Neurologic complications of open heart surgery. Computer-assisted analysis of 531 patients.
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Biomedical subjects
Publications and source records attributed to F G Estafanous.
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Significant hypertension can develop in 15 to 40 percent of patients undergoing various types of cardiac surgery. These hypertensive episodes can occur at almost any time before, during or after open or closed chest operations. The various hypertensions encountered in this context do not form a homogeneous entity; they are nt due to the same causes and do not necessarily develop by the same mechanisms. Their frequency and seriousness have been demonstrated by reports from many centers: hence, the urgent need for accurate definition of their various types to allow correct identification and therapy. A classification based on well defined clinical events is therefore proposed and possible mechanisms for the more common types of hypertension are reviewed. Prophylactic measures nclude reassurance, attention to details of anesthesia and maintenance of preoperative antihypertensive therapy when indicated; for patients with coronary artery disease, preventive nitrate therapy as well as prompt attention to chest pain is essential. Both general and specific antihypertensive measures to control the more common types of hypertension complicating cardiac surgery are outlined.
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The evolution of hemodynamic variables during the development of postcoronary bypass hypertension was investigated with use of serial cardiac output determination (indocyanine green dye) in 17 patients. Seven of the 17 patients remained normotensive (Group I) during the follow-up period of 4 to 6 hours after operation, whereas 10 (Group II) had a steady increase in blood pressure (173/101 mm Hg +/- 5.9/2.4 [mean +/- standard error] from 132/78 +/- 4.0/2.5 mm Hg immediately postoperatively, P less than 0.001) during the same time interval. Patients in Group I had no significant change in cardiac output, total peripheral resistance or heart rate. In contrast, patients who became hypertensive had a significant increase in total peripheral resistance (47 +/- 2.9 units/m2 from an initial level of 38 +/- 2.5 units/m2, P less than 0.001) with no significant change in cardiac index (2.73 +/- 0.17 versus 2.66 +/- 0.25 liters/min per m2, P greater than 0.10). Their heart rate, which was rapid initially (102 +/- 3.7 beats/min), remained unchanged during the hypertensive episode (103 +/- 3.0 beats/min). The mean rate of left ventricular ejection was not reduced by the increase in pressure and even tended to increase further in all but one patient. Central venous pressure (measured in all patients) and left atrial pressure (measured in eight patients) remained constant throughout the study in both Groups I and II. The results suggest that the mechanism underlying this type of hypertension is a generalized hemodynamic disturbance possibly related to overall sympathetic overdrive rather than the result of improved cardiac performance induced by myocardial revascularization.
Unilateral stellate ganglion block (right or left) was achieved by local injection of 15 ml of lidocaine in 27 patients with hypertension after coronary bypass surgery. The stellate block led to rapid and sustained control of blood pressure in 18 patients (9 of 15 with right stellate block and 9 of 12 with left stellate block). The reduction in arterial pressure was associated with significant (P less than 0.01) reductions in total peripheral resistance and heart rate but no significant changes in cardiac output or central venous or left atrial pressures. This hemodynamic pattern as well as effectiveness of a unilateral approach suggests that the stellate block reduced arterial pressure by interrupting the afferent limb of a pressor reflex from the heart or great vessels, or both. The procedure was free from side effects and helped avoid prolonged parenteral administration of potent antihypertensive drugs.
Paroxysmal hypertension occurred during the first 8 hours after cardiac valve replacement in 15 of 186 consecutive patients. The clinical characteristics of this hypertension were similar to those of hypertension after myocardial revascularization, except that this complication occurred much less frequently after valve replacement (8.1%) than after myocardial revascularisation (33%) (P less than 0.001). Hypertension resulting from hypoxia, hypercapnia, shivering, or arousal from anaesthesia was excluded from consideration. The rise in systemic arterial pressure (average 34/35 mmHg +/- 4.9/4.3 SE) was usually associated with a reduction in central venous pressure (12/15 patients) and a mild increase (2 to 4 cm saline) in left atrial pressure. The incidence of hypertension was not related to the valve replaced (aortic or mitral), type of lesion (stenosis or regurgitation), preoperative level of blood pressure, or use of hypothermia during operation. However, none of the 18 patients who had double valve replacement showed significant rise in blood pressure after operation. It is suggested that these hypertensive episodes may be related to pressor reflexes from the heart and/or great vessels.
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Hypertension immediately after coronary surgery is a problem in about one third of the patients so treated. This report discusses the possible causes of postoperative hypertension and describes several means of controlling the complication.
Respiratory care of patients undergoing open heart surgery should begin in the preoperative period. Patients must stop smoking, and if obese they are encouraged to lose weight. Pulmonary infection is treated and secretions must be eliminated. Postoperative hypoxemia, which is an expected event following anesthesia and surgery, is aggravated by circulatory instability and pulmonary complications. Following open heart surgery pulmonary complications such as atelectasis, congestion, edema, postperfusion lung, pneumothorax, pleural effusion, and hemothorax are common. Respiratory care should be planned to avoid these complications and to treat them promptly should they occur. Routinely every patient is mechanically ventilated for at least 12 to 18 hours following surgery. The type of ventilator used and its parameters are adjusted according to the clinical condition of the patient to maintain adequate oxygenation and to prevent any respiratory acidosis. When indicated, PEEP is applied to improve arterial oxygenation. Respiratory care is extended for at least 5 days after termination of artificial ventilation. Oxygen therapy is given with either a nasal catheter or a mask, according to the patient's need. IPPB and physiotherapy are continued until the patient shows no signs of pulmonary infection and is capable of effectively eliminating secretions. This routine management and extended postoperative respiratory care definitely contribute to the successful outcome of open heart surgery.
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