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Biomedical subjects

E C Rackow

Publications and source records attributed to E C Rackow.

At least 145 records · Page 8Linked to original sources
PubMed1983

Optimum left heart filling pressure during fluid resuscitation of patients with hypovolemic and septic shock.

The effect of increasing filling pressures on cardiac performance was examined in 15 patients undergoing fluid resuscitation for hypovolemic and septic shock. The initial significant increase in pulmonary artery wedge pressure (WP) from 7.0 +/- 2.0 to 11.9 +/- 1.6 mm Hg was associated with an increase in stroke volume index (SVI) from 24.2 +/- 9.8 to 34.7 +/- 12.4 ml/M2 (p less than 0.01), left ventricular stroke work index (LVSWI) from 16.9 +/- 7.8 to 28.5 +/- 11.6 g x m/M2 (p less than 0.01) and cardiac index (CI) from 2.25 +/- 0.68 to 3.06 +/- 0.85 L/min x M2 (p less than 0.01). Further significant increase in WP to 16.0 +/- 0.9 mm Hg did not result in any increase in SVI, LVSWI, or CI. The correlation between central venous pressure (CVP) and WP during fluid loading was only fair and the changes in CVP vs WP did not significantly correlate. We suggest that the optimum left heart filling pressure during fluid resuscitation of patients with hypovolemic and septic shock may not exceed a WP of 12 mm Hg.

Aged↗
PubMed1983

Fluid resuscitation in circulatory shock: a comparison of the cardiorespiratory effects of albumin, hetastarch, and saline solutions in patients with hypovolemic and septic shock.

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.

Aged↗
PubMed1982

Colloid osmotic pressure and fluid resuscitation with hetastarch, albumin, and saline solutions.

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.

Aged↗
PubMed1982

Neurogenic pulmonary edema.

This report presents a patient who developed fulminant pulmonary edema as a complication of an acute subarachnoid hemorrhage. Hemodynamic evaluation revealed low-normal pulmonary arteriolar resistances. Endobronchial fluid was freely suctioned from the patient over a two-day period and had a colloid osmotic pressure and protein content equal to the patient's plasma throughout the entire course. These findings suggest that neurogenic pulmonary edema in this patient was related to increased capillary permeability and may occur independent of pulmonary hemodynamics.

Adult↗
PubMed1982

The relationship of the colloid osmotic-pulmonary artery wedge pressure gradient to pulmonary edema and mortality in critically ill patients.

The relationship of serum colloid osmotic pressure (COP) and pulmonary artery wedge pressure (PAWP) to pulmonary edema and mortality was investigated in 76 critically ill patients. Forty patients suffered from circulatory shock and 36 did not. The COP-PAWP gradient and radiographic evidence of pulmonary edema were measured at the time of diagnosis. The COP-PAWP gradient was markedly decreased in both shock and non-shock patients with pulmonary edema. Decrease of the COP-PAWP gradient correlated with mortality only in those patients with shock. The shock patients who died had a significantly higher incidence of pulmonary edema than those who survived, whereas there was no difference in the incidence of pulmonary edema for surviving or dying non-shock patients. We conclude that marked decreases of the COP-PAWP gradient predict pulmonary edema in the critically ill, but predict mortality only for patients with circulatory shock.

Adult↗
PubMed1981

Hemodynamic and metabolic effects of abdominal aortic crossclamping.

The hemodynamic and metabolic effects of aortic crossclamping and declamping were studied in 10 patients undergoing abdominal aortic reconstructive surgery. After placement of pulmonary and radial arterial catheters, measurements were obtained preoperatively, during the procedure according to protocol, and postoperatively. Pulmonary arterial wedge pressure was maintained at 10 to 15 mm Hg throughout the operation. Aortic cross clamping produced a significant increase in systemic arteriolar resistance and systolic blood pressure, with no change noted in the left ventricular stroke work index. Declamping decreased systemic resistance and produced no change in the left ventricular stroke work index. Clamping and declamping resulted in elevations of serum lactate. Central venous pressure correlated with pulmonary arterial wedge pressure in each patient and in the entire group. Cardiac function is not decreased by aortic crossclamping, and central venous pressure can usually be used for hemodynamic monitoring in these patients.

