Possible mechanisms for the interaction of peripheral somatic nerve stimulation, tissue injury, and hemorrhage in the pathophysiology of traumatic shock.
Explore the source record for details and available documents.
Hemorrhage↗
Biomedical subjects
M Y Rady
Publications and source records attributed to M Y Rady.
Biphasic extrathoracic pressure CPR. A human pilot study.
HYPOTHESIS: Alternating intrathoracic pressure by means of a chest cuirass can cause perfusion and ventilation equal to or better than standard cardiopulmonary resuscitation (CPR) for humans in cardiac arrest. DESIGN: Nonrandomized, nonblinded, crossover pilot study. SETTING: Large urban emergency department. SUBJECTS: Five adult normothermic, nontraumatic, out-of-hospital cardiac arrest patients unresponsive to standard advanced cardiac life support. METHOD: Right atrial and aortic catheters were inserted for pressure measurement and blood gas analysis while the patient was receiving standard CPR by a pneumatic compression device (Thumper). The Thumper was then replaced by a chest cuirass (Hayek Oscillator). Pressure and blood gas measurements were then repeated. RESULTS: The coronary perfusion pressure increased from -1.2 +/- 8.6 mm Hg to 6.2 +/- 6.9 mm Hg for a mean change of 7.4 +/- 3.1 mm Hg (p = 0.006). The compression phase gradient increased 10.0 +/- 21.9 mm Hg (p = 0.364). The venous to arterial PCO2 gradient decreased 44.5 +/- 32.3 mm Hg (p = 0.070). The oxygen extraction ratio increased 1.6 +/- 9.4 percent (p = 0.761). The mean arterial PO2 and PCO2 changed from 252 to 240 mm Hg (p = 0.836) and from 53 to 66 (p = 0.172) mm Hg, respectively. CONCLUSION: The Hayek Oscillator chest cuirass produced a significant improvement in the coronary perfusion pressure. There was a trend for improved systemic perfusion as indicated by an improved compression phase gradient and venous to arterial PCO2 gradient, although this was not supported by the lack of improvement in the oxygen extraction ratio. The cuirass also adequately oxygenates and ventilates unassisted by positive pressure ventilation.
Cardiopulmonary Resuscitation↗
The effect of the total cumulative epinephrine dose administered during human CPR on hemodynamic, oxygen transport, and utilization variables in the postresuscitation period.
BACKGROUND: Studies evaluating the dose of epinephrine required to optimize return of spontaneous circulation and survival after CPR have shown that doses greater than recommended by advanced cardiac life support (ACLS) improve coronary perfusion pressure and short-term resuscitation rates. Since survival has not improved, it is possible that higher doses of epinephrine may be physiologically detrimental in the postresuscitation period. OBJECTIVE: The object of this study is to measure the effect of the total cumulative dose of epinephrine given during ACLS on the hemodynamic, oxygen transport, and utilization variables in the postresuscitation period. DESIGN: A prospective nonrandomized control trial of inception cohorts. SETTING: A large urban emergency department and intensive care unit. PATIENTS: Forty-nine successfully resuscitated witnessed, normothermic, nontraumatic, out-of-hospital patients, who had suffered cardiac arrests. INTERVENTIONS: All patients were treated according to ACLS guidelines; however, the epinephrine dose (0.01 to 0.2 mg/kg or 1 to 14 mg) was selected at the clinician's discretion and given through central venous access every 3 to 5 min. Hemodynamic, oxygen transport, and utilization variables were measured on a return of spontaneous circulation, and at least every 30 min thereafter under a standardized postresuscitation protocol. MAIN OUTCOME MEASURES: Hemodynamic, oxygen transport/utilization variables, and mortality in patients resuscitated from cardiac arrest. The total cumulative dose of epinephrine given during ACLS until a return of spontaneous circulation was recorded. RESULTS: A total cumulative epinephrine dose of 15 mg was found to best predict 24-h mortality. Of the 49 patients, 20 received less than 15 mg (group 1) and 29 received greater than 15 mg (group 2). Age, premorbid health status, sex, presenting rhythm, and duration of cardiac arrest were similar in both groups. The 24-h survival was 17 of 20 (85%) and 12 of 29 (41%) in group 1 and 2, respectively (p < 0.002). Over the first 6 h of the postresuscitation period, both groups had similar mean arterial pressure (MAP), mixed venous oxygen saturation, and systemic oxygen extraction ratio (all p > 0.1). Group 2, however, had a significantly lower cardiac index (CI), systemic oxygen consumption (VO2), and systemic oxygen delivery (DO2) (all p < 0.01). Systemic vascular resistance index (SVRI), initial and 6-h lactic acid levels were significantly higher in group 2 (all p < 0.03). CONCLUSIONS: The administration of all doses of epinephrine during the resuscitation of out-of-hospital cardiac arrest is associated with impairment of DO2 and VO2 in the postresuscitation period. Both duration and severity of these impairments correlate with the total cumulative epinephrine dose given during the resuscitation. Thus, inadvertent catecholamine toxicity represents a further complicating factor in the production of postresuscitation disease. Diagnostic and therapeutic interventions addressed toward mitigating these potentially reversible adverse effects may impact morbidity and mortality in out-of-hospital cardiac arrests.
