Decrease SA node automaticity
  • Slow conduction thru AV node
  • Decrease AV node rate of fire
  • Decrease contractility
166
Q

Drug type for VTAC?

A

Class III Antiarrhythmics – Potassium Channel Blockers

167
Q

What happens in an arrhythmia, how would you go about treating it, and how does each class of antiarrhythmic affect the physiology?

A
  • Problem w/conduction causes irregular beats
  • Target either myocyte AP or SA/AV nodal AP
    • Class I: Na+ Channel Blockers – Myocyte AP, decrease Phase 0 slope
    • Class II: Beta-blockers – Nodal AP, decrease Phase 4 slope
    • Class III: K+ Channel Blockers – Myocyte AP, elongate Phase 3 (increase QT)
    • Class IV: Non-DHP Ca2+ Channel Blockers – Nodal AP, increase Phase 0 slope
168
Q

What happens in each type of heart failure?

A
  • Generally: decreased CO → not enough O2 to tissues
  • Systolic: decreased inotropy (force of contaction) (weaker mm)
  • Diastolic: filling problem (bigger mm)
  • Left side: blood backs up into lungs → congestion
  • Right side: blood backs up into portal circulation → edema
169
Q

Cardiac myocyte AP

A
  • Phase 0: voltage-gated Na channels open → rapid depol
  • Phase 1: Na channels close, K channels open → initial repol
  • Phase 2: Ca channels open, balance K efflux → plateau + myocyte contraction
  • Phase 3: Ca channels close, voltage-gated K channels open → rapid repol
  • Phase 4: High K permeability → resting potential
170
Q

Cardiac Nodal AP

A
  • Phase 4: increased Na conductance → slow spontaneous depol (slope determines HR)
  • Phase 0: Ca channels open → rapid depol
  • Phase 3: Ca channels close, K channels open → rapid repol
171
Q

Compensation in Heart Failure

A
  • Increased SV
    • ADH, Aldosterone → increase filling volume → increase preload
    • Myocardial hypertrophy → increased force of contraction
  • Increased HR
    • SNS activation → increased rate of contraction
172
Q

Decompensation in Heart Failure

A

Compensatory mechanisms eventually lead to increased O2 demand, which exacerbates failure:

  • SNS overactivation → decreased receptor response
  • ADH/Aldosterone-mediated preload increase → increased myocardial O2 demand → cell death
  • Myocardial hypertrophy → increased myocardial O2 demand → cell death
173
Q

How would you treat the physiology of early heart failure?

A
  • Decrease preload (BP)
    • ACE inhibitors/ARBs
    • Hydralazine
    • Nitrates
  • Decrease SNS activation
    • Beta-blockers
174
Q

How would you treat the physiology of late heart failure?

A
  1. Aldosterone Antagonist Diuretics
    • Reduced fluid (congestion) and BP
  2. Ca2+ Channel Blockers
    • Arteriodilation + reduced HR (increased filling time)
  3. Digoxin
    • Increased contractility + reduced HR (increased filling time)
  4. ACE Inhibitors + Beta-blockers
    • Decreased BP
175
Q

CCB C/I

A
  • Heart failure (negative inotropic effect)
  • WPW (may accelerate conduction down accessory pathway → Vfib)
176
Q

1st line for most cases of Afib requiring rhythm control

A

Amiodarone (Class III K+ channel blocker)

177
Q

Drug of choice for acute paroxysmal supraventricular tachycardia?

178
Q

ACE inhibitors do this to the kidney

A

dilate efferent arteriole → reduce GFR → renal failure in pts w/existing problems (diabetics, renal aa stenosis)

179
Q

2 drugs that can decrease GFR

A
  • Acetazolamide (constrict afferent)
  • ACE inhibitors (dilate efferent)
180
Q

this beta blocker also acts as a direct vasodilator

A

Nevibolol → endothelial NO release

M2 - Pharm (10 decks)

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