INTRODUCTION Essay, Research Paper
Cardiac Location and StructuresThe heart is the driving force of the circulatory system, contracting about 70 times/minute to pump an adequate volume of blood with sufficient pressure to perfuse all body organs and tissues. The muscular organ, about the size of a clenched fist, weights from 300 to 400 g. It is located within the mediastinum of the thoratic cavity, above the diaphragm and between the lungs. This location subjects the heart?s activity to influence from all pressure variances during respiration, Fassler, (1991).Intrathoracic pressure varies with the respiratory cycle. On inspiration, the heart moves slightly vertically, and the increased negative pressure generated in the thoracic cavity increases venous blood return to the heart and pulmonary blood flow. On respiration, the heart moves slightly horizontally as the diaphragm rises, and a decreased negative pressure is generated.The pericardial sac is a fibrous membrane that doubles over onto itself to form two surfaces. A small amount of pericardial fluid in the sac allows the two surfaces to slide over each other without friction as the heart beats. The pericardium performs several functions. First, it provides shock-absorbing protection. Second, it acts as a protective barrier against bacterial invasion from the lungs. Third, because of its fibrous nature, it protects the heart from sudden overdistention and increase in size, Fassler, (1991).The heart has three tissue layers: the epicardium (outer layer), the myocardium (middle layer), and the endocardium (inner layer). The epicardium is the thin inner layer of the pericardium. The myocardium, thickest of the three layers, is composed of muscle fibers that contract, creating the pumping effect of cardiac activity. The endocardium, a smooth, membranous layer that lines all cardiac chambers and valve leaflets, is continuous with the intima, or lining, of the aorta and arteries, Fassler, (1991).The heart?s four chambers ? the right and left atria and left atria and the right and left ventricles ? are separated by the interatrial and interventricular septa. The atria are thin-walled, low-pressure chambers that serve primarily as reservoirs for blood flow into the ventricles. The ventricles are formed by muscle fibers that contract to eject blood to the pulmonary vasculature (right) and systemic circulation (left). Because the left ventricle must achieve the high pressure needed for systemic circulation, it is much thicker than the right ventricle, (Fig. #1), Fassler, (1991).The right atrium receives venous blood from the body via the venae cavae. The superior vena cava returns blood from the structures above the diaphragm, and the inferior vena cava drains venous blood from below the diaphragm. The coronary sinus returns venous blood to the right atrium. At the base of the right atrium is the tricuspid valve, which controls blood flow into the right ventricle and prevents back flow to the atrium during ventricular systole. The tight ventricle pumps blood through the pulmonary valve and the branches of the pulmonary artery to the lobes of the lungs, the pulmonary capillaries, and the alveolar capillaries that surround the alveoli, (Fig. #2), Fassler, (1991).At the alveolar capillaries, gas exchange occurs, that is, blood gives off carbon dioxide and receives oxygen. Then, oxygenated blood returns through the pulmonary veins to the left atrium. The mitral valve at the base of the left atrium controls blood flow to the left ventricle and prevents backflow to the left atrium. Both the mitral and the tricuspid valves are attached to the strong chorae tendineae, fibrous filaments that arise from the papillary muscles of the ventricle
Fig. (#1) Location of cardiac structures, Fassler, (1991).
Fig. (#2) Blood flow through the heart, Fassler, (1991).
and work to prevent eversion of the valves when the ventricle contracts, The left ventricle pumps blood through the aortic valve into the aorta, (Fig. #3), Fassler, (1991).The basic contractile unit in the myocardium, the sarcomere, is composed of actin and myosin filaments, which are contractile proteins. The degree to which actin and myosin overlap depends on the length of the sarcomere, which is determined by muscle stretch. Less overlap occurs during diastole, as the ventricle fills and the muscle stretches; more overlap occurs during diastole, when the muscle contracts. Contraction occurs when the action potential stimulates movement of calcium with energy release, causes the filaments to slide past each other and shorten sarcomere, Fassler, (1991).
