Stefan Bloechlinger

Haemodynamic variables and functional outcome in hypothermic patients following out-of-hospital cardiac arrest

AIM OF THE STUDY To evaluate the association between haemodynamic variables during the first 24h after intensive care unit (ICU) admission and neurological outcome in out-of-hospital cardiac arrest (OHCA) victims undergoing therapeutic hypothermia. METHODS In a multi-disciplinary ICU, records were reviewed for comatose OHCA patients undergoing therapeutic hypothermia. The hourly variable time integral of haemodynamic variables during the first 24h after admission was calculated. Neurologic outcome was assessed at day 28 and graded as favourable or adverse based on the Cerebral Performance Category of 1-2 and 3-5. Bi- and multivariate regression models adjusted for confounding variables were used to evaluate the association between haemodynamic variables and functional outcome. RESULTS 67/134 patients (50%) were classified as having favourable outcome. Patients with adverse outcome had a higher mean heart rate (73 [62-86] vs. 66 [60-78]bpm; p=0.04) and received noradrenaline more frequently (n=17 [25.4%] vs. n=9 [6%]; p=0.02) and at a higher dosage (128 [56-1004] vs. 13 [2-162] μgh(-1); p=0.03) than patients with favourable outcome. The mean perfusion pressure (mean arterial blood pressure minus central venous blood pressure) (OR=1.001, 95% CI =1-1.003; p=0.04) and cardiac index time integral (OR=1.055, 95% CI=1.003-1.109; p=0.04) were independently associated with adverse outcome at day 28. CONCLUSION Mean perfusion pressure and cardiac index during the first 24h after ICU admission were weakly associated with neurological outcome in an OHCA population undergoing therapeutic hypothermia. Further studies need to elucidate whether norepinephrine-induced increases in perfusion pressure and cardiac index may contribute to adverse neurologic outcome following OHCA.

Dysfunction of respiratory muscles in critically ill patients on the intensive care unit.

Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed ‘ventilator‐induced diaphragmatic dysfunction’ (VIDD) and should be distinguished from peripheral muscular weakness as observed in ‘ICU‐acquired weakness (ICU‐AW)’.

Left ventricular rotation: a neglected aspect of the cardiac cycle

PurposeTo describe the mechanics and possible clinical importance of left ventricular (LV) rotation, exemplify techniques to quantify LV rotation and illustrate the temporal relationship of cardiac pressures, electrocardiogram and LV rotation.Materials and methodsReview of the literature combined with selected examples of echocardiographic measurements.ResultsRotation of the left ventricle around its longitudinal axis is an important but thus far neglected aspect of the cardiac cycle. LV rotation during systole maximizes intracavitary pressures, increases stroke volume, and minimizes myocardial oxygen demand. Shearing and restoring forces accumulated during systolic twisting are released during early diastole and result in diastolic LV untwisting or recoil promoting early LV filling. LV twist and untwist are disturbed in a number of cardiac diseases and can be influenced by several therapeutic interventions by altering preload, afterload, contractility, heart rate, and/or sympathetic tone.ConclusionsThe concept of LV twisting and untwisting closely linking LV systolic and diastolic function may carry potential diagnostic and therapeutic importance for the management of critically ill patients. Future clinical studies need to address the feasibility of assessing LV twist and untwist as well as the relevance of its therapeutic modulation in critically ill patients.

