CORONARY BLOOD FLOW
Dr. David Lyness
@Gas_Craic
propofology.com
PART TWO
Sources:
http://ceaccp.oxfordjournals.org/content/5/2/61.full
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.
Critical stenosis occurs when coronary blood flow is unable to respond to an increase in metabolic demand
This usally when the diameter is reduced by 50%. Resting flow becomes affected if the diameter is reduced by 80%.
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.
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.
Flow diverted into a dilated parallel bed proximal to a stenosis is called coronary steal and can aggravate ischemia.
Flow in collaterals is also often pressure dependent.
Hypertension
The left ventricle undergoes hypertrophy in response to raised afterload (end-systolic wall stress).
Hypertension
The left ventricle undergoes hypertrophy in response to raised afterload (end-systolic wall stress).
The myofibrillar growth outstrips the capillary network, resulting in decreased capillary density.
Raised intramyocardial pressure lowers the subendocardial blood flow (coronary arteries that run deep within the myocardium)
The pressure load increases myocardial work and oxygen demand.
There is an impaired vasomotor response to hypoxia in hypertrophied tissue that makes it susceptible to ischaemia.
Heart failure
Impaired ejection results in larger diastolic volumes, raised LVEDP (preload) and lower coronary perfusion pressure.
Heart failure
Impaired ejection results in larger diastolic volumes, raised LVEDP (preload) and lower coronary perfusion pressure.
Sympathetic systemic vasoconstriction may help to improve the myocardial perfusion but increases pressure load and oxygen demand.
Antiplatelet drugs, anticoagulants and lipid lowering drugs
- These agents act inside the lumen to prevent further reduction in the vessel diameter.
- Statins inhibit HMG CoA reductase, an enzyme involved in cholesterol synthesis.
- Antiplatelet drugs prevent platelet aggregation, often the initial step in the formation of an occlusive thrombus.
- Antithrombin agents act at various sites in the coagulation cascade to inhibit thrombin formation.
Nitrates
- Nitrates produce vasodilatation in all vascular beds, mediated by nitric oxide release.
Nitrates
- Nitrates produce vasodilatation in all vascular beds, mediated by nitric oxide release.
- Relieve coronary vasospasm but their main benefit is to reduce preload, afterload and to increase maximal coronary dilation.
- Benefits may be offset by reflex tachycardia.
- Regional blood flow is improved due to dilatation of collaterals and a lower LVEDP.
Calcium channel blockers
- Compared to the non-dihydropyridines (verapamil and diltiazem) the dihydropyridines (nifedipine) produce
Calcium channel blockers
- Compared to the non-dihydropyridines (verapamil and diltiazem) the dihydropyridines (nifedipine) produce
more vasodilatation, less inhibition of the sinus and atrioventricular nodes, and less negative isotropy.
- The myocardial oxygen supply improves due to coronary dilatation and lower LVEDP.
- The oxygen demand is lessened because of decreases in contractility and pressure load.
Drugs acting on angiotensin
- ACEI's reduce conversion of angiotensin I to angiotensin II.
Drugs acting on angiotensin
- ACEI's reduce conversion of angiotensin I to angiotensin II.
- Reduce angiotensin-mediated vasoconstriction and enhance myocardial perfusion by vasodilatation without reflex tachycardia.
- Over time, it also regulates fibrous tissue formation after tissue injury.
- Drugs such as losartan are angiotensin receptor antagonists and enhance endothelial nitric oxide release (vasodilation)
Potassium channel openers
- Nicorandil is a novel anti-anginal agent.
Potassium channel openers
- Nicorandil is a novel anti-anginal agent.
- Increased potassium efflux results in reduced intracellular calcium and muscle relaxation.
- It dilates both normal and stenotic segments of the coronary arteries.
β-Blockers
- Coronary blood vessels contain β2 receptors.
β-Blockers
- Coronary blood vessels contain β2 receptors.
- Chronotropy and inotropy depends on β1 stimulation.
- β-blockers do not depress the cardiac output as much as originally thought.
- The reduction in the heart rate prolongs the diastolic perfusion time and they inhibit stress-induced rises in myocardial contractility.
- In patients on cardioselective β1-blockers, unopposed systemic β2 stimulation reduces the afterload, improves EF, and +ve inotropy'.
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.
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.
- In the failing heart, inotropes also reduce the LVEDP (preload) - remember the Frank-Starling curve.
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’.
In addition, coronary vasodilation and reduced afterload generally results in a favourable myocardial oxygen supply–demand ratio.
Isoflurane in particular causes coronary vasodilatation. Arterioles (resistance) are dilated more than epicardial (conductance) vessels.
Isoflurane in particular causes coronary vasodilatation. Arterioles (resistance) are dilated more than epicardial (conductance) vessels.
Isoflurane however, can provoke ischaemia in patients with coronary artery disease if tachycardia and hypotension is permitted.
Sevoflurane and halothane do not cause tachycardia or maldistribution of myocardial perfusion.
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
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
ANAESTHESIA
- The coronary circulation functions in a state of active vasodilatation.
- Abnormal endothelial nitric oxide production may play a role in diabetes, atherosclerosis and hypertension.
- Because CA's are end-arteries, there is little redundant blood flow, so blockages of vessels is critical.
- REMEMBER that: Flow down left coronary only occurs in diastole- hence tachycardia worsens ischaemia
