Cardiac tamponade (also known as pericardial tamponade) is a clinical syndrome in which the pressure from the excess pericardial fluid, or pericardial effusion, has increased to the point that the intrapericardial pressure exceeds the pressure within the cardiac chambers, resulting in inadequate cardiac filling, decreased cardiac output, and, ultimately, cardiogenic shock and death if not rapidly identified and appropriately treated.1-3
The normal pericardial sac contains approximately 10 to 20 mL of fluid, which acts as lubricant during cardiac motion (see Normal pericardium). Accumulation of pericardial fluid causes an increase in intrapericardial pressure. The pericardium can stretch to accommodate an increased fluid volume, but only if the accumulation is gradual.3 In such instances, intrapericardial pressure does not significantly increase, despite the increased intrapericardial fluid volume.3 During gradual accumulation, the pericardial fluid volume may exceed 1 L before the intrapericardial pressure finally exceeds the intracardiac pressure, leading to cardiac tamponade (see Cardiac tamponade).3,4
In instances when intrapericardial fluid accumulates rapidly, the pericardial sac cannot stretch to the degree needed to offset the increased intrapericardial pressure created by the excess fluid volume; thus, the intrapericardial pressure exceeds the intracardiac pressure.3,5,6 As little as 150 mL of intrapericardial fluid volume is sufficient to lead to cardiac tamponade if accumulation is acute.3,5,6
The incidence of cardiac tamponade in the US is estimated to be about 2 cases per 10,000. Approximately 2% of penetrating chest injuries are reported to result in cardiac tamponade.7
The causes of cardiac tamponade include all the causes of pericardial effusion or hemorrhage into the pericardium as well as iatrogenic etiologies. Infectious causes include viral, bacterial, fungal, and parasitic organisms. Noninfectious causes include autoimmune diseases, neoplasms, cardiac trauma, metabolic diseases, radiation, and rarely, drugs such as procainamide.8 Malignant diseases are the most common cause of cardiac tamponade.7
Signs and symptoms vary with the acuteness and underlying cause of the tamponade. A comprehensive review of the patient's history usually helps in identifying the probable etiology of a pericardial effusion; for example, patients with systemic or malignant disease present with weight loss, fatigue, or anorexia.9
Physical assessment findings in a patient with cardiac tamponade, such as tachypnea and dyspnea, are often nonspecific.1,3 Presenting signs will depend on the etiology and severity of cardiac tamponade.
The findings associated with Beck's triad, hypotension, dilated neck veins, and muffled heart sounds, are present in only a minority of patients with acute cardiac tamponade.10 When present, the neck vein distension is a result of increased right atrial pressure. The hypotension is caused by decreased stroke volume from decreased intracardiac chamber filling. The muffled or distant heart sounds result from soundwaves transmitted through fluid.1,6
Tachycardia is seen in almost all patients with cardiac tamponade, allowing for at least partial maintenance of cardiac output.10 A pericardial rub may be heard in patients with cardiac tamponade due to inflammatory pericarditis.10
Pulsus paradoxus or paradoxical pulse is a classic sign of cardiac tamponade. It is defined as an abnormally large decrease in systolic BP during inspiration (more than 10 mm Hg).1,3 (See Identifying pulsus paradoxus.)
Patients with possible cardiac tamponade should be evaluated with an ECG, chest X-ray, and echocardiography, depending on clinical status. Other imaging studies, such as computed tomography and cardiovascular magnetic resonance, are not usually necessary for diagnosis if bedside echocardiography is available.10
The ECG in patients with cardiac tamponade typically shows sinus tachycardia and may also show low voltage. Electrical alternans is characterized by beat-to-beat alterations in the voltage of the QRS complexes. Electrical alternans is relatively specific but not very sensitive for cardiac tamponade; it may be seen with very large pericardial effusions alone (see Electrical alternans).10
A chest X-ray showing an enlarged cardiac silhouette with clear lung fields may be seen in slowly developing cardiac tamponade. Cardiomegaly is not usually seen in acute cardiac tamponade since at least 200 mL of pericardial fluid must accumulate before the cardiac silhouette enlarges. In general, however, the findings on a chest radiograph are neither sensitive nor specific for the diagnosis of cardiac tamponade.10
Two-dimensional and Doppler echocardiography play major roles in the identification of pericardial effusion and in assessing its hemodynamic significance. In most cases of cardiac tamponade, a moderate to large effusion is present, and swinging of the heart within the effusion may be seen. Echocardiographic findings suggesting hemodynamic compromise are the result of transiently reversed right atrial and right ventricular diastolic transmural pressures. Cardiac chamber collapse typically occurs before clinical hemodynamic instability.10
Definitive treatment of cardiac tamponade is removal of the pericardial fluid, either by percutaneous (pericardiocentesis) or surgical drainage, to relieve the elevated intrapericardial pressure and improve hemodynamic status.1,6,11,12 The decision to use catheter-based or surgical intervention depends on many factors including degree of hemodynamic compromise, as well as relative contraindications and indications for each. Catheter pericardiocentesis is the treatment of choice in most patients. An indwelling catheter is generally left in the pericardial space until drainage is less than 25 mL/day, while a more extended drainage period is frequently preferred in malignant effusions.10
Additional interventions prior to therapeutic pericardial fluid drainage may include supplemental oxygen, volume expansion with agents such as blood, plasma, dextran (avoid dextran in patients with renal insufficiency because of the risk of renal failure), or saline, and vasopressors.3,13 Avoid positive pressure mechanical ventilation, if possible, because the positive intrathoracic pressures can further impair cardiac filling.3,6
It is crucial for critical care nurses to have a high index of suspicion for cardiac tamponade in patients who present with signs and symptoms of respiratory distress and hemodynamic compromise.14 Recognizing the classic signs such as Beck's triad (if present) and electrical alternans would aid prompt recognition of this medical emergency so that the healthcare provider can be alerted in a timely fashion.14,15 It is essential to establish venous access for fluid repletion and possible vasopressor therapy to support the patient's hemodynamics.14,15 Additional interventions include frequent monitoring of vital signs, continuous cardiac monitoring, supporting the patient during pericardiocentesis, and preparation of the patient for transport to the OR for surgical intervention if necessary.14,15
Cardiac tamponade is a medical emergency that requires a high index of suspicion for patients with potential risk factors and suspicious signs and symptoms. Rapid recognition and definitive treatment with pericardial fluid drainage can prevent cardiogenic shock and death.
The pericardium has two layers: a tough external fibrous layer called the fibrous pericardium and a parietal layer of serous pericardium that lines its inner surface. The pericardial cavity is a space between the visceral and parietal layers of the serous pericardium, and is lined by the mesothelial cells.
During inspiration, venous flow into the right heart increases, causing the interventricular septum to bulge into the left ventricle. This produces a decrease in left ventricular volume, with a subsequent decrease in stroke volume. In cardiac tamponade, the fluid in the pericardial sac produces further compression of the left ventricle, causing an exaggeration of the normal inspiratory decrease in stroke volume and systolic BP.
Rhythm strip showing electrical alternans caused by swinging movement of the heart within the pericardial sac.
Identifying pulsus paradoxus
Apply a BP cuff to the patient's arm. Inflate the cuff and as the patient breathes quietly, lower the cuff pressure to the systolic level. Note the pressure level at which the first sounds can be heard. Then drop the pressure very slowly until sounds can be heard throughout the respiratory cycle. Again, note the pressure level. The difference between these two levels is normally no greater than 3 or 4 mm Hg.
Source: Bickley L. Bates' Guide to Physical Examination and History Taking. 11th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2013.
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