New (direct) oral anticoagulants in VTE

Here is a recent review.

From the conclusion:

Selective thrombin and FXa inhibitors are a new class of anticoagulant drugs, designed to overcome the unmet needs of current therapy. They are orally active, reach full anticoagulant effects shortly after intake, have a relatively short half-life after discontinuation and, in most clinical circumstances, no regular laboratory monitoring or dose adjustment is required. These characteristics render these agents more manageable and appealing for both patients and physicians than heparins or VKAs, but apart these practical advantages of direct oral anticoagulants, what have we learnt from published phase III trials regarding their efficacy and safety in the clinical setting of VTE? A number of recently published systematic reviews and meta-analyses did pool data from randomised trials and performed indirect comparisons. Collectively, they showed that the four direct anticoagulants currently available have at least a similar efficacy for primary prevention and secondary prevention of VTE recurrence and all-cause mortality compared with standard treatments [50–54]. Pertaining to safety, the main issue is whether or not direct anticoagulants are associated with less bleeding complications that the traditional anticoagulants, particularly VKA antagonists. All in all, it was clearly and consistently shown that direct anticoagulants are associated with less intracranial bleeding than traditional agents, whereas the evidence of their superiority pertaining to other sites of bleeding is more uncertain [51].

Note that in the new ACCP guidelines DOACs are given preference over other oral anticoagulants in all non cancer related VTE.

Non invasive ventilation: ward or ICU?

Recently published:

Design: Prospective, observational, pragmatic study.

Setting: Ordinary wards of a teaching hospital.

Patients: Consecutive patients treated with noninvasive ventilation for acute respiratory failure.

Interventions: None.

Measurements and Main Results: Two-hundred and twenty-patients were enrolled. Mortality rates at 30-day, 90-days, and 1-year follow-up were 20%, 26%, and 34%. When excluding patients with “do-not-resuscitate” status, mortality rates were 13%, 19%, and 28%. The multivariate analyses identified solid cancer, pneumonia in hematologic patients, and do-not-resuscitate status as independent predictors of mortality with postoperative acute respiratory failure associated with improved survival. The same predictors were confirmed when excluding do-not-resuscitate patients from the analyses.

Conclusions: Noninvasive ventilation applied in ordinary wards was effective, with long-term outcomes not different from those reported for ICU settings. Solid cancer, pneumonia in hematologic malignancies, and do-not-resuscitate status predicted mortality, whereas patients with postoperative acute respiratory failure had the best survival rate. Additional studies are required to evaluate noninvasive ventilation efficacy in the wards compared with ICU.

Membrane active non cardiac drugs and the risk of cardiac arrest

From a poster presentation at AHA 2016:

Introduction: Drugs may increase risk of ventricular tachycardia/fibrillation (VT/VF) and sudden cardiac arrest (SCA) in susceptible individuals by blocking cardiac ion channels. This also applies to drugs prescribed for non-cardiac conditions (non-cardiac drugs) if these drugs possess such properties. A well-known example is non-cardiac drugs that block cardiac potassium channels and cardiac repolarization. These drugs may cause excessive QT-interval prolongation and VT/VF in individuals with reduced repolarization reserve (e.g., Long QT syndrome). Similarly, non-cardiac drugs that block cardiac sodium channels and cardiac depolarization increase VT/VF risk in individuals with reduced depolarization reserve (e.g., Brugada syndrome). We hypothesized that non-cardiac depolarization blocking drugs (DB-drugs) are associated with increased VT/VF risk in the general population.

Methods and results: A community based case-control study was performed. Cases were out-of-hospital SCA victims with documented VT/VF included in the ARREST study in June 2005 - December 2009…

We included 1787 SCA cases (mean age 66 years, 77% male) and matched them to 7666 non-SCA controls. Non-cardiac DB-drugs were used by 81 cases (4.5%) and 249 controls (3.2%), and were associated with a 41% increased SCA risk (ORadj: 1.41 [95% CI: 1.10-1.83] P less than 0.05). Use of two or more DB-drugs was associated with a 5.6-fold risk (OR: 5.63 [1.95-16.23] P less than 0.05)…

Conclusion: Current use of non-cardiac DB-drugs is associated with increased risk of SCA, especially when two or more DB-drugs are used simultaneously.

