IBHS 527 lecture 6

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VASUpharm14
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61403
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IBHS 527 lecture 6
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2011-01-23 03:27:50
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Cardiodynamics. richard. fun stuff
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  1. what is cardiodynamics?
    • 1. cardio:
    • how much blood does the heart eject in 60 seconds?
    • 2. dynamic:
    • how does the body increase of decrease this amount?
    • 3. what drugs increase of decrease this amount
    • -and how do they do it?
  2. cardiac output
    • volume of blood ejected by a heart pump in one minute; amount of blood pumped by each ventricle in one minute
    • use:
    • clinical measure of productivity = heart health
    • *volume ejected by each ventricle is about the same
  3. equation of cardiac output
    • C.O. = heart rate (HR) X stroke volume (SV)
    • cardiac output = ? L/min
    • -HR = # of contractions of the heart during one minute
    • *average HR = 75 beats/minute
    • -SV = amount of blood ejected from each ventricle during one beat
    • *average SV = 80 ml/beat
    • => 6 L/min is cardiac output
  4. combined cardiac output
    • L/min for both ventricles
    • *volume ejected by each ventricle is about the same
  5. 2 ways to change cardiac output (C.O.)
    • 1. influence the rate of the conduction system (nodes) to change the heart rate
    • 2. influence the strength of the contraction system (myocardium) to change the stroke volume
  6. heart rate while sleeping
    • 65 beats/min
    • *lower than average of 75 bpm
  7. maximum heart rate of person
    220 - age = maximum heart rate
  8. just increasing heart rate will have what fold increase in cardiac output (C.O.)?
    ~2.5 x
  9. what determines the heart rate?
    • SA nodal cells (top of the heart)
    • regulated by:
    • 1. nervous system (autonomic innervation)
    • 2. endocrine system (hormones)
  10. what determines the stroke volume?
    • ventricle muscle cells (bottom of the heart)
    • regulated by:
    • 1. cardiovascular system (end-diastolic volume)
    • 2. nervous and endo system (end-systolic volume)
  11. 3 receptors that detect blood change
    • 1. chemoreceptors
    • 2. baroreceptors
    • 3. stretch receptors
  12. context: 3 receptors that detect blood change
    chemoreceptors
    detect gas changes such as O2 and CO2
  13. context: 3 receptors that detect blood change
    baroreceptors
    detect changes in blood pressure (BP) and blood volume (BV)
  14. context: 3 receptors that detect blood change
    stretch receptors
    • detect distention of right atrium
    • "Bainbridge reflex"
  15. process of regulating cardiac output by Nervous system (autonomic innervation)
    • (1) blood changes detected by receptors (chemo/baro/stretch) --> (2) send action potential (AP) to medulla oblongata --> medulla oblongata sends action potential (AP) to heart --> neurotransmitters are released onto SA node
    • *sympathetic (spinal nerve) = norepinephrine = speed up
    • *parasympathetic (cranial nerve X/vagus nerve) = acetylcholine = slow down
  16. process of regulating cardiac output by Endocrine system (hormones)
    • (1) changes in blood detected (chemo/baro) --> (2) send action potential (AP) to medulla oblongata --> medulla oblongata sends action potential (AP) to adrenal medulla --> gland releases epi and norepi --> stimulates SA node
    • *stressful conditions - epistimulation
  17. How does ACh decrease the heart rate (HR)?
    parasympathetic --> ACh release --> bind to muscurinic receptors --> opens K+ channels (inside becomes less positive/more negative and RMP goes from -60 mV to -70 mV and now takes longer to create action potential (AP) --> slower APs => DEC. heart rate (HR)
  18. How does NE/E increase the heart rate (HR)?
    sympathetic --> Norepi/Epi release --> bind to beta-1 adrenergic receptors --> opens Ca2+ channels (inside becomes more positive/less negative and RMP goes from -60 mV to -50 mV and now is quicker to create action potential (AP) --> faster APs => INC. heart rate (HR)
  19. process of stroke volume
    (1) systole (action - squeezing) --> (2) end systolic volume (pause - left over volume in heart) --> (3) diastole (action - distending) --> (4) end diastolic volume (pause - volume gained in heart)
  20. equation of stroke volume
    • SV = EDV - ESV
    • *the difference between:
    • -EDV = end-diastolic volume (volume after diastole)
    • -ESV = end-systolic volume (volume after systole)
  21. 2 ways to detect ventricle volumes
    • 1. measure via Cardiac Conductance Catheterization (electrical impedance)
    • 2. estimate via echocardiogram (ultrasound)
  22. 2 ways to change stroke volume
    • 1. change end-diastolic volume (EDV)
    • 2. change end-systolic volume (ESV)
  23. context: 2 ways to change stroke volume
    change end-diastolic volume (EDV)
    • 1. INC. stroke volume:
    • INC. EDV (put more in heart- preload) 2 ways:
    • -INC. blood into heart by INC. venous return (INC. BV)
    • -INC. filling time (DEC. HR)
    • 2. DEC. stroke volume:
    • opposite of above
  24. context: 2 ways to change stroke volume
    change end-systolic volume (ESV)
    • 1. INC. stroke volume:
    • DEC. blood left in heart 3 ways:
    • -INC. EDV (Frank Starling's law) - more in more out
    • -INC. contractility (Epi, Norepi) with same amount of blood but with INC. calcium release
    • -DEC. afterload (vasodilation = less resistance)
  25. positive effectors of the heart
    • increase cardiac output (C.O.)
    • 1. increase HR (conduction):
    • -use positive chronotropic agents (affect SA node)
    • 2. increase SV (contraction):
    • -use positive inotropic agents (affect myocardial muscle cells)
    • *positive chronotropic/inotropic agents (affect node + muscle cells)
    • 1. endogenous/natural:
    • - epi/norepi - binds to beta-1 receptor --> open Ca2+ channels
    • 2. exogenous/drugs:
    • - epi pen
    • - beta-1 receptor agonists (like in CHF)
  26. negative effectors of the heart
    • decrease cardiac output (C.O.)
    • 1. decrease HR (conduction):
    • -use negative chronotropic agents (affect SA node)
    • 2. decrease SV (contraction):
    • -use negative inotropic agents (affect myocardial muscle cells)
    • *negative chronotropic/inotropic agents (affect node + muscle cells)
    • 1. endogenous/natural:
    • - ACh - binds to muscarinic receptors --> opens K+ channels
    • 2. exogenous/drugs:
    • (a) beta-1 receptor antagonists/beta blockers
    • ex:
    • - atenolol (Tenormin)
    • - metoprolol (Toprol, Lopressor)
    • (b) calcium channel blockers (with specificity for cardiac calcium channels (cc))
    • ex:
    • - verapamil (Calan SR, Verelan) - high specificity cardiac calcium channels (cc)
    • - diltiazem (Cartia) - medium specificity for cardiac calcium channels (cc)
  27. mixed effectors of the heart
    • digoxin
    • function:
    • 1. decreases HR (conduction)
    • negative chronotropic agent (affect SA node)
    • -inhibition of the Na+/K+ exchanger
    • -conduction cells can't recover membrane potential as fast
    • 2. increases SV(contraction)
    • positive inotropic agents (affect myocardial muscle cells)
    • -inhibition of the Na+/K+ exchanger
    • -Na+ builds up inside cell --> loss of Na+ gradient
    • -inhibition of Na+/Ca2+ exchanger
    • - calcium builds up inside cell --> more force generation
    • *uses in atrial fibrillation because don't want heart to beat too fast and also to not work too hard
    • -first choice are beta-blockers and calcium channel blockers

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