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).
Symptoms of arrhythmias include (4):
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 CBD’s 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).
CBD’s 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).
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.
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 Kraków, Os. Zlota Jesien 1 Poland Reviewers: Birmingham 3/99: B Groszek, H Kupferschmidt, N Langford, K Olson, J Pronczuk.