Raymond F. Raper

Epinephrine-induced lactic acidosis following cardiopulmonary bypass.

OBJECTIVE To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. DESIGN Prospective, randomized study. SETTING Postsurgical cardiothoracic intensive therapy unit. PATIENTS Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. INTERVENTIONS Randomized administration of either epinephrine or norepinephrine by infusion. MEASUREMENTS AND MAIN RESULTS Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p < or = .01). Blood glucose concentration was higher in the epinephrine group at time 2 (p = .02), while the cardiac index (p < .03) and the mixed venous Po2 (p = .04) were higher at time 1. compared with the norepinephrine group, the patients receiving epinephrine had higher femoral venous lactate concentrations (p = .03), increased lower limb blood flow (p = .05), and increased femoral venous oxygen saturations (p = .04). CONCLUSIONS The use of epinephrine after cardiopulmonary bypass precipitates the development of lactic acidosis in some patients. This phenomenon is presumably a beta-mediated effect, and is associated with an increase in whole-body and lower limb blood flow and a decrease in whole-body and transfemoral oxygen extraction. The phenomenon does not appear to be related to reduced tissue perfusion and does not have the poor outlook of lactic acidosis associated with shock.

The 'cuff-leak' test for extubation.

The ‘cuff‐leak’ test, which involves demonstrating a leak around a tracheal tube with the cuff deflated, has been advocated to determine the safety of extubation in patients with upper airway obstruction. In 62 such patients we were able safely to extubate all patients with a cuff leak. Two patients extubated without cuff leak required reintubation and in five patients who repeatedly failed the test, tracheostomy was performed. Subsequently, we extubated 10 patients who were stable on spontaneous ventilation and did not have cuff leak; three later required tracheostomy and seven were uneventfully extubated. While the presence of cuff leak demonstrates that extubation is likely to be successful, a failed cuff‐leak test does not preclude uneventful extubation and if used as a criterion for extubation may lead to unnecessarily prolonged intubation or to unnecessary tracheostomy.

PROFOUND REVERSIBLE MYOCARDIAL DEPRESSION AFTER ANAPHYLAXIS

Profound myocardial depression developed in 2 patients after severe anaphylactic reactions following the induction of anaesthesia in 1 case and a bee-sting in the other. Neither patient had pre-existent cardiac disease. In both patients haemodynamic assessment, radionuclide ventriculography, and two-dimensional echocardiography confirmed the clinical impression of profound systolic myocardial dysfunction. Haemodynamic stability was attained by intra-aortic balloon counterpulsation, which was probably life-saving in both cases. Cardiac function improved rapidly although some contractile depression persisted for several days. At follow-up both patients had normal cardiac function with no evidence of underlying heart disease.

Osteosclerotic Myeloma Complicated by Diffuse Arteritis, Vascular Calcification and Extensive Cutaneous Necrosis

Widespread, progressive skin necrosis developed in a 42-year-old male with a 5-year history of osteosclerotic myeloma. Biopsy of the necrotic lesions demonstrated a leucocytoclastic vasculitis with extensive vascular calcification. Radiological investigations demonstrated widespread arterial calcification. Clinical improvement of the established skin lesions followed the institution of a forced calciuresis and parathyroid hormone suppression by induced hypermagnesaemia and phosphate depletion. No further cutaneous necrosis developed. Subsequent treatment with oral immunosuppressive therapy and the diphosphonate, EHDP, has been associated with a complete 18-month remission. The relationship of this apparently unique pathological process to the osteosclerotic myeloma is discussed, together with the rationale for the therapeutic regime instituted.

Alterations in anion gap following cardiopulmonary bypass.

