Cardiac tamponade is the result of compression of the myocardium by fluid, gas, pus, blood, or at combination of substances.
It occurs in a physiologic continuum reflecting the amount of fluid, the rate of accumulation, and the nature of the heart.
The result is increased pericardial pressure, which causes decreased ventricle compliance and decreased flow of blood into the right ventricle which eventually leads to a decreased cardiac output.
Conditions that may predispose a patient to pericardial effusion and tamponade include:
- radiation exposure
- Tb pericarditis
- renal failure (uremic pericarditis)
- autoimmune diseases
- drugs that induce a lupus-like syndrome
- hypothyroidism, or
- ovarian hyperstimulation syndrome.
Clinical presentations of cardiac tamponade
- Chest pain and dyspnea
- Pulsus paradoxus >10 mm Hg
- Beck’s triad includes low blood pressure, elevated jugular venous distention, decreased heart sounds
- In the absence of hypotension and tension pneumothorax in a patient with PEA, the diagnosis of cardiac tamponade.
- Bedside ultrasound,
- Blood gases,
- Serum Electrolytes,
- Pericardial fluid analysis-biochemistry, microbiology and cytology,
- Serum creatinine and urea and/or
- Chest Xray
Treatment for cardiac tamponade
- Perform both primary and secondary assessment and provide appropriate interventions.
- Give oxygen if hypoxic or increased work of breathing.
- Connect the patient to a cardiac monitor and obtain vital signs.
- Pericardiocentesis is the definitive management
A: 0.9% sodium chloride (IV): to increase right sided filling pressure
Adults: 1-2 Litres
All patients with cardiac tamponade require inpatient management in an intensive care unit setting/HDU.