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Cardiology > 08: Drugs that Affect Vasculature > Flashcards

08: Drugs that Affect Vasculature Flashcards

1
Q

List the classes of cardiovascular drugs.

A
  1. Inotropic drugs and vasopressors
  2. Vasodilator drugs
  3. Antiadrenergic drugs
  4. Antiarrhythmic drugs
  5. Diuretics
  6. Antithrombotic drugs
  7. Lipid regulating drugs
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2
Q

What classes of drugs are used in the treatment of congestive heart failure?

A
  • Diuretics
  • Vasoactive drugs
  • Beta-blockers
  • Drugs affecting RAAS
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3
Q

What classes of drugs are used in the treatment of hypertension?

A
  • Diuretics
  • Adrenergic inhibitors
  • Direct vasodilators
  • Calcium channel blockers
  • RAAS blockers
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4
Q

What are the sub-classes of vasodilator drugs, and what are some examples under each?

A
  • _Venodilators _(↓pulmonary congestion)
    • Nitrates
  • Mixed vasodilators
    • ​Nitroprusside
    • ACE inhibitors & ARBs
    • alpha-adrenergic blockers
    • alpha-2-central agonists
    • Nesiritde
  • ​Arteriolar dilators (↑CO)
    • Hydralazine
    • Minoxidil
    • Calcium channel blockers
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5
Q

What drugs affect the vasculature?

A
  • Direct-acting vasodilators
  • Nitrates and phosphodiesterase-5 inhibitors
  • Calcium channel blockers (CCBs)
  • Anti-adrenergic drugs
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6
Q

List the four types of direct-acting vasodilators.

A
  1. Hydralazine
  2. Minoxidil
  3. Sodium nitroprusside
  4. Fenoldopam
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7
Q

Hydralazine

  1. Class
  2. Mechanism
  3. Net effect
  4. Indication
  5. Pharma
  6. SFx
  7. Other
A
  1. Direct vasodilator (precapillary arterioles)
  2. Unknown
  3. Fall in BP
  4. HTN w/ ↑creatinine (want to avoid ACEi or ARB); combo w/ isosorbide dinitrate to treat **systolic heart failure **(especially in black patients)
  5. Low bioavailability (extensive first pass hepatic metabolism); 50% of pts. fast acetylators; short half-life (2-4hr)–> take 2-3x/day but Fx persist up to 12 hr b/c bind avidly to vascular tissue
  6. Fall in BP –> baroreceptor-mediated ↑sympathetic outflow –> reflex tachy (palpitations); caution in patients with CAD (could precipitate myocardial ischemia); H/A, flushing, nausea, anorexia, **lupus-like syndrome **(slow acetylators)
  7. Primarily used in black CHF patients
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8
Q

Minoxidil

  1. Class
  2. Mechanism
  3. Net effect
  4. Indication
  5. Pharma
  6. SFx
  7. Other
A
  1. Direct vasodilator (arteriolar)
  2. ↑potassium channel permeability –> SMC hyperpolarization & relaxation
  3. ↓BP
  4. Severe/refractory HTN
  5. Good, reliable GI absorption; metabolized by hepatic glucuronidation; short half-life but longer pharma Fx
  6. Reflex adrenergic stimulation –>↑HR; decreased renal perfusion; **hypertrichosis **(XS hair growth); pericardial effusion (rare)
  7. Co-administer diuretic to increase renal perfusion
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9
Q

Sodium nitroprusside

  1. Class
  2. Mechanism
  3. Net effect
  4. Indication
  5. Pharma
  6. SFx
  7. Other
A
  1. Direct vasodilator (potent balanced)
  2. Broken into NO (vasodilation) and cyanide (converted to thiocyanate by liver and renally excreted)
  3. ↓arterial/systemic resistance, ↑venous capacitance
    • Normal LV funct: ↓CO 2/2 ↓venous return
    • Reduced LV funct: ↓systemic resistance (afterload) –> improved forward flow (CO)
  4. HTN emergency (potent & rapid; take with beta-blocker); severe CHF
  5. Continuous IV infusion; onset in 30 sec, peak in 2 min; Fx wane in minutes of discontinuation
  6. Thiocyanate accumulation/toxicity (blurred vision, tinnitus, disorientation, nausea); higher risk in setting of renal impairment
  7. Monitor serum levels if drug used for more than 24 hrs.
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10
Q

Nitrates

  1. Mechanism
  2. Net effect
  3. Indication
  4. Pharma
  5. SFx
  6. Other
A
  1. Vascular smooth muscle relaxation
  2. Venodilation (venous pooling, ↓venous return, ↓L/R sided filling), systemic arterial resistance unaffected, ↓CO 2/2 ↓preload; arteriolar dilation at higher doses (coronary arteries)
  3. Angina pectoris (↓LV preload –> ↓LV wall stress –> ↓myocardial O2 demand), acute coronary syndromes (e.g., coronary artery spasm), HF, angina pectoris prophylaxis, chronic management of CAD (long-acting nitrates: oral = isosorbide mono/dinitrate; transdermal patch or topical paste)
  4. Sublingual/sprays: peak action in 3 min, offset in 15-30min (liver deactivation)
  5. Drug tolerance develops, therefore “drug holiday” necessary to avoid tachyphylaxis
  6. Intravenous nitroglycerin given for acute treatment of hospitalized patient with unstable angina, pulmonary edema or heart failure (SFx = HoTN, reflex tachy, H/A, flushing)
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11
Q