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

ZusammenfassungHINTERGRUND: 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 veranlassen.SummaryBACKGROUND: While viral myocarditis and heart failure are recognized and feared complications of seasonal influenza A infection, only limited information is available for 2009 influenza A(H1N1)-induced heart failure. METHODS AND MAIN FINDINGS: This case series summarizes the disease course of four patients with 2009 influenza A(H1N1) infection who were treated at our institution from November 2009 until September 2010. All patients presented with severe cardiac dysfunction (acute heart failure, cardiogenic shock or cardiac arrest due to ventricular fibrillation) as the leading symptom of influenza A(H1N1) infection. Two patients most likely had pre-existent cardiac pathologies, and three required catecholamine therapy to maintain hemodynamic function. Except for one patient who died before influenza A(H1N1) infection had been diagnosed, all patients received antiviral therapy with oseltamivir and supportive critical care. Acute respiratory distress syndrome due to influenza A(H1N1) infection developed in one patient. Heart function normalized in two of the three surviving patients but remained impaired in the other one at hospital discharge. CONCLUSIONS: Influenza A(H1N1) infection may be associated with severe cardiac dysfunction which can even be the leading clinical symptom at presentation. During an influenza pandemic, a thorough history may reveal flu-like symptoms and should indicate testing for H1N1 infection also in critically ill patients with acute heart failure.

Effect of PEEP, blood volume, and inspiratory hold maneuvers on venous return.

According to Guytons model of circulation, mean systemic filling pressure (MSFP), right atrial pressure (RAP), and resistance to venous return (RVR) determine venous return. MSFP has been estimated from inspiratory hold-induced changes in RAP and blood flow. We studied the effect of positive end-expiratory pressure (PEEP) and blood volume on venous return and MSFP in pigs. MSFP was measured by balloon occlusion of the right atrium (MSFPRAO), and the MSFP obtained via extrapolation of pressure-flow relationships with airway occlusion (MSFPinsp_hold) was extrapolated from RAP/pulmonary artery flow (QPA) relationships during inspiratory holds at PEEP 5 and 10 cmH2O, after bleeding, and in hypervolemia. MSFPRAO increased with PEEP [PEEP 5, 12.9 (SD 2.5) mmHg; PEEP 10, 14.0 (SD 2.6) mmHg, P = 0.002] without change in QPA [2.75 (SD 0.43) vs. 2.56 (SD 0.45) l/min, P = 0.094]. MSFPRAO decreased after bleeding and increased in hypervolemia [10.8 (SD 2.2) and 16.4 (SD 3.0) mmHg, respectively, P < 0.001], with parallel changes in QPA Neither PEEP nor volume state altered RVR (P = 0.489). MSFPinsp_hold overestimated MSFPRAO [16.5 (SD 5.8) vs. 13.6 (SD 3.2) mmHg, P = 0.001; mean difference 3.0 (SD 5.1) mmHg]. Inspiratory holds shifted the RAP/QPA relationship rightward in euvolemia because inferior vena cava flow (QIVC) recovered early after an inspiratory hold nadir. The QIVC nadir was lowest after bleeding [36% (SD 24%) of preinspiratory hold at 15 cmH2O inspiratory pressure], and the QIVC recovery was most complete at the lowest inspiratory pressures independent of volume state [range from 80% (SD 7%) after bleeding to 103% (SD 8%) at PEEP 10 cmH2O of QIVC before inspiratory hold]. The QIVC recovery thus defends venous return, possibly via hepatosplanchnic vascular waterfall.

Preprocedural High-Sensitivity Cardiac Troponin T and Clinical Outcomes in Patients With Stable Coronary Artery Disease Undergoing Elective Percutaneous Coronary Intervention

