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Pharmacotherapeutics > Antihypertensive Drugs, Treatment of Angina Pectoris, Arrhythmias & CHF > Flashcards

Antihypertensive Drugs, Treatment of Angina Pectoris, Arrhythmias & CHF Flashcards

1
Q

What are the two main components of blood pressure that antihypertensive medications work to change? (Think about the BP equation)

A

Cardiac output & total peripheral resistance (BP = CO x TPR)

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2
Q

What is the difference between Primary & Secondary HTN?

A

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)

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3
Q

What is Metabolic Syndrome?

A

Combination of metabolic abnormalities including impaired glucose metabolism, hyperinsulinemia, dyslipidemia, & abdominal obesity. Associated with hypertension

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4
Q

Common HTN Drug Management (5)

A

(1) Diuretics, (2) Sympatholytics, (3) Vasodilators, (4) Calcium-Channel Blockers & (5) Drugs that inhibit Renin-Angiotensin System

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5
Q

Diuretics - Mechanism of Action

A

Increase renal excretion of water and sodium in order to decreased fluid volume within the body

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6
Q

What is something that needs to be monitored in patients that are on diuretics?

A

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)

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7
Q

Types of Diuretics (3)

A

Thiazide (Hydrochlorothiazide), Loop Diuretics (Lasix), & Potassium Sparing Diuretics

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8
Q

What population should Thiazide diuretics NOT be given to?

A

Geriatric population - Patients need to have good kidney function for this form of diuretic

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9
Q

What are the adverse effects of Diuretics?

A

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

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10
Q

Sympatholytic Drugs (4)

A

(1) Beta blockers, (2) Alpha blockers, (3) Presynaptic adrenergic inhibitors & (4) Centrally acting agonists

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11
Q

Beta Blockers

A

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

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12
Q

What are some potential side effects of Beta Blockers?

A

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

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13
Q

Alpha Blockers

A

Promote decreased vascular resistance by binding to vascular smooth muscle. Improve blood lipid profiles by decreasing triglycerides & total cholesterol

Examples: Doxazosin & Prazosin

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14
Q

What are the adverse effects of Alpha Blockers?

A

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

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15
Q

What type of patients should AVOID using Alpha Blockers?

A

Patients at risk for heart failure or cardiac disease

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16
Q

Presynaptic Adrenergic Inhibitors

A

Decrease blood pressure by inhibiting release of NE from presynaptic terminals which decreases sympathetic excitation of the heart and vasculature

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17
Q

What are some adverse effects of Presynaptic Adrenergic Inhibitors?

A

Bradycardia, arrhythmias, drowsiness, & GI disturbances

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18
Q

Centrally Acting Agents

A

Decrease blood pressure & cardiovascular stimulation by inhibiting sympathetic discharge from brainstem

Example: Clonidine

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19
Q

What are potential side effects of Centrally Acting Agents?

A

Dry mouth, dizziness & sedation

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20
Q

General side effects of Vasodilators

A

Reflexive tachycardia, dizziness, orthostatic hypotension, weakness, nausea, fluid retention, & headache

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21
Q

What is Renin?

A

Enzyme produced in the kidneys that is released when the body senses a decrease in blood pressure

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22
Q

What occurs when Renin & Angiotensinogen combine?

A

Transform into Angiotensin I

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23
Q

What is the function of Angiotensin Converting Enzyme?

A

Converting Angiotensin I into Angiotensin II which is a strong vasoconstrictor (increases blood pressure)

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24
Q

What are the three types of Renin-Angiotensin System Inhibitors?

A

(1) ACE Inhibitors (2) Angiotensin II Receptor Blockers/Antagonists (ARBs) & (3) Direct Renin Inhibitors

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25
Q

ACE Inhibitors

A

Cause vasodilation in order to decrease BP.

Inhibit the enzyme used to convert Angiotensin I into Angiotensin II (vasoconstrictor).

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26
Q

Angiotensin II Receptor Blockers (ARBs)

A

Block receptor for Angiotensin II, which restricts it from causing vasoconstriction. Results in vasodilation and decreased BP.

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27
Q

Direct Renin Inhibitors

A

Inhibit conversion of Renin & Angiotensinogen into Angiotensin I. Result in vasodilation & decreased BP.

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28
Q

Adverse Effects of Renin-Angiotensin System Inhibitors

A

Dry & persistent cough! (NOT ARBs)

Allergic reaction (rash), angioedema, hyperkalemia, & GI problems

29
Q

Calcium Channel Blockers

A

Block Ca2+ entry into vascular smooth muscle cells which inhibit contractility and lead to vasodilation/decreased resistance

Examples: Amlodipine, Diltiazem, Verapamil

30
Q

Adverse Effects of Calcium Channel Blockers

A

Excessive vasodilation (swelling), orthostatic hypotension, & heart rate abnormalities

31
Q

Stages of Hypertension (4)

A

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

32
Q

HTN Progression of Treatment

A

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)

33
Q

Rehab Implications for HTN

A

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!

