Vasopressin in vasodilatory shock: ensure organ blood flow, but take care of the heart!

Supplementary arginine vasopressin infusion in advanced vasodilatory shock may be accompanied by a decrease in cardiac index and systemic oxygen transport capacity in approximately 40% of patients. While a reduction of cardiac output most frequently occurs in patients with hyperdynamic circulation, it is less often observed in patients with low cardiac index. Infusion of inotropes, such as dobutamine, may be an effective strategy to restore systemic blood flow. However, when administering inotropic drugs, systemic blood flow should be increased to adequately meet systemic demands (assessed by central or mixed venous oxygen saturation) without putting an excessive beta-adrenergic stress on the heart. Overcorrection of cardiac index to hyperdynamic values with inotropes places myocardial oxygen supply at significant risk

The relationship between extravascular lung water and oxygenation in three patients with influenza A (H1N1)-induced respiratory failure

Zusammenfassung: Diese Fallsammlung berichtet über die Korrelation zwischen extravaskulärem Lungenwasser (EVLW) und dem arteriellen Sauerstoffpartialdruck/fraktionierten inspiratorischen Sauerstoffkonzentration (PaO2/FiO2) Quotienten bei drei Patienten mit schwerem Influenza A (H1N1)-induziertem Lungenversagen. Alle Patienten erlitten eine ausgeprägte Hypoxie (PaO2, 26-42 mmHg), mussten mit dem Biphasic Airway Pressure Mode (PEEP, 12-15 mmHg; FiO2, 0,8-1) mechanisch beatmet werden und wurden in 12 stündlichen Intervallen in die Bauchlage gedreht. Alle Patienten waren während 8-11 Tagen mit dem PICCO® System monitorisiert. Während der mechanischen Beatmung wurden ingesamt 62 simultane Bestimmungen des PaO2/FiO2 Quotienten und des EVLW durchgeführt. Es zeigte sich ein signifikanter Zusammenhang zwischen dem EVLW und dem PaO2/FiO2 Quotienten (Spearman-rho Korrelationskoeffizient, -0,852; p < 0,001). Bei allen Patienten war eine Abnahme des EVLW von einer Verbesserung der Oxygenation begleitet. Die Serumkonzentrationen der Laktatdehydrogenase waren bei allen Patienten erhöht und korrelierten signifikant mit dem EVLW während des Intensivaufenthaltes (Spearman-rho Korrelationskoeffizient, 0,786; p < 0,001). Zusammenfassend erscheint es, dass das EVLW bei Patienten mit schwerem H1N1-induziertem Lungenversagen erhöht ist und dabei eng mit Einschränkungen der Oxygenationsfunktion korrelier

Arterial blood pressure during early sepsis and outcome

Objective: To evaluate the association between arterial blood pressure (ABP) during the first 24h and mortality in sepsis. Design: Retrospective cohort study. Setting: Multidisciplinary intensive care unit (ICU). Patients and participants: A total of 274 septic patients. Interventions: None. Measurements and results: Hemodynamic, and laboratory parameters were extracted from a PDMS database. The hourly time integral of ABP drops below clinically relevant systolic arterial pressure (SAP), mean arterial pressure (MAP), and mean perfusion pressure (MPP=MAP−central venous pressure) levels was calculated for the first 24h after ICU admission and compared with 28-day-mortality. Binary and linear regression models (adjusted for SAPS II as a measure of disease severity), and a receiver operating characteristic (ROC) analysis were applied. The areas under the ROC curve were largest for the hourly time integrals of ABP drops below MAP60mmHg (0.779 vs. 0.764 for ABP drops below MAP55mmHg; P≤0.01) and MPP 45mmHg. No association between the hourly time integrals of ABP drops below certain SAP levels and mortality was detected. One or more episodes of MAP<60mmHg increased the risk of death by 2.96 (CI 95%, 1.06-10.36, P=0.04). The area under the ROC curve to predict the need for renal replacement therapy was highest for the hourly time integral of ABP drops below MAP75mmHg. Conclusions: A MAP level≥60mmHg may be as safe as higher MAP levels during the first 24h of ICU therapy in septic patients. A higher MAP may be required to maintain kidney functio

Arteriolar vasoconstrictive response: comparing the effects of arginine vasopressin and norepinephrine

INTRODUCTION: This study was designed to examine differences in the arteriolar vasoconstrictive response between arginine vasopressin (AVP) and norepinephrine (NE) on the microcirculatory level in the hamster window chamber model in unanesthetized, normotonic hamsters using intravital microscopy. It is known from patients with advanced vasodilatory shock that AVP exerts strong additional vasoconstriction when incremental dosage increases of NE have no further effect on mean arterial blood pressure (MAP). METHODS: In a prospective controlled experimental study, eleven awake, male golden Syrian hamsters were instrumented with a viewing window inserted into the dorsal skinfold. NE (2 μg/kg/minute) and AVP (0.0001 IU/kg/minute, equivalent to 4 IU/h in a 70 kg patient) were continuously infused to achieve a similar increase in MAP. According to their position within the arteriolar network, arterioles were grouped into five types: A0 (branch off small artery) to A4 (branch off A3 arteriole). RESULTS: Reduction of arteriolar diameter (NE, -31 ± 12% versus AVP, -49 ± 7%; p = 0.002), cross sectional area (NE, -49 ± 17% versus AVP, -73 ± 7%; p = 0.002), and arteriolar blood flow (NE, -62 ± 13% versus AVP, -80 ± 6%; p = 0.004) in A0 arterioles was significantly more pronounced in AVP animals. There was no difference in red blood cell velocities in A0 arterioles between groups. The reduction of diameter, cross sectional area, red blood cell velocity, and arteriolar blood flow in A1 to A4 arterioles was comparable in AVP and NE animals. CONCLUSION: Within the microvascular network, AVP exerted significantly stronger vasoconstriction on large A0 arterioles than NE under physiological conditions. This observation may partly explain why AVP is such a potent vasopressor hormone and can increase systemic vascular resistance even in advanced vasodilatory shock unresponsive to increases in standard catecholamine therapy

