The Electrocardiography In Pericarditis Biology Essay

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The electrocardiography pattern in patients with pericarditis has been known for several decades. These electrocardiographic abnormalities produced by pericarditis evolve through several distinct stages that reflect different clinical and pathological phases of the disease.

The electrocardiographic abnormalities produced by pericarditis can be attributed to 3 different factors (Surawicz, 1970);

1) The presence of effusion.

2) The "injury" of the superficial myocardium by the pressure of fluid, and

3) Superficial myocarditis.

TABLE: ELECTROCARDIOGRAM IN PERICARDITIS

FACTORS AFFECTING ELECTROCARDIOGRAM

ELECTROCARDIOGRAPHIC CHANGES

1. Pericardial effusion

Low voltage: cyclic variation of amplitude.

2. Pressure (fluid, fibrin on myocardium)

Current of injury' leading to deviation of S-T segment from the base line.

3. Superficial Myocarditis

Abnormal T-wave vector without lengthening of the Q-Tc interval.

EFFECTS OF PERICARDIAL EFFUSION:

1) Low voltage: this has always been considered to be a valuable sign and is thought to depend on the pressure of a lake of fluid about the heart causing short circuiting effect. Low voltage is said to be present when the QRS amplitude is 5 mm or less in each lead. If the voltage remains low after the removal of fluid the decreased amplitude of the electrocardiographic deflections is probably due to the insulating effect of fibrin (Lepeachkin, 1951). The low amplitude of the ventricular complex is frequently associated with normal amplitude of the P-wave in the limb leads. This may be explained by the absence of effusion over the posterior surface of atria, which is a part devoid of pericardial duplication (Holzmann, 1965).

2) Electrical alternans: The variations in the amplitude of the ventricular complex may be similar to the "electrical alternans" produced by an alternating configuration of the ventricular action potential or by alternating changes in intraventricular conduction. However, in pericarditis the "alternans" is apparently due to changes in cardiac position which result from the rotational, pendular motion of the heart. Normal rotation of the heart along the axis is attributed to the contraction of spiral muscle and the uncoiling of the large vessels. The motion is normally restrained by the relaxation filling and gentle pressure of the lung and mediastinum. The presence of effusion removes these normal restraints, and the heart has more freedom of rotation during systole and fewer tendencies to complete restoration during diastole (Mc Gregor, 1955). Littmann (1963) termed this type of motion "Cardiac Nystagmus". Subtle variations in the amplitude of the ventricular and occasionally the atrial complexes occur in most cases of large effusion, but marked variations are characteristically associated with the presence of cardiac tamponade. The variation in amplitude differs from the typical alternans pattern in that they occur gradually over more than 2 consecutive complexes. However, true alternans pattern may occasionally be present. Such alternans occur when the natural frequency of pendular motion happens to be approximately half the heart rate (Mc Gregor, 1955).

EFFECT OF PRESSURE:

Produced by fluid or fibrin: S-T deviation: Pressure on the myocardium produces a "Current of injury" that is manifested by deviation of the S-T segment from the base line. The resulting S-T vector is directed inferiorly and anteriorly. In horizontal heart the S-T vector tends to be parallel to the lead II axis and in vertical hearts to the lead III axis. The S-T deviation in pericarditis is usually less pronounced than in the early states of myocardial infarction. It is seldom greater than 4-5 mm and monophasic patterns do not occur (Schwab, 1935; Hull, 1961). This suggests that the injury current in pericarditis is probably smaller than in acute myocardial infarction. At the same time, reciprocal depression of the S-T segment in pericarditis is recorded in fewer standard leads than in infarction.

Differentiation from myocardial infarction: In myocardial infarction the terminal portion of the QRS complex is frequently obliterated and incorporated into the S-T segment. In pericarditis the configuration of the QRS complex remains unchanged, but the S wave may be pulled up by the elevated ST segment (Lepeachkin, 1951). The shape of the T wave in patients with the elevation of the S-T segment may be of greater diagnostic importance than the pattern of pulled S wave. In acute stage of pericarditis the amplitude and shape of t wave is usually changed and the elevated ST segment is concave, but in acute infarction. The T wave is frequently obliterated and the elevated S-T segment is convex.

CHANGES ATTRIBUTED TO SUPERFICIAL MYOCARDITIS:

Characteristically, the T wave vector in pericarditis is directed to the right and superiorly. The T wave in pericarditis is usually is inverted in more standard leads than in infarction. In typical cases of pericarditis the T wave becomes inverted in all standard leads with the exception of aVR and V1. However in pericarditis the T waves are usually less deeply or less completely inverted than in myocardial infarction. An incompletely inverted T-wave such as a diphasic wave or a notched T wave is a characteristic feature of the electrocardiographic pattern in pericarditis (Noth, 1940; Winternitz, 1930). T-wave abnormalities of pericarditis can be differentiated from t-wave abnormalities of myocardial infarction because of following factors:

1) The myocardial surface responsible for the abnormal T wave vector is greater in pericarditis than in myocardial infarction.

2) The muscle mass responsible for the T wave vector is smaller in pericarditis than in myocardial infarction.

3) The inflammatory changes associated with pericarditis appear to produce myocardial damage more slowly and insidiously than the ischemic changes associated with myocardial infarction.

Incidence and severity of electrocardiographic abnormalities: The incidence and the severity of the electrocardiographic abnormalities in pericarditis depend upon the origin of disease. Patients with chronic effusion may have no signs of pericarditis except for low voltage and low T-wave amplitude (Bedford, 1964). The typical pattern with ST segment and T wave changes occur in almost all the children (Nadas, 1961) and in all patients with traumatic pericarditis (Tabatzinita, 1961), acute non-specific and purulent pericarditis (Lepeschkin, 1951).

The changes appear less frequently in rheumatic, uraemic and neoplastic pericarditis and in pericarditis after myocardial infarction and cardiac surgery. The lower incidence of characteristic electrocardiographic pattern in this type of pericarditis is due to a lower incidence or lesser severity of accompanying myocarditis.

The duration of electrocardiographic changes produced by pericarditis depends on the cause and the extent of myocardial damage. Permanent electrocardiographic abnormalities occur more frequently after purulent, tuberculous and other type of pericarditis resulting in persistent adhesive or constrictive pericarditis. Atrial fibrillation or flutter is usually present in advanced stages of disease. Patients with sinus rhythm frequently have intra atrial conduction disturbances that produce "P" mitrale of mitral stenosis. However in patients with mitral stenosis and "P" mitrale the mean QRS axis is usually deviated to the right but in those with constrictive pericarditis the QRS vector is usually has an intermediate or left axis.

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