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This study evaluates the utility of arterial blood gas (ABG) parameters and chest radiography in predicting intubation need in patients with burn injuries with suspected inhalation injury.Patients with suspected inhalation injury admitted to a single centre, Burn Intensive Care Unit, between April 4th 2016 and July 5th 2019, were included. Admission ABG parameters and chest radiograph opacification were compared with whether the patient received an appropriate intubation: defined as intubation for a duration of over 48 h. Area under the receiver operator characteristic curve was calculated (AUROC).Eighty-nine patients were included. The majority (84%; n = 75) were intubated, of which 81% (n = 61) received appropriate intubations. pH had an AUROC of 0.88 and a pH of7.30 had an 80% sensitivity and specificity for detecting appropriate intubation. P/F ratio had an AUROC of 0.81 and a P/F ratio of40 had a 70% sensitivity and specificity for appropriate intubation. Chest radiograph opacification had poor utility in this regard (AUROC = 0.69). Adding pH and P/F ratio to the ABA criteria improved their sensitivity in detecting appropriate intubations (sensitivity: ABA + pH + P/F = 0.97 vs ABA = 0.86; p = 0.013), without altering their specificity.In patients suspected inhalation injury, pH and P/F ratio were good predictors for appropriate intubations. Incorporating the parameters into the ABA criteria improved their clinical utility.

It is unclear whether the association between vasopressor dose and mortality is affected by duration of administration. We examined whether prognostication in septic shock is feasible through the use of daily median vasopressor doses. We undertook a single-centre retrospective cohort study. We included patients with a diagnosis of septic shock admitted to the intensive care unit at Queen Elizabeth Hospital, Birmingham, UK, between April 2016 and July 2019. The primary outcome measure was 90-day mortality. We defined vasopressor dose as the median norepinephrine equivalent dose (equivalent infusion rates of all vasopressors and inotropes) recorded for each day, for the first four days of septic shock. We divided patients into groups by vasopressor dose quintiles and calculated their 90-day mortality rate. We examined area under the receiver operator characteristic curves for prognostic ability. In total, 844 patients were admitted with septic shock and had a 90-day mortality of 43% (n = 358). Over the first four days, median vasopressor dose decreased in 93% of survivors and increased in 56% of non-survivors. The mortality rate associated with a given vasopressor dose quintile increased on sequential days of septic shock. The area under the receiver operator characteristic curves of daily median vasopressor dose against mortality increased from day 1 to day 4 (0.67 vs. 0.86, p 0.05 μg.kg-1 .min-1 had an 80% sensitivity and specificity for mortality. The prognostic utility of vasopressor dose improved considerably with shock duration. Prolonged administration of small vasopressor doses was associated with a high attributable mortality.

The risk of upper gastrointestinal bleeding (UGIB) after transesophageal echocardiography (TEE) in patients with high grade esophageal varices (EV) that are undergoing Orthotopic Liver transplantation (OLT) is poorly understood. This was a retrospective single-centre cohort study in all patients that underwent OLT at Queen Elizabeth Hospital Birmingham between September 2016 and September 2018. The primary outcome was to determine the incidence of UGIB in patients that have undergone OLT with EV that received TEE. 401 patients were included in the study, of which 320 (80%) received TEE. The incidence of post-operative UGIB in patients that received TEE was 1.6% (5/320) in the entire cohort: 2.7% (4/149) in patients with no evidence of EV and 0.6% (1/171) in patients with EV. UGIB occurred in 1 patient with grade 2 EV and did not occur in patients with grade 1 or 3 EV. The incidence of UGIB in patients that received TEE was not statistically different to patients that did not: 1.6% (5/320) vs. 3.7% (3/81) p = 0.218. In conclusion, in patients that underwent OLT, intra-operative TEE use was associated with low rates of UGIB, even in cohorts with high grade EV. This suggests that TEE is a relatively safe method of haemodynamic monitoring in patients undergoing OLT.

Acute respiratory distress syndrome (ARDS) is a highly heterogeneous clinical condition. Shock is a poor prognostic sign in ARDS, and heterogeneity in its pathophysiology may be a barrier to its effective treatment. Although right ventricular dysfunction is commonly implicated, there is no consensus definition for its diagnosis, and left ventricular function is neglected. There is a need to identify the homogenous subgroups within ARDS, that have a similar pathobiology, which can then be treated with targeted therapies. Haemodynamic clustering analyses in patients with ARDS have identified two subphenotypes of increasingly severe right ventricular injury, and a further subphenotype of hyperdynamic left ventricular function. In this review, we discuss how phenotyping the cardiovascular system in ARDS may align with haemodynamic pathophysiology, can aid in optimally defining right ventricular dysfunction and can identify tailored therapeutic targets for shock in ARDS. Additionally, clustering analyses of inflammatory, clinical and radiographic data describe other subphenotypes in ARDS. We detail the potential overlap between these and the cardiovascular phenotypes.

