Democratizing Cardiac Hand Held Ultrasound

More and more sub specialties use echocardiography at the POC and bedside. I have attended some of these echo courses during Critical Care Meetings. I have also seen Intensivists go beyond the interpretation that are taught in these classes and I have seen some truly scary conclusions that they draw , thinking they understand fully what they are looking at or measuring.

The wider adoption of hand-held ultrasound is inhibited not by the lack of special training, but more by the attenuation of imaging skills of the non-imaging cardiologist.  Democratizing ultrasound by providing ubiquitous axis devoid of formal studies interpreted by echocardiographers is truly scary.  A hand-held ultrasound performed by somewhat with insufficiency skills is probably worse than no information at all.  Perhaps this attenuation skills will be less marked as the generations of the fellow's in training would have had access to hand-held ultrasounds but your through their careers although, this development would be welcome, we have not seen evidence of it yet.

I have seen truly scary interpretations  in the assessment of diastolic dysfunction for example.  Diastolic dysfunction is grossly and oversimplify divided into 4 grades, but truly classifying the function is extremely difficult, dependent on multiple parameters, and in some cases actually impossible to place the results in a particular class.  Assessment of left atrial pressure which is closely bound to this assessment is even more difficult and should be left to cardiologist with many years of experience in reading echocardiograms.  In particular bedside hand-held ultrasounds will often give fraudulent data.

For example assessment of IVC size and respirophasic changes is useless in patients on mechanical ventilation, yet an assessment is regularly made this way to define filling pressures.

The American College of cardiology has developed multiple algorithms to classify diastolic dysfunction and determine left atrial pressure.  They are not easy to remember and each has variable accuracy [sensitivity and specificity].

See attached article 1 and 2 and my slide presentation.

Critical Care Ultrasound Handbook

For those at the bedside this book may come in handy , also the BLUE protocol on lung ultrasound is well explained

 CAC Book from the Fluid Academy website

Back to the Drawing Board on ARDS

Prone positioning in severe ARDS now debated: some feel it can be more harmful than beneficial - has the pendulum swung? If so, there is no particular therapy left for ARDS - discussions at @ISICEM - #ISICEM19

— Jean-Louis Vincent (@jlvincen) March 6, 2019

I suspect with further studies we will see regression to the mean ....and proning likely may improve oxygenation but not mortality , similar as we saw in the ARDS Network with higher Tidal Volumes : improved oxygenation with higher tidal volumes but over time a higher mortality 

The Troponin Leak During Sepsis

Practitioners may be able to influence the risk of postinfection myocardial infarction if they remain mindful of the increased risk of myocardial infarction during and after acute infections and if they do not dismiss elevated troponin levels as “troponin leak.” Among patients with acute infection who have clinical indications for statins and aspirin, these medications should be continued (if the patient is already receiving them) or may be initiated if no contraindications are present.

Published in NEJM

The Future and Current Status of Vasopressors in Septic Shock

Two excellent articles recently published Online only and in the European Journal of Intensive Care Medicine

1. Challenges in the management of septic shock: a narrative review


2.A global perspective on vasoactive agents in shock



I actually use vasopressin way early when NE is still at levels < 10 mcg/ min in elderly patients generally with known paroxysmal AF/AFL, LV dysfunction and/or recent ECHO shows LAE ( >40 mm); younger patients with H/O rheumatic heart disease I would include ,also- essentially anybody I thought would be at higher then normal risk for new onset or recurrent AF/AFL

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

Ejection Fraction Pros and Cons

Ejection fraction (EF) reflects both cardiac function and remodeling, and is widely recognized as a valuable diagnostic and prognostic tool. Its use in a variety of settings, ranging from heart failure and myocardial infarction to valvular heart disease, has made it a cornerstone of modern cardiology, pervading guidelines and practice. However, the development of the test was in another era, with younger patients and a lower prevalence of heart failure with preserved EF. The performance expectations of EF in the current era are also demanding—in relation to detection of subclinical LV dysfunction, and especially relating to recognition of changes in LV function on sequential testing—for example in patients taking cardiotoxic drugs. This review discusses whether the impressive evidence base for EF justifies its ongoing use in the context of newer markers of LV function, and the sophisticated questions posed by modern cardiology.

