Acute pericarditis -pericardial effusion


Acute pericarditis
It is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial ECG changes. A pericardial effusion (increased pericardial fluid) is commonly-but not always-present.
Viral infection is the most common cause of acute pericarditis. The disease is usually self-limited with a relatively short duration (about 1-3 weeks). Viruses that can cause pericarditis include coxsackievirus B, echovirus, adenoviruses, influenza A and B viruses, enterovirus, Epstein-Barr, herpes simplex virus (HSV) type 1, varicella-zoster virus, measles virus, parainfluenza virus, respiratory syncytial virus (RSV), cytomegalovirus (CMV), hepatitis viruses A, B, and C and human immunodeficiency virus (HIV).
Idiopathic acute pericarditis, i.e. acute pericarditis with no clearly identified cause, is common. There are no differences in clinical features distinguishing idiopathic cases from viral pericarditis. Most cases of idiopathic pericarditis are propably undiagnosed viral infections. Seasonal peaks occur in spring and fall.

 Other causes of pericarditis include connective tissue disease (systemic lupus erythematosus, rheumatoid arthritis), myocardial infarction, postpericardiotomy syndrome, radiation, trauma, bacterial infection, tuberculosis, uremic pericarditis, malignancy, etc. Malignancy is a cause that we should have in mind in the process of differential diagnosis, especially in patients with moderate to large pericardial effusions. In patients presenting with acute pericarditis or pericardial effusion, 4-7% have an unsuspected malignancy. Most cases of neoplasm-related pericarditis result from metastatic disease, because primary neoplasms of the heart and pericardium are rare.
Symptoms of acute pericarditis: Chest pain, which may be intense, and usually is sharp, pleuritic (this means that the pain increases with deep respiration), and positional (worse when lying flat, relieved by leaning forward). The pain may also increase with body movements. Chest pain is usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. Fever is common.
Other symptoms are due to pressure on adjacent structures from a pericardial effusion and may include dyspnea (common symptom in pericarditis or pericardial effusion), cough, dysphagia and hiccups.
Physical Findings: Tachycardia is a usual finding. There is often a pericardial friction rub, a coarse high pitched sound with a scratching quality, described as two pieces of leather being rubbed together. This sound is best heard at the left sternal border at end-expiration with the patient sitting and leaning forward. It can have up to three components which correspond to the movement of the heart (a systolic component, an early diastolic component corresponding to the movement of the heart due to rapid ventricular filling and a late diastolic component at atrial systole). It is present in about 85% of the patients with acute pericarditis. The rub may be intermittent.
If you click on this video you can listen to a pericardial friction rub.
From: You Tube channel Rombero 123

Electrocardiogram : In acute pericarditis there is diffuse ST segment elevation (concave upward) usually present in almost all leads, except aVR and V1. PR-segment depression may be present, but in aVR there is a PR-segment elevation ( this is useful to differentiate from early repolarization and myocardial infarction).
Days later, ST segments return to baseline before T-wave inversion develops.
A useful feature in the differentiation of the concave ST segment elevation of acute pericarditis from the similar ST elevation present in early repolarization, is the following: In early repolarization there is also an increased amplitude of the T wave, so that the ratio of the elevation of the ST segment to the height of the T wave (ST-T ratio) < 0.25 . This ratio in acute pericarditisis is usually > 0.25.
Moreover, in acute pericarditis depression of the PR segment is often present and ST elevation is more diffuse ( compared to the ST elevation of early repolarization, or acute myocardial infarction).
In ST elevation myocardial infarction (STEMI) the leads with ST elevation correspond to a specific left ventricular wall (depending on the blocked coronary artery) and the elevated ST segment usually has a convex morphology. Often reciprocal ST segment depression in leads with an opposite orientation is also present in STEMI. These features differ from the pattern seen in acute pericarditis.

