Antihypertensive Drugs, Treatment of Angina Pectoris, Arrhythmias & CHF Flashcards
What are the two main components of blood pressure that antihypertensive medications work to change? (Think about the BP equation)
Cardiac output & total peripheral resistance (BP = CO x TPR)
What is the difference between Primary & Secondary HTN?
Primary accounts for 90% of patients and has no clear cause but is related to risk factors like diet, stress, genetics, smoking, alcohol and obesity that impact the SNS. Secondary accounts for 10% of patients and is the product of a different abnormality within the body (ex: chronic kidney disease, renal artery stenosis, and endocrine disorders)
What is Metabolic Syndrome?
Combination of metabolic abnormalities including impaired glucose metabolism, hyperinsulinemia, dyslipidemia, & abdominal obesity. Associated with hypertension
Common HTN Drug Management (5)
(1) Diuretics, (2) Sympatholytics, (3) Vasodilators, (4) Calcium-Channel Blockers & (5) Drugs that inhibit Renin-Angiotensin System
Diuretics - Mechanism of Action
Increase renal excretion of water and sodium in order to decreased fluid volume within the body
What is something that needs to be monitored in patients that are on diuretics?
Potassium levels. Along with sodium & water, renal excretion leads to a loss of potassium. Patients should be on potassium supplements and/or get their blood levels checked for potassium to ensure appropriate levels (reduce risk of arrhythmias)
Types of Diuretics (3)
Thiazide (Hydrochlorothiazide), Loop Diuretics (Lasix), & Potassium Sparing Diuretics
What population should Thiazide diuretics NOT be given to?
Geriatric population - Patients need to have good kidney function for this form of diuretic
What are the adverse effects of Diuretics?
Fluid depletion, electrolyte imbalance, hyponatremia, hypokalemia (Loop & Thiazide), orthostatic hypotension, impaired glucose/lipid metabolism, fatigue
“Up all night peeing” - Increased urinary frequency (fall risk for elderly)
Can increase CO & TPR due to decreased blood volume related to fluid depletion
Sympatholytic Drugs (4)
(1) Beta blockers, (2) Alpha blockers, (3) Presynaptic adrenergic inhibitors & (4) Centrally acting agonists
Beta Blockers
Reduce HTN by decreasing CO (lower myocardial contractility) and slowing HR
Compliment other hypertensive drugs - Used frequently in combination
Examples: Ending in “-lol”
Carvedilol, Propranolol & Metoprolol
What are some potential side effects of Beta Blockers?
Excessive decrease in HR, orthostatic hypotension, impaired glucose/lipid metabolism, depression, fatigue, GI issues, allergic reactions, blunted exercise HR.
Nonselective blockers will impact more than just the heart - can cause bronchoconstriction
Alpha Blockers
Promote decreased vascular resistance by binding to vascular smooth muscle. Improve blood lipid profiles by decreasing triglycerides & total cholesterol
Examples: Doxazosin & Prazosin
What are the adverse effects of Alpha Blockers?
Reflex Tachycardia (Reaction of baroreceptors after fall in TPR - *Wont happen if used with beta blocker)
Orthostatic hypotension & increased risk of cardiac disease and congestive heart failure due to vasodilation causing increased heart workload
What type of patients should AVOID using Alpha Blockers?
Patients at risk for heart failure or cardiac disease
Presynaptic Adrenergic Inhibitors
Decrease blood pressure by inhibiting release of NE from presynaptic terminals which decreases sympathetic excitation of the heart and vasculature
What are some adverse effects of Presynaptic Adrenergic Inhibitors?
Bradycardia, arrhythmias, drowsiness, & GI disturbances
Centrally Acting Agents
Decrease blood pressure & cardiovascular stimulation by inhibiting sympathetic discharge from brainstem
Example: Clonidine
What are potential side effects of Centrally Acting Agents?
Dry mouth, dizziness & sedation
General side effects of Vasodilators
Reflexive tachycardia, dizziness, orthostatic hypotension, weakness, nausea, fluid retention, & headache
What is Renin?