Magnesium levels, magnesium supplementation and neurological outcome following cardiac arrest

From a poster presentation at AHA 2016:

Introduction: Therapeutic hypothermia (TH) improves neurological outcomes after cardiac arrest by mitigating cerebral reperfusion injury. Plasma magnesium (Mg) inhibits glutamate release, restores blood brain barrier integrity and decreases brain edema. The neuroprotective role of Mg in cardiac arrest patients undergoing TH is not well established. We sought to determine the relationship of plasma Mg and neurologic outcomes in these patients.

Methods: A cohort of 384 consecutive patients who completed TH (33°C) from 2007 to 2016 was retrospectively studied. We evaluated favorable neurologic outcomes as a function of Mg levels before, during, and after TH as well as the relationship between neurologic outcomes and Mg supplementation during TH…

Patients with favorable neurologic outcomes had lower Mg levels at presentation (2.1 mEq/L vs. 2.2 mEq/L, p=0.031). Mg levels on presentation inversely correlated with favorable neurologic outcomes (r=-0.107). A larger percentage of patients who received magnesium supplementation had favorable neurologic outcomes (33% vs. 22%, p=0.033). We also stratified patients based on Mg levels in increments of 0.2 mEq/L to evaluate neurologic outcomes. A non-statistically significant trend towards worse neurologic outcomes was noted in patients with Mg less than 1.6 mEq/L at 24 hours and greater than 2.7 mEq/L at 24 and 48 hours…

Discussion: Lower Mg levels at presentation and magnesium supplementation during TH were associated with favorable outcomes. Intracellular shift and increased renal excretion of Mg have been associated with TH and could worsen hypomagnesemia on presentation after a cardiac arrest. Mg supplementation may potentiate the beneficial effects of TH.

Early repolarization pattern in families of victims of sudden arrhythmic death

From a recent study:

Background—The early repolarization (ER) pattern is associated with sudden death and has been shown to be heritable. Its significance when identified in families affected by sudden arrhythmic death syndrome (SADS) remains unclear…

Conclusions—The ER pattern is more common in SADS family members than controls adjusted in particular for relatedness. The increased prevalence is irrespective of ER subtype and the presence of other inherited arrhythmia syndromes. ER may therefore represent an underlying heritable arrhythmia syndrome or risk factor for sudden death in the context of other cardiac pathology.

Cobalt cardiomyopathy: it may be coming back

Report here.

Dilated cardiomyopathy review in Circulation

The review is open access full text. I have highlighted some sections below that are of particular interest.

Definitions

From the review:

The term dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders that are characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease.5

In clinical practice, the pathogenesis of heart failure (HF) has often been placed into 2 categories: ischemic and nonischemic cardiomyopathy. The term nonischemic cardiomyopathy has been interchangeably used with DCM. Although this approach might be practical, it fails to recognize that nonischemic cardiomyopathy can include cardiomyopathies caused by volume or pressure overload (such as hypertension or valvular heart disease) that are not conventionally accepted under the definition of DCM.1,5

The diagnostic evaluation

Figure 1 is very helpful and should be viewed in the original. A few key points from the figure follow:

Family history is an extremely important part of the initial evaluation given the frequency of familial DCM.

An ischemic work up is indicated if there are ischemic signs, symptoms or risk factors. In some patients over 35 lacking these features it still may be necessary if the etiology remains unknown after evaluation.

Myocardial biopsy for the diagnosis of giant cell/fulminant myocarditis is indicated in any of the following situations: acute decompensation requiring inotropic or mechanical support; type 2 heart block; sustained or symptomatic VT; lack of response of the heart failure syndrome to guideline based medical management within 2 weeks.

Biopsy may be indicated in occasional other situations where certain specific myocardial diseases are considered (see text).

Cardiac MRI may be indicated, particularly for infiltrative diseases.

