The effects of CO
2
inhalation were determined on 23 stroke patients with and without hypertension who underwent clinical, cardiohemodynamic, cerebral blood flow (hemispheric mean and regional), cerebral metabolic rate and cerebral angiographical studies.
Cardiac output, heart rate, systemic and pulmonary arterial blood pressures and cardiac work rose in essentially all patients during CO
2
inhalation, and fell to below baseline levels in approximately half of the patients studied after CO
2
, inhalation was discontinued.
Baseline cardiac output was normal in normotensive stroke patients without cardiac dysfunction, but was low in hypertensive stroke patients.
A statistically significant increase in cerebral blood flow occurred during CO
2
, inhalation, with an observed decrease in cerebrovascular resistance. The percentage increase in cerebral blood flow exceeded the increase in cardiac output.
Since hypercarbia causes a rise in systemic and pulmonary arterial blood pressure, CO
2
inhalation should be used cautiously in patients with systemic or pulmonary hypertension. The rise in cardiac work during CO
2
inhalation could jeopardize patients with coronary heart disease and those with heart failure.
Following cessation of CO
2
inhalation, blood pressure and cardiac output may fall below baseline levels, with a risk of posthypercapnic fall in cerebral blood flow. Occasionally, cardiac arrhythmia occurs during or following CO
2
inhalation.
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