Background: The cardiopulmonary effects of the combination of abdominal and thoracic pressures in humans have not been well delineated. Objective: To study the cardiopulmonary effects of 15 mm Hg of intra-abdominal pressure in the presence and absence of 10 cm H 2 O of positive end-expiratory pressure (PEEP). Design: Prospective. Setting: University hospital. Methods: Nine patients undergoing laparoscopic cholecystectomy had pulmonary compliance, cardiac output, exhaled carbon dioxide, and preload (left ventricular end-diastolic volume) determined at 4 points while undergoing ventilation with (1) no PEEP before pneumoperitoneum; (2) 10 cm H 2 O of PEEP and no pneumoperitoneum; (3) no PEEP and 15 mm Hg of pneumoperitoneum; and (4) 10 cm H 2 O of PEEP and 15 mm Hg of pneumoperitoneum. Preload and cardiac output were determined by means of transesophageal echocardiog-raphy. Pulmonary compliance and exhaled carbon dioxide were determined by an attachment to the end of the endotracheal tube. Main Outcome Measures: Preload, cardiac output, exhaled carbon dioxide, and pulmonary compliance. Results: There was no significant change from baseline in preload, cardiac output, or pulmonary compliance when either PEEP or pneumoperitoneum was applied separately. However, there was a significant decrease in preload (PϽ.01), cardiac output (P = .01), and exhaled carbon dioxide (P = .04) when PEEP and pneumoperitoneum were applied together. Pulmonary compliance was not significantly affected at any of these points. Conclusions: There was a significant reduction in preload and cardiac output when there was intra-abdominal pressure of 15 mm Hg in the presence of 10 cm H 2 O of PEEP. This combination of pressures may pose a contraindication to laparoscopic surgery.
(1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.
The changes in total pressure-length loop area were compared with changes in effective shortening area, systolic lengthening area and postsystolic shortening area (defined with respect to end-diastolic and end-systolic lengths) of the pressure-length loop during myocardial ischemia in seven anesthetized dogs instrumented for measurement of left ventricular pressure and regional segmental wall motion (sonomicrometry) in the minor axis of the apical region of the left ventricle. Ischemia was induced by gradual tightening of a micrometer-controlled snare around the left anterior descending coronary artery, which supplied the apical myocardium. Data were obtained at normal flow, after critical constriction (loss of pulsatile coronary flow), mild ischemia (ischemia 1: onset of regional dysfunction, i.e., postsystolic shortening and mild hypokinesia) and moderate ischemia (ischemia 2: marked hypokinesia). At each stage, acute afterloading was performed by partially occluding the descending thoracic aorta. The pressure-length loops were analyzed in terms of four areas: total loop area, effective shortening area, postsystolic shortening area and systolic lengthening area. Total loop area decreased only when marked hypokinesia was present (176 +/- 18.3 mm Hg x mm at ischemia 2 versus 245.1 +/- 26.9 mm Hg x mm at ischemia 1, p less than 0.05). However, effective shortening area (98.2 +/- 0.8% of total loop area at baseline; 93.8 +/- 2.4% at critical constriction; 76.3 +/- 7.2% at ischemia 1; 51.9 +/- 12.2% at ischemia 2) and postsystolic shortening area (1.8 +/- 0.8% of total loop area at baseline; 5.2 +/- 1.9% at critical constriction; 14.3 +/- 3/4% at ischemia 1; 23.8 +/- 5.1% at ischemia 2) changed significantly with each progressive stage of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
During human hepatic transplantation, ionized calcium (ICa) measured in whole blood with an ion-selective electrode varied greatly from ICa predicted from total calcium (TCa), protein, albumin, and pH, by means of recently published nomograms. Measurement of ICa was necessary because the interaction of citrate in transfused blood and calcium chloride (administered to offset citrate binding) caused large variations in TCa. During hepatic transplantation, ICa and electrolyte measurements were obtained at approximately 15-minute intervals or more frequently if indicated by changing cardiac status. In one patient, hemodynamic instability was accompanied by a large decrease in ICa, which then was followed by cardiac arrest aggravated by myocardial depression from inadequate ICa. Cardiovascular phenomena associated with ionized hypocalcemia suggest that the critical value for ICa should be no more than 0.4 mmol/L (1.6 mg/dL) below the reference range mean. The authors propose critical limits for ICa and discuss their significance in clinical management of tetany, hypotension, arrythmias, and cardiac arrest.
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