Transcript Chapter 21 Muscle Blood Flow and Cardiac Output During Exercise

Chapter 21
Muscle Blood Flow and Cardiac
Output During Exercise; the
Coronary Circulation and Ischemic
Heart Disease
Flow rate in muscle
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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
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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
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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
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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
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Increases force to drive blood (by 30%).
Dilates vessels, decreasing resistance (can
double flow rate).
Coronary Circulation
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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
Arterial Plexus
Pressure
Control of Coronary Circulation
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Metabolic (e.g. O2, Adenosine, Adenosine
phosphates, K+, H+, C02, bradykinin)
Arteriolar Muscle “fatigue.”
Nervous control:
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Parasympathetic (vagal) dilation
Constrictor (alpha) receptors
Dilator (beta) receptors [also stimulate
contraction]
Loss of Adenosine
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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)
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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
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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
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Decreased cardiac output – shock.
Failure of kidneys to excrete enough urine.
Ventricular fibrillation (post-event):
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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
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Tissue may be:
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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
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Can be caused by exercise (stable
angina).
Can occur “randomly” (unstable angina)
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May be as a result of thrombus formation and
dissolution.
Treatment: Vasodilators (nitroglycerine)
Or Beta blockers (vasoconstrictors, but they
slow down the heart).
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Cardiac Surgery
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Coronary bypass surgery
Coronary angioplasty (balloon, laser
ablation, mechanical).
Coronary stents (to hold the lesion open).
Drug eluding stents (e.g. NO donors).