Disease specific considerations: amyloidosis

The section on amyloidosis is long and loaded with good practical information such that I cannot do justice to it here. I will make these points:

First, I have reviewed cardiac amyloidosis extensively in prior posts. [1] [2] [3] [4] [5] [6] [7] [8]

Also there was this concerning unique aspects of pharmacologic management of heart failure due to cardiac amyloidosis:

Digoxin should be avoided in patients with amyloidosis (Level of Evidence C). Digoxin binds to amyloid fibrils and thus can predispose to toxicity even in the setting of normal serum digoxin levels.56

Calcium channel antagonists (nifedipine or verapamil) should not be administered, because they bind to amyloid fibrils and can result in exaggerated hypotensive and negative inotropic responses (Level of Evidence C).57

Alcoholic cardiomyopathy

In addition to standard guideline based treatment of heart failure there is no disease specific treatment other than alcohol cessation.

Cocaine related cardiomyopathy

Some general considerations, from the review:

Although cocaine abuse has been associated with acute coronary events and regional myocardial injury, long-term cocaine use also has been associated with global DCM without the presence of coronary artery disease (CAD) .. This has been termed cocaine-related cardiomyopathy and implies direct toxicity of cocaine on the myocardium.

Concerning treatment:

Recommendations With Moderate Level of Consensus for Cocaine-Related Cardiomyopathy

It is reasonable to treat patients with cocaine-related cardiomyopathy who have demonstrated abstinence for greater than 6 months with standard therapy for LV dysfunction, including β-blockers (Level of Evidence C).

In patients at risk for relapse for cocaine abuse, nonselective β-blocker treatment with α1-, β1-, or β2-receptor antagonism is reasonable because of potential protection against the unopposed α-agonism effects of cocaine with β1-receptor antagonist treatment alone (Level of Evidence C).

Methamphetamine and related drugs

Cessation of use is the only disease specific recommendation. I have previously reviewed this topic here.

Chemotherapeutic agents

The major culprits are anthracyclines but there are others. Cardiotoxicity may occur at lower doses than previously thought. This may be due to greater sensitivity of detection. A troponin leak acutely after first administration is predictive of clinical cardiac toxicity. Early implementation of guideline based therapies may improve function and prognosis. Much more in the full text.

Peripartum cardiomyopathy

Prognosis is variable. Up to two thirds may recover. A few progress to transplant. Treatment is according to the general heart failure guidelines with the exception of drugs contraindicated in pregnancy and during lactation. Bromocriptine as a disease specific adjunct has yet to be established.

Sarcoidosis

Here are a few points from the article:

Autopsy series suggest that 20% to 50% of patients with sarcoidosis have some degree of cardiac involvement228,232,233; however, only a fraction of these patients have clinically recognized cardiac sarcoidosis…

Diagnostic criteria for cardiac sarcoidosis have been proposed that rely on pathological demonstration of cardiac granulomas or noninvasive evidence of cardiac involvement in a patient with pathologically proven extracardiac sarcoidosis…

In patients with clinically evident cardiac sarcoidosis, complete heart block is a common finding…

Because the myocardial lesions in cardiac sarcoidosis are patchy, and many involve only the LV, an RV EMB provides diagnostic evidence of cardiac sarcoidosis in only 25% to 50% of autopsy-confirmed cases.232 Cardiac MRI with late gadolinium enhancement has emerged as a valuable imaging tool for the diagnosis of cardiac involvement in sarcoidosis…

Corticosteroids are the mainstay of therapy for sarcoidosis.228,229,231 ..Although there are no randomized controlled trials that have established the efficacy of corticosteroids in cardiac sarcoidosis, retrospective studies suggest benefit .. On the basis of observational studies, steroid therapy in patients with established cardiac sarcoidosis and active inflammation should be initiated before LV systolic function declines..Corticosteroids are commonly initiated at a high dose (prednisone 40–60 mg daily) and tapered off slowly over a period of months if clinical and imaging features remain stable or improve…