Nitrates

  1. Mechanism
  2. Net effect
  3. Indication
  4. Pharma
  5. SFx
  6. Other
A
  1. Vascular smooth muscle relaxation
  2. Venodilation (venous pooling, ↓venous return, ↓L/R sided filling), systemic arterial resistance unaffected, ↓CO 2/2 ↓preload; arteriolar dilation at higher doses (coronary arteries)
  3. Angina pectoris (↓LV preload –> ↓LV wall stress –> ↓myocardial O2 demand), acute coronary syndromes (e.g., coronary artery spasm), HF, angina pectoris prophylaxis, chronic management of CAD (long-acting nitrates: oral = isosorbide mono/dinitrate; transdermal patch or topical paste)
  4. Sublingual/sprays: peak action in 3 min, offset in 15-30min (liver deactivation)
  5. Drug tolerance develops, therefore “drug holiday” necessary to avoid tachyphylaxis
  6. Intravenous nitroglycerin given for acute treatment of hospitalized patient with unstable angina, pulmonary edema or heart failure (SFx = HoTN, reflex tachy, H/A, flushing)
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12
Q

Sildenafil

  1. Class
  2. Mechanism
  3. Net effect
  4. Indication
  5. Other
A
  1. Phosphodiesterase-5 inhibitor
  2. Inhibits breakdown of cGMP in pulmonary vasculature
  3. Decreased pulmonary vascular resistance –> ↑vasodilation & oxygenation
  4. Pulmonary HTN
  5. Do not use with nitrates: results in severe systemic HoTN 2/2 ↓preload
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13
Q

Verapamil

  1. Class
  2. Net effect
  3. Indication
  4. Pharma
  5. SFx
A
  1. Non-dihydropyridine CCB
  2. Vasodilation (+), negative inotropy (+++), AV node suppression (+++)
  3. Angina pectoris, coronary artery spasm, hypertension, supraventricular arrhythmias
  4. PO, renal excretion
  5. HoTN, brady, AV block, constipation
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14
Q

Diltiazem

  1. Class
  2. Net effect
  3. Indication
  4. Pharma
  5. SFx
A
  1. Non-dihydropyridine CCB
  2. Vasodilation (++), negative inotropy (++), AV node suppression (++)
  3. Angina pectoris, coronary artery spasm, HTN, supraventricular arrhythmias
  4. PO, hepatic excretion
  5. HoTN, brady, peripheral edema
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15
Q

Alpha-2 Agonists

  1. Class
  2. Examples
  3. Distribution
  4. Net effect
  5. Other
A
  1. Anti-adrenergics
  2. Clonidine, alpha-methyldopa, guanabenz, guanfacine
  3. Presynaptic adrenergic nerve terminals, vascular SMCs (coronary & renal arterioles)
  4. ↓sympathetic outflow from medulla –> ↓PVR & ↓cardiac stimulation –> ↓BP, ↓HR
  5. Disuse leads to rebound HTN
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16
Q

Sympathetic Nerve-Ending Antagonists

  1. Class
  2. Examples
  3. Mechanism
  4. Net effect
  5. Pharma
  6. Other
A
  1. Anti-adrenergics
  2. Reserpine
  3. Inhibit uptake of NE into storage vesicles in postganglionic and central neurons –> NE degradation –> catecholamine depletion –> ↓TPR
  4. ↓TPR
  5. CNS toxicity (sedation, imparied concentration, psychotic depression)
  6. Rarely, if ever, prescribed
17
Q

Peripheral Alpha-Adrenergic Receptor Antagonists

  1. Class
  2. Examples
  3. Indications
  4. SFx
A
  1. Anti-adrenergics
  2. Selective (A-1): Prazosin, terazosin, doxazosin; non-selective (A-1, A-2): Phentolamine, phenoxybenzamine
  3. Selective: HTN (except doxazosin –>CHF; tx w/ thiazide diuretic), benign prostatic hypertrophy; non-selective: pheochromocytoma (rarely used otherwise)
  4. Non-selectives block presynaptic alpha 2 receptor –> interference w/ normal feedback inhibition of NE release –> pronounced reflex symp SFx (tachy, arrhythmias); Selectives: H/A, dizziness; Both: orthostatic HoTN
18
Q

Nifedipin

  1. Class
  2. Net effect
  3. Indication
  4. Pharma
  5. SFx
A
  1. Dihydropyridine CCB
  2. Vasodilation (+++), negative inotropy (0/+), AV node suppression (0)
  3. Coronary artery spasm, HTN
  4. PO, renal excretion
  5. HoTN, H/A, flushing, peripheral edema
19
Q

What is the general mechanism of calcium channel blockers (CCBs)? What are the two main groups?

A
  • Impede influx of calcium through membrane channels in cardiac and smooth muscle cells (particularly, L-type channels)
  • Decrease intracellular calcium concentration available to contractile proteins
    • Vascular SMCs: vasodilation
    • Cardiac cells: negative inotropic effect
  • Two main groups:
    • Non-dihydropyridines
    • Dihydropyridines

Cardiology (13 decks)

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