It is the most sensitive test for detection of pericardial effusion, which commonly (but not always) accompanies acute pericarditis.
If there is a drop in ejection fraction, one must suspect that myocardial involvement is also present and the diagnosis of concomitant inflammatory disease of the myocardium (myocarditis) is made. In this case blood tests usually show a marked elevation of troponin and CKMB. This condition (concomitant pericarditis and myocarditis) is called myopericarditis.

Treatment of acute pericarditis

The first line therapy for acute pericarditis is the administration of non steroidal anti-inflamatory drugs (NSAIDs):
High-dose aspirin 650 mg -1 g x 3-4 times per day, or ibuprofen 600 mg PO x 3 times per day, or indomethacin 75 mg PO x2 times per day).
Useful is the co-administration with an H2-antagonist (e.g. ranitidine) or proton pump inhibitor (e.g. pantoprazol, lansoprazol etc)  to reduce the risk of gastrointestinal bleeding.
Concomitant administration of colchicine (combined with the administration of NSAIDS) can reduce the chances of recurrent
pericarditis. ( Dosage : 1–2 mg for the first day followed by 0.6–1 mg/day for 3 months).
For recurrent pericarditis, colchicine can be used with NSAIDs or instead of NSAIDs (1–2 mg/day followed by 0.6–1 mg/day).
Colchicine side effects: It can cause gastrointestinal symptoms (in that case the lower dose may be selected). Infrequently it can cause bone marrow suppression (chronic kidney disease is a risk factor for this side effect).
In acute pericarditis strenuous physical activity should be limited for at least 2 months.
Corticosteroids should be avoided as a treatment for pericarditis, since recurrence rate is increased with steroid treatment.
Steroids can be considered in cases of failure of NSAID and colchicine therapy. (Prednisone 0.2 - 0.5 mg/kg/day) for 4 weeks until symptoms and elevated C-reactive protein have resolved). The dose of corticosteroids is gradually reduced before discontinuation of this treatment. 
Avoid anticoagulants in the acute phase of pericarditis (if they are not absolutely necessary for a serious reason) to decrease the risk of intrapericardial hemorrhage and tamponade.

 Pericardial effusion
Causes of a pericardial effusion (an abnormal accumulation of pericardial fluid) include all the causes of acute pericarditis listed above but occasionaly it also occurs with some non-inflamatory states that induce fluid retention or increased cardiac filling pressures and consequently an increased central venous pressure (heart failure, pulmonary hypertension, renal failure, or cirrhosis). Other causes: hypothyroidism, amyloidosis, hemopericardium.

Hemopericardium is bleading into the pericardial sac, due to trauma (blunt or penetrating), as a complication of dissection of the ascending aorta, left ventricular rupture due to myocardial infarction, or as a complication of cardiac interventions.
Accumulation of pericardial fluid leads to a rise in intrapericardial pressure, which in turn can cause a rise in right and left atrial pressure and in right and left ventricular diastolic pressures. 
Cardiac tamponade is the condition in which pericardial fluid causes a rise in intrapericardiac pressure that significantly impairs diastolic filling of the heart, in other words when the fluid compresses the heart and reduces diastolic filling with subsequent hemodynamic compromise. This is a medical emergency. In severe tamponade diastolic pressures in all 4 cardiac chambers typically equalize and become equal to the intrapericardial pressure (about 15-20 mmHg). As the pressure exerted on the heart by the pericardial fluid increases, cardiac volumes progressively decline and the decreased ventricular end diastolic volumes lead to a reduction in stroke volume (because of Frank-Starling law). This leads to a reduction in cardiac output. A compensatory mechanism to the decreased cardiac output is sympathetic stimulation producing tachycardia and increased contractility. 
For clinical symptoms (caused by increased intrapericardial pressure) to develop, two main factors are significant:
 rate of fluid accumulation. This is the most important factor, since rapid accumulation of a moderate quantity of fluid, such as 80-200 ml, will result in markedly increased intrapericardial pressures and can often cause symptoms or even the full clinical picture of cardiac tamponade. On the other hand, gradual accumulations of up to 1 to 2 L are often well tolerated, because the pericardium in such cases has enough time to dilate.
2) The fluid volume. A large pericardial effusion is much more likely to cause symptoms than a small one, although the rate of fluid accumulation plays a major role.

