The parietal pericardium is a fibrous membrane surrounding the heart, to which it normally is not adherent. The pericardium encompasses a relatively fixed intrapericardiac volume that includes a small volume of pericardial fluid (20–50 mL in adults), the heart, and blood. As a result, the pericardium normally limits acute dilation of the ventricles and promotes diastolic coupling of the two ventricles (distention of one ventricle interferes with filling of the other). The latter effect is also due to the inter-ventricular septal wall they share. Moreover, diseases of the pericardium or larger pericardial fluid collec-tions can seriously impair cardiac output.
Cardiac tamponade exists when increased pericar-dial pressure impairs diastolic filling of the heart. Cardiac filling is ultimately related to the diastolic transmural (distending) pressure across each cham-ber. Consequently, any increase in pericardial pres-sure relative to the pressure within the chamber reduces filling. Pressure is applied equally to each cardiac chamber when the problem is a pericardial fluid collection; or, it can be applied “selectively,” as for example when an isolated pericardial blood clot compresses the left atrium. In general, the thin-walled atria and the right ventricle are more sus-ceptible to pressure-induced abnormalities of filling than the left ventricle.
Pericardial pressure is normally similar to pleu-ral pressure, varying with respiration between –4 and +4 mm Hg. Elevations in pericardial pressure are most commonly due to increases in pericar-dial fluid volume (as a consequence of effusions or bleeding). The magnitude of the increased pressure depends on both the volume of fluid and the rate of fluid accumulation; sudden increases exceeding 100–200 mL precipitously increase pericardial pres-sure, whereas very slow accumulations up to 1000 mL allow the pericardium to stretch with minimal increases in pericardial pressure.
The principal hemodynamic features of car-diac tamponade include decreased cardiac output from reduced stroke volume with an increase in central venous pressure. In the absence of severe left ventricular dysfunction, equalization of dia-stolic pressure occurs throughout the heart (right atrial pressure [RAP] = right ventricular end-diastolic pressure [RVEDP] = left atrial pressure [LAP] = left ventricular end-diastolic pressure [LVEDP]).
The central venous pressure waveform is char-acteristic in cardiac tamponade. Impairment of both diastolic filling and atrial emptying abolishes the y descent; the x descent (systolic atrial filling) is normal or even accentuated. Ref lex sympathetic
activation is a prominent compensatory response in cardiac tamponade. The resulting increases in heart rate and contractility help maintain cardiac output. Arterial vasoconstriction (increased SVR) supports systemic blood pressure, whereas sympathetic acti-vation reduces vascular capacitance, having the effect of an autotransfusion. Because stroke volume remains relatively fixed, cardiac output becomes pri-marily dependent on heart rate.
Acute cardiac tamponade usually presents as sudden hypotension, tachycardia, and tachypnea. Physical signs include jugular venous distention, a narrowed arterial pulse pressure, and muffled heart sounds. The patient may complain of an inability to lie flat. A friction rub may be audible. A prominent pulsus paradoxus (a cyclic inspira-tory decrease in systolic blood pressure of more than 10 mm Hg) is typically present. The latter actually represents an exaggeration of a normal phenomenon related to inspiratory decreases in intrathoracic pressure. (A marked pulsus para-doxus may also be seen with severe airway obstruc-tion or right ventricular infarction.) The heart may appear normal or enlarged on a chest radiograph. Electrocardiographic signs are generally nonspe-cific and are often limited to decreased voltage in all leads and nonspecific ST-segment and T-wave abnormalities. Electrical alternans (a cyclic altera-tion in magnitude of the P waves, QRS complex, and T waves) may be seen with large pericar-dial effusions and is thought to be due to pendu-lar swinging of the heart within the pericardium. Generalized ST-segment elevation may also be seen in two or three limb leads as well as V2 to V6 in the early phase of pericarditis. Echocardiography is invaluable in diagnosing and measuring pericardial effusions and cardiac tamponade, and as a guide for accurate needle insertion for pericardiocentesis. Signs of tamponade include diastolic compression or collapse of the right atrium and right ventricle, leftward displacement of the ventricular septum, and an exaggerated increase in right ventricular size with a reciprocal decrease in left ventricular size during inspiration.
Pericardial effusions may be due to viral, bac-terial, or fungal infections; malignancies; bleeding after cardiac surgery; trauma; uremia; myocardial infarction; aortic dissection; hypersensitivity or autoimmune disorders; drugs; or myxedema.
