I used my Alivecor heart monitor to record the event, send it in for an analysis and the results were afib with rapid ventricular response sustained. After reseaching what RVR is and after reading this article I am now convinced that marijuanna does have an ill effect on the heart. One study implicated cannabis in ‘cardiac asystole’ that basically means the heart stops beating. A patient was noted to have heart pauses of almost 6 seconds long on cardiac monitoring with the pauses related to periods of cannabis inhalation. Upon stopping use of cannabis, repeat monitoring showed that there were no further pauses.
Cannabinoids appear to have many functions in the digestive system including the inhibition of gastric acid production, GI motility, secretion and ion transport, and the attenuation of visceral sensation and inflammation (reviewed inReference 33). Perturbations in the levels of various components of the ECS have been noted in experimental animal models of GI disorders, as well as in clinical studies (reviewed inReference 33). The sections below summarize the information regarding the uses of cannabis and cannabinoids in the treatment of various disorders of the GI system.
Pre-clinical studies suggest that THC and CBD may protect against excitotoxicity, oxidative stress and inflammation in animal models of Alzheimer’s disease (AD). Significant evidence from pre-clinical, clinical and epidemiological studies supports an association between cannabis (especially THC-predominant cannabis) and THC, and an increased risk of psychosis and schizophrenia. Pre-clinical studies suggest certain cannabinoids (e.g. THC) may alleviate opioid withdrawal symptoms. Pre-clinical studies suggest CB1 receptor agonism (e.g. THC) may help increase the reinforcing properties of alcohol, increase alcohol consumption, and increase risk of relapse of alcohol use, as well as exacerbate alcohol withdrawal symptom severity. However, while limited evidence from short-term clinical studies suggests a potential for oral THC and nabilone to decrease certain symptoms of PTSD, there are no long-term clinical studies for these preparations or any clinical studies of smoked/vapourized cannabis for PTSD.
The recreational use of cannabis has sharply increased in recent years in parallel with its legalization and decriminalization in several countries. Commonly, the traditional cannabis has been replaced by potent synthetic cannabinoids and cannabimimetics in various forms. Despite overwhelming public perception of the safety of these substances, an increasing number of serious cardiovascular adverse events have been reported in temporal relation to recreational cannabis use. These have included sudden cardiac death, vascular (coronary, cerebral and peripheral) events, arrhythmias and stress cardiomyopathy among others.
Evidence shows marijuana users are much less likely to develop metabolic syndrome, a significant risk factor for obesity, diabetes, and heart disease. New discoveries reported at ICRS symposium highlight CBD’s potential for treating anxiety, cancer, heart disease, substance abuse, brain injuries, and more. This episode was meant to simply start the dialogue and make afibbers aware of the potential positive and negative effects of marijuana on their atrial fibrillation.
In mice, it was shown that hexahydrocannabinols could, as is typically observed with THC, produce cataleptogenic effectsReference 429. The clinical implications of this conversion of CBD to THC and hexahydrocannabinols are the subject of heated debate and currently unclear. Whereas the acute effects on the CNS and physiological effects occur within minutes by the smoking route or by vapourizationReference 149Reference 417, the acute effects proceed on a time scale of hours in the case of oral ingestionReference 417Reference 418. Acute oral administration results in a slower onset of action, lower peak blood levels of cannabinoids, and a longer duration of pharmacodynamic effects compared to smokingReference 78. The psychotropic effect or "high" occurs much more quickly by the smoking than by the oral route, which is the reason why smoking appears to be the preferred route of administration by many, especially among non-medical usersReference 419.
No statistically significant differences were observed between placebo and all CBD doses for UPDRS scores CBD gummies for sale, plasma BDNF levels or H1-MRS measures. However, the 300 mg CBD dose was associated with a statistically significant difference in mean total scores from placebo in the PDQ-39 suggesting that the 300 mg daily CBD dose is associated with an improvement in QoL measures in PD patients with no psychiatric comorbidities. With regard to clinical studies, one double-blind, placebo-controlled, 15-week, crossover trial of 15 patients with HD taking 10 mg/kg/day of oral CBD did not report improvement in symptoms associated with HDReference 258. A randomized, double-blind, placebo-controlled, crossover pilot study found little or no beneficial effect of 1 or 2 mg nabilone over placebo in 37 patients with HDReference 245. However, nabilone was well tolerated in this patient population and did not appear to exacerbate chorea or HD-associated psychosis, although some adverse effects such as drowsiness and forgetfulness were noted.
Symptoms of a dronabinol overdose may include dry mouth, extreme drowsiness, feeling extremely happy or sad, fast heartbeat, memory problems, urinating less than usual or not at all, disorientation, unusual thoughts or behaviors, problems with speech or coordination, panic, fainting, or seizure (convulsions). Dronabinol should never be given to another person, especially someone who has a history of drug abuse or habitual marijuana use.
In contrast, another study concluded that nabiximols treatment, in cannabis-naïve MS patients, was not associated with cognitive impairmentReference 699. However, the study did raise the possibility that higher dosages could precipitate changes in psychological disposition, especially in those patients with a prior history of psychosis. In any case, important information is generally lacking regarding the long-term adverse effects of chronic cannabinoid use in MS patients, and more generally in patients using for therapeutic purposes. The reasons behind the apparent discrepancies between subjective and objective measures are not clear; however, a number of possible explanations may be found to account for the differences.
Protective effects associated with exposure to CBD included the prevention of additional histological damage to arthritic hind-paw joints, suppression of TNF release from arthritic synovial cells, attenuation of lymph node cell proliferation, suppression of production of reactive oxygen intermediates and attenuation of lymphocyte proliferation. A recent systematic review and meta-analysis of clinical studies examining the strength of the existing evidence for the "opioid-sparing" effect of cannabinoids in the context of analgesia concluded that there was an absence of randomized, well-controlled clinical studies that provide evidence of an "opioid-sparing" effect of cannabinoidsReference 852. Furthermore, the existing data from clinical trials looking at the "opioid-sparing" ability of cannabis are mixed.