Long-term survival and functional capacity in cardiac surgery patients after prolonged intensive care.
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Biomedical subjects
Publications and source records attributed to R Replogle.
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Cardiac (or myocardial) failure, a major health problem, can be defined using physiologic criteria that consider the adequacy of O2 delivery relative to the body's O2 requirements. In clinical terms, cardiac failure may be described in terms of its chronicity or the extent to which signs and symptoms of right- versus left-sided heart failure are dominant. Congestive heart failure is a clinical syndrome that consists of a constellation of signs and symptoms that arise from congested organs and hypoperfused tissues. Acute cardiac failure occurs because of a decrease in myocardial contractility that can be offset by the Frank-Starling mechanism. In chronic cardiac failure dilatation and myocardial hypertrophy serve to restore ventricular function. Other compensatory responses that are invoked include a salt avid kidney, which mediates an expansion of the intravascular space, and the activation of the adrenergic nervous and renin-angiotensin-aldosterone systems and an increase in circulating arginine vasopressin. The management of acute and chronic cardiac failure can be derived from an understanding of the pathophysiologic mechanisms responsible for their appearance and include improving cardiac performance, as well as the distribution of systemic blood flow to tissues based on physiologic priorities and moment to moment variations in O2 requirements.
Cardiac tamponade is an important complication after cardiac surgery, yet little has been published on the echocardiographic diagnosis of this situation. The two-dimensional echocardiograms of 11 patients who required surgical relief of cardiac tamponade complicating cardiac surgery were therefore reviewed. Four had nonloculated pericardial effusions surrounding both ventricles. The other seven patients had a loculated posterior pericardial effusion; in three of these the effusion altered left ventricular posterior wall contour so that it was concave toward the effusion in the long-axis view; in two, a strikingly abnormal motion of the left ventricular posterior wall was noted, such that the width of the posterior pericardial space diminished in systole and widened abruptly in early diastole. The quantity of pericardial contents (fluid, blood or clot) evacuated surgically was smaller than usually encountered in patients with tamponade due to various "medical" conditions. Thus, unlike tamponade with other pericardial effusions, tamponade after cardiac surgery is due to a pericardial effusion that is smaller in volume, often loculated posteriorly and associated with certain unique two-dimensional echocardiographic features.
What is thought to be the first case of coronary artery bypass in a patient on lithium carbonate prophylaxis is presented. A postcardiotomy delirium developed on day 2 and appeared unrelated to the underlying manic-depressive illness. A 2-year follow-up indicated apparent resolution of pre-existing psychological difficulties and no recurrence of somatic symptoms. It is suggested that lithium carbonate prophylaxis be continued with appropriate monitoring during coronary artery bypass procedures.
Symptoms equated with "threatened" or "near-miss" sudden infant death syndrome (SIDS) were noted during feedings in 4 infants. In each case, barium esophagrams revealed dysmotility. Acute "near-miss" symptoms required cardiopulmonary resuscitation during esophagography in 2 infants. The authors suggest that esophageal dysmotility is a cause of "near-miss" SIDS and most likely is responsible for more fatalities than commonly realized. The cause-and-effect relationship is explained by a vagovagal reaction. Etiologies of esophageal dysmotility and possible prophylactic measures are discussed.
The authors review the relationship between esophageal dysfunction (dysmotility) and the unusual cardiopulmonary and neurological manifestations equated with the symptoms of the "near-miss" sudden infant death syndrome (SIDS). Six beagle puppies were studied to see whether esophageal irritation and dilatation could provoke any cardiac dysrhythmia. Some of the cardiographic irregularities observed in 10 of 11 trials occasionally precede fatal ventricular dysfunction. The authors conclude that esophageal irritation can be responsible for cardiac arrest and that one important cause of SIDS is esophageal dysmotility.
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A coronary arteriovenous fistula was diagnosed in a 20-year-old white male because of a continuous murmur atypically located along the left sternal border. Cardiac catheterization revealed a large left-to-right shunt, and selective coronary arteriography established the precise anatomic diagnosis. The patient was treated successfully by surgical reimplantation of the anomalous coronary artery into the aorta and ligation of its origin at the pulmonary artery. The embryological and clinical features of this anomaly are discussed, and mechanisms for its production are suggested. Attention is called to our observation of an apparent male sex predilection of this anomaly from review of the literature, in addition to the present patient. This is apparently the fourth patient with this anomaly whose condition was diagnosed antemortem by selective coronary arteriography and the fourth to have been treated by aortocoronary anastomosis providing an additive supply for both the present and the future. This is also the second case in the literature to have the transplanted right anomalous coronary artery demonstrated by selective coronary arteriography. It is likely that, with increasing use of selective coronary arteriography inthe diagnostic work-up of cardiac patients, more cases will be discovered and treated surgically.
