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Less Frequent Conditions Requiring Surgical Intervention

Heart Failure Requiring Transplantation

Indications for heart transplantation are outlined in Table 50-8 . Although the causes of end-stage heart failure are protean (ischemia, end-stage valvular disease, viral, post-irradiation, post-chemotherapy, idiopathic), all patients will be receiving maximal medical therapy and various combinations of converting-enzyme inhibitors, anticoagulants, antiplatelet agents, β-blockers, calcium antagonists, diuretics, digoxin, amiodarone, and other drugs.

1965


Figure 50-26 Proposed mechanisms of initiation of aortic dissection. In both cases, cystic medial necrosis is present. In A, an intimal tear is the initial event and is allowing aortic blood to enter the media. In B, the primary event is hemorrhage into the media, with secondary rupture of the overlying intima. A, adventitia; I, intima; M, media.

The perioperative implications of antiplatelet drug administration and heparin use are discussed elsewhere in this chapter. Although some patients with end-stage heart failure and liver congestion may, to a certain extent, be autoanticoagulated, most patients undergoing transplantation are taking oral anticoagulants. These drugs require perioperative reversal. In addition to being a source of antithrombin III, fresh frozen plasma is also a direct source of those coagulation factors inhibitable by oral anticoagulants and thus vitamin K1 -dependent factors (factors II [prothrombin], VII, IX, and X). Vitamin K1 (other vitamin K analogs are largely ineffective) administration begins to have an effect on liver enzyme kinetics only after 3 to 6 hours,[158] [159] even when given intravenously. Hence, vitamin K1 administration is not likely to have a significant influence on immediate hemostasis. In addition, vitamin K1 administration may result in resistance to re-anticoagulation with oral anticoagulants for several days postoperatively. Thus, some authors do not recommend administering vitamin K1 as an antidote to oral anticoagulants and confine its use to patients with over-dose when re-anticoagulation is not an issue. However, the risks associated with blood and blood product (i.e., fresh frozen plasma) transfusion may alter the threshold for administration. Several reports now support the efficacy of low-dose (0.5 to 1 mg) intravenous vitamin K to reverse anticoagulants without causing subsequent resistance to oral anticoagulation.

Pulmonary vascular congestion, pulmonary hypertension, and depending on the duration and severity, elevated pulmonary vascular resistance are inevitable and intrinsic features of end-stage heart failure. Severe pulmonary hypertension with elevated pulmonary vascular resistance has, depending on its magnitude, been a contraindication to heart transplantation. The upper limits of acceptability vary among centers. An upper limit of pulmonary vascular resistance of 6 Wood units is used at most centers.[160] (Wood resistance units are calculated as the quotient of the pulmonary vascular pressure gradient, measured in mm Hg, divided by flow, measured in L/m.) The degree of reversibility of elevated pulmonary vascular resistance is


Figure 50-27 Commonly used classification systems for aortic dissection. (From Isselbacher EM, Eagle KA, Desanctis RW: Diseases of the aorta. In Braunwald E [ed]: Heart Disease. A Textbook of Cardiovascular Medicine, 5th ed. Philadelphia, WB Saunders, 1980, pp 1546–1581.)

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TABLE 50-7 -- Commonly used classification systems to describe aortic dissection

Site of Origin and Extent of Aortic Involvement
DeBakey
Type I Originates in the ascending aorta and propagates at least to the aortic arch and often beyond it distally
Type II Originates in and is confined to the ascending aorta
Type III Originates in the descending aorta and extends distally down the aorta or, rarely, retrogradely into the aortic arch and ascending aorta
Stanford
Type A All dissections involving the ascending aorta, regardless of the site of origin
Type B All dissections not involving the ascending aorta
Descriptive
Proximal Includes DeBakey types I and II or Stanford type A
Distal Includes DeBakey type III or Stanford type B
From Isselbacher EM, Eagle KA, Desanctis RW: Diseases of the aorta. In Braunwald E (ed): Heart Disease. A Textbook of Cardiovascular Medicine, 5th ed. Philadelphia, WB Saunders, 1980, pp 1546–1581.

