1. Muscle Blood Flow and Cardiac Output During Exercise;
به نام خدا
Muscle Blood Flow and Cardiac Output During Exercise;
the Coronary Circulation
and Ischemic Heart Disease
Dr. Radmanesh

2. Blood Flow in Skeletal Muscle and Blood Flow Regulation During Exercise
Dr. Radmanesh

3. 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
Dr. Radmanesh

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5. Control of Blood Flow Through the Skeletal Muscles
Local Regulation—Decreased Oxygen in Muscle Greatly Enhances Flow
Nervous Control of Muscle Blood Flow
Dr. Radmanesh

6. Total Body Circulatory Readjustments During Exercise
(1) mass discharge of the sympathetic nervous system throughout the body with consequent stimulatory effects on the entire circulation
(2) increase in arterial pressure
(3) increase in cardiac output
Dr. Radmanesh

7. Coronary Artery Disease
Coronary Circulation
Coronary Artery Disease
Dr. Radmanesh

8. Coronary Artery Anatomy
Dr. Radmanesh

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11. small anterior cardiac veins
The left coronary artery supplies mainly the anterior and left lateral portions of the left ventricle, whereas
the right coronary artery supplies most of the right ventricle as well as the posterior part of the left ventricle in 80 to 90 per cent of people.
coronary sinus
small anterior cardiac veins
Through very minute thebesian veins, which empty directly into all chambers of the heart.
Dr. Radmanesh

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13. Pericardium (Epicardium)
Epicardial Vessel
Subepicardium
Myocardium
Subendocardium
Dr. Radmanesh

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18. Myocardial Oxygen Supply
Dr. Radmanesh

19. Resting O2 Consumption of Various Organs
Dr. Radmanesh

20. Myocardial Oxygen Supply
Regulation of Coronary Blood Flow
Dr. Radmanesh

21. Coronary Blood Flow Metabolic control Autoregulation
Endothelial control of coronary vascular tone
Extravascular compressive forces
Neural control
Dr. Radmanesh

22. 1. Myocardial metabolic level ↑cardiac activity, ↑cardiac
consumption O2 ,↓PO2,
adenosine
CO2, H+, lactic acid, K+,
prostaglandins.
Dr. Radmanesh

23. Endothelial Control of Coronary Vascular Tone
Dr. Radmanesh

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25. When Damage to Endothelium Occurs
Damage to endothelial cells will lead to:
Decreased Nitric Oxide and Prostacyclin production
Increased Endothelin production
This will lead to:
Vasoconstriction
Vasospasm
Thrombosis
Dr. Radmanesh

26. Neural Control Sympathetic Control Parasympathetic Control
Alpha = constrict coronary vessels
Beta = dilate coronary vessels
Parasympathetic Control
Acetylcholine
Vasodilation in healthy subjects
Vasoconstriction in patients with atherosclerosis
Dr. Radmanesh

27. Coronary Artery Disease
Myocardial ischemia occurs when myocardial availability is inadequate to meet metabolic requirements.
Dr. Radmanesh

28. Disorders
Most stem from atherosclerosis = fatty deposits (plaque) builds up on walls of arteries, obstructing blood flow, increasing blood pressure and risk of blood clots
Dr. Radmanesh

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31. Myocardial Infarction
the infarcted area takes on a bluish-brown hue, and the blood vessels of the area appear to be engorged despite lack of blood flow.
In later stages, the vessel walls become highly permeable and leak fluid the local muscle tissue becomes edematous,
and the cardiac muscle cells begin to swell because of diminished cellular metabolism.
Within a few hours of almost no blood supply, the cardiac muscle cells die
Dr. Radmanesh

32. Subendocardial Infarction
the blood vessels in the subendocardium are intensely compressed by systolic contraction of the heart
Dr. Radmanesh

33. Causes of Death After Acute Coronary Occlusion
(1) decreased cardiac output
(2) damming of blood in the pulmonary blood vessels and then death resulting from pulmonary edema;
(3)fibrillation of the heart
(4) rupture of the heart
Dr. Radmanesh

34. Decreased Cardiac Output—Systolic Stretch and Cardiac Shock
Dr. Radmanesh

35. Fibrillation of the Ventricles After Myocardial Infarction
rapid depletion of potassium from the ischemic musculature
“injury current : the ischemic musculature often cannot completely repolarize its membranes after a heart beat .
Powerful sympathetic reflexes
Cardiac muscle weakness caused by the myocardial infarction often causes the ventricle to dilate excessively
increases the pathway length for impulse conduction
abnormal conduction pathways
Dr. Radmanesh

36. Rupture of the Infarcted Area
the dead muscle fibers begin to degenerate
systolic stretch becomes greater and greater until finally the heart ruptures
Cardiac tamponade—that is, compression of the heart from the outside by blood collecting in the pericardial cavity
blood cannot flow into the right atrium, and the patient dies of suddenly
decreased cardiac output
Dr. Radmanesh

37. Myocardial Ischemia Systolic and diastolic dysfunction Angina
CHF or Pulmonary Edema
Arrythmias
Myocardial Infarction
Ventricular Rupture or VSD
Cardiogenic Shock
Death
Dr. Radmanesh

38. Stages of Recovery from Acute Myocardial Infarction Replacement of Dead Muscle by Scar Tissue
Dr. Radmanesh

39. Value of Rest in Treating Myocardial Infarction
The degreeof cardiac cellular death is determined by
the degree of ischemia and the workload on the heart muscle
“coronary steal” syndrome
Dr. Radmanesh

40. Pain in Coronary Heart Disease Angina Pectoris
Ischemia causes the muscle to release
acidic substances, such as lactic acid
other pain-promoting products,
such as histamine, kinins, or cellular proteolytic enzyme
Dr. Radmanesh

41. Drugs Used for Treatment of Ischemia
Oxygen
Beta-Blockers
Nitrates
Antiplatelet/Anticoagulant Drugs
Calcium-Channel Blockers
Dr. Radmanesh

42. Interventions for the Treatment of Myocardial Ischemia
Coronary Artery Bypass surgery (CABG)
Coronary Balloon Angioplasty
metal Sleeve
Laser
Dr. Radmanesh

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