Although numerous clinical, laboratory, and pharmacological variables have been reported as significant risk factors for critical illness polyneuromyopathy (CIPM), there is still no consensus on the aetiology of this condition. Objectives of the study were to assess the clinical and electrophysiological incidence and risk factors for CIPM.A cohort of critically ill patients was observed prospectively for a one-month period and the association between neuromuscular involvement and various potential risk factors was evaluated. Sixty one critically ill patients completed the follow-up (30 women, 31 men, median age 59 years).CIPM development was detected clinically in 17 patients (27.9 %) and electrophysiologically in 35 patients (57.4 %). CIPM was significantly associated with the presence and duration of systemic inflammatory response syndrome and the severity of multiple, respiratory, central nervous, and cardiovascular organ failures. The median duration of mechanical ventilation was significantly longer in patients with CIPM than in those without (16 vs 3 days, p<0.001). Independent predictors of CIPM obtainable within the 1(st) week of critical illness were the admission sequential organ failure assessment score (odds ratio [OR], 1.15; 95% confidence interval [CI], 1.02-1.36), the 1(st) week total sequential organ failure assessment scores (OR, 1.14; 95 % CI, 1.06-1.46) and the 1(st) week duration of systemic inflammatory response syndrome (OR, 1.05; 95% CI, 1.01-1.15). They were able to correctly predict the development of CIPM at the end of the 1(st) week in about 80% of critically ill cases.In conclusion, the presence and duration of systemic inflammatory response syndrome and the severity of multiple and several organ failures are associated with increased risk of the development of CIPM.

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The bioavailability of clopidogrel in critically ill patients after cardiopulmonary resuscitation is significantly impaired compared with stable patients. Therefore, other drugs, preferentially administered intravenously, should be considered.

Introduction Measurement of ventilatory efficiency, defined as minute ventilation per unit carbon dioxide production (V E /VCO 2 ), by cardiopulmonary exercise testing (CPET) has been proposed as a screen for hyperventilation syndrome (HVS). However, increased V E /VCO 2 may be associated with other disorders which need to be distinguished from HVS. A more specific marker of HVS by CPET would be clinically useful. We hypothesized ventilatory control during exercise is abnormal in patients with HVS. Methods Patients who underwent CPET from years 2015 through 2017 were retrospectively identified and formed the study group. HVS was defined as dyspnea with respiratory alkalosis (pH >7.45) at peak exercise with absence of acute or chronic respiratory, heart or psychiatric disease. Healthy patients were selected as controls. For comparison the Student t-test or Mann-Whitney U test were used. Data are summarized as mean ± SD or median (IQR); p<0.05 was considered significant. Results Twenty-nine patients with HVS were identified and 29 control subjects were selected. At rest, end-tidal carbon dioxide (P ET CO 2 ) was 27 mmHg (25–30) for HVS patients vs. 30 mmHg (28–32); in controls (p = 0.05). At peak exercise P ET CO 2 was also significantly lower (27 ± 4 mmHg vs. 35 ± 4 mmHg; p<0.01) and V E /VCO 2 higher ((38 (35–43) vs. 31 (27–34); p<0.01)) in patients with HVS. In contrast to controls, there were minimal changes of P ET CO 2 (0.50 ± 5.26 mmHg vs. 6.2 ± 4.6 mmHg; p<0.01) and V E /VCO 2 ((0.17 (-4.24–6.02) vs. -6.6 (-11.4-(-2.8)); p<0.01)) during exercise in patients with HVS. The absence of V E /VCO 2 and P ET CO 2 change during exercise was specific for HVS (83% and 93%, respectively). Conclusion Absence of V E /VCO 2 and P ET CO 2 change during exercise may identify patients with HVS.