EKG II - HYPERTROPHY / ENLARGEMENT - Tufts University

Updated 03/30/2020

ELECTROCARDIOGRAPHY - HYPERTROPHY / ENLARGEMENT

JohnE. Rush,DVM,MS,DACVIM(Cardiology),DACVECC Cummings School of Veterinary Medicine At Tufts University

OBJECTIVES List stimuli for physiologic and pathophysiologic cardiac hypertrophy. Describe the cellular changes and gross morphologic differences with eccentric vs. concentric hypertrophy. Be able to explain, using the Law of LaPlace, how myocardial hypertrophy alters wall tension. List ECG criteria and be able to identify ECG enlargement patterns of left atrial enlargement (P mitrale), right atrial enlargement (P pulmonale), left ventricular enlargement, and right ventricular enlargement in the dog and the cat. Identify electrocardiographic patterns for axis deviation (right axis deviation, left axis deviation) and bundle branch blocks (right bundle branch block, left bundle branch block and left anterior fascicular block). *** Includes especially important concepts

ELECTROCARDIOGRAPHY II Hypertrophy/Enlargement and Bundle Branch Block Physiology/pathophysiology, biochemistry, pathology of cardiac hypertrophy 1. Established causes of cardiac hypertrophy include:

a. postnatal growth b. increased workload (increased preload/afterload) c. ischemia/injury to myocardium d. hereditary factors e. hypothermia f. increased circulating/local levels of catecholamines g. increased circulating/local levels of angiotensin II levels h. pregnancy i. exercise j. anemia k. hyperthyroidism l. Many diseases

*Physiologic vs pathologic hypertrophy - cardiac hypertrophy can be induced by physiologic adaptation to needs of the organism by an otherwise healthy myocardium. These conditions are not usually associated with early biochemical (relative energy depletion) or mechanical malfunction of the heart that is seen with instances of pathologic hypertrophy (i.e. cardiac chamber enlargement secondary to a stenotic or incompetent heart valve).

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2. A stimulus for hypertrophy of cardiac muscle in cases of increased preload (volume overload; ex. mitral insufficiency) and/or increased afterload (pressure overload; ex. aortic stenosis, systemic hypertension) is thought to be an increase in wall stress (tension). ***

a. A chain of events is set into motion that results in compensation (a decrease towards normal of ). This process involves hypertrophy of the cardiac muscle, and this increase in wall thickness results in a diminution of wall tension according to the physical principles defined in the Law of LaPlace. ***

wall stress

P x r

2X wall thickness

P = pressure, r = radius of curvature

b. In the event that the cellular/subcellular compensatory mechanisms are unable to completely counteract an increase in wall stress, induced by an incompetent valve, stenotic valve or otherwise injured myocardium, a progressive process eventually resulting in myocardial failure may result.

c. The stimulus for cardiac hypertrophy is complex, is not always triggered exclusively by wall stress, and may be related to catecholamines, angiotensin, ischemia, an upset in the balance in energy (ATP) production and utilization, and many other factors.

? Individual myocytes undergo morphologic change soon after the stimuli for hypertrophy are encountered. This is associated with some increase in the number of nuclei/cell, increase in the sarcomere numbers and some longitudinal

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splitting of myocytes. Early and progressive increase in interstitial tissue (fibrosis) is associated with certain diseases that cause myocardial hypertrophy.

o Physiologic studies demonstrated that hypertrophy of the myocardium is associated with a depressed force-generating capacity per unit cross section of myocardium at any given muscle length, but that hypertrophied myocardium has a greater than normal overall force-generating capacity due to an increased number of weaker cross-sectional units.

