The Heart Functions as a Pump. How is the pump action controlled by regulated waves of cell-cell depolarization within the pump? 2/1 - PowerPoint PPT Presentation


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The Heart Functions as a Pump. How is the pump action controlled by regulated waves of cell-cell depolarization within the pump? 2/1


The Heart Functions as a Pump. How is the pump action controlled by regulated waves of cell-cell depolarization within the pump? 2/1 Review: What are the steps to a ... – PowerPoint PPT presentation

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Title: The Heart Functions as a Pump. How is the pump action controlled by regulated waves of cell-cell depolarization within the pump? 2/1

The Heart Functions as a Pump. How is the pump
action controlled by regulated waves of cell-cell
depolarization within the pump? 2/1
  • Review What are the steps to a cardiac cycle of
  • How do the heart valves maintain one-way blood
    flow in two separate circulatory loops?
  • How does the heart work as a pump?
  • What is the pathway taken by the wave of
    depolarization in the heart?
  • What is the difference between nodal and
    contractile depolarization?
  • What is a pacemaker potential?
  • How are cells initially become depolarized?
  • How does the action potential pass between
    adjacent cells? (PASSAGEelectrical syncitium)

Your heart pumps blood using a five step Cardiac
  • Remember the two equal cycles Pulmonary AND
  • 1) Diastolic Filling of Atria and Ventricles (V.
  • 2) Atrial Systole (VIP occurs towards the end of
    V. Diastole)
  • 3) Isovolumetric Ventricular Contraction (V.
  • 4) Ventricular Ejection (V. Systole)
  • 5) Isovolumetric Ventricular Relaxation (V.
  • Remember the two ventricles BOTH do these
    activities at about same time with the same
    volumes at two different pressures!
  • While Atrial Systole does occur, it is not as
    clinically important because the atria only do
    about 5 of the work done by the ventricles, so
    they just dont use as much ATP or need as much

Remember that the AV and semilular valves close
to prevent flow of blood from high to low
pressure back into the atria or ventricles!
How does pressures change in the heart chambers
and arteries during the cardiac cycle when you
are healthy? Memorize List!
  • Units of Pressure measured in mmHg is the
    ability of fluid pressure to maintain a column of
    mercury. Yes its archaic but its the unit used!
  • Pressure gradients let blood move! ?
    gradient?movement point A?B
  • Atrial Pressures Simply create enough P to load
    blood into ventricle
  • -Right Atrium 0-10 mmHg and the Left Atrium
    0-10 mmHg
  • Ventricles MUST generate enough pressure to load
    blood into arteries
  • Right Ventricle 0 to 15-25 mmHg
  • Left Ventricle 0 to 120mmHg
  • If pressure in ventricle is not great enough?No
    Blood Exits Ventricle
  • Arterial Pressures Systolic pressure is from
    Vent Systole and Diastolic is pressure just
    before next loading from ventricle (Contraction).
  • -Always expressed Systolic mmHg/Diastolic mmHg
  • -Pulmonary Artery 15-25/8 ? tough to feel (a
    very short circuit)
  • -Aorta 120/80?felt as a Pulse (a long-high
    resistance circuit)
  • Venous Pressures always very very low (sometimes
    even negative)!
  • -VenaCava and Pulmonary Veins 5/0 or lower

The volume of blood pumped by a ventricle per
minute is the cardiac output of that ventricle!
How is CO calculated? Memorize!
  • How do we get the ventricle ready to push blood
  • Most ventricular filling passively occurs as
    blood drains from vena cava and pulmonary veins
    through atria and into the apex (down hill) by
    simple gravity and draining..water pours out of
    a glass onto the floor by the same effect.
  • End Diastolic Volume(EDV) ml of blood in
    ventricle after the kick Pre-systole (130 ml)
  • Mostly from passive filling during Vent and
    Atrial diastole, plus a small bonus from atrial
    systole (about 100 ml 30 ml from kick)
  • Isovolumetric Contraction no volume change
  • AV Valves just closed and Semilunars are not yet
    able to open!
  • Volume in ventricle does not change but pressure
    on this 130 ml goes up until pressure in
    ventricle is greater than in the artery in the
    blood on other side of the semilunar valve!

