Biomarkers in low cardiac output syndrome after open cardiac surgery in children

Background Corrective cardiac surgery is the standard management for complex congenital heart disease. Cardiopulmonary bypass surgery and post-surgical intensive care may lead to low cardiac output syndrome (LCOS), as a major complication after open heart surgery. To diagnose early LCOS, lactate level, pCO2 gap, and mixed venous oxygen saturation (SvO2) are parameters reported to have correlations with decreased cardiac output, morbidity, and post-cardiac surgery mortality. Objective To determine the usefulness of lactate level, pCO2 gap (arterial-vein), and SvO2 for early detection of LCOS in children post-open heart surgery. Methods This prospective cohort study was done from August to October 2017 in the ICU of the Integrated Cardiac Center, Dr. Cipto Mangunkusumo Hospital, Jakarta. Subjects were pediatric patients who underwent cardiac surgery. After surgery, patients underwent monitoring in the ICU for clinical signs of LCOS and examinations for lactate levels, pCO2 gap, and SvO2 at 15 minutes, 4 hours and 8 hours. Results Thirty-three open heart surgery patients were the subjects. Lactate level at 4 hours and 8 hours post-operative were significantly higher in the LCOS group compared to non-LCOS group. For the pCO2 gap, only the 4-hour post-operative results were significantly higher in LCOS group compared to non-LCOS groups. In addition, only SvO2 at 4 hours after surgery was significantly lower in LCOS group compared to non-LCOS group. Conclusion Elevated lactate, high pCO2 gap, as well as decreased SvO2 at 4 hours post-operatively are the most reliable markers of LCOS after pediatric open heart surgery.

Changes in central venous to arterial carbon dioxide gap (PCO2 gap) in response to acute changes in ventilation

BackgroundEarly diagnosis of shock is a predetermining factor for a good prognosis in intensive care. An elevated central venous to arterial PCO2 difference (∆PCO2) over 0.8 kPa (6 mm Hg) is indicative of low blood flow states. Disturbances around the time of blood sampling could result in inaccurate calculations of ∆PCO2, thereby misrepresenting the patient status. This study aimed to determine the influences of acute changes in ventilation on ∆PCO2 and understand its clinical implications.MethodsTo investigate the isolated effects of changes in ventilation on ∆PCO2, eight pigs were studied in a prospective observational cohort. Arterial and central venous catheters were inserted following anaesthetisation. Baseline ventilator settings were titrated to achieve an EtCO2 of 5±0.5 kPa (VT = 8 mL/kg, Freq = 14 ± 2/min). Blood was sampled simultaneously from both catheters at baseline and 30, 60, 90, 120, 180 and 240 s after a change in ventilation. Pigs were subjected to both hyperventilation and hypoventilation, wherein the respiratory frequency was doubled or halved from baseline. ∆PCO2 changes from baseline were analysed using repeated measures ANOVA with post-hoc analysis using Bonferroni’s correction.Results∆PCO2 at baseline for all pigs was 0.76±0.29 kPa (5.7±2.2 mm Hg). Following hyperventilation, there was a rapid increase in the ∆PCO2, increasing maximally to 1.35±0.29 kPa (10.1±2.2 mm Hg). A corresponding decrease in the ∆PCO2 was seen following hypoventilation, decreasing maximally to 0.23±0.31 kPa (1.7±2.3 mm Hg). These changes were statistically significant from baseline 30 s after the change in ventilation.ConclusionDisturbances around the time of blood sampling can rapidly affect the PCO2, leading to inaccurate calculations of the ∆PCO2, resulting in misinterpretation of patient status. Care should be taken when interpreting blood gases, if there is doubt as to the presence of acute and transient changes in ventilation.

The Forgotten Hemodynamic (PCO2 Gap) in Severe Sepsis

Background. Central venous-arterial carbon dioxide difference (PCO2 gap) can be a marker of cardiac output adequacy in global metabolic conditions that are less affected by the impairment of oxygen extraction capacity. We investigated the relation between the PCO2 gap, serum lactate, and cardiac index (CI) and prognostic value on admission in relation to fluid administration in the early phases of resuscitation in sepsis. We also investigated the chest ultrasound pattern A or B. Method. We performed a prospective observational study and recruited 28 patients with severe sepsis and septic shock in a mixed ICU. We determined central venous PO2, PCO2, PCO2 gap, lactate, and CI at 0 and 6 hours after critical care unit (CCU) admission. The population was divided into two groups based on the PCO2 gap (cutoff value 0.8 kPa). Results. The CI was significantly lower in the high PCO2 gap group (P=0.001). The high PCO2 gap group, on admission, required more administered fluid and vasopressors (P=0.01 and P=0.009, respectively). There was also a significant difference between the two groups for low mean pressure (P=0.01), central venous O2 (P=0.01), and lactate level (P=0.003). The mean arterial pressure was lower in the high PCO2 gap group, and the lactate level was higher, indicating global hypoperfusion. The hospital mortality rate for all patients was 24.5% (7/28). The in-hospital mortality rate was 20% (2/12) for the low gap group and 30% (5/16) for the high gap group; the odds ratio was 1.6 (95% CI 0.5–5.5; P=0.53). Patients with a persistent or rising PCO2 gap larger than 0.8 kPa at T = 6 and 12 hours had a higher mortality change (n = 6; in-hospital mortality was 21.4%) than patients with a PCO2 gap of less than 0.8 kPa at T = 6 (n = 1; in-hospital mortality was 3%); this odds ratio was 5.3 (95% CI 0.9–30.7; P=0.08). The PCO2 gap had no relation with the chest ultrasound pattern. Conclusion. The PCO2 gap is an important hemodynamic variable in the management of sepsis-induced circulatory failure. The PCO2 gap can be a marker of the adequacy of the cardiac output status in severe sepsis. A high PCO2 gap value (>0.8 kPa) can identify situations in which increasing CO can be attempted with fluid resuscitation in severe sepsis. The PCO2 gap carries an important prognostic value in severe sepsis.