Hypercapnia-induced cerebral hyperperfusion: an underrecognized clinical entity

Abstract

Background and purpose: The incidence of cerebral hyperperfusion and hypoperfusion, respectively, resulting from hypercapnia and hypocapnia in hospitalized patients is unknown but is likely underrecognized by radiologists and clinicians without routine performance of quantitative perfusion imaging. Our purpose was to report the clinical and perfusion imaging findings in a series of patients confirmed to have hypercapnic cerebral hyperperfusion and hypocapnic hypoperfusion.

Materials and methods: Conventional cerebral MR imaging examination was supplemented with arterial spin-labeled (ASL) MR perfusion imaging in 45 patients during a 16-month period at a single institution. Patients presented with an indication of altered mental status, metastasis, or suspected stroke. Images were reviewed and correlated with arterial blood gas (ABG) analysis and clinical history.

Results: Patients ranged in age from 1.5 to 85 years. No significant acute findings were identified on conventional MR imaging. Patients with hypercapnia showed global hyperperfusion on ASL cerebral blood flow (CBF) maps, respiratory acidosis on ABG, and diffuse air-space abnormalities on same-day chest radiographs. Regression analysis revealed a significant positive linear relationship between cerebral perfusion and the partial pressure of carbon dioxide (pCO(2); beta, 4.02; t, 11.03; P < .0005), such that rates of cerebral perfusion changed by 4.0 mL/100 g/min for each 1-mm Hg change in pCO(2).

Conclusions: With the inception of ASL as a routine perfusion imaging technique, hypercapnic-associated cerebral hyperperfusion will be recognized more frequently and may provide an alternative cause of unexplained neuropsychiatric symptoms in hospitalized patients. In a similar fashion, hypocapnia may account for a subset of patients with normal MR imaging examinations with poor ASL perfusion signal.

Fig 1.

Typical clinical ASL map for a normocapnic 57-year-old patient with mild age-related degenerative changes. Normal CBF is depicted throughout GM with a GM CBF mean of 62.9 mL/100 g/min. The pCO₂ measured 38.8 mm Hg.

Fig 2.

ASL CBF perfusion map in a hypocapnic 58-year-old patient suspected of having an acute infarct. No abnormality was detected on conventional imaging, but the patient had marked global hypoperfusion (mean GM CBF, 25.5 mL/100 g/min). ABG showed pCO₂ of 34.4 mm Hg.

Fig 3.

ASL CBF map performed as part of the MR imaging examination demonstrated markedly increased blood flow in all GM and white matter structures consistent with global hyperperfusion (mean GM CBF, 175.2 mL/100 g tissue/min). Chest radiograph from the same date was significant for emphysema, and ABG analysis revealed a pCO₂ of 56.3 mm Hg (normal range, 35–45 mm Hg).

Fig 4.

Graph demonstrates global rates of CBF (mL/100 g/min) in GM, expressed as mean ± SD, for 3 groups (hypercapnia, normocapnia, and hypocapnia) on the basis of ABG measures of pCO₂. The asterisk (*) indicates a statistically significant difference from the normocapnia group. The cross (†) indicates a statistically significant difference between the hypercapnia and hypocapnia groups. Global rates of CBF are 106.1% higher in the hypercapnia group and 38.6% lower in the hypocapnia group compared with normocapnic control subjects.

Fig 5.

Graph of percent change versus pCO₂ for all groups shows a strong linear relationship between global GM CBF and pCO₂ with slight differences between male (red) and female (blue) patients.