Flow rate in muscle

1. Chapter 21Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and Ischemic Heart Disease

2. Flow rate in muscle • 4 ml/min/100 g to 80-100 ml/min/100 g • Intermittent as a result of contraction of muscle • Exercise opens capillaries • Flow strongly controlled by O2 concentration • Also vasoconstrictor nerves

3. Vasoconstrictor Nerves • Secrete norepinephrine (important during shock) • NE – vasoconstrictor • Epinephrine – secreted by adrenal medullae gives vasodilator effect during exercise • Cat vasodilator fibers secrete acetylcholine, inducing vasodilation.

4. Effects of Exercise on Muscle Circulation • Increased heart rate & pumping strength • Aterioles constricted in most of periphery (but not in coronary and cerebral systems). • Active muscle arterioles dilated • Vein muscle walls constricted (increased filling pressure, hence, increased venous return).

5. Local vs Whole Body Exercise • Local (e.g. lifting weight): Mainly vasoconstriction – high increase in BP (up to 170 mm Hg). • Whole body (e.g. running): vasodilation in a large mass of muscles leads to more slight increase in BP (maybe 20-40 mm Hg).

6. Effect of Arterial Pressure Rise • Increases force to drive blood (by 30%). • Dilates vessels, decreasing resistance (can double flow rate).

7. Coronary Circulation • Supply from inside the heart only reaches the inner 100 microns of the muscle. • Coronary arteries lie on outside of the heart. • Coronary arteries leave from the sinus of valsalva. • Empty into the sinus, the right atrium or the thebesian veins.

8. 300 Q (ml/min) Systole Diastole Coronary Flow Waveform Time

9. Coronary Capillary System Epicardial Subendocardial Arterial Plexus Pressure

10. Control of Coronary Circulation • Metabolic (e.g. O2, Adenosine, Adenosine phosphates, K+, H+, C02, bradykinin) • Arteriolar Muscle “fatigue.” • Nervous control: • Parasympathetic (vagal) dilation • Constrictor (alpha) receptors • Dilator (beta) receptors [also stimulate contraction]

11. Loss of Adenosine • ATP is degraded to ADP, AMP and Adenosine • Under ischemia, Adenosine can be lost. • After ~30 minutes too much has been lost to recover in a reasonable amount of time. • This mechanism is thought to be the cause of cardiac muscle death caused by an infarct.

12. Myocardial Infarction (Heart Attack) • Atheroscelrosis (Athere: “Gruel”; Sclerosis: “Hardening”) • Thrombosis: Sudden occlusion or embolus. • Local spasm • Slowly progressing disease allows collaterals to be developed. • Most common first symptom of coronary artery disease is sudden death.

13. Basal Coronary Requirements • Coronary muscle gets about 8 ml/min/100 g of tissue. • To stay alive it needs about 1.3 ml/min/100 g. • The heart can remain alive at ~20% of its normal flow. • Subendothelium is usually the first to go because of high compression.

14. Causes of Death by Heart Attack • Decreased cardiac output – shock. • Failure of kidneys to excrete enough urine. • Ventricular fibrillation (post-event): • Rapid depletion of potassium • Injury current (muscle cannot repolarize) • Sympathetic reflex stimulation • Abnormal conduction. • Rupture of the heart (leading to cardiac tamponade)

15. Recovery from Myocardial Infarction • Tissue may be: • Dead • Non-functional • Mildly ischemic • Dead muscle -> scar tissue (normal areas of the heart may become hypertrophic to compensate for lost function) • Non-functional muscle -> functional • Mildly ischemic muscle recovers quickly.

16. Angina Pectoris • Can be caused by exercise (stable angina). • Can occur “randomly” (unstable angina) • May be as a result of thrombus formation and dissolution. • Treatment: Vasodilators (nitroglycerine) Or Beta blockers (vasoconstrictors, but they slow down the heart).

17. Cardiac Surgery • Coronary bypass surgery • Coronary angioplasty (balloon, laser ablation, mechanical). • Coronary stents (to hold the lesion open). • Drug eluding stents (e.g. NO donors).