Before the development of left ventricular (LV) imaging, the assessment of cardiac function was limited to the measurement of pressure and flow. The development of left ventriculography and indicator dilution techniques in the early 1960s enabled estimation of LV volumes, and ejection fraction (EF) as stroke volume indexed to end-diastolic volume . The resulting measurement of cardiac function is now a keystone of modern cardiology, pervading guidelines and practice. This review discusses whether this evidence base justifies its ongoing use in the context of newer markers of LV function, and the more sophisticated questions posed by modern cardiology.

Proposed Decision Process About When to Trust and Distrust Ejection Fraction

Explanation GLS see link below to my Drive 

There is broad value in gathering global longitudinal strain (GLS) in every case, but the enclosed scenarios summarize where this measurement is most useful. 3D = 3-dimensional; EF = ejection fraction; HF = heart failure; ICD = implantable cardioverter-defibrillator; LV = left ventricular; MI = myocardial infarction.

Assessment of the Athlete’s Heart

This athlete showed severe LV enlargement with mild dysfunction on the basis of 2DE (LV end-diastolic 143 ml/m2, LV end-systolic 77 ml/m2, stroke volume 119 ml, EF 0.46) and 3DE (LV end-diastolic 136 ml/m2, LV end-systolic 70 ml/m2, stroke volume 118 ml, EF 0.48) (A). Stroke volume is validated with pulsed-wave Doppler (117 ml) (A). Medial and lateral tissue velocity (mean 12 cm/s) and global longitudinal strain (19%) are consistent with normal myocardial function (B). 2DE = 2-dimensional echocardiography; 3DE = 3-dimensional echocardiography; EF = ejection fraction; LV = left ventricular.

This asymptomatic, but inactive, elderly patient with type 2 diabetes mellitus (T2DM) shows normal LV size and ejection fraction (0.59%), but impaired GLS (15%) (A). The presence of myocardial disease is supported by LA enlargement (38 ml/m2), and mild concentric remodeling (LV mass 121 g, relative wall thickness 0.44), despite normal diastolic function and tissue Doppler (B). This pattern of impaired GLS without diastolic dysfunction accounts for a subgroup of T2DM patients with LV dysfunction LA = left atrial;

The time to peak LV deformation in all myocardial segments provides a measure of contractile dispersion. This is predictive of arrhythmias. Reproduced with permission from Haugaa et al. ECG = electrocardiogram; ICD = implantable cardioverter-defibrillator; SD = standard deviation;

There can be few parameters in the whole of medicine that have had such a ubiquitous role in the characterization and management of disease as EF in cardiology. Despite its limitations, it is hard to anticipate a situation in which EF would no longer be used for the detection of LV systolic dysfunction and the consequent prognostic implications of this condition. Advances are continuing in the main alternative methodologies; new CMR protocols are shorter, potentially reducing cost, whereas improvements in 3DE have enabled many echo acquisitions to be performed using a single beat, thereby removing the need for breath-holding and potential stitch artifacts. Moreover, in the age of machine learning, automation is already being seen in the process of tracing the endocardium. Nonetheless, caution is necessary concerning the use of semiautomatic algorithms to calculate volumes and EF, regardless whether from 2D or 3D data. Manual correction is important, although it has been made difficult by the presentation of only thumb-sized LV images with most software. Other improvements can be expected that might ensure that appropriate 2D image planes are selected, or cross-correlation with other measurements (e.g., Doppler).

Nonetheless, disease phenotypes have changed from the era when EF was developed, and we now have an expectation of identifying disease at an early stage. In many situations, the information provided by EF is inadequate; this is especially the case in the assessment of HFpEF and the recognition of SBHF, but is also pertinent to amyloidosis, hypertrophic cardiomyopathy, and the recognition of LV impairment in various valvular heart diseases, including regurgitant lesions and AS. There is a risk that classification by EF will be a barrier to deeper phenotyping of these illnesses—which is essential to develop targeted treatment strategies. Thus, the best way forward seems to be to retain EF because of its historical role and evidence base, but to accept that in a number of circumstances, EF alone is insufficient (Central Illustration). New and more sensitive markers of LV dysfunction, especially GLS, should be used when EF appears to be normal, or when particular diagnoses are sought where EF is unsuitable.

2D speckle tracking and GLS  : a simple primer 

Further data in JAMA Cardiology, published online February 27, 2019,   regarding GLS and certain patterns correlate with specific disease processes. Global longitudinal strain provides potentially incremental information at all stages of HF and across the realms of prognostic evaluation, diagnosis, management guidance, and follow-up. Multicenter studies using GLS are in progress, but especially in relation to HFpEF, the adoption of GLS in clinical trials has been slow. 

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.