Aetiology
The aetiology of cardiac tamponade varies widely, as pericardial effusions have several different causes, and is affected by factors such as demographic characteristics, clinical settings, or geographical distribution. In up to 60% of patients, known previous conditions can be identified as the cause of pericardial effusion.[16]
Common aetiologies include:[12][14][15][18][16][19][20][21][22]
Malignancy (particularly lung and breast cancer)
Idiopathic pericardial effusion
Viral infection (pericarditis)
Tuberculosis (in endemic regions)
Trauma
Iatrogenic (secondary to cardiac surgery or intervention)
Uraemia
Radiation-induced pericarditis
Collagen vascular disease
Hypothyroidism/myxoedema
Pathophysiology
Cardiac tamponade is determined by the rate of pericardial fluid accumulation, pericardial stretch, and the effectiveness of compensatory mechanisms.[23][24]
In classic cardiac tamponade, pericardial pressures are raised because of fluid accumulation in the pericardial space. Ventricular diastolic, right atrial, and wedge pressures all rise to equal pericardial pressures in response to compression countering chamber collapse.[2] This equalisation of pressures is the haemodynamic hallmark of tamponade. Once the pericardial pressure exceeds intra-chamber pressures, the chamber collapses.[2]
When the pericardium is stretched, full of fluid and inelastic, typical respiratory variation in left and right ventricular filling is greatly exaggerated. Inspiration increases negative intra-thoracic pressures and augments venous return to the right heart. This increased volume in the right heart forces the intra-atrial and intra-ventricular septums into the left heart. This is known as 'ventricular interdependence'.[25] Thus, the volumes within the left heart will be decreased with inspiration, resulting in an exaggerated decrease in systemic cardiac output and a drop in systemic blood pressure. Clinically, this is known as the pulsus paradoxus, a drop in systemic blood pressure >10 mmHg with inspiration.
On echocardiogram, ventricular interdependence is demonstrated by diastolic collapse of the right ventricle or septal shift with the act of respiration (septal bounce), or when there is more than 30% variation in transmitral inflow velocities during inspiration, and/or greater than 60% for transtricuspid inflow velocities.[4] The impaired diastolic filling is best appreciated in the right heart chambers, given the lower filling pressures. In cases of severe pulmonary hypertension, with severely raised right atrial and ventricular pressures, the changes in diastolic filling may be first seen in the left heart chambers.
Classification
Clinical classification of cardiac tamponade
Acute tamponade
This rapid-onset tamponade is seen in cardiac/great vessel trauma or as a complication of invasive cardiac procedures.
Presents with the classic features of the Beck's triad (hypotension, jugular venous distention, and distant heart sounds).
Effusion may be small, given the relative inelasticity of the pericardium.[3]
Subacute tamponade
A more gradual process of fluid accumulation, allowing for stretching of the pericardium and much larger effusions than seen with acute tamponade.[4]
Is the most common type of tamponade encountered in practice.
Typically seen in patients with neoplastic disease, tuberculosis, uraemia, or idiopathic disease. Symptoms may be more subtle and some or all of the Beck's triad may be absent.[4]
Regional tamponade
Caused by a loculated pericardial effusion or a compressing pericardial haematoma that mechanically impinges on a chamber of the heart, impairing normal filling.[4][5]
Symptoms vary and diagnosis may be difficult with echocardiography.
Seen localised in the ventricular after myocardial infarction and in the posterior atria after open-heart surgery.[5]
Low-pressure tamponade
Low-pressure physiology caused by concomitant large pericardial effusion and hypovolaemia.[6][7] Right atrial pressures fall, and a small rise in intra-pericardial pressure with pericardial effusion may result in chamber collapse.
Can be seen in hypovolaemic states associated with haemorrhage, haemodialysis/ultrafiltration, reduced oral intake and vomiting (usually in patients with cancer), or over-diuresis.[4][5][6]
Typical signs and symptoms of haemodynamic instability are often absent.[4][6]
Effusive constrictive pericarditis
An uncommon and distinct classification of tamponade. Presents with features of acute effusive pericarditis concomitant with cardiac tamponade and chronic constrictive pericarditis.[4][8]
Tamponade develops due to a combination of effusion and restriction as a result of inflamed/scarred pericardium.
Occurs more frequently in those with malignancy or prior radiation exposure.[9]
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