2020A04 Compare and contrast the effects of sevoflurane and nitrous oxide on the cardiovascular system.

	Sevoflurane	Nitrous oxide
Summary:
	Dose-dependent depression	Minimal overall effect Use to spare sevoflurane (e.g. haemorrhaging patient)
Mechanism:
Direct effects	↓L-Ca²⁺ activity ↑NO activity	Minimal Some negative inotropy
Indirect effects	Baroreceptor reflex -> ↑HR	↑SNS outflow from brainstem Transient (<1 hour)
Heart:
Rate	↑	↔↑
Contractility	↓	↔
Output	↔	↔↑
Circulations:
Systemic circulation	↓SVR ↓mAP	↔↑SVR ↔↑mAP
Pulmonary circulation	↓PVR (including ↓HPV)	↑PVR Exaggerated if already PHTN
CNS circulation	Dose-dependent*	↑CMRO₂ -> CBF Avoid if ↑ICP
Special:
Anaesthetic preconditioning	Yes^	No
QTc prolongation	Yes	No

Sevo CBF*

· <0.5MAC: ↓CBF (↓CMRO₂ predominates)

· 0.5-1MAC: CBF normalises

· >1MAC: ↑CBF (vasodilatation predominates)

Sevo preconditioning^

· Activation of mitochondrial and sarcolemmal ATP-sensitive K⁺ channels -> hyperpolarization

· Occurs at MAC >0.25

· Mimics ischaemic preconditioning

Note disagreements between Peck & Hill, Stoelting, Hemmings & Egan etc.