INTOX Home Page
    

CBD for Arrhythmia

Can CBD help with arrhythmia, and if so, how?

Arrhythmia and Its Symptoms

An arrhythmia (also called irregular heartbeat) is a problem with the rate or rhythm of a heartbeat. It means that the heart beats too fast, too slowly, or with an irregular pattern (1).

In healthy adults, the heart regularly beats at a rate of 60 to 100 times per minute (2).

Cardiac arrhythmias can be classified according to their effect on the heart rate, with bradycardia indicating a heart rate of fewer than 60 beats per minute and tachycardia indicating a heart rate of more than 100 beats per minute (3).

Why People Are Turning to CBD for Arrhythmia

According to a study published in the British Journal of Pharmacology, drastic cannabidiol or CBD administration suppressed irregular heartbeat caused by ischemia-induced heart arrhythmias (inadequate blood supply in the heart) (5). Thus, CBD provides the heart with protection.

The American Heart Association describes ischemia as a condition characterized by a restricted or reduced blood flow (which also restricts the flow of oxygen) (6).

In the said study, irregular heartbeats were monitored during ischemia before periods of CBD perfusion (passage of fluid through the circulatory system).

The size of the infarct (a localized area of dead tissue) or obstructed blood supply and cell damage in the heart were also examined through the drawing of blood from the arteries.

According to an article published by the University of Rochester Medical Center, as a result of long-term stress, high cortisol blood levels can raise blood cholesterol, blood pressure, triglycerides, and blood sugar (7). These are the common risk factors for arrhythmia and other heart diseases.

Meanwhile, CBD has been shown to possess anti-anxiety properties that may help combat stress.

Published in Neurotherapeutics Journal, a 2015 review of 49 studies demonstrated CBDs efficacy in reducing anxiety behaviors linked to multiple disorders (8).

In some cases that contribute to the development of ventricular tachycardia, open-heart surgery may be needed. An example of such a case is when there are blockages in the blood vessels (9).

After surgery or a heart attack, an individual may experience loss of appetite due to surgical pain, which can eventually lead to low levels of calcium and potassium, slowing down long-term recovery (10). Electrolyte imbalances can also make an individual susceptible to arrhythmia (11).

Fortunately, when it comes to pain relief, CBD may be useful. A study published in Chemistry and Biodiversity showed that a 1:1 ratio of CBD and THC helped with pain and sleep problems (12).

Meanwhile, results from a study, which examined the interaction between cannabinoids and cannabinoid receptors, showed evidence of how the endocannabinoid system can regulate appetite (13).

CBDs potent anti-inflammatory properties were also demonstrated in a 2018 study published in the Journal of Pharmacology and Experimental Therapeutics (14).

Working directly with the cannabinoid receptors of the body to help suppress inflammation, CBD may help people with myocarditis experience pain relief as well as reduced signs and symptoms.

Myocarditis is an inflammation of the heart muscle, which causes arrhythmias (15).

Conclusion

Studies have shown the amazing health benefits of CBD. This non-psychoactive cannabinoid from the cannabis plant may help prevent arrhythmia by providing its potential therapeutic properties.

However, there are side effects that come with CBD use, such as possible interactions with drugs used to promote the health of the cardiovascular system.

According to Mayo Clinic, other possible side effects of CBD use include drowsiness, dry mouth, diarrhea, fatigue, and reduced appetite (16).

Thus, before using CBD or any CBD products (such as tincture, gummies, salves, patches, or lotions) as a supplement to an existing therapy or as a remedy for specific heart conditions like arrhythmias, consult with a doctor experienced in cannabis use for advice.

