Fra sykepleier Nils Harald Gunnerød, Høgskolen i Oslo har vi fått følgende spørsmål:

Viser til artikkel hvor det står at hyperventilering etter ROSC (Return of Spontaneous Circulation - dvs. etter at hjertet har startet igjen) er skadelig. Nå er det mange år siden jeg var i klinikk som sykepleier, men var det noe vi gjorde med hodeskader var det å hyperventilere pasienter for å få bedret sirkulasjonen i en allerede skadet hjerne (ødemer). Hva er årsaken til at en hjerne som er skadet p.g.a. hjertestans (det går jeg ut fra) ikke skal hyperventileres? Er ikke vasokonstriksjon å foretrekke siden hjernen vil få ødemer etter stans? Vil ikke det bedre sirkulasjonen til hjernen?

Kristian Lexow fra Norsk Resuscitasjonsråd svarer

Det er et betimelig spørsmål du stiller. Svaret er todelt:

Hvis pasienten blir hyperventilert etter at hjertet har startet igjen (etter ROSC), vil vasokonstriksjonen pga. lav PCo2 ytterligere redusere blodstrømmen og forverre den cerebrale ischemien i den sene reperfusjonsfasen.

Hyperventilering kan lett øke luftveistrukket og gi auto-PEEP som fører til økning av det venøse trykket i hjernen som igjen gir nedsatt sirkulasjon i hjernen og dermed forverring av ischemien.

Normoventilering (dvs. 12 innblåsinger pr. minutt hos voksne) anbefales både under pågående HLR og etter at hjertet har startet. Hyperventilering bør unngås! Man kan lese mer om bakgrunnen for dette i kapittelet om “Advanced Cardiovascular Life Support” I Guidelinesboka (Guidelines on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, An International Consensus on Science. Circulation 2000;102:I1-I384. Resuscitation 2000; 46:1-448 eller Resuscitation 2001;48:199-239):

Ventilatory Parameters
Recent evidence supports the theory that sustained hypocapnea (low Pco2) may worsen cerebral ischemia (23, 24 and 25). After cardiac arrest, restoration of blood flow results in an initial hyperemic blood flow response lasting 10 to 30 minutes, which is followed by a more prolonged period of low blood flow. During this period of delayed hypoperfusion a mismatch between blood flow (oxygen delivery) and oxygen metabolism may occur. If the patient is hyperventilated at this stage, the additional cerebral vasoconstriction resulting from a low Pco2 may further decrease cerebral blood flow and worsen cerebral ischemia. There is no evidence that hyperventilation protects vital organs from further ischemic damage after cardiac arrest. The potential risk for further brain ischemia is real, and hyperventilation after cardiac arrest should be avoided. Safar et al (26) also showed indirectly that hyperventilation results in worse neurological outcome. After cardiac arrest, dogs treated with mild hypothermia enhanced by hypertension and ventilated to normocarbia had improved outcome with this clinical management.

Hyperventilation may generate airway pressures and auto-PEEP, leading to an increase in cerebral venous and intracranial pressures (27 and 28). The increase in cerebral vascular pressure results in a decreased cerebral blood flow and a further worsening of brain ischemia. This mechanism is independent of the effects of Pco2 or pH on cerebral vessel reactivity.

In summary, after either cardiac arrest or head trauma, ventilate the comatose patient to achieve normocarbia (Class IIa). Routine hyperventilation may be detrimental and should be avoided (Class III). In specific situations hyperventilation to achieve hypocarbia may be beneficial. Treat cerebral herniation syndrome with hyperventilation (Class IIa). Hyperventilation may also have a role when pulmonary hypertension is the cause of arrest (Class IIa). With restoration of cardiac output, metabolic acidosis usually corrects over time, and hyperventilation should not be used as a primary treatment modality. The use of buffer therapy is also not indicated and should be used for specific indications only (see above) (29 and 30).


23. A. Ausina, M. Baguena, M. Nadal, S. Manrique, A. Ferrer, J. Sahuquillo and A. Garnacho, Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?. Acta Neurochir Suppl 71 (1998), pp. 1–4.

24. M.N. Diringer, K. Yundt, T.O. Videen, R.E. Adams, A.R. Zazulia, E. Deibert, V. Aiyagari, R.G. Dacey, Jr, R.L. Grubb, Jr and W.J. Powers, No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury. J Neurosurg 92 (2000), pp. 7–13. Abstract-ScienceDirect Navigator

25. K.D. Yundt and M.N. Diringer, The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury. Crit Care Clin 13 (1997), pp. 163–184. Abstract-ScienceDirect Navigator