Manny J

Hepatic--portal venous gas in adults: etiology, pathophysiology and clinical significance.

The roentgenographic finding of hepatic-portal venous gas (HPVG) has been reported extensively in the pediatric and radiology literature. The surgical implications and clinical significance have yet to be fully defined. This study reviews the 60 reported cases in the literature and adds four new cases. HPVG appears as a branching radiolucency extending to within 2 cm of the liver capsule. HPVG is associated with necrotic bowel (72%), ulcerative colitis (8%), intra-abdominal abscess (6%), small bowel obstruction (3%), and gastric ulcer (3%). Mucosal damage, bowel distention and sepsis predispose to HPVG. The current mortality rate of 75% represents an improvement from previous experience. Analysis of survivors indicates that the finding of HPVG requires urgent surgical exploration except when it is observed in patients with stable ulcerative colitis.

Volume loading and vasodilators in abdominal aortic aneurysmectomy

Preoperative infusion of volume to increase the wedge pressure will maintain stable flow and arterial pressure at the time of aortic declamping. Usually 1,500 ml of balanced salt solution given with 75 g of albumin is sufficient to accomplish this purpose. Pressor or inotropic agents are not required. In our experience 14 percent of patients will have a down-slope in the preoperative myocardial performance curves. In these persons, volume infusions should be adjusted to keep the pulmonary arterial wedge pressure on the ascending portion of the curve. The use of vasodilator agents in normotensive patients has a deleterious effect on cardiac performance.

The Association of Lung Distention, Peep and Biventricular Failure

Although positive and expiratory pressure (PEEP) is known to depress the cardiac output, the mechanism remains debated. Two series of experiments were designed to explore this mechanism. In the first study, the application of 15 cm H2O of PEEP to nine anesthetized, ventilated dogs led to a reduction of cardiac index from (mean ± one standard error of the mean) 2.71 L/min m ± 0.35 to 2.19 L/min m ± 0.22 (p <.05) and a drop in mean arterial pressure (MAP) from 117 mm Hg ± 8 to 91 mm Hg ± 11 (p <.01). The mean net (vascular minus pleural pressure) pulmonary artery pressure (MPAP) rose from 15.3 mm Hg ± 1.2 to 20.6 mm Hg ± 1.8 (p <.02). The mean net central venous pressure (CVP) rose from 5.2 mm Hg ± 0.9 to 8.4 mm Hg ± 0.9 (p <.05) and the net pulmonary arterial wedge pressure (PAWP) rose from 6.7 mm Hg ± 0.7 to 9.5 mm Hg ± 0.9 (p <.01). There was a nonsignificant rise in the mean net left atrial pressure (LAP). As PEEP was raised in increments from 0 to 20 cm H2O, both LAP and PAWP increased. The rise in PAWP was always greater than the increase in LAP. The difference between PAWP and LAP was strongly correlated with the increase in MPAP (r = 0.98). This relationship was useful in correcting the PAWP during PEEP. The problem of cardiac depression was evaluated in a second series of eight dogs. These animals underwent complete chest wall excision to eliminate any possible direct effects of increased pleural pressure on the heart and great vessels. The absence of the chest wall permitted hyperexpansion of the lungs, particularly with positive end expiratory pressure. At 15 cm H2O of PEEP, the mean cardiac index fell in these animals from 2.36 L/min m± 0.26 to 1.47 L/min m± 0.18 (p <.01) and the MAP fell from 105 mm Hg ± 16.2 to 68 mm Hg ± 4.8 (p <.001). The CVP rose from a mean of 5.5 mm Hg ± 0.4 to 8.3 mm Hg ± 0.6 (p <.01) and the LAP rose from 6.3 mm Hg ± 0.8 to 8.0 mm Hg ± 1.1 (p <.05). The MPAP rose from 18.0 mm Hg ± 0.6 to 23.3 mm Hg ± 1.6 (p <.01). Comparison of Group I and II showed a significantly greater depression of the cardiac output and MAP in the open-chested animals. At the same time LAP was significantly higher. These data strongly suggest that PEEP and particularly pulmonary hyperinflation induce biventricular failure.

