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69 Cards in this Set
- Front
- Back
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blood flow through skeletal muscles during rest and during extreme exercise in a well-conditioned athlete |
3-4 ml/min/100g muscle versus 50-80 ml/min/100 g muscle
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when is blood flow highest in muscle during rhymical muscular contration
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very high for a few seconds at the end of contractions, then fades to normal
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what occurs during strong tetanic contraction
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blood flow can almost be stopped, but this also causes rapid weakening of the contraction
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one of most important chemical effects to cause arterioles to dilate with increased skeletal muscle activity
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reduction in oxygen in muscle tissues
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oxygen deficiency causes release of what vasodilator substances
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adenosine is most important
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how long can adenosine sustain vasodilation in skeletal muscle
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about 2 hours
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what vasodilators continue to maintain increased capillary blood flow once insentitive to adenosine
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1) potassium 2) ATP 3) lactic acid 4) CO2; not sure what role each of these play
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what do sympathetic vasoconstrictor nerve fibers secrete at their nerve endings
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norepinephrine
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how much can sympathetic vasoconstrictor nerve fibers decrease blood flow in resting muscles
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one half to one third normal
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when is the sympathetic vasoconstrictor of high physiologic importance
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circulatory shock and furing other periods of stress (need to maintain normal or high arterial pressure)
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what secretes large amounts of norepineprine and even more epinephrine into the blood during strenuous exercise
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medullae of the two adrenal glands
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what is the effect of epinephrine on muscle vessels
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slight vasodilating due to exitation of beta adrenergic receptors
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what receptors does norepinephrine act on in muscle vessels
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alpha vasoconstrictor receptors
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3 major effects that occur during exercise to supply muscle
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1) mass discharge of sympathetic nervous system 2) increase in arterial pressure 3) increased CO
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what occurs to heart during sympathetic stimulation
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increased rate and pumping strength along with normal parasympathetic inhibition
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what accounts for an additional 2L/min of extra blood flow to muscle during strenuous exercise
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arterioles of peripheral circulation strongly contracted, except those of active muscle ('lend' their blood supply)
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what two peripheral circulatory systems are spared vasoconstrictor effects
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coronary and cerebral systems; both have poor vasoconstrictor innervation
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what increases mean systemic filling pressure during exercise
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veins are powerfully contracted
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how is arterial pressure increased during exercise
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1) vasoconstriction of arterioles 2) increased heart pumping 3) increased mean systemic filling pressure via venous constriction
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what determines how high the arterial pressure is increased
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number of muscles being used and how strenuous the activity; standing on ladder hammering (170 mmHg high), swimming/running (20-40 mmHg higher)
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why doesn't arterial pressure increase more during whole body strenuous exercise
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extreme vasodilation in large masses of active muscle
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why does the slope of the venous return curve rotate upwards
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decreased resistance in virually all the blood vessels in active muscle tissue
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what part of the endocardial surface can receive nutrition directly from the blood inside cardiac chambers
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inner 1/10 mm
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what does the left coronary artery generally supply
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anterior and left lateral portions of the L ventricle
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what does the right coronary artery generally supply
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most of R ventricle, posterior part of L ventricle in 80-90% of people
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coronary sinus carries what percent of total coronary blood flow
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75 percent
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what does the coronary venous blood from the right ventricle return through
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small anterior cardiac veins that flow directly into the right atrium
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thebesian veins
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minute coronary veins that empty directly into all chambers of the heart (very small amount of coronary venous blood goes via this route)
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average coronary resting blood flow
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225 ml/min (4-5% total CO)
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Why does efficiency of the cardiac energy utilization have to increase as work load increased
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blood flow does not increase in proportion to increased work-load (6-9 fold increase in work load may cause 3-4 fold increase blood flow)
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proposed mechanism of adenosine release in cardiac cells
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oxygen decreases, large proportion of ATP degrades to AMP, small portions of AMP degraded and release adenosine into tissue fluids, vasodilation occurs
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other vasodilators identified in cardiac muscle
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adenosine, K+, H+, CO2, bradykinin, maybe NO and prostaglandins
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direct and indirect effects of autonomic nerve stimulation on coronary blood flow
