Successful Treatment of Right Ventricular Failure with Atrial Septostomy

Successful Treatment of Right Ventricular Failure with Atrial 8eptostomy· Michael]. Swanson, D.O.; Anthony G. Fabaz, D.O.; and [ia Y. lung, M.D.

In the case reported, a patient with severe right ventricular failure following coronary revascularization was successfully weaned from cardiopulmonary bypass following creation of an atrial septal defect. This technique facilitated rapid decompression of the failing right ventricle by shunting blood to the more compliant left ventricle, thus augmenting left ventricular preload and enhancing cardiac output. Recovery of right ventricular function was demonstrated by progressive hemodynamic improvement, as well as reduction of right-to-left intracardiac shunting and resolution of arterial hypoxemia.

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erioperative right ventricular failure is a difficult surgical problem with high mortality and limited therapeutic options. The normal right ventricle is a low-pressure volume pump, which, like the left ventricle, may be severely compromised by ischemia, infarction, volume overload and afterload mismatch. Loss of the normal compliance and contractility of the right ventricle may lead to circulatory embarrassment and efforts must be made to decompress the acutely failing right ventricle, as well as improving systemic circulation. Immediate therapeutic measures include correction of any underlying acidosis, hypoxemia, electrolyte imbalance as well as volume loading, administration of positive inotropic agents and pulmonary vasodilators, atrial or A-V sequential pacing and intra-aortic balloon counterpulsation. Beyond this there is no standard form of surgical therapy, although at the present time, emphasis is on the use of right ventricular assist devices and pulmonary artery balloon counterpulsation.' CASE REPORT

A 57-year-old white man with a history of stable angina since suffering an acute anterolateral myocardial infarction six years earlier, underwent cardiac catheterization following recent worsening of anginal symptoms. An anatomically dominant right coronary artery was found to be diffusely diseased, while there was 90 percent narrowing in the mid- and distal portions of the left anterior descending coronary artery and moderately diffuse disease involving the left circumflex coronary artery. The left ventricle was mildly enlarged and exhibited focal anterior wall dyskinesia. Left ventricular end-diastolic pressure was moderately elevated at 20 mm Hg. Cardiac index was 2.1 L'min/rn! and the ejection fraction was approximately 50 percent. Pulmonary artery pressures were normal (15/7 mm Hg) and mean pulmonary capillary wedge pressure was 6 mm Hg. Right atrial and right ventricular pressures were normal. The patient was taken to surgery electively for coronary revascularization. A left internal mammary artery pedicle graft was anastomosed to the left anterior descending coronary artery, a sequential reversed saphenous vein graft to the first and second obtuse marginal branches of the left circumflex coronary artery, and

·From the Thoracic and Cardiovascular Surgery Institute, Ingham Medical Center, Lansing, Michigan 950

