Vasopressor Medications Can Trigger Pulmonary Hypertension by Redistributing Blood Into Lungs
Vasopressor medications can trigger pulmonary hypertension by increasing blood volume rather than constricting blood vessels in the lungs, according to a study.
This insight may improve the management of patients treated with vasopressors, particularly those who also have heart disease, researchers said. Vasopressors are used to treat extremely low blood pressure. They do so by narrowing blood vessels, which increases blood pressure.
The study, “Vasopressors induce passive pulmonary hypertension by blood redistribution from systemic to pulmonary circulation,” was published in the journal Basic Research in Cardiology.
Vasopressor medications are commonly used when patients have heart failure or sepsis, a life-threatening condition that arises when the body’s response to infection injures its own tissues and organs. The treatments are also used in resuscitating patients.
Although vasopressors save lives, their use can have a serious downside: increasing pressure in the lungs. This causes pulmonary hypertension, reducing the right side of the heart’s ability to work properly.
Researchers do not know why vasopressors trigger high blood pressure in the lungs. Some studies suggest they do so by constricting small blood vessels in the lung, as they do in the rest of the body.
But researchers at West China Hospital, Sichuan University thought it might be a different process: passive re-routing of blood into the lung blood vessels to increase blood volume.
To test this idea, the research team gave the vasopressor phenylephrine to dogs, then measured a range of blood circulation parameters.
They found that the treatment increased blood volume in the lungs by 63 percent, and elevated blood pressure both in lung circulation and in the rest of the body.
The team noted that while the medication increased blood-vessel resistance in areas of the body outside the lungs, the resistance in lung blood vessels was only slightly higher than normal. This suggested that blood vessel constriction did not cause the increased lung pressure.
To test their hypothesis that larger blood volume caused the increase in pressure, the researchers slowly withdrew 5% to 10% of the total blood volume from the left atrium. That is the heart chamber that receives oxygenated blood from the lungs, and is exposed to elevated lung blood pressure.
Lowering blood volume reduced the pressure in the heart chamber and reversed lung hypertension, researchers found.
Other experiments confirmed the findings. They also demonstrated that the processes caused by vasopressor drugs are similar to those occurring in patients with left heart disease, where blood is redistributed from systemic circulation to lung circulation. Systemic circulation covers all other body parts but the lungs.
“In conclusion, we have identified a new type of passive PH [pulmonary hypertension] induced by vasopressors. Its lack of detection may underestimate the occurrence. Recognition of vasopressor-induced PH and understanding its underlying mechanisms may help improve patient care when vasopressors are used for patients with septic shock, especially with coexisting heart disease,” the team concluded.