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Biomedical subjects

R M Hardaway

Publications and source records attributed to R M Hardaway.

At least 37 records · Page 2Linked to original sources

Pulmonary artery pressure versus pulmonary capillary wedge pressure and central venous pressure in shock.

Evidence is presented from 43 dogs and 30 patients that under conditions of severe hemorrhagic, traumatic or septic shock, there may be partial obstruction of the pulmonary microcirculation due to disseminated intravascular coagulation (DIC) particularly in the pulmonary venules. This may cause the left atrial pressure to fall and the pulmonary artery pressure to rise, in some cases drastically. Pulmonary edema may result. This dangerous rise in pulmonary artery pressure is not reflected by the wedged pulmonary artery catheter which will monitor only the status of the left heart. Central venous pressure (CVP) may remain within normal limits even after pulmonary artery pressure has risen to dangerous levels with the development of pulmonary edema. It is only with right ventricle failure against the high pulmonary pressure that CVP rises. It is concluded that pulmonary artery pressure measurements are very important in monitoring intravenous fluid administration in severe shock. Wedged pulmonary artery pressures monitor the left heart but may be misleading if taken alone. Central venous pressure gives a delayed response to fluid overload.

Aged↗

Expansion of the intravascular space in severe shock.

Hypovolemic shock, if untreated for a while or if severe, results in an increase in intravascular capacity due to the opening of all capillaries at once. This expansion of the vascular capacity in patients with severe or untreated shock requires much more intravenous fluids for adequate treatment than the volume of blood lost. Fluid volume requirements should be determined by results (normal blood pressure and urinary output) and by central venous pressure or pulmonary arterial pressure for maximum tolerable administration. Blood volume measurements are useless. The vascular space shrinks to normal after adequate resuscitation, creating relative hypervolemia.

Adolescent↗

Overcompensation syndromes.

As a result of severe injury or illness, a complex series of metabolic changes takes place in the body to enable it to cope with the stress and recover. Although these changes are beneficial and necessary, at times they are more extensive than desirable and may result in metabolic alkalosis, hypertension, disseminated intravascular coagulation, and fibrinolysis.

Acidosis↗

Prediction of survival or death of patients in a state of severe shock.

In previously normal patients in a state of severe shock, a prolongation of partial thromboplastin time above 100 seconds due to shock, an elevation of lactic dehydrogenase above 500 units per milligram, an elevation of serum glutamicoxalacetic transaminase above 125 units per milliliter, an elevation of serum glutamic-pyruvate transaminase above 60 units per milliliter, an elevation of lactate above 52 milligrams per milliliter are grave signs and predict a probable mortality. This does not apply to patients in a state of acute traumatic and hemorrhagic shock in extreme vasoconstriction or treated with vasoconstrictors. An arterial pO2-alveolar pO2 ratio of below 15 per cent indicates a probable mortality, above 30 per cent, a probable recovery. Cardiac index, arterial pH, arterial pO2, blood volume and systemic blood pressure have little correlation with survival. Monitoring coagulation and the intensity of its activity seem to be an effective index of mortality in severe shock in previously normal patients.

Alanine Transaminase↗

Mechanism of traumatic shock.

Although many attempts have been made to demonstrate the existence of a shock-producing toxin, little success has been attained. Traumatic shock is generally believed to be caused by simple loss of blood. Evidence is presented that tissue trauma causes hemolysis. Although hemoglobin is harmless, the stroma of the broken red cells is a clotting stimulant which, in the presence of the slow capillary flow of hemorrhagic shock, sustains a continuing disseminated intravascular coagulation. This disseminated intravascular coagulation produces a clotting defect, morbidity and death. The condition is not responsive to intravenously administered fluids but is responsive to fibrinolysin therapy.

Animals↗

Influence of fibrinogen levels in dogs on mortality from hemorrhagic and traumatic shock.

1) Fibrinogen levels appear related to the outcome of hemorrhagic shock in dogs. 2) Fibrinogen levels can vary with different animals based on location, disease, stress, nutrition, or other factors. 3) Any experiments in hemorrhagic shock (or anything else) should utilize simultaneous and paired controls of animals from the same source or they may be subject to major error.

Animals↗

Treatment of severe shock with phenoxybenzamine.

Phenoxybenzamine is a safe and effective vasodilator which usually causes an increase in arterial blood pressure, an increase in cardiac index, an increase in urine output and a decrease in pulmonary artery pressure and central venous pressure in states of severe shock if hypovolemia has been corrected. Phenoxybenzamine does not produce detrimental effects if given in appropriate instances. Phenoxybenzamine should be given only after other appropriate treatments, including adequate intravenous volume administration, have failed to produce an adequate arterial blood pressure and urinary output. It should be given only in the presence of a high normal central venous pressure and a high pulmonary artery pressure. Its administration should be closely monitored. It may be repeated once or twice at 24 hour intervals, if necessary. At present, phenoxybenzamine is available for intravenous use only as an investigative drug.

Blood Pressure↗

Importance of capillary perfusion.

Perfusion is more critical than oxygen in the maintenance of cell viability. A high hematocrit or high fibrinogen level increases blood viscosity and predisposes to disseminated intravascular coagulation. It is recommended that a hematocrit of about 30 be maintained in periods of circulatory stress such as shock or extracorporeal circulation.

Animals↗

The danger of hemolysis in shock.

Intravascular hemolysis is sometimes harmful and often fatal. Other times it is harmless. Dogs were paired and subjected to hemorrhagic shock. One of the pair was given 2 ml/kg of autologous hemolyzed blood before bleeding. The other of the pair was given 2 ml/kg of heparinized autologous blood. All of the animals given heparinized blood survived, whereas, all of the animals given hemolyzed blood died. The animals given hemolyzed blood developed coagulation changes indicative of Disseminated Intravascular Coagulation (DIC), whereas, the dogs given nonhemolyzed blood did not. It is concluded that hemolysis in the presence of shock (slow capillary flow) causes DIC and death. Hemorrhagic shock alone or hemolysis alone was harmless.

Animals↗

Monitoring of the patient in a state of shock.

Patients in a state of shock require careful monitoring to carry out intelligently appropriate treatment. Many methods of monitoring are available. Some are required for all patients in a state of shock, some are only required in severe or refractory shock, some are of little value, some are valuable but difficult or expensive and some are confusing and may mean the opposite of what they seem to indicate.

Animals↗

Treatment of shock.

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Acid-Base Equilibrium↗

Viet Nam wound analysis.

A statistical study is reported of 17,726 wounded American soldiers in Viet Nam over 15 months from March 1966 to July 1967. Causes, location, treatment, and results were analyzed for various regions, organs, and tissues. Results of treatment were remarkably good, the best in the history of military surgery. Major problems of resuscitation and treatment of local tissue injury which had not before been treated on a large scale were treated with excellent results.

Abdominal Injuries↗