Adult↗
Triage and resuscitation of critically ill patients in the emergency department: current concepts and practice.
Recognition of tissue hypoxia or cumulative oxygen debt is of fundamental importance for the triage and resuscitation of critically ill patients during the 'golden hour' in the emergency department. Vital signs, shock index and invasive monitoring of mean arterial pressure and central venous pressure have limited roles in evaluating cumulative oxygen debt and systemic oxygen balance in an acute critical illness. The measurement of central venous blood oxygen saturation, arterial lactate concentration, cardiac output and systemic oxygen delivery and consumption can enhance the detection of the clinically occult cumulative oxygen debt in critically ill patients. Organ-specific oxygenation indices such as gastric tonometry and renal function can supplement indicators of systemic oxygen balance to detect ischaemia-hypoxia of non-vital organs. Systemic oxygenation and organ-specific indices can guide the choice of therapy to optimize resuscitation of the macro- and microcirculation in critically ill patients in the emergency department.
Critical Illness↗
A comparison of the effects of skeletal muscle injury and somatic afferent nerve stimulation on the response to hemorrhage in anesthetized pigs.
The effect of skeletal muscle injury (SMI) on cardiovascular and O2 transport responses to hemorrhage (HS) were examined in anesthetized pigs. Bilateral hindlimb muscle was injured 75 minutes before HS was started at a rate of 0.75 mL/min.kg until a total of 30 mL/kg (40% estimated total blood volume) had been removed. The reductions in cardiac index (CI), left ventricular stroke work, and oxygen delivery (Do2) and the increase in plasma lactate concentration following HS were exacerbated by SMI such that although oxygen consumption was maintained after HS it fell after SMI + HS. The deleterious effect of SMI on the response to HS was greater than that recorded previously following somatic brachial nerve stimulation (BNS). Thus, in order to achieve a given reduction in CI and Do2 or a rise in Shock Index (heart rate divided by systolic blood pressure) to approximately 3, a blood loss of 40% was needed after HS; this was reduced to 36% by the addition of BNS, whereas a loss of only 29% was needed when SMI was introduced. The mechanism of the deleterious effect of SMI is unclear although a change in the distribution of regional blood flow and a rise in the critical oxygen delivery may be implicated.
Anesthesia↗
Measurement of oxygen consumption after uncomplicated acute myocardial infarction.
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.
Aged↗
Early cardiorespiratory findings after severe blunt thoracic trauma and their relation to outcome.
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.
Cardiac Output↗
Resuscitation fluids and oxygen transport in haemorrhagic shock.
