Arrhythmias Quiz Part (1)

When circulated blood returns to the heart via venous circulation, blood enters the right atrium. Right atrial contraction and changes in right ventricular pressure result in delivery of blood to the right ventricle through the tricuspid valve. Right ventricular contraction pumps blood through the pulmonic valve through the pulmonary arteries to the lungs, where blood becomes oxygenated. The blood then flows through the pulmonary veins into the left atrium. Left atrial contraction and changes in left ventricle (LV) pressure result in delivery of blood through the mitral valve into the LV. Contraction of the LV results in pumping of blood through the aortic valve and to the tissues of the body. Mechanical activity of the heart (contraction of the atria and ventricles) occurs as a result of the electrical activity of the heart.

The pacemaker of the heart is not the SA node

The SA node has the greatest degree of automaticity

Ventricular myocyte resting membrane potential is usually –70 to –90 mV

During each action potential cycle, the potential of the membrane rapidly increases to a threshold potential due to a rapid influx of sodium into the cell

When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to enter the cell rapidly

This rapid influx of positive ions creates a vertical upstroke of the action potential. This previous is considered as phase 0, which represents ventricular depolarization. At this point, the fast sodium channels become inactivated.

Ventricular depolarization begins, consisting of phases 1 through 3 of the action potential.

Phase 1 repolarization occurs primarily as a result of an influx of potassium ions.

During phase 2, potassium ions continue to exit the cell, but the membrane potential is balanced by an influx of calcium and sodium ions, transported through slow calcium and slow sodium channels, resulting in a plateau.

During phase 3, the efflux of potassium ions greatly exceeds calcium and sodium influx, resulting in the major component of ventricular repolarization.

During phase 4, Calcium ions gradually enter the cell, increasing the threshold again to –60 to –80 mV and initiating another action potential.

Cardiac arrhythmias are caused by

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity

Abnormal atrial automaticity will not result premature atrial contractions, atrial tachycardia or atrial fibrillation

The mechanism of abnormal impulse conduction is traditionally referred to as :

Reentry is often initiated as a result of an abnormal premature electrical impulse (abnormal automaticity); therefore, in these situations, the mechanism of the arrhythmia is both abnormal impulse formation (automaticity) and abnormal impulse conduction (reentry).

These three conditions are  (1) at least two pathways for the impulse to travel  (2) a “unidirectional block” in one of the conduction pathways                                                                                     (3) slowing of the velocity of impulse conduction down the other conduction pathway.

Under normal circumstances, when a premature impulse is initiated, it cannot be conducted in either direction down either pathway because :

A premature impulse may be conducted down both pathways if it is only slightly premature and arrives after the tissue is no longer refractory

Myocardial ischemia does not alter impulse conduction velocity

Class (I) drugs primarily increase ventricular automaticity and speed up conduction velocity.

He class I drugs are subdivided into classes IA, IB, and IC

The class IC drugs have the greatest potency for slowing ventricular conduction

Class IA drugs have intermediate potency, and class IB drugs have the lowest potency