Pericardial Disease (Pericarditis and Pericardial Tamponade)

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Chapter 31 Pericardial Disease (Pericarditis and Pericardial Tamponade)

Stuart F. Sidlow, MD , C. William Hanson, III , MD

1 What is the structure of the pericardium?

The pericardium is a two-layered structure surrounding the heart and consisting of the fibrous and serous layers. The fibrous layer is a stiff, inelastic structure, which has little ability to accommodate fluid accumulation over a short time course. The serous layer consists of two layers, the parietal and visceral pericardium. The parietal layer is adherent to the fibrous pericardium, and the visceral layer is part of the epicardium or external layer of the heart wall. When pericardial effusion occurs, it normally is between the parietal and visceral layers of the serous pericardium. The pericardial space normally holds 15 to 50 mL of an ultrafiltrate of plasma.

2 Why do hemodynamic changes occur with the buildup of fluid between the layers of the serous pericardium?

When fluid accumulates in the pericardial space, the fibrous pericardium has little ability to stretch. As the volume increases in this space, further inflow into the right side of the heart is impaired, which results in decrease in filling of the left side of the heart, and thus preload is decreased.

3 What general types of pericardial disease exist?

Acute fibrinous pericarditis (acute pericarditis)

Pericardial effusion without hemodynamic compromise

Cardiac tamponade

Constrictive pericarditis

5 Describe the clinical manifestation of acute pericarditis (history and physical examination)

Patient may complain of pleuritic chest pain worse on inspiration. Pain is exacerbated by supine position and relieved by sitting up. Dyspnea may be present. A pericardial friction rub is highly specific to acute pericarditis. Many are seen initially with high fever (temperature > 38° C) and new cardiomegaly on chest radiograph. Pleural effusions are frequently observed.

6 What is on the differential diagnosis of acute pericarditis?

Differential diagnosis of acute pericarditis consists of acute myocardial infarction, pulmonary embolus, gastroesophageal reflux, and musculoskeletal pain.

7 How is acute pericarditis manifested on electrocardiography (ECG)?

There is a progression of four stages on ECG, but for diagnosis one should evaluate for concave-up ST segments throughout most leads (exceptions include aV_R and V₁).

8 What other diagnostic tests are useful in diagnosis of acute pericarditis?

Serum cardiac troponin I and creatine kinase, myocardial bound (CKMB) levels should be evaluated. Usually mild troponin increases occur in the absence of increased CKMB levels. The increase is due to inflammation of myocardium. Other tests may include (on the basis of suspicion and other findings) antinuclear antibodies, tuberculin skin test, human immunodeficiency virus serology, and blood cultures.

9 How is pericardiocentesis used in diagnosing or treating acute pericarditis?

Pericardiocentesis or surgical drainage should be performed for one of three reasons:

If moderate to severe tamponade is present, resulting in hemodynamic compromise (class I recommendation)

If purulent, TB or neoplastic effusion is suspected (class IIa recommendation)

If a persistently symptomatic effusion is present

10 Does echocardiography play a role in the diagnosis of acute pericarditis?

Echocardiography should be performed in all patients suspected of having acute pericarditis. The echo is often normal, but when an effusion is seen it supports the diagnosis of acute pericarditis. The absence of effusion does not rule it out. The use of echocardiography was given a class I recommendation by the American Heart Association, American College of Cardiology, and American Society of Echocardiography.

11 How is therapy decided for treatment of acute pericarditis?

Treatment is based on the cause of acute pericarditis as follows:

Neoplastic: Drainage if hemodynamic compromise, and appropriate chemotherapy.

Viral: Symptomatic and supportive care.

Autoimmune: Nonsteroidal antiinflammatory drugs (NSAIDs) are the mainstay of treatment (class I); corticosteroids may be used if refractory to NSAID therapy.

Bacterial or TB: Antibiotics as appropriate by blood or pericardial fluid culture.

Uremia: Reversal of uremic state.

12 What is constrictive pericarditis?

Constrictive pericarditis is a chronic condition by which the parietal and visceral layers of the pericardium fuse and are often calcified. Causes are similar to those with acute pericarditis. It is usually well tolerated until advanced stages, at which point diastolic filling becomes impaired. Patients have dyspnea and Kussmaul sign (described in question 15), peripheral edema is usually present, and a pericardial knock may be heard.

13 What is pericardial tamponade?

Pericardial tamponade is a process in which fluid (blood or serous fluid) accumulates in the pericardial space, either acutely or over time.

14 What is Beck triad?

Beck triad consists of falling arterial blood pressure, elevated systemic central venous pressure (CVP), and a small, quiet heart.

15 What is Kussmaul sign?

Kussmaul sign is a paradoxical increase in CVP with inspiration. It is observed in any condition that restricts venous return to the heart.