Enzyme produced in the kidneys that is released when the body senses a decrease in blood pressure
What occurs when Renin & Angiotensinogen combine?
Transform into Angiotensin I
What is the function of Angiotensin Converting Enzyme?
Converting Angiotensin I into Angiotensin II which is a strong vasoconstrictor (increases blood pressure)
What are the three types of Renin-Angiotensin System Inhibitors?
(1) ACE Inhibitors (2) Angiotensin II Receptor Blockers/Antagonists (ARBs) & (3) Direct Renin Inhibitors
ACE Inhibitors
Cause vasodilation in order to decrease BP.
Inhibit the enzyme used to convert Angiotensin I into Angiotensin II (vasoconstrictor).
Angiotensin II Receptor Blockers (ARBs)
Block receptor for Angiotensin II, which restricts it from causing vasoconstriction. Results in vasodilation and decreased BP.
Direct Renin Inhibitors
Inhibit conversion of Renin & Angiotensinogen into Angiotensin I. Result in vasodilation & decreased BP.
Adverse Effects of Renin-Angiotensin System Inhibitors
Dry & persistent cough! (NOT ARBs)
Allergic reaction (rash), angioedema, hyperkalemia, & GI problems
Calcium Channel Blockers
Block Ca2+ entry into vascular smooth muscle cells which inhibit contractility and lead to vasodilation/decreased resistance
Examples: Amlodipine, Diltiazem, Verapamil
Adverse Effects of Calcium Channel Blockers
Excessive vasodilation (swelling), orthostatic hypotension, & heart rate abnormalities
Stages of Hypertension (4)
Normal: <120/80 mmHg
Pre-Hypertensive: 120-139/80-89 mmHg
Stage 1 Hypertension: 140-159/90-99 mmHg
Stage 2 Hypertension: >159/99 mmHg
HTN Progression of Treatment
Stage 1 HTN treated with one form of medication (diuretic, calcium channel blocker, ACE inhibitor or ARB)
Stage 2 HTN treated with two “first line of defense” drugs (2 of the above medications)
Rehab Implications for HTN
Monitor for Hypotension & Orthostatic Hypotension
Avoid activity that will increase widespread vasodilation (Whirlpool/Hubbard tanks)
Potential for blunted HR response to exercise – Use RPE scales!
What is Angina Pectoris?
Intense compression and tightness in the sternal region occurring during ischemic heart disease. Can radiate to the jaw or left arm.
Result of myocardial oxygen supply & demand imbalance leading to increased lactic acid accumulation
Drug Treatments for Angina Pectoris (3)
(1) Organic Nitrates (2) Beta Blockers & (3) Calcium Channel Blockers
Organic Nitrates
Convert into nitric oxide within vascular smooth muscle to cause vasodilation. Decreases cardiac preload
Examples: Nitroglycerin, isosorbide dinitrate, & isosorbide mononitrate
Therapeutic Effect of Nitroglycerin
Therapeutic effect sets in within 2 minutes (usually sublingually) - AVOIDS the first pass effect of the liver and is able to initiate its effects quickly
Adverse Effects of Nitroglycerin/Organic Nitrates
Headache, dizziness, & orthostatic hypotension (result of increased vasodilation)
Anticoagulants for Angina Pectoris
Prevent coronary arteries from becoming completely blocked by clot formation. Examples: Aspirin, Plavix, & Heparin
Stable Angina
Exertional Angina - Certain point of onset with activity. Result of myocardial oxygen demand greatly exceeding oxygen supply
Treatment for Stable Angina
Beta blockers (preventative & initial treatment), calcium channel blockers, & organic nitrates (acute episodes)
Variant Angina
Vasospasm causes decrease in myocardial oxygen. Occurs at rest & with activity. Environmental & emotional stimuli may play a role as well.
Treatment for Variant Angina
Calcium channel blockers are most effective
Unstable Angina
Most severe form of angina. Sudden rupture of atherosclerotic plaques within the coronary arteries causing vasoconstriction & thrombus formation.
