Card Set Information

2011-01-07 21:31:03

muscle blood flow and cardiac output during exercise
Show Answers:

  1. Why is exercise so stressful on the circulatory system?
    Large amount of muscle mass that needs perfused
  2. Increase in cardiac output during exercise?
    • 4-5 times normal
    • 6-7 times in an athlete
  3. rate of blood flow through the muscles?
    • 3-4 ml/min/100g
    • during exercise in an athlete 50-80 ml/min/100g
  4. blood flow during muscle contraction?
    • during the contraction the pressure of the muscle decreases blood flow
    • during tetanic contractions the flow can be almost stopper, the causes rapid weakening of the muscle
  5. capillary availability
    • at rest some muscle capillaries have little to no flow
    • during exercise dormant capillaries open up to decrease the distance nutrients must travel
    • 2-3 fold increase in capillary surface area
  6. What causes arteriole dilation during muscle activity?
    • chemical substances
    • lack of O2
  7. How does lack of oxygen cause vasodilation in arterioles?
    • without oxygen arterial smooth muscle can not sustain vascular tone
    • the lack of oxygen causes the release of vasodilator substances
  8. Most important vasodilator substance in arterioles
    • adenosine
    • only last for 2 hours
  9. After muscles become insensitive to adenosine what vasodilators take over?
    • potassium ions
    • ATP
    • lactic acid
    • carbon dioxide
  10. sympothetic vasoconstricter
    • noreinephrine
    • can decrease blood flow to as little as one half to one third normal
    • important during shock and times of stress
    • maintains a normal arterial pressure
  11. secretions of the adrenal medula
    • norepinephrine, vaso constriction
    • epinephrine, slight vasodilator due to activation of beta and alpha, slightly more beta
  12. Three major effects on circulation during exercise
    • mass discharge of the sympathetic nervous system
    • increase in arterial pressure
    • increase in cardiac output
  13. Three major effects of mass sympathetic discharge
    • the heart is stimulated to increase rate and contraction strength.
    • most of the peripheral arterials are constricted except those to active muscles. Can account for up to 2L/min extra blood flow to muscles
    • The muscle wall of the veins contract, this greatly increases filling pressure by increasing venous return and therefore increases cardiac output.
  14. What two systems have poor vasoconstrictor innervation
    coronary and cerebral
  15. How is arterial pressure increased during exercise, 3?
    • vasoconstriction of arterials and small arteries
    • increased pumping activity of the heart
    • increase in filling pressure and cardiac output
    • pressure can become very high if only a few muscles are used since only those muscles become vasodilator
    • lower arterial pressure if doing whole body exercise, running swimming, since for vasodialtion is occurring in large masses of muscle
  16. Why is increased arterial pressure during exercise important?
    • it increases the force in which blood is moved into the tissue
    • The extra pressure stretches the walls of the vessels to allow more flow
  17. Two factors that increase cardiac output?
    increased rate and increased strength of contraction
  18. What must happen to venous return to be able to increase cardiac output?
    it must increase
  19. What two factors cause the venous return to increase during exercise
    • sympathetic stimulation contracts the veins
    • tensing of the abdominal and skeletal muscle compresses internal vessels providing more compression of the capacitive vascular system
    • from 7mmhg to 30mmhg
  20. What happens to right atrial pressure during increased cardiac output of exercise
    it raises very little because of the greatly increased sympathetic stimulation of the heart
  21. where on the heart do main coronary arteries lie?
    • on the surface
    • only the inner 1/10 of a millimeter of endocardium receives nutrition through diffusion
  22. where does most coronary venous blood return to
    • coronary sinus with a small amount going directly to the right atrium through the anterior veins
    • thebesian veins enter the closest chamber
  23. What is the resting coronary blood flow?
    225 ml/min 4-5 % of total CO
  24. During exercise how does the increased workload of the heart get its nutrition
    coronary blood flow can increase 3-4 fold, the rest of the needed energy comes from the increased efficiency of cardiac energy utilization
  25. Phasic changes of cardiac blood flow
    • in the left ventricle blood is supplied during diastole and is slowed during systole due to muscle contraction
    • the same is true of the right heart but to a much lesser extent, the right ventricle does not contract as strongly
  26. What are the different layers of the coronary arteries
    • epicardial, intramuscular branches, subendocardial plexus
    • the subendocardial vessels compensate for the lack of flow during systole with there great number
  27. Indirect vs direct nervous control of the coronary vessels
    • direct- neurotransmitter stimulation
    • indirect- has much more effect, if the sympathetic nervous system increases cardiac out the increase in metabolic products will cause vasodilation even in the presence of norepi, a vasoconstrictor
  28. There is much more sympathetic innervation of the heart then parasympathetic
  29. location of receptors of the coronary vasculature
    • alpha is on epicardial
    • beta is on intramuscular
  30. What happens if nervous stimulation alter blood flow in the wrong direction
    the metabolic requirements will over ride the nervous innervation
  31. What is the hearts energy source of choice?
    • fatty acids instead of carbohydrates
    • more oxygen is needed for fatty acid metabolism to ATP then with carbs
  32. What is a cause of pain in ischemic heart tissue
    build up of lactic acid
  33. What happens to ATP during metabolism
    • first it is metabolized to ADP then to AMP and then to adenosine
    • the cellular membrane is permeable to adenosine and it leaves the cell