This study examined the cardiovascular and oxygen transport/consumption relationships in haemorrhagic shock and resuscitation using Human Albumin and Gelatin solutions in a porcine haemorrhagic shock model. Immature pigs (17-25 kg) were anaesthetised and ventilated with nitrous oxide, oxygen and isoflurane. Aortic pressure monitoring and monitoring of pulmonary pressures and cardiac output via a Swan-Ganz catheter were instituted. A controlled haemorrhage of 40% of blood volume at 1% blood volume per minute was followed 30 minutes later by resuscitation with 60% of blood volume of 4.5% Human Albumin (Immuno) or 4% Modified Fluid Gelatin (Gelofusine). Haemorrhage caused marked decreases in (CI), mean arterial pressure and oxygen delivery (DO2). Oxygen consumption (V02) remained unchanged. Resuscitation with Albumin and Gelatin raised CI to values 60% to 70% above control though only Albumin restored DO2. Deterioration was more rapid in the Gelatin group due to the estimated half a life of 3 hours in this model. Oxygen extraction was 10% higher in the Gelatin group 2 hours after resuscitation. The role of oxygen radicals in haemorrhagic shock is discussed.
Albumins↗
Continuous central venous oximetry and shock index in the emergency department: use in the evaluation of clinical shock.
Initial therapy of shock in the emergency department (ED) emphasizes the normalization of physiologic variables such as heart rate (HR), mean arterial pressure (MAP), and central venous pressure (CVP) rather than restoration of adequate tissue oxygenation. After hemodynamic stabilization of MAP, CVP, and HR, the authors examined tissue oxygenation as indicated by continuous central venous oximetry (SCVO2), lactic acid concentration, and shock index (SI). Sixteen consecutive nonrandomized patients presenting to the ED of a large urban hospital in shock (MAP < 60 mm Hg, HR > 120 beats/min, and altered sensorium) were initially resuscitated with fluid, blood, inotropes, and/or vasoactive drug therapy to normalize MAP, CVP, and HR. In addition, SCVO2, arterial lactate concentration, and SI were measured after completion of resuscitation in the ED. Eight patients (group no. 1) had inadequate tissue oxygenation reflected by low SCVO2 (less than 65%). Four patients in group no. 1 had elevated arterial lactic acid concentration. All group no. 1 patients had an elevated SI (> 0.7) suggesting persistent impairment of left ventricular stroke work. Eight patients (group no. 2) had normal or elevated SCVO2 (> 65%). In group no. 2, arterial lactic acid concentration was elevated in six and SI in seven patients. Normalization of hemodynamic variables does not adequately reflect the optimal endpoint of initial therapy in shock in the ED. Most (94%) of these patients continue to have significant global ischemia and cardiac dysfunction as indicated by reduced SCVO2 and elevated lactic acid concentration and SI. Systemic tissue oxygenation should be monitored and optimized in the ED in these critically ill patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The clinical implications of continuous central venous oxygen saturation during human CPR.
STUDY OBJECTIVE: The purpose of this study was to observe, measure, and describe the changes in central venous oxygen saturation during CPR and immediately after return of spontaneous circulation. It also was to examine the clinical utility of continuous central venous oxygen saturation monitoring as a indicator of return of spontaneous circulation during CPR in human beings. DESIGN AND SETTING: Eight-month, prospective, non-outcome, observational, nonrandomized case series in the ED of a large urban hospital. TYPES OF PATIENTS: Adult normothermic, nontraumatic, out-of-hospital cardiopulmonary arrests. INTERVENTIONS: All patients were managed according to advanced cardiac life support guidelines. A proximal aortic and double-lumen central venous catheter was placed. Central venous oxygen saturation was measured continuously spectrophotometrically with a fiberoptic catheter in the central venous location. MEASUREMENTS: Aortic blood pressure and central venous oxygen saturation were simultaneously measured throughout each resuscitation. Return of spontaneous circulation was defined as a systolic blood pressure of more than 60 mm Hg for more than five minutes. RESULTS: One hundred patients who experienced 68 episodes of cardiac arrest were studied. Patients with return of spontaneous circulation had a higher initial and statistically higher mean and maximal central venous oxygen saturation than those without return of spontaneous circulation (P = .23, .0001, and .0001, respectively; P less than .05 is significant). No patient attained return of spontaneous circulation without reaching a central venous oxygen saturation of at least 30%. Only one of 68 episodes of return of spontaneous circulation was attained without reaching a central venous oxygen saturation of at least 40%. A central venous oxygen saturation of greater than 72% was 100% predictive of return of spontaneous circulation. CONCLUSION: Continuous central venous oxygen saturation monitoring can serve as a reliable indicator of return of spontaneous circulation during CPR in human beings.