Adult↗
PubMed1981

The spectrum of pulmonary edema: differentiation of cardiogenic, intermediate, and noncardiogenic forms of pulmonary edema.

Pulmonary edema fluid and serum samples were obtained from 20 patients with cardiac and noncardiac pulmonary edema, and total protein, albumin, and globulin concentrations were measured. The mean edema fluid to serum protein ratio in patients with pure cardiogenic pulmonary edema was 0.37 +/- 0.09. In contrast, the patients with pure noncardiogenic pulmonary edema had protein ratios of 0.84 +/- 0.12 (p less than 0.001). Another group of patients with both cardiac and noncardiac causes for edema demonstrated edema fluid to serum protein ratios that were significantly higher than those found in the cardiogenic patients and lower than the protein ratios in the noncardiogenic patients (0.60 +/- 0.07) (p less than 0.01) A cardiac or noncardiac causes of pulmonary edema could be determined in all patients, using edema fluid to serum total protein ratios in conjunction with globulin ratios. Cardiogenic and noncardiogenic pulmonary edema represent the extremes in the spectrum of pulmonary edema. A combination of increased permeability and hydrostatic pressure may account for an intermediate form of pulmonary edema.

Adult↗
PubMed1980

Pulmonary edema; a complication of diabetic ketoacidosis.

Hemodynamic evaluation in two patients and analysis of pulmonary edema fluid in one patient with diabetic ketoacidosis and acute pulmonary edema were performed. Pulmonary arterial wedge pressures in both patients were low or normal (1 and 9 mm Hg). In one patient the colloid osmotic pressure of the pulmonary edema fluid was 68 percent of the value of the serum. The serum colloid osmotic pressure-pulmonary arterial wedge pressure gradient in the second patient was markedly reduced. Pulmonary edema complicating diabetic ketoacidosis may be the result of increased permeability of pulmonary capillary membranes and altered intravascular colloid-hydrostatic forces.

Adult↗
PubMed1978

Uremic pulmonary edema.

Pulmonary edema fluid analyses and hemodynamic evaluations were performed in two uremic patients with acute pulmonary edema. The colloid osmotic pressure of the pulmonary edema fluid ranged from 57 per cent to 93 per cent that of the serum. Although cardiac function was normal in both patients, the serum colloid osmotic pressure--pulmonary artery wedge pressure gradients were markedly reduced. Uremic pulmonary edema is the result of alterations of pulmonary intravascular Starling forces and increases in pulmonary capillary membrane permeability, allowing for the efflux of protein-rich fluid from the capillaries into the lung.

Adult↗
PubMed1978

Acute pulmonary edema in Plasmodium falciparum malaria.

This report describes a patient who developed acute pulmonary edema as a complication of Plasmodium falciparum malaria. Hemodynamic evaluation revealed a pulmonary artery wedge pressure of 3 mm Hg and a cardiac index of 4.6 liter per min per m2. The patient exhibited an acute decrease in serum colloid osmotic pressure from 25.1 mm Hg to 16.8 mm Hg. These findings suggest that pulmonary edema in this patient was the result of altered capillary membrane permeability.

Acute Disease↗
PubMed1977

Colloid osmotic pressure as a prognostic indicator of pulmonary edema and mortality in the critically ill.

The relationship of colloid osmotic pressure (COP) to pulmonary edema and mortality in 128 critically ill patients was investigated in our critical care unit, and confirms previously reported observations. The COP in the 86 survivors was 22.0 (+/- 0.4 SEM) mm Hg versus 17.2 (+/- 0.6 SEM) mm Hg in the 42 who died (P less than 0.001). The patients were divided into three groups: 71 with no pulmonary edema, COP of 21.5 (+/- 0.5 SEM) mm Hg; 40 with cardiogenic pulmonary edema, COP of 21.4 (+/- 0.4 SEM) mm Hg; and 17 with noncardiogenic pulmonary edema, COP OF 13.6 (+/- 0.8 SEM) mm Hg. Colloid osmotic pressure was significantly lower in patients with noncardiogenic pulmonary edema (P less than 0.001). In 36 patients in whom pulmonary artery wedge pressures (PWP) were available, a COP-PWP gradient of 4.0 mm Hg or less was always associated with pulmonary edema, while a COP-PWP gradient greater than 4.0 mm Hg was never associated with pulmonary edema. Colloid osmotic pressure is a useful prognostic indicator of pulmonary edema and mortality in the critically ill.

