Chapter 44 Cardiotonic Agents

Front 1

Cardiotonic Agents

Back 1

Drugs used to increase contractility of heart
Used to treat heart failure (HF) – also called congestive heart failure (CHF)
Cardiac cycle
Treatment – try restore system balance

Front 2

Congestive Heart Failure (CHF) Definition

Back 2

Condition in which the heart fails to effectively pump blood around the body

Front 3

Congestive Heart Failure (CHF) Primary treatment

Back 3

Helping the heart muscle to contract more efficiently to restore system balance

Front 4

Composition of the Sarcomere

Back 4

Protein fibers
Thin actin fibers
Thick myosin fibers

Front 5

Underlying Problems in CHF Involving Muscle Function

Back 5

The muscle could be damaged
Atherosclerosis or cardiomyopathy
The muscle could be forced to work too hard to maintain an efficient output
Hypertension or valvular disease
The structure of the heart could be abnormal
Congenital cardiac defects

Front 6

Causes of Congestive Heart Failure (CHF) Coronary artery disease (CAD)

Back 6

Leading cause of CHF
Insufficient supply of blood to meet O2 needs
Muscles become hypoxic – no longer function efficiently
Can evolve into MI – muscle cells die or are damaged – leads to inefficient pumping effort

Front 7

Causes of Congestive Heart Failure (CHF) Cardiomyopathy – enlargement of muscles

Back 7

Viral infection
Alcoholism
Anabolic steroid abuse
Collagen disorder

Front 8

Causes of Congestive Heart Failure (CHF)

Back 8

Causes muscle alterations and ineffective contraction and pumping

Front 9

Causes of Congestive Heart Failure (CHF) Hypertension

Back 9

Leads to enlarged cardiac muscle d/t excess workload
Places constant, increased demand for O2 on system

Front 10

Causes of Congestive Heart Failure (CHF) Valvular heart disease

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Leads to overload of the ventricles (valves don’t close tight)
Allows blood to leak backward into ventricles
Overload causes muscle stretching and increased demand for O2 and energy
Heart muscle has to constantly contract harder

Front 11

Compensatory Mechanisms in CHF

Back 11

Baroreceptors stimulated causing a sympathetic stimulation
Increase in heart rate, blood pressure, and rate and depth of respirations, increased force of contraction, and an increase in blood volume
Stimulates release of renin from kidneys – increases blood pressure and blood volume

Front 12

Cellular Changes

Back 12

Myocardial cells changed with prolonged HF
Lack ability produce energy
Movement calcium ions no longer effective
Leads further deterioration
Unable contract effectively and deliver blood

Front 13

Left Sided CHF

Back 13

Reflects engorgement of pulmonary veins
Difficulty breathing (tachypnea, dyspnea, orthopnea)
Coughing and hemoptysis
Rales may be present (fluid in lung tissue)
Pulmonary edema – fluid prevents gas exchange

Front 14

*Right Sided CHF

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Usually occurs from COPD or other lung dz
Venous return to heart is decreased
Causes congestion and backup of blood systemically
Distended neck veins
Liver enlarges – pain and tenderness
Dependent edema(legs and feet)
Pitting edema lower extremities
Increased urine output (nocturia)

Front 15

Treatments for Congestive Heart Failure Vasodilators (ACE inhibitors and nitrates)

Back 15

Decrease workload of overworked cardiac muscle

Front 16

Treatments for Congestive Heart Failure Diuretics

Back 16

Decrease blood volume, which decreases venous return and blood pressure

Front 17

Treatments for Congestive Heart Failure Beta-adrenergic agonists

Back 17

Stimulate the beta-receptors in the sympathetic nervous system, increasing calcium flow into the myocardial cells and causing increased contraction

Front 18

Effects of Cardiac Glycosides

Back 18

Increased force of myocardial contraction
Increased cardiac output and renal perfusion
Increased urine output and decreased blood volume
Slowed heart rate
Decreased conduction velocity through the AV node

Front 19

Cardiac Glycosides Actions

Back 19

Increase intracellular calcium, allowing more calcium to enter the myocardial cell during depolarization; cause positive inotropic effect, increasing renal perfusion with a diuretic effect and decreasing renin release; and slow conduction through the AV node

Front 20

Cardiac Glycosides Indications

Back 20

Treatment of CHF and atrial fibrillation

Front 21

Cardiac Glycosides Pharmacokinetics

Back 21

Rapidly absorbed and widely distributed throughout the body
Primarily excreted unchanged in the urine

Front 22

Cardiac Glycosides Contraindications

Back 22

Allergy
Ventricular tachycardia or fibrillation, heart block, and sick sinus syndrome
Idiopathic hypertrophic subaortic stenosis
Acute MI, renal insufficiency, and electrolyte abnormalities

Front 23

Cardiac Glycosides Cautions

Back 23

Pregnancy and lactation
In pediatric and geriatric patients
theraputic dose is close to toxic dose

Front 24

Cardiac Glycosides Adverse effects

Back 24

Headache, weakness, drowsiness, and *vision changes*
GI upset and anorexia
Arrhythmia development

Front 25

Cardiac Glycosides Drug-to-drug interactions

Back 25

Verapamil, amiodarone, quinidine, quinine, erythromycin, tetracycline, and cyclosporine
Potassium-losing diuretics
Cholestyramine, charcoal, colestipol, bleomycin, cyclophosphamide, and methotrexate

Front 26

Phosphodiesterase Inhibitors Classification

Back 26

Second class of drugs that act as cardiotonic (inotropic) agents

Front 27

Phosphodiesterase Inhibitors Types

Back 27

Inamrinone (Inocor): approved for use only in patients with CHF that has not responded to digoxin, diuretics, and vasodilators
Milrinone (Primacor): short-term management of CHF in patients who are receiving digoxin and diuretics

Front 28

*Phosphodiesterase Inhibitors Actions

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*Block the enzyme phosphodiesterase*, leading to an increase in myocardial cell cyclic adenosine monophosphate (cAMP), *which increases calcium levels in the cell, causing a stronger contraction* and prolonged response to sympathetic stimulation; directly relax vascular smooth muscle

Front 29

Phosphodiesterase Inhibitors Indication

Back 29

Short-term treatment of CHF in patients unresponsive to digitalis, diuretics, and vasodilators

Front 30

Phosphodiesterase Inhibitors Pharmacokinetics

Back 30

Widely distributed after injection
Metabolized in the liver and excreted in the urine

Front 31

Phosphodiesterase Inhibitors Contraindications

Back 31

Allergy
Severe aortic or pulmonic disease, MI, fluid volume deficit, and ventricular arrhythmias

Front 32

Phosphodiesterase Inhibitors Cautions

Back 32

Pregnancy and lactation
In the elderly

Front 33

Phosphodiesterase Inhibitors Adverse effects

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Arrhythmia
Hypotension
Nausea, vomiting
Thrombocytopenia
Pericarditis
Pleuritis
Fever
Chest pain
Burning at injection site

Front 34

Phosphodiesterase Inhibitors Drug-to-drug interaction

Back 34

Furosemide