Chapter 22 Flashcards
afterload
a measure of the vascular resistance that the left ventricle must overcome in order to eject blood during contraction
cardiac glycoside (Digitalis Glycosides)
drug obtained from plants of the genus digitalis
-considered, a second-line drug
cardiac output (CO)
the amount of blood pumped per minute by the heart
chronic heart failure (CHF)
condition in which the heart is unable to pump sufficient blood to the tissues of the body
digitalization
method of dosage with cardiac glycosides that rapidly produces effective drug levels
ectopic beat
extra heartbeat, a type of cardiac arrhythmia
hypercalcemia
high serum calcium
hyperkalemia
high serum potassium
maintenance dose
daily dosage of cardiac glycoside that maintains effective drug levels in the blood
Na/K adenosine triphosphatase (Na/K ATPase)
enzyme that energizes the sodium/potassium pump and is inhibited by cardiac glycosides
preload
refers to venous return, the amount of blood returning to the heart that must be pumped
Vasodilators
cardiac glycoside (Digitalis Glycosides)
increase cardiac output by
- dilating blood vessels-reduces work load on the heart
- dilate veins-decrease venous return- decrease preload
- dilate arteries- reduce BP and peripheral resistance- decrease afterload
Diuretics
cardiac glycoside (Digitalis Glycosides)
prevent retention fluid accumulation
Beta- Blockers
cardiac glycoside (Digitalis Glycosides)
reduce heart rate and sympathetic activation
What is the therapeutic effect of Diuretics in CHF?
elimination of excess sodium and water by the kidneys
- reduces edema and congestion
- produces vasodilation effect
Thiazide Diuretics
Block sodium reabsorption increase sodium & water excretion in urine
Potency is moderate and Used in mild to moderate cases of CHF
May cause hypokalemia
Loop Diuretics
Most potent, used in treating severe heart failure or impaired renal function
Cause increase of sodium & water excretion and loss of potassium
Effects last for 4 to 8 hours.
Aldosterone Antagonist
Weak diuretics, act on the collecting ducts of the nephron
Known as potassium-sparing diuretics
-Increase sodium excretion and retain potassium
Reduce mortality
Often prescribed with thiazide an loop diuretics to counter balance the loss of K+
Adverse Effects of Diuretics
Thiazides and loop diuretics
-Nausea, hypotension, hypokalemia, hyperuricemia, and hyperglycemia
Potassium-sparing diuretics
-Hyperkalemia
What are the therapeutic effects of Vasodilators?
Vasodilators dilate blood vessels
- Lower peripheral resistance and blood pressure
- Decrease cardiac work and oxygen consumption and increase cardiac output
Arterial dilator - Hydralazine
- Decreases blood pressure and reduces afterload
- Adverse effects are mostly due to excessive decrease in bp
- Nausea, postural hypotension, headache, and reflex tachycardia
Venodilators
Nitroglycerine and isosorbide dinitrate
-Reduction in amount of blood returning to the heart -Reduce venous return and preload; this enables the heart to pump more forcefully and increase co
Adverse effects
-Headache, dizziness, vasomotor flushing, postural hypotension, and reflex tachycardia
Balanced vasodilators
- Preferred agents for the treatment of CHF
- Dilate arteries and veins
- Angiotensin-converting enzyme (ACE) inhibitors
- Reduce the formation of angiotensin II
- Decrease bradykinin inactivation
- Angiotensin receptor blockers (ARBs)
- Block the actions of angiotensin II
(Angiotensin-converting Enzyme (ACE) Inhibitors & Angriotensin receptor blockers (ARBS)-Inhibit the actions of angiotensin II, which causes vasoconstriction, release of aldosterone and release of ADH. Aldosterone and ADH cause retention of sodium and water
Adverse effects of ACEIs and ARBs
- Headache, dizziness, hypotension, hyperkalemia, and GI disturbances
- ACEIs can cause dry cough and allergic reactions, including angioedema.
What is the Therapeutic use of Adrenergic Beta-Blockers in CHF?
Block beta-1 receptors on the heart
-Decrease heart rate ( allow heart to fill) and force of contraction (fx more efficiently)
Block beta-1 receptors in the kidneys (juxtaglomerular cells that release renin)
-Reduce release of renin and activation of RAA mechanism
Preferred beta-blockers
Metoprolol, bisoprolol, nebivolol, and carvedilol
Cardiac Glycoside- Digoxin
Pharmacological effects
- Increases force of myocardial contractions
- Stimulates the vagus nerve
Special considerations
-Patient’s pulse should be between 60 and 100 beats per minute before drug administration.
Mechanism of Action of Digoxin
- Digoxin binds to and inhibits Na/K ATPase.
- Inhibition of Na/K ATPase increases intracellular concentration of Na+ ions
- Increased intracellular Na+ decreases the Na+/Ca++ exchanger and allows intracellular Ca++ concentrations to increase
- Increased intracellular Ca++ increases the formation of actinomyosin and increases the force of myocardial contractions
- https://www.youtube.com/watch?v=ljm1JSubTOc
Pharmacokinetics
Cardiac Glycoside - Digoxin
Administration follows the sequence of digitalization and maintenance.
Administered orally or intravenously depending on the urgency of the situation
Changes in the serum electrolytes affect drug actions.
Cardiac Glycoside - Digoxin
- Hypokalemia can lead to increased incidence of arrhythmias.
- Hyperkalemia antagonizes therapeutic effects.
- Hypercalcemia enhances drug action.
- Patients treated with diuretics should increase potassium intake.
Adverse effects
Cardiac Glycoside - Digoxin
Mild symptoms - Nausea, vomiting, headache, visual disturbances, and rashes
Toxic effect - Cardiac arrhythmias and premature ventricular contractions
-Antidote - Digoxin Immune Fab
Clinical indications
Cardiac Glycoside - Digoxin
Treatment of CHF – to increase force of contraction
Used in cases of atrial flutter and atrial fibrillation
Drug interactions
Cardiac Glycoside - Digoxin
Antacids, laxatives, kaolinpectin, and cholestyramine
-Decrease the absorption of digoxin from the GI tract
Quinidine increases digoxin plasma levels.
Calcium channel blockers (verapamil and diltiazem) and beta-blockers
- Decrease heart rate and force of contraction
- Diuretics cause loss of potassium.
Other drugs that increase myocardial interaction
Cardiac Glycoside - Digoxin
Adrenergic drugs (dopamine and dobutamine) -Increase force of contraction
Amrinone and milrinone
-Increase calcium concentrations in heart muscle and produce vasodilation
What is the Preferred Therapy for Chronic Heart Failure?
Mild CHF - Restriction of sodium intake and diuretic therapy
Severe CHF - ACEIs or ARBs should be additionally administered.
- Tachycardia - Low-dose beta-blockers
- Digoxin therapy is considered when diuretic and vasodilator therapy do not control symptoms.
