Left ventricular outflow tract obstruction-be prepared!

The current trend to treat hypotension in critically ill patients is to place a greater emphasis on inotropic support and less on fluid resuscitation in order to limit the potential harm from fluid overload. This combination may trigger left ventricular outflow tract obstruction (LVOTO) in susceptible patients. Although LVOTO is classically described in patients with hypertrophic cardiomyopathy it has been reported in other conditions including septic shock, apical ballooning syndrome, myocardial infarction, respiratory failure, and post valvular surgery. It is more common in the elderly, females, and in patients with hypertension, diabetes, and chronic vascular disease because of predisposing anatomical conditions such as left ventricular hypertrophy, small left ventricle size, sigmoid septum and alterations in the positions of the aortic and mitral valve annular planes. The onset of LVOTO is largely unpredictable due to a complex interplay between preload, afterload, heart rhythm and rate in susceptible patients. The consequences of missing this treatable condition may lead to life-threatening hypotension refractory to, or exacerbated by, a further increase in inotropic support. Dynamic LVOTO should be considered in any hypotensive intensive care patient. Echocardiography is perhaps the best tool to assess LVOTO and its underlying pathophysiology in the critically ill. Detection of LVOTO is a relatively simple task using a combination of two-dimensional, M-mode and spectral Doppler imaging by an operator alert to the possible diagnosis.

Does left ventricular tissue Doppler peak systolic velocity (Sm) reflect cardiac output in the critically ill?

Cardiac output (CO) is dependent on a number of factors, in particular, the systolic function of the heart. Tissue Doppler (TD) is a modality in echocardiography that measures myocardial velocity and is related to contractility. TD can therefore be used to measure the systolic function of the heart. This study sought to establish whether the systolic component of TD can be used to estimate CO in critically ill patients. Retrospective data was obtained from a total of 80 patients: 29 patients with a normal echocardiogram, and 51 intensive care unit patients; 28 septic and 23 with heart failure. The mean TD peak systolic velocity (Sm) was significantly lower in the heart failure patients (P <0.05) compared to both normal and septic group. The mean CO was significantly higher in septic patients when compared to heart failure patients. A mild to moderate positive correlation was found between Sm and CO in the heart failure group and with all patients combined (r2=0.19, P <0.001). Subsequent analysis of Sm versus stroke volume again showed a mild positive correlation in the heart failure group and combined results (r2=0.18, P <0.001). Sm was weakly correlated to heart rate only in the normal group but not in the combined cohort. Our data confirms a weak to moderate correlation between Sm and CO, probably resulting from a positive correlation of Sm and stroke volume. This correlation is not strong enough to support the use of an individual's Sm to estimate CO in intensive care patients.

[Impact of pandemic H1N1 2009 influenza virus on critical care in Australia: a single centre case series]. / Onemocnení pandemickým chripkovým virem HIN1 2009 vyzadující intenzivní péci: soubor nemocných z jednoho centra v Austrálii.

INTRODUCTION: In late May 2009, an outbreak of the novel swine - influenza A virus (H1N1) was identified in the Southern hemisphere. We describe the clinical and epidemiologic characteristics ofpatients infected with H1N1 requiring intensive care (ICU) admission at a Sydney University Hospital. METHODS: We retrospectively reviewed medical charts and laboratory results ofall patients who tested positively for H1N1 by viral polymerase chain reaction (PCR) on nasopharyngeal smear or endobronchial secretions. RESULTS: From June 1st until August 31st, 2009 a total of 17 patients required admission to the Intensive Care Unit at Nepean Hospital, a tertiary teaching hospital. There were 9 males and 8 females with a mean age of 42 years. The majority of patients were admitted to the ICU within 48 hours of hospital presentation. All patients had flu like symptoms and most presented with respiratory distress and tachycardia. More than half of patients had patchy alveolar infiltrates on chest X ray. Patients who developed acute lung injury and acute respiratory distress syndrome (ALI/ARDS) typically presented with normal leukocyte count, lymphopenia, raised C-reactive protein, creatinkinase, transaminases but normal urea and creatinine. Fourteen patients required intubation while two received non-invasive ventilation. Several patients tested negative for H1N1 on nasopharyngeal smear PCR but tested positive on endobronchial secretions and the rapid flu antigen test proved unreliable. Two patients died during hospital admission but neither from respiratory failure or its consequences. The median duration of intensive care stay was 12 days while hospital stay was 18 days. DISCUSSION: The Nepean Hospital's patient profile and outcomes are similar to the data for all H1N1 associated ICU admission in Australia and New Zealand. H1N1 is capable of causing severe respiratory infection especially in the young to middle aged and the impact on intensive care units is disproportionate to seasonal flu. To reliably test for H1N1 in intubated patients we recommend performing viral PCR on endobronchial secretions.

