Elizabeth Valentine, MD Nina Singh-Radcliff, MD
BASICS
DESCRIPTION
• The 12-lead EKG is a noninvasive test that provides information on the electrical function of the heart and aids in the diagnosis of pathophysiologic processes.
• Serves as a baseline for perioperative changes and as a screening tool to identify cardiac abnormalities.
• Continuous 3- or 5-lead EKG is an American Society of Anesthesiologists (ASA) standard monitor used for general anesthesia and monitored anesthesia care.
PHYSIOLOGY PRINCIPLES
• P wave (80 ms): Denotes atrial depolarization. Myocardial depolarization is normally initiated by spontaneous sinoatrial (SA) node depolarization. The signal is quickly and efficiently conducted along a specialized conduction pathway. In the atria, this pathway is via interatrial tracts (anterior, middle, and posterior); they begin by depolarizing the right, followed by the left, atria. The conduction cells depolarize adjacent myocardial cells, which have a different histology.
• QRS (80–120 ms): Denotes the varying stages of ventricular depolarization. The Q wave is the initial negative deflection and results from septal depolarization. The R wave follows and is the first positive deflection. It results from depolarization of the larger, more muscular left ventricle; right ventricular depolarization is normally obscured. The S wave is the final negative deflection caused by lateral wall depolarization.
• T wave: Denotes ventricular repolarization. The beginning of the wave represents a period of absolute refractoriness, where a subsequent depolarization (no matter how strong) cannot initiate a aberrant rhythm. The latter portion of the wave is a time of relative refractoriness, where a strong enough depolarization can result in a runaway rhythm.
• PR interval (120–200 ms): Time from the start of atrial depolarization to atrioventricular (AV) nodal conduction to conduction through the His-Purkinje system.
• QRS width: Represents the time for ventricular depolarization
• J point: Describes the intersection between the QRS complex and ST segment. When the heart rate is increased, atrial repolarization may be observed at the very end of the QRS complex as J point depression.
• ST segment: Denotes the end of depolarization to the beginning of repolarization and is usually isoelectric
• QT interval (QTc <440 ms): Beginning of ventricular depolarization to the end of ventricular repolarization. Time for ventricular repolarization is heart rate dependent; thus, the QT is usually corrected for heart rate (QTc).
• Rate: Typically measured between sequential R waves; the RR interval (0.6–1.2 s) is useful
due to its prominent wave that allows for easy detection. A rate <60 bpm is bradycardia; a axis is between 0 and 100° in the frontal plane. Left or right axis deviation can suggest underlying pathophysiology.
ANATOMY
• A total of 12 leads allows for “visualizing” the electrical function from different angles through the heart. Considering the leads in different combinations can aid in clinical diagnosis.
• Standard limb leads (I, II, III): Form the points of Einthoven’s triangle, an equilateral triangle whose vertices lie at the left and right shoulders and the pubic region and whose branch block or left anterior hemiblock, inferior MI, or left ventricular hypertrophy.
Common causes of a right axis deviation include right ventricular hypertrophy, chronic lung disease, right bundle branch block, or lead reversal.
• Bundle branch blocks: A prolonged QRS suggests either a right (RBBB) or a left bundle branch block (LBBB). They are described as either partial (QRS <120 ms) or complete (QRS
>120 ms). Although a RBBB can represent pulmonary or right heart disease, it is more commonly benign. Alternatively, a LBBB is more likely to indicate underlying cardiac pathology (CAD, CMO, valvular disease). A new onset LBBB should prompt a thorough cardiac workup. The anterior or posterior fascicle of the left bundle may be blocked in isolation (termed hemiblock). A nonspecific intraventricular conduction delay describes a nonpathologic widening of the QRS complex that does not meet the criteria for either LBBB or RBBB.
• AV blocks: Impaired conduction between the atria and ventricles of the heart are described
as first, second, and third degree. First-degree AV block is defined as a PR interval >0.2 s.