Cardiac CycleThe heart ejects blood during ventricular systole, which comprises approximately one-third of the cardiac cycle. The cardiac muscles relax during diastole, which comprises the remaining two-thirds of the cardiac cycle. The first phase of systole, called isovolumetric contraction, begins with closure of the tricuspid and mitral valves. Pressure in the walls of the ventricles builds in preparation for mechanical contraction. When ventricular pressure becomes higher than pressure in the aorta and pulmonary artery, the pulmonary and aortic valves open, allowing for paid ejection of blood. Blood is ejected rapidly at first and then more slowly as pressure decreases. Pressure in the ventricles continues to fall until the aortic and pulmonary valves close. Closure of the valves begins the first phase of diastole, called isovolumetric relaxation. During this time, ventricular pressure continues to decrease. When pressure in the ventricles becomes less than atrial pressure, the tricuspid and mitral valves open, permitting rapid ventricular fillings. The ventricle continues to fill until atrial contraction occurs. Atrial
Fig. (#3) Coronary Artery Circulation, Fassler, (1991)
contraction contributes the final volume for ventricular filling, Fassler, (1991).
Pulmonary CirculationThe right side of the cardiac pump, consisting of the right atrium and right ventricle, delivers venous blood to the lungs for oxygenation. The thin-walled pulmonary vessels have little medial muscle and offer six times less resistance than systemic blood vessels. Since the pulmonary vessels offer little resistance, the right ventricle is considered a low-pressure pump, Fassler, (1991).
Systemic CirculationThe left side of the cardiac pump, consisting of the left atrium and left ventricle, generates the high pressures necessary to overcome peripheral vascular resistance and to deliver oxygenated arterial blood to all body tissues. Because the left ventricle has a larger muscle mass than the right ventricle, must generate more pressure, and contract with greater strength, it has a greater need for oxygen. Thus, the left ventricle is particularly susceptible to the effects of deficient oxygen supply, Fassler, (1991).
Coronary CirculationCoronary artery circulation delivers oxygenated blood to the heart, primarily during diastole. The small coronary arteries branch off the aorta and encircle the heart at the epicardial layer.The arteries continue to branch and enter the myocardium and endocardium, becoming arterioles and then capillaries. The right coronary artery branches to the right from the aorta and supplies blood to the right atrium, the right ventricle, the sinoatrial (SA) and atrioventricular (AV) nodes of the conduction system, and, in most people, the inferior-posterior wall of the left ventricle. The left coronary artery bifurcates into the left anterior descending and circumflex coronary supplies the left atrium and the left ventricle. In some people, the circumflex artery also provides oxygenated blood to the posterior surfaces of the left atrium and left ventricle, Fassler, (1991).
HemodynamicsCardiac output refers to the volume of blood ejected by the left ventricle into the aorta in 1 minute-normally, about 4 to 6 liters/minute at rest. Cardiac output is a product of the heart rate multiplied by the stroke volume, the amount of blood ejected from the left ventricle with each beat. The heart rate may vary form second to second or minute to minute. The stroke volume may vary from beat to beat, Fassler, (1991).
Heart RateA change in heart rate can dramatically affect cardiac output. For instance, when the heart rate increases, cardiac output may double or triple. In a person with heart disease, such an increase can be dangerous because it decrease diastolic filling time, increases oxygen demand, and decreases coronary artery perfusion time. Conversely, if the heart rate falls below 50 beats/minute, cardiac output usually decreases, Fassler, (1991).
Stroke VolumeVariables influencing the stroke volume include preload, afterload and contractility. Preload is the volume of blood that fills the ventricle at the end of diastole. An increase in diastolic volume increases muscle stretch and subsequent stroke volume. Either excessive or inadequate preload can increase the heart?s work load and decrease the stroke volume. Afterload, the resistance to flow from the ventricle, increase secondary to vasoconstriction in the peripheral blood vessels or to increased resistance, such as aortic stenosis. Increases in afterload result in greater oxygen demand because the heart must use more contractile energy to eject blood. Contractility refers to the ability of cardiac muscle fibers to shorten. Calcium within the cell allows protein fibers to be attracted to each other causing muscle shortening. The contractile (or inotropic) state of the myocardium can be influenced by many factors. For instance, epinephrine, dopamine, and sympathetic nervous system stimulation exert a positive inotropic effect (increase contractility), whereas hypoxemia, acidosis, and such drugs as propranolol (Inderal) exert a negative inotropic effect (decrease contractility), Fassler, (1991).
