Chapter 21 Muscle Blood Flow and Cardiac Output

Muscle Blood Flow and Cardiac Output During Exercise

• Focuses on blood flow to skeletal muscle and coronary arteries, regulated by local vascular resistance responsive to metabolic needs
• Discusses cardiac output control during exercise, heart attack characteristics, and angina pectoris pain

Blood Flow Regulation in Skeletal Muscle

• Strenuous exercise requires significant blood flow to skeletal muscles and cardiac output increases
• Cardiac output increases 4-5 times in non-athletes and 6-7 times in well-trained athletes

Skeletal Muscle Blood Flow Rate

• Resting blood flow averages 3-4 ml/min/100 g of muscle
• Extreme exercise blood flow can increase 25-50 fold, up to 100-200 ml/min/100 g of muscle
• Peak flows of 400 ml/min/100 g reported in endurance-trained athletes' thigh muscles

Blood Flow During Muscle Contractions

• During rhythmic exercise, blood flow increases and decreases with each muscle contraction
• Flow remains high briefly after contractions, then returns to normal
• Lower flow cause during contraction from blood vessel compression
• Strong tetanic contraction can almost stop blood flow, causing rapid weakening

Increased Blood Flow in Muscle Capillaries

• During exercise, dormant capillaries open, reducing oxygen diffusion distance
• Capillary surface area increases 2-3 fold, improving oxygen and nutrient diffusion

Control of Skeletal Muscle Blood Flow

• Increased flow is caused by locally released chemicals, especially reduced oxygen levels, leading to arteriolar vasodilation

Other Vasodilator Factors

• Vasodilator factors sustain increased capillary blood flow during exercise if adenosine is not effective
• Includes potassium ions, adenosine triphosphate (ATP), lactic acid, and carbon dioxide

Nervous Control of Muscle Blood Flow

• Skeletal muscles have sympathetic vasoconstrictor nerves
• In some animals, sympathetic vasodilator nerves are present
• Norepinephrine decreases blood flow in resting muscles to one-half to one-third normal when maximally activated
• Important in circulatory shock and stress

Adrenal Glands

• Medullae secrete norepinephrine plus epinephrine during strenuous exercise
• Circulating norepinephrine causes vasoconstriction
• Epinephrine can cause vasodilation by exciting beta-adrenergic receptors

Circulatory Readjustments During Exercise

• Essential adjustments to supply blood flow include sympathetic nervous system activation, arterial pressure increase, and cardiac output increase

Effects of Sympathetic Activation

• Signals from the brain and attenuated parasympathetic signals result in increased heart rate and pumping strength
• Arterioles in most of the peripheral circulation strongly contract, except in active muscles
• Blood flow is temporarily reduced in nonmuscular areas, directing it to muscles
• Coronary and cerebral systems are spared from vasoconstriction
• Vein walls contract, increasing mean systemic filling pressure

Sympathetic Stimulation and Arterial Pressure

• Sympathetic stimulation increases arterial pressure during exercise
• Due to multiple effects- vasoconstriction, increased pumping activity/venous contraction
• Increase ranges from 20 mm Hg to 80 mm Hg

Importance of Increased Arterial Pressure

• When muscles are stimulated maximally in labs, muscle blood flow does not rise more than eightfold without allowing arterial pressure to rise
• During exercise, increases arterial pressure push blood through tissue vessels, along with locally released vasodilators and higher blood pressure to increase muscle blood flow

Importance of Increased Cardiac Output During Exercise

• Increased cardiac output delivers oxygen and nutrients during exercise
• Ability of circulatory system to increase cardiac output sets the limit for continued muscle work

Graphic Analysis of Changes in Cardiac Output

• Heavy exercise requires changes in both cardiac output and venous return curves
• Sympathetic stimulation increases heart rate (up to 170-190 beats/min) and contraction strength

Venous Return Curves During Heaving Exercise

• Mean systemic filling pressure rises partly from sympathetic stimulation and tensing of skeletal muscles
• Abdominal and skeletal muscle compress, increasing mean systemic filling pressure from 7 mm Hg to 30 mm Hg
• Decreased resistance in active muscle tissue rotates the venous return curve upward
• Combination raises the entire venous return level

Equilibrium Points

• New equilibrium occurs in changes to venous return and cardiac output curves
• Stronger heart, right atrial pressure may fall below normal during exercise
• Weaker heart marked increase in right atrial pressure even with moderate exercise

Coronary Circulation

• Coronary artery disease causes one-third of deaths in industrialized countries
• Older adults have impaired coronary artery circulation

Physiologic Anatomy of Coronary Blood Supply

• Main coronary arteries lie on the heart's surface, penetrating into the muscle mass
• Heart receives its nutritive blood supply through these
• Left coronary artery supplies the anterior and left lateral left ventricle
• Right coronary artery supplies right ventricle/posterior left ventricle

Normal Coronary Blood Flow

• Normal average blood flow is 70 ml/min/100 g of heart weight, 225 ml/min or 5% of cardiac output
• During exercise, cardiac output increases, coronary flow increases to use extra heart nutrients

Cardiac Muscle Compression

• Coronary capillary blood flow the left ventricle falls to a low point during systole
• Due to compression of intramuscular blood vessels during contraction
• Blood flows rapidly during diastole as the muscle relaxes
• Contraction effects right ventricle are only partial

Epicardial vs Subendocardial Coronary Blood Flow

• Epicardial arteries supply most muscle tissue
• Intramuscular arteries from epicardial vessels penetrate the needed nutrients muscle
• Subendocardial arteries lie beneath the endocardium
• Blood flow reduced in subendocardial plexus with ventricular contraction
• Extra vessels compensate for subendocardial reduction

