Comparison of critical care by family physicians and general internists.
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Biomedical subjects
Publications and source records attributed to M T Haupt.
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A wide variety of colloidal and crystalloidal fluids, as well as blood and blood products, are available to the clinician for treatment of the hypovolemic patient. These fluids vary with respect to the size, shape, and concentrations of electrolytes, colloidal molecules, and/or cellular components, duration of volume-expanding effects, incidence of allergic reactions, and effect on the coagulation system. When these fluids are administered intravenously, their distribution in the vascular, interstitial, and cellular compartments can be predicted from fundamental physiological principles as well as from the results of laboratory and clinical research. It is thus recognized that colloidal fluids and blood provide more rapid expansion of the intravascular space when compared with crystalloidal fluids. Similar volumes of crystalloidal fluids more rapidly expand the interstitial and intracellular spaces. These principles guide therapy in hypovolemic shock. A logical decision regarding intravenous fluid therapy may be based on the nature of the volume deficit (blood, plasma, or selective protein loss, loss of free water and/or electrolytes) and the predicted changes in cellular and extracellular compartments.
To evaluate the effects of reorganizing physician resources in a medical intensive care unit (MICU), we studied the impact of these changes in patients with septic shock. Patients were compared during two consecutive 12-month periods: (1) an interval in which faculty without critical care medicine (CCM) training supervised the MICU (before CCM, n = 100) and (2) following staffing with physicians formally trained in CCM (after CCM, n = 112). Acute Physiology and Chronic Health Evaluation scores were utilized to compare severity of illness and were similar for each group (29 +/- 11 before CCM vs 28 +/- 10 after CCM). However, mortality was significantly lower during the post-CCM interval (74% vs 57%, respectively). There was no significant difference in the frequency of use of mechanical ventilation (83% vs 87%), although pulmonary artery catheters (48% vs 64%) and arterial catheters (24% vs 73%) were employed more frequently after CCM. The number of subspecialty consultations and MICU and hospital length of stay were similar for both intervals. We conclude that the implementation of dedicated staffing by CCM physicians in a university hospital MICU was associated with a favorable impact on patients with septic shock.
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Fifty-four patients with systemic sepsis and signs of circulatory shock were prospectively investigated immediately before and after 1 of 3 therapeutic interventions chosen to increase systemic oxygen delivery (DO2): colloidal fluid loading (Group I, n = 20), blood transfusion (Group II, n = 17), or catecholamine infusion (dopamine or dobutamine, Group III, n = 17). Patients in Groups I and II with normal blood lactate concentrations (less than 2.2 mmol/L) exhibited no significant increases in systemic oxygen consumption (VO2) in response to the increases in DO2. However, significant increases in VO2 were noted in patients in Groups I and II with elevated lactate concentrations (greater than 2.2 mmol/L). In contrast to patients in Groups I and II, patients in Group III with and without lactic acidosis exhibited significant increases in VO2 after catecholamine administration. Lactic acidosis, a clinical marker of anaerobic metabolism or oxygen debt, appears to predict increases in VO2 in response to increases in DO2 in septic patients receiving fluid and catecholamines increase VO2 without regard for the presence or absence of anaerobic metabolism. The results of this clinical trial therefore suggest that catecholamines may exert a direct effect on oxidative metabolism.
Anaphylactic, anaphylactoid, and related forms of shock are true medical emergencies characterized by bronchial reactivity, airway edema, and hypovolemia. These reactions are attributed to the immunologic and nonimmunologic activation of mast cells and basophils, which results in the acute release of a variety of biochemical mediators that influence vascular tone and permeability. The therapeutic approach to these reactions is guided by the understanding of associated cellular and biochemical changes.
We prospectively evaluated 20 patients with systemic sepsis and signs of circulatory failure to determine if fluid loading was associated with increases in systemic oxygen delivery (DO2) and consumption (VO2). Fluid loading led to an increase in DO2 in 14 patients (70%). Patients who demonstrated increased DO2 with a corresponding increase in VO2 (Group A, n = 8) had significantly higher (p less than 0.05) initial blood lactate levels (4.9 +/- 2.9 mmol/L, mean +/- SD) than did patients without an increase in VO2 (Group B, n = 6, 1.9 +/- 1.0 mmol/L). A decrease in DO2 that was attributed to hemodilution was noted in the remaining 6 patients (Group C). Group C exhibited elevated lactate levels (5.1 +/- 2.4 mmol/L) and no significant changes in VO2. We conclude that lactic acidosis, a marker of anaerobic metabolism, predicts increases in VO2 in septic patients who respond to fluid loading with an increase in DO2.
