The ten pitfalls of lactate clearance in sepsis

Lactate as a goal of what?

The complexity of lactate as a molecule, substrate, biomarker, energy source, component of some intravenous fuids, and major modulator of cellular bioenergetics during physiological stress is formidable

Such complexity makes it impossible to defne what goal it should be a marker or target of. Seeking to lower lactate levels (by whatever means given the multiple events that regulate its blood levels) has no credibility and no logic in terms of hemodynamics, bioenergetics, or tissue protection. In fact, it could make more biological sense to assist the natural process of lactate utilization and generation during sepsis or during other physiological stress situations by administering lactate. Until we are able to define the goals that we wish to achieve by manipulating lactate and have the means of measuring whether we have achieved such goals or not, the idea of seeking to lower lactate by increasing its “clearance” in sepsis is both an illusion and a folly.


Jan Bakker, Department of Intensive Care, Erasmus MC University Medical Center, Rotterdam, Netherlands

Fourth Universal Definition of Myocardial Infarction

The following are key points to remember from this Expert Consensus Document on the Fourth Universal Definition of Myocardial Infarction (MI):

1. The current (fourth) Universal Definition of MI Expert Consensus Document updates the definition of MI to accommodate the increased use of high-sensitivity cardiac troponin (hs-cTn).
2. Detection of an elevated cTn value above the 99th percentile upper reference limit (URL) is defined as myocardial injury. The injury is considered acute if there is a rise and/or fall of cTn values.
3. The criteria for type 1 MI includes detection of a rise and/or fall of cTn with at least one value above the 99th percentile and with at least one of the following:
1. Symptoms of acute myocardial ischemia;
2. New ischemic electrocardiographic (ECG) changes;
3. Development of pathological Q waves;
4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology;
5. Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy.
4. The criteria for type 2 MI includes detection of a rise and/or fall of cTn with at least one value above the 99th percentile and evidence of an imbalance between myocardial oxygen supply and demand unrelated to coronary thrombosis, requiring at least one of the following:
1. Symptoms of acute myocardial ischemia;
2. New ischemic ECG changes;
3. Development of pathological Q waves;
4. Imaging evidence of new loss of viable myocardium, or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
5. Cardiac procedural myocardial injury is arbitrarily defined by increases of cTn values (>99th percentile URL) in patients with normal baseline values (≤99th percentile URL) or a rise of cTn values >20% of the baseline value when it is above the 99th percentile, but it is stable or falling.
6. Coronary intervention-related MI is arbitrarily defined by elevation of cTn values >5times the 99th percentile URL in patients with normal baseline values. In patients with elevated pre-procedure cTn in whom the cTn levels are stable (≤20% variation) or falling, the post-procedure cTn must rise by >20%. However, the absolute post-procedural value must still be at least five times the 99th percentile URL. In addition, one of the following elements is required:
1. New ischemic ECG changes;
2. Development of new pathological Q waves;
3. Angiographic findings consistent with a procedural flow-limiting complication such as coronary dissection, occlusion of a major epicardial artery or a side branch occlusion/thrombus, disruption of collateral flow or distal embolization.
7. Coronary artery bypass grafting (CABG)-related MI is arbitrarily defined as elevation of cTn values >10 times the 99th percentile URL in patients with normal baseline cTn values. In patients with elevated pre-procedure cTn in whom cTn levels are stable (≤20% variation) or falling, the post-procedure cTn must rise by >20%. However, the absolute post-procedural value still must be >10 times the 99th percentile URL. In addition, one of the following elements is required:
1. Development of new pathological Q waves;
2. Angiographic documented new graft occlusion or new native coronary artery occlusion;
3. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.
8. It is increasingly recognized that there is a group of MI patients with no angiographic obstructive coronary artery disease (≥50% diameter stenosis in a major epicardial vessel), and the term “myocardial infarction with non-obstructive coronary arteries (MINOCA)” has been coined for this entity.
9. Patients may have elevated cTn values and marked decreases in ejection fraction due to sepsis caused by endotoxin, with myocardial function recovering completely with normal ejection fraction once the sepsis is treated.
10. Arriving at a diagnosis of MI using the criteria set forth in this document requires integration of clinical findings, patterns on the ECG, laboratory data, observations from imaging procedures, and on occasion pathological findings, all viewed in the context of the time horizon over which the suspected event unfolds.

The Future of Haemodynamic Monitoring

Webinar presented 1/24 2019 by ESICM , F. Michard , MD, PhD

Dr. Michard shows in this presentation Multiple noninvasive techniques are currently available on the horizon ,  measuring fluid responsiveness, cardiac output and tissue perfusion.  An interesting technique in the operating room is the use of arecruitment maneuver and assessment of stroke volume or cardiac output [noninvasively] applying the 3×30 rule to predict fluid responsiveness. 

Techniques with micro-sensors, both for S VO2 and carotid blood flow are also available already.  A wearable collar as real-time detects change in chest impedance, could be very valuable in anticipating increased extravascular lung water/pulmonary edema.  

In cardiology similar techniques were already available, but by means of invasive techniques through the MIMS pulmonary artery monitor or measurement of thoracic impedance, OptiVol, available on many new or implantable defibrillators and CRT- P devices.

I posted the video on YouTube to the web this morning as an easy reference.

I apologize, I forgot to turn of my microphone and created a painful "echo" but the video is still audible ( i hope) 

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