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INTRODUCTION

Alterations in heart rhythm and rate can have sweeping and at times ultimately fatal hemodynamic consequences perioperatively. Thus, the rapid interpretation of abnormal rhythms and their correction is critical in cardiac anesthesia practice.

THE ELECTROCARDIOGRAM

The electrocardiogram (ECG) remains one of the main monitors used by anesthesiologists. It is primarily employed in anesthesia practice to detect heart rate and rhythm changes and perioperative myocardial ischemia. The ECG detects electrical currents generated by the electrical activity of the heart. ECG leads are placed in different positions and provide various perspectives (depending upon where the lead is placed) of the electrical activity of the heart as electrical vectors point toward or away from the examining leads. Examining the ECG in multiple leads provides the anesthesiologist the ability to discern if perceived changes in the ECG pattern are widespread (found in multiple leads) or are perhaps less significant (motion artifact). At the end of diastole, atrial depolarization generates the “P” wave and is followed by atrial contraction. Following atrial contraction, the ventricle is loaded awaiting systole. Systole commences at the QRS beginning with isovolumetric contraction following a 120- to 200-ms conduction delay at the AV node. Subsequently, intracavitary pressure builds, the atrioventricular valves (e.g., mitral or tricuspid) close, and the arterioventricular valves (e.g., aortic, pulmonic) open resulting in ventricular ejection of the stroke volume (SV). The QRS represents the electrical activity generated by the depolarization of the left and the right ventricles. Depolarization proceeds from the AV node through the interventricular septum via the His-Purkinje fibers. The QRS segment lasts approximately 120 milliseconds. Repolarization of the ventricles produces the ST segment and the T wave. Electrolyte abnormalities (e.g., hypocalcemia) and drug effects (e.g., droperidol) can delay repolarization leading to a prolonged QT interval. This can result in potentially life-threatening ventricular arrhythmias (see Figures 3–1 and 3–2).

Figure 3–1.

Conducting system of the heart. Left: Anatomic depiction of the human heart with additional focus on areas of the conduction system. Right: Typical transmembrane action potentials for the SA and AV nodes, other parts of the conduction system, and the atrial and ventricular muscles are shown along with the correlation to the extracellularly recorded electrical activity, that is, the electrocardiogram (ECG). The action potentials and ECG are plotted on the same time axis but with different zero points on the vertical scale for comparison. AV, atrioventricular; LAF, left anterior fascicle; SA, sinoatrial. (Data from Donahue JG, Choo PW, Manson JE, et al. The incidence of herpes zoster. Arch Intern Med. 155:1605–1609, 1995; Choo PW, Galil K, Donahue JG, et al. Risk factors for postherpetic neuralgia. Arch Intern Med. 1997;157:1217–1224.)

Figure 3–2A,B.

The progression of cardiac conduction in the heart during a cardiac cycle. (Adapted with permission from Rushmer RF: Cardiovascular Dynamics, 2nd ed. Philadelphia, PA: Saunders; 1961.)

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