Sepsis Guidelines Backlash

Why it  takes so long for common sense to set in is sometimes mind boggling.


2018 Update to Surviving Sepsis Guidelines: Cue Backlash

Tidal Volumes in non-ARDS

Completely suspected these results . Extending low tidal volume strategy in non-  ARDS population had no rational. A positive finding in one population , suddenly becomes a " general standard ".
Hanging on to certain ICU metrics is like staring in black hole.

Jama Network 2018

https://drive.google.com/file/d/1UJnOs5qus7qJyScgWiLIx_GJWKH1TFIJ/view?usp=drivesdk

Automated Impella Controller (AIC) Interpretation in the ICU

How to Interpret the Automated Impella® Controller

Vin Barry, Director of Product Development at Abiomed joins Dr. George Vetrovec to discuss how physicians should interpret the Automated Impella Controller (AIC) while making rounds. The AIC algorithm includes:

1. Alarm Window
2. Catheter Model
3. Performance Level
4. Mean Flow
5. Placement Signal Waveform
6. Motor Current Waveform

Additionally, Vin Barry  presents a case-based example of AIC management. Watch the video to learn how you can approach the AIC and successfully manage patients on Impella® heart pump support.

Subscribe or join the conversation by following  Twitter: @ProtectedPCI

AIC-041-17

To learn more about the Impella® platform of heart pumps, including important risk and safety information associated with the use of the devices,  visit: www.protectedpci.com/indications-use-safety-information/

VT storm Treatment

Chatzidou et al. prospectively randomized 60 patients with implantable cardioverter-defibrillators (ICDs) and electrical storm (ES) in a 1:1, double-blind design to therapy with propranolol (40 mg orally every 6 h) versus metoprolol (50 mg orally every 6 h). Secondary causes for the index presentation were excluded and all subjects received amiodarone. The authors found that patients treated with propranolol had a shorter length of stay with significantly reduced arrhythmic burden and ICD discharges at 48 h. The results clearly indicate that propranolol is a better antiarrhythmic drug than metoprolol for acute treatment of ES in those patients who have already received amiodarone.

As to why propranolol (a nonselective β-blocker) is more effective than metoprolol (a selective β1-blocker), the authors pointed to the down-regulation of β1 and up-regulation of β2 receptors in heart failure β2 receptor activation induces hypokalemia, and increases QT interval and dispersion of repolarization in the ventricular myocardium . Na-K pump inhibition by even moderate hypokalemia plays a critical role in promoting early afterdepolarization (EAD)–mediated arrhythmias by inducing a positive feedback cycle, activating Ca/calmodulin-dependent protein kinase II and enhancing late
INa . Therefore, the β2-blocking effects of propranolol in heart failure could be antiarrhythmic by preventing epinephrine-induced hypokalemia.

Could something else help explain the results of the study? Propranolol was first synthesized over a half century ago and helped win the Nobel Prize for Sir James Black . Because of the focus on its β-blocking effects, its other actions are often not appreciated. Propranolol (but not metoprolol) blocks both the peak and the late (persistent) INa, flattens the APD restitution curve, and decreases the number of activation fronts during VF . Reduced INa could also reduce Ca overload, which may reduce the IKAS thus helping to suppress recurrent VT or VF. However, INablock occurs at higher propranolol drug concentrations than are required for beta-adrenergic antagonist. Because propranolol plasma concentrations were not measured in the present study, whether INa blocking effects contributed to the results remains unclear.
Propranolol, the most lipophilic beta blocker, can easily cross the lipid cell and blood-brain barrier and may cause seizures in overdose cases. Sodium channel blocking beta blockers are said to possess “membrane stabilizing activity” which potentiates toxicity in overdose.

Propranolol Versus Metoprolol for Treatment of Electrical Storm in Patients With Implantable Cardioverter-Defibrillator

Albumin in Sepsis

Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial

Summary

Background

Acute acidaemia is frequently observed during critical illness. Sodium bicarbonate infusion for the treatment of severe metabolic acidaemia is a possible treatment option but remains controversial, as no studies to date have examined its effect on clinical outcomes. Therefore, we aimed to evaluate whether sodium bicarbonate infusion would improve these outcomes in critically ill patients.