Arterial Blood PressureThe pressure exerted on the arterial wall as blood flows through the arteries is called arterial blood pressure, a product of the cardiac output and the total peripheral resistance, which is determined by blood viscosity and by the length and internal diameter of the vessels. Arteries have a medial or muscle layer in their wall that permits constriction or dilation of the vessel. Thus, peripheral vascular resistance and blood pressure are affected by vasoconstriction and vasodilation, Fassler, (1991).
Cardiac InnervationInnervation of the heart involves the autonomic nervous system and the baroreceptor and Bainbridge reflexes.
Autonomic Nervous SystemThe autonomic nervous system influences cardiac activity through sympathetic and parasympathetic verve fibers. Sympathetic fibers are found in the atrial and ventricular walls, the SA and AV nodes. The sympathetic effect on the heart is mediated through beta receptor sites and release of norepinephrine. Stimulation of beta receptors increase heart rate, conduction velocity, and contractility. The major effects are usually on the SA node, increasing heart rate, and the myocardial muscle. The sympathetic nervous system also has receptor, sites, primarily alpha and beta receptors in peripheral blood vessels. When the sympathetic nervous system is stimulated, the alpha effects predominate in the blood vessels and cause vasoconstriction. The parasympathetic effects on the heart are mediated through release of acetylcholine at nerve endings in the SA node, atrial muscle, and AV node. Parasympathetic or vagal stimulation decrease heart rate and conduction velocity, Fassler, (1991).
Baroreceptor and Bainbridge ReflexesThe baroreceptor reflex mediates heart rate as well as peripheral vascular resistance. The baroreceptors-specialized ?pressure-sensitive? tissue located in the aortic arch and carotid sinuses-increase their rate of discharge when they are stretched by increase blood pressure. Impulses are transmitted to the cardiovascular center in the medulla. The cardiovascular center decreases sympathetic stimulation and increases parasympathetic stimulation, thereby decreasing heart rate initiating blood vessel dilation. Conversely, baroreceptors also respond to decreasing blood pressure by increasing heart rate and vasoconstriction, Fassler, (1991).The Bainbridge reflex is thought to be mediated by stretch receptors in the atria. These receptors may respond to increased volume and cause an increase in heart rate. Contractility is unaffected by the Bainbridge reflex, Fassler, (1991).
CORRELATION OF PHYSIOLOGIC EVENTS TO ELECTRICAL EVENTS RECORDED ON THE ECG
Through out the cardiac cycle the heart produces a series of action potentials. This sequence of action potential produces a series of deflections that represents different events within the cardiac cycle. The classic series of deflections constituting one cardiac cycle is: P wave, QRS complex, and T wave. The significance of these deflections (and the intervals between) is explained as follows, (Graph #1), (Fig. #4), Murphy, (1991).
P WaveThe first wave of the cycle, the P wave, represents the spread of electrical depolarization throughout the atria, Murphy, (1991).
PR IntervalThe PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It represents the time it takes for the electrical impulse to travel from the atria to the ventricles. Thus the PR interval has two components: (1) the P wave (time needed to depolarize the atria) and (2) the PR segment (end of P wave to beginning of the QRS complex, representing the time the impulse spends in the AV node), Murphy, (1991).
QRS Complex
Fig. (#4) Normal cardiac intervals, Murphy, (1991).
The QRS complex represents the spread of electrical depolarization throughout ventricular muscle. The QRS complex is composed of several ?wave? outlined in detail below, Murphy, (1991).Q WaveThe Q wave is the first negative deflection preceding an R wave (regardless of the size of the deflection). A Q wave is always downward in direction. This wave usually represents depolarization of the muscular interventricular septum in the frontal leads (I, II, III, aVR, aVL, aVF). Abnormally deep Q waves in these leads are often seen with myocardial infarction, Murphy, (1991).
R WaveThe R wave is the first positive deflection of the complex. In the frontal leads this wave represents depolarization of the main bulk of ventricular muscle. An R wave is always directed upward regardless of a preceding Q wave, Murphy, (1991).
S WaveThe S wave is the negative deflection following an R wave. An S wave usually represents the late depolarization of the last bit of left ventricular muscle. In the anterior precordial leads(V, to V3) the S wave is large because of the normal slightly posteriorly directed mean QRS vector, Murphy, (1991).
