RNSG 1018B Unit 4 Pharmacology Flashcards

Vocabulary flashcards covering classes of antihypertensive drugs, antihypotensives, vasopressors, heart failure medications, and antiarrhythmics based on Unit 4 lecture tables.

ACE Inhibitors

Class of antihypertensives (e.g., Lisinopril, Benazepril, Enalapril) that blocks conversion of Angiotensin I to Angiotensin II, decreases aldosterone, and reduces afterload/preload. Characterized by persistent dry cough, hyperkalemia, angioedema, and a Black Box warning for teratogenicity.

Angiotensin II Receptor Blockers (ARBs)

Class of antihypertensives (e.g., Losartan, Valsartan) that selectively blocks Angiotensin II binding at smooth muscle and adrenal receptors. Serves as an alternative for patients who develop an ACE-inhibitor cough; carries teratogenic risks.

Direct Renin Inhibitors

Antihypertensive drug (Aliskiren) that inhibits renin directly, stopping conversion of angiotensinogen to Angiotensin I. Has poor oral absorption and must not be taken with high-fat meals or concurrent ACEi/ARBs.

Calcium Channel Blockers (CCBs)

Drug class (e.g., Amlodipine, Diltiazem, Verapamil, Nicardipine) that inhibits $\text{Ca}^{2+}$ movement across cardiac/vascular smooth muscle membranes, causing vasodilation and decreased cardiac workload. Patients must avoid grapefruit juice.

Vasodilators

Antihypertensive agents (e.g., Hydralazine, Nitroglycerin, Nitroprusside) that directly relax vascular smooth muscle to reduce systemic vascular resistance. Nitroprusside infusions require close monitoring for cyanide toxicity.

SNS Blockers / Adrenergic Antagonists

Drug class including Beta-blockers, Alpha-1 blockers, and Central Alpha-2 agonists that blocks sympathetic drive to lower HR, contractility, and vascular resistance. Must not be stopped abruptly due to risk of rebound hypertensive crisis.

Sympathetic Adrenergic Agonists (Vasopressors)

First-line agents for shock and severe refractory hypotension (e.g., Norepinephrine, Dopamine, Vasopressin) that stimulate $\alpha$- and $\beta$-adrenergic receptors to cause vasoconstriction and increase cardiac output. Administered via central line.

Midodrine

Oral selective $\alpha_1$-agonist causing arterial and venous constriction, indicated for symptomatic orthostatic hypotension. Doses must be avoided within $4\,\text{hours}$ of bedtime to prevent supine hypertension.

Droxidopa

Prodrug converted to norepinephrine by dopa-decarboxylase, indicated for neurogenic orthostatic hypotension. Carries a boxed warning for supine hypertension and requires sleeping with the head of the bed elevated.

Cardiac Glycosides (Digoxin)

Heart failure drug providing positive inotropic and negative chronotropic effects. Requires checking apical pulse for $1\,\text{full minute}$ (hold if $\text{HR} < 60\,\text{bpm}$) and maintaining a therapeutic range of $0.5\text{--}2.0\,\text{ng/mL}$. Antidote is Digoxin Immune Fab (Digifab).

Phosphodiesterase (PDE) Inhibitors (Milrinone)

Heart failure drug that blocks the PDE enzyme to increase intracellular $\text{cAMP}$ and $\text{Ca}^{2+}$, increasing contractility and vasodilation. Administered IV only for short-term management of acute decompensated heart failure in ICU settings.

HCN Channel Blockers (Ivabradine)

Drug that inhibits $I_f$ pacemaker current in the SA node to slow heart rate without affecting contractility. Indicated to lower heart failure hospitalization risk in patients with resting $\text{HR} \ge 70\,\text{bpm}$ on max-tolerated beta-blocker dose; causes luminous phenomena (phosphenes).

Angiotensin Receptor-Neprilysin Inhibitors (ARNI)

Combination medication Entresto (Sacubitril/Valsartan) where Sacubitril inhibits neprilysin and Valsartan blocks ARB receptors. Requires a $36\text{-hour}$ washout period when switching from an ACE inhibitor to prevent severe angioedema.

Class 1 Antiarrhythmics

Sodium channel blockers that act as membrane-stabilizing agents by inhibiting fast sodium channels during $\text{Phase 0}$ of the cardiac action potential.

Class 1A Antiarrhythmics

Sodium channel blockers (Quinidine, Procainamide, Disopyramide) that depress $\text{Phase 0}$ and prolong action potential duration and repolarization. Procainamide requires long-term monitoring for positive ANA titers and drug-induced Lupus-like syndrome.

Class 1B Antiarrhythmics

Sodium channel blockers (Lidocaine, Mexiletine) that depress $\text{Phase 0}$ slightly and shorten action potential duration. Effective only against ventricular arrhythmias; slurred speech, confusion, or twitching indicates Lidocaine toxicity requiring immediate infusion stoppage.

Class 1C Antiarrhythmics

Sodium channel blockers (Flecainide, Propafenone) that markedly depress $\text{Phase 0}$ with no effect on action potential duration. Strictly contraindicated in structural heart disease or prior MI due to sudden cardiac death risk (CAST Trial).

Class 1D Antiarrhythmics (Ranolazine)

Antiarrhythmic drug that inhibits late inward sodium current ($\text{INaL}$) for chronic angina. Does not significantly affect HR or BP, but can prolong QT interval.

Class 2 Antiarrhythmics (Beta-Blockers)

Drugs (Metoprolol, Propranolol, Esmolol, Atenolol) that competitively block $\beta_1$-adrenergic receptors, depressing $\text{Phase 4}$ automaticity and slowing AV node conduction. Carries a Black Box Warning against abrupt discontinuation.

Adenosine

Antiarrhythmic agent that slows conduction time through the AV node to rapidly convert Paroxysmal Supraventricular Tachycardia (PSVT) to sinus rhythm. Efficacy is reduced by caffeine and theophylline.

Class 3 Antiarrhythmics

Potassium channel blockers (Amiodarone, Sotalol, Dofetilide, Ibutilide) that prolong $\text{Phase 3}$ repolarization and effective refractory period. Amiodarone requires baseline chest X-ray, PFTs, LFTs, and thyroid panels due to organ toxicity risk.

Verapamil

Class 4 antiarrhythmic selective for cardiac tissue, causing pronounced negative inotropic and negative dromotropic effects. Common side effect is severe constipation; elevates serum digoxin levels by $50\text{--}70\%$.

Diltiazem

Class 4 antiarrhythmic with balanced selectivity between cardiac tissue and vascular smooth muscle, acting as a moderate negative inotrope and strong depressant of SA and AV node conduction.