Methods

We did a multicentre, open-label, randomised controlled, phase 3 trial. Local investigators screened eligible patients from 26 intensive care units (ICUs) in France. We included adult patients (aged ≥18 years) who were admitted within 48 h to the ICU with severe acidaemia (pH ≤7·20, PaCO2 ≤45 mm Hg, and sodium bicarbonate concentration ≤20 mmol/L) and with a total Sequential Organ Failure Assessment score of 4 or more or an arterial lactate concentration of 2 mmol/L or more. We randomly assigned patients (1:1), by stratified randomisation with minimisation via a restricted web platform, to receive either no sodium bicarbonate (control group) or 4·2% of intravenous sodium bicarbonate infusion (bicarbonate group) to maintain the arterial pH above 7·30. Our protocol recommended that the volume of each infusion should be within the range of 125–250 mL in 30 min, with a maximum of 1000 mL within 24 h after inclusion. Randomisation criteria were stratified among three prespecified strata: age, sepsis status, and the Acute Kidney Injury Network (AKIN) score. The primary outcome was a composite of death from any cause by day 28 and the presence of at least one organ failure at day 7. All analyses were done on data from the intention-to-treat population, which included all patients who underwent randomisation. This study is registered with ClinicalTrials.gov, number NCT02476253.

Findings

Between May 5, 2015, and May 7, 2017, we enrolled 389 patients into the intention-to-treat analysis in the overall population (194 in the control group and 195 in the bicarbonate group). The primary outcome occurred in 138 (71%) of 194 patients in the control group and 128 (66%) of 195 in the bicarbonate group (absolute difference estimate −5·5%, 95% CI −15·2 to 4·2; p=0·24). The Kaplan-Meier method estimate of the probability of survival at day 28 between the control group and bicarbonate group was not significant (46% [95% CI 40–54] vs 55% [49–63]; p=0·09. In the prespecified AKIN stratum of patients with a score of 2 or 3, the Kaplan-Meier method estimate of survival by day 28 between the control group and bicarbonate group was significant (63% [95% CI 52–72] vs 46% [35–55]; p=0·0283). Metabolic alkalosis, hypernatraemia, and hypocalcaemia were observed more frequently in the bicarbonate group than in the control group, with no life-threatening complications reported.

Interpretation

In patients with severe metabolic acidaemia, sodium bicarbonate had no effect on the primary composite outcome. However, sodium bicarbonate decreased the primary composite outcome and day 28 mortality in the a-priori defined stratum of patients with acute kidney injury.

Funding

French Ministry of Health and the Société Française d'Anesthésie Réanimation.

Fewer Episodes of Atrial Fibrillation When Vasopressin Is Combined with Norepinephrine

Association of Vasopressin Plus Catecholamine Vasopressors vs Catecholamines Alone With Atrial Fibrillation in Patients With Distributive ShockA Systematic Review and Meta-analysis

Alexandra P. Lengyel¹; Ludhmila Hajjar, MD²; Anthony C. Gordon, MD^3,4; François Lamontagne, MD, MSc⁵; Jeff S. Healey, MD, MSc¹; Richard P. Whitlock, MD, PhD¹; Emilie P. Belley-Côté, MD, MSc¹

JAMA. 2018;319(18):1889-1900. doi:10.1001/jama.2018.4528

Results  Twenty-three randomized clinical trials were identified (3088 patients; mean age, 61.1 years [14.2]; women, 45.3%). High-quality evidence supported a lower risk of atrial fibrillation associated with vasopressin treatment (RR, 0.77 [95% CI, 0.67 to 0.88]; risk difference [RD], −0.06 [95% CI, −0.13 to 0.01]). For mortality, the overall RR estimate was 0.89 (95% CI, 0.82 to 0.97; RD, −0.04 [95% CI, −0.07 to 0.00]); however, when limited to trials at low risk of bias, the RR estimate was 0.96 (95% CI, 0.84 to 1.11). The overall RR estimate for RRT was 0.74 (95% CI, 0.51 to 1.08; RD, −0.07 [95% CI, −0.12 to −0.01]). However, in an analysis limited to trials at low risk of bias, RR was 0.70 (95% CI, 0.53 to 0.92, P for interaction = .77). There were no significant differences in the pooled risks for other outcomes.

Conclusions and Relevance  In this systematic review and meta-analysis, the addition of vasopressin to catecholamine vasopressors compared with catecholamines alone was associated with a lower risk of atrial fibrillation. Findings for secondary outcomes varied.