Cardiac tamponade is the pericardial syndrome occurring when pericardial effusion impairs diastolic filling of the heart till reducing cardiac output and producing signs and symptoms. The impairment of diastolic filling is continuous through the entire diastole. The size of the effusion as well as its distribution may be variable [1, 2].

Since the pericardium is relatively stiff, if a pericardial fluid collects quickly, such as in haemopericardium, the limit of pericardial stretch is reached soon with volumes of 200–300 mL; on the contrary a slowly accumulating pericardial effusion may reach 1–2 L before the development of cardiac tamponade [3, 4]. This pathophysiology explains that cardiac tamponade is a last-drop phenomenon. Thus a small increase of pericardial volume may precipitate the syndrome, and also the aspiration of small amounts of pericardial fluid may greatly improve the clinical condition in urgent pericardiocentesis [5].

Usually pericardial effusions are circumferential, but after trauma or cardiac surgery, they may be loculated and even be responsible for localized compression and the development of cardiac tamponade.

The classical presentation of cardiac tamponade has been described by the thoracic surgeon, Beck in 1935 (Fig. 14.1) [5, 6]. Beck identified a triad including hypotension, increased jugular venous pressure and a small and quiet heart.

This triad was classically identified in “surgical tamponade” with acute cardiac tamponade due to intrapericardial haemorrhage because of trauma and myocardial or aortic rupture. The Beck triad may be lacking in patients with “medical tamponade” with slowly accumulating pericardial fluid. Hypotension is absolute or relative. Acute cardiac tamponade is usually associated with low blood pressure (<90 mmHg) but only slightly reduced in subacute and chronic tamponade. Hypertensive patients may have normal to mildly elevated blood pressure concomitant to cardiac tamponade [5, 6].

On physical examination, classical signs include neck vein distention with elevated jugular venous pressure at bedside examination, pulsus paradoxus and diminished heart sounds on cardiac auscultation. Pulsus paradoxus has been described for the first time by Kussmaul in 1873 as a palpable reduction of radial pulse on inspiration in patients with cardiac tamponade. The so-called paradox was the “waxing and waning” of the peripheral pulse, in contrast to the unvarying strength of the apical cardiac impulse. Pulsus paradoxus is classically defined as an inspiratory reduction of at least 10 mmHg of the systolic blood pressure. It can be easily detected by recording the systolic pressure at which Korotkoff sounds are first audible and the systolic pressure at which they are audible through the whole respiratory cycle (Fig. 14.2) [5, 6].

Pulsus paradoxus is due to exaggerated ventricular interdependence occurring in cardiac tamponade when overall volume of cardiac chambers becomes fixed and any change in the volume of one side of the heart causes the opposite changes in the other side (i.e. inspiratory increase of venous return and right chambers with decreased left chambers volume and reduced systemic blood pressure) (Fig. 14.3). On ECG, the patient usually shows tachycardia, low QRS voltages and electrical alternans. Both ECG signs are non-specific and are considered related to the damping effect of pericardial fluid and swinging heart [5, 6].

All the causes of pericardial effusion are also possible causes of cardiac tamponade. In clinical practice the most common aetiologies include cancer, tuberculosis and purulent infections, trauma, iatrogenic complication of cardiovascular interventions (e.g. ablation of arrhythmias, pacemaker implantation, percutaneous coronary intervention), acute aortic disease, systemic inflammatory diseases and renal failure [4, 5].

The diagnosis of cardiac tamponade is a clinical diagnosis based on the combination of a suggestive history and symptoms (typically dyspnoea on exertion progressing to orthopnoea, chest pain and/or fullness) together with elevated jugular venous pressure at bedside examination, pulsus paradoxus, diminished heart sounds and often hypotension. The clinical suspicion of cardiac tamponade should be confirmed by echocardiography. Echocardiography can be performed bedside and in urgent/emergency situations and demonstrates moderately large or large circumferential pericardial effusion, signs of right atrial and/or right ventricular compression and abnormal respiratory variation in right and left ventricular dimensions and in tricuspid and mitral valve flow velocities usually associated with inferior vena cava plethora (Table 14.1 and Fig. 14.4) [3–5].