Acute pericarditis

Question 1

Cardiac tamponade definition?

Answer 1

In this condition, pericardial fluid accumulates under high pressure, compresses the
cardiac chambers, and severely limits filling of the heart. As a result, ventricular stroke volume and
cardiac output decline, potentially leading to hypotensive shock and death.

Question 2

Etiology?

Answer 2

Any etiology of acute pericarditis can progress to cardiac tamponade, but the most common causes
are neoplastic, postviral, and uremic pericarditis. Acute hemorrhage into the pericardium is also an
important cause of tamponade, which can result
(1) from blunt or penetrating chest trauma,
(2) from
rupture of the left ventricular (LV) free wall following MI, or (3) as a complication of a dissecting
aortic aneurysm .

Question 3

Pathophysiology (result of the surrounding tense pericardial fluid)?

Answer 3

As a result of the surrounding tense pericardial fluid, the heart is compressed, and the diastolic
pressure within each chamber becomes elevated and equal to the pericardial pressure. Because the compromised cardiac chambers cannot accommodate normal venous return, the systemic and pulmonary venous
pressures rise. The increase of systemic venous pressure results in signs of right-sided heart failure
(e.g., jugular venous distention), whereas elevated pulmonary venous pressure leads to pulmonary
congestion. In addition, reduced filling of the ventricles during diastole decreases the systolic stroke
volume, and the cardiac output declines. These derangements trigger compensatory mechanisms
aimed at maintaining tissue perfusion, initially through activation of the sympathetic nervous system
(e.g., elevation of the heart rate). Nonetheless, failure to evacuate the effusion leads to inadequate
perfusion of vital organs, shock, and ultimately death.

Question 4

Clinical features?

Answer 4

Cardiac tamponade should be suspected in any patient with known pericarditis, pericardial effusion,
or chest trauma who develops signs and symptoms of systemic vascular congestion and decreased
cardiac output. The key physical findings include
(1) jugular venous distention;
(2) systemic
hypotension; and
(3) a “small, quiet heart” on physical examination, a result of the insulating effects
of the effusion. Other signs include sinus tachycardia and pulsus paradoxus. Dyspnea and tachypnea
reflect pulmonary congestion and decreased oxygen delivery to peripheral tissues. If tamponade
develops suddenly, symptoms of profound hypotension are evident, including confusion and
agitation. However, if the effusion develops more slowly, over a period of weeks, then fatigue
(caused by low cardiac output) and peripheral edema (owing to right-sided heart failure) may be the
presenting complaints.
Pulsus paradoxus is an important physical sign in cardiac tamponade that can be recognized at the
bedside using a standard blood pressure cuff. It refers to a decrease of systolic blood pressure (more
than 10 mm Hg) during normal inspiration.