CASE 10. What would the ST segment of this ECG look like? On which leads would you see this ST segment change? What does the T wave represent?

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1 CASE 10 A 57-year-old man presents to the emergency center with complaints of chest pain with radiation to the left arm and jaw. He reports feeling anxious, diaphoretic, and short of breath. His past history is significant for type II diabetes mellitus and hyperlipidemia. On examination, the patient appears to be in moderate distress and anxious. His electrocardiograph (ECG) shows evidence of acute myocardial injury in the inferior leads. The emergency room physician suspects that the left anterior descending artery is involved. What would the ST segment of this ECG look like? On which leads would you see this ST segment change? What does the T wave represent?

2 88 CASE FILES: PHYSIOLOGY ANSWERS TO CASE 10: ELECTROCARDIOGRAPHY Summary: A 57-year-old man has chest pain and ECG evidence of acute myocardial injury (ST-segment elevation) in the inferior leads (leads II, III, and av F ). ST-segment appearance: Elevation of the ST segments. Inferior leads: II, III, and av F. T wave: Represents ventricular polarization. CLINICAL CORRELATION This 57-year-old man has risk factors for coronary heart disease: diabetes mellitus and hyperlipidemia. His history is very suspicious for an acute coronary event. Oxygen should be administered quickly, followed by an aspirin to chew. Nitroglycerin can be given if the patient continues to have chest pain. The ECG often is helpful; however, a subset of patients with a myocardial infarction (MI) will not have ECG findings. Thus, a normal ECG does not rule out an MI. Cardiac enzymes should be drawn. These markers are sensitive indicators of myocardial injury. Interpretation of an ECG is essential in managing patients with chest pain because a patient s clinical problem often can be determined from the ECG. Various abnormalities can be recognized, including cardiac arrhythmias, infarction, ischemia, and hypertrophy. This patient has typical symptoms of an MI. An ECG of a patient with an MI often will show elevated ST segments acutely and the presence of Q waves after several days. The location of ECG changes in certain leads helps localize where the injury may be occurring. In this case, leads II, III, and av F were affected and represent the inferior portion of the heart. When a patient with stable angina undergoes an exercise stress test, an ECG is performed, and the appearance of ST-segment depression or elevation will indicate cardiac ischemia and therefore be a positive stress test. Cardiac hypertrophy often leads to changes in the mean electrical axis, which can be determined by comparing the relative magnitude of the QRS complex on different leads. APPROACH TO ELECTROCARDIOGRAPHY PHYSIOLOGY Objectives 1. Know the ECG leads and electrical vectors. 2. Be able to understand the correspondence of parts of the ECG to the cardiac cycle. 3. Know the effects of heart block, hypertrophy, and acute MI on the ECG.

3 CLINICAL CASES 89 Definitions ECG segment: Part of the ECG record measured in terms of voltage, usually relatively flat (e.g., the ST segment). ECG interval: Part of the ECG record measured in terms of time (e.g., the QT interval). First-degree heart block: Prolongation of the time taken for action potentials to propagate through the AV node (abnormally long PR interval). Second-degree heart block: Failure of some but not all action potentials to propagate through the AV node (greater number of P waves than QRS complexes). Third-degree heart block: Failure of all action potentials to propagate through the AV node (no correlation between P waves and QRS complexes). DISCUSSION The electrocardiogram records small extracellular signals on the surface of the body that are produced by action potentials generated synchronously by large regions of the heart. To obtain the standard 12-lead ECG, an electrode is attached to each forearm and ankle, and six electrodes are placed on standard locations across the chest (see Figure 10-1). The electrodes on the extremities are used to define six limb leads [three standard (I, II, and III) and three augmented (av R,aV L, and av F )], and the chest electrodes define six precordial leads (V 1 to V 6 ). Individual leads refer to the potential difference measured between one electrode and one or more of the others. Each lead provides information from a unique angle. The six limb leads monitor electrical vectors (having magnitude and direction) in the frontal plane, and the six precordial leads monitor vectors in the transverse plane. Together, the leads provide a dynamic representation of the three-dimensional electrical vector resulting from the net flow of current from action potentials across the heart. During the cardiac cycle, characteristic events are exhibited on most leads. The electrical signal depends on the mass of cardiac tissue in which current is flowing, and so electrical signals corresponding to events in small nodal regions are not detected by the leads. It also should be remembered that the ECG displays changes in potential (produced by changes in current) and not steady-state absolute values. When little net current is flowing (when most cells are at resting potential or in the plateau phase of the action potential), the ECG will be at its baseline value. The cycle begins with the P wave, generated by roughly synchronous depolarization of atrial muscle cells (see Figure 10-2). This is followed by a return to the isoelectric baseline during the period when action potentials are conducted through the atrioventricular (AV) node, bundle of His, and Purkinje fibers, which have relatively little mass. The sharp QRS complex then occurs when the large mass of ventricular muscle cells initiate, nearly synchronously, their fast action potentials: very large currents