Patients with cardiac sarcoidosis and reduced LVEF or symptomatic HF should also be treated with standard HF therapy.1 However, because fatal arrhythmias account for 25% to 65% of deaths caused by cardiac sarcoidosis, particular attention is needed to identify patients who would benefit from placement of a permanent pacemaker with an ICD.228,229,231 Although limited, current evidence suggests that ICDs could prevent death caused by dangerous arrhythmias or sudden cardiac death in patients with reduced LVEF, as well as those with relatively preserved LVEF.2,231 In support of this recommendation, the 2012 American College of Cardiology Foundation (ACCF)/AHA/Heart Rhythm Society guidelines for device-based therapy listed cardiac sarcoidosis as a reasonable indication for ICD implantation, with a Class IIa recommendation.240,241

Myocarditis

This section of the paper is very dense and should be read in the original. I will list only a few points here.

The term myocarditis means inflammation of the myocardium. It does not point to a specific etiology. Some specific myocardial diseases such as sarcoidosis covered separately above may be considered forms of myocarditis.

The indications for biopsy are controversial. The paper gives a reasonable approach. There is a set of noninvasive clinical criteria that can be applied if biopsy is considered impractical. These criteria are provided in the text.

Concerning treatment, note this from the paper:

Myocarditis that presents as DCM should be treated per current guidelines for systolic HF.1,3 Individual trials and a meta-analysis suggest that immunosuppression is generally not indicated for the management of acute lymphocytic myocarditis in adults. In cases of giant cell myocarditis, cardiac sarcoidosis, or eosinophilic myocarditis, treatments directed at modifying the immune response should be considered…

Device therapy may be indicated for certain malignant ventricular arrhythmias but not solely for low EF, since ventricular function may improve as inflammation subsides.

HIV can cause DCM

In the heart failure work up, patients with DCM and risk factors for HIV should be tested for HIV as a possible etiology of DCM.

Chagas diseases

Patients who present with DCM and have epidemiologic risk factors should be screened.

Connective tissue and autoimmune diseases

From the paper:

Autoimmune diseases have long been established as rare causes of cardiomyopathy and HF. There are several proposed mechanisms, including immune-mediated myocarditis, progressive fibrosis, and apoptosis with resultant restrictive and dilated phenotypes, progressive atherosclerosis with subsequent ischemic cardiomyopathy, and HF as a result of therapies used for the primary rheumatologic disorder.289 The more well-described associations between autoimmune/rheumatologic disorders and HF include systemic lupus erythematosus (SLE), scleroderma, RA, dermatomyositis, and polyarteritis nodosa (PAN). Sporadic case reports have also associated HF with ankylosing spondylitis, psoriatic arthritis, celiac sprue, vasculitis, and inclusion body myositis through a variety of mechanisms.

Obesity cardiomyopathy

The association of obesity with heart failure is now well enough recognized to warrant this designation. However, according to the article:

Although the concept of a cardiomyopathy related to obesity has been described previously,355–357 severe LV systolic dysfunction occurs uncommonly because of obesity alone, and the presence of LV systolic dysfunction should trigger an investigation for other contributory factors before it is attributed to obesity alone.

Multiple mechanisms were discussed in the paper. Beyond those, obesity can be a cause of the syndrome of high output heart failure. In a recent series, for example, obesity was identified as the etiology of high output heart failure in 31%. Additional factors include obesity's now well known association with atrial fibrillation [9] [10] and the disturbed sodium balance inherent in obesity due to lowered levels of natriuretic peptides.

Thyroid cardiolyopathy

The pathogenesis is incompletely understood. From the article:

Triiodothyronine (T3) generally increases the force and speed of systolic contraction and the speed of diastolic relaxation, through its effects on myosin isoforms and calcium-handling proteins.368–370 In addition, T3 decreases vascular resistance, including coronary vascular tone, and increases coronary arteriolar angiogenesis. Thyroid hormones can also promote both physiological and pathological myocardial hypertrophies.371 Hypothyroidism promotes myocardial fibrosis by stimulating fibroblasts, whereas the reverse is seen in hyperthyroidism..Hyperthyroidism and hypothyroidism can both lead to cardiovascular injury, including HF. However, a DCM related only to the thyroid disorder is present only in a small proportion of these patients.