T WaveT wave represents ventricular repolarization.ST SegmentThe ST segment is measured from the end of th
QT IntervalThe QT interval is measured from the beginning of the QRS complex to the end of the T wave. This interval represents the entire time required for ventricular depolarization and repolarization, Murphy, (1991).
U WaveThe U wave is an infrequent finding on a normal ECG. The U wave appears after the T wave. It is small and of low voltage. Its exact significance in the normal ECG is unknown. It has been postulated as representing repolarization of the Purkinje fiber conduction system. Several pathologic states give rise to U waves, the most common of which is hypokalemia, Murphy, (1991).
The Conduction SystemThroughout the heart runs a system of highly specialized tissues capable of conducting impulses more rapidly than surrounding muscle tissue. These special tissues are capable of conducting impulses many times faster than normal cardiac muscle tissue and have an extremely short refractroy period. Furthermore, portions of the conduction system possess inherent automaticity that allows spontaneous depolarization at certain characteristic rates. Because the SA node is the tissue with the fastest inherent automaticity, it usually functions as the primary pacemaker of the heart. If the SA node is blocked or damaged, the fastest viable site becomes the primary pacemaker of the heart, (Fig. #5), Murphy, (1991).
Fig. (#5) The electrical conduction system of the heart, Murphy, (1991).
ELECTRODES AND LEADS
Because the heart is surrounded by tissue and body fluids (electrolyte solutions), the electrical action potentials produced in the heart are widely conducted throughout the body. However, ECG tracings are recorded from electrodes positioned at several specific points, Murphy, (1991).An electrode is a sensing device that detects changes in electrical potential at a given point. The electrode is connected to a galvanometer, which measures and records these potential differences. Each electrode thus becomes a different ?eye? through which the heart?s electrical activity may be viewed. Whenever the electrical axis of the heart points primarily toward a positive electrode, a positive (upward) deflection is recorded on the ECG. If the axis is directed away from a positive electrode, the deflection on the ECG is negatively (downwardly) directed. Leads are another term for these electrodes. Three ?types? of leads are currently in use today: (1) Standard bipolar limb leads, (2) Augmented unipolar limb leads, and (3) Unipolar precordial leads, Murphy, (1991).
Standard Bipolar Limb Leads (I, II, III)The standard limb leads, designated I, II, and III by convention, represent true bipolar leads, That is, they detect differences in electrical potential between two different points. Lead I connects the two arms, lead III the left arm and the left leg, and lead II (the hypotenuse of the triangle) connects the left leg and right arm. The result is the well known Einthoven?s triangle. If each of the sides is now pushed to the center of the triangle, three intersecting lines of reference are produced, which make up the triaxial reference system, (Fig #6), Murphy, (1991).
Fig. (#6) Triaxial reference system, Murphy, (1991).
Augmented Unipolor Limb Leads (aVR, aVL, aVF)The second set of leads, the augmented unipolar limb leads, are so called because they detect potential differences at a single point. Each lead has one point that serves as a positive electrode and three other points connected to a resistor that serves as the negative electrode. The lines of reference produced between each augmented limb lead and the heart produce a new set of axes. This new triaxial system is about 30 degrees out of phase with that generated by the standard limb leads, I, II and III. When the two triaxial systems are combined, the hexaxial reference system is produced, (Fig. #7), Murphy, (1991).The hexaxial reference system is the standard limb lead system used today. This system represents a 360 degrees circle used to map the frontal electrical axis of the heart. Each of the six poles represents 60 degrees of the circle. By convention the poles are assigned designations for axis determination, (Fig. #8), Murphy, (1991).
Unipolar Precordial Leads (V1 to V6)The precordial electrodes provide a second dimension for determining the heart?s electrical axis and six more ?views? of its anterior and lateral aspects. Like the augmented leads, the precordial leads are unipolar, detecting potential differences at a single point. V4 to V6 are all on the same horizontal plane. V1 and V2 are likewise on a horizontal plane. V3 is situated midway between V2 and V4. These leads determine whether the electrical axis of the heart points ?forward? (positive) or ?backward? (negative), (Fig. #9), Murphy, (1991).Additionally, the precordial leads provide six more electrical ?views? in a horizontal plane across the anterior and lateral aspects of the heart.
