Heart Failure and Liver Disease Cardiohepatic Interactions

The heart and the liver are in close relation to each other. Impairment of cardiac function may leadtohepatic dysfunction and vice versa (Central Illustration). Liver hypoperfusion and hepatic congestionarethe 2 central pathophysiological mechanisms, both in acute cardiogenic liver injury and hepatic congestion. Cirrhotic cardiomyopathy is a syndrome that includes systolic, diastolic, and electrophysiological abnormalities that develop in the setting of liver cirrhosis. Altered LXR signaling contributes to the development of HF comorbidities. Because the liver is the first organ exposed to the gut toxic molecules produced in HF, gut–liver interaction in the setting of HF has been an exciting new research field. Management of deranged cardiohepatic interactions remains challenging.

Cardiac and Liver Dysfunction Often Co-ExistCo-existence is the result of systemic disorders and diseases affecting both organs (e.g., alcohol abuse, drugs, inflammation, autoimmunity, infections) as well as complex cardiohepatic interactions. The latter interactions include development of acute cardiogenic liver injury and congestive hepatopathy in HF as well as cardiac dysfunction and HF in the setting of liver cirrhosis (cirrhotic cardiomyopathy), nonalcoholic fatty liver disease, and sequelae following liver transplantation. Finally, altered LXR signaling may contribute to the pathogenesis of HF co-morbidities. HF = heart failure; LXR = liver X receptor.

Schematic Relating LXR Signaling to HF Development

In the cell nucleus, LXR form an obligate heterodimer complex with the RXR that binds to regulatory regions of target genes. Following ligand binding, the LXR/RXR complex undergoes a conformational change that leads to the release of co-repressors and recruitment of co-activators, which modulates target gene expression. Altered LXR/RXR signaling contributes to development of HF risk factors and co-morbidities and, consequently, HF. HF = heart failure; LXR = liver X receptor; RXR = retinoid X receptor.

Challenges in the management of septic shock: a narrative review

Why I really like this article 

It may not be a bad idea to keep this sentence on a sticky note for intervention answers, if you have to deal with the same endless questions in regards to therapy:
1.  Urine output is a good marker of shock at a very early onset but not a good marker for resuscitation.  Is neither sensitive nor specific for improvement in renal perfusion.
Use this for the same intervention question: Oliguria, only 15 mL this shift… Suggestions?
2.  Another good one is also: Lactate is going up… You want me to give a fluid bolus?
Answer:" I am awaiting randomized trials" [should with target lactate reduction, and to which magnitude, or lactate normalization AND your headache will also be better.

GUIDANCE FOR ANTICOAGULATION REVERSAL

This fact sheet provides clinical guidance for the administration of reversal agents, when needed, for patients on anticoagulation for any indication.

Reversal of anticoagulants may be required for a life-threatening or critical site bleed, or in situations in which bleeding cannot be controlled with other measures.   JACC 2018-Summary 

Trauma patient and cardiac surgery patient may benefit from TEG, but interpretation on anticoagulants can be difficult.

The full recommendation from JACC 2018 can be found here

These Pocket Guidelines in PDF are also quite helpful on the fly:  Clinical Practice Guide on Antithrombotic Drug Dosing and Management of Antithrombotic DrugAssociated Bleeding Complications in Adults February 2014*
by the American Society of Hematology

In Memory of a Giant in Anticoagulation and Hemophilia, Professor Harold Roberts. Attached is his Berry Hill Lecture at UNC Chapel Hill from 2003

Use of Medication for Cardiovascular Disease During Pregnancy

Cardiovascular disease complicating pregnancy is rising in prevalence secondary to advanced maternal age, cardiovascular risk factors, and the successful management of congenital heart disease conditions. The physiological changes of pregnancy may alter drug properties affecting both mother and fetus. Familiarity with both physiological and pharmacological attributes is key for the successful management of pregnant women with cardiac disease. This review summarizes the published data, available guidelines, and recommendations for use of cardiovascular medications during pregnancy. Care of the pregnant woman with cardiovascular disease requires a multidisciplinary team approach with members from cardiology, maternal fetal medicine, anesthesia, and nursing.



Volume 73, Issue 4, February 2019 DOI: 10.1016/j.jacc.2018.10.075

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)