1000-2000 5 ьшò

Rapid reduction in tissue hypoxia with 100% oxygen via nonrebreathing reservoir facemask (2)[A] until COHb is normal (<3%) and patient is asymptomatic, regardless of oxygen saturation or PO2

ADDITIONALTHERAPIES

Hyperbaric oxygen is controversial (2,3)[A]. Existing trials do not establish whether hyperbaric reduces the incidence of adverse neurologic outcomes (3) [A].

Hyperbaric oxygen currently recommended for:

–Age > 36 years

–Levels >25–30%

–Exposure >24 hours

–Loss of consciousness (4)[C]

–Abnormal neuropsychiatric testing

–Evidence of cardiac involvement

–Severe acidosis (4)

Hyperbaric oxygen is safe in pregnant woman, but there have been no prospective studies of efficacy (2)[A]. International consensus favors it for treating pregnant women (4)[C].

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Patients whose symptoms do not improve after 4 to 5 hours of 100% O2

should be transported to the nearest hyperbaric oxygen facility. Hospitalize patients with ECG or laboratory evidence of severe poisoning, evidence of end-organ damage, or other concerning medical or social factors.

Admit comatose patients and patients with CO poisoning after smoke inhalation to the ICU.

Patients with mild symptoms from accidental poisoning can be managed in the ED and safely discharged.

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

All patients treated for acute CO poisoning should be seen in follow-up in 1 to 2 months after discharge (2). Patients should undergo neuropsychological

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testing if there are behavioral or cognitive concerns.

Behavioral assessment is crucial following intentional CO poisoning.

Patient Monitoring

Measurement of COHb levels

Arterial blood gases

PATIENT EDUCATION

Professional installation and maintenance of combustion devices: 1-800-638- 2772; Consumer Products Safety Commission hotline

CO detector installation in homes, especially near bedrooms and potential CO sources

Annual furnace inspections (5)[B]

PROGNOSIS

Most survivors recover completely, with only a minority developing chronic neuropsychiatric impairment.

COMPLICATIONS

Cardiac:

–Myocardial infarction

–Dysrhythmia

Pulmonary:

–Pulmonary edema

–Pneumonia (aspiration)

Neurologic:

–Anoxic encephalopathy

–Intellectual deterioration

–Memory impairment

–Parkinsonism

Behavioral:

–Irritability

–Aggressiveness

–Violence

–Moodiness

Geriatric Considerations

Higher incidence of cardiovascular and neurologic disease, increasing

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complications

REFERENCES

1.Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009;360(12):1217–1225.

2.Hampson NB, Piantadosi CA, Thom SR, et al. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning. Am J Respir Crit Care Med. 2012;186(11):1095–1101.

3.Buckley NA, Juurlink DN, Isbister G, et al. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041.

4.Rupert DJ, Poehlman JA, Damon SA, et al. Risk and protective behaviours for residential carbon monoxide poisoning. Inj Prev. 2013;19(2):119–123.

5.Sircar K, Clower J, Shin MK, et al. Carbon monoxide poisoning deaths in the united states, 1999 to 2012. Am J Emerg Med. 2015;33(9):1140–1145.

ADDITIONALREADING

Centers for Disease Control and Prevention: http://www.cdc.gov/co

Centers for Disease Control and Prevention. Carbon monoxide poisoning after a disaster. http://www.cdc.gov/disasters/carbonmonoxide.html. Accessed October 2, 2017.

Iqbal S, Clower JH, Hernandez SA, et al. Areview of disaster-related carbon monoxide poisoning: surveillance, epidemiology, and opportunities for prevention. Am J Public Health. 2012;102(10):1957–1963.

United States Consumer Product Safety Commission: http://www.cpsc.gov

United States Environmental Protection Agency: http://www.epa.gov/iaq/co.html

World Health Organization: http://www.who.int/gho/phe/chemical_safety/poisons_centres/en/index.html

CODES

ICD10

T58.91XAToxic effect of carb monx from unsp source, acc, init

T58.8X1AToxic effect of carb monx from oth source, accidental, init T58.01XAToxic effect of carb monx from mtr veh exhaust, acc, init

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CLINICALPEARLS

If there is a concern for CO poisoning, remove individuals from the source and deliver 100% oxygen by high-flow face mask or endotracheal tube.

During pregnancy, there is disproportionate impact on the fetus due to CO binding by fetal hemoglobin.

Consider CO poisoning in younger patients with chest pain or ischemia or if patients who present in case clusters with similar symptoms and a potential CO source exposure.

COHb levels do not correlate well with symptoms or severity of illness.

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CARDIOMYOPATHY

Timothy P. Fitzgibbons, MD, PhD Theo E. Meyer, MD,

DPhil

BASICS

DESCRIPTION

Cardiomyopathy encompasses a large group of diseases of the myocardium that commonly result in mechanical pump dysfunction. The current classification scheme attempts to differentiate between myocardial diseases confined to the myocardium (primary) and those due to systemic disorders (secondary). Specific causes of myocardial dysfunction due to other cardiovascular disorders are considered a third, separate category (1). Classification of cardiomyopathy

–Primary Genetic

■Hypertrophic cardiomyopathy (HCM)

■Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D)

■Left ventricular (LV) noncompaction (LVNC)

■Glycogen storage (Danon type, PRKAG2)

■Conduction defects

■Mitochondrial myopathies

■Ion channel disorders: long QT syndrome (LQTS), Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular

tachycardia (CPVT), Asian SUNDS Mixed

■Dilated cardiomyopathy (DCM) (genetic or nongenetic)

■Restrictive

Acquired

■Myocarditis, stress cardiomyopathy, peripartum, tachycardia-induced, infants of type 1 diabetic mothers

–Secondary (see list below) Specific

■Ischemic

■Valvular

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■Hypertensive

■Congenital heart disease

Patients with end-stage cardiomyopathy have stage D heart failure or severe symptoms at rest refractory to standard medical therapy.

