Nitrates, Antianginals, and Calcium Channel Blockers

Vocabulary practice flashcards covering coronary artery disease pathophysiology, types of angina, organic nitrates, beta-adrenergic antagonists, thrombolytics, myocardial infarction management, and the physiology and classification of calcium channel blockers.

Myocardial Ischemia

A condition in which the heart receives an insufficient amount of oxygen to meet its metabolic demands, resulting from an imbalance between myocardial oxygen supply and demand.

Atherosclerosis

A disease of the arteries characterized by the deposition of plaques of fatty, fibrous material (atheromas) on their inner walls, serving as the most common cause of coronary artery disease.

Arteriosclerosis

A vascular disorder characterized by the thickening and hardening of the inner and central walls of the artery.

Angina Pectoris

Acute chest pain caused by myocardial ischemia, classically presenting as a crushing sensation in the anterior chest that radiates to the left arm and scapula (or to the jaw in females), usually precipitated by physical exertion or emotional distress.

Stable Angina

A form of angina pectoris characterized by episodes that are fairly predictable in frequency, intensity, and duration, and are relieved by rest.

Vasospastic (Prinzmetal's) Angina

A type of angina caused by coronary artery spasms that may or may not involve atherosclerotic plaque.

Silent Angina

Myocardial ischemia that occurs in the absence of chest pain (asymptomatic), which carries a high risk for acute myocardial infarction and sudden death.

Unstable Angina

A medical emergency characterized by unexpected, suddenly occurring angina episodes that happen at rest.

Organic Nitrates

Drugs that release nitric oxide in vascular smooth muscle, dilating veins to reduce preload and dilating coronary arteries to terminate acute anginal episodes or prevent recurrent attacks.

Partial Fatty-Acid Oxidation Inhibitors

Antianginal agents that reduce the inflow of sodium and calcium ions into the myocardium, decreasing cellular metabolic rate and myocardial oxygen demand.

Methemoglobinemia

A serious potential adverse effect associated with organic nitrate pharmacotherapy.

Beta-Adrenergic Blockers (in Angina)

First-line prophylactic drugs for stable angina that selectively block $\beta_1$-adrenergic receptors in the heart to lower blood pressure, slow heart rate, reduce contractility, and decrease cardiac workload.

Myocardial Infarction (MI)

The complete cessation of blood flow to a portion of the myocardium—often following the rupture of an atherosclerotic plaque and clot formation—leading to myocardial muscle death.

Thrombolytics

Medications like alteplase (Activase) administered in early MI (ideally within $30\text{ minutes}$, effective between $20\text{ minutes}$ and $12\text{ hours}$, but of no benefit after $24\text{ hours}$) to dissolve occlusive clots and restore myocardial perfusion.

Cardiac Remodeling

A series of molecular, cellular, and interstitial changes altering the size, shape, mass, geometry, and function of the heart after injury; suppressed post-MI using ACE inhibitors such as captopril or lisinopril.

Cardiopulmonary Arrest

The complete cessation of cardiac and respiratory activity, commonly resulting from a dysrhythmia or pulseless ventricular tachycardia.

Vasopressors (in Cardiopulmonary Arrest)

Sympathomimetic agents, primarily epinephrine (or vasopressin as an alternative), administered following cardiac arrest to elevate blood pressure and reestablish coronary and cerebral perfusion.

Sarcolemma

The plasma membrane of muscle fibers that undergoes depolarization during an action potential, opening voltage-gated ion channels to permit calcium influx.

L-Type Calcium Channel

The primary, relatively slow voltage-gated calcium channel located on the sarcolemma of cardiac and vascular smooth muscle, responsible for sustained calcium entry during muscle contraction.

T-Type Calcium Channel

Low-voltage calcium channels found in vascular smooth muscle and the sinoatrial (SA) node; selectively blocked by ethosuximide (Zarontin).

N-Type Calcium Channel

Neuronal calcium channels distributed throughout the nervous system that regulate neurotransmitter release and pain transmission in the spinal cord; selectively blocked by ziconotide.

Negative Inotropic Effect

A reduction in the contractility or force of myocardial contraction, produced by decreased inward calcium influx during the plateau phase of the action potential.

Negative Chronotropic Effect

A decrease in heart rate resulting from fewer action potentials generated by the SA node and reduced automaticity.

Negative Dromotropic Effect

A reduction in the conduction velocity of electrical impulses through the atrioventricular (AV) node.

Dihydropyridines

A subclass of calcium channel blockers that bind reversibly to closed-type L-type calcium channels, exerting high selectivity for relaxing arterial smooth muscle with no clinically significant effect on cardiac inotropy, chronotropy, or dromotropy.

Non-Dihydropyridines

A subclass of calcium channel blockers (including verapamil and diltiazem) that bind open-type L-type calcium channels on both vascular smooth muscle and myocardium, reducing contractility, slowing sinus node rate, and delaying AV node conduction.

Amlodipine (Norvasc)

A dihydropyridine calcium channel blocker featuring the longest half-life in its class and once-daily dosing, prescribed for hypertension, chronic stable angina, and Prinzmetal's variant angina.

Clevidipine (Cleviprex)

An intravenous injectable emulsion dihydropyridine CCB that rapidly lowers systemic blood pressure within minutes.

Isradipine

The most potent dihydropyridine calcium channel blocker, utilized alone or alongside a thiazide diuretic for treating hypertension.

Verapamil (Calan, Isoptin, Verelan)

A phenylalkylamine non-dihydropyridine calcium channel blocker that decreases myocardial contractility and AV conduction velocity, acting as an antihypertensive, antianginal, and Class IV antidysrhythmic.

Sick Sinus Syndrome

A cardiac condition where a damaged SA node fails to reliably fire electrical impulses; it serves as a strict contraindication to non-dihydropyridine calcium channel blockers.