Symptoms-clinical presentation

A patient with a pericardial effusion can be asymptomatic, or present with typical symptoms of pericarditis, or with symptoms related to compression of adjacent structures by the effusion, or the clinical picture of cardiac tamponade, which is an emergency.

Large effusions  can present with a sensation of dull chest pain or pressure, or a nonspecific sense of chest discomfort, or with dyspnea (dyspnea is a common symptom).

Other symptoms related to mechanical compression of adjacent structures may include dysphagia, cough, hoarseness (due to compression of the left recurrent laryngeal nerve), hiccups (compression of the phrenic nerve) and nausea.
On physical examination, in a large pericardial effusion, there is often reduced intensity of the heart sounds (muffled heart sounds) and the apex beat cannot be palpated.
In tamponade, symptoms include fatigue and lightheadedness (due to a low cardiac output caused by the restricted cardiac diastolic filling ) and dyspnea. Patients with tamponade are more comfortable sitting and leaning forward.
Physical signs of cardiac tamponade include tachycardia, hypotension, muffled heart sounds, elevated jugular venous pressure, loss of the Y descent in the jugular venous pulse and pulsus paradoxus (decrease in systolic blood pressure with inspiration greater than 10 mm Hg). Tachypnea may also be present.
Pulsus paradoxus is not entirely specific for cardiac tamponade. Other conditions that can cause pulsus paradoxus are constrictive pericarditis, pulmonary embolism, pulmonary emphysema and severe asthma.
In tamponade often there are also some signs commonly present in patients with reduced cardiac output, such as cool extremities, peripheral cyanosis, diaphoresis (sweating, due to compensatory sympathetic stimulation). 

The classic presentation of tamponade is referred to as Beck triad:
1) elevated jugular venous pressure,
2) arterial hypotension, and
3) quiet ("muffled") heart sounds.

The ECG in a large pericardial effusion or tamponade can show: reduced QRS voltage, nonspecific T-wave flattening, and electrical
alternans (often with sinus tachycardia).
Electrical alternans is the phenomenon of alternation of QRS complex amplitude or axis between beats. This is due to the swinging motion of the heart in the pericardial cavity causing a change in QRS voltage and axis from beat to beat.

Echocardiography in pericardial effusion : It takes advantage of the different acoustic properties of pericardial fluid as compared with the myocardium and parietal pericardium. Pericardial fluid is typically echolucent (black or almost black in the echo image), whereas myocardium and pericardial membrane are echodense (white or gray).Pericardial effusion is seen on 2D echocardiography as an echolucenr space surrounding the heart. Occasionaly fibrinous strands, and/or thrombus can be present in the effusion.
Pericardial effusions are not always completely echolucent and may have varying degrees of echogenicity when they contain fibrin or clot, protein, chyle, tumor cells, or bacteria.
The size of the pericardial effusion can be assessed in the parasternal long axis, apical four chamber and subcostal views. Measurements of the width (thickness) of a pericardial effusion are taken during end-diastole and according to these measurements the effusion is generally classified as:
Small if <1 cm
Moderate if between 1 to 2 cm
 Large if >2 cm.
Small pericardial effusions often can be seen only posteriorly (but sometimes they can also be seen as circumferential). Moderate-sized and large-sized effusions are circumferential.Epicardial fat occasionally can be confused with a pericardial effusion. It appears as a relatively echolucent space usually anteriorly from the heart (less often posteriorly). However, epicardial fat usually has more echogenicity than fluid, usually with a “stippled appearance” ( with multiple dots). Increased epicardial fat is more commonly seen in the elderly, particularly in obese women.
In case of an echolucent space posterior to the heart, we should distinguish if this is a pericardial or a left pleural effusion. The parasternal long-axis view shows pericardial fluid as an echolucent space located anterior to the descending aorta, whereas pleural fluid lies posterior to the descending thoracic aorta.

