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
300

Q
(ml/min)

Systole Diastole Time

Coronary Capillary System
Epicardial

Subendocardial Pressure
Arterial Plexus
 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).