Pharm110 Chp 17 Cardiac Stimulants and Depressants Flashcards
Cardiac Glycosides
Digoxin prefix “oxin”
- Positive inotropic (Increases stroke volume and cardiac output)
- Negative chronotropic (Slows heart rate)
- Negative dromotropic (Slows heart rate)
- Heart failure most common use
- Rapid digitalization (Pt. gets a loading dose)
- Gradual digitalization (Pt. gets a maintenance dose, allowing therapeutic drug blood levels to accumulate gradually)
Digitalis administration
-Before administering each dose of digoxin, take apical pulse rate for 60 seconds. If below 60 or over 100, withhold drug and notify Dr.
Digoxin toxicity
-Withhold drug and report following signs to Dr. immediately:
-Anorexia
-Abdominal pain
-Visual disturbances (blurred, yellow or green vision with white halos)
-Arrhythmias
-Serum digoxin levels greater than 2 nonograms/mL.
(Normal range 0.8-1.5 ng/mL)
Predisposition to cardiac glycoside toxicity:
- Hypokalemia (normal 3.5-5 potassium level)
- Renal impairment
- Rapid IV administration
Digoxin toxicity treatment
- Stop drug
- Check potassium level (administer if needed)
- Monitor heart rate (administer antiarrhythmics)
- Toxicity overdose antidote Digoxin immune fab (Digiband)
Antiarrhythmic drugs
Propanolol, Esmolol, Bretylium tosylate.
- Used only in emergencies
- Goal to restore normal cardiac function and prevent life threatening arrhythmias.
Work 3 ways
- Decrease automaticity of cardiac tissues in the ectopic sites
- Alter rate of conductions of electrical impulses through the heart
- Alter refractory period of cardiac muscle between consecutive contractions
Adverse effects
- Bronchoconstriction
- Heart failure
Types of arrhythmias
- Atrial flutter: (Rapid contraction of atria(up to 300 bpm) at a rate too rapid for the ventricles to pump efficiently)
- Atrial fibrillation: (Irregular and rapid atrial contraction, resulting in a quivering of the atria and causing an irregular and inefficient ventricular contraction).
- Clots can form due to blood pooling
- Premature ventricular contraction: (Ventricles contract before atria, resulting in a decrease in the amount of blood pumped to the body)
- Ventricular tachycardia: (Rapid heartbeat with a rate more than 100 bpm, usually originating in the ventricles)
- Ventricular fibrillation: (Rapid, disorganized contractions of the ventricles resulting in the inability of the heart to pump any blood to the body, which result in death unless treated immediately)
Beta-adrenergic blocking agents
- Inhibit beta1 and beta2 sympathetic receptors
- Reduce heart rate
- Reduce contractility
- Decrease supraventricular and ventricular rhythms
- Decrease blood pressure
Calcium channel antagonists
Verapamil
Reduce influx of calcium into the cell
- Prevention or reversal of spasms of the coronary blood vessels.
- Coronary artery dilation
- Reduction of myocardial oxygen consumption
Adenosine
-Slow conduction through the AV node
Adverse effects
- Shortness of breath
- Facial flushing
- Nausea and vomiting
Adrenergic or Smypathomimetic drugs
Epinephrine and norepinephrine levarterenol
Mimic epinephrine and/or norepinephrine
- affect alpha or beta adrenergic receptors
- Treat shock
- Cause vasoconstriction
- Reverse hypotension from shock
- BP and ECG must be closely monitored.
- Cardiac and urine output must be monitored
Inotropic
Chronotropic
Dromotropic
Inotropic (increase or decrease force of myocardial contraction)
Chronotropic (Increase or decrease heart rate by altering the rate of impulse at the SA node.)
Dromotropic (Increase or decrease the conduction of electrical impulses through the myocardium.