"Low And Slow" - Calcium Channel Blocker And Beta Blocker Overdose - Help From MCHD Paramedic Podcast And EMC Podcast

“Low And Slow” refers to the hypotension and bradycardia that can occur with calcium channel and beta blocker overdose.

Today I’m reviewing calcium channel blocker overdose and beta blocker overdose. The two resources below are out standing podcast. The first is from the MCDC Paramedic Podcast and the second is from Emergency Medicine Cases.

Here is the link to Episode 36 – Calcium Channel Blocker And Beta Blocker Toxicity from the MCDC Paramedic Podcast. And here are the show notes:

Cardiovascular medication poisoning can produce markedly unstable patient presentations. Dr. Patrick and Brad Ward review some of the basics and more recent therapeutic developments in the treatment and management of beta-blocker and calcium channel blocker toxicity.

References:

1. St-Onge M, Anseeuw K, Cantrell FL, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Critical Care Medicine. 2017;45(3):e306-e315.

2. Wax P, Erdman A, Chyka P, et al. Beta-blocker ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005; 43(3):131-146.

Here is the link to Episode 90 – Low and Slow Poisoning from Emergency Medicine Cases. And here are excerpts from the excellent show notes:

One of the things we need to think about whenever we see a patient who’s going low and slow with hypotension and bradycardia is an overdose. B-blockers, calcium channel blockers (CCB) and digoxin are some of the most frequently prescribed cardiovascular drugs. And inevitably we’re going to be faced with both intentional and unintentional overdoses from these drugs in the ED. On this EM Cases podcast the Medical Director of The Ontario Poison Control Centre and Emergency Physician at St. Michael’s Hospital, Dr. Margaret Thompson, along with Dr. Emily Austin, Emergency Physician and Toxicologist at St. Michael’s Hospital, help us to recognize these overdoses early and manage them appropriately.

Differential Diagnosis of Low and Slow

Non-toxicological causes:

MI with cardiogenic shock

Hyperkalemia

Myxedema coma

Spinal cord injury

Hypothermia

Toxicological causes:

Calcium channel blockers

Beta-blockers

Digoxin

Opiates

Alpha-2 antagonists (e.g., clonidine)

Sodium channel blockers (e.g., TCA, carbamazepine, flexeril, antipsychotics, propranolol, cocaine)

Management of Seizures in the Toxicology Patient

There are several modifications of the usual algorithm for treating adult seizures when it comes to the poisoned patient.

Avoid Sodium Channel Blockers

Benzodiazepines are the first line treatment for treating seizures in patients with an overdose. In toxicological seizures, do not treat with antiepileptic drugs that have sodium channel blockade (i.e., phenytoin, fosphenytoin) because many poisons block sodium channels and additional sodium channel blockade may result in cardiac instability. If seizures persist, even after large doses of benzodiazepines, consider advancing to phenobarbital or propofol.

Bicarbonate

In patients with an overdose who are seizing and have evidence of sodium channel blockade (wide QRS on EKG), give sodium bicarbonate.

Naloxone

Consider naloxone in patients who may have an opioid overdose and are seizing. Some opioids can cause seizures (i.e., meperidine). Opioids may also cause hypoperfusion, which can lead to seizures.

A) Fluids

Establish two IVs and give the patient a fluid bolus of normal saline (1-2 liters) to start.

B) Decontamination

Activated charcoal

Consider decontamination with a dose of activated charcoal. The dose of activated charcoal is determined by the dose of the drug ingested in a 10:1 ratio of charcoal to drug. For example, a single 240mg tablet of Diltiazem requires only 2.4g of activated charcoal.

Factors to consider in the decision to give activated charcoal:

Does the drug bind to charcoal?

Charcoal does not bind lithium or iron, therefore, should not be given for overdoses of these drugs.

Was the drug ingested within one hour?

For most drugs, activated charcoal is indicated within one hour of ingestion only.

Is the drug likely to stay in the stomach for a prolonged time (beyond the one hour post-ingestion)?

Some drugs will stay in the stomach or upper intestinal tract for a prolonged period of time. In overdoses that involve drugs with these properties, charcoal should still be considered even if the ingestion occurred more than one hour ago. Examples of such drugs would include medications that are extended release formulations, enteric-coated medications, opioids and anticholinergic medications that delay gastric emptying, ASA, and theophylline.

Is the patient protecting their airway?

Aspiration pneumonitis is the most common complication of activated charcoal administration. If you suspect that a patient not be able to protect their airway because of altered level of awareness or anticipated seizure, avoid the use of activated charcoal.

Gastric lavage should only be considered for a massive life-threatening ingestion if it can be undertaken within 60 minutes of ingestion, and if the size of the tablets taken is smaller than that of the lavage tube (36-40f). Remember that these patients will need their airway secured prior to placement of the lavage tube. There is no evidence to suggest that gastric lavage reduces mortality from overdose.

Whole bowel irrigation

There is no evidence that whole bowel irrigation improves outcomes in overdoses.

Consider whole bowel irrigation in 3 situations:

Large drugs not bound by charcoal: iron, lithium, potassium

Body packers

Massive overdoses of extended release medications

Go to Episode 5 for a discussion on body packer management

C) Atropine

Consider a trial of 0.5mg IV atropine in patients with bradycardia.

What about cardiac pacing? In the overdose patient, transcutaneous pacing is unlikely to be successful, but may be attempted. If transcutaneous pacing is unsuccessful, it is generally agreed that transvenous pacing should be avoided in the patient with a slow and low poisoning as it may precipitate dysrhythmias in the overdose patient with an ‘irritable’ heart.

C) Calcium

Calcium Gluconate 3 amps IV push or Calcium Chloride 1amp IV push if a central line is established followed by infusion if an effect is seen.

C) High Dose Insulin

High dose Regular Insulin 1 U/kg plus 2 amps D50W IV push

Follow with 1 U/kg/hr insulin drip with 0.5 g/kg/hr dextrose if serum glucose <11

Titrate up q15 mins by 0.25-0.5U/kg/hr until cardiac contractility is adequate based on POCUS findings and vital signs

B-blocker poisoning usually requires more insulin than CCB poisoning

Monitor serum glucose q15mins, then q1h once the glucose has stabilized Monitor serum potassium

Insulin takes about 30-45 minutes to work – so it needs be to started early

One of the biggest pitfalls in the management of B-blocker overdoses is not giving enough insulin. Patients may require up to 8-10U/kg/hr!

D) Vasopressors

Norepinepherine or epinephrine may be required for hemodynamic support until the insulin takes effect. The choice of medication will depend on cardiac contractility on point of care ultrasound (POCUS). Epinepherine is favored over norepinephrine in patients with evidence of myocardial depression on POCUS. Norepinepherine is favored in patients with normal contractility on POCUS.

E) Glucagon

Glucagon may be considered as a last resort. Our experts do not recommend the routine use of glucagon in beta blocker overdoses. It can worsen hypotension and bradycardia as well as cause vomiting which increases the risk of aspiration.

F) Lipid emulsion therapy

[I placed the section on lipid emulsion therapy in a separate blog post, Lipid Emulsion Therapy – Help From Emergency Medicine Cases Episode 90, Posted on March 15, 2019 by Tom Wade MD. I did this so that I could easily find the section on Lipid Emulsion Therapy using my website’s search function.]