Blood Circulation↗
Venous hyperoxia after cardiac arrest. Characterization of a defect in systemic oxygen utilization.
BACKGROUND: Supranormal mixed venous oxygen saturation (mixed venous hyperoxia), although reported, has never been characterized in humans resuscitated from cardiac arrest (postarrest cardiogenic shock). By contrast, cardiogenic shock without cardiopulmonary arrest (primary cardiogenic shock) is accompanied by mixed venous hypoxia under similar conditions of low oxygen delivery (DO2). The appearance of mixed venous hyperoxia indicates an excessive supply relative to demand in perfused tissue or cellular impairment of oxygen utilization, ie, low systemic oxygen consumption (VO2). Failure to improve VO2 has been associated with a poor outcome in other shock states. STUDY OBJECTIVE: This study evaluates the clinical significance of mixed venous hyperoxia and its implications for impaired systemic oxygen utilization. The oxygen transport patterns in surviving and nonsurviving cardiac arrest patients are compared for their prognostic and therapeutic implications. STUDY DESIGN: Consecutive, nonrandomized series. SETTING: Large urban emergency department (ED). PARTICIPANTS: Adult normothermic, nontraumatic out-of-hospital cardiac arrest patients presenting to the ED who develop a return of spontaneous circulation (ROSC). INTERVENTIONS: On arrival to the ED, a fiberoptic catheter was placed in the central venous position for continuous central venous oxygen saturation monitoring (ScvO2). A proximal aortic catheter was placed via the femoral artery for blood pressure monitoring. Upon ROSC, the fiberoptic catheter was advanced to the pulmonary artery. Mean arterial pressure (MAP), cardiac index (CI), VO2, DO2, systemic oxygen extraction ratio (OER), and systemic vascular resistance index (SVRI-dynes.s/cm5.m2) were measured immediately and every 30 min. The duration of cardiac arrest (DCA) in minutes and amount of epinephrine (milligrams) administered during ACLS was recorded. MEASUREMENTS AND RESULTS: Twenty-three patients were entered into the study. Survivors (living more than 24 h) and nonsurvivors (living less than 24 h) were compared. CONCLUSIONS: These findings indicate an impairment of systemic oxygen utilization in postarrest cardiogenic shock patients. In spite of a lower DO2 than survivors, the OER in nonsurvivors remained lower than expected. Venous hyperoxia is a clinical manifestation of this derangement. Epinephrine dose may have a causal relationship. The inability to attain a VO2 of greater than 90 ml/min.m2 after the first 6 h of aggressive therapy was associated with a 100 percent mortality in 24 h.
Aged↗
The effect of nociceptive stimulation on the changes in hemodynamics and oxygen transport induced by hemorrhage in anesthetized pigs.
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.
Animals↗
Full-length ureteric splintage in the management of bilharzial ureteric strictures.
Our experience with full-length ureteric splintage is reviewed with a note on the technique and its outcome. It is safe, effective and simple, easy to teach and easy to learn. It is recommended as the operation of choice in bilharzial ureteropathy.
Adult↗
Conventional open surgery for renal stones in the era of modern techniques.
Explore the source record for details and available documents.
Child, Preschool↗
Mass closure of abdominal incisions and the role of suture technique in wound healing.
Explore the source record for details and available documents.
Abdominal Muscles↗
Shock index: a re-evaluation in acute circulatory failure.