34
Q

What is Angina Pectoris?

A

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

35
Q

Drug Treatments for Angina Pectoris (3)

A

(1) Organic Nitrates (2) Beta Blockers & (3) Calcium Channel Blockers

36
Q

Organic Nitrates

A

Convert into nitric oxide within vascular smooth muscle to cause vasodilation. Decreases cardiac preload

Examples: Nitroglycerin, isosorbide dinitrate, & isosorbide mononitrate

37
Q

Therapeutic Effect of Nitroglycerin

A

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

38
Q

Adverse Effects of Nitroglycerin/Organic Nitrates

A

Headache, dizziness, & orthostatic hypotension (result of increased vasodilation)

39
Q

Anticoagulants for Angina Pectoris

A

Prevent coronary arteries from becoming completely blocked by clot formation. Examples: Aspirin, Plavix, & Heparin

40
Q

Stable Angina

A

Exertional Angina - Certain point of onset with activity. Result of myocardial oxygen demand greatly exceeding oxygen supply

41
Q

Treatment for Stable Angina

A

Beta blockers (preventative & initial treatment), calcium channel blockers, & organic nitrates (acute episodes)

42
Q

Variant Angina

A

Vasospasm causes decrease in myocardial oxygen. Occurs at rest & with activity. Environmental & emotional stimuli may play a role as well.

43
Q

Treatment for Variant Angina

A

Calcium channel blockers are most effective

44
Q

Unstable Angina

A

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

45
Q

Treatment for Unstable Angina

A

Anticoagulants & antiplatelet therapy is essential for prevention of MI.

ACE Inhibitors & statins are also used.

46
Q

Rehab Implications for Angina Pectoris

A

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

47
Q

What are the 3 basic abnormalities that can cause an arrhythmia?

A

(1) Abnormal impulse generation
(2) Abnormal impulse conduction
(3) Simultaneous abnormalities

48
Q

List the 4 classes of Anti-Arrhythmic Drugs

A

Class I: Sodium Channel Blockers
Class II: Beta Blockers
Class III: Drugs that prolong repolarization
Class IV: Calcium Channel Blockers

49
Q

Class I: Sodium Channel Blockers

A

Inhibit sodium channels in cardiac tissues to decrease membrane excitability and normalize rate of firing

Class IA, IB, & IC

50
Q

Most common side effect of Sodium Channel Blockers

A

Pro-arrhythmic effect - Tendency for increased rhythm disturbances. Others include dizziness, visual disturbances, and GI issues

51
Q

Class III: Drugs that prolong repolarization

A

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)

52
Q

Side effects of Amiodarone (Class III)

A

Pulmonary toxicity, thyroid problems, and liver damage. Can increase proarrhythmic effects

Combination of Class I, II, & III anti-arrhythmic drugs

53
Q

Class IV: Calcium Channel Blockers (What form of arrhythmia is commonly treated with these drugs?)

A

Atrial Fibrillation

Work by decreasing rate of SA node discharge and inhibiting conduction velocity through AV node

54
Q

Rehab Implications for Arrhythmias

A

Know signs of Cardiotoxicity (faintness & dizziness) and Hypotension

55
Q

What is important to do in patients with an arrhythmia?

A

Take pulse rate for the FULL 60 seconds

56
Q

2 main goals of Congestive Heart Failure treatment?

A
  1. Increase myocardial contractility (Positive Inotropic Agents)
  2. Decrease cardiac workload
57
Q

What drug is classified as a Positive Inotropic Agent?

A

Digoxin (Cardiac Glycosides)

58
Q

What drugs work to decrease cardiac workload?

A

ACE inhibitors, ARBs, Beta Blockers, Diuretics, & Vasodilators

59
Q

Cardiac Glycosides (DIGITALIS)

A

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

60
Q

What kind of effect does Digitalis have on the SNS?

A

Inhibitory effect - Decreases stress on heart, slows HR, and slows impulse conduction

61
Q

What do PTs need to be aware of when working with patients on Digitalis?

A

Digitalis Toxicity! Overdoses can become fatal.

62
Q

Signs of Digitalis Toxicity

A

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

63
Q

When are ACE inhibitors most effective in treating CHF?

A

When patients are experiencing heart failure due to reduced left ventricular function (systolic heart failure)

64
Q

What needs to be considered when using Diuretics in patients with CHF?

A

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

65
Q

Rehab Implications for CHF Treatment

A

Watch for S/S of acute congestive heart failure, digoxin toxicity, fluid/electrolyte depletion & hypotension

66
Q

Signs of Acute CHF

A

Increased cough, difficulty breathing, dyspnea, and abnormal respiratory sounds

67
Q

Signs of Digoxin Toxicity in Rehab

A

Dizziness, confusion, nausea, & arrhythmias

68
Q

Signs of Fluid/Electrolyte Depletion

A

Fatigue & weakness can be early signs

Pharmacotherapeutics (13 decks)

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