The hemodynamic effects of hyperthyroidism include decreased systemic vascular resistance, increased resting heart rate and LV contractility, and enhanced isovolumic ventricular relaxation.373 Decreased systemic vascular resistance stimulates renin release with activation of the angiotensin-aldosterone axis,…

Growth hormone disorders

Consider these if the clinical picture fits.

Stress cardiomyopathy, chronic tachycardia myopathy and PVC induced cardiomyopathy

I have discussed these entities extensively in earlier posts to numerous to link here.

LBBB induced cardiomyopathy

It is well known that myocardial diseases capable of producing DCM can cause LBBB. On the other hand, less well known is the fact that LBBB itself, even if initially an isolated finding, can lead to DCM. Device therapy (resynchronization) may be helpful.

Genetic causes

This section deals with, in addition to familial DCM and its several inheritance patterns, left ventricular non-compaction and arrhythmogenic cardiomyopathy, formerly known as arrhythmogenic right ventricular dysplasia. From the paper:

DCM was initially believed to be inherited in a small percentage of cases until Michels et al475 showed that ≈20% of patients had family members with echocardiographic evidence of DCM when family screening was performed. More recently, inherited familial DCM has been shown to occur in 30% to 50% of cases, with autosomal dominant inheritance being the predominant pattern of transmission; X-linked, autosomal recessive, and mitochondrial inheritance patterns are less common but occur.

Duchenne and Becker muscular dystrophy are genetic causes of DCM but were not mentioned.

Iron overload cardiomyopathy

This can be as a result of hereditary hemochromatosis or chronic transfusions or iron infusions. Screening for iron overload is recommended in the evaluation of new cases of DCM although by the time DCM presents due to iron overload it may be too late for disease specific treatment to be beneficial.

Eosinophilic syndromes

Although this category is included in a review of DCM, it presents initially as a restrictive CM. From the paper:

The diagnosis of hypereosinophilic syndrome is made in the presence of eosinophils greater than 1500/μL..Echocardiography and MRI can be helpful in the diagnosis of eosinophilic myocarditis; however, myocardial biopsy remains the gold standard. After diagnosis, evaluation for secondary causes is essential.. If hypereosinophilic syndrome is suspected, a hematology consultation is warranted.. Corticosteroid therapy is generally considered primary therapy for eosinophilic myocarditis, but its efficacy is not well supported.

Low tidal volume ventilation for ARDS: we have been slow on the uptake

From a recent study:

Objective: Low tidal volume ventilation lowers mortality in the acute respiratory distress syndrome. Previous studies reported poor low tidal volume ventilation implementation. We sought to determine the rate, quality, and predictors of low tidal volume ventilation use.

Design: Retrospective cross-sectional study.

Setting: One academic and three community hospitals in the Chicago region.

Patients: A total of 362 adults meeting the Berlin Definition of acute respiratory distress syndrome consecutively admitted between June and December 2013.

Measurements and Main Results: Seventy patients (19.3%) were treated with low tidal volume ventilation (tidal volume less than 6.5 mL/kg predicted body weight) at some time during mechanical ventilation. In total, 22.2% of patients requiring an FIO2 greater than 40% and 37.3% of patients with FIO2 greater than 40% and plateau pressure greater than 30 cm H2O received low tidal volume ventilation. The entire cohort received low tidal volume ventilation 11.4% of the time patients had acute respiratory distress syndrome. Among patients who received low tidal volume ventilation, the mean (SD) percentage of acute respiratory distress syndrome time it was used was 59.1% (38.2%), and 34% waited more than 72 hours prior to low tidal volume ventilation initiation. Women were less likely to receive low tidal volume ventilation, whereas sepsis and FIO2 greater than 40% were associated with increased odds of low tidal volume ventilation use. Four attending physicians (6.2%) initiated low tidal volume ventilation within 1 day of acute respiratory distress syndrome onset for greater than or equal to 50% of their patients, whereas 34 physicians (52.3%) never initiated low tidal volume ventilation within 1 day of acute respiratory distress syndrome onset. In total, 54.4% of patients received a tidal volume less than 8 mL/kg predicted body weight, and the mean tidal volume during the first 72 hours after acute respiratory distress syndrome onset was never less than 8 mL/kg predicted body weight.

