Cardiac arrhythmias and hypertensive emergencies are not uncommon in the intensive care unit. This chapter will discuss basic cardiac electrophysiology, cardiac conduction, electrocardiography (ECG) interpretation, tachyarrhythmias, bradyarrhythmias, and hypertensive crisis.
BASIC CARDIAC ELECTROPHYSIOLOGY
Mechanisms of arrhythmia initiation, maintenance, and termination are best understood by reviewing the basic electrophysiologic properties of the cardiac cells. The resting cardiac transmembrane potential is normally –50 to –95 mV (depending on the type of cardiac cell) and is maintained by the electrochemical equilibration of the sodium (Na+), potassium (K+), calcium (Ca2+), and chlorine (Cl–) ions. From an electrophysiological standpoint, cardiac cells can be classified into fast-response (contractile cells) and slow-response (automatic) cells. Sinus node and atrioventricular (AV) node cells are considered slow response cells. The electrophysiological properties during diastole (resting phase) and systole (activation phase) are different.
The cardiac transmembrane action potential of fast response cells consists of 5 phases (Fig. 5-1):
Phase 0: Rapid depolarization is caused by a sudden influx of Na+ ions.
Phase 1 (absent in slow-response cells): Early rapid repolarization due to inactivation of the inward Na+ channels and simultaneous activation of outward K+ channels, resulting in a net efflux of positive ions.
Phase 2 (absent in slow-response cells): The plateau phase may last several hundred milliseconds and is mainly due to the outward K+ and Cl– ion current with an inward current of Na+ and Ca2+.
Phase 3: Final rapid repolarization occurs due to opening of slow delayed rectifier K+ channels and simultaneous closure of inward Na+ and Ca2+ channels, resulting in a net efflux of positive ions.
Phase 4: The resting membrane potential is reached. It is usually rectilinear in fast-response cells due to inward Na+ and Ca2+ currents and outward K+ currents.
In slow-response cells, resting transmembrane potential is slightly less negative (around –60 mV) and is followed by gradual diastolic depolarization, which is responsible for the property of automaticity. Diastolic depolarization is caused predominantly by an inward current of both Na+ and Ca2+ with slow/small outward current of K+.
Different classes of antiarrhythmics have their effects on 1 or more phases (Table 5-1).
TABLE 5-1Classes of Antiarrhythmics and Effects on Phases ||Download (.pdf) TABLE 5-1Classes of Antiarrhythmics and Effects on Phases
|Class ||Effect on Phases ||Example Drugs |
|Class Ia ||Depress phase 0, prolong repolarization ||Quinidine, procainamide, disopyramide |
|Class Ib ||Depress phase 0, shorten repolarization ||Lidocaine, phenytoin, mexiletine |
|Class Ic ||Depress phase 0, minimal effect on repolarization ||Flecainide, propafenone, moricizine |
|Class II ||Decrease slope of phase 4 ||Propranolol, esmolol, timolol, metoprolol, atenolol |
|Class III ||Prolong phase 3 ||Amiodarone, sotalol, ibutilide, dofetilide |
|Class IV ||Prolong phase 2 ||Verapamil, diltiazem |