Background—Cardiac troponin detected by new-generation, highly sensitive assays predicts clinical outcomes among patients with stable coronary artery disease (SCAD) treated medically. The prognostic value of baseline high-sensitivity cardiac troponin T (hs-cTnT) elevation in SCAD patients undergoing elective percutaneous coronary interventions is not well established. This study assessed the association of preprocedural levels of hs-cTnT with 1-year clinical outcomes among SCAD patients undergoing percutaneous coronary intervention. Methods and Results—Between 2010 and 2014, 6974 consecutive patients were prospectively enrolled in the Bern Percutaneous Coronary Interventions Registry. Among patients with SCAD (n=2029), 527 (26%) had elevated preprocedural hs-cTnT above the upper reference limit of 14 ng/L. The primary end point, mortality within 1 year, occurred in 20 patients (1.4%) with normal hs-cTnT versus 39 patients (7.7%) with elevated baseline hs-cTnT (P<0.001). Patients with elevated hs-cTnT had increased risks of all-cause (hazard ratio 5.73; 95% confidence intervals 3.34–9.83; P<0.001) and cardiac mortality (hazard ratio 4.68; 95% confidence interval 2.12–10.31; P<0.001). Preprocedural hs-TnT elevation remained an independent predictor of 1-year mortality after adjustment for relevant risk factors, including age, sex, and renal failure (adjusted hazard ratio 2.08; 95% confidence interval 1.10–3.92; P=0.024). A graded mortality risk was observed across higher tertiles of elevated preprocedural hs-cTnT, but not among patients with hs-cTnT below the upper reference limit. Conclusions—Preprocedural elevation of hs-cTnT is observed in one fourth of SCAD patients undergoing elective percutaneous coronary intervention. Increased levels of preprocedural hs-cTnT are proportionally related to the risk of death and emerged as independent predictors of all-cause mortality within 1 year. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCT02241291.

Heart–lung interactions during neurally adjusted ventilatory assist

IntroductionAssist in unison to the patient’s inspiratory neural effort and feedback-controlled limitation of lung distension with neurally adjusted ventilatory assist (NAVA) may reduce the negative effects of mechanical ventilation on right ventricular function.MethodsHeart–lung interaction was evaluated in 10 intubated patients with impaired cardiac function using esophageal balloons, pulmonary artery catheters and echocardiography. Adequate NAVA level identified by a titration procedure to breathing pattern (NAVAal), 50% NAVAal, and 200% NAVAal and adequate pressure support (PSVal, defined clinically), 50% PSVal, and 150% PSVal were implemented at constant positive end-expiratory pressure for 20 minutes each.ResultsNAVAal was 3.1 ± 1.1cmH2O/μV and PSVal was 17 ± 2 cmH20. For all NAVA levels negative esophageal pressure deflections were observed during inspiration whereas this pattern was reversed during PSVal and PSVhigh. As compared to expiration, inspiratory right ventricular outflow tract velocity time integral (surrogating stroke volume) was 103 ± 4%, 109 ± 5%, and 100 ± 4% for NAVAlow, NAVAal, and NAVAhigh and 101 ± 3%, 89 ± 6%, and 83 ± 9% for PSVlow, PSVal, and PSVhigh, respectively (p < 0.001 level-mode interaction, ANOVA). Right ventricular systolic isovolumetric pressure increased from 11.0 ± 4.6 mmHg at PSVlow to 14.0 ± 4.6 mmHg at PSVhigh but remained unchanged (11.5 ± 4.7 mmHg (NAVAlow) and 10.8 ± 4.2 mmHg (NAVAhigh), level-mode interaction p = 0.005). Both indicate progressive right ventricular outflow impedance with increasing pressure support ventilation (PSV), but no change with increasing NAVA level.ConclusionsRight ventricular performance is less impaired during NAVA compared to PSV as used in this study. Proposed mechanisms are preservation of cyclic intrathoracic pressure changes characteristic of spontaneous breathing and limitation of right-ventricular outflow impedance during inspiration, regardless of the NAVA level.Trial registrationClinicaltrials.gov Identifier: NCT00647361, registered 19 March 2008

Left Ventricular Torsion Abnormalities in Septic Shock and Corrective Effect of Volume Loading: A Pilot Study

