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78 Cards in this Set
- Front
- Back
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resting blood flow through skeletal muscle
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4ml/min/100g muscle
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exercise blood flow through cardiac muscle
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100-200ml/min/100g muscle
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when is blood flow lower through muscles
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contraction
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cause of lower blood flow during muscle contraction
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compression of vessels when muscle contracts
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what causes blood flow increase during exercise
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vasodialative agents acting on arterioles
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two main agents of vasodilation in skeletal muscle under stress
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lack of oxygen and adenosine from ATP degredation
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what are the minor vasodilative agents involved with maintaining vessel vasodilation in skeletal muscle
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potassium ions, ATP, lactic acid and carbon dioxide
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what are the methods of nervous vasoactive control in skeletal muscle blood vessels
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sympathetic vasoconstrictor and vasodilator nerves
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function of noepinephrine in sympathetic vasoconstriction
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causes constriction in the PERIPHERAL circulation and RESTING muscles, binds to alpha receptors
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function of epinephrine in sympathetic vasodilation
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causes a weak vasodilation effect because of stimulation of the beta-adrenergic receptors
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what are the three total body readjustments that occur during exercise
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discharge of sympathetic nervous system, increase in cardiac output, increase in arterial pressure
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how does the body gain more blood during strenuous exercise
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acute vasoconstriction of vessels in resting muscles increases systemic flow to active muscles as much as 2L/min
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what is spared the blood harvesting effect
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coronary and cerebral circulation due to little vasoconstrictor (alpha receptors)
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mean systemic filling pressure
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where you constrict the venous return to the heart and systemically increase the preload to the right ventricle
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ways in which you can increase arterial pressure
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vasoconstriction of vessels in relaxed muscles, increased cardiac output, increase in mean systemic filling pressure
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which would cause a larger change in systemic arterial blood pressure, swimming, or hammering a nail
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hammering a nail because selective vasoconstriction is taking place increasing the amount of blood going to a smaller amount of vessels, swimming would increase only marginally due to the large increase in vasodilation
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what rises majorly at the beginning of strenuous exercise
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mean systemic filling pressure due to sympathetic stimulation of vessels
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what causes an upward slope in the venous return curve
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decreased systemic or acute resistance to blood flow causes an increase in the amount of blood that is delivered to the right atrium
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in light of everything, what happens to the right atrium of a marathon runner when he is running uphill at mile 23
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his right atrial pressure will actually be BELOW normal because of severely increased cardiac rate
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left coronary artery supply
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anterior and left lateral portions of the left ventricle
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right coronary artery supply
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right ventricle, and posterior portion of the left ventricle
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how does venous blood from the left ventricle return to the right atrium
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coronary sinus
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veins that empty coronary venous blood back into the heart
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thebsian veins
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flow of blood through ventricles through systole and diastole
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when in systole blood flow is lessened in right, almost stopped in left due to muscular contraction, flow is restored in systole
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what supplies the outer surface of the heart muscle
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epicardial arteries
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what supplies the inner portions of the heart muscle
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subendocardial arteries
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which of the two cardiac arterial systems is most compromised during systole
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subendocardial because intramuscular
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how does the subendocardial plexus compensate for systolic compression
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lots of collateral vessels and anastamoses
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what is the main regulator of blood flow through the coronary system
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local arteriolar vasodilation in response to nutritional needs of the cardiac muscle (oxygen)
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what substances are responsible for vasodilation in cardiac arteries
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lack of oxygen, adenosine, nitric oxide
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stimulation of the autonomic nervous system can affect the heart how
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directly and indirectly
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direct autonomic actions
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response of neurotransmitters directly on the vessels
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indirect autonomic actions
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secondary changes in coronary blood flow caused by increased or decreased activity of the heart
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vagal parasympathetic distribution to the ventricular system is...