The three types of leads (bipolar, augmented unipolar, and precordial provide a total of 12 different electrical ?views of the heart. This is of great clinical importance in evaluating the many varieties of cardiac pathology manifested on the ECG, Murphy, (1991).
Normal ElectrocardiogramThe ECG is generally recorded on graph paper at a standard speed of 25 mm/sec. In the standard ECG recording, 0.1 mV produces a 1-mm positive (upward) deflection, (Graph #2), Mosby, (1983).Although the SA node normally is the pacemaker of the heart, it does not contain enough mass the produce a voltage detectable by the surface ECG. The P wave, caused by depolarization of the atria, is the first evidence of electrical activity in the cardiac cycle. After the P wave the ECG returns to baseline as the depolarization wave is slowed in the tissue of the AV node. When the ventricular muscle depolarizes, the QRS complex is produced. An initial downward or negative deflection is termed a q wave, whereas an initial upward or positive deflection is termed an R wave. A positive deflection following a q wave is also termed an R wave. By convention, r indicated a small upward deflection and R a large upward deflection. The S wave is a negative deflection following an R wave. If a QRS complex has only a negative deflection without a positive deflection it is known as a QS complex. In a QRS complex with more than one R wave, the additional positive deflection is labeled R. Once the ventricles are completely depolarized, the ECG returns to the baseline (ST segment). The T wave that follows represents ventricular repolarization and may sometimes be followed by a small U wave. Atrial repolarization is generally lost in the PR interval and QRS complex because of the small amount of force produced, Mosby, (1983).
DRUG AND ELECTROLYTE EFFECTS
Various drugs and alterations in electrolyte levels can affect cellular electrophysiology. For instance, digoxin (Lanoxin) in a therapeutic dose may cause a downward cove, or recession, of the ST segment that mimics ST segment depression. Digoxin toxicity may produce numerous arrhythmias, including bradycardias, AV blocks, ventricular ectopy, atrial fibrillation, and atrial flutter, Kessler, (1995).At high blood levels, Class 1A antiarrhythmic agents, such as quinidine sulfate (Quindex) and procainmaide, can affect the ECG. The most common effects are a widened QRS complex and a lengthened QT interval. Widening of the QRS complex by 50% or more is a sign of toxicity. Class II antiarrhythmic agents (beta blockers) may widen the PR interval, and Class IV agents (calcium channel blockers) may slow conduction and lengthen the QT interval, Fassler, (1991).Abnormal serum potassium levels also effect the ECG. Hyperkalemia widens the QRS complex; produces tall peaked or tented T waves; alters repolarization; and eventually slow the heart rate. Acute hyperkalemia may produce ventricular fibrillation. Hypokalemia affects cell membrane competency, may produce premature ventricular complexes, enhances the toxic effects of digoxin, and causes short or flattened T waves and U waves, Fassler, (1991).
DigitalisDigitalis is given to cardiac patients for two major reasons; (1) to slow conduction through the AV node, and (2) to increase myocardial contractility in heart failure.Slowing of AV conduction is useful in atrial fibrillation, where it brings the ventricular response down to a reasonable rate, and in supraventricular tachyarrhythmias that involve conduction through the AV node, such as PSVT, where it may interrupt the arrhythmia, Huang, (1993).The normal effect of digoxin is sagging or scooping ST- segment depression. A prolonged PR interval also can be seen.The effects of toxic levels of digoxin are many and include sinus bradycardia, AV block (first, second, or third degree), atrial fibrillation with slow ventricular response, accelerated junctional tachycardia, PAT, often with AV block, and ventricular ectopy, VT, VF, Huang, (1993).Patients in atrial fibrillation who develop accelerated junctional tachycardia go from an irregular rhythm (AF) to a regular rhythm (junctional tachycardia); because they still have no P waves, they are often said to have regularization of ventricular response. This arrhythmia should immediately raise the suspicion of digoxin toxicity, although other causes that irritate the junctional tissues may lead to the same rhythm, Huang, (1993).
QuinidineNormal quinidine effects include QRS prolongation, ST-segment depression, T- wave inversion, and QT prolongation. Toxic rhythms include ventricular ectopy and polymorphous VT, which in the setting of a prolonged QT interval is torsades de pointes, Huang, (1993).
