Management of septic shock.
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Biomedical subjects
Publications and source records attributed to J D Edwards.
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There have been important advances in the resuscitation of patients in septic shock in recent years. Survival can be improved by earlier recognition and therefore eradication of the sepsis combined with logical supportive measures. As with any acutely ill patient consultation with intensive care unit staff may be useful. Consultation with the intensive care unit does not necessarily imply the need for admission and mechanical ventilation; helpful advice may be forthcoming. Equally, referral to the intensive care unit does not mean an admission of failure but merely a recognition that additional skills and technical facilities are necessary for the patient's survival.
Blunt trauma involving the innominate and carotid arteries is a rare occurrence that can be lethal or have serious neurologic sequelae. To our knowledge this is the first reported case in the international literature describing the association of posttraumatic innominate artery aneurysm with total occlusion and thrombosis of the common carotid artery at its origin by an intimal flap. The diagnostic problems created by this unusual injury are discussed. In this case the patency of the distal portion of the common and internal carotid arteries was demonstrated by magnetic resonance angiography (MRA), whereas color duplex and digital arteriographic studies were unsuccessful. This demonstration was crucial to patient management. Since no studies are available comparing color duplex imaging, conventional arteriography, and MRA in the evaluation of blunt carotid trauma, this case study is presented to demonstrate the utility of MRA in emergency situations. In addition, we analyze the possible pathogenesis and discuss the surgical treatment.
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University of Wisconsin (UW) and Eurocollins (EC) solutions are widely used for preservation of organs before transplantation. However, effect of storage solutions on vascular interface for transplant success is not known. In this study, we have used rat aorta as a model and assessed the effects of cold storage in UW and EC solutions on smooth muscle and endothelial function and the morphology. Smooth muscle and endothelial functions of the rat aorta were assessed using in vitro isometric tension measurement. Morphologic studies were done with scanning and transmission electron microscopy. No significant difference in contractile response to either norepinephrine (NE) or potassium chloride was observed between control aorta and aorta stored in UW solution for 1 hr or 24 hr. In contrast, sensitivity, but not the reactivity to NE and KCl, was increased in aorta stored in EC solution for 1 hr. If the tissues were stored in EC solution for 24 hr, both sensitivity and reactivity to NE and KCl were significantly reduced. Relaxatory response to acetylcholine, in endothelium-intact vessels were reduced in aortas stored in EC solution, but not in UW solution. The magnitude of relaxations observed in tissues stored in the EC solution for 24 hr was less than in tissues stored for 1 hr. Sodium nitroprusside elicited similar relaxatory response in endothelium-denuded control tissue and in tissues stored in UW and EC solution. Electron microscopy data revealed marked swelling of the cell, loss of mitochondria and other intracellular organelles, and striking calcium deposits after preservation of the vessels in EC for 1 or 24 hr. In aorta stored in UW solution for 24 hr, endothelial and smooth muscle cells were intact, with moderate-size vacuoles in the cytoplasm. These results suggest that the UW solution is more suitable than EC solution for short-term preoperative storage of blood vessels.
BACKGROUND: Oxygen consumption (VO2) has been shown to be decreased after acute myocardial infarction (AMI) complicated by cardiogenic shock. STUDY OBJECTIVE: To evaluate early measurement of VO2 by indirect calorimetry after an uncomplicated AMI (UAMI). STUDY DESIGN: Prospective nonrandomized case study. SETTING: Emergency department of a large urban hospital. PARTICIPANTS AND INTERVENTIONS: Twenty-six consecutive patients presenting with confirmed UAMI. VO2 was measured by indirect calorimetry (Deletrac, Datex Ins,) which is noninvasive. All patients received buccal or intravenous nitroglycerin and thrombolytic therapy, and none received opiates before VO2 measurement. RESULTS: Two groups of patients were identified by subsequent development of cardiogenic shock. Group 1 did not develop cardiogenic shock, and group 2 developed shock within 24 h of admission. Group 1 (n = 22) had a significantly higher VO2 compared to group 2 (n = 4), mean 154(SD 25) vs mean 100(SD 13) ml/min.m2, p < 0.002. Group 1 had a significantly higher increase in basal metabolic rate than group 2, mean 30 percent (SD 11) vs mean 10(SD 15) percent, p < 0.007. There was no significant difference in age, heart rate (HR), shock index (SI), or rate-pressure product (RPP) between groups 1 and 2. All patients in group 2 developed cardiogenic shock despite thrombolytic therapy, and two died within 24 h of admission. CONCLUSION: VO2 is increased in UAMI and represents increased metabolic demands of peripheral tissues and not cardiac oxygen uptake. A reduction in VO2 (< 100 ml/min.m2) after AMI may be an early predictor of subsequent development of cardiogenic shock. Measurement of VO2 in UAMI by indirect calorimetry in the emergency department may be of value to identify patients at high risk and could influence their management.