Second-degree AV block may be Type 1 (Mobitz 1, Wenckebach), defined as progressive prolongation of the PR interval with eventual dropped QRS; or Type II (Mobitz 2), where the PR remains unchanged prior to the sudden failure of conduction of a P wave and a dropped ventricular beat. In third-degree AV block, there is no association between P waves and QRS complexes. While first-degree and Mobitz I AV block are generally benign conditions, Mobitz II (can progress to complete heart block) and third-degree AV blocks are indications for cardiac pacing.
• P waves: Abnormal P wave morphology may indicate an ectopic atrial rhythm, whereas a changing P wave morphology may suggest either a wandering atrial pacemaker or multifocal atrial tachycardia. An irregular rhythm with no clear P waves suggests atrial fibrillation. A regular “saw tooth” pattern may suggest atrial flutter.
• Arrhythmias: A narrow QRS suggests a supraventricular (above the ventricles) rhythm while a wide QRS suggests either a ventricular source or aberrant conduction of a supraventricular rhythm.
• QT prolongation: Prolonged QTc is a risk factor for developing ventricular arrhythmias (Torsades de Pointes) and is an independent risk factor for sudden cardiac death. QTc may rate-slowing property of the AV node, thus allowing for extremely fast heart rates and potential hemodynamic instability. The combination of cardiac arrhythmias and an accessory pathway may degenerate into ventricular fibrillation. vector. A large R wave in aVR is quite sensitive for TCA toxicity; may also see an increased QRS and QTc interval.
– Hyperkalemia: EKG changes are due to delayed depolarization and hastened
repolarization. Changes commonly progress in order from symmetrically peaked T waves
→ widened QRS → prolonged PR interval → loss of P wave → loss of R wave → ST depression → EKG that resembles sine wave → ventricular fibrillation → asystole.
– Hypocalcemia: QTc prolongation and cardiac irritability leading to arrhythmias – Hypercalcemia: Shortened ST segment and QTc interval
– Hypomagnesemia: PR and QT interval prolongation, cardiac irritability – Hypermagnesemia: May see PR prolongation and QRS widening
PERIOPERATIVE RELEVANCE
• Intraoperative bovie, electrical interference, patient shivering, tremors, or movement may closely resemble an intraoperative arrhythmia. Close inspection may reveal the QRS
“marching through” the interference; other times, it may be indistinguishable from a true arrhythmia. Close evaluation of other monitors (blood pressure, pulse oximetry or arterial plethysmograph, verification of palpable peripheral pulses) may provide clues in this circumstance.
• Malpositioning of leads may result in the appearance of ST changes. Thus, it is good practice to place leads in proper position if it does not interfere with the surgical field and to note baseline abnormalities in the EKG tracing.
• Body habitus: Large breasts or obesity may result in low-voltage EKG.
• Pulmonary artery catheters and central lines: For patients with LBBB, there is a risk of complete heart block with insertion. In this circumstance, it is prudent to have pacing capabilities readily available. Similarly, in patients with WPW, the pulmonary artery catheter or a wire for central line placement can induce a hemodynamically intolerable tachyarrhythmia.
• Extracorporeal shock wave lithotripsy: Older machines time shocks to be delivered during the R wave to prevent R on T phenomenon.
• Cardioversion: Machines synchronize the delivery of electrical discharge to the R wave to prevent R on T phenomenon.
GRAPHS/FIGURES
FIGURE 1. EKG waves, segments, and intervals
FIGURE 2. The 12 leads allow for assessment of the electrical function of the three-dimensional heart.
REFERENCES
1. Correll DJ, Hepner DL, Chang C, et al. Preoperative electrocardiograms: Patient factors predictive of abnormalities. Anesthesiology. 2009;110(6):1217–1222.
2. Eagle KA, Berger PB, Calkins H, et al. Practice advisory for preanesthesia evaluation: An updated report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology. 2012;116:522–538.