Endotoxin stimulated interleukin-10 production is enhanced by adenosine. Possible key to septic shock associated immune deficiency?

The aim of this bench study was to investigate whether adenosine influences secretion of interleukin-10 (IL-O) in human whole blood culture stimulated with lipopolysaccharide. Whole blood from healthy human volunteers was mixed ex vivo in 1:1 ratio with RPMI 1640 culture medium and subsequently cultured at 37 degrees C with or without adenosine (total of 120 microM added in four aliquots over two hours) in the presence or absence of 100 ng/ml lipopolysaccharide for four and eight hours, respectively. There was only a minimal IL-10 production after four hours of culture regardless of the experimental conditions. However, lipopolysaccharide stimulated whole blood cultures with added adenosine released large amounts of IL-lO after eight hours. The response was similar whether adenosine was added before (5.99 pg/ml/10(6) leucocytes) or after (10.35 microg/ml/10(6) leucocytes) stimulation with lipopolysaccharide and interindividual variation was present. In conclusion adenosine enhances lipopolysaccharide stimulated IL-10 production in whole human blood and may contribute to the IL-10 mediated immune dysfunction in sepsis.

Increased B-type natriuretic peptide (BNP) level is a strong predictor for cardiac dysfunction in intensive care unit patients.

Patients admitted to an Intensive Care Unit (ICU) frequently have underlying cardiac dysfunction. Early interventions are sometimes difficult to initiate because of diagnostic uncertainty as to whether cardiac failure is present As B-type natriuretic peptide (BNP) has been shown to be increased in cardiac dysfunction, we sought to demonstrate whether BNP can be used as a screening tool for cardiac dysfunction in patients admitted to ICU. All patients admitted to a combined medical and surgical ICU over a four-week period were included in the study. BNP was measured on the point of admission using a hand-held meter. Clinicians were blinded from the measurement when diagnoses were made as to whether or not the patients had clinically significant cardiac dysfunction. Patients with cardiac dysfunction had a significantly higher level of BNP when compared to the non-cardiac dysfunction group: 516 +/- 385 pg/ml (n = 26) v 67 +/- 89 pg/ml (n = 58) (P < 0.0001) A BNP cut-off value at 144 pg/ml exhibited a 92% sensitivity, 86% specificity and 96% negative predictive value. The sensitivity improved to 96% when the analysis was confined to patients > or = 55 years. At this cut-off value, BNP is a strong predictor of cardiac dysfunction. BNP measurement offers a rapid and affordable way to screen for cardiac dysfunction in patients admitted to ICU. An increased BNP level warrants further cardiac investigations so as to implement early interventions for cardiac decompensation in ICU patients.

Arterial and mixed venous xenon blood concentrations in pigs during wash-in of inhalational anaesthesia.

There are no data available on the kinetics of blood concentrations of xenon during the wash-in phase of an inhalation anaesthesia aiming at 1 MAC end-expiratory concentration. Therefore, we anaesthetized eight pigs with continuous propofol and fentanyl and measured arterial, mixed venous and end-expiratory xenon concentrations by gas chromatography-mass spectrometry 1, 2, 3, 4, 5, 7, 10, 15, 20, 30, 60 and 120 min after starting the anaesthetic gas mixture [67% xenon/33% oxygen; 3 litre x min(-1) during the first 10 min, thereafter minimal flow with 0.48 (SD 0.03) litre x min(-1)]. End-expiratory xenon concentrations plateaued (defined as <5% change from the preceding value) at 64 (6) vol% after 7 min, and arterial and mixed venous xenon concentrations after 5 and 15 min respectively. The highest arterio-venous concentration difference occurred after 3 min. Using the Fick principle, we calculated a mean xenon uptake of 3708 (829) and 9977 (3607) ml after 30 and 120 min respectively.

Impact of enteral feeding on gastric tonometry in healthy volunteers and critically ill patients.