References

  1. MedlinePlus. (2016, August 15). Arrhythmia. Retrieved from https://medlineplus.gov/arrhythmia.html.
  2. Harvard Health Publishing. (2019, Feb). Cardiac Arrhythmias. Retrieved from https://www.health.harvard.edu/a_to_z/cardiac-arrhythmias-a-to-z.
  3. Ibid.
  4. MedlinePlus. (2016, August 15). Arrhythmia. Retrieved from https://medlineplus.gov/arrhythmia.html.
  5. Walsh SK, Hepburn CY, Kane KA, Wainwright CL. Acute administration of cannabidiol in vivo suppresses ischaemia-induced cardiac arrhythmias and reduces infarct size when given at reperfusion. Br J Pharmacol. 2010;160(5):12341242. DOI:10.1111/j.1476-5381.2010.00755.x.
  6. American Heart Association. (2015, July 31). Silent Ischemia and Ischemic Heart Disease. Retrieved from https://www.heart.org/en/health-topics/heart-attack/about-heart-attacks/silent-ischemia-and-ischemic-heart-disease.
  7. University of Rochester Medical Center Rochester. Stress Can Increase Your Risk for Heart Disease. Retrieved from https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=1&ContentID=2171.
  8. Blessing EM, Steenkamp MM, Manzanares J, Marmar CR. Cannabidiol as a potential treatment for anxiety disorders. Neurotherapeutics. 2015;12(4):825836. doi: 10.1007/s13311-015-0387-1.
  9. Mayo Clinic. (2018, Oct 4). Ventricular tachycardia. Retrieved from https://www.mayoclinic.org/diseases-conditions/ventricular-tachycardia/diagnosis-treatment/drc-20355144.
  10. Parham WA, Mehdirad AA, Biermann KM, Fredman CS. Hyperkalemia revisited. Tex Heart Inst J. 2006;33(1):4047.
  11. Gettes LS. Electrolyte abnormalities underlying lethal and ventricular arrhythmias. Circulation. 1992;85(1 Suppl):I70I76.
  12. Russo EB, Guy GW, Robson PJ. Cannabis, pain, and sleep: lessons from therapeutic clinical trials of Sativex, a cannabis-based medicine. Chem Biodivers. 2007;4(8):17291743. DOI:10.1002/cbdv.200790150.
  13. Kirkham TC. Cannabinoids and appetite: food craving and food pleasure. Int Rev Psychiatry. 2009;21(2):163171. DOI:10.1080/09540260902782810.
  14. Petrosino S et al. Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis. Journal of Pharmacology and Experimental Therapeutics June 2018, 365 (3) 652-663; DOI: https://doi.org/10.1124/jpet.117.244368.
  15. Mayo Clinic. (2019, Mar 16). Myocarditis. Retrieved from https://www.mayoclinic.org/diseases-conditions/myocarditis/symptoms-causes/syc-20352539.
  16. Bauer, B. (2018, Dec 20). What are the benefits of CBD and is it safe to use? Retrieved from https://www.mayoclinic.org/healthy-lifestyle/consumer-health/expert-answers/is-cbd-safe-and-effective/faq-20446700.



    HYPOKALAEMIA



    DEFINITION



    A serum potassium concentration less than 3.5 mmol/L (mEq/L).



    A serum potassium concentration of less than 2 mmol/L is regarded as

    severe hypokalaemia.



    TOXIC CAUSES



    Hypokalaemia in acute poisonings a consequence of one the following

    mechanisms:



    Secondary to shift of potassium from extracellular to intracellular

    space

         Competitive blockade of K+ channels

              Barium

              Chloroquine

         Increased Na+/K+ ATPase activity

              Beta 2 agonists (e.g. albuterol/salbutamol, terbutaline,

                epinephrine)

              Caffeine 

              Insulin 

              Theophylline, 

         Toxic metabolic alkalosis or respiratory alkalosis



    Secondary to increased renal losses of potassium

         Chronic glucocorticoid administration

         Chronic toluene abuse

         Liquorice and carbenoxolone

         Potassium-losing diuretics



    Secondary to increased gastrointestinal losses of potassium

         Any acute poisoning associated with protracted vomiting or

           diarrhoea.



    Secondary to increased potassium loss in sweat

         Cholinergic syndrome with severe sweating



    NON-TOXIC CASES



    Secondary to shift of potassium from extracellular to intracellular

      space

         Insulinoma

         Metabolic or respiratory alkalosis

         Total parenteral nutrition



    Secondary to increased gastrointestinal losses of potassium

         Anorexia nervosa/bulimia

         Diarrhoea

         Prolonged gastric suction

         Toxic megacolon 



         Villous adenoma of colon

         Vomiting, protracted

         Zollinger-Ellison syndrome



    Secondary to increased renal losses of potassium

         Cushing's syndrome 

         Hyperaldosteronism, primary or secondary

         Increased urinary flow (postobstructive diuresis, large 

           IV infusions)

         Magnesium deficiency

         Renal tubular acidosis



    Inadequate dietary intake of potassium

         Alcoholism

         Anorexia nervosa

         Intravenous infusion of potassium-free fluid 

         Malnutrition



    CLINICAL FEATURES



    At serum potassium concentrations between 2.5 and 3.5 mmol/L the

    patient may be asymptomatic or experience mild symptoms, including

    weakness and muscle fatigue.  As serum potassium concentration falls

    below 2.5 mmol/L, clinical manifestations may progress to include

    severe muscle weakness, ileus, respiratory paralysis and atrial and

    ventricular arrhythmias.  The patient with severe hypokalaemia is at

    risk of sudden death from respiratory or cardiac arrest (ventricular

    tachycardia).



    Hypokalaemia alters the resting membrane potential and slows

    repolarisation.  These changes are reflected in the electrocardiogram

    by depression of ST segments, flattening of the T wave, and prominence

    of the U wave (rarely).  The absence of a visible T wave and the

    presence of a U wave may mimic QT prolongation. 



