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

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

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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.

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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).

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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).

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Effect of Arterial Pressure Rise

• Increases force to drive blood (by 30).
• Dilates vessels, decreasing resistance (can
  double flow rate).

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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.

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Coronary Flow Waveform
Time
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Coronary Capillary System
Epicardial
Subendocardial Arterial Plexus
Pressure
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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

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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.

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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.

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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.

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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)

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Recovery from Myocardial Infarction

• Tissue may be
• Dead
• Non-functional
• Mildly ischemic
• Dead muscle -gt scar tissue (normal areas of the
  heart may become hypertrophic to compensate for
  lost function)
• Non-functional muscle -gt functional
• Mildly ischemic muscle recovers quickly.

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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).

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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).