[Hypothermia and cerebral protection after head trauma. Influence of blood gases modifications]. / Hypothermie et protection cérébrale après traumatisme crânien. Influence des gaz du sang.

The usefulness of therapeutic hypothermia is highly debated after traumatic brain injury. A neuroprotective effect has been demonstrated only in experimental studies: decrease in cerebral metabolism, restoration of ATP level, better control of cerebral edema and cellular effects. Despite negative multicenter clinical studies, therapeutic hypothermia is still used to a better control of intracranial pressure. However, important issues need to be clarified, particularly the level and duration of hypothermia, the depth and modalities of sedation. A clear understanding of blood gases variations induced by hypothermia is needed to understand the cerebral perfusion and oxygenation changes. It is essential to recognize and to use hypothermia-induced physiological hypocapnia and alkalosis under strict control of cerebral oxygen balance (jugular venous saturation or tissue PO(2)) and also to take into account the increased affinity of hemoglobin for oxygen. Management of post-traumatic intracranial hypertension using hypothermia, directed by intracranial pressure level, and consequently for long duration, is potentially beneficial but needs further clarification.

Respiratory alkalosis: a quick reference.

This article serves as a quick reference for respiratory alkalosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Role of C5a in multiorgan failure during sepsis.

In humans with sepsis, the onset of multiorgan failure (MOF), especially involving liver, lungs, and kidneys, is a well known complication that is associated with a high mortality rate. Our previous studies with the cecal ligation/puncture (CLP) model of sepsis in rats have revealed a C5a-induced defect in the respiratory burst of neutrophils. In the current CLP studies, MOF occurred during the first 48 h with development of liver dysfunction and pulmonary dysfunction (falling arterial partial pressure of O(2), rising partial pressure of CO(2)). In this model an early respiratory alkalosis developed, followed by a metabolic acidosis with increased levels of blood lactate. During these events, blood neutrophils lost their chemotactic responsiveness both to C5a and to the bacterial chemotaxin, fMLP. Neutrophil dysfunction was associated with virtually complete loss in binding of C5a, but binding of fMLP remained normal. If CLP animals were treated with anti-C5a, indicators of MOF and lactate acidosis were greatly attenuated. Under the same conditions, C5a binding to blood neutrophils remained intact; in tandem, in vitro chemotactic responses to C5a and fMLP were retained. These data suggest that, in the CLP model of sepsis, treatment with anti-C5a prevents development of MOF and the accompanying onset of blood neutrophil dysfunction. This may explain the protective effects of anti-C5a in the CLP model of sepsis.

Autotriggering caused by cardiogenic oscillation during flow-triggered mechanical ventilation.

OBJECTIVES: We noticed that in some patients after cardiac surgery, when flow triggering was used, cardiogenic oscillation might be autotriggering the ventilatory support. In a prospective study, we evaluated the degree of cardiogenic oscillation and the frequency rate of autotriggering. We suspected that autotriggering caused by cardiogenic oscillation was more common than clinically appreciated. DESIGN: Prospective, nonrandomized, clinical study. SETTING: Surgical intensive care unit in a national heart institute. PATIENTS: A total of 104 adult patients were enrolled after cardiac surgery. INTERVENTIONS: During the study period, patients were paralyzed and ventilated with intermittent mandatory ventilation at a rate of 10 breaths/min, pressure support of 10 cm H2O, and flow triggering with a sensitivity of 1 L/min. MEASUREMENTS AND MAIN RESULTS: Because the patients would not be able to breathe spontaneously, we counted pressure-support (PS) breaths as instances of autotriggering. Then, we classified the patients into two groups according to the number of PS breaths: an "AT group" (PS breaths of >5/min) and a "non-AT group" (PS breaths of < or =5/min). If autotriggering occurred, we decreased the sensitivity so autotriggering disappeared (threshold triggering sensitivity). The intensity of cardiogenic oscillation was assessed as the flow and airway pressure at the airway opening. A total of 23 patients (22%) demonstrated more than five autotriggered breaths/min. During mechanical ventilation, the inspiratory flow fluctuation caused by cardiogenic oscillation was significantly greater in the AT group than in the non-AT group (4.67+/-1.26 L/min vs. 2.03+/-0.86 L/min; p<.01). The AT group also showed larger cardiac output, higher ventricular filling pressures, larger heart size, and lower respiratory system resistance than the non-AT group. As the inspiratory flow fluctuation caused by cardiogenic oscillation increased, the level of triggering sensitivity also was increased to avoid autotriggering. In the AT group with 1 L/min of sensitivity, the respiratory rate increased (19.9+/-2.7 vs. 10+/-0 breaths/min, p<.01), Paco2 decreased (30.8+/-4.0 torr [4.11+/-0.36 kPa] vs. 37.6+/-4.3 torr [5.01+/-0.57 kPa]; p < .01), and mean esophageal pressure increased (7.7+/-3.0 vs. 6.9+/-3.0 cm H2O; p<.01) compared with the threshold triggering sensitivity. CONCLUSIONS: Autotriggering caused by cardiogenic oscillation is common in postcardiac surgery patients when flow triggering is used. Autotriggering occurred more often in patients with more dynamic circulation. Autotriggering caused respiratory alkalosis and hyperinflation of the lungs.

Extracorporeal CO2 Removal in severe adult respiratory distress syndrome.

Sixty-five per cent survival has been achieved in a group of patients with severe ARDS and a predicted mortality of 92%, by the use of Gattinoni's technique of extracorporeal CO2 removal. In patients and animals the technique has usually resulted in rapid improvement in the radiographic appearance and lung function. There are several possible mechanisms by which the technique may facilitate lung repair, including improvement of lung tissue oxygenation, the avoidance of high airway pressures and regional alkalosis in the lung, a reduction in oxygen toxicity, and the frequency observed reduction in pulmonary artery pressure. The apparent effectiveness of the technique and other associated evidence have implications which should lead us to reconsider some aspects of our conventional management of patients with severe ARDS.

Does intermittent mandatory ventilation correct respiratory alkalosis in patients receiving assisted mechanical ventilation?

One of the claimed advantages of intermittent mandatory ventilation (IMV) over assisted mechanical ventilation (AMV) (assist-control) is the avoidance or correction of acute respiratory alkalosis, ostensibly by allowing patients to achieve normal alveolar ventilation (VA) and PaCO2 through the function of an intact ventilatory drive. However, although respiratory alkalosis in patients being hyperventilated with controlled mechanical ventilation (CMV) can be corrected by a change to IMV, CMV is seldom appropriate for patients with acute respiratory failure, and whether IMV affects respiratory alkalosis in patients triggering the ventilator in the AMV mode has not previously been tested. We studied 26 patients with acute respiratory alkalosis (pH greater than or equal to 7.48) while receiving AMV. Measurements of arterial blood gases and CO2 production (VCO2), and calculation of VA, were performed after 30 min of AMV, repeated after 30 min of IMV at a mandatory rate one half the previous AMV rate, and then repeated again 30 min after a return to the original AMV settings. Mean arterial pH decreased slightly from 7.51 during AMV to 7.48 during IMV, and returned to 7.51 on resumption of AMV (p less than 0.05 for both changes); corresponding mean values for PaCO2 were 28.6, 29.7, and 27.5 mmHg, respectively. These changes were related to an increase in VCO2 during IMV as compared with AMV (p less than 0.05), without a significant alteration in VA. When the mandatory rate was further reduced during IMV from one half to one fourth the prior, triggered AMV rate in 10 patients, no additional reduction in pH occurred.(ABSTRACT TRUNCATED AT 250 WORDS)