The association between body-mass index and patient outcome in septic shock: a retrospective cohort study

Zusammenfassung: HINTERGRUND: Es bestehen keine Daten über die Assoziation zwischen dem Body Mass Index (BMI) bzw. BMI Kategorien und der Mortalität von septischen Schock-patienten. METHODEN: Die Datenbank einer interdisziplinären Intensivstation wurde retrospektiv nach erwachsenen Patienten mit septischem Schock durchsucht. Von allen Patienten wurde der BMI, demographische, klinische und laborchemische Parameter gemeinsam mit Outcomevariabeln dokumentiert. Die Studienpatienten wurden wie folgt anhand des BMI kategorisiert: BMI 30 kg/m2, Fettleibigkeit. Bivariate und multivariate logistische Regressionsmodelle wurden verwendet, um den Zusammenhang zwischen dem BMI und Outcome-variabeln zu untersuchen. RESULTATE: 301 septische Schockpatienten wurden identifiziert. Der BMI war bivariat mit der Mortalität auf der Intensivstation assoziiert (OR, 0,91; 95% CI, 0,86-0,98; p = 0,007). Es gab keine signifikante Assoziation zwischen dem BMI und der Mortalität auf der Intensivstation. Allerdings waren höhere BMI Werte trendmässig mit einer niedrigeren Intensivstations-mortalität assoziiert (OR, 0,93; 95% CI, 0,86-1,01; p = 0,09). Während übergewichtige (OR, 0,43; 95% CI, 0,19-0,98; p = 0,04) und fettleibige (OR, 0,28; 95% CI, 0,08-0,93; p = 0,04) Patienten ein unabhängig niedrigeres Risiko auf der Intensivstation zu versterben hatten als normalgewichtige Patienten, gab es keinen Unterschied im Sterberisiko zwischen normal- und untergewichtigen Patienten (p = 0,22). Ein hoher BMI war unabhängig mit einer geringen Häufigkeit eines akutem Deliriums (p = 0,04) und einer geringeren Intensivwieder-aufnahmerate (p = 0,001), aber mit mehr Harnwegsinfektionen (p = 0,02) assoziiert. SCHLUSSFOLGERUNG: Bis zu einem BMI von 50 kg/m2 scheint keine Assoziation zwischen BMI und schlechterem Überleben auf der Intensivstation oder im Krankenhaus bei septischen Schockpatienten zu bestehen. Im Gegenteil, hohe BMI Werte könnten sogar das Risiko am septischen Schock zu versterben reduziere

Antifactor Xa activity in critically ill patients receiving antithrombotic prophylaxis with standard dosages of certoparin: a prospective, clinical study

INTRODUCTION: Deep venous thrombosis with subsequent pulmonary embolism or post-thrombotic syndrome is a feared complication in the intensive care unit. Therefore, routine prophylactic anticoagulation is widely recommended. Aside from unfractionated heparin, low molecular weight heparins, such as certoparin, have become increasingly used for prophylactic anticoagulation in critically ill patients. In this prospective study, we evaluated the potency of 3,000 IU certoparin administered once daily to reach antithrombotic antifactor Xa (aFXa) levels of 0.1 to 0.3 IU/ml in 62 critically ill patients. METHODS: AFXa levels were determined 4, 12 and 24 h after injection of certoparin. Prothrombin time, activated partial thromboplastin time, antithrombin, fibrinogen, hemoglobin, platelet count, serum urea and creatinine concentrations were documented before and 12 and 24 h after injection of certoparin. RESULTS: Four hours after certoparin injection (n = 32), 28% of patients were within the antithrombotic aFXa range. After 12 and 24 h, 6% achieved antithrombotic aFXa levels. Because of a severe pulmonary embolism in one study patient, an interim analysis was performed, and the dosage of certoparin was increased to 3,000 IU twice daily. This regime attained recommended antithrombotic aFXa levels in 47%, 27%, 40% and 30% of patients at 4, 12, 16 and 24 h, respectively, after twice daily certoparin injection (n = 30). Antithrombin and fibrinogen concentrations slightly increased during the observation period. Low antithrombin concentrations before certoparin were independently correlated with underdosing of certoparin. Patients with aFXa levels <0.1 IU/ml 4 h after certoparin injection required vasopressors more often and had lower serum concentrations of creatinine and urea than patients with antithrombotic aFXa levels. CONCLUSION: Standard dosages of certoparin of 3,000 IU given once or twice daily are ineffective for attaining the recommended aFXa levels of 0.1 to 0.3 IU/ml in critically ill patients. Low antithrombin levels before certoparin administration were independently associated with low aFXa levels. Renal function and vasopressor therapy may further influence the effectiveness of certoparin in ensuring adequate antithrombotic prophylaxis