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

Influenza A(H1N1) infection and severe cardiac dysfunction in adults: A case series

Zusammenfassung: HINTERGRUND: Während die virale Myokarditis und das Herzversagen anerkannte und gefürchtete Komplikationen einer saisonalen Influenza A Infektion sind, liegen bislang nur wenig Informationen über ein durch das 2009 Influenza A(H1N1) Virus induziertes Herzversagen vor. METHODEN UND HAUPTERGEBNISSE: Diese Fallsammlung fasst den Krankheitsverlauf von vier Patienten mit 2009 Influenza A(H1N1) Infektion zusammen, welche an unserer Klinik im Zeitraum von November 2009 bis September 2010 behandelt wurden. Alle Patienten präsentierten sich mit einer schweren kardialen Funktionsstörung (akutes Herzversagen, kardiogener Schock oder Herzkreislaufstillstand im Rahmen eines Kammerflimmerns) als das führende Symptom einer Influenza A(H1N1) Infektion. Zwei Patienten waren mit hoher Wahrscheinlichkeit kardial vorerkrankt, und drei benötigten eine Katecholamintherapie, um die hämodynamische Funktion zu stabilisieren. Mit Ausnahme eines Patienten der vor der Diagnosestellung der Influenza A(H1N1) Infektion verstarb, wurden alle Patienten mit einer antiviralen Therapie mit Oseltamivir und supportiver Intensivtherapie behandelt. Ein Acute Respiratory Distress Syndrom infolge der Influenza A(H1N1) Infektion trat bei einem Patienten auf. Die Herzfunktion normalisierte sich bei zwei Patienten und war bei einem Patienten noch bei Krankenhausentlassung eingeschränkt. SCHLUSSFOLGERUNG: Eine Influenza A(H1N1) Infektion kann mit einer schweren kardialen Funktionseinschränkung assoziiert sein. Diese kann sich sogar als führendes klinisches Symptom darstellen. Während einer Influenza Pandemie kann eine genaue Anamneseerhebung Grippeähnliche Symptome hervorbringen und sollte auch bei kritisch kranken Patienten mit akutem Herzversagen eine Diagnostik auf H1N1 Infektion veranlasse

Fulminant systemic capillary leak syndrome due to C1 inhibitor deficiency complicating acute dermatomyositis: a case report

INTRODUCTION: Dermatomyositis is a chronic inflammatory disorder characterized by muscular and dermatologic symptoms with variable internal organ involvement. This is the first report on a patient with acute dermatomyositis and fulminant systemic capillary leak syndrome. CASE PRESENTATION: A 69-year-old Caucasian woman with chronic dermatomyositis presented with clinical signs of severe hypovolemic shock and pronounced hemoconcentration (hematocrit, 69%). Her colloid osmotic pressure was 4.6mmHg. Following a bolus dose of prednisolone (500mg), fluid resuscitation was initiated. During volume loading, anasarca and acute respiratory distress rapidly developed. Echocardiography revealed an underfilled, hypokinetic, diastolic dysfunctional left ventricle with pericardial effusion but no signs of tamponade. Despite continued fluid resuscitation and high-dosed catecholamine therapy, the patient died from refractory shock 12 hours after intensive care unit admission. A laboratory analysis of her complement system suggested the presence of C1 inhibitor deficiency as the cause for systemic capillary leakage. The post-mortem examination revealed bilateral pleural, pericardial and peritoneal effusions as well as left ventricular hypertrophy with patchy myocardial fibrosis. Different patterns of endomysial/perimysial lymphocytic infiltrations adjacent to degenerated cardiomyocytes in her myocardium and necrotic muscle fibers in her right psoas major muscle were found in the histological examination. CONCLUSIONS: This case report indicates that acute exacerbation of chronic dermatomyositis can result in a fulminant systemic capillary leak syndrome with intense hemoconcentration, hypovolemic shock and acute heart failure. In the presented patient, the cause for diffuse capillary leakage was most probably acquired angioedema, a condition that has been associated with both lymphoproliferative and autoimmunologic disorders

Hemodynamic variables and mortality in cardiogenic shock: a retrospective cohort study

INTRODUCTION: Despite the key role of hemodynamic goals, there are few data addressing the question as to which hemodynamic variables are associated with outcome or should be targeted in cardiogenic shock patients. The aim of this study was to investigate the association between hemodynamic variables and cardiogenic shock mortality. METHODS: Medical records and the patient data management system of a multidisciplinary intensive care unit (ICU) were reviewed for patients admitted because of cardiogenic shock. In all patients, the hourly variable time integral of hemodynamic variables during the first 24 hours after ICU admission was calculated. If hemodynamic variables were associated with 28-day mortality, the hourly variable time integral of drops below clinically relevant threshold levels was computed. Regression models and receiver operator characteristic analyses were calculated. All statistical models were adjusted for age, admission year, mean catecholamine doses and the Simplified Acute Physiology Score II (excluding hemodynamic counts) in order to account for the influence of age, changes in therapies during the observation period, the severity of cardiovascular failure and the severity of the underlying disease on 28-day mortality. RESULTS: One-hundred and nineteen patients were included. Cardiac index (CI) (P = 0.01) and cardiac power index (CPI) (P = 0.03) were the only hemodynamic variables separately associated with mortality. The hourly time integral of CI drops 0.05). The hourly time integral of CPI drops 0.05). CONCLUSIONS: During the first 24 hours after intensive care unit admission, CI and CPI are the most important hemodynamic variables separately associated with 28-day mortality in patients with cardiogenic shock. A CI of 3 L/min/m2 and a CPI of 0.8 W/m2 were most predictive of 28-day mortality. Since our results must be considered hypothesis-generating, randomized controlled trials are required to evaluate whether targeting these levels as early resuscitation endpoints can improve mortality in cardiogenic shock

Association of arterial blood pressure and vasopressor load with septic shock mortality: a post hoc analysis of a multicenter trial

INTRODUCTION: It is unclear to which level mean arterial blood pressure (MAP) should be increased during septic shock in order to improve outcome. In this study we investigated the association between MAP values of 70 mmHg or higher, vasopressor load, 28-day mortality and disease-related events in septic shock. METHODS: This is a post hoc analysis of data of the control group of a multicenter trial and includes 290 septic shock patients in whom a mean MAP > or = 70 mmHg could be maintained during shock. Demographic and clinical data, MAP, vasopressor requirements during the shock period, disease-related events and 28-day mortality were documented. Logistic regression models adjusted for the geographic region of the study center, age, presence of chronic arterial hypertension, simplified acute physiology score (SAPS) II and the mean vasopressor load during the shock period was calculated to investigate the association between MAP or MAP quartiles > or = 70 mmHg and mortality or the frequency and occurrence of disease-related events. RESULTS: There was no association between MAP or MAP quartiles and mortality or the occurrence of disease-related events. These associations were not influenced by age or pre-existent arterial hypertension (all P > 0.05). The mean vasopressor load was associated with mortality (relative risk (RR), 1.83; confidence interval (CI) 95%, 1.4-2.38; P 70 mmHg by augmenting vasopressor dosages may increase mortality. Future trials are needed to identify the lowest acceptable MAP level to ensure tissue perfusion and avoid unnecessary high catecholamine infusions

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