System(s) affected: cardiovascular; renal

Pediatric Considerations

Etiology: idiopathic, viral, congenital heart disease, and familial

Pregnancy Considerations

May occur in women postpartum

EPIDEMIOLOGY

Predominant age: Ischemic cardiomyopathy is the most common etiology; predominantly in patients aged >50 years. Consider uncommon causes in young.

Incidence

60,000 patients <65 years old die each year from end-stage heart disease.

35,000 to 70,000 people might benefit from cardiac transplant or chronic support.

Prevalence

Most rapidly growing form of heart disease

ETIOLOGYAND PATHOPHYSIOLOGY

Ischemic heart disease: most common etiology; up to 66% of patients

Hypertension

Valvular heart disease

Primary genetic causes

Congenital heart disease

Peripartum/postpartum Endocrine

–Diabetes mellitus

–Hyperthyroidism

–Hypothyroidism

–Hyperparathyroidism

–Pheochromocytoma

–Acromegaly

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Nutritional deficiencies

– Beriberi, pellagra, scurvy, selenium, carnitine, kwashiorkor Autoimmune/collagen

–Systemic lupus erythematosus

–Dermatomyositis

–Rheumatoid arthritis

–Scleroderma

–Polyarteritis nodosa

Infectious causes

–Viral (e.g., HIV, coxsackievirus, adenovirus)

–Bacterial and mycobacterial (e.g., diphtheria, rheumatic fever)

–Parasitic (e.g., toxoplasmosis, Trypanosoma cruzi)

Infiltrative (2)

–Amyloidosis

–Gaucher disease

–Hurler disease

–Hunter disease

–Fabry disease

Storage

–Hemochromatosis

–Fabry disease

–Glycogen storage disease (type II, Pompe)

–Niemann-Pick disease

Neuromuscular/neurologic

–Duchenne and Emery-Dreifuss muscular dystrophies

–Friedreich ataxia

–Myotonic dystrophy

–Neurofibromatosis

–Tuberous sclerosis

Toxic

–Alcohol

–Drugs and chemotherapy: anthracyclines, cyclophosphamide, Herceptin

–Radiation

–Heavy metal, chemical agents

Inflammatory (granulomatous):

– Sarcoidosis

Idiopathic

Endomyocardial

– Endomyocardial fibrosis

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– Hypereosinophilic syndrome (Loeffler endocarditis)

Genetics

Autosomal dominant HCM is the most common form of primary genetic cardiomyopathy (1/500 in the general population). Genetic causes of DCM are less common, accounting for 1/3 cases, with mostly autosomal dominant inheritance. LVNC and ARVC are also inherited in an autosomal dominant fashion in addition to LQTS and other ion-channel disorders.

RISK FACTORS

Hypertension

Hyperlipidemia

Obesity

Coronary artery disease

Diabetes mellitus

Smoking

Physical inactivity

Excessive alcohol intake

Dietary sodium

Obstructive sleep apnea

Chemotherapy

GENERALPREVENTION

Reduce salt and water intake; home BPand daily weight measurement

DIAGNOSIS

HISTORY

Dyspnea at rest or with exertion

Paroxysmal nocturnal dyspnea

Orthopnea

Postprandial dyspnea

Right upper quadrant pain or bloating

Fatigue

Syncope

Edema

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PHYSICALEXAM

Tachypnea

Cheyne-Stokes breathing

Low pulse pressure

Cool extremities

Jugular venous distention

Bibasilar rales

Tachycardia

Displaced point of maximal impulse (PMI)

S3 gallop

Blowing systolic murmur

Hepatosplenomegaly

Ascites

Edema

DIFFERENTIALDIAGNOSIS

Severe pulmonary disease

Primary pulmonary hypertension

Recurrent pulmonary embolism

Constrictive pericarditis

Some advanced forms of malignancy

Anemia

DIAGNOSTIC TESTS & INTERPRETATION

ECG: LV hypertrophy, interventricular conduction delay, atrial fibrillation, evidence of prior Q-wave infarction

Hyponatremia

Prerenal azotemia

Anemia

Mild elevation in troponin

Elevated B-type natriuretic peptide (BNP) or pro-BNP

Mild hyperbilirubinemia

Elevated liver function tests

Elevated uric acid

Initial Tests (lab, imaging)

ECG

Chest radiograph

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–Cardiomegaly

–Increased vascular markings to the upper lobes

–Pleural effusions may or may not be present.

Echocardiography

–In DCM, four-chamber enlargement and global hypokinesis are present.

–In HCM, severe LV hypertrophy is present.

–Segmental contraction abnormalities of the LV are indicative of previous localized myocardial infarction.

Cardiac MRI

– May be useful to characterize certain nonischemic cardiomyopathies Stress myocardial perfusion imaging (MPI)

–Recommended in those with new-onset LV dysfunction or when ischemia is suspected

Diagnostic Procedures/Other

Cardiac catheterization

Helpful to rule out ischemic heart disease

Characterize hemodynamic severity

Pulmonary artery catheters may be reasonable in patients with refractory heart failure to help guide management.

TREATMENT

See “Heart Failure, Chronic” for detailed treatment protocols.

GENERALMEASURES

Reduction of filling pressures

Treatment of electrolyte disturbances

MEDICATION

First Line

Systolic failure syndromes

–Either an ACE inhibitor or an ARB are equally effective and should be considered in all patients; initiate at low doses and titrate as tolerated to target doses (3)[A].

–Entresto, a combination drug containing a neprilysin inhibitor and valsartan (ARNI), was recently approved for the treatment of systolic heart failure

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