also important in evaluating the suitability of recipients for heart transplantation. Pulmonary vascular resistance values less than 6 Wood units should be demonstrated before heart transplantation is undertaken. Elevated pulmonary vascular resistance may be reversible with pulmonary vasodilators. A significant systemic vasodilator effect (>20% decrease in systemic blood pressure) in response to a vasodilator, without a decrease in pulmonary vascular resistance, demonstrates a lack of reversibility. Inhaled NO
TABLE 50-8 -- Indications and criteria for cardiac transplantation
End-state heart disease not amenable to other medical or surgical therapy
Class III–IV symptoms with optimal medical therapy and prognosis for 1-year survival less than 50%
Age ≤ 60–65
Healthy apart from heart disease
Emotionally stable, well motivated to resume active lifestyle
Compliant with medical advice
Supportive family/companions willing and able to make similar long-term commitments
From Kasper EK, Achuff SC: Clinical evaluation of potential heart transplant recipients. In Baumgartner W, Reitz B, Kasper E, Theodore J (eds): Heart and Lung Transplantation, 2nd ed. Philadelphia, WB Saunders, 2002, pp 57–63.

can also be used to assess reversibility. However, it is expensive and the absence of a response does not allow one to distinguish between the lack of reversibility and an inadequate dose because inhaled NO will not induce systemic hypotension. Patients with increased pulmonary vascular resistance pose potentially significant problems. They are at increased risk of succumbing to the pulmonary vascular effects of CPB (i.e., exacerbation of elevated pulmonary vascular resistance and accentuated pulmonary vasoreactivity). Thus, the donor right ventricle is at increased risk of failure because of a mismatch in afterload. Moreover, the donor ventricle in a transplanted heart is at risk of some degree of ischemic insult during the interval between explantation and implantation, thereby compounding the risk of right ventricular failure.

Increasingly, patients are placed on mechanical circulatory support systems as a bridge to transplantation, which has obvious implications for the timing and difficulty of surgery. These patients pose a management dilemma. The nature of the surgery makes it desirable to use aggressive antifibrinolytic therapy such as aprotinin. Although re-exposure to aprotinin places patients at increased risk for antibody/immune-mediated reactions, clinical experience and antibody data indicate that such reactions are less frequent than would be predicted, especially as the interval between exposures increases.

Cardiac Tamponade

Common causes of cardiac tamponade are listed in Table 50-9 . Though often and understandingly viewed by the anesthesiologist as an acute life-threatening event requiring urgent surgical intervention, cardiac tamponade can have a wide spectrum of clinical manifestations ranging from mild to severe. The rapidity of fluid accumulation in the pericardium and the related variable of pericardial sac compliance are the primary determinants of the physiologic impairments that occur with tamponade ( Fig. 50-28 ). Acute accumulation of a relatively small volume of fluid in a noncompliant "compartment" can lead to rapid cardiovascular collapse. In contrast, larger
TABLE 50-9 -- Common causes of cardiac tamponade
Hemorrhagic pericarditis caused by
  Aortic dissection
  Ventricular free wall rupture after myocardial infarction
  Anticoagulant-induced hemopericardium
  Trauma (stab wounds, central venous catheters)
  Cardiac surgery
Uremic pericarditis
Neoplastic pericarditis (especially mesothelioma or lymphoma)
Serous pericarditis (rheumatoid disorders, irradiation, viral infection)
From MacVeigh I: Anesthesia for the surgical management of pericardial disease. In Thys DM (ed): Textbook of Cardiothoracic Anesthesiology. New York, McGraw-Hill, 2001, pp 630–643. Copyright © by McGraw-Hill, Inc. Used by permission of McGraw-Hill Book Company.

1967


Figure 50-28 Pressure-volume relationship of the pericardium in the presence of pericardial effusion. A, hyperacute cardiac tamponade (gunshot or stab wounds to the heart); B, subacute cardiac tamponade—the effusion developed over a period of a few days; C, effusion that has developed over a period of several weeks to months; D, chronic effusive pericarditis—pericardial pressure is slightly elevated but does not cause major hemodynamic impairment. (From Smith T: Cardiovascular Therapeutics: A Companion to Braunwald's Heart Disease. Philadelphia, WB Saunders, 1996, p 774.)

accumulations occurring over time can be well tolerated. Cardiac tamponade that occurs after cardiac surgery develops in the absence of an intact pericardium and results from blood accumulation in the "closed" space around the heart and ineffective chest tube drainage. Moreover, in this setting, relatively small accumulations may have significant hemodynamic consequences if the low-pressure cavities (i.e., the atria) of the heart are preferentially compressed.

