Hypertesive

β₁-blocker

slow heart rate, dialate vessels

Hypertesive

centrally acting α₂  blocker

decrease BP by decreasing symp outflow from medulla

emergencies

ACE inhibitor

prevent ACE from producing agiotension II

decrease blood volume and pressure

Angiotension II receptor blocker

block vasoconstriction and aldostersone secretion

decrease BP by antagonizing effects of angiotension in vascular SM

Class IV (Ca²⁺ channel blocker) - vasodilation, increase O2 supply, slow conduction at AV node

vasodialation (relax SM), decrase heart rate

Stabilize dysrhythmia, HTN, & angina

Vasodialators

relaxation of vascular SM to decrease peripheral resistance, increase blood flow, decrease BP

inadequate as sole therapy, must be combo with β-blocker or diuretic

Peripherally acting α-blocker

depletes NE storage

decreases vascular tone and BP

only used for severe emergencies

Peripherally acting α-blocker

depletes NE storage

decreases vascular tone and BP

only used for severe emergencies

Peripherally acting irreversible α-blocker

decreases vascular tone and BP

only used for severe emergencies, longer lasting

Loop Diuretic

inhibit Na & Cl reabsorption

increase Na, Cl, K, & H₂0 excretion

rapid H₂0 loss, O₂ toxicity

Loop Diuretic

inhibit Na & Cl reabsorption

increase Na, Cl, K, & H₂0 excretion

rapid H₂0 loss, O₂ toxicity

Potassium sparing diuretic

block Na⁺ channel for reabsorbtion in DCT and collecting duct

mild diuresis, paired with another diuretic

nicotinic antagonist

used for hypertensive emergencies during surgery

renin inhibitor

inhibitits conversion of angiotensinogin to angiotension I, so angiotension II and aldosterterone are not produced, thus brain not signaled to increase BP

Miscellaneous

Decrease in live triglyceride synthesis, required for VLDL, LDL

Decrease VLDL, LDL, and total cholesterol

Nitrate

Dilate blood vessels, decrease O2 demand, increase O2 supply

stop acute angina attack

Nitrate

Dilate blood vessels, decrease O2 demand, increase O2 supply

Use for all type of angina pectoris

β₁ - blocker

decreases rate and force of heart contractions

rapid onset, short duration

Anginal and Anti-Dysrhythmic Agents

Class 1a - bind to sodium channel; intermediate onset & offset

slows conduction velocity (mild), prolongs AP

Anti-Anginal and Anti-Dysrhythmic Agents

Class 1b - bind to sodium channel; short effects

Anti-Anginal and Anti-Dysrhythmic Agents

Class 1c - bind to sodium channel; prolonged effects

Anti-Anginal and Anti-Dysrhythmic Agents

Class III - block K⁺ (and some Na⁺⁾ channels

stabilize dysrhythmia by slowing conduction at AV node

Can cause deposit on cornea, optic neuritis, and colon deposits

Cardiac Glycosides

Inhitbit ATPase, increase intracellular [Ca²⁺]

Decrease heart size, increase renal blood flow

Use for CHF, atrial fibrillation and flutter

Low therapeutic index

Phosphodiesterase inhibitor

increase myocardial contractions and cause vasodilation

used in short term acute heart failure

Phosphodiesterase inhibitor

increase myocardial contractions and cause vasodilation

used in short term acute heart failure

Aldosterone Antagonist

used for management of chronic heart failure for myocardial infarction

K⁺ sparing diuretic