ObjectivesTo evaluate the changes in the anion gap and their relation to hyperlactatemia and alterations in plasma proteins after cardiopulmonary bypass. DesignProspective study. SettingCardiothoracic intensive therapy unit. PatientsOne hundred eleven consecutive patients after cardiopulmonary bypass. Measurements and Main ResultsData were collected before cardiopulmonary bypass and every 6 hrs for 24 hrs after cardiopulmonary bypass. Results were analyzed for the entire cohort and for hyperlactatemic subgroups. The major finding of this study was that the anion gap decreased significantly at all sampling periods relative to precardiopulmonary bypass values, despite the presence of clinically important hyperlactatemia. No correlation between the decrease in plasma protein concentrations and the decrease in anion gap could be demonstrated. ConclusionsThe decrease in anion gap after cardiopulmonary bypass appears to represent a balance between the influences of increased serum chloride and lactate concentrations and reduced plasma protein concentrations. This analysis demonstrates the limitations of the anion gap in the evaluation of a metabolic acidosis after cardiopulmonary bypass. (Crit Care Med 1992; 20:52)

Changes in myocardial blood flow rates during hyperdynamic sepsis with induced changes in arterial perfusing pressures and metabolic need

ObjectiveTo determine whether hyperdynamic sepsis is associated with dysregulation in the control of myocardial blood flow rates unrelated to hypotension or the use of anesthetic agents. DesignProspective, nonrandomized, controlled trial. SettingExperimental laboratory. SubjectsFifteen mature male sheep (34 to 61 kg). InterventionsData were recorded in study subjects before and after the induction of sepsis following cecal ligation and perforation. Data were then recorded during: a) an infusion of prostaglandin E1 (PGE1), which decreased mean arterial perfusing pressure; and b) an infusion of zymosan-activated plasma, which increased mean pulmonary arterial pressures. Measurements and Main ResultsMyocardial blood flow rates were measured by the radiolabeled microsphere technique and cardiac index was measured by the thermodilution technique. Cardiac index (change Δ) postcecal ligation and perforation minus baseline (+2.3 ± 1.0 L/min/m2; p <.01) was increased in the septic study. Blood flow rate to the left ventricle was simultaneously increased, and was not further affected when the PGE1 infusion decreased the mean arterial perfusing pressures (-19 ± 4%). During the infusion of zymosan-activated plasma, mean pulmonary arterial pressures increased (50 ± 30%) and right ventricular blood flow was increased (zymosan minus postcecal ligation and perforation study: Δ17.8 ± 50 mL/100 g/min; p <.01). ConclusionsIn this model of hyperdynamic sepsis, increases in blood flow to both the left and right ventricles were positively coupled to changes in respective ventricular work. From the interventional PGE1 and zymosan-activated plasma infusion studies, we found no evidence to support previous suggestions that the regulation of myocardial blood flow rates according to changes in perfusing pressure and/or metabolic oxygen need is significantly altered during hyperdynamic sepsis. (Crit Care Med 1993;21:1192–1199)

Sedation in Intensive Care

The term “sedation” as used by intensivists carries a number of meanings. While traditionally sedation is defined as use of hypnotic-sedative drugs to produce drowsiness, this term is misleading and dates from the days in which barbiturates were the only such drugs available [1]. With the development of “tranquilizers”, the traditional sedative-hypnotic drugs have come to play a lesser role in daytime sedation, although the drugs traditionally classified as tranquilizers are more commonly used in psychiatric disorders than in the intensive care unit (ICU). Indeed, in the ICU the demand for and indication for sedation cover a wide spectrum, and the majority of drugs used have general depressant properties.

Pulmonary oedema, acid aspiration, bronchospasm and anaphylaxis

In this chapter, four disorders associated with acute hypoxaemia during anaesthesia are presented. While these four may at first glance seem unrelated, each may be a significant factor in anaesthetic morbidity and mortality. Moreover, there is some considerable clinical overlap between the four so that it may be difficult in any given situation to identify the primary event and to distinguish cardiovascular from respiratory causes of hypoxia. To some extent, at least, each of the four entities is both preventable and often easily managed if considered and recognized appropriately.