Under normal conditions, venous return to the heart is facilitated by the decrease in intracavity pressure that occurs post-systole. Fluid accumulation around the heart decreases and eliminates the transmural distending pressure that promotes cardiac filling. If severe, diastolic pressures increase. Moreover, diastolic pressures in the atria and ventricles tend to equalize. Impaired cardiac filling results in impaired cardiac output and activation of reflex neurohumoral mechanisms (autonomic nervous system, catecholamine release, vasopressin release, activation of the renin-angiotensin system) in an attempt to maintain adequate organ perfusion. Predictably, hypovolemia exacerbates the hemodynamic effects of tamponade. As a corollary, optimizing volume status, as well as having access to allow one to accomplish this, is a key feature of the perioperative management of these patients. Moreover, anesthetic regimens should be designed to use pharmacological tools that minimally attenuate (as much as possible) the sympathetic response that is the essential mechanism by which cardiac output and blood pressure are maintained (albeit inadequately) in these patients.

Constrictive Pericarditis

Constrictive pericarditis is most frequently idiopathic or viral. Other causes include radiation therapy, post-cardiac surgery, post-myocardial infarction (Dressler's syndrome), connective tissue disorders, and renal failure. As with tamponade, diastolic filling of the heart is restricted in constrictive pericarditis. Depending on the cause, level of progression, and severity of the process, varying degrees of pericardial calcification, pericardial effusion, and myocardial and/or coronary involvement may be present. In severe cases, the latter may be manifested as myocardial atrophy (and thus systolic dysfunction), whereas coronary involvement is probably mediated by scar-induced compression of the coronary arteries. The symptoms and signs of constrictive pericarditis are a function of impaired cardiac output (fatigue, malaise) and limitations in venous return to the left (dyspnea, cough) and/or the right (enlarged liver, ascites) sides of the heart. As in tamponade, intracavitary pressure measurements reveal equalization of diastolic pressures, but a more pronounced decrease in pressure in early diastole (corresponding to a pronounced y descent on CVP), thereby giving rise to the so-called square root sign ( Fig. 50-29 ).

Primary Cardiac Tumors

Primary cardiac tumors are rare.[161] [162] Among primary cardiac tumors, benign tumors are much more common, and of benign tumors, myxomas are by far the most common. Approximately 85% of these usually solitary tumors occur in the left atrium.

Cardiac tumors may be manifested clinically in one or more of three ways: (1) nonspecific systemic features, (2) thromboembolic phenomena, and (3) local cardiac effects. Nonspecific systemic manifestations include fever, malaise, cachexia, arthralgia, rash, and behavioral changes. Mechanistically, there is good evidence to suggest that interleukin-6 synthesis by tumor tissue mediates

1968


Figure 50-29 Simultaneous recordings of right and left ventricular pressure showing "dip and plateau" waveforms and equalization of right and left ventricular diastolic pressure. (From Baim DS, Grossman W: Cardiac Catheterization, Angiography, and Intervention, 5th ed. New York, Lippincott Williams & Wilkins, 1995 p 419.)

these nonspecific systemic symptoms.[163] [164] [165] The combination of intracavity location and the friable nature of myxomatous tissue underlies thromboembolic complications. If the primary tumor occurs in the left side of the heart, systemic emboli occur. If it occurs in the right side, pulmonary emboli occur. The local effects of a tumor depend on its specific location in the heart. For example, myocardial tumors most often cause conduction disturbances, whereas the most common tumor and its location (i.e., a left atrium myxoma) are likely to cause changes in normal mitral valve function (i.e., cause symptoms similar to those occurring in mitral stenosis). Dyspnea on exertion, orthopnea, cough, and hemoptysis are common manifestations.

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