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Chapter 27 Reproductive Endocrinology

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Chapter 27 Reproductive Endocrinology Powered By Docstoc
					                                                  Chapter 18 Cardiac Physiology
                                                                Heart Anatomy
•   heart chambers
     –   R L atrium
     –   R L ventricle
•   valves
     –   R atrioventricular valve      =        tricuspid
     –   L atrioventricular            =        bicuspid = mitral
     –   aortic semilunar valve
     –   pulmonary semilunar valve
•   other
     –   interventricular septum
     –   interatrial septum

                                                                Heart Anatomy
•   blood vessels
     –   SVC , IVC                     into R atrium
     –   pulmonary veins               into L atrium
     –   pulmonary trunk               out of R ventricle
     –   aorta                         out of L ventricle

                                                              cardiac muscle tissue
•   striated (sarcomeres)
•   short cells , branched
•   intercalated discs        specialized connections betw cells
     –   gap junctions        allow ions to pass betw cells
     –   desmosomes           prevents separation of cells
•   many mitochondria         aerobic respiration
                              huge O2 requirement

•   functional syncytium all cells contract simultaneously
•   autorhythmic cells        cells depolarize without stimulus

                                                       cardiac vs skeletal muscle tissue
•   cardiac muscle doesn’t fatigue
     –   long refractory period
     –   more time to make ATP

•   contraction
     –   skeletal muscle               motor units
     –   cardiac muscle                entire myocardium

•   nerve connections
     –   skeletal                      each cell requires a neuron
     –   cardiac                       contract without neurons
                                                            cardiac muscle contraction - 1
•   contracts like skeletal muscle :
     –   resting membrane potential -90mV
     –   stimulus (+ ions)
          • opens fast Na+ channels (voltage-gated)
     –   depolarization          ( -90mV to +30 mV)
          • + opens Sarcoplasmic reticulum
          • Ca++ stimulates sarcomere to contract
     –   repolarization          K+ channels (voltage-gated) open
•   only different :
                                                            cardiac muscle contraction - 2
•   resting membrane potential                    -90mV
•                            +
    stimulus opens fast Na channels (voltage-gated)
•   depolarization ( -90mV to +30 mV)
     –   depolarization opens slow Ca++ channels
     –   cell stays depolarized longer =          plateau
     –     ++
         Ca opens SR         = Calcium stimulated Calcium release
     –     ++
         Ca stimulates sarcomere to contract
•   decreased K+ permeability                     delays repolarization
•   repolarization
     –   K+ channels open
     –   Ca++ pumped into SR                      Ca – ATPase pump
     –     ++
         Ca pumped out of cell                    Na – Ca antiport (20)

                                                            cardiac muscle contraction - 3
•   much longer contraction in cardiac muscle
     –   skeletal                2–5 ms
     –   cardiac                 300 ms

•   cardiac depolarized longer
     –   skeletal                Na+ depol                   last 1-5 ms
     –   cardiac                   ++
                                 Ca depol                    lasts 150-200ms

•   long refractory period 250 ms vs skeletal 2-3ms
          • prevents summation
          • prevents fatigue
          • prevents tetany
                                                                functional syncytium
•   entire atria contract simultaneously
•   entire ventricles            contract simultaneously
•   gap junctions                                 = electrical synapse
     –   cell stimulates all adjacent cells

                                                            heart contracts without nerves
•   non-contractile cardiac cells act like neurons
•   initiate and spread action potential for entire myocardium
•   autorhythmic                 depolarize automatically
•   conduction pathway           connected autorhythmic cells
                                                                 autorhythmic cells
•   spontaneous depolarization
•   pacemaker potential       unstable resting potential
•   hyperpolarized at         - 60 mV
•   HCN channels (pacemaker channels) = slow Na+ channel
•   hyperpolar opens HCN channels                 Na+ leaks in
•   threshold                           - 40 mV
•   fast (voltage-gates) Ca++ channel open            depolarization
•                      +
    voltage gated K channels open                 repolarization
•   hyperpolarization (-60mV) opens HCN channel

