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Biomedical subjects

H B Hechtman

Publications and source records attributed to H B Hechtman.

At least 199 records · Page 11Linked to original sources
PubMed1980

Aortic aneurysm repair. Reduced operative mortality associated with maintenance of optimal cardiac performance.

Recent advances in the operative management of aortic aneurysms have resulted in a decreased rate of morbidity and mortality. In 1972, we hypothesized that a further reduction in operative mortality might be obtained with controlled perioperative fluid management based on data provided by the thermistor-tipped pulmonary artery balloon catheter. From 1972 to 1979 a flow directed pulmonary artery catheter was inserted in each of 110 consecutive patients prior to elective or urgent repair of nonruptured infrarenal aortic aneurysms. The slope of the left ventricular performance curve was determined preoperatively by incremental infusions of salt-poor albumin and Ringer's lactate solution. With each increase in the pulmonary arterial wedge pressure (PAWP), the cardiac index (CI) was measured. The PAWP was then maintained intra- and postoperatively at levels providing optimal left ventricular performance for the individual patient. There were no 30-day operative deaths among the patients in this series and only one in-hospital mortality (0.9%), four months following surgery. The five-year cumulative survival rate for patients in the present series was 84%, a rate which does not differ significantly from that expected for a normal age-corrected population. Since the patient population was unselected and there were no substantial alterations in operative technique during the present period, these improved results support the hypothesis that operative mortality attending the elective or urgent repair of abdominal aortic aneurysm can be minimized by maintenance of optimal cardiac performance with careful attention to fluid therapy during the perioperative period.

Adult↗
PubMed1980

Is respiratory failure a consequence of blood transfusion?

The pulmonary entrapment of microaggregates, platelets, and white cells in stored blood is thought to contribute to abnormalities in lung function. Washing of red cells removes these potentially damaging elements. This prospective, randomized, double-blind study compares the pulmonary function of patients undergoing abdominal aortic aneurysmectomy who received either washed or unwashed red cell concentrates. Both groups received equivalent volumes of blood, albumin, and balanced salt solution duing surgery. Postoperatively, no differences were observed in the physiologic shunt, QS/QT, pulmonary artery pressure, pulmonary vascular resistance, or effective dynamic compliance. The cardiac index at equivalent left ventricular filling pressures was the same. The results indicate that it is unlikely that microaggregates or other formed elements in stored blood lead to compromised pulmonary function.

Aged↗
PubMed1979

Intrapulmonary clotting and fibrinolysis during abdominal aortic aneurysm surgery.

Intravascular clotting and fibrinolysis (C and F) are events which often accompany major surgical trauma. Their role in inducing cardiopulmonary failure is debated and prompted this study of 13 patients undergoing elective AAA. Following intubation, anesthesia and pressure breathing fibrinolytic activity (FA) in arterial blood exceeded that in mixed venous blood (p < 0.001) indicating pulmonary secretion of proteolytic activity. Fibrinogen, plasminogen and fibrin degradation products (FDPs) were normal. During surgery, fibrinogen and plasminogen fell (p < 0.001) while nonplasmin mediated FA and FDPs rose (p < .001). Despite heparinization (5000 U IV) aortic clamping (avg 56 min) led to evidence of C and F within the lungs. Arterial fibrinogen was 33.2 mg/ml lower than mixed venous blood (p < 0.01) and plasminogen was 0.47 Sherry units lower (p < 0.001). Soluble fibrin monomer appeared in arterial blood (p < 0.01). At the same time nonplasmin mediated FA was consumed within the lungs (p < 0.01) and FDPs were produced (44.6 microg/ml higher in arterial blood, p < 0.001). Similar changes were noted after aortic declamping. The transient 5.3 ml/cm H(2)0 fall in dynamic compliance was unrelated to C and F. Pulmonary vascular resistance and arterial pressure were unchanged. During wound closure intrapulmonary C and F ceased. Postoperatively (6 h), the physiologic shunt of 15.1% was similar to tbe preoperative value of 13.3%. All C and F factors returned to normal except FDPs which remained elevated. An average of 0.2 U blood was given prior to aortic clamping and 3.1 U during clamping. Neither the volume nor the type of blood (7 patients received washed RBCs) influenced pulmonary C and F. The results show that pressure breathing will alter pulmonary metabolism from clearance to secretion of fibrinolytic activity. Surgery leads to systemic C and F while intrapulmonary C and F is triggered by aortic clamping despite IV heparin. Delayed functional consequences of C and F are possible. Immediate postoperative effects are not apparent.