Conclusions: More than 12 years after publication of the landmark low tidal volume ventilation study, use remains poor. Interventions that improve adoption of low tidal volume ventilation are needed.

Though I had long sensed something like this I was surprised that the utilization was that low.

Pooled analysis of ODYSSEY trials: LDL reduction (even extreme reduction) matters, even with non-statin treatments

From the paper, published in Circulation:

Background: A continuous relationship between reductions in low-density lipoprotein cholesterol (LDL-C) and major adverse cardiovascular events (MACE) has been observed in statin and ezetimibe outcomes trials down to achieved levels of 54 mg/dL. However, it is uncertain whether this relationship extends to LDL-C levels less than 50 mg/dL. We assessed the relationship between additional LDL-C, non–high-density lipoprotein cholesterol, and apolipoprotein B100 reductions and MACE among patients within the ODYSSEY trials that compared alirocumab with controls (placebo/ezetimibe), mainly as add-on therapy to maximally tolerated statin.

Methods: Data were pooled from 10 double-blind trials (6699 patient-years of follow-up). Randomization was to alirocumab 75/150 mg every 2 weeks or control for 24 to 104 weeks, added to background statin therapy in 8 trials. This analysis included 4974 patients (3182 taking alirocumab, 1174 taking placebo, 618 taking ezetimibe). In a post hoc analysis, the relationship between average on-treatment lipid levels and percent reductions in lipids from baseline were correlated with MACE (coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, or unstable angina requiring hospitalization) in multivariable analyses.

Results: Overall, 33.1% of the pooled cohort achieved average LDL-C less than 50 mg/dL (44.7%–52.6% allocated to alirocumab, 6.5% allocated to ezetimibe, and 0% allocated to placebo). In total, 104 patients experienced MACE (median time to event, 36 weeks). For every 39 mg/dL lower achieved LDL-C, the risk of MACE appeared to be 24% lower (adjusted hazard ratio, 0.76; 95% confidence interval, 0.63–0.91; P=0.0025). Percent reductions in LDL-C from baseline were inversely correlated with MACE rates (hazard ratio, 0.71; 95% confidence interval, 0.57–0.89 per additional 50% reduction from baseline; P=0.003). Strengths of association materially similar to those described for LDL-C were observed with achieved non–high-density lipoprotein cholesterol and apolipoprotein B100 levels or percentage reductions.

Conclusions: In a post hoc analysis from 10 ODYSSEY trials, greater percentage reductions in LDL-C and lower on-treatment LDL-C were associated with a lower incidence of MACE, including very low levels of LDL-C (less than 50 mg/dL). These findings require further validation in the ongoing prospective ODYSSEY OUTCOMES trial.

Ectopy captured on the 12 lead ECG and future events

From an abstract at AHA 2016:

Methods: We sought to determine if the presence of at least one PAC would predict AF and at least one PVC would predict HF using a single standard (10-second) ECG ...

Results: Among 5,577 CHS participants followed for a median 12 years, a 12-lead ECG PAC (4%) was associated with 60% increased risk of AF (HR 1.6; 95% CI 1.3-2.0; P less than 0.001; Figure) and a PVC (5%) with a 30% increased risk of HF (HR 1.3; 95% CI 1.0-1.6; P = 0.021) and a decline in left ventricular ejection fraction (OR 2.8, 95% CI 1.3-6.1, p=0.008) after multivariable adjustment...

Conclusions: Based on a single standard ECG, the presence of any atrial ectopy predicted AF and any ventricular ectopy predicted HF.

Dexmedetomidine versus haloperidol in delirious non intubated ICU patients

From a recent paper:

Objectives: To evaluate the clinical effectiveness, safety, and cost of dexmedetomidine for the treatment of agitated delirium refractory to haloperidol in nonintubated critically ill patients.

Design: Nonrandomized, controlled trial.

Setting: Intensive care department of a tertiary care nonprofit hospital.