OBJECTIVES To evaluate the cause and prognosis of hyperdynamic left ventricular ejection fraction in critically ill patients with sepsis. DESIGN Retrospective, single-center cohort study. SETTING University Hospital ICU, Birmingham, United Kingdom. PATIENTS ICU patients who received a transthoracic echocardiogram within 7 days of sepsis between April 2016 and December 2019. INTERVENTION None. MEASUREMENTS AND MAIN RESULTS The 90-day mortality rates of normal (55-70%), depressed ( 70%) were compared. Multivariate logistic regression analysis was performed to determine the association of left ventricular ejection fraction phenotypes with mortality and the association of clinical variables with left ventricular ejection fraction phenotypes. One-thousand fourteen patients met inclusion criteria and were 62 years old (interquartile range, 47-72), with mostly respiratory infections (n = 557; 54.9%). Ninety-day mortality was 32.1% (n = 325). Patients with hyperdynamic left ventricular ejection fraction had a higher mortality than depressed and normal left ventricular ejection fraction cohorts (58.9% [n = 103] vs 34.0% [n = 55] vs 24.7% [n = 167]; p < 0.0001, respectively). After multivariate logistic regression, hyperdynamic left ventricular ejection fraction was independently associated with mortality (odds ratio, 3.90 [2.09-7.40]), whereas depressed left ventricular ejection fraction did not (odds ratio, 0.62 [0.28-1.37]). Systemic vascular resistance was inversely associated with hyperdynamic left ventricular ejection fraction (odds ratio, 0.79 [0.58-0.95]), and age, frailty, and ischemic heart disease were associated with depressed left ventricular ejection fraction. CONCLUSIONS Hyperdynamic left ventricular ejection fraction was associated with mortality in septic ICU patients and may reflect unmitigated vasoplegia from sepsis. Depressed left ventricular ejection fraction was not associated with mortality but was associated with cardiovascular disease.

Supplemental Digital Content is available in the text., OBJECTIVES: To assess whether right ventricular dilation or systolic impairment is associated with mortality and/or disease severity in invasively ventilated patients with coronavirus disease 2019 acute respiratory distress syndrome. DESIGN: Retrospective cohort study. SETTING: Single-center U.K. ICU. PATIENTS: Patients with coronavirus disease 2019 acute respiratory distress syndrome undergoing invasive mechanical ventilation that received a transthoracic echocardiogram between March and December 2020. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: Right ventricular dilation was defined as right ventricular:left ventricular end-diastolic area greater than 0.6, right ventricular systolic impairment as fractional area change less than 35%, or tricuspid annular plane systolic excursion less than 17 mm. One hundred seventy-two patients were included, 59 years old (interquartile range, 49–67), with mostly moderate acute respiratory distress syndrome (n = 101; 59%). Ninety-day mortality was 41% (n = 70): 49% in patients with right ventricular dilation, 53% in right ventricular systolic impairment, and 72% in right ventricular dilation with systolic impairment. The right ventricular dilation with systolic impairment phenotype was independently associated with mortality (odds ratio, 3.11 [95% CI, 1.15–7.60]), but either disease state alone was not. Right ventricular fractional area change correlated with Pao2:Fio2 ratio, Paco2, chest radiograph opacification, and dynamic compliance, whereas right ventricular:left ventricle end-diastolic area correlated negatively with urine output. CONCLUSIONS: Right ventricular systolic impairment correlated with pulmonary pathophysiology, whereas right ventricular dilation correlated with renal dysfunction. Right ventricular dilation with systolic impairment was the only right ventricular phenotype that was independently associated with mortality.

IntroductionAcute respiratory distress syndrome (ARDS) is the major cause of mortality in patients with SARS-CoV-2 pneumonia. It appears that development of ‘cytokine storm’ in patients with SARS-CoV-2 pneumonia precipitates progression to ARDS. However, severity scores on admission do not predict severity or mortality in patients with SARS-CoV-2 pneumonia. Our objective was to determine whether patients with SARS-CoV-2 ARDS are clinically distinct, therefore requiring alternative management strategies, compared with other patients with ARDS. We report a single-centre retrospective study comparing the characteristics and outcomes of patients with ARDS with and without SARS-CoV-2.MethodsTwo intensive care unit (ICU) cohorts of patients at the Queen Elizabeth Hospital Birmingham were analysed: SARS-CoV-2 patients admitted between 11 March and 21 April 2020 and all patients with community-acquired pneumonia (CAP) from bacterial or viral infection who developed ARDS between 1 January 2017 and 1 November 2019. All data were routinely collected on the hospital’s electronic patient records.ResultsA greater proportion of SARS-CoV-2 patients were from an Asian ethnic group (p=0.002). SARS-CoV-2 patients had lower circulating leucocytes, neutrophils and monocytes (pDiscussionThe clinical syndromes and respiratory mechanics of SARS-CoV-2 and CAP-ARDS are broadly similar. However, SARS-CoV-2 patients initially have a lower requirement for vasopressor support, fewer circulating leukocytes and require prolonged ventilation support. Further studies are required to determine whether the dysregulated inflammation observed in SARS-CoV-2 ARDS may contribute to the increased duration of respiratory failure.

