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					 Chapter 20


the heart
Anatomy review

Electrical activity of the whole heart (EKG)

Electrical activity of the heart cells

The Cardiac Cycle

Cardiac Input and Output (dynamics)
Heart review

         4 chambers
              2 atria         receive
              2 ventricles    send

         4 valves
              2 AV valves
              2 semilunar valves

         2 circuits
               systemic
               pulmonary
            external heart anatomy




fig. 20-9
            internal heart anatomy




fig. 20-6
100 keys (pg. 678)
  “The heart has four chambers, two associated
  with the pulmonary circuit (right atrium and right
  ventricle) and two with the systemic circuit (left
  atria and left ventricle). The left ventricle has a
  greater workload and is much more massive
  than the right ventricle, but the two chambers
  pump equal amounts of blood. AV valves
  prevent backflow from the ventricles into the
  atria, and semilunar valves prevent backflow
  from the aortic and pulmonary trunks into the
  ventricles.”
cardiac conduction system
    modified cardiac muscle cells

        •SA node (sinoatrial node)
             wall of RA
        •AV node (atrioventricular node)
             between atrium and ventricle
        •conducting cells
             AV bundle (of His)
             conducting fibers
             Purkinje fibers
              conducting system of heart




fig. 20-12a
prepotential

   cannot maintain steady resting potential
   gradually drift toward threshold


           SA node       80-100 bpm

           AV node       40-60 bpm
fig. 20-12b
because SA node is faster…

     …it controls the heart rate
                     (pacemaker)

but heart rate is normally slower
than 80-100 bpm
           (parasympathetics)

if SA node is damaged, heart can still
continue to beat, but at a slower rate
if heartbeat is slower than normal…

          … bradycardia



if heartbeat is faster than normal…

          … tachycardia
impulse conduction




          fig. 20-13
impulse conduction

     SA node
         atria get signal - contract
         signal to AV Node
               AV node sends signal
               to ventricles (time delay)
                     ventricles contract
                          after atria are done


       damage to any part of conducting
       system may result in abnormalities   (EKG)
ECG’s        electrocardiagram
EKG’s

  recording of the electrical activity of the
  heart (from the surface of the body)




         fig 20-14
ECG’s
   different components:

        P wave
            depolarization of the atria
        QRS complex
            depolarization of the ventricles
                 bigger
                 stronger signal
        T wave
            repolarization of the ventricles
ECG’s




        fig 20-14 EKG
ECG’s
   to analyze:

        size of voltage changes
        duration of changes
        timing of changes



                 intervals
ECG’s




        fig 20-14 EKG
ECG’s
  intervals:

        P-R interval
            from start of atrial depolarization

                to start of QRS complex

        time for signal to get from atrium to
        ventricles

        if longer than 200 msec can mean
        damage to conducting system
ECG’s
  intervals:

        Q-T interval
          time for ventricular depolarization
                  and repolarization
                 (ventricular systole)

           if lengthened, may indicate, [ion]
           disturbances, medications,
           conducting problems, ischemia, or
           myocardial damage.
ECG’s
  intervals:

        T-P interval

        from end of ventricular repolarization

         to start of next atrial depolarization


        the time the “heart” is in diastole
        the “isoelectric line”
fig 20-14 EKG
                  T-P
                interval
ECG’s
  intervals:
    abnormalities cardiac electrical activity

                = cardiac arrhythmias


           some are not dangerous

           others indicate damage to heart
100 keys (pg. 688)
  “The heart rate is normally established by cells of
  the SA node, but that rate can be modified by
  autonomic activity, hormones, and other factors.
  From the SA node the stimulus is conducted to
  the AV node, the AV bundle, the bundle
  branches, and Purkinjie fibers before reaching
  the ventricular muscle cells. The electrical
  events associated with the heartbeat can be
  monitored in an electrocardiagram (ECG).”
Electrical activity of the heart cells
    99 % of heart is contractile cells

    similar to skeletal muscle

    AP leads to Ca2+ around myofibrils
     Ca2+ bind to troponin on thin filaments
       initiates contraction (cross-bridges)

        but there are differences…
              nature of AP
              location of Ca2+ storage
              duration of contraction
Electrical activity of the heart cells
    The action potential

         resting potential of heart cells
                   ~ -90mV

         threshold is reached near
              intercalated discs

         signal is AP in an adjacent cell
              (gap junctions)
Electrical activity of the heart cells
    The action potential

         review skeletal muscle




    fig. 20-15
Electrical activity of the heart cells
    The action potential

         once threshold is reached the action
         potential proceeds in three steps.
Electrical activity of the heart cells
    The action potential - step 1

         rapid depolarization
             (like skeletal muscle)