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This study examined the initial haemodynamic and oxygen transport patterns in 24 patients with severe blunt thoracic trauma in whom immediate monitoring with femoral and pulmonary artery catheters was required after admission to the intensive care unit. All patients required mechanical ventilation and were studied before receiving inhalational anaesthesia and within 12 h of injury. Two groups of patients were identified; nine patients (group 1) had an impaired left ventricular stroke work index (LVSWI) and 15 patients had a normal LVSWI (group 2). There were no significant differences in the abbreviated injury scale score for the chest, the total injury severity score, or the mean ages of the two groups. There were significant differences in stroke volume index, 32 versus 56 ml m-2 (P less than 0.001), and cardiac index, 3.2 versus 5.3 l min-1 m-2 (P less than 0.001), and therefore in oxygen delivery, 469 versus 852 ml min-1 m-2 (P less than 0.001), despite apparently adequate volume expansion using the same protocol and clinical criteria in both groups. Oxygen consumption was not significantly different in the two groups, 135 versus 157 ml min-1 m-2, because of a higher oxygen extraction ratio in group 1, 29 versus 19 per cent (P less than 0.001), and hence lower mixed venous oxygen saturation, 73 versus 82 per cent (P less than 0.02). Seven patients in group 1 died (78 per cent) compared with two in group 2 (13 per cent). Early depression of cardiac function is associated with poor outcome in patients with thoracic trauma, and measurements of oxygen transport variables may influence resuscitation and the timing of surgical procedures.
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OBJECTIVE: To identify any plateau in oxygen consumption (VO2) when oxygen delivery (DO2) is increased in patients with the adult respiratory distress syndrome (ARDS). DESIGN: Clinical prospective study; multiple regression analysis was done to assess the relationship between VO2 and DO2 for pooled data and for each individual patient. SETTING: University hospital ICU. PATIENTS: Twenty consecutive patients aged 18 to 78 yrs (mean 43.5) in whom ARDS was present during their ICU stay. INTERVENTIONS: Multiple measurements were obtained in individual patients (mean number of measurements 40, range 20 to 83) and mathematical models were fitted to both pooled and individual patient data. DO2 ranged from 212 to 1550 mL/min.m2 with a maximum of 758 to 1550 mL/min.m2 (mean 1136). Because of the large variations between patients, it was not justifiable to describe a relationship for the pooled data and each case was analyzed individually. MEASUREMENTS AND MAIN RESULTS: We found the optimal regression model to be linear in 13 patients, cubic in four, and either cubic or linear in one. Two patients demonstrated no significant relationship. The relationship for the group was determined from each patient's data and was best described by linear regression. CONCLUSIONS: In no patient was there evidence of a plateau, despite high levels of DO2 being achieved in all patients.
OBJECTIVE: To review clinical studies of oxygen transport in cardiogenic and septic shock. DESIGN: Descriptive and prospective studies. SETTING: University hospital multi disciplinary ICU. PATIENTS: Critically ill cardiogenic and septic shock patients greater than 18 and less than 80 yrs of age. INTERVENTIONS: The responses to volume loading with colloid or crystalloid and infusion of catecholamines are documented with baseline hemodynamic and oxygen transport measurements before and after administration of catecholamines. MEASUREMENTS AND MAIN RESULTS: Nineteen patients in cardiogenic shock were studied. In three patients, invasive systemic mean arterial pressure was greater than 80 mm Hg and cardiac index was greater than 2.0 L/min.m2. In all patients, there were increases in oxygen extraction ratio that averaged 48 +/- 18 (SD) %. However, in 30 septic shock patients, extraction ratio was 24 +/- 2%. In both groups, the response to therapy was an increase in mixed venous oxygen saturation from 54 +/- 16% to 69 +/- 8% in cardiogenic patients (p less than .001) and from 75 +/- 2% to 80 +/- 1% in septic shock (p less than .01). CONCLUSIONS: There are widely differing oxygen transport patterns in cardiogenic and septic shock that may have implications for therapy.
