This middle aged gentleman has presented with an ominous collection of symptoms: worsening dyspnea and chest discomfort, tachycardia, hypotension, an elevated jugular venous pressure (JVP), pulsus paradoxus, and muffled heart sounds. The above collection of signs and symptoms is almost pathognomonic of cardiac tamponade; this is supported by the electrocardiographic (ECG) findings of low-voltage QRS complexes and electrical alternans. Urgent bedside echocardiography is an essential next step; this confirms the presence of a pericardial effusion, and also reveals the presence of right atrial collapse during a significant part of the cardiac cycle, end-diastolic right ventricular collapse, and vena caval plethora; these signs indicate cardiac hemodynamic compromise and confirm the clinical diagnosis. Note that contrast computed tomography (CT) of the thorax and cardiac magnetic resonance imaging (CMR) will not affect his acute management and are best avoided right now. As he is hemodynamically unstable, pericardiocentesis (under imaging guidance) should be performed as soon as feasible; administration of intravenous (IV) fluids will help maintain him until that time. Inotropic therapy in cardiac tamponade is controversial, and is probably best avoided here; in the absence of evidence of a clear infective etiology, IV antibiotics are not indicated either.
Cardiac tamponade is a medical emergency where accumulation of fluid in the pericardial cavity results in cardiac compression, thus giving rise to diminished cardiac filling, decreased cardiac output, and ultimately, cardiogenic shock. In the United States, the incidence of cardiac tamponade is 2 per 10,000 individuals; furthermore, ~2% of penetrating chest injuries result in the condition. Note that cardiac tamponade can occur acutely (i.e. within minutes to hours), sub-acutely, or chronically. Acute tamponade is usually a result of intrapericardial haemorrhage secondary to trauma, myocardial or aortic rupture; the subacute and chronic variants may be due to a range of causes, both benign and malignant. To comprehend the underlying pathophysiology, one must first understand that the pericardial space (which lies between the visceral and parietal pericardium) is usually a potential space, typically containing between 10 to 50 cc of fluid. Where a pericardial effusion occurs, the pericardial space slowly fills up to the pericardial reserve volume (i.e. the volume at which the pericardial sac is fully distended). Following this, further accumulation of fluid results in stretching of the parietal pericardium. At this point, a key physiologic principle kicks in - which is that the compliance of the parietal pericardium is more or less fixed in the short term (hours to days), but can slowly increase over time (weeks to months). Thus, acute pericardial effusions which exceed the pericardial reserve volume (typically ~200 cc) are forcibly bounded by the inelastic parietal pericardium, resulting in compression of the cardiac chambers and a rapid onset of tamponade. However, in the case of subacute and chronic effusions, the parietal pericardium has time to slowly stretch, thus allowing a larger effusion to accumulate before tamponade occurs. As might also be apparent, intra-pericardial pressures rise very slowly while the pericardial reserve volume is being filled, and while the parietal pericardium is stretchable. However, once the limit of parietal pericardial compliance is reached, intra-pericardial pressures rise extremely rapidly. This explains why tamponade is a 'last-drop phenomenon' (i.e. the last few drops give rise to the highest increments in pressure, and drainage of the first few drops results in the greatest decompression). Another phenomenon which should be discussed at this point is pulsus paradoxus; this is defined a fall of systolic blood pressure of >10 mmHg during inspiration. To understand this, one must recall that in inspiration, the right ventricle fills up more than the left, as the decrease in intrathoracic pressure promotes emptying from the vena cavae, while also reducing blood flow from the pulmonary veins into the left ventricle. The resulting distension of the right ventricle results in displacement of the interventricular septum towards the left side, resulting in further underfilling of the left heart, and a subsequent reduction in systolic blood pressure. In expiration, the converse occurs; the entirety of this phenomenon is termed "ventricular interdependence". That said, in normal individuals, the difference in systolic blood pressures between inspiration and expiration is usually <10 mmHg. In a patient with cardiac tamponade, the pressure on the right ventricle forces it to mainly distend into the left ventricle (thus reducing filling far more than in normal persons); this explains the exaggerated difference in systolic blood pressures. Cardiac tamponade can