a reversed saphenous vein graft to the distal right coronary artery. Myocardial protection included systemic cooling to 20°C, intermittent topical cooling with iced saline solution, and oxygenated blood cardioplegia (1,000 ml), Myocardial temperatures were not monitored. Aortic occlusion time was 97 minutes, and the patient was easily weaned from cardiopulmonary bypass after 2 hours and 58 minutes. Mean graft flows were 100 mllmin to the left circumflex sequential graft and 107 mllmin to the right coronary artery vein graft. Hemodynamic parameters were stable upon closure of the chest and transfer to the intensive care unit (BP 135/55, LAP 12 mm Hg). Immediately following transfer to the ICU the patient spontaneously developed ventricular fibrillation and failed to respond to DC countershock and therapy with intravenous antiarrhythmics. The chest was reopened, open cardiac massage initiated, and an intra-aortic balloon pump was placed percutaneously. Sinus rhythm was re-established after approximately 15 minutes of cardiac massage and drug therapy, with satisfactory systemic blood pressure (102/55 mm Hg) and elevated left atrial pressure (26 mm Hg). The right atrium and right ventricle were both cyanotic, distended and dyskinetic. The patient was returned to the surgical suite where cardiopulmonary bypass was resumed. With the primary problem at this time appearing to be right ventricular infarction, an occluded right coronary artery vein graft was suspected. The right coronary artery vein graft was then taken down and revised; thus, a subsequent mean graft flow of 100 mllhr was obtained. The patient was again weaned from cardiopulmonary bypass; however, it was not possible to generate left atrial pressure greater than 12 mm Hg or systemic blood pressure greater than 86/40 mm Hg without right heart distention. Cardiopulmonary bypass was resumed and an atrial septal defect was created to facilitate decompression of the right ventricle. With the patient on full cardiopulmonary bypass and both superior and inferior vena cavae cannulated, a pursestring suture was placed in the right atrial appendage and the latter incised. An incision was then made in the interatrial septum and bluntly spread with a hemostat to approximately 1.5 em in diameter. The atrial pursestring was then secured with a Rummel tourniquet. Dilation of the atrial septostomy was required with persistent right heart distention; however, following this, the patient was weaned from cardiopulmonary bypass with satisfactory hemodynamic parameters (BP 123/51, LAP 9 mm Hg, RAP 9 mm Hg) and marked improvement in right ventricular contractility. The heart remained distended and edematous in appearance. Therefore, it was not possible to close the chest or remove the chest retractor without hemodynamic compromise. A sterile occlusive dressing was placed over the chest retractor and the patient was transferred to the ICU with stable hemodynamic parameters (RAP 9 mm Hg, LAP 9 mm Hg, BP 135/60 mm Hg). Antiarrhythmic therapy was continued postoperatively, and hemodynamic parameters were stabilized with intra-aortic balloon counterpulsation and inotropic support. There was initial arterial hypoxemia (Po 2 48); however, peripheral perfusion was good and there was no cyanosis. The arterial hypoxemia gradually improved (Table 1), and left atrial oxygen saturation demonstrated the hypoxemia to be secondary to intracardiac shunting and not a pulmonary defect. The chest retractor was removed on the second postoperative day, at which time the atrial pursestring suture was ligated and the skin was closed. The sternum was closed and the intra-aortic balloon pump removed on the fifth postoperative day. Convalescence thereafter was complicated by supraventricular arrhythmias, but these were controlled with administration of digitalis and calcium channel blockers. There was no deterioration of renal function and no infectious complication. Alternations in mental status were transient. The postoperative electrocardiogram exhibited diffuse precordial Q waves consistent with extensive anteroseptal and lateral myocardial infarction. Serum creatine phosphokinase measured 24 hours following the precipitating episode of ventricular fibrillation SuccessfulTreatment of Right Ventricular Failure (Swanson, Fabaz, Jung)

Table I-Resolution

Preop Day 1 Day 6 Day 13 Day 18

ofArterial Hypoxemia

with Recovery ofHight Ventricular Function Following Atrial Septostomy for Right Ventricular Failure

FIo 2

PaOz

LA(%)

.21 .70 .60 .40 .2

86 53 62 80

94.5 93.2 94*

Oxygen Saturation

SA(%) 94.4 80.8 90.6 94.4

~02 Content (LA-SA), Vol %

2.02 0.43

Shunt R-L 3.0

*By ear oximetry was markedly elevated at 1722 U/L (7.74 percent MB), substantiating a diagnosis of perioperative myocardial infarction. The patient was discharged on the 20th postoperative day and was able to resume normal activities thereafter. An echocardiogram was performed nine months later and was remarkable for what appeared to be a right atrial thrombus. Oral anticoagulation therapy was initiated at that time, and the patient continued to do well clinically. DISCUSSION

Causes of acute right ventricular failure are rarely identified specifically and are generally considered to be multifactorial in nature. 1 The most common cause may be global ischemic insult to the myocardium, which may be secondary to inadequate myocardial protection, ventricular fibrillation, air or particulate emboli to the right coronary artery, acute graft occlusion, volume overloading, afterload mismatch or reperfusion injury. It has been clearly demonstrated that the right ventricle is more difficult to protect than the left ventricle in open cardiac procedures. Also, there is significant evidence to suggest that inadequate right ventricular hypothermia can precipitate acute right ventricular failure." The maintenance of right ventricular myocardial temperatures below 25°C appears to be critical in maintaining adequate protection of the myocardium." Severe right coronary artery stenoses clearly limit the delivery of cardioplegic solution to the right ventricle. 3 The traditional concept of the right ventricle as a passive conduit allowing for unimpeded blood flow from the venous capacitance system to the pulmonary circulation developed from experimental studies in which cautery-mediated injury to the entire right ventricular free wall failed to impair cardiac function or significantly alter hemodynamic parameters." The interventricular septum, however, appears to be virtually indispensable for both right and left ventricle pump function and it appears to be global right ventricular dysfunction, ie, including the septum that precipitates right ventricular failure." Studies suggest that the isolated right atrium may act as an effective pump when beating with physiologic preload against low afterload, but becomes progressively less efficient as preload and afterload are increased. 6 This has been well demonstrated clinically by the Fontan procedure. Elevated pulmonary vascular resistance increases right ventricular afterload and is clearly a cause of acute right ventricular failure." The acute increase in right ventricular volume and pressure produces increased oxygen demand secondary to the LaPlace relationship and there is a reduction in coronary blood flow to the endocardium due to increased transmural gradient. However, right ventricular