•   rhythm of spontaneous depolarization

                                                           intrinsic conduction pathway
•   Sino-atrial (S-A) node
•   Atrio-ventricular (A-V) node
•   A-V bundle (bundle of His)
•   bundle branches
•   Purkinjie fibers

                                                                       conduction
•   gap junctions spread depolarization along pathway
•   Ca++ causes threshold in adjacent cells

                                                                       S-A node
•   sino-atrial node                              =         pacemaker
•   right atrium
•   fastest autorhythmic tissue         ~ 90+ / min
•   sets pace for entire myocardium

•   sinus rhythm                        normal
     –   slowed by P-ANS                ~ 70 – 75 / min
     –   vagal tone

                                                                       A-V node
•   atrio-ventricular node
•   internodal pathway                  from S-A node
     –   atrium contracts

•   delay ~ 0.1 msec

•   50 / min w/o S-A node


•   atrioventricular bundle             (bundle of His)
     –   only electrical connection from atria to ventricles

•   R & L bundle branches
•   Purkinjie fibers
•   bundle to Purkinjie       =         ventricular contraction
•   contraction begins at apex and moves upward
                                                                           ANS effects
•   S-ANS, epinephrine
     –   autorhythmic cells                   opens HCN channels
                                               rate
     –   myocardial cells                     open Ca channels
                                               contractility
     –   via ß receptors                      cAMP
•   P-ANS
     –   autorhythmic cells                   open K channels
                                               rate
          • via muscarinic receptors
     –   myocardial cells                     no effect

                                                                                ECG
•   electrocardiogram
•   ECG is record of all electrical events of heart
•   waves :
     –   P wave                   -           atrial depolarization
     –   QRS complex              -           ventricular depolarization
     –   T wave                   -           ventricular repolarization
•   intervals :
     –   P-Q interval                         begin atrium to begin ventricle
                                              entire conduction system
     –   S-T segment                          ventricular plateau
     –   Q-T interval                         entire ventricular events
     –   R-R interval                         1 beat               heart rate

                                                                           Arrhythmia
•   irregular heart beat
•   bradycardia       slow rate < 60
•   tachycardia       fast rate       > 100
•   palpitation       brief, temporary arrhythmia
•   flutter           fast, consistent heart rate > 200
•   fibrillation      fast, uncoordinated          > 300
                      ventricles contract w/o filling
•   PVC = premature ventricular contraction
       occassional, irreg. ventricular contraction
       cardiac muscle become conductive
•   asystole                      no contractions
                                                                      innervation of heart
•   vital signs       -           what part of brain ?
•   cardioaccelerator center
     –   S-ANS to S-A node and pathway                     -   increase rate
     –   S-ANS to myocardium                              stronger contract
•   cardioinhibitory center
     –   P-ANS to S-A node and A-V node -                      decrease rate
     –   vagal tone               constant

•   hypothalamus                  limbic system
                                  cerebrum
                                                                     Heart valves
•   function :                   prevent backflow
•   open and close by pressure of moving blood
•   A-V valves
     –    open :        weight of blood from atria
     –    close : pressure of ventricular contraction

•   Semilunar valves
     –    open :        pressure of ventricular contraction
     –    close :       weight of blood in artery (aorta ; pulmonary )


                                                                    Heart sounds
•   closing of valves
•   1st    =            A-V valves close
           • forces blood against valves
           • ventricular systole
•   2nd    =            Semilunar valves close
           • gravity from blood in arteries
           • ventricular diastole
                                                                    heart murmurs
•   abnormal heart sounds                  abnormal blood flow
•   defective valves
     –    mitral stenosis                  thickened mitral valve
     –    regurgitation                    fail to close

•   septal defects
     –    interatrial
     –    patent ductus arteriosus

                                                                    Cardiac cycle
•   1 “heartbeat”
•   all events of blood flow
•   systole             =        contraction
     –    atrial systole
     –    ventricular systole
•   diastole            =        relaxation
     –    atria and ventricles relax

