Electrocardiography – Pericarditis, Pericardial Effusion and Cardiac Tamponade

Patients with pericardial effusions may quickly progress to cardiac tamponade. These conditions are often difficult to d iagnose, although physical examination and chest radiography are known to be poorly diagnostic of pericardial effusion. Advanced imaging techniques can accurately detect and quantify the size of pericard ial effusions. Unfortunately, these advanced techniques are expensive and are often not feasible as screening tests for pericardial effusion. In contrast, 12-lead electrocard iogram is inexpensive and is easily performed, but to our knowledge, its diagnostic value for pericardial effusion and cardiac tamponade has not been systematically examined. Pericarditis, pericardial effusion, and cardiac tamponade are associated with various electrocardiographic signs. Low voltage, PR segment depression, ST-T changes and electrical alternans have each been diagnostic of pericardial effusion and / or cardiac tamponade. However, many of the studies that previously investigated these electrocardiographic signs examined patient populations. The diagnostic value of 12-lead electrocardiogram for pericarditis, pericard ial effusion and cardiac tamponade has been reviewed in this article.


Introduction
This clinician relies heavily on techniques in diagnosing pericardial d isease that demonstrate the presence of pericardial effusion. Currently available investigative tools that aid in the detection of pericardial effusion include electrocardiography, echocardiography, chest X-ray, cardiac fluoroscopy, computerized to mography, magnetic resonance imaging, radionuclide scanning and pericardiocentesis. Routine 12-lead electrocardiography and chest X-ray are available and the most commonly used screening investigations in card iac assessment. Accordingly, the review was undertaken to mechanisms of these electrocardiographic changes in the detection of pericardial effusion and its complications [1].
The elect rocard iog ram (EC G) in card iac tamponade shows sinus tachycardia, lo w voltage, and, if pericard itis is present, the elect rocard iog ram find ings typical o f that disorder. Electrical alternans is relatively specific but not very sensitive for tamponade; rarely, this phenomenon is seen with very large pericardial effusions alone [2,3]. The beat-to-beat alterations in the QRS comp lex is characteristic of electrical alternans and other electrocard iog raph ic changes reflect the swinging of the heart in the pericard ial flu id. It is suggested that low QRS voltage in patients with a pericardial effusion is actually a specific man ifestation of tamponade, not of the effusion.
In 90% of cases electrocardiogram abnormalities are seen and typically progress through four distinct stages. Stage 1. is ST seg ment elevation, with concavity upwards, or 'saddle-shaped'. This electrocardiographic pattern is seen in all the leads except in V1 and A VR. Stage 2. is ST segment resolution. Stage 3. is widespread T wave inversion and Stage 4. is resolution of T wave. In 50% of cases depression of the PR interval occurs and is caused by atrial inflammat ion. It often appears in the early stages and is regarded as a pathognomonic feature of pericard itis. The ECG changes of pericardit is can be confused with those of acute myocardial infarction. However, changes in pericardit is are global and have no reciprocal ST depression or loss of R wave amplitude or Q wave format ion [4].

Electrocardiography in Pericarditis
The electrocard iography pattern in patients with pericardit is has been known for several decades. These electrocardiographic abnormalities produced by pericarditis evolve through several distinct stages that reflect different clin ical and pathological phases of the disease. The electrocardiographic abnormalities produced by pericarditis can be attributed to 3 different factors as shown in (Table.1) [5]. A nu mber of factors cause pericarditis including viral or bacterial in fection, metastatic tumours, collagen vascular diseases, myocardial infarction, card iac surgery, and uraemia The electrocardiographic changes of acute pericarditis are same in some ways that seen with acute myocardial infarction [5,6]  Current of injury' leading to deviation of S-T segment from the base line.

Superficial myocarditis
Abnormal T-wave vector without lengthening of the Q-T c interval.

ST Segment Elevati on
Acute pericarditis is usually characterized by ST segment elevations due to alterations in ventricular repolarisation in early phase of pericard itis. Th is electrocardiographic pattern is due to current of injury resulting fro m concomitant inflammat ion of the epicardiu m. ST elevation also occurs in acute myocardial infarction (M I) and early repolarisation.

