It can be injected, sniffed, or smoked (NDA,2014). Cigarette smoke is an irritant and results in low-grade inflammation of the airways and alveoli, with increased numbers of inflammatory cells notably macrophages and neutrophils. These in turn produce elastases, which are proteolytic enzymes that destroy elastin, the protein that is found in lung tissue. The irritant effect of cigarette smoke increases the level of elastases in the lungs beyond the body’s ability to neutralize the elastases. Over the years, the elastin within the lungs is lost, tissue becomes destroyed, and emphysema is the resulting condition (Stockley RA, 1995). This combined with the heroin additive increases a person’s chances of developing emphysema. It is thought that the damage is caused due to heroin burning at a higher temperature than tobacco.This Inflammation in the airways and repeated cycles of inflammation and repair leads to the remodelling of the tissues of the airways (P.Walker, …show more content…
This proves to be difficult as pre-hospital clinicians do not carry air nebulisers. Instead, we use low doses of oxygen, which has now been proven to worsen hypercapnia. NWAS states that to prevent the over-oxygenation of deteriorating patients, oxygen driven nebulisers are limited to six minutes. This will reduce the risk of hypercapnia (NWAS,2016). Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. End tidal C02 monitoring is available in the pre-hospital setting. It correlates well against the hospital tests such as arterial blood gas testing which is painful and invasive (Ross, et al,