Please enable JavaScript.

Coggle requires JavaScript to display documents.

Heart Physiology (Blood Pressure (Systemic Circulation (Veins…

- - - - Almost 0
  - - - atrial kick
        
        ventricles full/EDV
        
        130 mL
        
        EDP
        
        Increased with
        
        venous return, total blood volume
        
        decreases w/
        
        HR
        
        preload #
        
        Frank-Starling Mechanism
        
        The greater the heart muscle is stretched during filling, the greater the force and volume of contraction.
        
        20-30% of EDV
  - - - Venous blood through pulmonary valve to artery
        
        Ventilation& diffusion
        
        pulmonary veins passively drain to
        
        LA
    - - After IVP exceeds IA pressure
    - - same V of blood as RV
      - 60% EDV (ejection fraction) normally ejected
      - V out= Stroke V
        
        70-80 mL, leaving 60-70
      - afterload
        
        P against which the ventricles (especially the left ventricle) exert their contractile force and must overcome in order to eject the stroke volume.
  - - - Have thick muscular walls; high pressure, high velocity.
      - 13% blood
    - - adjustable flow thanks to muscles
    - - 64% Systemic
      - Delayed Compliance for spike in V
      - Valves
      - Venous/Muscle Pump
        
        Aided by gravity increasing P on periphary
        
        Varicose Veins
      - Intra abdominal P spikes Venous P
    - - Diastolic & Systolic about the same
      - Hydorstatic
        
        Difusion into interstitial space
        
        10% to
        
        90% to venules
      - Oncotic/Osmotic
        
        reabsorption
    - - Inverse to Cross sectional area
    - - Blood 3-4x's as viscous as H2O
      - Men
        
        42-45%
      - Women
        
        37-39%
      - anemia low
      - polycemia high
        
        Tx w/ phlebotomy
  - - - preload
      - afterload
      - Contractiity beta 1
        
        decrease in MI
        
        NorEpinephrine & Thyroxine increase them. Thryroxine improves epi use
      - 70-80 mL
      - Increased by venous return
  - - - Drops in exercise due to vasodilation
      - Increases in CO drop
        
        Alpha 1 vasoconstriction
- - - - 50% comorbidity w/ CAD
    - - Carotid
    - - best heard in aortic position
      - slower peaking=worse
  - - - May be from MI damaging papillary muscle
- - - - Contracts when stretched
  - - - Interstitial oncotic P
      - Cap Hydrostatic P
    - - cap oncotic P
  - - - Both LE & LUE
    - - RUE
- - - - AV node
        
        inferior atrium
        
        .03 s to arrive
        
        less gap junctions
        
        .09 s to get through node, .03-4 through AV fiber
        
        delay+ fibrous AV barrier= impulse can't go back
        
        His Bundle
        
        R& L purkinje fibers
        
        Ventricular depolarization+contraction
        
        1 more item...
        
        More gap junctions=FAST just .03 s
        
        40-60bpm rythmic rate
    - - More excitable
      - L channels
        
        slow influx of Na+ & Ca2+
        
        self excitation
    - - Not all have it
      - Left atrium
    - - Pacemaker other than SA node
      - Atrial Escape Rythym 60-80 bpm atrial foci take over
        
        Junctional Escape Rythym 40-60 bpm AV node or other junction takes over
        
        Ventricular Escape Rythyms 20-40 bpm Bundles or Purkinje's
        
        idioventricular rythym
        
        idiojunctional rythym
  - - - V depolarization
        
        Longer if hypertrophied
    - - Atrial depolarization/systole
    - - V repolarization/isovolemic relaxation
    - - SA node fires-Purkinje fibers fire
      - Delay caused by AV node
    - - HR/time between pulses
    - - Time v are depolarized
    - - v depolarization-repolarization time contracted
  - - - Ca rushes into the cardiac cell,
        
        opens voltage-gated Ca channels on the Sarcoplasmic Reticulum.
        
        more Ca on sarcoplasm-> troponin contractile action
  - - - Vagus
        
        May drop Cardiac Output to almost 0
        
        Mostly via HR
        
        Mostly to atrium
        
        Acytlcholine
    - - Sympathetic Chain
        
        may increase Cardiac Output over 100%
        
        target of Beta-Blockers
        
        Norepinephrine
- - - - serous pericardium
        
        Parietal
        
        Visceral
        
        Fibrous pericardium
        
        inflexible
        
        Cardiac tamponade
        
        Tx saw sternum
        
        Secretes serous fluid
        
        lubrication
      - forms syncytium
    - - less turbulence