Tricylic Anitdepressants and PhenothiazinesTricyclic antidepressants and phenothiazines have similar effects as quinidine. They prolong the QRS duration and the QT interval and cause ST-segment depression and T-wave inversion. In overdoses of tricyclic antidepressants, the QRS duration is more progranstically important than the absolute level of the drug. The QRS duration acts as a bioassay of the effects of the drug, Huang, (1993).
HyperkalemiaIncreasing serum concentration so potassium lead the following changes: tall peaked T waves, AV conduction problems and flat P waves that may be difficult to see, prolonged QRS complex duration, ST-segment depression and T-wave inversion, VT and VF, Huang, (1993).
HypokalemiaHypokalemia leads to ST-segment depression and T-wave flattening. With serum potassium levels less than 3.0, prominent U waves will be seen. These are due to continues ventricular repolarization, but they follow the T wave, Huang, (1993).
HypercalcemiaHypercalcemia leads to a shortened QT interval, with the T wave rising from the QRS.
HypocalcemiaHypocalcemia leads to a prolonged QT interval. However, in contrast to the effects of quinidine, the T-wave duration remains normal and the ST segment is prolonged. If the hypocalcemia is severe, there may be T-wave inversion as well, Huang, (1993).
PericarditisPericarditis is an inflammation of the pericardium. The changes seen on ECG are ST-segment elevation and PR-interval depression. The baseline of the tracing should be taken as the segment between one T wave and the next P wave. If the PR segment is below this level, there is PR-interval depression, Huang, (1993).
Pericardial EffusionPericardial effusions may cause low voltage because of the fluid that comes between the heart and the electrodes on the chest. There also may be electrical alternans, in which the size of the QRS complex varies from beat to beat, Huang, (1993).
CONCLUSION
Electrocardiography is an essential feature of modern coronary care and of arrhythmia diagnosis; no cardiologic workup is complete without it, Parker, (1996)Previous studies have shown that electrocardiograms (ECGs), are not likely to change the diagnosis of a skilled cardiologist who determines that a patient has heart disease on the basis of history and physical examination. Swenson and colleagues conducted a prospective study to determine whether physicians are more likely to change their diagnosis if they use ECGs in the evaluation of a patient referred for chest pain or heart murmur, Huffman, (1991).Children between one month and fourteen years of age were included in this study if they were referred to a cardiology group for evaluation of either a heart murmur (79 percent) or chest pain (21 percent). The cardiologist made a diagnosis of no heart disease, possible heart disease or definite heart disease based on his or her findings on the history and physical examination. Definite heart disease was defined as any cardiac lesion that would potentially require follow-up or endocarditis prophylaxis, or that could cause morbidity. ECGs were then performed in all of the patients. Results were reviewed by the cardiologist, who changed the original diagnosis if necessary or ordered an echocardiogram if indicated, Huffman, (1991).Overall, four children (7 percent) who were initially thought to have no heart disease were found to have heart disease. Most (68 percent) of the 25 patients initially diagnosed with possible heart disease had normal ECGs. In nearly one half (48 percent) of the patients, the diagnosis of possible heart disease was changed to no heart disease (28 percent) or definite heart disease (20 percent) based on the ECG results. Finally, in the group initially diagnosed with definite heart disease, ECGs confirmed these findings in one third of the patients, Huffman, (1991).The authors conclude that the information provided by routine ECGs are valuable in the evaluation of patients with heart murmurs or chest pain, Huffman, (1991).
BIBLIOGRAPHY
Fassler, M. (1991). Electrocardiogram Interpretation and Emergency Intervention.Springhouse, Pennsylvania: Springhouse Corporation
Huang, P. (1993). Introduction to Electrocardiography. Philadelphia, Pennsylvania:W.B. Saunders Company
Huffman, G. (1997). ?Radiographs and ECGs for assessing pediatric chest pain.? AmericanFamily Physician. June, pp. 28-41.
Kaye, D. (1983). Fundamentals of Internal Medicine. St. Louis, Missouri: C. V. MosbyCompany
Kessler, D. (1995). ?Ambulatory Electrocardiography.? Archives of Internal Medicine.January 23, 1995, pp 165-170.
Murphy, K. (1991). ECG Essentials. Chicago, Illinois: Quintessence Publishing Co.