Cardiac Medications: What’s With the Mixing & Matching? Michele B. Collins MSN RN CCRN September 2009
Sodium OUTSIDE cell &
Potassium INSIDE cell before depolarization
Cell has NEGATIVE charge & must CONTRACT to become POSITIVE
SA node has less negativity so it serves as pacemaker
With cell stimulation, cell permeability allows sodium INTO cell & potassium OUT of cell
With sodium, can only have STAT (“fast channel”) contraction
Calcium (“fast channel”) also enters cell,
leading to total controlled contraction
Na+ - K+ pump uses energy (ATP) so SODIUM LEAVES cell and POTASSIUM RETURNS to cell
Calcium also leaves cell at this time
If the S-A node does not generate an impulse, another cardiac site WILL (“reentry phenomenon”)
Statistically, if you take six different drugs, you have an 80% percent chance of at least one drug-drug interaction.
Wayne K. Anderson, Dean, State University of New York School of Pharmacy
Beta Blockers Ace Inhibitors
Calcium Channel Blockers
Angiotensin II Receptor Blockers (ARB)
Why so Many?
In atrial fibrillation, used to suppress arrhythmias
Often done to relieve the symptoms associated with loss of the atrial component to ventricular filling ( atrial kick ) due to atrial fibrillation or flutter .
In individuals with ventricular arrhythmias, used to suppress arrhythmias. Antiarrhythmic agents may be considered the first-line therapy in the prevention of sudden death in certain forms of structural heart disease
Refers to a cardiac muscle cell firing off an impulse on its own
All cardiac cells can initiate an action potential , however, only some of these cells are designed to routinely trigger heart beats
Found in the 'conduction system' of the heart and include the SA node, AV node, Bundle of HIS and Purkinje fibers
S inoatrial node is a single specialized location in the atrium which has a higher automaticity (a faster pacemaker) than the rest of the heart, and therefore is usually responsible for setting the heart rate, and initiating each heart beat.
Occurs when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping
If conduction is abnormally slow in some areas, part of the impulse will arrive late and potentially be treated as a new impulse
Can produce a sustained abnormal circuit rhythm. Re-entry circuits are responsible for atrial flutter , most paroxysmal supraventricular tachycardia , and dangerous ventricular tachycardia .
Conditions that increase automaticity include sympathetic nervous system stimulation and hypoxia
Resulting heart rhythm depends on where the first signal begins
if in sinoatrial node, the rhythm remains normal but rapid
if an ectopic focus, many types of dysrhythmia may ensue.
THE EFFECTS OF STIMULATING ADRENERGIC RECEPTORS
RECEPTOR SITE ACTION
alpha peripheral blood vessels vasoconstriction of peripheral arterioles
Block movement of calcium into smooth muscle cells in vessel walls
Calcium required for muscle contraction; calcium channel blockers cause relaxation and dilatation of arteries
By this mechanism, lower BP
Dilate the coronary arteries so also used in treatment of
R educe cardiac contractility, PVR, & myocardial O2 needs. Effective on reentrant dysrhythmias that require AV nodal conduction for their continuation
In contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.
Some have a slowing effect on the heart rate and are used in the treatment of arrhythmia
Used in treatment of hypertension, arrhythmia, and angina
Paroxysmal SVT, rate control for a-fib and flutter
Dilate coronary arteries/decreases BP
Potentiates effects of digoxin
Change position slowly.
Usually go away within a few hours to a day or so and are not said to be permanent once the medication has "washed out" of the system
Common side effects of these drugs include constipation, dizziness, and weakness
Swelling of the feet and ankles
Excessive lowering of the blood pressure
Most common with first dose
Change position slowly
Rarely an excessively slow heart beat
Worsening of HF
Many calcium channel blockers come in an extended release or sustained release preparation ( XL, SR) that is convenient for once a day dosing. These tablets should not be cut in half or crushed, as this would affect the rate of drug release into the bloodstream.
Less negative inotropic activity than verapamil
D ilates the coronary arteries
Treatment of supraventricular arrhythmias
Oral diltiazem is effective in treatment of reentry tachycardia
A dverse Effects : fewest adverse effects of this category of drugs
- AV Block if patient is on Beta Blocker therapy
Verapamil (Calan, Isoptin): severe hypotension & bradycardia