CORONARY BLOOD FLOW
Factors of disease, drugs and anaesthesia alter coronary flow
Part One explains how coronary blood flow is maintained, regulated and calculated
Coronary artery disease
Deposits of lipids, smooth muscle proliferation and endothelial dysfunction reduce the luminal diameter.
With increasing stenosis, distal arterioles dilate maximally to preserve flow up to the point where the vascular bed is maximally dilated. Further stenosis leads to a drop in flow and flow becomes pressure dependent.
The left ventricle undergoes hypertrophy in response to raised afterload (end-systolic wall stress).
Impaired ejection results in larger diastolic volumes, raised LVEDP (preload) and lower coronary perfusion pressure.
Antiplatelet drugs, anticoagulants and lipid lowering drugs
- These agents act inside the lumen to prevent further reduction in the vessel diameter.
- Nitrates produce vasodilatation in all vascular beds, mediated by nitric oxide release.
Calcium channel blockers
- Compared to the non-dihydropyridines (verapamil and diltiazem) the dihydropyridines (nifedipine) produce
Drugs acting on angiotensin
- ACEI's reduce conversion of angiotensin I to angiotensin II.
Potassium channel openers
- Nicorandil is a novel anti-anginal agent.
- Coronary blood vessels contain β2 receptors.
Vasopressors and inotropes
- Restore coronary perfusion pressure in hypotensive patients and benefit patients heading towards the lower end of autoregulation range. - Any ↑ in aortic diastolic pressure may be offset by an ↑ in myocardial oxygen demand related to higher workload, contractility and HR.
DRUGS - Seven Considerations
Halogenated anaesthetic agents activate ATP-sensitive potassium channels and lower intracellular calcium.
This results in negative inotropy and mimic the protective effect of discrete episodes of myocardial ischaemia before a sustained ischaemic insult, so-called ‘ischaemic preconditioning’.
Isoflurane in particular causes coronary vasodilatation. Arterioles (resistance) are dilated more than epicardial (conductance) vessels.
Perioperative stress results in sympathetically mediated tachycardia, hypertension, increase in shear forces and increased myocardial oxygen demand. Central neuraxial block obtunds this potentially harmful response but any substantial fall in blood pressure will lower the coronary perfusion pressure. Thoracic epidural analgesia also blocks sympathetic outflow to the heart. Sympathetic stimulation produces coronary vasodilatation in healthy individuals but vasoconstriction in patients with coronary artery disease
- The coronary circulation functions in a state of active vasodilatation.
- Abnormal endothelial nitric oxide production may play a role in diabetes, atherosclerosis and hypertension.