VIDEO  A cardiology case of a postoperative (loculated) pericardial effusion. The chest x ray, echocardiography and treatment are being shown.

Echocardiographic findings suggestive of tamponade 
Pericardial tamponade is mainly a clinical diagnosis, but the following echocardiographic findings are suggestive of tamponade:
1 Right atrial collapse: An inward displacement of the right atrial (RA) free wall seen in the apical 4 chamber view or the subcostal (subxiphoid) view, in late diastole, or in systole. This is due to compression from the pericardial fluid, when intrapericardial pressure exceeds RA pressure. This sign appears earlier than right ventricular (RV) collapse, since RA pressure is smaller than RV pressure.
2 Right ventricular (RV) early diastolic collapse (an inward motion of the RV free wall because of compression from the pericardial fluid).
3 Marked respiratory variation in Doppler inflow velocities across mitral and tricuspid valves. (This finding is also seen in constrictive pericarditis). This can be assessed more easily if you slow the sweep speed (at the doppler menu) to 25 cm/s, to allow for an increased number of cardiac cycles to be displayed. In tamponade, in inspiration there is an increase in tricuspid valve inflow velocity of  40% or greater and a decrease in mitral inflow velocity of  25% or
greater .
4 Dilatation of the inferior vena cava, because of increased central venous pressure (due to the pressure exerted by the pericardial effusion on the RA).

Hemodynamic features of cardiac tamponade include an elevated right atrial pressure with marked reduction or absense of the Y descent in right atrial pressure curve (or central venous pressure curve) . The loss of the Y descent is explained as following: The Y descent is a drop in central venous pressure at the time of early diastolic filling of the right ventricle. In tamponade heart volume is fixed (restricted) as a result of compression of the heart by pericardial fluid. So blood can move from the central veins into the heart only when its volume reduces (only when blood is leaving from the heart), that is during systole and not in diastole. For this reason the Y descent in tamponade is lost, but the X descent is not lost. 

In tamponade  RA pressure, diastolic RV pressure, and pulmonary capillary wedge pressures are almost equal, with a difference  5 mmHg (This finding, called equalization of pressures, is also observed in constrictive pericarditis, but in constrictive pericarditis the Y descent is not reduced, on the contrary there is a prominent X and Y descent ).
Treatment of tamponade
Cardiac tamponade is a medical emergency. Evacuation of the pericardial fluid is needed promptly via needle pericardiocentesis with the insertion of an intrapericardial catheter, or via surgical treatment. A useful temporary measure, that helps to stabilize  blood pressure before pericardial fluid evacuation, is expansion of intravascular volume with intravenous infusion of saline (normal saline 0,9%).

A case of a large pericardial effusion due to pericarditis. A video by the EchoWeb. Link:


Useful links and bibliography

Lazaros G, Imazio M, Brucato A, Tousoulis D. 
Untying the Gordian knot of pericardial diseases: A pragmatic approach. Hellenic J Cardiol. 2016;57(5):315-322. doi: 10.1016/j.hjc.2016.11.024. 

Kyriakakis CG, Mayosi BM, de Vries E, Isaacs A, Doubell AF.An approach to the patient with suspected pericardial disease. S Afr Med J. 2016 Feb;106:151-155.

2015 ESC Guidelines for the diagnosis and management of pericardial diseases

Yusuf SW, Hassan SA, Mouhayar E, Negi SI, Banchs J, O'Gara PT. Pericardial disease: a clinical review. Expert Rev Cardiovasc Ther. 2016; 14:525-539.

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