How Long Should You Hold In Weed?

How Long Should You Hold In Weed
Why Maintaining Cannabis Smoke Doesn’t Get You Higher – Many individuals say that the longer they inhale cannabis, the stronger the effect. However, more than 90% of the cannabinoids are immediately absorbed upon inhalation. The sensation of getting high from keeping it in has nothing to do with the cannabis itself; rather, it is caused by oxygen deprivation to the brain.

Depriving your brain of oxygen by holding in your cigarette might cause you to feel dizzy. Carbon monoxide and poisons from combustion enhance the lightheadedness caused by smoking and keeping it in. More you keep in, the higher your heart rate rises and the faster blood is pushed in to compensate for the low oxygen levels, which contributes to the sensation of receiving more from your cigarette.

In reality, smoking for longer than necessary results in the absorption of undesirable smoke and tars. Using joints and bongs to consume cannabis and inhaling the smoke causes tar to adhere more strongly to the lungs. However, if you inhale the vapor from a vaporizer, you run a decreased chance of tar clinging to your lungs, since this mode of cannabis ingestion has been shown to be cleaner.

How long should vape be inhaled?

How Long Should You Hold In Weed There is a common misconception that when vaping or smoking marijuana, you should hold your breath after taking a puff. It is also a cliche in television and film that holding in smoke for a longer period of time results in a more intense high. However, this notion is false and not supported by science.

  • Theoretically, if you want to extract the maximum THC and CBD from your cannabis, you should inhale the smoke or vapor for a longer period of time.
  • Before breathing, some individuals advise waiting 10 seconds, 20 seconds, or even a couple of minutes if possible.
  • It seems sense that doing so would increase the potency of your cannabis.

However, the reality is more complex.

WHAT HAPPENS WHEN YOU BREATHE IN CANNABIS SMOKE? Taking massive hits or keeping them in for an extended amount of time has no influence on the “effectiveness” of your marijuana. Let’s examine the real mechanisms underlying the absorption of cannabis in smoke or vapor.

What is bong lung?

A report on a case of “bong lung” in a patient with cystic fibrosis 7000, Australia 1 Departments of Respiratory Medicine, Royal Hobart Hospital, Liverpool Street, Hobart, Tasmania 7000, Australia 1 Departments of Respiratory Medicine, Royal Hobart Hospital, Liverpool Street, Hobart, Tasmania Locate papers authored by 2 Radiology, Royal Hobart Hospital, Liverpool Street, Hobart, Tasmania, 7000, Australia. 7000, Australia 1 Departments of Respiratory Medicine, Royal Hobart Hospital, Liverpool Street, Hobart, Tasmania 7000, Australia 2 Radiology, Royal Hobart Hospital, Liverpool Street, Hobart, Tasmania 7000 Australia, Hobart, Tasmania, Discipline of Pathology, University of Tasmania Medical School, Collins Street Author who connects with readers.

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Zoe Gao: ; Richard Wood-Baker: ; Robin Harle: ; Kon Muller: ; Jenny Hauser: ; David W Reid: 21 October 2009 receipt; 19 November 2010 acceptance. ©2010 Gao et al; licensee BioMed Central Ltd. This is an Open Access article given under the Creative Commons Attribution License (), which enables unlimited use, distribution, and reproduction in any form, as long as the original work is appropriately credited.

Recently, marijuana or “bong” lung has been described. Subjects are susceptible to spontaneous pneumothoraces and often develop big peripheral paraseptal lung bullae. Bullae development is likely caused by direct lung toxicity and repetitive barotrauma as a result of numerous valsalva maneuvers performed by smokers in an attempt to have a stronger pharmacological impact.

  • We report a possible instance of “bong lung” in a 23-year-old Caucasian male with cystic fibrosis who had a history of recurrent pneumothoraces and atypical sputum cytology abnormalities.
  • Our example demonstrates the need of asking young adults with cystic fibrosis about illegal drug use and the value of sputum cytology and computed tomography scanning when patients arrive with pneumothoraces and clinical worsening.

Recent research has shown marijuana use as a risk factor for bullous lung disease and recurrent pneumothoraces. The buildup of carbon-laden alveolar macrophages (AM) and polymorphonuclear cells (PMNs) in the airway lumen and lung parenchyma is indicative of an inflammatory response induced by the deposition of heated particulate matter in the upper lobe lung following inhalation.

  • Cannabis inhibits the capacity of AM to phagocytose microorganisms, increasing the risk of airway infection and lung abscesses.
  • There are also indications that smoking marijuana raises the risk of lung cancer, but this has not been conclusively confirmed.
  • We present the case of a 23-year-old Caucasian male with cystic fibrosis (CF) with recurrent pneumothoraces, most likely related to “bong lung” and the presence of atypical sputum cytology results.

A 23-year-old Caucasian male with cystic fibrosis was hospitalized with a one-week history of pleuritic chest discomfort, an increased cough, and purulent sputum, along with moderate hemoptysis. FEV 1 decreased to 2.01L (42% projected) from 2.76L (57% predicted) when lungs were healthy.

  1. On inspection, he was found to be clubbed, emaciated (BMI = 18), but not cyanosed.
  2. His chest auscultation demonstrated broad inspiratory crackles over both upper lobes.
  3. The patient was diagnosed with an infectious aggravation of bronchiectasis.
  4. His intravenous ceftazidime and tobramycin, physiotherapy, and nutritional supplements were maintained.