         Na+ into cell
            through voltage-gated channels
                        (fast channels)
Electrical activity of the heart cells
    The action potential - step 2

        the plateau

        Na+ channels close
        Ca2+ channels open for a “long” time
             (slow calcium channels)
        Ca2+ in balances Na+ pumped out
Electrical activity of the heart cells
    The action potential - step 3

        repolarization

        Ca2+ channels begin closing
        slow K+ channels begin opening
        K+ rushes out restoring resting pot.
Electrical activity of the heart cells
    The action potential - step 3

        repolarization

        Na+ channels are still inactive
        cell will not respond to stimulus

                         = refractory period
fig. 20-15a
Electrical activity of the heart cells
    The role of calcium

        extracellular Ca2+ enters cells
          during the plateau phase (20%)

        Ca2+ entering triggers release of
          Ca2+ from sarcoplasmic reticulum

        ... heart is highly sensitive to
               changes in [Ca2+] of the ECF
Electrical activity of the heart cells
    The role of calcium

        in skeletal muscle, refractory period
        ended before peak tension developed…
                   …summation was possible
                             …tetanus.

        in cardiac muscle refractory period lasts
        until relaxation has begun…
                   …no summation
                              …no tetanus.
Clinical note:        Heart attacks

    blockage of coronary vessels

    myocardium without blood supply…

                 …cells die
                                 (infarction)

    myocardial infarction (MI) = heart attack
Clinical note:        Heart attacks

    blockage of coronary vessels

          due to:
               CAD (coronary artery disease)
                         (plaque in vessel wall)

                 blocked by clot (thrombosis)
Clinical note:           Heart attacks

    blockage of coronary vessels

          as O2 levels fall, cardiac cells will:

                 accumulate anaerobic enzymes
                 die and release enzymes

   LDH           lactose dehydrogenase
   SGOT          serum glutamic oxaloacetic transaminase
   CPK           creatine phosphokinase
   CK-MB         cardiac muscle creatine phosphokinase
to here 3/26
lec # 31
Clinical note:     Heart attacks

    anticoagulants (aspirin)
    clot-dissolving enzymes

    quick treatment will help reduce damage
    due to blockage
Clinical note:      Heart attacks
  risk factors:
         smoking
         high blood pressure
         high blood cholesterol       any 2
         high [LDL]                 more than
         diabetes                    doubles
         male                       your risk
                                      of MI
         severe emotional stress
         obesity
         genetic predisposition
         sedentary lifestyle
The cardiac cycle


     contraction               relax
      (systole)              (diastole)


     fluid (blood) moves

     always moves from higher pressure…

                    …toward lower pressure
fig. 20-16
The cardiac cycle


        atrial systole
        atrial diastole
                                  together
        ventricular systole
        ventricular diastole


                generic heart rate 75 bpm
fig. 20-17
The cardiac cycle


        atrial systole (100 msec)

 1+2       blood in atria is pushed through AV
           valves into ventricles

                (follows path of least resistance)

           “tops off” the ventricles
           blood in ventricles is called EDV
                        (end diastolic volume)

           end of atrial systole
   3…
           ventricular diastole begins
The cardiac cycle


          ventricular systole (270 msec)
              pressure start to rise in ventricle
   …3         when it is greater than pressure in
              atria, the AV valves will close
                    (chordae tendineae and papillary m.)

                                                      “lubb”
              pressure continues to build until it can
      4
              force open the semilunar valves
The cardiac cycle


         ventricular systole (270 msec)
             up until now, ventricles have been
     4       contracting but no blood has
             flowed:
                   isovolumetric contraction

             ventricular volume has not changed
             but the pressure has increased
The cardiac cycle


         ventricular systole (270 msec)
             when pressure in ventricle is
             greater than pressure in the
             arteries, the semilunar valves will
             open

     5       ventricular ejection
                    stroke volume
             some blood left behind
             end systolic volume (ESV)
The cardiac cycle


         ventricular systole (270 msec)
             as pressure drops below that of
     6       arteries, the semilunar valves will
             close again
                                   “Dupp”
The cardiac cycle


         ventricular diasatole (430 msec)
             semilunar valves are shut
     7       AV valves are shut too (temporarily)

                    isovolumetric relaxation

             when pressure gets below atrial
     8       pressure, AV valves will open
             and ventricle will begin to fill
             passively
fig. 20-17
Heart sounds

     auscultation

             stethoscope



      lubb                 lubb
             DUPP                 DUPP
Heart sounds

     lubb

     closing of the AV valves
          as ventricular contraction begins
Heart sounds