ARDS is the major cause of mortality in patients with SARS-CoV-2 pneumonia. We report a single-centre study comparing the characteristics of ARDS patients with and without SARS-CoV-2. A greater proportion of SARS-CoV-2 patients were from an Asian ethnic group (p=0.002). SARS-CoV-2 patients had lower circulating leukocytes, neutrophils and monocytes (p

This study compares the ability of liberal vs restrictive intubation criteria to detect prolonged intubation and inhalation injury in burn patients with suspected inhalation injury. Emerging evidence suggests that using liberal criteria may lead to unnecessary intubation in some patients. A single-center retrospective cohort study was conducted in adult patients with suspected inhalation injury admitted to intensive care at Queen Elizabeth Hospital, Birmingham between April 2016 and July 2019. Liberal intubation criteria, as reflected in local guidelines, were compared to restrictive intubation criteria, as outlined in the American Burn Association guidelines. The number of patients displaying positive characteristics from either guideline was compared to the number of patients who had prolonged intubation (more than 48 hours) and inhalation injury. In detecting a need for prolonged intubation (n = 85), the liberal criteria had greater sensitivity (liberal = 0.98 [0.94–1.00] vs restrictive = 0.84 [0.75–0.93]; P = .013). However, the restrictive criteria had greater specificity (restrictive = 0.96 [0.89–1.00] vs liberal = 0.48 [0.29–0.67]; P < .001). In detecting inhalation injury (n = 72), the restrictive criteria were equally sensitive (restrictive = 0.94 [0.87–1.00] vs liberal = 0.98 [0.84–1.00]; P = .48) and had greater specificity (restrictive = 0.86 [0.72–1.00] vs liberal = 0.04 [0.00–0.13]; P < .001). In patients who met liberal but not restrictive criteria, 65% were extubated within 48 hours and 90% did not have inhalation injury. Liberal intubation criteria were more sensitive at detecting a need for prolonged intubation, while restrictive criteria were more specific. Most patients intubated based on liberal criteria alone were extubated within 48 hours. Restrictive criteria were highly sensitive and specific at detecting inhalation injury.

Key points Animal studies suggest an anti‐fibrillatory action of the vagus nerve on the ventricle, although the exact mechanism is controversial.Using a Langendorff perfused rat heart, we show that the acetylcholine analogue carbamylcholine raises ventricular fibrillation threshold (VFT) and flattens the electrical restitution curve.The anti‐fibrillatory action of carbamylcholine was prevented by the nicotinic receptor antagonist mecamylamine, inhibitors of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by the nitric oxide (NO) donor sodium nitroprusside.Carbamylcholine increased NO metabolite content in the coronary effluent and this was prevented by mecamylamine.The anti‐fibrillatory action of both carbamylcholine and sodium nitroprusside was ultimately dependent on muscarinic receptor stimulation as all effects were blocked by atropine.These data demonstrate a protective effect of carbamylcholine on VFT that depends upon both muscarinic and nicotinic receptor stimulation, where the generation of NO is likely to be via a neuronal nNOS–sGC dependent pathway. Abstract Implantable cardiac vagal nerve stimulators are a promising treatment for ventricular arrhythmia in patients with heart failure. Animal studies suggest the anti‐fibrillatory effect may be nitric oxide (NO) dependent, although the exact site of action is controversial. We investigated whether a stable analogue of acetylcholine could raise ventricular fibrillation threshold (VFT), and whether this was dependent on NO generation and/or muscarinic/nicotinic receptor stimulation. VFT was determined in Langendorff perfused rat hearts by burst pacing until sustained VF was induced. Carbamylcholine (CCh, 200 nmol l–1, n = 9) significantly (P, Key points Animal studies suggest an anti‐fibrillatory action of the vagus nerve on the ventricle, although the exact mechanism is controversial.Using a Langendorff perfused rat heart, we show that the acetylcholine analogue carbamylcholine raises ventricular fibrillation threshold (VFT) and flattens the electrical restitution curve.The anti‐fibrillatory action of carbamylcholine was prevented by the nicotinic receptor antagonist mecamylamine, inhibitors of neuronal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by the nitric oxide (NO) donor sodium nitroprusside.Carbamylcholine increased NO metabolite content in the coronary effluent and this was prevented by mecamylamine.The anti‐fibrillatory action of both carbamylcholine and sodium nitroprusside was ultimately dependent on muscarinic receptor stimulation as all effects were blocked by atropine.These data demonstrate a protective effect of carbamylcholine on VFT that depends upon both muscarinic and nicotinic receptor stimulation, where the generation of NO is likely to be via a neuronal nNOS–sGC dependent pathway.