Cardiac tamponade: causes, symptoms, diagnosis and treatment
Cardiac tamponade, what is it? The pericardium is a protective saccular structure surrounding the heart and consists of two leaflets: the parietal pericardium (the fibrous outer layer) and the visceral pericardium (the inner layer, in contact with the myocardial surface)
The two leaflets delimit the ‘pericardial space’, which contains 5-15 ml of fluid: when this fluid accumulates abnormally, it is called a ‘pericardial effusion’.
If the fluid accumulates slowly, the pericardial space can accommodate up to 2 litres of fluid without a significant increase in pericardial pressure, whereas an effusion that accumulates rapidly, as in haemopericardium caused by trauma, can cause what is called ‘cardiac tamponade’ even with a small collection of fluid, e.g. 100-200 ml.
Cardiac tamponade therefore occurs when the accumulation of fluid in the pericardial space exerts excessive pressure on the heart
Initially, cardiac tamponade leads to an increase in intracardiac filling and venous pressures.
As the heart’s diastolic and intrapericardial filling pressures equalise, ventricular filling is reduced and systolic output decreases.
Adrenergic activation leads to an increase in heart rate, myocardial contractility and systemic vascular resistance: this is the system our body has available to compensate for the tamponade.
Eventually, however, these compensatory mechanisms are unable to maintain normal cardiac output, and systemic blood pressure falls.
The haemodynamic consequences of a pericardial effusion depend largely on the rate at which the fluid accumulates.
In addition, the restrictive characteristics of the pericardium (i.e. a normal pericardium is relatively distensible) and intravascular volume status may influence the amount of pericardial fluid sufficient to induce tamponade.
For example, when hypovolaemia is present, compressive effusions induce tamponade faster than in isovolaemic or hypervolaemic states.
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Cardiac tamponade is caused by pericardial effusion, which in turn can be caused by:
- Pericarditis
- Cardiac tumours
- Myocardial infarction
- Influenza
- Kidney failure
- Hypothyroidism
- Histoplasmosis
- Leukaemia
- Lymphoma
- Tuberculosis
- Liver cancer
- Lung cancer
- AIDS
- Amyloidosis
- Rheumatoid arthritis
- Breast cancer
- Echinococcosis
- Foetal Erythroblastosis
- Lassa fever
- Systemic lupus erythematosus
- Melanoma
- Pleural mesothelioma
- Myocarditis
- Myxoma
- Mononucleosis
- Sjögren’s syndrome
- Heart failure
- Toxoplasmosis.
The symptoms complained of by patients in cardiac tamponade are attributable to reduced cardiac output
When tamponade develops slowly, symptoms typically include dyspnoea, asthenia and light-headedness.
In contrast, patients with acute tamponade are often critical patients, with symptoms and signs of cardiogenic shock.
Diagnosis
On physical examination, patients appear anxious and pale, with tachypnoea and diaphoresis.
Tachycardia is a compensatory sign and helps maintain cardiac output.
Paradoxical pulse (drop in systolic pressure of more than l0 mmHg on inspiration) is a characteristic finding in patients with cardiac tamponade.
Under normal conditions, right ventricular filling increases with inspiration when intrathoracic pressure is reduced, resulting in distension of the right ventricle with minimal involvement of the left ventricular inflow.
With cardiac tamponade, the compressive effects of pericardial fluid limit the expansion of the right ventricle.
As a result, the interventricular septum protrudes into the left ventricular cavity to allocate the increased blood volume into the right ventricle.
This action subsequently prevents left ventricular filling, causing a reduction in systolic output and a fall in systolic pressure.
However, the paradoxical pulse is non-specific to cardiac tamponade and can occur with other disease states such as chronic obstructive pulmonary disease, asthma, severe congestive heart failure, pulmonary embolism and, in some cases, with constrictive pericarditis.
The jugular veins are distended due to high pressures in the right ventricle.
The negative x-wave is typically prominent, while the negative y-wave is absent.
Pulmonary fields are clear. Cardiac examination usually reveals quiet heart tones, although fretting may be heard.
Chest X-ray examination may reveal, if the effusion is abundant, a cardiac silhouette with a globular configuration.
The ECG may reveal reduced voltage or electrical alternation. Echocardiography is the reference examination for non-invasive assessment.
The right atrium and right ventricle are low-pressure, thin-walled cardiac chambers and are very susceptible to the effects of increased intrapericardial pressures.
As a result, when intrapericardial pressures exceed the filling pressures of the right sections of the heart, collapse of these chambers is observed.
In addition, the kinetic characteristic of the interventricular septum varies with respiration as does the filling and output of the left ventricle, and the inferior vena cava is typically distended.
Despite the usefulness of echocardiography, right heart catheterisation may be necessary to document the haemodynamic significance of a pericardial effusion.
Typical findings of tamponade include an increase and equalisation of atrial and ventricular diastolic pressures.
If the intrapericardial pressure is measured simultaneously, it is elevated and equal to the ventricular and atrial filling pressures.
Cardiac tamponade is a medical emergency and requires immediate treatment
Intravenous hydration is one of the most important measures.
Vasopressor drugs may be necessary to stabilise the patient while the definitive strategy to perform pericardiocentesis is worked out.
If the effusion is conspicuous and circumferential, pericardiocentesis can quickly restore haemodynamic stability.
If the effusion is saccaric or recurrent, surgical drainage with the formation of a pericardial window may be necessary.
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