Cardiac I – Pharmacology & Physiology Vocabulary

This set covers key vocabulary from the Cardiac I review: physiology (baroreceptors, RAAS), pathophysiology, major cardiovascular drug classes, prototypes, mechanisms, side effects, and critical nursing considerations.

Baroreceptors

Pressure-sensitive nerve endings in the carotid sinus and aortic arch that sense stretch and help regulate blood pressure.

Mean Arterial Pressure (MAP)

Average arterial pressure during a single cardiac cycle; primary indicator of tissue perfusion.

Cardiac accelerator/inhibitor centers

Regions in the medulla oblongata that adjust heart rate via sympathetic and parasympathetic (vagal) nerves.

Renin-Angiotensin-Aldosterone System (RAAS)

Hormonal cascade activated by low blood pressure or volume to raise BP and retain sodium and water.

Renin

Kidney enzyme that converts angiotensinogen to angiotensin I, initiating RAAS.

Angiotensinogen

Liver-produced plasma protein that is the substrate for renin.

Angiotensin-Converting Enzyme (ACE)

Lung-derived enzyme that converts angiotensin I to potent vasoconstrictor angiotensin II.

Angiotensin I

Inactive decapeptide formed from angiotensinogen; converted to angiotensin II by ACE.

Angiotensin II

Active octapeptide that causes vasoconstriction, stimulates aldosterone release, and triggers ADH secretion.

Aldosterone

Adrenal cortex hormone that increases renal re-absorption of Na⁺ and H₂O and excretion of K⁺.

Antidiuretic Hormone (ADH)

Posterior pituitary hormone that promotes water re-absorption in kidneys to raise blood volume.

RAAS Triggers

Low fluid volume, low sodium, or a drop in blood pressure.

RAAS Goals

Restore blood pressure, expand circulating volume, and conserve sodium.

Vasoconstriction

Narrowing of blood vessels, increasing systemic vascular resistance and blood pressure.

Sodium and Water Reabsorption

Process whereby kidneys reclaim Na⁺; water follows osmotically, expanding plasma volume.

Conditions Worsened by RAAS

Hypertension, atherosclerosis/CAD, diabetes, metabolic syndrome, LV hypertrophy, cardiac remodeling, heart failure.

ACE Inhibitors (ACEi)

“-pril” drugs that block ACE, lowering angiotensin II; treat HTN, HF, MI; adverse cough, hyperkalemia, angioedema.

Angiotensin II Receptor Blockers (ARBs)

“-sartan” drugs that block angiotensin II receptors; less cough, risk of angioedema & hyperkalemia.

ARNi (Sacubitril/Valsartan)

Combination that blocks angiotensin II receptors and prevents BNP breakdown to enhance natriuresis; used in HF.

Lisinopril

Prototype ACE inhibitor; monitor BP, K⁺, renal function; watch for cough and angioedema.

Losartan

Prototype ARB; lowers BP without ACE-induced cough; monitor for hypotension & hyperkalemia.

Entresto

Brand of Sacubitril/Valsartan; indicated for chronic heart failure with reduced EF.

Loop Diuretic

High-ceiling diuretic acting in ascending loop of Henle to block Na⁺/Cl⁻ reabsorption; potent fluid removal.

Furosemide

Prototype loop diuretic; rapid onset; risks: hypokalemia, dehydration, ototoxicity; push IV ≤20 mg/min.

Thiazide Diuretic

Diuretic acting in early distal tubule; moderate diuresis; ineffective with low GFR.

Hydrochlorothiazide

Prototype thiazide; common for HTN; watch photosensitivity, hypokalemia, dehydration.

Potassium-Sparing Diuretic

Weak diuretic that conserves K⁺ in late distal tubule/collecting duct; often combined with loops or thiazides.

Spironolactone

Aldosterone antagonist; risks hyperkalemia & endocrine effects (gynecomastia, hirsutism).

Osmotic Diuretic

Agent like mannitol that creates osmotic force, pulling water into renal tubule; used for cerebral edema.

Mannitol

IV osmotic diuretic; may cause peripheral edema, headache, electrolyte imbalance.

Orthostatic Hypotension

Drop in BP upon standing; common with diuretics & alpha blockers; teach slow position changes.

Hypokalemia

Serum K⁺ <3.5 mEq/L; risk with loop & thiazide diuretics; potentiates digoxin toxicity.

Hyperkalemia

Serum K⁺ >5.5 mEq/L; risk with ACEi, ARBs, potassium-sparing diuretics, salt substitutes.

Ototoxicity

Hearing damage linked to rapid IV furosemide administration; avoid pushing >20 mg/min.

Digoxin

Cardiac glycoside that increases intracellular Ca²⁺ to improve contractility; narrow range 0.8–2 ng/mL.

Digoxin Therapeutic Range

Serum level 0.8–2 ng/mL; toxicity signs: GI upset, visual halos, arrhythmias; monitor K⁺ & HR.

Calcium Channel Blockers (CCB)

Drugs that inhibit Ca²⁺ influx in vascular smooth muscle/myocardium; subclasses dihydropyridines and non-dihydropyridines.

Dihydropyridines (e.g., Amlodipine)

CCBs ending in “-dipine” that primarily vasodilate; minimal effect on HR.

Non-Dihydropyridines (Verapamil, Diltiazem)

CCBs that reduce HR and contractility; useful for rate control.

Nitroglycerin (NTG)

Short-acting nitrate for acute angina; take 1 tab SL, repeat q5 min up to 3 while seeking EMS.

Isosorbide Mononitrate

Long-acting oral nitrate (ImDur) for chronic angina prevention.

Hydralazine

Arterial vasodilator for hypertensive emergencies; often combined with beta blocker to prevent reflex tachycardia.

HMG-CoA Reductase Inhibitors (Statins)

Drugs that block cholesterol synthesis; reduce LDL; adverse myopathy, ↑T2DM risk.

Myopathy (Statin Adverse Effect)

Muscle pain or weakness; rare progression to rhabdomyolysis; report immediately.

Terazosin

Alpha-1 blocker for BPH; on Beers List due to risk of orthostatic hypotension in elders.

Clonidine

Central alpha-2 agonist that lowers sympathetic outflow; SE: drowsiness, dry mouth, bradycardia.

Beta Blockers (BB)

Drugs that lower HR and contractility; used in HTN, HF, post-MI; check HR before dosing.

Nursing Diuretic Considerations

Give early in day, monitor weight, I&O, BP, electrolytes (especially K⁺); educate on orthostatic safety.