Approach to Bradycardia

Approach to Bradycardia

Last week we discussed an approach to bradycardia at morning report.

When there is an abnormality in a vital sign, the first step is to ensure stability.  

1.       Assess the ABCs, get monitors on, IV access

a.       Bradycardia is defined as a heart rate less than 60 beats per minute

2.       Ask yourself, is this unstable bradycardia?

a.       If yes à go down the unstable bradycardia ACLS algorithm

b.      If no à there is time to perform a focused history, physical and get investigations

3.       How do you define unstable bradycardia?

a.       Bradycardia that is causing one of the following symptoms:

                                                               i.      Hypotension

                                                             ii.      Acute altered mental status

                                                            iii.      Signs of shock

                                                           iv.      Ischemic chest discomfort

                                                             v.      Acute heart failure

4.       If there is unstable bradycardia, follow the ACLS algorithm including considering:

a.       Atropine

b.      Transcutaneous pacing

c.       Dopamine or epinephrine infusions

5.       If it is stable bradycardia, there is time to collect more information with a focused history, physical and get investigations

6.       An ECG is a key investigation!

7.       Two main question are:

a.       What type of rhythm is it?

b.      What is causing the bradycardia?

Rhythms associated with bradycardia

Bradycardia is an umbrella term that means that the heart rate is less than 60 beats per minute. But there can be several different rhythms that can cause a heart rate of less than 60 bpm.

-          Bradycardias can be classified narrow complex or wide complex (and as regular or irregular)

Narrow complex bradycardias

-          Sinus bradycardia

-          Junctional bradycardia

-          Sinus-node dysfunction

-          Second degree AV block, type I or II

-          Complete AV block (third degree AV block) with junctional escape

-          Atrial flutter or atrial fibrillation with high degree block/slow ventricular response

Wide complex bradycardia

-          Idioventricular rhythm

-          Complete AV block (third degree AV block) with ventricular escape

-          Any other causes of narrow complex bradycardia with aberrancy or bundle branch block

Causes of bradycardia

There are many causes of bradycardia. While not a fully inclusive list, causes can include:

Cardiac disease

-          Myocardial ischemia/MI

-          Myocarditis

-          Cardiomyopathies

-          Congenital disorders (such as muscular dystrophy)

Metabolic

-          Electrolyte disturbances (i.e. hypo- or hyper-kalemia)

-          Hypothyroidism

-          Hypothermia

Drugs

-          Medications (i.e. digoxin, beta blockers, calcium channel blockers, etc)

-          Toxidromes (cholinergic)

Iatrogenic

-          Post-cardiac procedure, surgery or transplantation  

Infectious

-          Endocarditis

-          Lyme disease

-          Typhoid fever

-          Chagas Disease

Autoimmune

-          Systemic lupus erythematosus

-          Rheumatoid arthritis

-          Scleroderma

Infiltrative

-          Sarcoidosis

-          Amyloidosis

-          Hemochromatosis

Physiological causes

-          Athletes

-          Vagal stimuli

Other causes

-          Hypoxia

-          Obstructive Sleep Apnea

-          Increased intracranial pressure (i.e. Cushing response)

References:

1.       Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342(10):703-9.

2.       Life in the Fastlane. Bradycardia. https://lifeinthefastlane.com/resources/bradycardia-ddx/

Alcohol withdrawal

Yesterday we discussed alcohol withdrawal.

Alcohol use can have effects on the body from head to toe. Complications of alcohol use can include:

-          Thiamine deficiency

o   Causing Wernicke encephalopathy characterized by the triad of encephalopathy, oculomotor dysfunction, and ataxia, or Korsakoff syndrome, the chronic consequence of Wernicke encephalopathy

-          Malnutrition and refeeding syndrome

-          Alcoholic ketoacidosis

-          Hypertension and cardiovascular disease

-          Cardiomyopathy

-          Liver disease including cirrhosis and hepatitis

-          Pancreatitis

-          Gastritis and esophagitis

-          Peripheral neuropathy

-          Bone marrow suppression

-          Injury/trauma

-          Malignancies, including GI, liver, and breast cancer

-          Psychiatric disorders

Another complication of alcohol use is alcohol withdrawal. There are several different phases of alcohol withdrawal. As such, the timing of symptoms compared to the last drink is helpful piece of information on history.

Manifestations of alcohol withdrawal:

-          Early alcohol withdrawal (onset 1-48 hours after last drink) can include symptoms such as insomnia, tremulousness, anxiety, GI upset, anorexia, headache, diaphoresis and palpitations.

-          Alcohol withdrawal seizures (onset 6-48 hours after last drink) are usually generalized, tonic-clonic seizures. Don’t forget basic principles such as accuchecks to ensure it is not a hypoglycemic seizures and reporting to the Ministry of Transportation for seizures. First line treatment of alcohol withdrawal seizures is benzodiazepines

-          Alcoholic hallucinosis (onset 12-48 hours after last drink) usually involves visual, auditory or tactile hallucinations. Importantly, orientation and vital signs are normal and that is what distinguishes alcoholic hallucinosis from delirium tremens.

-          Delirium tremens (onset 24-96 hours after last drink) is a serious manifestation of alcohol withdrawal characterized by delirium, agitation, tachycardia, hypertension, fever and diaphoresis. It is a medical emergency.

Principles of the management of alcohol withdrawal include:

1.       Rule out other causes of symptoms. Depending on the clinical presentation, for example confusion or change in level of consciousness, don’t forget to investigate for other causes of the presentation such as infection, co-ingestions, metabolic derangement, liver failure, GI bleeds, pancreatitis, and injuries (such as subdural hematoma) to name a few.