Pericarditis versus Acute Myocardial Infarction
The major difference between the electrocardiographic changes in pericarditis and acute myocardial infarction is their pattern of distribution. The ST segment elevations in acute myocardial infarct ion are characteristically limited to the localized area of the infarct that is anterolateral leads (I, aVL, V1 to V6) or the inferio r (II, III, aVF) leads. But in pericardit is the ST-T changes are more generalized, occurring in both anterior and inferior leads.
Pericardit is does not produce abnormal Q waves as seen with myocardial infarcts. The abnormal Q wave in myocardial infarction is due to death of heart muscle which leads due to loss of positive depolarizat ion voltages. Pericardit is causes only superficial inflammation but not frank myocardial necrosis. So, abnormal Q waves are not seen unless there is associated myocarditis. The mo rphology and distribution sequence of the ST-T abnormalities help in distinguishing acute pericarditis fro m acute MI. The ST segment elevation in acute pericarditis is at the J point with its normal concavity upwards. The characteristic ECG pattern of acute MI is ST elevation often associated with convexity upwards (do me-shaped).

Pericarditis Versus Early Repol arisation
The electrocardiographic changes in acute pericard itis must also be differentiated fro m those in the early repolarisation normal variant. One d ifferentiating feature is that ST elevations occur in both the limb and precord ial leads in most c, whereas about one-half of normal variants have no ST deviations in the limb leads [7]. In addition, PR deviation is present in acute pericardit is and evolution of the ST-T changes is not seen in early repolarisation.
Another most reliable electrocardiographic pred ictor to differentiate between acute pericardit is and early repolarisation is the ratio of ST elevation to T wave amp litude in lead V6 which was more than 0.24 in acute pericardit is in a prospective study done by Gin zton, LE and La ks, M. [8].

PR Seg ment Elevation
The repolarisation of the atria is also affected by acute pericardit is, which occurs during the PR segment that is fro m the end of the P wave to beginning of the QRS co mp lex. Acute inflammat ion pericard iu m causes an atrial current of injury, wh ich is reflected ECG by PR segment elevation in lead aVR and PR segment depression in other limb leads and in the left chest leads V5 and V6). Thus, PR segment and ST segment changes are typically in opposite directions in acute pericardit is. For examp le, in aVR, the PR segment is elevated (often by only 1 mm o r so) while the ST segment is usually slightly depressed and other leads may show PR depression and ST elevation [9].

T Wave Inversion
The ST segment elevations which are seen with acute pericardit is after a variable time is followed by T wave inversions, which may resolve co mpletely with t ime with normalizat ion of the ECG. But however, in some patients, the T wave inversions may persist for a prolonged period as in chronic pericardit is. This sequence of ST elevation followed by T wave elevation is the same as that described with myocardial infarction [9].

Effects of Pericardial Effusion
Pericardit is usually the results to occurrence pericard ial effusion. The major hemodynamic co mp licat ion of pericardial effusion is cardiac tamponade. The most co mmon ECG finding of pericardial effusion with or without cardiac tamponade is low voltage QRS co mplexes, probably due to short-circuiting of card iac potentials by the flu id surrounding the heart. The presence of low voltage and sinus tachycardia should always raise concern about pericardial effusion with tamponade. Another ECG change that can occur with pericardial effusion and tamponade is electrical alternans. Electrical alternans with sinus tachycardia is a h ighly specific ECG finding of card iac tamponade, but its absence does not exclude pericardial tamponade.

Low Voltage
This has always been considered to be a valuable sign and is thought to depend on the pressure of a lake of flu id about the heart causing short circuiting effect. Low voltage is said to be present when the QRS amp litude is 5 mm or less in each lead. If the voltage remains low after the removal of flu id the decreased amplitude of the electrocardiographic deflections is probably due to the insulating effect of fibrin [10]. The low amplitude of the ventricular co mp lex is frequently associated with normal amp litude 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.
Internal short circuiting of the electrical currents by the accumulated fluid within the pericard ial space change in the position of the heart [11], increasing distance fro m the current generator to the recording electrodes [12,13], decrease in cardiac chamber size and volume [14,15] and changes in the generation and propagation of electrical currents in the myocardiu m [14] are the several mechanisms have been proposed to explain the association between pericardial effusion and low QRS voltage. The mechanisms of low QRS voltage with pericard ial effusion in an experimental approach have tried to clarify only by few investigators like Karatay [14], Fried man [16], Schlant and Hurst [17] and others.

Electrical Al ternans
The variations in the amplitude of the ventricular co mp lex 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 pericardit is the "alternans" is apparently due to changes in cardiac position which result fro m 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 (Figure 1).

Figure 1. Effects of pericardial effusion
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 [18]. Litt mann, in 1963 termed this type of motion as "Card iac Nystagmus" [19]. Subtle variations in the amplitude of the ventricular and occasionally the atrial co mplexes occur in most cases of large effusion, but marked variations are characteristically associated with the presence of card iac tamponade. The variation in amp litude differs fro m the typical alternans pattern in that they occur gradually over more than two 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 [18].