The effects of somatic nociceptive afferent stimulation on aspects of cardiac function and oxygen transport were examined in a model of hemorrhage in anesthetized pigs. The brachial nerves were stimulated (BNS) alternately to obtain a rise in heart rate of 18% and in mean arterial pressure of 17%. This stimulation was started 75 minutes before the start of hemorrhage and maintained throughout and after the withdrawal of blood. The animals were bled at a rate of 0.75 ml/min.kg until a total of 30 ml/kg had been removed. At the end of hemorrhage the reductions in cardiac index (CI), stroke volume (SV), and left ventricular stroke work (LVSW) were greater in the BNS group compared with controls. The nociceptive stimulation also elicited greater reductions in oxygen delivery (DO2I) and oxygen consumption (VO2) and a greater rise in the arterial plasma lactate concentration. Thus it seems that nociceptive stimulation exacerbates the changes in systemic oxygen transport and cardiac function induced by hemorrhage.
Fifteen consecutive patients who had been resuscitated from cardiac arrest and transferred immediately to an Intensive Care Unit were studied. Measurements of intraarterial pressure, cardiac output and systemic vascular resistance demonstrate that 'cuff' blood pressure may not always be related to intraarterial pressure or cardiac output and cannot be used for diagnostic, therapeutic, or prognostic purposes. Following resuscitation, a palpable pulse was present in each of these patients, but did not correlate with adequacy of cardiac output. Too often we hear during a cardiac arrest the question 'Does the patient have an output?', when we should really be asking 'Does the patient have a pulse?'. The palpation of a pulse is a simple and important indication of spontaneous cardiac activity. However cardiac output must be measured and it's adequacy cannot be inferred from this basic clinical measurement.
Various mechanisms have been proposed to explain the shock sometimes associated with right ventricular infarction, but only small numbers of patients with clinical shock have been studied. The haemodynamic profiles of seven patients with clinical cardiogenic shock after right ventricular myocardial infarction were studied prospectively. They were selected because all had a stable cardiac rhythm and none had absolute hypovolaemia during the study period. In all of them the mean right atrial pressure exceeded the pulmonary artery occlusion pressure. After treatment with varying combinations of dopamine, dobutamine, and glyceryl trinitrate (titrated to achieve the optimum haemodynamic response) the mean systemic arterial pressure increased, as did the cardiac index. There was an associated increase in the left ventricular stroke work index but the right ventricular stroke work index was unchanged. There was no significant change in heart rate, mean right atrial pressure, or pulmonary artery occlusion pressure. This suggests that the probable mechanism of the shock associated with right ventricular infarction is concomitant severe left ventricular dysfunction.
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There are few data on oxygen transport in cardiogenic shock after acute myocardial infarction. This prospective study examined oxygen transport variables in 19 such patients and assessed their responses to treatment. Femoral and pulmonary arterial catheters were inserted before any therapy except correction of hypoxemia by mechanical ventilation in 8 patients, defibrillation (3 patients) or pacing (5 patients). In 3 patients mean arterial pressure was greater than 80 mm Hg and cardiac index greater than 2.1 liters/min/m2 with normal mixed venous oxygen saturation despite simultaneous clinical shock. They recovered with no further treatment. Sixteen patients were treated with varying combinations of intravenous fluids and dobutamine (37 +/- 25 mu/kg/min) and 14 survived long enough for a second set of measurements to be completed. Mean heart rate increased from 83 +/- 22 to 101 +/- 20 beats/min and mean cardiac index from 1.4 +/- 0.5 to 2.5 +/- 0.4 liters/min/m2 (p less than 0.001). Oxygen consumption (VO2) was maintained even when oxygen delivery (DO2) was less than 330 ml/min/m2. After treatment DO2 increased from 230 +/- 69 to 397 +/- 60 ml/min/m2 (p less than 0.001) and VO2 from 103 +/- 31 to 124 +/- 27 ml/min/m2 (p less than 0.05). Mean mixed venous oxygen saturation increased from 54 +/- 16 to 69 +/- 8% (p less than 0.001) and mean oxygen extraction ratio decreased from 48 +/- 16 to 31 +/- 6% (p less than 0.001). There was no correlation between cuff systolic blood pressure and mean arterial pressure before or after resuscitation. Thirteen patients survived to hospital discharge. When cardiogenic shock responds to treatment, large increases in DO2 lead to small increases in VO2 but large increases in mixed venous oxygen saturation, reflecting improved tissue oxygen availability.
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The APACHE II severity of illness scoring system was prospectively studied on 756 patients admitted to a general intensive care unit (ICU) from January 1986 to June 1988. Admission data were used. Individual and group risk of death were calculated for 3 diagnostic categories commonly seen in the A&E department and requiring admission to an ICU. The APACHE II score on admission tended to underestimate the risk of death following operative and non-operative trauma, and self-poisoning. This may have been related to the use of an analysis not yet validated against values obtained on admission to ICU. Such validation is urgently needed on a UK population if APACHE II scoring is to be of value in the A&E department.