  • VentricularEjection/StrokeVolume(SV) blood
    leaving vent. (70ml)
  • Ejection Fraction (EF)
  • EFSV/EDV X 100 70ml/130ml X 100 54
  • SV can be larger and EF can be up to 90 during
  • End Systolic Volume (ESV) Amount left in vent.
    After systole
  • ESVEDV-SV130ml-70ml 60 ml (amt. remaining
    during isovolumetric relaxation)
  • Heart disease a weak ventricle so the EF is
    small and ESV large
  • Cardiac Output (CO) amount pumped by a
  • CO SV X HR 70 ml/beat X 75 beats/min 5,000
  • COSV X HR 100 ml/min X 50 beats/min 5,000
  • (X2 for whole heart Rt/Lt ventricles pump
    equal volumes 5X210 L/min)
  • Range (cardiac reserve) CO can get up to 35
    L/min/Ventricle for Olympic Athletes! Your Blood
    volume (4-7 L) must be recycled many times/min at
    35 L/min

Will I need to do the math for the calculation we
just looked at on a lab or lecture test?
Answer Yes Will I get to use a calculator
NoWill math be easy Yes
  • Formulas should be understood for what they
    are.a logical prediction of what the body does.
  • Know basic formulas we just looked at.
  • Know normal values we just looked at.
  • Know how to calculate missing information given a
    set of known facts.

SA Node--gt(Atrial depolarization/contraction)?AV
Node?Bundle of His?Lt/Rt Bundle
Branch?Pukinje?Myocardium (Depol./Contract)
How do depolarizations pass between cardiac cells?
  • Intercalated discs hold adjacent cardiac cells
    together and the gap junctions create tiny pores
    in the discs between the cells allowing passage
    of ions like Na and Ca, this unites all
    cardiac cells into an electrical syncitium (all
  • Conduction Path SA Node?Atria?AV Node?Common
    bundle branch?Bundle of His? R/L Bundle Branches?
    Purkinje fibers ? Myocardium (contractile cells
  • Note the Conduction rates and Consequence of
    rates in different locations in the pathway are
    not the samethis is very important!
  • Then the wave of depolarization (excitation)
    spreads from endocardium to epicardium (Inside to
  • V.I.P. Atrioventricular septum is normally
    non-conductive to depolarization! Depol only
    passes through the AV-Node!
  • V.I.P. There is a bit of contraction in the
    interventricular septum prior to the walls of the
    ventricles (this is clinically significant!)
  • Heart Rhythm is the heart conduction
  • Nodal vs. Arrhythmia vs. Ectopic Foci
    vs. Fibrillation

  • HUGE Functional Difference Pacemaker Cell vs.
    Contractile Cell
  • SA NodalCell(AV nodal or conduction)(no
    contractile force)
  • Cardiac Myocyte (force generationcontractile)
  • Speed of Na leak determines rate of
    depolarization for SA/AV-Nodes Very
    Steep?Depolarizes Fast?Rapid Heart Rate
  • Not Steep Cells depolarize slowly? take more
    time to reach threshold for voltage gated Na
    channels to open? Slow Heart Rate
  • Absolute refractory period determines rate of
    depolarization by determining time the cell must
    wait until it can be depolarized again
  • Myocytes and Timing Why a delay in the onset of
  • Na channels must open and let Na into cell
  • Ca gets inside myocytes
  • Ca must find troponin and pull it off actin
  • Actin must find/bind myosin
  • Actin must ratchet across myosin and generate
  • Ca Slow to exit myocytes
  • These all add to the x-axis (time) of contraction
  • This generates force in ventricle Isovolumetic
    Contraction? Ejection

SA Nodal cells are non-contractile and
rhythmically depolarize themselves and adjacent
cells. Nodal cells eventually depolarize
adjacent contractile cells via gap junctions. As
a result, the depolarizations of contractile and
non-contractile cells are very different!
Non-Contractile Cells!
Remember this is depolarization in single cells,
not the whole heart!
Agents like epinephrine speed up the heart rate
and the parasympathetic NS (ACH) slows the heart
down. What happens to the rate of membrane
leakage (pacemaker potential) to accomplish this
change in heart rate at the SA Node?
Before and after Sympathetic Stimulation?
pacemaker potential Longer period between
depol Shorter period between depol
Longer time to next depolarization
Stimulation of the parasympathetic NS slows down
the heart rate by hyperpolarizing the SA node and
decreasing its leakiness (pacemaker potential)