Cardio 10 Deck 3 Flashcards
Arrhythmias are caused by
physiological and/or anatomical consequences to prevent normal cardiac action potentials.
Normal HR depends on
the intrinsic electrical impulses initiated at the sinoatrial (SA) node and conducted to the AV node and over the ventricles.
Absolute refractory period
Regardless of the strength of a stimulus, the cell cannot be depolarized.
Relative refractory period
Stronger-than-normal stimulus can induce depolarization
Refractoriness
State of the cardiac cell which determines depolarization.
Damaged heart cells
may maintain a constant rate of refractoriness or may not be refractory at all.
Spontaneously depolarizing cells
SA nodes, AV nodes, His-Purkinje, special atrial cells
Automaticity
Ability of a heart cell to spontaneously depolarize and generate an action potential
Automaticity may be
altered, enhanced, decreased by:
Cell damage, biochemical disturbance, pharmacological agents, environmental toxins
Automacity is the target
Target for antiarrhythmic drugs
Reentry Phenomena
Reentry is the cause of some arrhythmias.
It depends on two anatomically or physiologically distinct electrical pathways.
Normally, impulses from the
AV node are conducted down both pathways in the same direction, bifurcating to cover the entire ventricle.
Sometimes this will get interupted and go out of order and this is wher eyou will have atopic irregular beats. Reentry phenomena
Reentry Phenomena
If a block is encountered
by the action potential in one of the pathways, then the impulse can only be conducted down the other pathway.
The impulse can return to the initial point of bifurcation and reexcite the myocardium
Short-circuiting conducting tissue can occur
and cause premature contraction.
PVC and PAC
If reentry is
repetitive, sustained ventricular arrhythmias, such as ventricular tachycardia, can occur.
Class I: sodium channel blockers
MOA
A: lengthen the duration of action potential
B: shorten the duration of action potential
C: minimally increase action potential
Class II: beta blockers
MOA
Reduce adrenergic activity in the heart Sotalol: considered a class II and III drug
Class III: potassium channel blockers
MOA and example
Prolong effective refractory period and reduce speed of conduction
Amiodarone
Class IV calcium channel blocker MOA
Block the influx of calcium, reduce contractility (negative inotropism), decrease SA and AV node conduction
Significantly reduce afterload but little effect on preload
Class IV calcium channel blocker example
Verapamil, diltiazem, bepridil
potassium will
prolong the effect of refractory period to reduce the speed of conduction. This can stop the heart.
I. Membrane-stabilizing agents (sodium channel blockers)
examples A,B,C
Quinidine, procainamide, disopyramide
Lidocaine, phenytoin
Encainide, Iorcainide, flecainide
Beta blocker examples
Propranolol, metoprolol, sotalolol, and others
III. Agents that prolong duration of the action potential (potassium channel blockers)
examples
Amiodarone, bretylium
. Agents that prolong duration of the action potential (potassium channel blockers)
examples
Amiodarone, bretylium
IV. Calcium channel blockers
examples
Verapamil, diltiazem, bepridil
Pharmacological management of arrhythmias requires
an office that is prepared, ready, and able to handle emergencies.
Drugs for arrhythmias you will see these patients for
infections, depression, anemia, fatigue, and so on. Be aware of actions and adverse drug interactions.
Beta Adrenergic Blockers various types include
include nonspecific beta antagonists, selective beta-antagonists, and those with or without intrinsic sympathomimetic activity (ISA)
Beta blockers are commonly seen in
In post-MI patients, cardioselective agents without ISA are preferred.
some beta blockers are used as
aniarrhythmics
Drugs with ISA may help
avoid a decrease in cardiac output (CO) and HR. May be preferred for patients who experience bradycardia with other BBs.
Beta Adrenergic Blockers more effective in
African American and older patients
BBs may NOT be
abruptly withdrawn, because it will increase beta receptor sensitivity
BB are no longer
first-line HTN drug choice
Amiodarone class
III antiarrhythmic
Amiodarone onset of action
oral – 2 days to 3 weeks
Amiodarone duration of action
7 to 50 days
Amiodaraone excreted in
feces, 1% in urine
Amiodarone watch out for
for use of grapefruit juice!
inhibits the absorption and will cause the pts to get the wrong dose.
Dose of Amiodarone
Ventricular arrhythmias: 800 to 1,600 mg twice daily for 1 to 3 weeks, then decreased to 300 to 400 mg twice daily, maintenance 400 mg/day
Amiodarone ARR
thyroid, neurological, blue skin discoloration, bradycardia, lung damage not evident until advanced
Amiodarone drug interactions
many
For All Antiarrhythmics Monitoring
Potassium, blood urea nitrogen (BUN), creatinine, therapeutic drug levels
Electrocardiography (ECG)
For All Antiarrhythmics Patient education
Take exactly as prescribed; do not double doses.
Be aware of food–drug interactions.
Monitor HR for regularity of rate and rhythm.
Monitor BP at home.
