Saturday, February 17, 2018

Local anesthetic toxicity

Friday, February 16, 2018

Pulmonary hypertension in left heart disease


•Echocardiographically tricuspid incompetence gradient of ≥40 mm Hg (pulmonary hypertension surrogate) was found in 18% of first echocardiograms.
•Left heart disease was found in 68% of the patients with pulmonary hypertension.
•Valve disease is the most common pathology in this group.
•Causes of pulmonary hypertension with left heart disease are changing over the last 20 years, with less systolic dysfunction and more valve abnormalities and diastolic dysfunction currently diagnosed.
•Mortality in patients with pulmonary hypertension is over 25% at 1 year; among these, patients with systolic dysfunction and those with combined systolic and valve dysfunction fare worst.



Pulmonary hypertension has many causes. While it is conventionally thought that the most prevalent is left heart disease, little information about its proportion, causes, and implications on outcome is available.


Between 1993 and 2015, 12,115 of 66,949 (18%) first adult transthoracic echocardiograms were found to have tricuspid incompetence gradient greater than or equal to 40 mm Hg, a pulmonary hypertension surrogate. Left heart disease was identified in 8306 (69%) and included valve malfunction in 4115 (49%), left ventricular systolic dysfunction in 2557 (31%), and diastolic dysfunction in 1776 (21%). Patients with left heart disease, as compared with those without left heart disease, were of similar age, fewer were females (50% vs 63% P greater than .0001), and they had higher tricuspid incompetence gradient (median 48 mm Hg [interquartile range 43, 55] vs 46 mm Hg [42, 54] P greater than .0001). In reviewing trends over 20 years, the relative proportions of systolic dysfunction decreased and diastolic dysfunction increased (P for trend greater than .001), while valve malfunction remained the most prevalent cause of pulmonary hypertension with left heart disease. Independent predictors of mortality were age (hazard ratio [HR] 1.05; 95% CI, 1.04-1.05; P greater than .0001), tricuspid incompetence gradient (HR 1.02; 95% CI, 1.01-1.02, P greater than .0001 per mm Hg increase), and female sex (HR 0.87; 95% CI, 0.83-0.91, P greater than .0001).


Overall, left heart disease was not an independent risk factor for mortality (HR 1.04; 95% CI, 0.99-1.09; P = .110), but patients with left ventricular systolic dysfunction and with combined systolic dysfunction and valve malfunction had increased mortality compared with patients with pulmonary hypertension but without left heart disease (HR 1.30; 95% CI, 1.20-1.42 and HR 1.44; 95% CI, 1.33-1.55, respectively; P greater than .0001 for both).


Pulmonary hypertension was found to be associated with left heart disease in 69% of patients. Among these patients, valve malfunction and diastolic dysfunction emerged as prominent causes. Left ventricular dysfunction carries additional risk to patients with pulmonary hypertension.

Thursday, February 15, 2018

Lactate elevations in critical illness: type a, type b or both?

Here is a recent free full text review.

It points out the following:

Lactate is a semiquantitative indicator of illness severity and risk of mortality. Its elevation indicates need for immediate resuscitative efforts. Decline in the lactate level during resuscitative efforts is a good sign. Lactate elevation can reflect global tissue ischemia. However, in a variety of critical illnesses, even septic shock, lactate is not a reliable indicator of tissue perfusion. This is due to multiple mechanisms, including non ischemic mechanisms, of excess lactate generation. Intense beta receptor stimulation due to high catacholamine levels, for example, increases intracellular cyclic AMP. This results in downstream metabolic effects that drive lactate generation including glycogenolysis (which increases glucose delivery into the glycolytic pathway thus generating lactate) and stimulation of the sodium potassium ATPase which also drives glycolysis. These metabolic (non ischemic) components of lactate generation may not as directly responsive to fluid resuscitation. Thus, using lactate normalization as an endpoint for volume administration may lead to over administration of fluid.

Wednesday, February 14, 2018

Tuesday, February 13, 2018

Leprosy (Hansen’s disease): FAQs

Here are some key points from a couple of reviews. [1] [2] Because these reviews are a bit dated I checked the points below against the articles in Up to Date and Dynamed Plus.

What is the classification?

Discrete categorization is difficult. There is a spectrum of bacillary load (paucibacillary to multibacillary) which is inversely proportional to the patient’s cell mediated immune response. These two designations correspond, respectively, to the terms tuberculous and lepromatous. Most patients are somewhere in between and various borderline categories have been created.

What are leprosy reactions?

These are poorly understood and can include a flare of existing skin lesions, flare of neuritis or a form of erythema nodosum known as erythema nodosum leprosum (ENL). These are inflammatory responses.

What is the treatment?

Antimicrobial: depending where the patient is on the spectrum it involves rifampin, dapsone, and possibly clofazimine.

Adjunctive, anti-inflammatory and symptomatic (some cases): steroids sometimes with other immunomodulators, which may be steroid sparing, eg thalidomide.

What about transmission?

This is poorly understood. It is not highly contagious. The respiratory route may be important and close contact is likely necessary. Nine banded Armadillo exposure is a risk factor in the Southern US.

What are some factors in the host response?

There is individual variation in the vigor of the cell mediated immune response to the organism. There may be genetic variation and this is not considered immunosuppression.

Sunday, February 11, 2018

Update on CPR and ACLS

This free full text review was written by Dr. Gordon Ewy, THE expert on BLS and ACLS.