Physiologic effects of colloidal (5% albumin, 6% hydroxyethylstarch, 6% dextran-70) and crystalloidal (Ringer's lactate) fluids were examined in rats (six in each fluid group) after infusion of an LD99 of rattlesnake venom, previously shown to produce shock secondary to increased vascular permeability. Venom infusion (iv, 2.0 mg/kg, 30 min) was followed by fluid infusion (iv, 30 min) in quantities sufficient to reverse venom-induced hemoconcentration. Venom infusion decreased mean arterial pressure, increased blood lactate, and increased hematocrit in all animals (p less than .01). Fluid infusion reversed these changes, although six times the volume of crystalloid was required to produce hemodilution comparable to the colloidal fluids (120 ml/kg Ringer's lactate, 20 ml/kg colloids). Although no significant changes in the respiratory parameters were noted after administration of the three colloids, Ringer's lactate produced decreases in PaC2 (107 +/- 6 torr, mean +/- SEM to 72 +/- 7, p less than .05), increases in PaCO2 (30 +/- 4 torr to 55 +/- 5, P less than .001), decreases in plasma colloid osmotic pressure (14.2 +/- 0.8 torr to 6.6 +/- 0.9, p less than .001) at the end of fluid infusion. These changes were associated with significantly increased wet-dry lung ratios (p less than .001) in identically prepared animals, sacrificed after fluid infusion. In spite of the development of pulmonary edema in the crystalloid-treated animals, survival was similar for each group (6/6 for albumin and dextran, 5/6 for hydroxyethylstarch and Ringer's lactate). We thus conclude that both colloidal and crystalloidal fluid resuscitation leads to survival in permeability shock. Resuscitation with crystalloidal fluid, however, requires significantly greater volumes and is associated with the development of pulmonary edema.
The hemodynamic characteristics of 36 febrile patients were studied when temperature was greater than 100 degrees F and after resolution of fever (temperature less than or equal to 100 degrees F). The patients were divided into those with bacterial infection (group I, n = 26) and those whose fever was noninfectious in etiology (group II, n = 10). Analysis of patients likely to have coronary artery disease (CAD) (subset A, n = 12) and those unlikely to have CAD (subset B, n = 7) was carried out. To maintain constant preload, pulmonary artery wedge pressure varied by not more than 2 mm Hg in all patients. Resolution of fever was associated with a 23% increase in stroke volume index (SVI) and 37% increase in left ventricular stroke work index (LVSWI) for group I (p less than 0.01). Group II showed a 27% increase in SVI and a 38% increase in LVSWI (p less than 0.05). Both subsets A and B showed significant increases in LVSWI after resolution of fever. We found evidence of decreased left ventricular performance during the febrile state in patients with and without infections. Since all groups and subsets maintained a normal or high cardiac index associated with increased heart rate during the febrile state, the tachycardic response of the febrile patient may serve to maintain cardiac output when myocardial performance is impaired.
Twenty-six consecutive patients in hypovolemic shock were randomized to fluid challenge with 5% albumin (A), 6% hetastarch (H), or 0.9% saline (S) solutions. Fluid challenge consisted of 250 ml of test fluid every 15 min until the pulmonary artery wedge pressure (WP) reached 15 mm Hg. Thereafter, WP was maintained at 15 mm Hg for an additional 24 h with infusions of the same test fluid. Vital signs, hemodynamic and respiratory variables, as well as arterial lactate and colloid osmotic pressure (COP) were monitored according to protocol. Chest x-rays were performed by standardized technique before fluid challenge and at 12 and 24 h of maintenance fluid therapy and were evaluated for evidence of pulmonary edema. Cardiac function and hemodynamic stability were restored by fluid challenge with A, H, and S. Two to 4 times the volume of S as A or H was required to achieve similar hemodynamic endpoints. COP was increased by fluid challenge with A or H but was markedly reduced by fluid challenge with S and throughout the 24-h maintenance period. Fluid challenge resulted in reductions in COP-WP gradient of 62% in the A, 43% in the H, and 125% in the S groups. Resuscitation with S resulted in a significantly higher incidence of pulmonary edema (87.5%) than did resuscitation with A (22%) or H (22%). Urine output was not different among the groups at any time during the study. We conclude that 6% H performs as well as 5% A as a resuscitative fluid and that resuscitation with either of these colloids is associated with a lower incidence of pulmonary edema than is resuscitation with 0.9% S.
The effects of fluid resuscitation with 6% hetastarch, 5% albumin, or 0.9% saline solutions on plasma colloid osmotic pressure (COP) were examined in 26 patients with hypovolemic circulatory shock. One liter of hetastarch produced a 36% increase in COP compared to an 11% increase after 1 L of albumin (p less than 0.001). One liter of saline resulted in a 12% decrease in COP (p less than 0.05). The mean COP increased from 16.3 +/- 1.6 (SE) mm Hg to a maximum of 23.7 +/- 1.4 mm Hg during the first 24 h of hetastarch resuscitation (p less than 0.01), and from 17.0 +/- 1.1 to 22.3 +/- 1.5 mm Hg with albumin (p less than 0.001). Saline resuscitation decreased the COP from 17.1 +/- 1.1 mm Hg to a minimum of 12.7 +/- 1.1 mm Hg (p less than 0.02). These changes persisted from 2-5 days after resuscitation. Saline resuscitation required significantly larger amounts of fluid. The authors conclude that fluid resuscitation of circulatory shock with colloid solutions increases COP and requires less volume of resuscitative fluid.