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Haemodynamics during inhalation of a 50% nitrous‐oxide‐in‐oxygen mixture with and without hypovolaemia
Author(s) -
HAHN R. G.,
RIDDEZ L.,
BRISMAR B.,
STRANDBERG Å.,
HEDENSTIERNA G.
Publication year - 1997
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1997.tb04728.x
Subject(s) - medicine , inhalation , anesthesia , cardiac output , hemodynamics , nitrous oxide , blood volume , oxygen transport , oxygen , ventilation (architecture) , respiratory minute volume , vascular resistance , stroke volume , blood flow , arterial blood , respiratory system , blood pressure , heart rate , chemistry , mechanical engineering , organic chemistry , engineering
Background: Inhalation of a gas mixture containing 50% nitrous oxide in oxygen (N 2 O/O 2 ) is widely used for pain relief in emergency situations, which may also be associated with blood loss. The aim of this study was to evaluate the haemodynamic effects of this gas mixture in normo‐ and hypovolaemic subjects. Methods: Six healthy males were studied during inhalation of N 2 O/O 2 before and after withdrawal of 900 ml of blood. On each occasion, we measured systemic and pulmonary arterial pressures, cardiac output, blood gases, extravascular lung water, and the blood flow and oxygen consumption in the whole body, liver and kidneys. Results: Inhalation of N 2 O/O 2 reduced the stroke volume and increased peripheral resistance. Oxygen uptake decreased in the liver (‐30%) and in the whole body (‐23%). Blood withdrawal reduced the pulmonary arterial and central venous pressures (‐30 to ‐50%) and further decreased stroke volume and the blood flows to the liver and the kidney (‐15%). The extravascular lung water tended to increase both during inhalation of N 2 O/O 2 and during hypovolaemia. Conclusion: N 2 O/O 2 aggravated the hypokinetic circulation induced by hypovolaemia. However, the oxygen consumption decreased only during inhalation of N 2 O/O 2 . This opens up the possibility that the cardiodepression associated with N 2 O/O 2 is caused by a change in metabolic demands.