Indian Journal of Thoracic and Cardiovascular Surgery 1985-86; 4 : 19-22

Anaesthetic Management of Cardiac Tamponade after Open Heart Surgery K MURALIDHAR', A ROUT*, K MOHANDAS ~

ABSTRACT : The anaesthetic management of cardiac tamponade following open heart surgery in 82 patients has been reviewed. The overall incidence was 4.1 per cent in 2000 open heart cases. In individual disease groups, the highest incidence was found in patients with endomyocardial fibrosis (14.55% in 55 cases), followed by Ebstein's anomaly (l I. 11% in 18 cases) and tetralogy of Fallot (9.37% in 256 cases). The anaesthetic technique used was that of judicious administration of anaesthetic agents, volume expansion, correction of metabolic acidosis, inotropic infusion, and careful IPPV to avoid excessive inflation pressures.

KEY WORDS ." anesthesia, anesthetics, cardiac tamponade, heart diseases, postoperative complications.

INTRODUCTION

A low cardiac output state following open heart surgery may be due to a variety of causes, amongst which cardiac tamponade is a surgi- cal emergency, especially when associated with profound cardiovascular collapse. It is a low output state caused by impairment of diastolic filling of the heart resulting from an unchecked rise in the intrapericardial pressure ~. Severe hypo- tension and cardiac arrest have been reported during

"Lecturer, +Assistant Professor, '~Professor and Head of the Department.

From the Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India.

Address for correspondence : Dr. K Mohandas, Professor, Department of Anaesthesiology, SCTIMST. Trivandrum 695 011, India.

administration of general anaesthesia in such pa- tients. Most of the anaesthetic agents are myocardial depressants and many are peripheral vasodilators as well. Judicious administration of these drugs is therefore necessary to avoid serious haemodynamic decompensation. This paper reviews the periopera- tive management of patients with cardiac tamponade after open heart surgery over a 10 year period.

PATIENT PROFILE

Between June 1976 and June 1986, there were 82 cases of proven cardiac tamponade following open heart surgery. Cases of myocardial failure with suspected cardiac tamponade, where no tamponade was found on re-exploration of the chest, were excluded from the study.

Clinical diagnosis of cardiac tamponade was confirmed in 82 (4.1%) out of 2000 cases of open- heart surgery. There were 45 males and 37 females.

20 Muralidhar et al

Most of the patients belonged to the second and third decades.

TABLE. I Incidence of tamponade in relation to the type of surgery performed

TABLE II Time-lag between surgery and re- exploration

CLINICAL PRESENTATION

Most patients presented with a low output state with elevated CVP and enlarged cardiac silhouette in the chest radiograph. The highly sensitive indices for early detection were falling urinary output, and/or increasing doses of diuretics to keep up the renal output, and fall in the peripheral temperature. These signs were detectable even in the absence of actual fall in the systemic arterial pressure. The typical features of pericardial effusion such as Kussmaul's sign, paradoxical pulse, and muffling of heart sounds were not reliable. One patient had bradycardia and one had cardiac arrest in the ][CU before the tamponade could be relieved. Patients with late tamponade presented with non specific symptoms like weakness, anorexia, diaphoresis, chest pain and cold extremities; the diagnosis could be confirmed by chest x-ray and echocardiography.

The distribution of patients who developed postoperative tamponade and the time-lag between surgery and re-exploration are summarised in Tables I and II respectively. The maximum incidence (80.5%) of postoperative tamponade occurred within the first 48 hours after the initial surgery. Late tamponade manifesting 7 days or later after the initial operation :'3 occurred in 8 patients, 7 of whom underwent palliative procedures (valve replacement, endocardiectomy) for endomyocardial fibrosis and one had undergone aortic valve replacement with VSD closure.

ANAESTHETIC MANAGEMENT

The anaesthetic techniques used are summarised in Table III. The supportive measures used were :

�9 blood volume expansion by rapid infusion of colloids or crystalloids

�9 inotropic infusion comprising isoprenaline, isoprenaline-adrenaline, dopamine, or dopamine- adrenaline at a rate to maintain an adequate or acceptable blood pressure

Anaesthesia for postoperative tamponade 21

�9 correction of metabolic acidosis

�9 use of diuretics to maintain adequate urinary flow

TABLE llI Anaesthetic technique employed a Tamponade presenting within 72 hrs of surgery

b Tamoonade presenting beyond 72 hrs of surgery

The perioperative monitoring included EKG, direct arterial pressure, CVP, urinary output, ventilatory parameters, temperature, arterial blood gases, serum electrolytes, haematocrit, coagulation profile and chest x-ray.

