Volume 2 Supplement 1

18th International Symposium on Intensive Care and Emergency Medicine

Open Access

Cerebral blood flow velocities in hypoxemic patients

  • F Chiappini1,
  • L Fuso1,
  • G Pagliari1,
  • M Visocchi2,
  • B Cioni2 and
  • M Meglio2
Critical Care19982(Suppl 1):P071

https://doi.org/10.1186/cc201

Published: 1 March 1998

Full text

According to the literature, in normocapnic hypoxia cerebral blood flow (CBF) increases in order to maintain a steady oxygen (O2) delivery as well as to prevent a significant drop in cerebral venous O2 tension. The aim of the present study is to investigate transcranial Doppler (TCD) velocitometric patterns in hypoxemic patients. CBF velocity was evaluated before and after inhalation of an O2 enriched mixture in order to detect differences in O2 delivery when chronic hypoxia was corrected. Eight patients (mean age 71.4 ± 2.2 yrs) with respiratory failure (RF) (hypoxemia without hypercapnia), were studied before starting a long-term oxygen therapy. None had a history of cardiovascular and/or hematologic diseases. A group of 8 healthy subjects, matched for age and gender, were also studied as reference group. Both patients with RF and normal subjects underwent a CBF velocity measurement, in supine position, by using TCD (Quantascope, Toshiba T2100, Vital Science, Amsterdam, The Netherlands) both in basal conditions (while breathing room air) and during the inhalation of an O2 enriched mixture through a Venturi mask for at least 30 min. Heart rate was recorded and arterial blood gases were measured with a emogasanalyzer ABL-330 (Radiometer, Copenhagen) before the assessment of CBF velocity both in basal conditions and during the inhalation of the O2 enriched mixture. A significant increase of PaO2 and SaO2 during the inhalation of the O2 enriched mixture in comparison with basal conditions was found both in patients with RF (PaO2: 54.1 vs 84.9 mmHg, P = 0.004; SaO2: 86.6 vs 95.8%, P = 0.003) and in normal subjects (PaO2: 82.9 vs 112.2 mmHg, P = 0.0004; SaO2: 95.6 vs 97.8%, P = 0.003). The CBF velocities decreased in both groups (32.2 vs 27.9 cm/s, P = 0.011 in RF patients; 29.8 vs 19.9 cm/s, P = 0.0003, in normal subjects). However, the reduction of CBF velocities was lower in RF patients in comparison with the normal subjects (-4.3 ± 3.5 vs -10 ± 4.4 cm/s, respectively, P = 0.012).

In conclusion, the lower decrease of the CBF velocities in RF patients during the inhalation of an O2 enriched mixture seems to indicate that chronic hypoxia induces a quite maximal vasodilatation to protect CBF and, thus, to maintain an adequate O2 delivery to the brain.

Authors’ Affiliations

(1)
Department of Respiratory Physiology, Catholic University Rome
(2)
Department of Neurosurgery, Catholic University Rome

Copyright

© Current Science Ltd 1998

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