STUDY OBJECTIVE: To evaluate the relationship between the shock index SI (ratio of heart rate to systolic arterial pressure) and cardiac function and oxygen transport in an experimental model of hemorrhage and clinical septic shock. METHODS AND RESULTS: This study was conducted in a hypovolemic circulatory failure model; 40% hemorrhage in the anesthetized pig and normovolemic hyperdynamic septic patients in the intensive care unit (ICU). Hemodynamic and oxygen transport variables were measured and their relationships to SI was examined. SI was inversely related to blood loss, cardiac index (CI), stroke volume (SV), mean arterial pressure (MAP) and left ventricular stroke work (LVSW) (r = -0.73, -0.75, -0.89 and -0.75, respectively P less than 0.01) following hemorrhage in the anesthetized pig. Oxygen transport variables, i.e. oxygen delivery (DO2) and mixed venous oxygen saturation (SvO2P) (r = -0.68 and -0.74, respectively, P less than 0.01) were also inversely related to the SI. Oxygen consumption (VO2) increased initially with increasing SI and fell when SI was greater than 3.0. In clinical septic shock and following blood volume expansion, the SI was not correlated to CI, SVI, MAP or systemic vascular resistance (SVR) (r = -0.01, -0.47, -0.34 and -0.14, respectively, P-value NS) but was inversely related to LVSWI (r = -0.68, P less than 0.01). There were no relationships between the SI and oxygen transport variables (DO2, SvO2) (r = -0.02 and -0.17, P-value NS) in septic shock. CONCLUSION: SI provides a non-invasive means to monitor deterioration or recovery of LVSW during acute hypovolemic and normovolemic circulatory failure and its therapy. SI may be of limited value in the assessment of systemic oxygen transport and response to therapy in clinical shock.
Animals↗
The role of central venous oximetry, lactic acid concentration and shock index in the evaluation of clinical shock: a review.
Initial therapy of shock in the emergency department emphasizes the normalization of hemodynamic variables e.g. heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP) rather than optimization of systemic and regional oxygenation. Central venous oximetry (ScvO2), arterial lactic acid concentrations (Lact) and the shock index (SI) were examined during initial hemodynamic stabilization of clinical shock in the emergency room. Although initial therapy normalized MAP, CVP and HR; ScvO2, Lact and SI continued to be abnormal indicating inadequate systemic oxygenation and left ventricular (LV) performance. Measurement of ScvO2, Lact and SI may provide valuable additional information on the adequacy of systemic oxygenation and LV function during initial therapy of shock. This may identify patients who require further monitoring and intervention to optimize systemic oxygen transport and cardiac performance and reduce their morbidity and mortality.
Blood Pressure↗
Hemodynamics of interposed abdominal compression during human cardiopulmonary resuscitation.
OBJECTIVE: Clinical studies of interposed abdominal compression CPR (IAC-CPR) have had diverse outcomes. This study compared the hemodynamics of standard CPR and IAC-CPR in humans. METHODS: A 24-month prospective nonrandomized analysis of hemodynamic parameters was performed in a convenience cohort of 20 adults who had out-of-hospital, nontraumatic, normothermic cardiac arrests. The study took place in the resuscitation unit of a large urban hospital. Thoracic aortic and right atrial catheters were inserted and pressures were recorded during standard CPR and IAC-CPR. Coronary perfusion pressures (CPPs) were determined during standard CPR and IAC-CPR. The patients were separated into two groups based upon their responses to IAC-CPR. Responders had increases in CPP during IAC-CPR; nonresponders had decreases or no change in CPP during IAC-CPR. Aortic relaxation, right atrial relaxation, aortic compression, and right atrial compression phase pressures were compared between the two groups. RESULTS: CPPs increased in 13 patients and decreased in seven patients. The mean change in CPP with IAC-CPR was an increase of 5.8 +/- 15.1 torr. An elevated right atrial compression phase pressure (RaComp) during standard CPR was predictive of an increase in CPP during IAC-CPR (p = 0.047). In those patients who showed improvements in CPP during IAC-CPR, mean aortic relaxation phase pressures (AoRelax) increased by 9.5 +/- 14.2 torr (p = 0.026) and mean right atrial relaxation phase pressures (RaRelax) decreased by 2.6 +/- 6.2 torr (p = 0.099) during IAC-CPR. CONCLUSIONS: The variable effects of IAC-CPR on CPP appear to be multifactorial. The improvement in CPP that occurred in responders to IAC-CPR was secondary to an increase in AoRelax as well as a decrease in RaRelax.
Abdomen↗