•   systole + diastole = cardiac cycle

                                                                 cardiac cycle - basic
•   atrial systole                         atria contract
•   ventricular systole                    ventricles contract
     –    (atrial diastole)
•   diastole                               all chambers relax
                                                                  cardiac cycle - details
•   ventricular filling
     –   passive filling                atrium to ventricle
     –   atrial systole                                       “
•   ventricular systole
     –   isovolumetric contraction      no blood movement yet
                                        A-V valves close
     –   ventricular ejection           ventricle to artery
                                        SL valves open
•   diastole
     –   isovolumetric relaxation       SL valves close

                                                                     Cardiac output
•   = amt. blood pumped / minute / ventricle
•   Cardiac output = stroke volume x heart rate
                        CO = SV x HR

•   heart rate       =     pulse        =         beats / min
•   stroke volume = amount pumped / beat / ventricle


•   “resting stroke volume” ~ 70 ml/beat
•   HR                                   ~    70 beat / min
•   CO =         70ml x 70 beat/min = 4900 ml/min                       ~ 5 liters/ min

•   stronger heart ( SV )  slower heart rate
     –       100ml x 50 beat/min = 5000 ml\min
•   weak heart requires  HR (more work)

                                                                    regulation of HR
•   positive chronotropic factors                 increase HR
     –   S-ANS                  stim Beta receptors
                                open HCN channels
     –   epinephrine
     –   thyroxine
•   negative chronotropic factors                 decrease HR
     –   P-ANS                  stim muscarinic receptors
                                open K channels = vagal tone
     –   Beta blockers

                                                                    why change HR ?
•   to maintain CO
     –   blood pressure                  BP                 reflex  HR
                 – baroreceptors
     –    SV                  reflex  HR
•   to  CO
     –    metabolic demand
     –   emotion
     –   danger
     –   exercise
                                                                    stroke volume
•   EDV end diastolic volume            after filling
•   ESV end systolic volume             after contraction
•
•   SV = EDV - ESV
•   SV     = 120 ml - 50 ml       =    70 ml

•   ejection fraction                   ~ 60 % of EDV
     –   relatively constant, as EDV varies
     –   since  EDV   SV

                                                                    physics of SV
•   What moves blood?
     –   ΔP                             pressure gradient
     –   fluids move from high to low pressure

•   ventricular P > aortic P            blood moves out
•   ventricular P = aortic P            blood stops moving

•   increase vent P                     contractility                 increase SV
•   increase aortic P                   resistance                    decrease SV


                                                                regulation of SV
•   strength of contraction
     –   intrinsic control              preload             = EDV
     –   extrinsic control              contractility

•   afterload                  = resistance

                                                             intrinsic factors of SV
•   Preload
     –   length-tension relationship
     –   Frank-Starling’s Law of the Heart
          • increase stretch  increase contraction
          •  EDV   SV
•   venous return                       amt blood entring heart
     –   skeletal muscle pump
     –   S-ANS                 systemic vasoconstriction
•        due to: exercise
                  slow HR
•    due to:       very fast HR
                    blood loss , dehydration

                                                             extrinsic factors of SV
•   = contractility
•   positive inotropic factors                     contractility
          • S-ANS ; epinephrine                   open Ca channels
          • thyroxine
          • Ca++
          • digitalis
•   negative inotropic factors                    contractility
          • K+
          • H+ (pH)
          • Calcium channel      blockers


                                                                      afterload
•   afterload    = total peripheral resistance
•   ventricles pump against resistance in aorta
•    BP (aorta)        SV

•   self corrects
     –    BP         SV                   EDV         contract
          HR
•   myocardial hypertrophy
     –   systemic hypertension                   L ventricle
     –   pulmonary hypertension                  R ventricle

                                                                   cardiac disease
•   MI                                 myocardial infarction
•   ischemia                           decreased blood supply
•   infarct                            destroyed myocardium
•   CAD                                coronary artery disease        CABG
•   CHF                                congestive heart failure
•   MVP                                mitral valve prolapse
•   Mitral stenosis                    decreased size of opening in valve
•   Angina                             brief pain of coronary artery origin
•   Rheumatic heart disease            Strept infection
•   arrhythmia                         irregular heart rate
•   Atherosclerosis                    decreased lumen due to plaques
•

				
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posted:11/1/2011
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