Pharmacological Management Of Heart And Vascular Disease Flashcards
Alpha Adrenergic Antagonists
Action: causes dilation of arterioles/veins and ↓ BP
MOA: Reduce peripheral vascular tone by blocking alpha-1-adrenergic receptors
PT implication: slow positions changes 2 º dizziness/OH
Angiotensin-Converting Enzyme (ACE) Inhibitors
Action: limits vasoconstriction (↓ BP and afterload)
MOA: suppress enzyme that converts angiotensin I to II
PT implications: slow position changes 2 º dizziness/ fainting, Pts with heart failure should avoid rapid ↑ in HR
Angiotensin II Receptor Antagonists
Action: limit vasoconstriction
MOA: block angiotensin II receptors
PT implications: none
Antiarrhythmic Agents (Class I-IV)
Action: control cardiac arrhythmias
MOA:
Class I: sodium channel blockers
Class II: inhibit sympathetic activity by blocking B-adrenergic receptors
*Class III: prolong repolarization by inhibiting K/Ca channels most effective
Class IV: depress depolarization and slows conduction through AV node
PT implications: adherence to dose schedule
Anticoagulant Agents
Action: blood thinner and slows clot formation
MOA: inhibits platelet aggregation and thrombus formation
PT implications: avoid injuries 2 º ↑ bleeding/bruising risk
Antihyperlipidemia Agents
Action: modifies lipids
MOA: statins inhibit enzyme action in cholesterol synthesis, ↓ LDL and triglycerides, and ↑ HDL, most commonly used
PT implications: aerobic exercise can also aid in ↑ HDL
Antithrombotic/Antiplatelet Agents
Action: prevents clot formation
MOA: inhibits platelet aggregation and clot formation
PT implications: avoid injuries 2 º ↑ bleeding/bruising risk
Beta Blocker Agents (Beta-Adrenergic Blocking Agents)
Action: decrease myocardial O2 demand by ↓ heart rate/contractility
MOA: blocks B-adrenergic receptors
PT implications: ↓ HR/BP response with activity, use RPE, OH
Calcium Channel Blockers
Action: ↓myocardial contraction, vasodilation, ↓ O2 demand of heart
MOA: ↓ Ca++ entry into smooth muscle
PT Implications: ↓ HR/BP response with activity, OH, s/s of heart failure (ie peripheral edema, dyspnea, weight gain)
Diuretic Agents
Action: ↓ BP
MOA: increase excretion of Na/urine
PT implication: OH, s/s electrolyte imbalance, muscle weakness, cramping
Nitrate Agents
Action: decrease ischemia
MOA: smooth muscle relaxation and vasodilation
PT Implications: OH, sublingual administration for acute angina attack
Positive Inotropic Agents
Action: increase force/velocity of myocardial contraction, ↓ HR
MOA:↓ conduction through AV node, ↓ SNS activation
PT Implications: monitor HR during activity, seek HCPs if rate < 60 or > 100 bpm
Thrombolytic Agents
Action: clot dissolution, reopens vessels to maintain blood flow
MOA: conversion of plasminogen to plasmin.
PT Implications: Avoid trauma due to altered clotting