4 90 CASE FILES: PHYSIOLOGY Lead I Lead II Lead III Lead av L Lead av R Lead av F V 4 V V 1 V 3 2 V 5 V 6 Figure A diagram of the 12-lead placement for the ECG. The frontal plane is represented on leads I, II, and III as well as augmented leads av R,aV L, and av F. The cross-sectional plane is depicted on the precordial leads of the chest.

5 CLINICAL CASES 91 R P T Q S Atrium SA node AV node Ventricle Figure Major waves of the ECG. The P, QRS, and T waves are shown corresponding to characteristic action potentials in the key cardiac structures. are produced by the coordinated opening of numerous Na + channels across the ventricles. Another isoelectric period follows during the prolonged plateau (phase 2) of the ventricular action potentials, when little net current flows. The T wave then occurs, produced by the less synchronous repolarization (phase 3) of the ventricular muscle cells. First-degree heart block, which is produced by slowing of conduction through the AV node, is demonstrated on the ECG by a prolongation of the PR interval. Second-degree heart block occurs when a fraction of the action potentials fail to propagate through the AV node. This is demonstrated by a larger number of P waves than QRS complexes. Every QRS complex is associated with a preceding P wave, with the PR interval either remaining fixed or progressively increasing during successive cycles until a QRS complex is dropped. Third-degree, or complete, heart block occurs when no action potentials propagate through the AV node. In this case, the P waves and QRS complexes are independent of each other, and the QRS complexes occur less frequently than do the P waves because the latent ventricular pacemaker that takes over has a longer intrinsic cycle period. All

6 92 CASE FILES: PHYSIOLOGY three degrees of heart block can be produced transiently by parasympathetic stimulation of the AV node as well as by other causes, such as tissue injury. Ectopic pacemakers can lead to atrial or ventricular tachycardia and to occasional premature contractions. Premature atrial contractions display an early P wave, often with an abnormal shape because the atrial discharge is initiated in a different part of the atrium than is normally the case. The following RR interval is usually normal. Premature ventricular contractions display an early QRS complex without any preceding P wave. The QRS complex is abnormal (broadened and sometimes inverted) because of the abnormal site of initiation and the lack of normal activation of the Purkinje fiber system. If reentry in the atria leads to atrial fibrillation, all P waves are lost and replaced by irregular voltage fluctuations and the RR interval becomes irregularly irregular. In ventricular fibrillation, all regular electrical signals in the ECG are lost while the ventricles quiver ineffectively. Hypertrophy increases the mass of tissue that generates action potentials. If the hypertrophy is localized to one part of the heart, it alters the heart s mean electrical axis. This axis is determined by estimating the area under the QRS complex in different leads and plotting the vectors or by simply noting which lead is at right angles to the lead that is recording the minimal deflection. The normal mean electrical axis is down and to the left because the left ventricle has the greatest mass. In left ventricular hypertrophy, the axis would be shifted farther to the left. In right ventricular hypertrophy, it would be shifted to the right. Acute MI can cause a sustained, partial depolarization of surviving myocardial cells in the region of injury, and this depolarization generates an injury current between those cells and normal cells in the heart. Because the ECG measures only changes in potential produced by changes in current, not absolute potentials, this steady injury current has no effect on the baseline of the ECG. However, during the plateau of the ventricular action potentials (the ST segment), membrane potential during the plateau phase of cells in the depolarized region will be close to that of cells in the remainder of the ventricle that are also in the plateau phase, and the recorded potential will be close to true zero. Because the baseline is not at true zero (because of the injury current), the ST segment will be elevated or depressed from the baseline (depending on the location of the injury and the lead examined) during an acute MI. COMPREHENSION QUESTIONS Choose one of these answers (A E) for questions 10.1 through 10.3: A. P wave B. PR interval C. QRS complex D. ST segment E. T wave

