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

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

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

Dr. Radmanesh

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

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

Coronary Artery Disease Coronary Circulation Coronary Artery Disease Dr. Radmanesh

Coronary Artery Anatomy Dr. Radmanesh

Dr. Radmanesh

Dr. Radmanesh

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

Dr. Radmanesh

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

Dr. Radmanesh

Dr. Radmanesh

Dr. Radmanesh

Dr. Radmanesh

Myocardial Oxygen Supply Dr. Radmanesh

Resting O2 Consumption of Various Organs Dr. Radmanesh

Myocardial Oxygen Supply Regulation of Coronary Blood Flow Dr. Radmanesh

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

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

Endothelial Control of Coronary Vascular Tone Dr. Radmanesh

Dr. Radmanesh

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

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

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

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

Dr. Radmanesh

Dr. Radmanesh

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

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

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

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

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

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

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

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

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

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

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

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

Dr. Radmanesh