BACKGROUND: Enteral feeding may interfere with gastric tonometry measurement. The effect of enteral nutrition on gastric tonometry has not been fully documented. METHODS: Seven healthy volunteers and nine stable intensive care unit (ICU) patients with poor tolerance of gastric feeding were investigated. Consecutive continuous postpyloric and gastric feeding, both at two different rates (40 and 100 ml. h-1, respectively), and an intragastric 200 ml nutrition bolus were studied. Gastric intramucosal PCO2 (PiCO2) was measured by air tonometry and in patients a gastric intramucosal-arterial PCO2 difference (PCO2 gap) was calculated. Hemodynamics and blood gases were also measured. RESULTS: In volunteers, PiCO2 remained stable during the postpyloric phase. During continuous gastric feeding PiCO2 did not change significantly, although in 4 volunteers PiCO2 increased >0.5 kPa. PiCO2 decreased significantly after gastric bolus from 6.9+/-0.4 to 6.1+/-0.5 kPa (P<0.05). Eight patients had an increased PCO2 gap (>1 kPa) at baseline (1.8+/-0.6 kPa). PCO2 gap changes during the whole study were not statistically significant. However, during the postpyloric phase (or immediately afterwards), the PCO2 gap increased by more than 0.5 kPa in 5 patients. After gastric bolus, a decrease in PCO2 gap >0.5 kPa was seen in 5 patients. CONCLUSION: In volunteers, postpyloric feeding does not interfere with gastric tonometry measurement and gastric bolus leads to a PiCO2 decrease. The impact of postpyloric and gastric feeding on gastric tonometry in ICU patients with compromised gut is variable.

Effects of ultrafiltration, dialysis, and temperature on gas exchange during hemodiafiltration: a laboratory experiment.

To study gas exchange in the filter during continuous venovenous hemodiafiltration (CVVHDF), an air-tight heated mixing chamber with adjustable CO2 supply was constructed and connected to a CVVHDF monitor. Bicarbonate-free crystalloid (Part 1) and packed red blood cell (Part 2) solutions were circulated at 150 ml x min(-1). Gas exchange expressed as pre-postfilter difference in CO2 and O2 contents was measured at different CVVHDF settings and temperatures of circulating and dialysis solutions. Ultrafiltration was most efficacious for CO2 removal (at 1,000 ml x h(-1) ultrafiltration CO2 losses reached 13% of prefilter CO2 content). Addition of dialysis (1,000 ml x h(-1)) increased CO2 loss to 17% and at maximal parameters (filtration 3,000 ml x h(-1), dialysis 2,500 ml x h(-1)), the loss of CO2 amounted to 35% of prefilter content. Temperature changes of circulating and/or dialysis fluids had no significant impact on CO2 losses. The O2 exchange during CVVHDF was negligible. Currently used CVVHDF is only marginally effective in CO2 removal. Higher volume ultrafiltration combined with dialysis can be expected to reach clinical significance.

[Acute respiratory distress syndrome]. / Akutní respiracní distress syndrom.

Acute respiratory distress syndrome (ARDS) is the general term used for severe acute respiratory failure of diverse aetiology. It is associated with a high morbidity, mortality (50-70%), and financial costs. Regardless of aetiology, the basic pathogenesis of ARDS is a systemic inflammatory response leading to a diffuse inflammatory process that involves both lungs, thus causing diffuse alveolar and endothelial damage with increased pulmonary capillary permeability and excessive extravascular lung water accumulation. ARDS is commonly associated with sepsis and multiple organ failure. The clinical picture involves progressive hypoxaemia, radiographic evidence of pulmonary oedema, decreased lung compliance and pulmonary hypertension. Despite the scientific and technological progress in critical care medicine, there is no specific ARDS therapy available at the moment and its management remains supportive. Therapeutic goals include resolution of underlying conditions, maintenance of acceptable gas exchange and tissue oxygenation and prevention of iatrogenic lung injury. Many new specific therapeutic strategies have been developed, however, most of them require further scientific evaluation. The paper reviews definition, basic pathogenesis and pathophysiology of ARDS and discusses current concepts of therapeutic possibilities of ARDS.

Continuous venovenous hemodiafiltration (CVVHDF) with citrate anticoagulation in the treatment of a patient with acute renal failure, hypercalcemia, and thrombocytopenia.

A 72-year-old patient with multiple myeloma was admitted to the intensive care unit because of hypercalcemic crisis and acute renal failure. After 7 days of comprehensive therapy including diuretics steroids, calcitonin, and intermittent hemodialysis (IHD) with low-calcium dialysate, calcium still reached high levels between IHD treatments and thrombocytopenia developed after chemotherapy. CVVHDF with calcium-free bicarbonate dialysate was started. Anticoagulation with 2.2% citrate was performed in order to chelate calcium, and thus treat the hypercalcemia, and to provide regional anticoagulation, and thus reduce the risk of bleeding due to thrombocytopenia. CVVHDF with citrate anticoagulation was continued for 6 days, and standard heparin anticoagulation was started when the hypercalcemia and thrombocytopenia abated.