pump failure may occur with normal pulmonary vascular resistance in the presence of right ventricular infarction, 8 septal ischemia," and ischemic papillary muscle dysfunction." Initial therapy for acute right ventricular failure includes correction of any underlying pathophysiology. Atrial or A-V sequential pacing should be considered in all patients. Volume loading to elevate right atrial pressure to 20-25 mm Hg may help optimize preload, but is not likely to be beneficial with septal dysfunction." Optimal pharmacologic support includes the utilization of positive inotropic agents and pulmonary vasodilators. Isoproterenol may be the drug of choice in that it is both a potent inotrope that will enhance right ventricular contractile force and a potent pulmonary vasodilator that will reduce right ventricle afterload. The combined right atrial infusion of prostaglandin E 1 (30-150ng! kg/min) and left atrial infusion of norepinephrine (up to 1 fJ.g/ kg/min) has been utilized to successfully treat right ventricular failure." Ibuprofen, a potent cyclo-oxygenase inhibitor, has produced significant and selective right ventricular afterload reduction in conditions where pulmonary vasoconstriction is elicited by thromboxane formation. 12 Failure of volume loading, physiologic pacing, drug therapy and intraaortic balloon counterpulsation to improve cardiac index above 1.8 L'min/m" with a normal left atrial pressure requires direct therapeutic intervention to assist the right ventricle and pulmonary circulation. There are several reports of successful pulmonary artery balloon counterpulsation for treatment of intraoperative right ventricular failure. This method, however, has the inherent risk of injury to the vessel endothelium and optimal timing is required to produce hemodynamic benefits." Right ventricular bypass pumps offer maximum circulatory support while the right ventricle recovers. 14 The creation of an interatrial septal defect to provide relief of experimentally produced right ventricular strain was reported in 1951,15 but only anecdotal clinical experience has been reported." There is substantial rationale and experience in utilization of atrial septostomy in certain congenital cardiac lesions. Creation of a surgical atrial septal defect facilitates right ventricular afterload reduction by way of a right-to-left intracardiac shunt, thus enhancing left ventricular preload and cardiac output at the expense of arterial oxygen saturation. The optimal size and placement of the surgically created ASD are not known. Studies by Brecher and Opdyke" suggest that a defect as small as 5 mm in diameter may be sufficient to relieve right heart distention, while defects greater than 2 em in diameter may adversely alter atrial dynamics. With improvement in right ventricular CHEST I 92 I 5 I NOVEMBER, 1987

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function, flow should be redirected to the low-pressure, lowimpedance puhnonary circulation and the shunt should reverse from left-to-right or resolve. Right ventricular performance improves more rapidly than that of the left ventricle following acute ischemic injury, with reversal of depressed right ventricular ejection fraction within 72 hours of injury in 10 of 11 patients (91 percent). 17 Once hemodynamic stability has been achieved, the primary problem created by atrial septostomy is that of arterial hypoxemia. Efforts to improve oxygenation should be directed toward improving right ventricular function and decreasing pulmonary vascular resistance. A flow-directed pulmonary artery catheter may optimize hemodynamic management. Positive end-expiratory pressure may increase functional residual capacity and improve gas exchange; however, these benefits may occur at the expense of worsening hypoxemia as the degree of right-to-left shunting may increase with elevated pulmonary vascular resistance. Evaluation of the shunt by measuring the pulmonary vein (left atrial) to systemic artery oxygen stepdown excludes any puhnonary source of shunt or desaturation, and resolution of the stepdown in oxygen saturation is consistent with decreased right-to-Ieft shunting and improved right ventricular function. The potential problems of a residual atrial septal defect and paradoxic emboli are significant, but should be considered within the larger risk/benefit framework of right ventricular failure. ACKNOWLEDGMENT: Special thanks to Steven J. R. Phillips, M. D. for his encouragement in publishing this report, and to my wife Deborah for her support and assistance. REFERENCES