7 CLINICAL CASES 93 [10.1] Period when ventricular action potentials are in their plateau phase. [10.2] Prolonged during first-degree heart block. [10.3] Produced by depolarization of atrial fibers. [10.4] An emergency room physician performs carotid massage in an attempt to slow the heart rate of a patient with supraventricular tachycardia. The physician explains to the patient that this maneuver is expected to increase vagal stimulation. A dramatic increase in activity of vagal preganglionic axons is most likely to result in which of the following? A. Decrease the RR interval B. Decrease the number of QRS complexes relative to the number of P waves C. Decrease the PR interval D. Decrease the duration of the ST segment E. Shift the mean electrical axis of the heart to the right Answers [10.1] D. Ventricular cells are in the plateau phase of the action potential during the ST segment, which is isoelectric (remaining at baseline) because there is no change in current flow and the net amount of current is very small. [10.2] B. The PR interval is prolonged because conduction through the AV node is slowed significantly during first-degree heart block. [10.3] A. The P wave is produced by atrial depolarization. The P wave is slower and shorter than the QRS complex because the atria lack a fast conducting system corresponding to the bundle of His-Purkinje fiber system to synchronize the depolarization of the atrial working fibers. [10.4] B. Dramatically increased release of acetylcholine (ACh) from postganglionic neurons strongly excited by vagal preganglionic axons will hyperpolarize AV nodal fibers sufficiently to block a fraction of the impulses being conducted through the AV node. This leads to partial (second-degree) or total (third-degree) heart block. Vagal activity also will decrease rather than increase heart rate (answer A) and conduction velocity through the AV node (answer C) and will have little effect on action potentials in the ventricles (answer D) because there is relatively little parasympathetic innervation of the ventricles. Parasympathetic stimulation has no effect on the mass of cardiac tissue in different regions of the heart and thus has no effect on the mean electrical axis of the heart (answer E).

8 94 CASE FILES: PHYSIOLOGY PHYSIOLOGY PEARLS The ECG, which often is monitored with 12 extracellular electrodes on the surface of the body, detects small potentials produced by the generation of large extracellular currents during synchronous discharge of action potentials by enormous populations of cardiac muscle cells. In a single cardiac cycle monitored on an ECG lead, the P wave represents action potential initiation in the atria, the QRS complex represents action potential initiation in the ventricles, and the T wave represents the repolarization of the ventricles. In first-degree heart block, the number of P waves equals the number of QRS complexes, but the PR interval is prolonged. In second-degree heart block, the number of P waves exceeds the number of QRS complexes, but each QRS complex is coordinated with a preceding P wave. In third-degree heart block, the P waves and QRS complexes are completely independent, and the frequency of P waves exceeds the frequency of QRS complexes. Hypertrophy of part of the heart shifts the mean electrical axis in the direction of the increased mass of cardiac tissue. REFERENCES Downey JM. The Electrocardiogram. In: Johnson LR, ed. Essential Medical Physiology. San Diego, CA: Elsevier Academic Press; 2003: Lederer JW. Cardiac electrophysiology and the electrocardiogram. In: Boron WF, Boulpaep EL, eds. Medical Physiology. Philadelphia, PA: Elsevier Science; 2003:

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