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not that great
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AcH has what direct effect on coronary arteries
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dilate the coronary arteries
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sympathetic innervation to coronary vessels is
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a lot
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constrictor receptors
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alpha
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vasodilator receptors
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beta
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epicardial vessels have more of what
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alpha = constrictor
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endocardial vessels have more of what
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beta = vasodilators
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sympathetics can constrict or dilate coronary arteries
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both, but constrict more
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cardiac cells use what as a form of energy on rest
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fatty acids
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cardiac cells use what form of energy during ischemic conditions
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glucose
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what are the negatives of using glucose as a heart supply fuel
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exhausts large quantities of blood glucose very quickly and also build up lactic acid - probably cause of ischemic pain
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during severe cardiac ischemia what does the heart tissue do to ATP
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convert ATP into adenosine
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what is the purpose of depleting ATP supply for adenosine
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adenosine is a potent local vasodilator
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what is the major consequence of using ATP for vasodilation
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in about 30 minutes, about half of the adenine base can be lost, leads to a severe defecit of ATP that can lead to cardiac ischemia
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what is the most frequent cause of diminished coronary blood flow
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atherosclerosis
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what are the indications for atherosclerosis
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overweight, obese, HBP, sedentary life style
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what is the most common area for atherosclerotic plaques to occur
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first few cm of major coronary arteries
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thrombus
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atherosclerotic plaque where the plaque itself breaks through the endothelium and attracts platelets
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coronary embolus
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where the clot breaks free and occludes a more distal vessel
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spasm of vessel wall can lead to what
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secondary thrombosis of the vessel
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what is one factor that determines the degree of damage done to heart tissue during an ischemic episode
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degree of collateral circulation
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why do patients recover from small areas of coronary occlusion within a month
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collateral circulation takes about a month to fully dilate and reach the original flow rates of coronary vessels
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what phenomenon occurs when occlusions form slowly
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collateral circulation builds up at the same time, patients may not even be aware of occlusions due to collateral circulation building up at the same time
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when a muscle has zero blood flow
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infarcted
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why does infarcted tissue have a brown bluish hue
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due to hemoglobin deoxygenation
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fun fact: heart needs 1.3 ml of oxygen per 100 grams of muscle to remain alive, normally gets 8ml/100mg, even if you have 15 to 30% of total blood flow you still get perfectly functioning tissue
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dat shit cray
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what part of the heart is infarcted first
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subendocardial layer because of decreased perfusion
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4 main causes of death post MI
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decreased cardiac output, damming of blood in the lungs leading to pulmonary edema, fibrillation of the heart, rupture of the heart wall
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systolic stretch
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where an ischemic portion of the heart wall gets pushed outwards due to pressure increase during systole
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what happens when the heart is physically unable to pump enough blood into the peripheral vascular tree
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cardiogenic shock
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what happens to blood when it cannot be pumped into systemic circulation
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builds up in venous circulation
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what is the result of increased venous blood holding
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leads to kidney hypofusion which increases blood volume even more, can lead to lethal pulmonary edema a few days after appearing fine post MI
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what do many people with coronary occlusion die of
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ventricular fibrillation
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when are the two critical periods in which fibrillation can develop
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10 minutes post MI, then after an hour or so lasting for another couple hours
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4 factors leading to heart fibrillation
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loss of blood supply causes an increase in cardiac extracellular potassium levels, injury currents where ischemic musculature cannot repolarize, sympathetic reflexes induce fibrillation due to low blood pressure, excessive ventricle dilation causes distension of conduction pathways
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when is the patient most at risk for cardiac wall rupture
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a few days post MI when the wall has had time to dead muscle degenerates
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how long does it take for nonfunctional muscle fibers to become refunctional after MI (assuming they did not infarct)
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few days to 3 weeks
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how does the heart compensate for loss of muscular tone
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hypertrophy of remaining muscle
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coronary steal syndrome
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where a patient recovering from infarctions is under too much stress so sympathetic stimulation robs blood from smaller vessels for coronary arteries - can lead to worsening MI
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cardiac reserve
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heart pumps 300-400% more blood than necessary, even if damaged can still be fine if not stressed too much
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what causes cardiac pain
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possibly by lactic acid buildup, pain impulses through sensory afferent fibers into the CNS
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angina pectoris
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where load on heart becomes more than curreent oxygen delivery can handle
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how do you treat angina pectoris
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nitro w/ B blockers
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aortic coronary bypass
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taking arm or leg veins and grafting back into heart to bypass clots, only value in patients with not that severe muscle infarctions
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baloon angioplasty
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where you break occlusions with a baloon tipped catheter, will eventually require repeat stents or procedure in about 24-40% of patients often within 6 months - due to lots of scar tissue
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