3. The exact biochemical/subcellular pathogenesis of pathologic cardiac hypertrophy are complex.

4. The specific response of the myocardium to increased stress is determined in large part by the nature of the added work load that is present. These will be discussed further as they relate to increased workloads imposed upon the left ventricle. However, it should be understood that similar changes can and do occur in the right ventricle when cardiovascular disorders have a predominant effect on the right side of the heart. a. Concentric hypertrophy *** ? Increased afterload (i.e. aortic or subaortic stenosis, systemic hypertension or increased systemic vascular resistance). ? Enlargement is primarily due to an increase in the size, particularly the width of the fibers. There is some evidence using election microscopy that hypertrophy is accompanied by both splitting and addition of sarcomeres in parallel. ? Increased O2 consumption ? Beneficial effects o Total force may be increased as a result of a greater muscle mass. o Increased ejection fraction. b. Eccentric hypertrophy (dilatation) *** ? Increased preload (i.e. intra- and extracardiac shunts, aortic insufficiency, mitral incompetence). ? Chamber enlargement is initiated by dilatation with secondary hypertrophy. Dilatation is associated with an increase in cell size and length, a rearrangement and shifting (i.e. "slippage") of myofibrils within the myocardial cells and possibly an increase in the number of sarcomeres in series. ? Increased O2 consumption ? Beneficial effects o Increased velocity and extent of myocardial fiber shortening o Normal or increased ejection fraction o Greater proportion of contractile energy is expended in shortening than in tension development

Electrocardiographic Alterations in Cardiac Enlargement/Hypertrophy Clinical recognition of cardiac enlargement normally incorporates a good physical examination and a series of noninvasive diagnostic procedures. As a rule, thoracic radiography, electrocardiography and echocardiography are the procedures most useful in obtaining this information. However, each of these diagnostic procedures has certain inherent limitations which tend to reduce their usefulness and in certain circumstances. An example of these limitations: In patients with concentric hypertrophy, the external size of the left ventricle on thoracic radiographs may be normal or minimally enlarged. However, the increased LV muscle mass that accompanies this condition usually can be identified by electrocardiography and echocardiography. On the other hand, when eccentric hypertrophy and its associated LV

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dilatation is present, thoracic radiography and electrocardiography are frequently able to identify its presence. The degree of cardiac enlargement or hypertrophy, patient cooperation and the presence of other intrathoracic processes (i.e. pleural effusion) may limit the diagnostic capabilities of each procedure. The real value of electrocardiography lies in its capability of being able to provide quality information that cannot be obtained by other means. In addition to its usefulness in providing information regarding cardiac chamber enlargement/ hypertrophy, electrocardiography also can contribute the following: (1) identification of cardiac arrhythmias and conduction disturbances, (2) recognition of ventricular ischemia, (3) information regarding drug effect/toxicity and (4) insight to certain electrolyte abnormalities. In the discussion that follows, we will concentrate on the electrocardiographic recognition of cardiac enlargement/ hypertrophy. Unfortunately, due to differences between the activation process of Type A species (including dog cat and primates) vs. the extensive Purkinje fiber penetration in Type B species (hooved animals like horses, cattle), the evaluation of cardiac enlargement in the Type B animals is neither sensitive or specific, so the information that follows is only applicable to dogs and cats and primates. Measurements are usually made from ECG tracings of lead II at 50 mm/sec paper speed with 1mV = 1cm Atrial Enlargement 1. P pulmonale or Right Atrial Enlargement Pattern - PII: duration < 0.04 sec; amplitude >

0.4mV dogs, > 0.2mV cats. *** P pulmonale is associated with right atrial enlargement. In dogs it can also been seen with chronic respiratory disease. In some cats, with severe left atrial enlargement may have P pulmonale (right atrial enlargement pattern on ECG) instead of P mitral (left atrial enlargement pattern on ECG).

LEAD II, (50 mm/sec)

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2. P mitrale or Left Atrial Enlargement Pattern- PII: duration > 0.04 sec; amplitude < 0.4mV dogs, < 0.2mV cats.*** Is associated with left atrial enlargement and called P mitrale since disease of the mitral valve is often associated with left atrial enlargement. There can be a notch associated with the widened P wave, especially in dogs.

P mitrale or left atrial enlargement in a dog 50 mm/sec

3. Biatrial enlargement - PII: duration > 0.04 sec; amplitude > 0.4mV dogs, 0.2mV cats (beware over interpretation of P mitrale) 5

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