BACKGROUND Ventricular torsion is an important component of cardiac function. The effect of septic shock on left ventricular torsion is not known. Because torsion is influenced by changes in preload, we compared the effect of fluid loading on left ventricular torsion in septic shock with the response in matched healthy control subjects. METHODS We assessed left ventricular torsion parameters using transthoracic echocardiography in 11 patients during early septic shock and in 11 age- and sex-matched healthy volunteers before and after rapid volume loading with 250 mL of a Ringers lactate solution. RESULTS Peak torsion and peak apical rotation were reduced in septic shock (10.2 ± 5.2° and 5.6 ± 5.4°) compared with healthy volunteers (16.3 ± 4.5° and 9.6 ± 1.5°; P = 0.009 and P = 0.006 respectively). Basal rotation was delayed and diastolic untwisting velocity reached its maximum later during diastole in septic shock patients than in healthy volunteers (104 ± 16% vs 111 ± 14% and 13 ± 5% vs 21 ± 10%; P = 0.03 and P = 0.034, respectively). Fluid challenge increased peak torsion in both groups (septic shock, 10.2 ± 5.3° vs 12.6 ± 3.9°; healthy volunteers, 16.3 ± 4.5° vs 18.1 ± 6°; P = 0.01). Fluid challenge increased left ventricular stroke volume in septic shock patients (P = 0.003). CONCLUSIONS Compared with healthy volunteers, left ventricular torsion is impaired in septic shock patients. Fluid loading attenuates torsion abnormalities in parallel with increasing stroke volume. Reduced torsional motion might constitute a relevant component of septic cardiomyopathy, a notion that merits further testing in larger populations.

Unusual cause of myocardial infarction and congestive heart failure in a patient with prosthetic valve endocarditis

In a patient with staphylococcus lugdunensis prosthetic aortic valve endocarditis and coronary septic embolism accompanied by antero‐lateral myocardial infarction, embolic material was successfully aspirated from the bifurcation of the left anterior descending coronary artery and the first diagonal branch. A good angiographic result was documented six months thereafter when the patient presented with a second complication, pulsatile compression of the left main coronary artery by an abscess cavity originating between the aortic and mitral annulus, leading to congestive heart failure. The patient underwent successful surgical replacement of the aortic valve prosthesis with concomitant patch reconstruction of the annulus as well as tricuspid annuloplasty.

Baseline serum bicarbonate levels independently predict short-term mortality in critically ill patients with ischaemic cardiogenic shock

Background: Cardiogenic shock is a feared complication of acute myocardial infarction with high mortality rates. Data on the predictive role of acid base dysregulation in this clinical setting are sparse. We therefore embarked on investigating the predictive role of serum bicarbonate in critically ill intensive care unit (ICU) patients with cardiogenic shock. Methods: A total of 165 ischaemic cardiogenic shock patients (118 men, aged 68.4 years (interquartile range 59.0–77.4), APACHE II score 26.0 (interquartile range 21.0–29.0), after percutaneous coronary intervention were included in a single-centre analysis. Percutaneous coronary intervention-related data such as left ventricular ejection fraction and laboratory indices were recorded and routine clinical follow-up was obtained at hospital discharge and at one year. All-cause mortality was assessed and data were analysed using univariate and multivariate models. Results: All-cause mortality was highest (17%) during the first 48 hours following ICU admission (28-day mortality rate 43%). In a multiple regression model, age (hazard ratio (HR) 1.035, 95% confidence interval (CI) 1.011–1.059, P=0.004), APACHE II score (HR 1.036, 95% CI 1.002–1.072, P=0.037) and baseline serum bicarbonate levels (HR 0.93, 95% CI 0.866–0.998, P=0.046) independently predicted 28-day mortality (overall model fit χ2 22.9, P<0.0001). The HR for patients in the lowest baseline serum bicarbonate tertile for 365-day mortality was HR 2.06 (95% CI 1.20–3.53). Conclusions: In a large cohort of consecutive cardiogenic shock patients hospitalised in the ICU, low serum bicarbonate levels at admission independently predicted mortality. Given the widespread availability of blood gas analysers in ICUs, we propose baseline serum bicarbonate levels as an additional biomarker for identification and stratification of cardiogenic shock patients at risk.