Symptomatic cardiac tamponade requires evacua-tion of the pericardial fluid, either surgically or by pericardiocentesis. The latter is associated with a risk of lacerating the heart or coronary arteries and of pneumothorax. Traumatic postoperative (following thoracotomy) cardiac tamponade is nearly always treated surgically, whereas tamponade from other causes may more often be amenable to pericardio-centesis. Surgical treatment is also often undertaken for large recurrent pericardial effusions (infec-tious, malignant, autoimmune, uremic, or radiation induced) to prevent tamponade. Simple drainage of pericardial fluid may be achieved through a subxi-phoid approach, whereas drainage combined with pericardial biopsy or pericardiectomy may be per-formed via a left anterior thoracotomy or median sternotomy. Drainage and biopsies can also be accomplished through left-sided thoracoscopy.
The anesthetic approach must be tailored to the patient. For the intubated postoperative cardiac patient in extremis, the chest may be reopened immediately in the ICU. For awake conscious patients who will undergo left thoracotomy or median ster-notomy, general anesthesia and endotracheal intuba-tion are necessary. Local anesthesia may be used for patients undergoing simple drainage through a sub-xiphoid approach or pericardiocentesis. Removal of even a small volume of fluid may be sufficient to greatly improve cardiac output and allow safe induc-tion of general anesthesia. Small doses (10 mg intra-venously at a time) of ketamine also provide excellent supplemental analgesia.
Induction of general anesthesia in patients with cardiac tamponade can precipitate severehypotension and cardiac arrest. We find it useful to have an epinephrine infusion available and we sometimes initiate it before induction.
Large-bore intravenous access is mandatory. Monitoring of intraarterial pressure is useful, but placement of monitors should not delay pericardial drainage if the patient is unstable. The anesthetic technique should maintain a high sympathetic tone until the tamponade is relieved; in other words, “deep” anesthesia is not the object. Cardiac depression, vasodilation, and slowing of the heart rates should be avoided. Similarly, increases in mean airway pressures can seriously jeopardize venous return. Awake intubation with mainte-nance of spontaneous ventilation is theoretically desirable, but coughing, straining, hypoxemia, and respiratory acidosis are equally detrimental and should be avoided. Thoracoscopy requires one-lung anesthesia.
Ketamine is the agent of choice for induction and maintenance until the tamponade is relieved. Small doses of epinephrine (5–10 mcg) may be useful as a temporary inotrope and chronotrope. Generous intravenous fluid administration is useful in maintaining cardiac output.
Constrictive pericarditis may develop as a sequela of acute or recurrent pericarditis. Pathologically, the pericardium is thickened, fibrotic, and often calcified. The parietal pericardium is typically adherent to the visceral pericardium on the heart, often obliterating the pericardial space. The stiff-ened parietal pericardium limits diastolic filling of the heart to a fixed and reduced volume. In contrast to acute cardiac tamponade, filling during early diastole is typically accentuated and manifested by a prominent y descent on the central venous pres-sure waveform.
Patients with constrictive pericarditis display jugular venous distention, hepatomegaly, and often ascites. Liver function may be abnormal. In con-trast to acute tamponade, constrictive pericardi-tis prevents respiratory fluctuations in pericardial pressure; because venous return to the heart does not increase during inspiration, a pulsus paradoxus is uncommon. In fact, venous pressure does not fall or may paradoxically rise during inspiration (Kussmaul’s sign). The chest radiograph will often reveal pericardial calcification. Low QRS voltage and diffuse T-wave abnormalities are usually pres-ent on the ECG. Atrial fibrillation and conduction blocks may be present. Echocardiography may be helpful in making the diagnosis.
Pericardiectomy is usually reserved for patients with moderate to severe disease. The procedure is usu-lly performed through a median sternotomy. It is complicated by the necessity for extensive manipu-lations of the heart that interfere with cardiac filling and ejection, induce frequent arrhythmias, and risk cardiac perforation. CPB may be required.
Selection of specific anesthetic agents is less important than avoiding excessive cardiac depres-sion, vasodilation, and bradycardia. Cardiac output is generally rate dependent. Adequate large-bore intravenous access and direct arterial and central venous pressure monitoring are usu-ally employed. Although cardiac function usually improves immediately following pericardiectomy, some patients display a persistently low cardiac output and require temporary postoperative ino-tropic support.
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