Produced by Flui d or Fi brin
Pressure on the myocardium produces a "Current of injury" that is manifested by deviation of the S-T segment fro m 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 a xis. The S-T deviat ion in pericarditis is usually less pronounced than in the early stages of myocardial infarct ion. It is seldom greater than 4-5 mm and monophasic patterns do not occur [20]. This suggests that the injury current in pericardit is is probably smaller than in acute myocardial infarct ion. At the same time, recip rocal depression of the S-T segment in pericarditis is recorded in fewer standard leads than in infarct ion.

Differentiation from Myocardial Infarcti on
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 S-T segment [10]. 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 pericard itis the amp litude and shape of T-wave is usually changed and the elevated S-T segment is concave, but in acute infarct ion. The T-wave is frequently obliterated and the elevated S-T segment is convex. The most reliable method for distinguishing between pericarditis and myocardial infarction, however, is by calculating the ratio of the height of the ST-segment elevation in millimetre to the height of the T-wave amplitude in millimetre in lead V6. A ratio g reater than 0.25 strongly suggests acute pericarditis [21].

Changes Attri buted to Superficial Myocarditis
Characteristically, the T-wave vector in pericard itis is directed to the right and superiorly. The T-wave in pericardit is is usually is inverted in more standard leads than in infarct ion. In typical cases of pericard itis the T-wave becomes inverted in all standard leads with the exception of aVR and V1. However in pericardit is the T-waves are usually less deeply or less comp letely inverted than in myocardial infarction. An inco mpletely inverted T-wave such as a diphasic wave or a notched T-wave is a characteristic feature of the electrocardiographic pattern in pericardit is [22,23]. T-wave abnormalities of pericardit is can be differentiated fro m T-wave abnormalities of myocardial infarct ion because of following factors: 1) The myocardial surface responsible for the abnormal T-wave vector is greater in pericarditis than in myocardial infarct ion.
2) The muscle mass responsible for the T-wave vector is smaller in pericard itis than in myocardial infarct ion.
3) The inflammatory changes associated with pericarditis appear to produce myocardial damage more slowly and insidiously than the ischemic changes associated with myocardial infarction (Figure 2).

Incidence and Severity of ECG Abnormalities
The incidence and the severity of the electrocardiographic abnormalities in pericardit is depend upon the origin of disease. Patients with chronic effusion may have no signs of pericardit is except for lo w voltage and low T-wave amp litude [24]. The typical pattern with S-T segment and T-wave changes occur in almost all acute non-specific or purulent pericardit is [10], in children [25] and in all patients with trau matic pericardit is [26].
The changes appear less frequently in rheu matic, uraemic and neoplastic pericard itis and in pericarditis after myocardial in farction and cardiac surgery. The lower incidence of characteristic electrocard iographic pattern in this type of pericardit is is due to a lower incidence or lesser severity of accompanying myocarditis.
The duration of electrocardiographic changes produced by pericardit is 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 fibrillat ion 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 mit ral stenosis and "P" mitrale the mean QRS axis is usually deviated to the right but in those with constrictive pericardit is the QRS vector is usually has an intermediate or left axis.
Pericardial diseases can present clinically as acute pericardit is, pericard ial effusion, cardiac tamponade, and constrictive pericardit is. Patients can subsequently develop chronic or recurrent pericardit is. Structural abnormalities including congenitally absent pericardiu m and pericard ial cysts are usually asymptomatic and are uncommon. Clin icians are often faced with several diagnostic and management questions relating to the various pericard ial syndromes [27].

Conclusions
The diagnosis and management of pericardial d iseases remains difficult because of the wide spectrum of clinical man ifestations. This review article describes the usefulness of electrocard iographic diagnostic criteria and outline evidence-based treatment of major pericardial diseases. The typical electrocardiographic find ings in acute pericarditis, including widespread upward concave ST-segment elevation and PR-segment depression. Sinus tachycardia, low-voltage QRS co mplex and electrical alternans electrocardiographic findings associated with cardiac tamponade. The diagnosis can be made on history and clinical examination, electrocardiogram, and laboratory tests in acute pericard itis. But when there is evidence of hemodynamic co mpro mise and the diagnosis is equivocal additional imaging techniques like echocardiography, cardiac co mputed tomography and cardiac magnetic resonance imag ing can be used. Echocardiography is diagnostic in cardiac tamponade and first-line of treat ment in hemo-dynamically unstable patients is emergency pericardiocentesis.