Pancreatic insufficiency and persistent airway sepsis due to Pseudomonas aeruginosa infection comprised the patient’s medical history. At birth, he was identified as carrying the F508/1898 + G CF gene mutation. He was reported to suffer from osteoporosis and severe gastroesophageal reflux.

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In the past two years, he had been hospitalized twelve times due to acute exacerbations of his CF lung disease, and his forced expiratory volume in one second L (FEV 1) had decreased from 3.17 L (74% expected) to 2.76L (56% predicted) during this time. He also had a history of recurrent pneumothoraces on the left side.

During his hospitalization, he had soaring fevers and severe pleuritic discomfort. For the purpose of detecting pulmonary emboli, a CT pulmonary angiography was conducted. The CT scan revealed no emboli, but massive bilateral upper lobe lung bullae, more apparent on the right side, along with other bronchiectatic alterations (Figure ).

Microscopy of sputum revealed the predicted preponderance of PMNs as well as droplets of oily brown material encased in mucus. PMNs were seen to contain vacuoles containing this brown-pigmented material, and these droplets were also observed to be surrounded by palisades of PMNs (Figure ). On closer interrogation, the patient acknowledged to consuming marijuana through a bong for several years.

He denied tobacco usage. A tentative diagnosis of severe CF bronchiectasis complicated with “bong lung” was made. The patient made a sluggish recovery over the course of three weeks and got marijuana use counseling. His FEV 1 at discharge was 2.33L (48% of the anticipated value).

  1. Marijuana lung had previously been documented in heavy smokers, but not in CF patients.
  2. Our patient arrived with repeated spontaneous pneumothoraces and a fast decline in lung function, which led to frequent exacerbations.
  3. High-resolution computed tomography (HRCT) scans revealed that he had massive apical bullae, comparable to those commonly reported in marijuana users.

This is the first known instance of bong lung in a patient with cystic fibrosis, however the frequency of marijuana usage in CF has been estimated to be as high as 20%, suggesting that this ailment may be underdiagnosed. Adults with cystic fibrosis should consider Bong lung since pneumothorax is a rather prevalent consequence of the condition, accounting for 75 percent of occurrences in people over the age of 18.

On sputum microscopy, our case was remarkable for the formation of new palisades of PMNs surrounding and attempting to engulf/phagocytose marijuana particles. There have been no previous reports of airway PMNs containing unusual inclusion bodies in marijuana smokers. However, increased PMN recruitment and activation in cystic fibrosis due to inhalation of marijuana may exacerbate the already excessive innate immune response and promote further lung injury.

Our case demonstrates the need of examining drug misuse and marijuana use in individuals with cystic fibrosis, particularly in the setting of unusual paraseptal bullae, recurrent pneumothoraces, fast deterioration in lung function, and repeated hospitalizations with worsening airway sepsis.

When individuals with cystic fibrosis have an inexplicable decline in respiratory status, sputum cytology and CT scans should be considered. PMNs: polymorphonuclear cells The authors report having no conflicting interests. At the time of the patient’s presentation and diagnosis, DR was the consultant physician and ZG was a medical student connected to the respiratory unit.

ZG discovered the case’s distinctiveness and drafted the initial case report draft. As did his colleagues RWB, KM, and RH, DR participated to the preparation of the case report. KM was responsible for interpreting the sputum cytology, while RH was responsible for interpreting the radiography.

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JH elaborated on the history of substance usage and contributed to the text evaluation. The final paper has been reviewed and approved by all writers. The patient provided written informed consent for the publishing of this case report and any related pictures. The written permission is available for evaluation by the journal’s editor-in-chief.

SW Hii, JD Tam, BR Thompson, and MT Naughton. Bullous lung disease linked to marijuana.2008’s Respirology 13:122–127. doi: 10.1111/j.1440-1843.2007.01186.x. Hii S, M.T. Naughton, and A. Young. Marijuana lung. Internal Medicine Journal 2006; 36:270–271. doi: 10.1111/j.1445-5994.2006.01040.x.

Tashkin DP. Marijuana smoking as a cause of lung damage. Monaldi Arch Chest Dis.2005; 63:93–100. Hamadeh R., A. Ardehali, R.M. Locksley, and M.K. York. A bone marrow transplant patient developed fatal aspergillosis after smoking tainted marijuana. Chest.1988; 94:432–433. doi: 10.1378/chest.94.2.432. PE Mann, AB Cohen, TN Finley, and AJ Ladman.

Alveolar macrophages. Differences in structure and function between nonsmokers and marijuana and tobacco smokers. Lab Invest.1971; 25:111–120. RA Sewell, AJ Cohn, and MC Chawarski. There are questions over cannabis’ role in triggering lung cancer. Eur Respir J.2008; 32:815–816.

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Psychoactive drug usage for recreational purposes by patients with cystic fibrosis. J Pediatr.1987; 111:293–299. doi: 10.1016/S0022-3476(87)80090-2. Stenbit A, Flume PA. Pulmonary problems in adult cystic fibrosis patients. American Journal of Medical Sciences 335 (2008):55–59.

What exactly is a dry hit?

Dry hits occur when the cotton (or other wicking material) in your vaporizer is not saturated with e-liquid. This might be due to a wicking issue, a coil being run at too high a wattage (or needing to be replaced), or a completely empty tank!

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