Fourteen infants with complete common atrioventricular canal (CCAVC) underwent open heart surgery under deep hypothermia and circulatory arrest. There were three operative deaths and two late deaths. Postoperative studies performed in seven of the nine survivors revealed nearly normal hemodynamics. There were no residual shunts, and excellent mitral valve function was observed in six patients. In one patient, residual mitral regurgitation was noted. The pulmonary artery pressures and pulmonary vascular resistances were normal except in one who had severe pulmonary vascular obstructive disease before surgery. The mean left ventricular end-diastolic volume changed from 175 +/- 24% (SEM) before surgery to 106 +/- 7% after surgery (P less than 0.01). The corresponding right ventricular end-diastolic volume changed from 166 +/- 16% to 102 +/- 19% (P less than 0.025). Left ventricular ejection fraction was mildly decreased before and after surgery (0.63 +/- 0.02). Surgical repair of CCAVC is possible during the first year of life, with likely normalization of cardiac size and function. Unsatisfactory results related to pulmonary vascular obstruction may be anticipated if repair is delayed much beyond the first year.
Twenty-eight dogs were subjected to 90 minutes of hypothermic (30 degrees C) cardiopulmonary bypass with moderate hemodilution. In 6 dogs the heart was vented and beating for 60 minutes. Eight dogs underwent ventricular fibrillation with coronary perfusion (VF + CP). In 14 dogs the aorta was cross-clamped for 60 minutes while the myocardium was protected by local cardiac hypothermia (ICA + LCH). Eighteen animals survived. Hemodynamic studies at seven weeks revealed no major differences among the three groups. At postmortem examination, no gross scarring was noted in any heart. Microscopical examination of 14 hearts was completely-normal. In the VF + CP group, 2 hearts had isolated microscopical scars. Similar linear subendocardial scars (less than or equal to 1.5 X 0.5 mm) were noted in 2 hearts subjected to ICA + LCH. Survival after 60 minutes of VF + CP or ICA + LCH did not result in long-term morphological injury to or functional impairment of the myocardium.
Surgical closure of a left coronary artery-left ventricular fistula in a 44-year-old black man is reported. The fistula was discovered by coronary arteriography after the patient was admitted to the hospital complaining of recurrent chest pain. The fistula was closed with cardiopulmonary bypass, ischemic arrest, and hypothermia, and there was an uneventful postoperative recovery. The previously reported five cases of fistulas terminating in the left ventricle that were closed surgically are reviewed. Four of these cases originated in the right coronary artery and one in the left coronary artery. Three of the six patients were symptomatic at the time of discovery of the lesion. Cardiopulmonary bypass was necessary in five of the six cases. One patient died in the postoperative period from intractable hemorrhage. It is recommended that coronary artery fistulas by closed upon establishment of the diagnosis because of the sequelae if they are allowed to remain open; these include premature atherosclerosis, aneurysmal dilatation of the coronary artery, and congestive heart failure.
An 8 week old infant with severe heart failure from type 1 truncus arteriosus underwent successful corrective surgery employing the Rastelli procedure with use of deep hypothermia and total circulatory arrest. Postoperative hemodynamic studies showed complete closure of the septal defect, disappearance of truncal stenosis, but presence of mild porcine valve stenosis. This procedure is possible even in very small subjects and is preferable to palliative pulmonary arterial banding.
A ventricular septal defect acquired from a penetrating injury to the membranous septum closed spontaneously, as documented by repeat cardiac catheterization. The patient was asymptomatic from the time the lesion was discovered until the present. We advise observation of these lesions for a period of time, provided that no evidence of cardiac decompensation or pulmonary hypertension is noted as determined by hemodynamic studies and clinical observation. Cardiac catheterization is mandatory to confirm the diagnosis, measure the magnitude of the shunt, and rule out associated intracardiac injuries. We believe the lesion should be closed on an elective basis, regardless of the absence of symptoms, if after a reasonable time there is no evidence that the ventricular septal defect is closing and a significant shunt is demonstrated.
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Isolated mitral insufficiency in children is quantitated angiographically by comparing the stroke volumes of the right ventricle and left ventricle. The disease results in greater enlargement of the left atrium than of the left ventricle and is accompanied by a significant increase in left atrial "distensibility." Right and left heart pressures may be normal or may be increased; they tend to be elevated in the group with regurgitant fractions of over 50%. Annuloplasty results in marked clinical and hemodynamic improvement and may even be corrective.
We present an infant with right-sided juxtaposition of atrial appendages who had open heart surgery for ventricular septal defect and patent ductus arteriosus. Of 12 cases thus far reported, ventricular d-loop was observed in nine, and normal position of great vessels in four. Contrary to previous views, this condition may not be accompanied by severe conotruncal anomalies.
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