Supporting hemodynamics: what should we target? What treatments should we use?

Assessment and monitoring of hemodynamics is a cornerstone in critically ill patients as hemodynamic alteration may become life-threatening in a few minutes. Defining normal values in critically ill patients is not easy, because 'normality' is usually referred to healthy subjects at rest. Defining 'adequate' hemodynamics is easier, which embeds whatever pressure and flow set is sufficient to maintain the aerobic metabolism. We will refer to the unifying hypothesis proposed by Schrier several years ago. Accordingly, the alteration of three independent variables - heart (contractility and rate), vascular tone and intravascular volume - may lead to underfilling of the arterial tree, associated with reduced (as during myocardial infarction or hemorrhage) or expanded (sepsis or cirrhosis) plasma volume. The underfilling is sensed by the arterial baroreceptors, which activate primarily the sympathetic nervous system and renin-angiotensin-aldosterone system, as well as vasopressin, to restore the arterial filling by increasing the vascular tone and retaining sodium and water. Under 'normal' conditions, therefore, the homeostatic system is not activated and water/sodium excretion, heart rate and oxygen extraction are in the range found in normal subjects. When arterial underfilling occurs, the mechanisms are activated (sodium and water retention) - associated with low central venous oxygen saturation (ScvO2) if underfilling is caused by low flow/hypovolemia, or with normal/high ScvO2 if associated with high flow/hypervolemia. Although the correction of hemodynamics should be towards the correction of the independent determinants, the usual therapy performed is volume infusion. An accepted target is ScvO2 >70%, although this ignores the arterial underfilling associated with volume expansion/high flow. For large-volume resuscitation the worst solution is normal saline solution (chloride load, strong ion difference = 0, acidosis). To avoid changes in acid-base equilibrium the strong ion difference of the infused solution should be equal to the baseline bicarbonate concentration

Clinical review : Extracorporeal membrane oxygenation

The H1N1 fl u pandemic led to a wider use of extracorporeal membrane oxygenation (ECMO), proving its power in hypoxemic emergencies. The results obtained during this pandemic, more than any randomized trial, led to the worldwide acceptance of the use of membrane lungs. Moreover, as centers that applied this technique as rescue therapy for refractory hypoxemia recognized its strength and limited technical challenges, the indications for ECMO have recently been extended. Indications for venovenous ECMO currently include respiratory support as a bridge to lung transplantation, correction of lung hyperinfl ation during chronic obstructive pulmonary disease exacerbation and respiratory support in patients with the acute respiratory distress syndrome, possibly also without mechanical ventilation. The current enthusiasm for ECMO in its various aspects should not, however, obscure the consideration of the potential complications associated with this life-saving technique, primarily brain hemorrhage

Contribution of red blood cells to the compensation for hypocapnic alkalosis through plasmatic strong ion difference variations

Introduction Chloride shift is the movement of chloride between red blood cells (RBC) and plasma (and vice versa) caused by variations in pCO2. The aim of our study was to investigate changes in plasmatic strong ion diff erence (SID) during acute variations in pCO2 and their possible role in the compensation for hypocapnic alkalosis.Methods Patients admitted in this year to our ICU requiring extracorporeal CO2 removal were enrolled. Couples of measurements of gases and electrolytes on blood entering (v) and leaving (a) the respiratory membrane were analyzed. SID was calculated as [Na+] + [K+] + 2[Ca2+] \u2013 [Cl\u2013] \u2013 [Lac\u2013]. Percentage variations in SID (SID%) were calculated as (SIDv \u2013 SIDa) x 100 / SIDv. The same calculation was performed for pCO2 (pCO2%). Comparison between v and a values was performed by paired t test or the signed-rank test, as appropriate. Results Analysis was conducted on 205 sample-couples of six enrolled patients. A signifi cant diff erence (P <0.001) between mean values of v\u2013a samples was observed for pH (7.41 \ub1 0.05 vs. 7.51 \ub1 0.06), pCO2 (48 \ub1 6 vs. 35 \ub1 7 mmHg), [Na+] (136.3 \ub1 4.0 vs. 135.2 \ub1 4.0 mEq/l), [Cl\u2013] (101.5 \ub1 5.3 vs. 102.8 \ub1 5.2 mEq/l) and therefore SID (39.5 \ub1 4.0 vs. 36.9 \ub1 4.1 mEq/l). pCO2% and SID% signifi cantly correlated (r2 = 0.28, P <0.001). Graphical representation by quartiles of pCO2% is shown in Figure 1. Conclusions As a reduction in SID decreases pH, the observed movement of anions and cations probably limited the alkalinization caused by hypocapnia. In this model, the only source of electrolytes are blood cells (that is, no interstitium and no infl uence of the kidney is present); it is therefore conceivable to consider the observed phenomenon as the contribution of RBC for the compensation of acute hypocapnic alkalosi