28 May Cocaine Use and Pulmonary Hypertension
Pulmonary hypertension is a term that doctors use to describe the presence of dangerously high blood pressure levels within the arteries that feed blood to the lungs. If left untreated, this pressure can eventually lead to an abnormal enlargement in part of the heart and the subsequent development of heart failure. Cocaine use can contribute to the onset of pulmonary hypertension, especially when the drug is taken intravenously or inhaled through the lungs as “crack.” Fully 20 percent of all people who die from cocaine use show clear signs of artery damage stemming from pulmonary hypertension’s effects.
Pulmonary Artery Basics
Pulmonary is a medical term meaning “lung-related.” The term pulmonary artery is used in one of two basic ways. Sometimes, doctors use the term to refer specifically to the main pulmonary artery, a large blood vessel that travels from the lower right portion of the heart to the lungs. This vessel carries oxygen-depleted blood, which gets replenished with new oxygen transferred from millions of tiny sacs within the lungs called alveoli. Doctors also sometimes refer more generally to the pulmonary arteries, a term that applies to both the main pulmonary artery and all of the smaller blood vessels that branch off from that artery into the lungs.
Pulmonary Hypertension Basics
Pulmonary hypertension occurs when abnormal constriction (narrowing) appears within the pulmonary artery or its secondary blood vessels. This narrowing decreases the amount of room available for the blood traveling through these arteries, and therefore increases the pressure required to make that blood flow. Since the blood that flows into the pulmonary arteries comes from the right side of the heart, it is this segment of the heart that bears the brunt of the pressure increase. Over time, the excessive force required to pump blood to the lungs enlarges and weakens the right side of the heart. Eventually, these structural changes can lead to the development of heart failure, a condition that occurs when the heart can’t take in enough blood—or pump out enough blood—to maintain the oxygen flow required to sustain all systems, organs, and tissues.
Some people develop a condition called primary pulmonary hypertension (PPH), which occurs unpredictably and usually has no clear or consistent underlying cause. Others develop hypertension as a result of such diverse problems as respiratory disease, inflammation or disease within the pulmonary arteries, sickle cell anemia, congenital heart disease, advancing HIV infection, rheumatoid arthritis, lupus, chronic liver disease, blood clots that form within the main pulmonary artery or its tributaries, or a condition called a pulmonary embolism, which occurs when a clot or some other material travels from elsewhere in the body and lodges in one of the lung’s blood vessels.
Cocaine use can contribute to the development of pulmonary hypertension in any one of several different ways. First, the presence of cocaine in the bloodstream can trigger excessive levels of activity in a nerve network, called the sympathetic nervous system, which normally helps keep the body’s blood vessels working properly. One consequence of this excessive activity is a blood vessel narrowing that can produce abnormally elevated pressure levels within the pulmonary arteries. In addition, overexcitement of the sympathetic nervous system can trigger an erratic, potentially severe condition called vasospasm, which involves a rapid narrowing in various blood vessels (including the pulmonary arteries) that can produce drastically high pressure levels by intermittently cutting off most or all normal blood flow.
People who use cocaine can also develop serious problems by inadvertently introducing chemical impurities into their bloodstreams in the form of mineral substances called talc and silica. Talc is sometimes purposefully added to powered cocaine; it also frequently appears as a secondary ingredient in pills that get crushed and injected along with cocaine. Silica comes from the burning and inhalation of crack. Once inside the body, both talc and silica can effectively mimic a pulmonary embolism and trigger hypertension by lodging within a pulmonary blood vessel. In addition, habitual use of cocaine can lead to direct damage in the lining of the pulmonary vessels; in turn, this damage can lead to inflammation that narrows the blood vessels, and thereby contributes to pulmonary hypertension.
One out of every five people who die from cocaine use has significant shrinkage in both the small and medium blood vessels that branch from the main pulmonary artery, according to a study review published in 2007 in RadioGraphics, a journal produced by the Radiological Society of North America. This type of shrinkage is clear physical evidence of pulmonary hypertension within the affected blood vessels. In people who use cocaine, damage to the pulmonary artery and its tributaries tends to occur at an unusually early age.
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