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 POi of 416 mm Hg was achieved. PEEP plasma reduced developed tension (Tpd) from 2.18 ± 1.0 to 1.90 ± 1.05 g (P < 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 < 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 μg/ml during PEEP (P < 0.1). Addition of pentobarbital to normal plasma led to a slight decrease in Tpd only when the concentration exceeded 99 μg/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. Ore Res 45: 460-467, 1979

The continuing clinical enigma of duodenal diverticulum

Seventy-one cases of duodenal diverticula were reviewed. Fifty-four or 76 percent were associated with symptoms of varying severity. Forty (74 percent) of the symptoms were considered serious. These included bleeding, severe abdominal pain, weight loss, chills, fever and jaundice, and evidence of right upper quadrant peritonitis. Nineteen patients were operated on and gallstones were found in 12. Multiple operative procedures because of recurring symptoms characterized the entire series. Relief of symptoms was achieved only in those who had diverticulectomy or a sidetracking operation. The difficulties of identifying this lesion as the source of the patients symptoms and the indications for its removal are emphasized.

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.

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 μg/ml higher in arterial blood, p < 0.001). Similar changes were noted after aortic declamping. The transient 5.3 ml/cm H2O 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 the pre-operative 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.

Cyclo-oxygenase products mediate hypoxic pulmonary hypertension

High-risk infants with a fetal pattern of circulation demonstrate hyperactivity of the pulmonary vascular bed in response to stimuli including mucous plugging, atelectasis, and endotrachial tube suctioning. The resultant increase in pulmonary vascular resistance (PVR) leads to pulmonary hypertension, severe right-to-left shunting, and hypoxemia. Stimuli that trigger pulmonary hypertension cause hypoxia, suggesting the importance of hypoxic pulmonary vasoconstriction (HPV). Although many humoral mediators of HPV have been hypothesized, none have been proven. This study investigates the possible role of the cyclo-oxygenase derivatives thromboxane A2 and prostacyclin as determinants of hypoxic pulmonary hypertension. Open-chested lambs were ventilated with 13% O2 prior to and following treatment with OKY 046, a selective thromboxane inhibitor. In untreated lambs, the partial pressure of arterial oxygen fell from 80 +/- 27 (mean +/- SD) to 35 +/- 13 mm HG (P less than .01). The mean arterial pressure (MAP) remained at 50 +/- 7 mm HG, and the cardiac output (CO) was unchanged at 0.8 +/- 0.2 L/min. The mean pulmonary arterial pressure (MPAP) rose from 11 +/- 4 to 20 +/- 4 mm HG (P less than .01) whereas the PVR increased 70% (P less than .01). TxB2 rose from 147 +/- 85 to 271 +/- 154 pg/mL (P less than .05), and 6-keto-PGF1 alpha rose from 105 +/- 96 to 142 +/- 110 pg/mL. These substances are the hydrolysis products of TxA2 and prostacyclin respectively. In animals treated with OKY 046 prior to ventilation with 13% O2, values for MAP, CO, and PVR were similar to those of the nontreatment period.(ABSTRACT TRUNCATED AT 250 WORDS)

Left Ventricular Filling Pressure as a Determinant of Subendocardial Blood Flow

Abstract The effect of ventricular diastolic pressure on subendocardial flow was studied during isovolumic contraction in an isolated heart. In 9 experiments flow averaged 95 ± 8 ml/min ˙ 100 gm of tissue (mean ± standard deviation). With balloon inflation to 50 ml, diastolic pressure increased from 1 ± 2 mm Hg to 14 ± 4 mm Hg ( p p p p p p r = −0.84; p r = 0.87; p r = 0.97; p

Pressure Breathing and Altered Fibrinolytic Activity

Abstract Twenty-one anesthetized dogs were intubated. Euglobulin lysis times, expressed as units of fibrinolytic activity, were obtained in 10 dogs (Group 1). During spontaneous breathing, fibrinolytic activity increased across the peripheral circulation from 3.2 ± 0.6 units (mean ± standard deviation) in femoral artery blood to 4.5 ± 0.9 in infrarenal vena cava blood ( p p p Positive inspiratory pressure (ZEEP 1 ) (rate, 12; tidal volume, 15 ml per kilogram of body weight) increased fibrinolytic activity in femoral artery blood to 5.8 ± 0.9, a value higher than in the blood in the pulmonary artery ( p 2 O PEEP), fibrinolytic activity in femoral artery blood rose to 8.5 ± 1.0, higher than during ZEEP 1 ( p 1 levels with removal of PEEP. During the study, fibrinolytic activity in infrarenal vena cava blood increased along with that in femoral artery blood ( r = 0.67; p 1 ( p p These results indicate that the lungs normally extract and perhaps store plasminogen activator, secreted in large part by the kidneys. Pressure breathing, particularly PEEP, causes the release of activator from the lungs with an increase in arterial and peripheral venous fibrinolytic activity.