Venous admixture in human septic shock: comparative effects of blood volume expansion, dopamine infusion and isoproterenol infusion on mismatching of ventilation and pulmonary blood flow in peritonitis.

A hemodynamic study with blood gas analysis was performed so we could observe changes induced by blood volume expansion, dopamine infusion and isoproterenol infusion in 20 adult patients suffering from peritonitis complicated with septic shock and acute respiratory failure. Blood volume expansion increased cardiac index (from 2.6 +/- 1.21/min/m2 to 3.4 +/- 1.31/min/m2; p less than 0.001), but also enhanced venous admixture (QS/QT) from 27 +/- 14% to 36 +/- 13%; p less than 0.01). Dopamine infusion increased cardiac index (from 2.6 +/- 0.9 1/min/m2 to 3.4 +/- 1 l/min/m2; p less than 0.001), but also enhanced venous admixture (from 25 +/- 11% to 31 +/- 12%, p less than 0.001). Isoproterenol infusion increased cardiac index (from 2.6 +/- 0.9 l/min/m2 to 3.6 +/- 1.1 l/min/m2; p less than 0.001), but also enhanced venous admixture (from 27 +/- 12% to 33 +/- 11%; p less than 0.001). This worsening in mismatching of ventilation and blood flow is correlated with the enhancement in pulmonary blood flow obtained by these three therapeutic procedures.

Effect of dopamine on intrapulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure.

The hemodynamic response to a dopamine HCl infusion (10 microgram/kg per min) was measured in 25 adult patients with severe sepsis: there were 6 patients with circulatory hyperdynamic states, 9 patients with myocardial failure, and 10 with hypovolemia. Each patient also had acute respiratory failure. Changes of intrapulmonary shunt fraction (Qs/Qt), arterial and mixed venous oxygen tension (PaO2 and PvO2), oxygen transport, and oxygen consumption (VO2) were evaluated before and after dopamine infusion. Dopamine infusion produced clinical improvement and increased cardiac output. The hemodynamic response seemed to differ slightly according to the pattern of circulatory failure: chronotropic effect appeared to be predominant in hyperdynamic states, whereas inotropic effect appeared to be predominant in myocardial failure or hypovolemia. Moreover, in hypovolemic patients we noted a rise in pulmonary capillary wedge pressure suggesting an additional increase in venous return. During this treatment, we also noted a worsening of the Qs/Qt despite the increase in pulmonary blood flow; this worsening did not prevent significant improvements in VO2, but the improvement in PVO2 was offset by increased Qs/Qt and PaO2 remained unchanged.

Hemodynamic factors influencing arterial hypoxemia in massive pulmonary embolism with circulatory failure.

Arterial hypoxemia is a common finding in acute pulmonary embolism, and its severity is generally assumed to be proportional to the extent of pulmonary artery obstruction. We studied blood gases (during room air breathing and 100% oxygen breathing) and hemodynamic data is seven patients with massive pulmonary embolism and circulatory failure. All measurements were made before and 30 minutes after medical therapy of shock. We observed that a low cardiac output state can result in a misleading improvement in arterial oxygenation during massive pulmonary embolism, and that an improved circulatory status resulting from medical therapy (including inotropic drug infusion with or without blood volume expansion) can paradoxically increase arterial hypoxemia. We conclude that severity of arterial hypoxemia may not reflect the severity of pulmonary artery obstruction in acute pulmonary embolism if shock is present.

Massive pulmonary embolism with circulatory failure: survival following sixty hours' support with a membrane lung.

A 62-year-old man had circulatory failure from massive pulmonary embolism following a road accident. Despite intensive therapy including urokinase infusion, inotropic drugs, and mechanical ventilation, the patient's circulatory status deteriorated. When it became impossible to maintain the mean systemic arterial pressure above 50 mm. Hg and the cardiac index above 1 L. per minute per square meter, circulatory support by partial cardiopulmonary bypass with a membrane lung was begun. Acute circulatory failure and acute pulmonary hypertension were promptly reduced by this procedure, and patient's status necessitated only intravenous heparin infusion and mechanical ventilation. After 60 hours of bypass the patient was weaned from the membrane lung, and 1 month later he was discharged from the hospital.

Immediate and middle-term cardiorespiratory effects of positive end-expiratory pressure in thirteen cases of non-haemodynamic pulmonary oedema.

Thirteen patients with severe acute respiratory failure were ventilated with positive end-expiratory pressure (PEEP) for 9 days. Haemodynamic measurements were performed after 15 min during 100% oxygen breathing, first with intermittent-positive pressure ventilation, secondly with positive end-expiratory pressure. The latter improved the Pa, O2 from 89 to 150 torr, decreased the QS/QT from 43% to 32% and decreased the Pa, CO2 from 37 to 34 torr; this improvement in gas exchange was accompanied by a decrease in cardiac index from 4.4 to 3.7 1 min-1m-2 without changing the systemic arterial pressure. Despite this beneficial effect on arterial blood oxygenation, it did not improve the survival rate of patients with severe acute respiratory failure.

[Hemodynamic profile in acute respiratory distress syndromes in the adult (author's transl)]. / Profil hémodynamique du syndrome de détresse respiratoire aiguë de l'adulte.

Hemodynamic, investigations carried out on 25 patients suffering from acute respiratory distress in the adult established a specific hemodynamic profile for that syndrome, including precapillary pulmonary artery hypertension and systemic arterial hypotension. The level of pulmonary vascular resistance (abnormally high) and systemic arterial resistance (abnormally low) were referred to the cardiac index (which may be increased in some patients due to infusions of Dopamine, or reduced in others due to an veno-arterial bypass). The observed hemodynamic disorders are not related to hypoxemia since this is corrected by permanent positive pressure breathing, or by extracorporeal oxygenation.