16 List common settings for acute pericardial tamponade

After cardiac operations, blunt or penetrating mediastinal trauma (especially stab wounds), acute myocardial infarction with free wall rupture, endovascular catheterization (including aortograms and carotid arteriograms) with perforation, and, uncommonly, central venous catheter placement (due to erosion of the catheter through a vessel wall)

17 Describe the changes in hemodynamic monitoring seen in a patient with pericardial tamponade

Generally referred to as pulsus paradoxus, on arterial line tracing one may see first subtle, then dramatic respiratory variation in the systolic pressure (> 10 mm Hg difference between expiration and inspiration). In a patient who does not have an endotracheal tube in place, as venous return increases to the right side of the heart with negative intrathoracic pressure during inspiration, the free wall of the right ventricle (RV) cannot expand outward into the pericardial space because of the fluid accumulation. The intraventricular septum is displaced into the left ventricle (LV) as the RV distends. As a result, filling of the LV is impaired, causing a decrease in LV preload. During pulmonary artery (PA) catheter monitoring, one sees equalization of diastolic pressures. The pressures of Right atrium = RV = PA diastolic = Wedge pressure (difference < 5 mm Hg).

19 How is pericardial tamponade diagnosed?

Tamponade is a clinical diagnosis based on history and physical examination results. It usually represents an emergency and can lead to pulseless electric activity (PEA) cardiac arrest if left undiagnosed and untreated. Some common features include jugular venous distention with increased CVP (Kussmaul sign), faint heart sounds, sinus tachycardia, and pulsus paradoxus. If one is unsure of the diagnosis, some studies are helpful in diagnosis. The ECG may demonstrate electrical alternans or sinus tachycardia with low-voltage QRS complexes. Chest radiograph may show an enlarged cardiac silhouette. Echocardiography is extremely useful in diagnosis of this condition and has been given a class I recommendation. On echo, right atrial collapse is more sensitive but less specific than RV collapse. If tamponade is highly suspected, one should not wait for an echo before instituting therapy. See Figure 31-2.

Figure 31-2 Electrical alternans.

20 Briefly describe the hemodynamic strategy in a patient with suspected pericardial tamponade

The hemodynamic strategy consists of “fast, full, and tight.”

Fast means allow the patient to have tachycardia (no β-blockers, please).

Full means to increase preload (fluids wide open).

Tight indicates treatment that allows the patient’s blood pressure to rise either by volume resuscitation or with vasopressors (norepinephrine, epinephrine, or phenylephrine) as indicated.

This strategy should be used until definitive management of the tamponade can be performed. Intubation should be avoided until the last possible moment to avoid cardiovascular collapse during anesthetic induction.

21 Why should intubation be avoided during initial treatment of tamponade?

Intubation should be deferred until the last possible moment because increasing intrathoracic pressure with positive pressure ventilation, and myocardial depression or vasodilation resulting from anesthetic agents, can decrease cardiac output by up to 25%, which may eliminate cardiac output in some patients.

22 What therapeutic maneuvers should be performed in a patient with pericardial tamponade?

After determination of the cause and rapidity with which the fluid accumulated, either pericardiocentesis, pericardial window (pericardotomy), or sternotomy (as in patients after cardiac surgery) should be performed.

23 List the contraindications for bedside pericardiocentesis

Severe coagulopathy or low platelet count

Stable effusion (i.e., blind, bedside pericardiocentesis should be performed only with impending cardiovascular collapse or during cardiopulmonary resuscitation)

24 What other conditions are included in the differential diagnosis of pericardial tamponade?

Other conditions to be considered when tamponade is suspected include massive pulmonary embolus, tension pneumothorax, massive myocardial contusion or myocardial ischemia resulting in cardiogenic shock, exacerbation of severe chronic obstructive pulmonary disease with air trapping, and constrictive pericarditis.

Key Points Characteristics of Pericardial Tamponade

1. It is usually a true medical emergency.

2. If left unnoticed or untreated, it results in PEA cardiac arrest.

3. It is a clinical diagnosis.

4. Most useful diagnostic tool is echocardiography, if time permits.

5. Life-saving measure consists of needle pericardiocentesis in emergent situation.

Websites

UpToDate online version 13.3 (www.uptodate.com):

Schiller N, Foster E: Echocardiographic evaluation of the pericardium

Shabetai R, Hoit B: Cardiac tamponade

Shabetai R, Imazio M: Evaluation and management of acute pericarditis

Shabetai R, Soler-Soler J, Corey GR: Etiology of pericardial disease

1 Benumof J. Anesthesia and Uncommon Diseases, 4th ed. Philadelphia: Saunders; 1998.

2 Moore K. Clinically Oriented Anatomy, 3rd ed. Philadelphia: Williams & Wilkins; 1992.

3 Murray M., Coursin D., Pearl R., et al. Critical Care Medicine—Perioperative Management, 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2002.

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