     DUPP

     closing of the semilunar valves
          as ventricular relaxation begins
Heart dynamics

     cardiac output

     heart rate        variation &
                      adjustments
     stroke volume
Heart dynamics     definitions


EDV       end diastolic volume
              ventricle is full
              beginning to contract
ESV       end systolic volume
              ventricle is done contracting
              (a little blood left inside)
Stroke volume
              SV = EDV - ESV
Heart dynamics    definitions


cardiac output (CO)

   CO = HR (heart rate) x SV

          how much blood the heart
          pumps in a minute


both the SV and the HR can vary
   Heart dynamics


    both the SV and the HR can vary




fig. 20-20
Heart dynamics


variation in HR

    autonomics

         dual innervation to SA node
Heart dynamics      HR


parasympathetics

    releases ACh
         opens K+ channels
              lowers the resting potential
                   (hyperpolarize cell)
                        slows heart rate

 controlled by cardioinhibitory centers in
 the medulla oblongatat
Heart dynamics     HR


parasympathetics

   controlled by cardioinhibitory centers in
   the medulla oblongata



   reflexes        hypothalamus
Normal:




Parasympathetics:




              fig 20-22
Heart dynamics     HR


sympathetics

   releases NE
        binds to beta-1 receptors
             opens Na+/Ca2+ channels
                  depolarize cell
                        speeds up heart rate
Heart dynamics        HR


sympathetics

   controlled by cardioacceleratory centers
   in the medulla oblongata



           reflexes        hypothalamus
Normal:




Sympathetics:




                fig 20-22
Heart dynamics       HR


atrial (Bainbridge) reflex

    increased venous return
         stretches atria
               stimulates stretch receptors
                    stimulates sympathetics
                         increase HR
                               (and CO)
Heart dynamics   HR


hormones

    E, NE, thyoid hormone
        affect SA node
              speed up HR
to here 3/30/07
lec# 33
Heart dynamics


stroke volume (SV)

    remember

         SV = EDV - ESV
Heart dynamics     SV


EDV

    the amount of blood in the ventricle at
    the end of its diastolic phase, just
    before contraction begins.
Heart dynamics    SV


EDV

          affected by the filling time
                       &
                venous return



                   preload
Heart dynamics       SV


EDV

    preload   the degree of stretching of the
              ventricle during diastole

    preload is proportional to EDV

    preload      affects heart muscles ability to
                 generate tension
Heart dynamics   SV


EDV

    preload
Heart dynamics      SV


EDV

    preload

         “more in = more out”

                 Frank-Starling principle
fig. 20-23
Heart dynamics      SV


ESV

    preload

    contractility

    afterload
Heart dynamics      SV


ESV

    contractility
           amount of force generated with
           a contraction

               increase   + inotropic action

               decrease   - inotropic action
Heart dynamics      SV


ESV

    contractility

          factors that influence:

                ANS
                hormones
Heart dynamics      SV
                           sympathetic NS

ESV                              NE, E
                          + inotropic effect
    contractility

          ANS
                         parasympathetic NS

                                  ACh
                          - inotropic effect
fig. 20-23
Heart dynamics      SV
                         NE, E, glucagon,
                         thyroid hormones
ESV

    contractility
                              dopamine,
          hormones           dobutamine
         (and drugs)        isoproterenol
                               digitalis


                         + inotropic effect
                          (hypertension)
Heart dynamics      SV
                            propanolol
                              timolol
ESV                             etc.,
                          (beta-blockers)
    contractility

          hormones           verapamil
         (and drugs)         nifedipine
                           (Ca2+ blocker)

                         - inotropic effect
fig. 20-23
Heart dynamics        SV


ESV

    preload

    contractility

    afterload       the amount of tension
                    needed to open semilunar
                    valves and eject blood
Heart dynamics      SV


ESV

    afterload    the amount of tension
                 needed to open semilunar
                 valves and eject blood

      greater afterload
           longer isovolumetric contraction
                 less ejected, larger ESV
Heart dynamics      SV


ESV

    afterload

    restrict blood flow       inc. afterload

         constrict peripheral vessels
         circulatory blockage
fig. 20-23
Summary

  Heart rate   hormones
               venous return

  EDV          filling time
               venous return

  ESV          preload
               contractility
               afterload

  SV = EDV-ESV
100 keys (pg. 703)

  “Cardiac output is the amount of blood
  pumped by the left ventricle each minute.
  It is adjusted on a moment-to-moment
  basis by the ANS, and in response to
  circulating hormones, changes in blood
  volume, and alternation in venous return.
         Most healthy people can increase
  cardiac output by 300-500 percent.”

				
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posted:10/25/2012
language:English
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