2.       Supportive care.

a.       Initial resuscitation including ABCs. Treat volume depletion.

b.      Treat any identified triggers or other causes of symptoms. There can be something else going on, such as pancreatitis or an infection, that led to reduced alcohol intake and then alcohol withdrawal.

c.       GIVE THIAMINE (before giving glucose) and a multivitamin  

d.      Nutritional support (may need to be NPO depending on level of consciousness to prevent aspiration) à consider other methods of nutritional support, get SLP and dietitian involved, and don’t forget to monitor for refeeding syndrome.

e.      Monitor severity of alcohol withdrawal with CIWA-Ar and clinical assessments.

                                                               i.      Items on the CIWA-Ar (Clinical Institute Withdrawal Assessment Scale for Alcohol, revised) include: nausea and vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile auditory and visual disturbances, headache, and orientation.  

f.        Treat alcohol withdrawal with benzodiazepines.

                                                               i.      Often diazepam or lorazepam are the benzodiazepines of choice and they are used in a symptom-triggered approach (administration and dose triggered by CIWA-Ar score)

                                                             ii.      Diazepam has a longer half-life so is usually the first choice to avoid recurrent withdrawal or seizures.

                                                            iii.      However, with cirrhosis or acute hepatitis, a benzodiazepine with a shorter halt-life such as lorazepam, may be preferred to avoid over-sedation.

                                                           iv.      Take a look and become familiar with the CIWA-Ar protocols at your institution.

                                                             v.      For refractory delirium tremens, barbiturates such as phenobarbital and/or propofol may be necessary.

References:

1.       Up-to-date “Management of moderate and severe alcohol withdrawal syndromes”. Hoffman et al. Last updated Jan 17, 2017.

2.       Schuckit M. Recognition and Management of Withdrawal Delirium. NEJM. 2014;371:2109-13. 

Clostridium difficile Infection

During morning report we discussed a case of Clostridium difficile Infection (CDI). Here are some key points about the risk factors, diagnosis, risk stratification, and management of CDI.

Pathophysiology and Risk factors:

-          Clostridium difficile is an anaerobic Gram-positive spore-forming bacillus

-          Transmitted through the fecal-oral route by spores that are resistant to heat, acid, and antibiotics

-          Colonizes the large intestine and makes exotoxins that cause colitis in susceptible patients

-          In a healthy host, colonization is prevented by barrier properties of a health fecal microbiota

-          Most of the risk factors for CDI have to do with a weakened fecal microbiota

-          Risk factors:

o   Antibiotics (Most important risk factor!)

§  Almost all antibiotics are a risk factor but classically think of fluoroquinolones, cephalosporins, clindamycin, ampicillin and amoxicillin (1)

§  Interestingly, a recent cohort study in JAMA Internal Medicine, showed that even the receipt of antibiotics by prior hospital bed occupants can increase the risk for CDI in subsequent patients who occupy the same bed! (2)

o   Advanced age

o   Chemotherapy

o   Underlying diseases (such as inflammatory bowel disease, immunosuppression) (1)

Diagnosis:

-          The diagnosis of CDI is usually made by C diff toxin assays in stool (either an enzyme immunoassay for toxins or a PCR test for microbial toxin genes)

-          Culturing Clostridium difficile in stool is not widely available and is not often used

-          Note that the C diff toxin assays may stay positive after a CDI is appropriately treated so a positive C diff stool test after an appropriate course of treatment for CDI needs to be interpreted with caution (i.e. involve the expertise of Infectious Disease)

Risk stratification and management:

-          How one treats CDI varies depending on the severity of the infection.

-          One resource I find very helpful is the Antimicrobial Stewardship Program of UHN/SHS best practices:

http://www.antimicrobialstewardship.com/antimicrobial-stewardship-best-practices (3)

-          This is their summary slide on C difficile severity Criteria:

Source: http://www.antimicrobialstewardship.com/antimicrobial-stewardship-best-practices (3)

-          And here is a summary of the treatment of CDI based on severity:

-           

Source: http://www.antimicrobialstewardship.com/antimicrobial-stewardship-best-practices (3)

-          Bottom line is that metronidazole is first-line for mild-moderate disease and ORAL vancomycin is first line for severe disease. Once there is complicated/fulminant disease, ORAL vancomycin and IV metronidazole are both given and General Surgery and Infectious Diseases consultations are key.

-          Keep in mind that the vancomycin needs to be given ORALLY! It is not absorbed in the GI tract and therefore will act in the colon where the infection is; IV vancomycin isn’t going to help.

-          There are subtleties to the treatment of recurrent CDI including much interest in fecal microbial transplantation, which has evidence supporting its effectiveness and cost-effectiveness in the treatment of recurrent CDI, including RCTs (4).

References:

1.       NEJM review article: Leffler D, Lamont JT. Clostridium difficile infection.  N Engl J Med. 2015;372(16):1539. http://www.nejm.org/doi/pdf/10.1056/NEJMra1403772

2.       Freedberg et al. Receipt of antibiotics in hospitalized patients and risk for Clostridium difficile infection in subsequent patients who occupy the same bed. JAMA Intern Med. 2016;176(12):1801-1808.

3.       Antimicrobial Stewardship Program of UHN/SHS best practices: http://www.antimicrobialstewardship.com/antimicrobial-stewardship-best-practices

4.       Health Quality Ontario. Fecal Microbiota therapy for Clostridium difficile infection: A health technology assessment. Ont Health Technol Assess Ser. 2016; 16(17):1-69.