    DIFFERENTIAL DIAGNOSIS



    Arrhythmias:  Hypoxia, use of digitalis or other drugs, myocardial

    injury, and other electrolyte disturbances (hypomagnesaemia).

    Muscle weakness: Myasthenia gravis, botulism, and central or

    peripheral neurological disease.



    RELEVANT INVESTIGATIONS



    Serum potassium

    Serum sodium, chloride, and bicarbonate

    Renal function tests (urea, creatinine)

    ECG

    Arterial blood gas analysis

    Urine potassium concentration (24 hour collection)



    TREATMENT



    Treatment is determined by the acuity and mechanism of the

    intoxication, as well as the serum potassium, the severity of

    symptoms, and the presence or absence of ECG abnormalities.  For

    patients with hypokalaemia due to chronic diuretic use or prolonged

    severe gastrointestinal or renal potassium losses, the total body

    potassium deficit may be as large as 300 to 500 mEq. On the other

    hand, hypokalaemia due to intracellular shift of potassium is

    associated with relatively small total body potassium deficit and may

    not warrant aggressive replacement.



    Mild hypokalaemia can usually be managed with oral potassium

    supplements.  Moderate-to-severely symptomatic patients require, in

    addition to management of the underlying condition, continuous cardiac

    monitoring and intravenous potassium supplementation.  Specific

    management of acute complications such as cardiorespiratory arrest,

    ventricular arrhythmias, respiratory failure and rhabdomyolyis is also

    indicated.



     Mild hypokalaemia (3 to 3.5 mmol/L)

         Oral potassium supplementation of 30 to 100 mmols/day is

         adequate.

         Elixir: 10% elixir provides 20 mmols/tablespoon; 2 to 3

         tablespoons/day is usually sufficient. Best tolerated when

         diluted with juice and taken with meals.

         Tablets: Wax matrix tablets contain 6 to 8 mmols/tablet and may

         be better tolerated than the liquid form.



     Moderate hypokalaemia (2.5 to 3 mmol/L)

         Oral potassium replacement as for mild hypokalaemia, if

         tolerated.  In symptomatic patients, and those unable to take

         oral potassium, administer up to 10 mmol of potassium per hour

         intravenously, with continuous cardiac monitoring and frequent

         monitoring (e.g. every 4 hours) of the serum potassium

         concentration.



     Moderately severe hypokalaemia (2 to 2.5 mmol/L)

         Oral potassium replacement as for mild hypokalaemia, if

         tolerated. In addition, administer up to 15 mmol of potassium per

         hour intravenously, with continuous cardiac monitoring and

         frequent monitoring (e.g. every 4 hours) of the serum potassium

         concentration.



     Severe hypokalaemia (<2 mmol/L)

         Oral potassium replacement as for mild hypokalaemia, if

         tolerated. In addition, administer up to 20 mmol of potassium per

         hour intravenously, with continuous cardiac monitoring and

         frequent monitoring (e.g. every 4 hours) of the serum potassium

         concentration.  In very severe cases, infusion rates as high as

         30 mmol/hour have been used, but caution should be exercised

         because of the potential for cardiotoxicity, especially if the

         potassium is administered via a central catheter.



     Pediatric dosing of potassium is based on the body weight, duration

    and mechanism of hypokalaemia, and the potassium level. In general,

    dosing should not exceed 0.25 mmol/kg per hour.



     Hypokalaemia associated with beta-2 adrenergic stimulation may be

    treated with beta-adrenergic blockers (eg, propranolol, esmolol).

    Caution should be used if the patient has a history of asthma. 



    CLINICAL COURSE AND MONITORING



    Continuous monitoring of cardiac rhythm together with careful

    monitoring of serum potassium and other electrolyte concentrations,

    acid-base status, and renal function is indicated until severe

    hypokalaemia and the underlying cause are controlled.



    Over-zealous infusion of potassium in the acute phase of hypokalaemia

    secondary to potassium channel blockade or beta-2-adrenergic

    stimulation may result in rebound hyperkalaemia during recovery.



    LONG-TERM COMPLICATIONS



    Hypoxic brain and other organ injury may occur as a result of cardiac

    or respiratory arrest secondary to hypokalaemia. 



    Acute renal failure may be associated with rhabdomyolysis secondary to

    hypokalaemia.



    AUTHOR(S)/REVIEWERS:



    Author:        Dr Barbara Groszek

                   Department of Clinical Toxicology, Jagiellonian

                   University

                   31-826 Krakw, Os. Zlota Jesien 1

                   Poland



    Reviewers:     Birmingham 3/99: B Groszek, H Kupferschmidt,

                   N Langford, K Olson, J Pronczuk.