Adolescent↗
PubMedDate not supplied

Fulminant noncardiogenic pulmonary edema in the critically ill.

The relationship between the serum colloid osmotic pressure (COPs), pulmonary artery wedge pressure (PWP), and pulmonary edema fluid colloid osmotic pressure was studied in six critically ill patients with fulminant noncardiogenic pulmonary edema. The relationship between COPs and PWP was also studied in 36 critically ill patients without pulmonary edema. The COPs-PWP gradient was normal in those patients without pulmonary edema. Three patients with noncardiogenic pulmonary edema had markedly reduced COPs-PWP gradients secondary to decreases in COPs. Their pulmonary edema fluid colloid osmotic pressure averaged 61% that of their serum colloid osmotic pressure. Three patients with noncardiogenic pulmonary edema had normal COPs-PWP gradients. Their pulmonary edema fluid colloid osmotic pressure averaged 92% that of their COPs. Noncardiogenic pulmonary edema in the critically ill patient may be caused by either a decrease of COPs-PWP gradient or an increase in capillary membrane permeability.

Adult↗
PubMedDate not supplied

Pathophysiology and treatment of septic shock.

The mortality from septic shock continues to range between 40% to 60% despite advances in cardiovascular support and antibiotic therapy. Impairment of host defenses predisposes to the development of both severe infection and septic shock. The activation of a myriad of cellular and plasma mediators by microbial toxins produces the systemic and metabolic manifestations of sepsis. The clinical presentation includes characteristic clinical, hemodynamic, and laboratory abnormalities. Multiple organ systems are involved during septic shock, with outcome dependent on the circulatory response and the development of sequential organ failures. Initial resuscitation is directed at restoring tissue perfusion with fluids and vasoactive drugs, guided by assessment of the patient's hemodynamic status. Identification of the site of infection and choice of appropriate antibiotics are critical to the success of therapy. Newer therapeutic modalities include immunologic interventions that attenuate mediator activity and modulate the immune response. Pharmacologic therapies are also being developed that are aimed at blocking the actions of specific mediators.

Energy Metabolism↗
PubMedDate not supplied

Colloid and crystalloid fluid resuscitation.

The choice of colloid or crystalloid solutions for fluid resuscitation of critically ill patients remains controversial. Marked reduction of extracellular water is considered an important defect in shock by proponents of crystalloid fluid therapy. Large volumes of crystalloid replenish this extracellular deficit. Hypovolemia is regarded as the primary defect in shock by those favoring colloid fluid therapy. Colloidal fluids promptly restore plasma volume and reestablish hemodynamic stability with substantially lesser volumes of fluid. However, only 8% of infused water and less than 25% of infused saline are retained in the intravascular fluid compartment after 1 h. On the other hand, almost the entire volume of iso-oncotic colloid is retained with the intravascular space after 1 h. Hypertonic saline decreases intracellular fluid volume. Hyperoncotic colloid decreases both interstitial and intracellular fluid volumes as it disproportionately expands intravascular volume. The choice of fluid is not only contingent on the restoration of intravascular volume, the rapidity with which it is accomplished and the duration of its effect, but also on the adverse effects that follow fluid resuscitation. This is of greatest moment in the fluid resuscitation of patients in whom circulatory shock follows volume depletion. Crystalloid fluid repletion which requires between 2- and 4-fold as much volume as colloidal fluid is of little risk in the young, traumatically injured patient. However, in older patients, the risk of pulmonary edema is increased.

Albumins↗