Patients: All consecutive admissions to a medical-surgical ICU with a diagnosis of agitated delirium.

Interventions: Initial haloperidol titration: all patients received IV bolus doses of haloperidol until agitation was controlled (Richmond Agitation Sedation Scale scoring range, 0 to −2) or reaching the maximum daily dose. Group comparison: patient responders to haloperidol (control group) were compared with nonresponders (dexmedetomidine group).

Measurements and Main Results: A total of 132 nonintubated patients were treated with haloperidol in the initial haloperidol titration phase. Forty-six patients (34.8%; 95% CI, 26.0–43.1%) did not respond to haloperidol, and 86 patients (65.2%; 95% CI, 56.3–73.0%) were responders. During the group comparison phase, dexmedetomidine achieved a higher percentage of time in satisfactory sedation levels than did haloperidol (92.7% [95% CI, 84.5–99.8%] vs 59.3% [95% CI, 48.6–69.3%], respectively; p = 0.0001). Haloperidol was associated with 10 cases (11.6% [95% CI, 6.5–21.2%]) of oversedation and two (2.0% [0.4–8%]) of corrected QT lengthening. Direct cost of dexmedetomidine was 17 times greater than haloperidol, but it achieved a mean savings of $4,370 per patient due to the reduction in length of ICU stay.

Conclusions: In the study conditions, dexmedetomidine shows to be useful as a rescue drug for treating agitation due to delirium in nonintubated patients in whom haloperidol has failed, and it seems to have a better effectiveness, safety, and cost-benefit profile than does haloperidol.

End of rotation hand-offs are risky

And the ACGME duty hour regs may have made it worse.

Common ECG findings and the risk of cardiac arrest

From a poster presentation at AHA 2016:

Methods: We cross-linked individuals who had an ECG recording between 2001 and 2011 in primary care with the Danish Cardiac Arrest Register and identified OHCAs of presumed cardiac cause. Multivariable cause-specific Cox regression was used to estimate the association between the ECG abnormalities and OHCA and calculate the absolute 10-year risk of OHCA for men and women with and without known cardiac disease for different age groupings…

Results: A total of 326,227 individuals were included in the study and of those 2,667 suffered an OHCA during a median follow-up of 4 years. The following ECG findings were strongly associated with OHCA: ST-depression without atrial fibrillation (AF), left bundle branch block, and non-specific intraventricular block.

A composite of commonly observed ECG markers may predict sudden cardiac arrest

–-according to an abstract presented at the AHA 2016 sessions.

Early coronary angiography after out of hospital cardiac arrest

---was associated with improved survival to hospital discharge in this systematic review and meta-analysis. (Poster presentation at AHA 2016).

Real world experience with the Medtronic Reveal monitor

From an abstract presented at the AHA 2016 sessions:

Results: A total of 233 patients were included in the study..The indications for implantation were syncope (37.3%), palpitations (24%), AF management (18%), near syncope (5.2%), cryptogenic stroke (3.9%), bradycardia (3.9%), NSVT (1.7%) and long QT (1.3%). A total of 89 (39%) had a diagnosis made during the follow-up time 8 ±4 months..Diagnoses made were AF 22(24.7%), SVT 17(19%), Sick sinus syndrome 10(11%), symptomatic bradycardia 2 (2%), advanced heart block 4 (4.4%), PVC 4 (4.4%), VT 1(1%), other 29 (32.5%). These diagnoses led to change in medication 19 (21%), office visits 17 (19%), radiofrequency ablation 23 (26%), pacemaker implantation 18 (20%), ICD implantation 4 (4%), and miscellaneous 9 (10%). 24 patients underwent device explantation. A total of 3440 CareLink transmissions occurred during the follow up (mean of 15 transmissions per patient).

Chemical defibrillation with IV potassium

From a presentation at AHA 2016:

Introduction: Potassium-based cardioplegia is used in the operating theater to induce asystole. This effect is rapidly reversed with wash-out of the potassium resulting in resumption of electrical activity. This retrospective study examined 5 patients with refractory ventricular fibrillation (VF) cardiac arrest who achieved normal sinus rhythm after chemical defibrillation with exogenous KCl or resolution of endogenous hyperkalemia.