Aorta, Abdominal↗
PubMed1979

Importance of oxygen transport in clinical medicine.

One or more of the several components of the oxygen transport system may function abnormally in critical illness. Arterial hypoxemia is an important feature of acute respiratory failure. Its prominence may obscure other limitations in oxygen availability such as low cardiac output, anemia, or an increased red cell affinity state. These several components of the oxygen transport system can be influenced by therapeutic maneuvers, but the result may not necessarily be a net benefit. For example, red blood cell transfusion therapy may correct anemia, but increase the red blood cell affinity state so as to adversely affect cardiac function. Treatment programs require consideration of the interaction of these several variables affecting oxygen transport.

Aged↗
PubMed1979

Presence of negative inotropic agents in canine plasma during positive end-expiratory pressure.

Application of positive end-expiratory pressure (PEEP) will reduce cardiac output (CO). Humoral mediation of this event by circulating negative inotropic agents was examined using a rat papillary muscle bioassay. Twenty-seven dogs were anesthetized with an iv pentobarbital infusion. Plasma was obtained before and after 30 minutes of PEEP. The plasma was oxygenated in a small (4.5-ml) papillary muscle chamber using a diffusion membrane. An average PO2 of 416 mm Hg was achieved. PEEP plasma reduced developed tension (Tpd) from 2.16 +/- 1.0 to 1.90 +/- 1.05 g (P less than 0.0001). A fall in Tpd was observed whether or not CO was maintained constant with fluid infusion. Resting tension was unchanged. The percent reduction in Tpd correlated with the fall in CO (r = 0.63, P less than 0.01) when fluid was not infused to maintain CO. Reapplication of control plasma restored Tpd. Barbiturate levels in anesthetized dogs rose from 17.3 to 19.4 microns/ml during PEEP (P less than 0.1). Addition of pentobarbital to normal plasma led to a slight decrease in Tpd only when the concentration exceeded 99 microns/ml. In three experiments on ex vivo perfused hearts, application of PEEP led to lowering of peak systolic pressure (PSP) within 5 minutes. Removal of PEEP restored PSP in a similar time. The results support the hypothesis that the decline in CO with PEEP is mediated in part by a circulating negative inotropic agent.

Acid-Base Equilibrium↗
PubMed1979

Abnormalities in organ blood flow and its distribution during positive end-expiratory pressure.

Current evidence is inconclusive regarding the possibility that positive end-expiratory pressure (PEEP) redistributes flow and may be directly responsible for systemic organ dysfunction. This study tests the hypothesis that PEEP may induce abnormalities in the distribution of cardiac output (CO). Eight anesthetized dogs were studied during (1) 0 cm H2O PEEP (Z1), (2) 15 cm H2O PEEP (P), (3) Z2, and (4) bleeding (B) to reduce the CO to the same level as P. At each of the four periods, a different 15 mu radiolabelled microsphere was injected into the left atrium. Another four dogs were used to varify that each type of microsphere had the same flow distribution. CO fell from 3.1 liters/min to 1.9 during P (P smaller than 0.01) and to 2.0 during B (P smaller than 0.01). Mean arterial pressure (MAP) declined from 102 to 83 mm Hg (P smaller than 0.01) and 86 mm Hg (P smaller than 0.01(, respectively. Left atrial pressure (LAP) rose from 5.0 to 7.9 mm Hg during P (P smaller than 0.01) and fell during B to 2.7 mm Hg. c0 and its distribution were the same during Z1 and Z2. P caused selective reductions in hepatic (52%), adrenal (25%), and bronchial (24%) blood flows (P smaller than 0.01). In contrast, total flow to these organs during B was the same as during Z. Total renal flow was unchanged by P or B, but the cortical:medullary flow ratio increased during P from 24 to 49 (P smaller than 0.01) and was unchanged by B. P induced a decrease in fundal nucosal flow as compared with Z (P smaller than 0.01). Total coronary flow fell from 100 to 64 ml/min during both P and B (P smaller than 0.01). P led to a selective fall in subendocardial flow (67 ml/min X 100 gm) as compared with B (82.5 ML/MIN X 100 gm, P smaller than 0.01) as well as in the subendocardial:subepicardial flow ratio (1.069 vs. 1.112 ml/min X 100 gm, P smaller than 0.05). It is likely that the higher left ventricular filling pressure (LAP) during P as compared with during B compressed the endocardium and induced relative ischemia. Similarly the high airway pressure during P may have impeded bronchial mucosal flow. The causes and consequences of the other P-induced variations in flow are speculative.

Animals↗