Precursor to acute MI - 1 of 3 conditions under Acute Coronary Syndrome
Treatment for Unstable Angina
Anticoagulants & antiplatelet therapy is essential for prevention of MI.
ACE Inhibitors & statins are also used.
Rehab Implications for Angina Pectoris
Increased myocardial oxygen demand during exercise can cause angina attack - Have nitroglycerin tablets available & do NOT overtax patients.
Blunted HR response to exercise is possible
What are the 3 basic abnormalities that can cause an arrhythmia?
(1) Abnormal impulse generation
(2) Abnormal impulse conduction
(3) Simultaneous abnormalities
List the 4 classes of Anti-Arrhythmic Drugs
Class I: Sodium Channel Blockers
Class II: Beta Blockers
Class III: Drugs that prolong repolarization
Class IV: Calcium Channel Blockers
Class I: Sodium Channel Blockers
Inhibit sodium channels in cardiac tissues to decrease membrane excitability and normalize rate of firing
Class IA, IB, & IC
Most common side effect of Sodium Channel Blockers
Pro-arrhythmic effect - Tendency for increased rhythm disturbances. Others include dizziness, visual disturbances, and GI issues
Class III: Drugs that prolong repolarization
Delay repolarization of cardiac cells in order to lengthen the time interval between action potentials - Slows and stabilizes heart rate
Treat ventricular arrhythmias (V-tach, V-fib, SVT)
Example: Amiodarone (properties of class I, II & III)
Side effects of Amiodarone (Class III)
Pulmonary toxicity, thyroid problems, and liver damage. Can increase proarrhythmic effects
Combination of Class I, II, & III anti-arrhythmic drugs
Class IV: Calcium Channel Blockers (What form of arrhythmia is commonly treated with these drugs?)
Atrial Fibrillation
Work by decreasing rate of SA node discharge and inhibiting conduction velocity through AV node
Rehab Implications for Arrhythmias
Know signs of Cardiotoxicity (faintness & dizziness) and Hypotension
What is important to do in patients with an arrhythmia?
Take pulse rate for the FULL 60 seconds
2 main goals of Congestive Heart Failure treatment?
- Increase myocardial contractility (Positive Inotropic Agents)
- Decrease cardiac workload
What drug is classified as a Positive Inotropic Agent?
Digoxin (Cardiac Glycosides)
What drugs work to decrease cardiac workload?
ACE inhibitors, ARBs, Beta Blockers, Diuretics, & Vasodilators
Cardiac Glycosides (DIGITALIS)
Two types: Digoxin (only one used in U.S.) & Digitoxin
Improves pumping action of heart by increasing intracellular calcium; increases CO and exercise tolerance. Decreases symptoms of heart failure & CHF hospitalizations
What kind of effect does Digitalis have on the SNS?
Inhibitory effect - Decreases stress on heart, slows HR, and slows impulse conduction
What do PTs need to be aware of when working with patients on Digitalis?
Digitalis Toxicity! Overdoses can become fatal.
Signs of Digitalis Toxicity
GI distress (N/V, diarreha), CNS disturbances (drowsiness/fatigue/confusion/visual disturbances), Cardiac function abnormalities (arrhythmia, PVC, v-tach, heart blocks)
Can lead to V-fib & death
When are ACE inhibitors most effective in treating CHF?
When patients are experiencing heart failure due to reduced left ventricular function (systolic heart failure)
What needs to be considered when using Diuretics in patients with CHF?
Whether or not they have chronic kidney disease/kidney issues as well. Diuretics can help CHF by increasing renal secretion but can make kidney function worse
Rehab Implications for CHF Treatment
Watch for S/S of acute congestive heart failure, digoxin toxicity, fluid/electrolyte depletion & hypotension
Signs of Acute CHF
Increased cough, difficulty breathing, dyspnea, and abnormal respiratory sounds
Signs of Digoxin Toxicity in Rehab
Dizziness, confusion, nausea, & arrhythmias
Signs of Fluid/Electrolyte Depletion
Fatigue & weakness can be early signs