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direct: acetylcholine from vagus nerves, epi/norepi from sympathetic nerves; indirect: local responses chreating secondary changes
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example of indirect effect
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acetylcholine slows heart, decreasing need for O2, causes constriction of coronary vessels
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direct effect of acetylcholine
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dilate coronary vessels
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constrictor receptors of blood vessels
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alpha receptors
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dilator receptors of blood vessels
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beta receptors
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epicardial coronary vessels have mostly what kind of receptos
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alpha receptors
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intramuscular arteries have mostly what kind of receptors
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beta receptors
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under resting conditions what does cardiac muscle normally consume for energy
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fatty acids (70%)
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when ischemic, what does cardiac tissue use for energy
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must use glycolysis and have blood glucose for energy; causes lactic acid build up---may be one of causes of ishemic pain
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what is believed to cause dilation of coronary arteries during coronary hypoxia
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adenosine-cardiac muscle cells are slightly permeable to and it diffuses into circulating blood
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what is deliterious effect of 'leaking' adenosine
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within 30 mins, 1/2 can be lost; can only be replaced 2% per hour
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how does leaked adenosine affect cardiac cells
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on of major causes of cardiac cellular death during myocardial ischemia
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what can cause muscular spasm of coronary artery
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direct irritation by edges of an arteriosclerotic plaque, local nervous reflexes that cause excess coronary vascular wall contraction
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wher are most anastamoses in the heart
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smaller arteries sized 20-250 um in diameter
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how much blood flow can anastamoses provide when heart is ishemic
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usually less than half needed to keep muscle alive
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how quickly do anastomoses dialate and reperfuse damaged areas
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dialate within seconds, don't enlarge much for 8-24 hours, then increase and double by 2nd or 3rd day; reach normal flow by ~ 1 month
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how much oxygen do cardiac cells require to stay alive
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1.3 ml O2 per 100 g muscle tissue per minute
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how much oxygen is delivered to a normal resting L ventricle each minute
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8 ml O2 per 100 g muscle
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what portion of the heart often becomes infarcted even when ther is no evidence on outer surface portions
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subendocardial muscle
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why is the subendocardial muscle most likely to suffer infarction
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blood vessels are intensely compressed by systolic contraction
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most common causes of death after acute MI
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1) decreased CO 2) damming of blood in pulmonary blood vessels 3) fibrillation of heart 4) rupture of heart
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systolic stretch
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ischemic portion forced outward by pressure inside ventricle
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when does cardiac shock almost always occur
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when more than 40% left ventricle infarcted
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death occurs in what percentage of patients who devlope cardiac shock
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85 percent
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when does pulmonary edema generally become a problem after MI
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a few days after when kidneys try to compensate for diminished CO
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two dangerous periods when fibrillation is most likely to occur
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1) 10 minutes after infarction 2) 1 hour or so later (lasting for several hours)
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4 factors for heart fibrillation tendancy
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1) rapid depletion of K+ 2) injury current 3) sympathetic reflexes 4) cardiac muscle weakness (causes dilation)
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when are patients most prone to rupture after MI
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few days after MI when dead muscle fibers degenerate
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how can you assess systomlic stretch
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cardiac imaging to see if worsening
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what does a rupture cause
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cardiac tamponade (compression of heart from outside from collecting blood)
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how long does the heart to make partial/complete recovery from MI
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within few months
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why is rest one of the most important treatments during MI recovery
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stress/exercise causes blood to flow to normal muscle and bypass anastamoses feeding ischemic muscle ('coronary steal')
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where is angina pectoralis generally felt
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beneath upper sternum over heart and often refered to left arm and left shoulder (also neck and side of face)
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pain desciption in angina pectoralis
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hot, pressing, constricting
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drugs used for prolonged treatment of angina pectoris
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beta blockers
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beta blocker mechanism
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block sympathetic beta adrenergic receptors; decreases heart need to have extra O2 during stressful conditions
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when would a patient be a good candidate for aortic-coronary bypass surgery
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constricted areas are located at only a few discrete points and normal/almost normal elsewhere
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