1. General Cardiovascular Flashcards

1
Q

Treatment of Essential HTN

A
  • Diuretics
  • ACE inhibitors
  • Angiotensin II receptor blockers (ARBs)
  • Ca channel blockers
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2
Q

Treatment of HTN in CHF

A
  • Diuretics (usually loop, sometimes K sparing)
  • ACE inhibitors
  • ARBs
  • Beta blockers (OK in compensated CHF, use cautiously in uncompensated CHF, do NOT use in cardiogenic shock)
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3
Q

Treatment of HTN in Diabetes Mellitus

A
  • ACE inhibitors (also protective against diabetic nephropathy)
  • ARBs
  • Ca channel blockers
  • Diuretics
  • Beta blockers
  • Alpha blockers
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4
Q

Treatment of Malignant HTN

A
  • Nitroprusside
  • Fenoldopam
  • Diazoxide
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5
Q

Hydralazine - MOA

A
  • Increase cGMP –> smooth muscle relaxation

- Vasodilate arterioles more than veins –> afterload reduction

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6
Q

Hydralazine - Clinical Use

A
  • Severe HTN, CHF
  • First line for HTN in pregnancy with methyldopa
  • Frequently coadministered with a b-blocker to prevent reflex tachycardia
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7
Q

Hydralazine - Toxicities

A
  • Compensatory tachycardia –> CI in angina / coronary artery disease
  • Fluid retention, nausea, headache, angina
  • Lupus-like syndrome
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8
Q

Ca Channel Blockers - Available Drugs

A

Dihydropyridines:

  • Nifedipine
  • Amlodipine

Non-dihydropyridines:

  • Verapamil
  • Diltiazem
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9
Q

Ca Channel Blockers - MOA

A
  • Block voltage dependent L-type Ca channels or cardiac and smooth muscle thereby reducing muscle contractility.
  • In heart reduce conduction velocity, increase effective refractory period, increase PR interval
  • Vascular selectivity - Nifedipine > Diltiazem > Verapemil
  • Heart selectivity - Verapemil > Diltiezam > Nifedipine
    “Verapemil - Ventricle”

[Nifedipine, Amlodipine, Verapamil, Diltiazem]

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10
Q

Ca Channel Blockers - Clinical Use

A
  • HTN
  • Angina (Nifedipine - effects similar to Nitrates) (Verapamil - effects similar to b-blockers, use in asthmatics)
  • Arrhythmias, prevention of nodal ie SVT (not Nifedipine)
  • Prinzmetal’s angina
  • Raynaud’s

[Nifedipine, Amlodipine, Verapamil, Diltiazem]

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11
Q

Ca Channel Blockers - Toxicities

A
  • Cardiac depression, Sinus node depression
  • AV block, CHF
  • Peripheral edema
  • Flushing
  • Dizziness
  • Constipation

[Nifedipine, Amlodipine, Verapamil, Diltiazem]

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12
Q

Nitroprusside - MOA

A
  • Short acting

- Increase cGMP via direct release of NO

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13
Q

Nitroprusside - Clinical Use

A

Malignant HTN

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14
Q

Nitroprusside - Toxicities

A

Can cause Cyanide toxicity - releases CN

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15
Q

Fenoldopam - MOA

A
  • Dopamine D1 receptor agonist –> relaxes vascular smooth muscle
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16
Q

Fenoldopam - Clinical Use

A
  • Malignant HTN
17
Q

Diazoxide - MOA

A
  • K channel opener –> hyperpolarizes and relaxes vascular smooth muscle
18
Q

Diazoxide - Clinical Use

A
  • Malignant HTN
19
Q

Diazoxide - Toxicities

A
  • Hyperglycemia - reduces insulin release
20
Q

Nitrates - Available Drugs

A
  • Nitroglycerin

- Isosorbide dinitrate

21
Q

Nitrates - MOA

A
  • Vasodilate by releasing nitric oxide in smooth muscle –> increase cGMP –> smooth muscle relaxation
  • Dilate veins much more than arterioles –> preload reduction

[Nitroglycerin, Isosorbide dinitrate]

22
Q

Nitrates - Clinical Use

A
  • Angina
  • Pulmonary edema
  • Also used as an aphrodisiac and erection enhancer

[Nitroglycerin, Isosorbide dinitrate]

23
Q

Nitrates - Toxicities

A
  • Reflex tachycardia
  • Hypotension
  • Flushing
  • Headache
  • “Monday disease” in industrial exposure –> development of tolerance (tachyphylaxis) for vasodilating action during work week and loss of tolerance over the weekend resulting in tachycardia, dizziness and headache on reexposure on Monday

[Nitroglycerin, Isosorbide dinitrate]

24
Q

Anti-anginal Therapy

A
  • Nitrates
  • b-Blockers (ie Metoprolol, Atenolol, Cavedolol) (NOT Pindolol or Acebutelol - they are partial agonists)
  • Ca channel blockers
    • Nifedipine effects similar to Nitrates
    • Verapamil effects similar to b-Blockers, can use in asthmatics
25
Q

Nitrates in Anginal Therapy

A

Affect preload

  • Decrease end-diastolic volume
  • Decrease BP
  • Reflex increase in contractility
  • Reflex increase in HR
  • Decrease in ejection time
  • Decrease in Myocardial O2 consumption (MVO2)
26
Q

b-Blockers in Anginal Therapy

A

Affect afterload

  • Increase end-diastolic volume
  • Decrease BP
  • Decrease in contractility
  • Decrease in HR
  • Increase in ejection time
  • Decrease in Myocardial O2 consumption (MVO2)
27
Q

Nitrate + b-Blocker in Anginal Therapy

A
  • Little effect on end-diastolic volume
  • Decrease BP
  • Little effect on contractility
  • Decrease in HR
  • Little effect on ejection time
  • Large decrease in Myocardial O2 consumption (MVO2)
28
Q

Cardiac Glycosides - Available Drugs

A

Digoxin

29
Q

Digoxin - MOA

A
  • Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca antiporter –> increases intracellular Ca –> Positive inotropy.
  • Stimulates Vagus nerve
30
Q

Digoxin - Clinical Use

A
  • CHF (increases contractility)

- Atrial fibrillation (decreased conduction at AV node and depression of SA node)

31
Q

Digoxin - Toxicities

A
  • Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh)
  • ECG - Increased PR, decreased QT, scooping, T wave inversion, arrhythmia, hyperkalemia

Toxicities worsened by:

  • Renal failure - decreased drug excretion
  • Hypokalemia - Permissive for digoxin to bind at K binding site on Na/K ATPase
  • Quinidine - Decreased Digoxin clearance, and displaces Digoxin from tissue binding sites.
32
Q

Digoxin Overdose Antidote

A
  • Slowly normalize K
  • Lidocaine
  • Cardiac pacer
  • Anti-Digoxin Fab fragments
  • Mg
33
Q

Digoxin - Kinetics

A
  • 75% bioavailability
  • 20-40% protein bound
  • Half life = 40h
  • Urinary excretion
34
Q

Nesiritide - MOA

A
  • Recombinant B-type natriuretic peptide (BNP) –> Increase in cGMP and vasodilation –> Increase diuresis, decrease TPR.
35
Q

Nesiritide - Clinical Use

A
  • Acute decompensated heart failure
36
Q

Nesiritide - Toxicities

A
  • Hypotension