    • Within 30 minutes of severe hypoxia half of the adenosine can be lost from the cell, it can only be produced at 2% an hour in the cell. Because of this after 30 minutes of ischemia relief may be to late
  34. The most frequent cause of congestive heart failure?
    slowly increasing coronary ischemia and weakening of the cardiac muscle
  35. Most frequent cause of diminished coronary flow
  36. Causes of athrosclerosis
    • genetics
    • large cholesterol intake
    • sedentary lifestyle
  37. Athrosclerotic plaque?
    • colesterolo depositino beneath the endothelium that becomes fibrosed and sometimes calcified
    • common site is the first few centimeters of a coronary artery
  38. When does acute coronary occlusion occur
    in a person who already has an underlying atherosclerotic coronary disease
  39. How does and acute coronary occlusion occur
    • the plaque can cause a thrombus which can then occlude the vessel, this usually occurs where the plaque has broken through the surface and is in direct contact with the blood. Can become an embolus
    • The plaque can irritate the smooth muscle of the wall and cause a vaso spasm
  40. What has an effect of the degree of damage of coronary occlusion
    • collateral flow
    • when an occlusion develops in a large artery the small collateral branches begin to dilate within seconds
    • after 24 hours the collateral flow will dilate enough for adequate flow to the muscle, doubling by the second. Can reach normal flow by 1 month
    • As the plaque grows this collateral flow will become to little and tissue will die
  41. Def of an infarct
    area of muscle with zero flow or so little it cannot sustain function
  42. What happens to the tissue directly after an infarction
    • collateral blood begins to seep into the area
    • the are becomes overfilled with stagnant blood
    • the muscle fibers use oxygen, causing the hemoglobin to become totally de-oxygenated
    • the infarct becomes bluish-brown
    • the local vessels begin to leak fluid and the area becomes edematous
    • cells begin to swell and lose function
    • cells die
  43. what is the oxygen requirement of cardiac muscle
    • 1.3ml/min/100g
    • during rest the normal delivery is 8ml/min/100g
  44. Why does the subendocardium infarct when there is no evidence of infarct on the outer surface
    • it has extra difficulty obtaining blood flow because of compression of contraction
    • this area will be damaged first with compromised blood flow
  45. four most common causes of death after MI
    • decreased cardiac output
    • damming of blood in the pulmonary blood vessels, death from pulmonary edema
    • fibrillation of the heart
    • rupture of the heart
  46. What is systolic stretch
    • when the normal portion of the ventricle contracts the ischemic portion of the muscle is forced outward by the intraventricular pressure
    • much of the pumping force is dissipated by the bulging of the non functional area
  47. When peripheral tissue becomes ischemic and dies?
    • this is due to lack of blood flow and is called cardiac shock
    • usually occurs when 40% of the LV is infarcted
    • death in 85% of patients
  48. How does damming of venous system affect body after MI
    • no effect for the first couple days
    • the blood flow to the kidneys is diminished and the kidneys fail to excrete enough urine
    • this will add to the total body fluid and lead to congestive heart failure
  49. What are the two most dangerous periods to develop v fib after an MI
    • first ten minutes
    • one hour after lasting for a few hours
  50. four factors that increase the tendency to fibrillate
    • an acute loss of blood supply to the heart causes depletion of K which increases the amount of extracellular K
    • Injury current develops, the ischemic muscle can not fully depolarize after a beat. The outer membrane of these cells is negative and this negativity can spread and depol other section of the heart
    • powerful sympathetic reflexes develop after massive infarct
    • the weakened muscle will dilate increasing the electrical pathway
  51. When will the muscle rupture after infarct
    • after a few days, the infarcted muscle needs time to degenerate and stretch out before rupturing
    • due to systolic stretch
  52. Using systolic stretch to asses the progress of an MI
    the amount of stretch is assessed every day
  53. Tamponade
    compression of the heart from the outside, this blocks the flow of blood into the rt atrium and the pt can die of decreased cardiac output
  54. Muscle damage with a small infarct?
    little to no death can occur, part of the muscle though can become non functional due to inadequate nutrition
  55. In the days following cardiac muscle death
    • the dead cells are replaced by fibrous scar
    • the ischemia will promote the development of a large quantity of fibroblasts
    • the scar will contract over the next year
    • the normal areas of the heart will hypertrophy to compensate for the muscle loss
  56. What determines the degree of cellular muscle death
    the degree of ischemia and the workload of heart muscle
  57. Coronary steal syndrome
    • after MI during excessive exercise the vessels of the healthy tissue will dilate and steal blood supply from the nonfunctional tissue
    • this will worsen the ischemic condition and lead to further cell death
  58. cardiac function after an MI
    • the pumping capacity is permanently diminished
    • the normal cardiac reserve at rest is 300-400% so even with a lose of function you can still perform normal activities
  59. causes of pain in ischemic tissue
    • lactic acid
    • histamine
    • kinins
    • proteolitic enzymes
  60. Pectoralis angina
    pain felt beneath the sternum when the demand of the heart is greater then the supply
  61. Reason for pain in the arm and neck from the heart
    during embryonic life the heart originates in the neck so the heart and arms and neck share the same spinal cord segments for pain fibers
  62. vasodilators used for pectorals angina
    nitroglycerine and nitrates
  63. beta blockers decrease
    the metabolic need on the heart