Ventilation and capnography
Arterial carbon dioxide tension ( PaCO 2
) is determined by the balance between alveolar ventilation and carbon dioxide ( CO 2
) delivery to the lungs from production in the body ( Schauvliege , 2016 ).
In a patient with no significant pulmonary disease or reduction in cardiac output , end-tidal carbon dioxide ( ETCO 2
) can be used as a non-invasive method of measuring arterial CO 2
, as the difference between
PaCO 2 and ETCO 2 will be less than 5 mmHg ( Armitage- Chan et al ., 2007 ). The normal values for PaCO 2 in a healthy patient are between 35 and 45 mmHg ( Schauvliege , 2016 ).
Most pre-anaesthetic and induction agents are dose-dependent respiratory depressants and can subsequently cause hypoventilation and hypercapnia ( PaCO 2
> 45 mmHg ) ( Egger , 2016 ). This hypercapnia causes cerebral vasodilation , resulting in increases in ICP ( Schirmer-Mikalsen et al ., 2016 ). As a result of this , it may be necessary to ventilate the lungs of patients with intracranial disease manually or mechanically .
Mechanical ventilation ( MV ) using positive endexpiratory pressure ( PEEP ) will improve oxygenation and prevent mechanical lung injury , as it increases functional residual capacity , which prevents atelectasis occurring ( Li et al ., 2020 ). An increased intrathoracic pressure during intermittent positive-pressure ventilation ( IPPV ) can reduce jugular venous drainage , decreasing venous return from the head ( Hammond & Murison , 2016 ).
Armitage-Chan et al . ( 2007 ) state that maintaining a peak inspiratory pressure below 25 cmH 2
O and PEEP less than 5 cmH 2
O prevents an increase in ICP that is clinically significant . However , peak airway pressure between 12 and 15 cmH 2
O in the healthy animal is normally adequate , and it is recommended that the pressure should not exceed 20 cmH 2
O ( Hammond &
Murison , 2016 ).
Hyperventilation and subsequent hypocapnia ( PaCO 2 between 26 and 30 mmHg ) causes cerebral vasoconstriction , reducing cerebral blood volume and reducing ICP ( Hammond & Murison , 2016 ). However , this can reduce cerebral perfusion and oxygenation , and increase the risk of ischaemia ( Armitage-Chan et al ., 2007 ). The brain ’ s storage of O 2 and substrates is limited and very sensitive to changes in cerebral blood flow ( severe reductions can cause neuronal death ) ( Greene , 2010 ).
Controlled hyperventilation is an extremely rapid method of reducing ICP , as a decrease in PaCO 2 of 10 mmHg can reduce ICP by up to 30 % in 15 seconds ( Armitage-Chan et al ., 2007 ). However , due to the severe risks mentioned above and the poor prognosis , controlled hyperventilation as a treatment to reduce ICP is not advocated . It should only be implemented as an emergency therapy in select cases when there is clear clinical evidence of increased ICP ( Hammond & Murison , 2016 ).
Control of body temperature
Anaesthesia causes depression of the thermoregulatory centre , a reduction in metabolic rate , peripheral vasodilation and muscle inactivity – all factors contributing to a decrease in body temperature ( Schauvliege , 2016 ). Previous recommendations for anaesthetising patients with raised ICP state that maintaining the patient moderately hypothermic ( 31 – 34 ° C ) would reduce the effects of global ischaemia , decrease metabolic rate , and decrease ICP ( Armitage-Chan et al ., 2007 ). However , hypothermia can cause serious complications , including an increased risk of infection , shivering and increased O 2 consumption during recovery .
The first reported use of therapeutic hypothermia outside a surgical setting in veterinary medicine was as a component of a dog ’ s seizure management plan , in which the patient made a full neurological recovery ( Hayes , 2009 ). However , targeted temperature management ( TTM ) is not currently recommended as standard care in patients with traumatic brain injury ( TBI ) in human medicine ( Brodeur et al ., 2017 ), and the effects of controlled hypothermia in veterinary patients are still being investigated and further trials are needed . The current recommendation is to keep patients normothermic ( Brodeur et al ., 2017 ).
Cushing reflex
The Cushing reflex is a protective action of the brain to preserve an adequate cerebral perfusion pressure despite an increased ICP ( Agrawal et al ., 2008 ). Increased ICP can cause compression of the vasomotor centre within the brain , causing hypoxia . This , in turn , increases sympathetic outflow and increases arterial blood pressure ( Leece , 2016 ) to promote cerebral blood flow ( Dewey , 2016 ). Cerebral vessels are vasodilated , and systemic blood pressure is increased by the vasoconstriction of peripheral vessels considered not essential to survival ( e . g . those in skin , muscle , mesentery ) ( Dewey , 2016 ). Baroreceptors then mediate a compensatory bradycardia , and so hypertension and bradycardia simultaneously can be interpreted as a warning sign for raised ICP ( Agrawal et al ., 2008 ).
These changes will be quite sudden and extremely notable ( Abelson , 2008 ). In cases of severely increased ICP , compression of vital medullary centres may occur , resulting in hypertension , bradycardia , and respiratory
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