Methods: From December 2015 to May 2016, 19 patients were transported to the University of Minnesota in ongoing refractory VF as part of the Minnesota Resuscitation Consortium Advanced Perfusion and Reperfusion Cardiac Life Support Strategy. ECMO was initiated on arrival. Coronary angiography was performed and significant coronary artery disease was treated as necessary. Three patients had continued VF despite multiple shocks and treatment with amiodarone, lidocaine, metoprolol, and propofol. These patients were given KCl 0.5 mEq/kg bolus as salvage therapy after 90-120 minutes of VF. Defibrillation was administered as needed…

Results: Of the 3 patients that received exogenous potassium bolus, 2 achieved sustained ROSC. The third patient suffered recurrent VF after 30 seconds of sinus rhythm and went on to die. One of the 2 patients that achieved ROSC survived to hospital discharge while 1 patient suffered severe anoxic brain injury and died. The average peak potassium level in these 3 patients was 7.2 mmol/L with normalization within 25 minutes. The EKG showed asystole immediately after treatment with spontaneous return of normal sinus rhythm within 10 minutes.

Bag the banana bag in favor of the optimal metabolic cocktail for critically ill alcoholics

From a recent review:

Objective: Patients with a chronic alcohol use disorder presenting to the ICU may be deficient in important vitamins and electrolytes and are often prescribed a “banana bag” as a reflexive standard of therapy. The difficulty of diagnosing Wernicke’s encephalopathy in the critical care setting is reviewed. Furthermore, whether the contents and doses of micronutrients and electrolytes in standard banana bags meet the needs of critically ill patients with an alcohol use disorder is assessed based on available evidence...

Study Selection and Data Extraction: Articles relevant to Wernicke’s encephalopathy, vitamin and electrolyte deficiencies in patients with alcohol use disorders, and alcoholic ketoacidosis were selected...

Data Synthesis: Of these deficiencies, thiamine is the most important for the practicing clinician to assess and prescribe replacement in a timely manner. Based on a pharmacokinetic assessment of thiamine, the banana bag approach likely fails to optimize delivery of thiamine to the central nervous system. Folic acid and magnesium may also merit supplementation although the available data do not allow for as strong a recommendation...

Conclusions: ..for patients with a chronic alcohol use disorder admitted to the ICU with symptoms that may mimic or mask Wernicke’s encephalopathy, we suggest abandoning the banana bag and utilizing the following formula for routine supplementation during the first day of admission: 200–500 mg IV thiamine every 8 hours, 64 mg/kg magnesium sulfate (approximately 4–5 g for most adult patients), and 400–1,000 μg IV folate. If alcoholic ketoacidosis is suspected, dextrose-containing fluids are recommended over normal saline.

Increasing use of advanced therapies, declining mortality in cardiac arrest

From a poster presentation at AHA 2016:

Methods: The Healthcare Cost and Utilization Project’s Nationwide Inpatient Sample was utilized to identify a cohort of adults hospitalized with CA, identified through International Classification of Diseases-9 codes…

Results: In-hospital all-cause mortality significantly decreased over the 7-year study period (65.5%, 63.4%, 59.3%, 57.9%, and 57.0%, 56.0%, and 56.3% from 2006-2012). From 2006-2012, there was an overall rise in the use of coronary angiogram (12.8%, 13.0%, 14.7%, 15.0%, 14.3%, 14.7%, and 15.8%), percutaneous coronary intervention (PCI) (7.5%, 7.1%, 8.4%, 8.1%, 8.1%, 8.4%, and 8.9%), TH (0.2%, 0.3%, 0.6%, 1.2%, 1.9%, 2.8%, and 3.0%), and ECMO (0.1%, 0.1%, 0.1%, 0.2%, 0.2%, 0.3%, and 0.4%)…

Conclusions: During 2006-2012, a decline in mortality was accompanied by a steady rise in use of advanced therapies, including ECMO, TH, coronary angiogram, and coronary revascularization. Patients of younger age and with CAD were more likely to receive these advanced therapies.