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Spence PA, Weisel RD, Salerno TA. Right ventricular failure: pathophysiology and treatment. Surgical Clinics of NA 1985; 65:689-97 Gonzalez AC, Brandon TA, Fortune RL, Casano SF, Martin M, Benneson DL, et al. Acute right ventricular failure is caused by inadequate right ventricular hypothermia. J Thorac Cardiovasc Surg 1985; 39:16-26 Christakis cr; Fremes SE, Weisel RD, Ivanov J, Madonik M, Seawright SJ, et al. Right ventricular dysfunction following cold potassium cardioplegia. J Thorac Cardiovasc Surg 1985; 90:243-50 Starr I. The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. Am Heart J 1943; 26:291-301 Farrar OJ, Compton PG, Hershon JJ, Fonger JD, Hill JD. Right heart interaction with the mechanically assisted left heart. World J Surg, 1985; 9:89-102 Murphy DA, Marble AE, Landymore R, Dajee H. Assessment of the isolated right atrium as a pump. J Thorac Cardiovasc Surg 1978; 76:485-88 Vlahakes GJ, Turley K, Hoffman JI. The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations. Circulation 1981; 63:87-95 Cohn JR, Guha NH, Broder MI, Limas CJ. Right ventricular infarction. Am J Cardio11974; 33:209-14 Agarwal JB, Yamazaki H, Bodenheimer MM, Banka VS, Helfant RH. Effects of isolated interventricular septal ischemia on global and segmental function of the right and left ventricle. Am Heart J 1981; 102:654-63 Huyghens L, Dupont A, DeWilde PL, Defoer F: Transient tricuspid valve insufficiency following acute inferior myocardial infarction. Acta Cardiol 1986; 41:63-7

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11 D'Ambra MN, LaRaia PJ, Philbin OM, \Vatkins WD, Hilgenberg AD, Buckley MJ. Prostaglandin E 1, a new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 1985; 89:567-72 12 Hasselstrern LJ, Eliasen K, Mogensen T, Anderson JB. Lowering pulmonary artery pressure in a patient with severe acute respiratory failure. Inten Care Med 1985; 11:48-50 13 Opravil M, Gorman AJ, Krejcie TC, Michaelis LL, Moran JM. Pulmonary artery balloon counterpulsation for right ventricular failure: Experimental results. Ann Thorac Surg 1984; 38:242-53 14 Dembitsky W~ Daily PO, Raney AA, Moores WY, [oyo C'f Temporary extracorporeal support of the right ventricle. J Thorac Cardiovasc Surg 1986; 91:518-25 15 Brecher GA, Opdyke DF: The relief of acute right ventricular strain by the production of an interatrial septal defect. Circulation 1951; 4:496-502 16 Aris A. Commentary on: Pulmonary circulatory support. A quantitive comparison offour methods. J Thorac Cardiovasc Surg 1984; 88:963 17 Steele ~ Kirch D, Ellis J, Vogel R. Battock D. Prompt return to normal of depressed right ventricular ejection fraction in acute inferior infarction. Br Heart J 1977; 39:1319-23

Management of Chronic Alveolar Hypoventilation with Nasal Positive Pressure Breathing* Anthony F. DiMarco, M.D., F.C.C.P.; Alfred F. Connors, M.D., F.C.C.P.; and Murray D. Altose, M.D., F.C.C.P.

Negative pressure ventilation is the most common method of providing assisted ventilation without a tracheostomy. Unfortunately, negative pressure devices have several disadvantages and are not well tolerated by all patients. We present a patient in whom intermittent assisted ventilation was applied successfully by using a nasal mask to provide positive pressure ventilatory support.

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atients suffering from chronic respiratory failure secondary to neuromuscular disease or idiopathic hypoventilation may require intermittent assisted ventilation to sustain adequate spontaneous ventilation.!" The most common method of providing assisted ventilation without tracheostomy is by means of negative pressure ventilation using either a tank, cuirass, or body wrap ventilator. Unfortunately, these devices restrict patient mobility," can produce upper airway obstruction and, in the case of the cuirass or body wrap, produce only limited inspired volumes. 5 In the present report, we describe the successful use of a nasal mask to provide intermittent positive pressure ventilation for a patient with chronic respiratory failure in whom negative pressure ventilatory support was unsuccessful. CASE REPORT

A 25-year-old woman first presented to Cleveland Metropolitan *From the Department of Medicine, Cleveland Metropolitan General Hospital and Case Western Reserve University, Cleveland. Reprint requests: Dr. Di Marco, 3395 Scranton Road, Cleveland

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Management of Chronic Alveolar Hypoventilation (DiMarco, Connors, A/tose)