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

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

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.

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).

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).

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

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.

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

Coronary Capillary System Epicardial Subendocardial Arterial Plexus Pressure

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]

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.

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.

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.

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)

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.

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).

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).