Local Muscle Metabolism

• Blood flow is regulated by local arteriolar vasodilation that responds to cardiac muscle needs

Oxygen Demand

• Major factor of local coronary blood flow regulation
• Blood flow is regulated by cardiac musculature for oxygen needs
• If oxygen cannot be supplied the blood flow increases

Vasodilators

• Decreases in oxygen concentration increases great vasodilator propensity that is adenosine
• Large amounts of ATP degrade to adenosine monophosphate
• Some is further degraded to adenosine, increasing local coronary blood flow
• Other vasodialators: phosphate compounds,hydrogen/potassium ions, prostaglandins, nitric oxide

Nervous Control of Coronary Blood Flow

• Autonomic nerves affect blood flow directly and indirectly
• Direct effects from acetylcholine and norepinephrine affect coronary vessels
• Indirect effects due to changes in heart regulation greatly affect coronary flow

Vasocontriction and vasodilation

• Norepinephrine/epinephrine can have constrictor or dilator effects, based on presence of receptors in blood vessel walls
• Alpha constrictor receptors, beta are dilator receptors beta receptors exist in coronary vessels
• Epicardial have alpha receptors, intramuscular beta
• Sympathetic stimulation of vasoconstriction

Contol of Flow

• Metabolic factors, especially myocardial oxygen consumption, control blood flow
• Overrides nervous effects

Cardiac Muscle Metabolism

• Cardiac muscle is like other tissues in metabolism
• Uses greater fatty acids to supply energy
• Uses anaerobic glycosis for energy
• Glycolysis consumes blood glucose creating lactic acid

ATP and Cardiac energy

• 95% of energy from foods is uses to form ATP in mitochondria
• ATP conveys energy for cardiac contraction and functions
• Severe coronary ischemia degrades ATP to AMP and adenosine
• Agent is released which causes dilation of coronary arterioles and hypoxia
• Adenosine is loss with reperfusion with ischemia
• Loss after 30 minutes is too late to assist cardiac cells after injury

Ischemic Heart Disease

• Is the top cause of death in western countries, results from insufficient coronary blood flow
• 35% of +65 ages die from the disease
• Caused by acute coronary occulsion or fibrillation as well as weakening of heart pumping

Atherosclerosis causes Heart Disease

• frequent diminishment of blood flow is atherosclerosis
• cholesterol deposits under endothelium
• Fibrous tissue invades tissue and becomes calcified
• atherosclerotic plaque results and protrudes into vessel lumens

Artery Occlusion Causes

• Can be in those with atherosclerosis with normal coronary function
• Atheroscerlotic can blood clot called thrombus. plaque breaks through
• Thrombus can flow distally called coronary embolus
• Muscular spasm can occur from plaque or nervous reflexes

Collateral Circulation Values

• Collateral circulation reduces damage to degree in heart
• Diameter are 20 -250 micrometers in normal heart
• Small arteries dialate in seconds of occlusion and is less than half flow
• 8 -24 collateral flow increases and doubles in 2-3 days to normal in one month
• Gradual atherscleortic over years form collateral vessels
• Collateral vessels increase to provide needed blood flow limited exercise output

Myocardial Infarction

• When blood flow cease after cornoary vessel occlusion is called infraction
• Zero flow is infarcted blood
• The process to the infarction is myocardial
• Small amount collateral blood comes in and area stagnant becoming over filled
• The area uses oxygen haemoglobin deoxygenated and is blueish brown hue
• Vessles are engorged with lack flow

Cardiac muscle

• Requires oxygen around 1.3 minutes g of tissue muscle for the alive
• Delivers about oxygen for normal left ventricle and so is okay at 15-30 % of normal flow
• Central potrtion with no collateral is lost muscle

Causes after occlusion of heart

• In subbendoardal muscled frequently and evidence is not available
• High consumtion uses extra oxygen with high difficult of blood
• Contraction intesively compressed due to systolilic contraction of heart
• Damage usually is first is usually subbendocardial then is the spreading damage
• Heart attack causes follows:
• Heart outpud decreased
• Domming heart by edema by lack flow of blood
• Then fribillation or occassional rupture

Sysolic Strech and Weakness

• Fibers dont work and have low force while effected
• Venticle forces outward to devop the pressure the systolic strech
• The force is the dissipated via nonfunctional muscle
• The condition with cardiac failure and ischemia called coronary shock
• Sysyolic strech happens with too much ventricle affected
• 70 % in the attack of cardiac

Cardiac Vein

• High blood volume during
• Kidneys fail
• Edema
• Patients will sudden fall death by symptoms

Drug Treatment

• Vasodialating drugs are ministered during shock and provide imemdiate relief
• Angiotension is used
• Other drug treatments
• Calcium channel blockers

Fibrilation of Ventricles

• The occusion will heart fibrilates
• The attack has high tendency fibrillation
• Also can be caused by
• Loss and low blood
• Ischmia
• Sympathetic
• Cardiac muscle weakness

Muscle

• The tissue will rupture the high loss volume with degenration
• The death muscles goes outwards to contract
• systolic strentches to rupture
• severe infraction
• Cardiac tamport to cause rapid development by outside heart

Recovery Stages

• Acute occulsion shows muscle effects
• Small portions ishecmia with muscle
• The part small musclses comes no full contraction
• Large ischemia the fibres that has lost rapidly supply blood
• The non function of muscle happens to spreads

Muscle death

• Muscle death happens and has new tissue
• Scar is forms to increase
• There is much muscle dead loss with high overloads and increases activity of heart
• The cardiac reserve happens is reduced load
• Reverses must is body must
• Reversse to stop