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1390-59 Intro to Pharmacology > Chapter 22 > Flashcards

Chapter 22 Flashcards

1
Q

afterload

A

a measure of the vascular resistance that the left ventricle must overcome in order to eject blood during contraction

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2
Q

cardiac glycoside (Digitalis Glycosides)

A

drug obtained from plants of the genus digitalis

-considered, a second-line drug

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3
Q

cardiac output (CO)

A

the amount of blood pumped per minute by the heart

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4
Q

chronic heart failure (CHF)

A

condition in which the heart is unable to pump sufficient blood to the tissues of the body

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5
Q

digitalization

A

method of dosage with cardiac glycosides that rapidly produces effective drug levels

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6
Q

ectopic beat

A

extra heartbeat, a type of cardiac arrhythmia

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7
Q

hypercalcemia

A

high serum calcium

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8
Q

hyperkalemia

A

high serum potassium

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9
Q

maintenance dose

A

daily dosage of cardiac glycoside that maintains effective drug levels in the blood

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10
Q

Na/K adenosine triphosphatase (Na/K ATPase)

A

enzyme that energizes the sodium/potassium pump and is inhibited by cardiac glycosides

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11
Q

preload

A

refers to venous return, the amount of blood returning to the heart that must be pumped

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12
Q

Vasodilators

cardiac glycoside (Digitalis Glycosides)

A

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
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13
Q

Diuretics

cardiac glycoside (Digitalis Glycosides)

A

prevent retention fluid accumulation

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14
Q

Beta- Blockers

cardiac glycoside (Digitalis Glycosides)

A

reduce heart rate and sympathetic activation

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15
Q

What is the therapeutic effect of Diuretics in CHF?

A

elimination of excess sodium and water by the kidneys

  • reduces edema and congestion
  • produces vasodilation effect
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16
Q

Thiazide Diuretics

A

Block sodium reabsorption  increase sodium & water excretion in urine

Potency is moderate and Used in mild to moderate cases of CHF

May cause hypokalemia

17
Q

Loop Diuretics

A

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.

18
Q

Aldosterone Antagonist

A

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+

19
Q

Adverse Effects of Diuretics

A

Thiazides and loop diuretics
-Nausea, hypotension, hypokalemia, hyperuricemia, and hyperglycemia

Potassium-sparing diuretics
-Hyperkalemia

20
Q

What are the therapeutic effects of Vasodilators?

A

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.
21
Q

What is the Therapeutic use of Adrenergic Beta-Blockers in CHF?

A

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

22
Q

Cardiac Glycoside- Digoxin

A

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.

23
Q

Mechanism of Action of Digoxin

A
  1. Digoxin binds to and inhibits Na/K ATPase.
  2. Inhibition of Na/K ATPase increases intracellular concentration of Na+ ions
  3. Increased intracellular Na+ decreases the Na+/Ca++ exchanger and allows intracellular Ca++ concentrations to increase
  4. Increased intracellular Ca++ increases the formation of actinomyosin and increases the force of myocardial contractions
  5. https://www.youtube.com/watch?v=ljm1JSubTOc
24
Q

Pharmacokinetics

Cardiac Glycoside - Digoxin

A

Administration follows the sequence of digitalization and maintenance.

Administered orally or intravenously depending on the urgency of the situation

25
Q

Changes in the serum electrolytes affect drug actions.

Cardiac Glycoside - Digoxin

A
  • Hypokalemia can lead to increased incidence of arrhythmias.
  • Hyperkalemia antagonizes therapeutic effects.
  • Hypercalcemia enhances drug action.
  • Patients treated with diuretics should increase potassium intake.
26
Q

Adverse effects

Cardiac Glycoside - Digoxin

A

Mild symptoms - Nausea, vomiting, headache, visual disturbances, and rashes

Toxic effect - Cardiac arrhythmias and premature ventricular contractions
-Antidote - Digoxin Immune Fab

27
Q

Clinical indications

Cardiac Glycoside - Digoxin

A

Treatment of CHF – to increase force of contraction

Used in cases of atrial flutter and atrial fibrillation

28
Q

Drug interactions

Cardiac Glycoside - Digoxin

A

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.
29
Q

Other drugs that increase myocardial interaction

Cardiac Glycoside - Digoxin

A 
Adrenergic drugs (dopamine and dobutamine)
   -Increase force of contraction

Amrinone and milrinone
-Increase calcium concentrations in heart muscle and produce vasodilation

30
Q

What is the Preferred Therapy for Chronic Heart Failure?

A

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.

1390-59 Intro to Pharmacology (17 decks)

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