MORTALITY

There was no case of intraoperative or early postoperative death. There were seven late post- operative deaths due to renal failure (5), brain death (1) and hepatic and renal failure (1).

DISCUSSION

Tamponade is more common and more danger- ous after cardiac surgery than is usually appreciated. Acute tamponade after cardiac surgery is usually due to haemorrhage combined with inadequate pericardial drainage and usually occurs within 48 hours of operation but may sometimes develop days or even weeks later, especially in patients on anticoagulants.

The incidence of cardiac tamponade after open heart surgery in our institute has been 4.1 per cent. Bentall et al 4 reported an incidence of 6.4 per cent in 327 patients and Craddock 5 5.4 per cent in 400 patients. The highest incidence (14.55%) of tamponade was in patients with endomyocardial fibrosis followed by those with Ebstein's anamoly (I1.11%). This is due to abnormalities of the coagulation profile following right heart failure and hepatic dysfunction and consequent excessive bleeding.

In the acute state, 150 to 250 ml of blood in an adult may be sufficient to cause tamponade 6. Since cardiac output in these patients is reduced, fixed, and dependent upon elevated venous filling pressure, anything which impairs cardiac contraction or venous return further depresses the cardiac output, even in the well compensated state. Hypotension and cardiac arrests have been documented in patients with tamponade after administration of most general anaesthetic agents and even premedication 7. In our experience drugs like nitrous oxide, diazepam, morphine, ketamine, pancuronium, etc. which have minimal effect on the haemodynamic stability, especially when used judiciously, appear to be safe. As even minimal degrees ofhypoxia and hypercarbia should be avoided, controlled ventilation is an essential part of general anaestheia; yet, IPPV may further aggravate tamponade s9 and we recommend that excessive inflation pressures not be used at least till the chest is open and tamponade relieved.

In conclusion, postoperative cardiac tamponade is a life threatening emergency which needs early diagnosis and prompt relief for the successful outcome of the open heart procedure. In this study, there were no deaths during the surgical procedure or in the immediate postoperative period.

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Anaesthetic techniques involving the use of agents which have minimal depressant action on the cardiovascular haemodynamics appear to be safe. Supportive measures should include blood volume expansion, inotropic infusion, correction of meta- bolic acidosis, maintenance of adequate urinary output and meticulous haemostasis.

A c k n o w l e d g e m e n t s

The authors wish to thank Prof. M.S. Valiathan, Di rec tor of the Inst i tute for permiss ion to publish this paper and the staff of the Medical Records Department of the Institute for their co-operation.

References

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2. MEkmL W, DAr~AHOO JS, BRAWLEY RK, TAYCOR D. Late cardiac tamponade: a potentially lethal complication after open heart surgery. J Thorac Cardiovasc Surg 1976; 72: 929-32.

3. HARDESTY RL, THOMPSON M, LERGERG DB et al. Delayed postoperative cardiac tamponade: diagnosis and management. Ann Thorac Surg 1978; 26: 155-64.

4. BENTALL HH, SMrm B, OMERI MA, MELROSE DG, ALLWORKS S. Blood loss after car, diopulmonary bypass. Lancet 1964; 2: 277-9.

5. CRADDOCK DR. Reoperation for haemorrhage follow- ing cardiopulmonary bypass. Br J Surg 1968; 55: 17-20.

6. EBERT PA. The Pericardium. In: Sabiston DC, Spencer FC eds. Gibbon's Surgery of the Chest, 4th ed. Philadelphia: WB Saunders, 1983: 995.

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GUNTItE-ROTIt WG, MORGAN BC, MULLIN S. Effect of respiration on venous return and stroke volume in cardiac tamponade. mechanism of pulsus paradoxus. Circulation Res 1967; 20: 381-90.

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