often be extremely tricky to suspect clinically. While the condition has classically been associated with 'Beck's Triad' (hypotension, elevated jugular venous pressure, and muffled heart sounds), the entire triad is only present in a minority of patients. While pulsus paradoxus (as explained above) is also cited as being a common finding, it is often difficult to elicit (and easy to miss); this might be why the incidence has been reported to vary from 12% to 75% of patients. Note that dyspnea is the commonest clinical finding, but is (obviously) highly nonspecific. Often, the clinical setting and history may aid the diagnosis; thus, in patients who have experienced acute trauma, or who have recently undergone a cardiac procedure, one or more of the above signs or symptoms should raise consideration of tamponade. Echocardiography is the diagnostic technique of choice; this will allow detection of the pericardial effusion and quantification of the size and extent, as well as assessment of the hemodynamic impact. Note that cardiac chamber collapse is a key finding indicating hemodynamic compromise; as the pressures in the right atrium and ventricle are considerably less than those of the left heart, these are preferentially affected. In particular, right atrial collapse which persists for more than one-third of the cardiac cycle is 100% sensitive and 82% specific for tamponade; right ventricular collapse in late diastole is also highly specific (84% to 100%), but is not sensitive. Other key echocardiographic findings include increased interdependence between the cardiac chambers, and the presence of a dilated and plethoric vena cava (due to backward transmission of the increased right heart pressures). Electrocardiography (ECG) may provide additional information in the form of low-voltage QRS complexes, and electrical alternans, while chest radiographs may help reveal cardiomegaly. Note that computed tomography (CT) of the thorax and cardiac magnetic resonance imaging (CMR) are not part of the routine evaluation of cardiac tamponade; however, they may be of use in ruling out concomitant diseases involving the mediastinum and lungs. There is general agreement that established cardiac tamponade requires pericardial drainage; where the patient is hemodynamically unstable, this should be performed as soon as possible; in stable patients, this should be conducted within 12 to 24 hours, after obtaining any necessary laboratory results. In this respect, note that the European Society of Cardiology (ESC) released a stepwise scoring system in 2014 to triage patients with tamponade; a score of ≥6 warrants immediate intervention. In the majority of patients, pericardiocentesis is appropriate; this is ideally performed under echocardiographic or fluoroscopic guidance, although blind needle insertion may need to be entertained if the patient is rapidly deteriorating, and facilities are unavailable. As mentioned earlier, tamponade is a last-drop phenomenon; thus aspiration of as little as 10 to 50 cc of liquid may result in dramatic improvement. However, in the case of large effusions (>1 litre), excessive drainage should not be performed at once, as this may precipitate acute pulmonary edema. This is because excessive drainage results in a rapid increase in right ventricular stroke volume and left ventricular filling, without giving enough time for the systemic arteries to relax (as they tend to significantly constrict during cardiac tamponade, so as to maintain the systemic blood pressure). Note that both thrombocytopenia and anticoagulant therapy are contraindications for pericardiocentesis, as is the presence of poor facilities for cardio-respiratory resuscitation. Surgery is preferred in the event of cardiac or aortic rupture or following acute chest trauma; this is because such lesions are often large, and unlikely to self-seal. Furthermore, surgical drainage is preferred for purulent effusions in unstable septic patients, and for loculated effusions which cannot be managed percutaneously. Until drainage can be performed, these patients should be kept in bed, preferably with their legs elevated (so as to improve venous return); inhaled oxygen therapy should also be commenced. Fluid resuscitation may be of benefit, particularly if hypotension (< 100 mmHg) is present, while vasopressor medications may be commenced to to improve perfusion pressure. Note that the use of inotropic drugs is controversial, because endogenous catecholamine stimulation is already maximal in these circumstances. Depending on the likely underlying etiology, further treatment may also be administered (for example, nonsteroidal anti-inflammatory drugs in the event of suspected viral pericarditis). In general, cardiac tamponade is universally fatal unless detected and treated on a timely basis. Following treatment, the long-term mortality depends on the underlying etiology.