The Cardiovascular System

  • Created by: rosieevie
  • Created on: 19-01-17 21:11

Why do we need a heart?

Diffusion too slow

Heart provides bulk flow circulation to all necessary tissues

Oxidative phospohrylation produces ATP so oxygen needs to be in constant supply as an electron acceptor

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Red Blood Cells

  • Increase oxygen carrying capacity (x40)
  • Oxygen solubility in plasma too low
  • PO2 lungs < PO2 inspired air because of exchange between in and out air
  • PO2 expired air never 0mmHg
  • Alveoli equillibrium with pulmonary blood flow = PO2 almost same
  • Haemoglobin can bind to 4 O2 molecules at one time - one for each protein molecule
  • Haemoglobin dissociates cooperatively - easier to remove later O2 molecules
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Oxygen Dissociation Curve


  • Blood leaving lungs and entering systemic arteries - PO2 95mmHg (97%)
  • Venous blood returning from peripheral tissues - PO2 400mmHg (75%)
  • Heavy excersise - as low as PO2 15mmHg
  • Utilization coefficient - % oxygen haemoglobin gives up to tissues = 25% (exercise <75%)
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Human Heart Structure

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The Heart

  • Beats from 20 days after conception - continously pumps blood during formation
  • Orginially tubular - over time ventricles expand and start to twist
  • (
  • Myogenic - beats by itself - inherent pacemaker ability
  • Same volume of blood on both sides
  • Heart contraction increases pressure
  • Left ventricle has more muscle - pumps blood to body (more pressure)
  • Valves prevent blood backflow
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Cardiac Muscle

Specialised and distinct from other 2 types:

  • Branched cells with intercalated discs that join back of cells together
  • Discs allow ion flow = strong mechanism
  • Each myocyte (cell) can have multiple nuclei
  • Cardiac myocyte beat regularly


Three types:

  • Atrial
  • Ventricular
  • Excitory and conductive fibres - can't contract, specialised to conduct signals at same time as muscle contraction

Artial and ventricular contract similarly to skeletal muscle - duration longer

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Action Potentials and Excitation/Contraction Coupl

  • Atrial and venticular syncytium (cytoplasmic mass) seperated
  • Action potentials very long with 'plateau' phase
  • Action potentials conducted between fibres

Excitation/contraction coupling similar to skeletal muscle:

  • Action potential enters adjacent cell
  • Voltage-gated Ca2+ channels open and Ca2+ enters cell
  • Ca2+ induces more Ca2+ release through ryanodine receptor channels
  • Accumulation of Ca2+ as SR is emptied (SR Ca2+ reservoir)
  • Ca2+ binds to troponin - initates contraction
  • Ca2+ flux persists for 200ms
  • Action potential stops and Ca2+ pumped back into SR - muscle relaxation
  • Na+/K+ pump creates gradient
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Excitatory and Conductive Muscle Fibres

  • Specialised fibres (syncytical cells) with few contractive fibrils 
  • Pacemaker cells (in SA and AV nodes) spontanously produce rhythmical action potentials
  • Conductive fibres (bundle of His) spread excitation
  • Produces coordinated efficient beating of heart

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AV Node

  • The penetrating portion of AV bundles delays signal
  • Undergoes regressive repolarisation - long absolute refractory period
  • (
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Heart Valves and Pressure

  • Heart murmur - when valves don't seal


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Cardiac Output

  • Systole - heartbeat phase where muscle contracts
  • Diastole - heartbeat phase where muscle relaxes
  • End-diastolic volume - filing of ventricles from venous return to about 110-120mls blood (can be 150-180mls during large blood flow)
  • End-systolic volume - remaining volume of blood in ventricles (~40-50mls, can be 10-20mls in strong contraction
  • Ejection volume - fraction of the end-systolic volume that is ejected
  • Stoke volume output - volume of blood pumped from ventricles during contraction
  • Cardiac outpud - volume of blood pumped through the circulatory system in 1 minute

Increased end-diastolic and end-systolic volumes can lead to up to double normal stroke volume output

Cardiac Output = (EDV-DSV) x Heart Rate

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Global Control of the Heart

  • Otherwise energetically expensive
  • Allow us to match to tissue demand
  • Match to ventilation perfusion

Controlled by the autonomic nervous system

Sympathetic divsision - stimulates heart

  • Inotropic effects - modifying speed
    • Increase force and stroke volume -> increased Ca2+ entry and CATPase activity
  • Chronotropic effects - modifying rate
    • Increase Na+ and Ca2+ -> increased depolarisation -> increased heart rate

Parasympathetic division - slows heart

  • Chronotropic effects - modifies rate
    • Increase K+ and decrease Ca2+ -> hyperpolarisation and decreased depolarisation -> decreased heart rate
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Three seperate circulations - pulmonary, peripheral and cardiac (heart needs its own blood supply)

Venous return - rate of blood flow back to the heart (normally limits cardiac output)

Heart generates force and causes blood pressure

Circulation controls flow, tissue perfustion, venous return - affected by circuit resistance

Blood pressure - force genrated by heart - normal 120/80mmHg

  • Top number = systolic pressure
  • Bottom number = diastolic pressure
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Circulatory Pressure


Cardiac output = Pressure difference/Total peripheral resistance

  • Heart generates pressure difference
  • Pressure drop at arterioles, before this it oscillates
  • All main arteries have elastic wall to accomodate pressure changes - smooths flow
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Blood Vessel Structure


  • Thich elastic wall - high pressure so prevents bursting
  • Endothelial cells line lumen - prevent clotting
  • Connective tissue surrounds endo cells
  • Circular smooth muscle - strong and regulates contraction 
  • Exracellular matrix cells - rough and act as coating

Reduce vessel size - thinner walls due to less pressure


  • Small (size of RBC) for effective diffusion
  • Beds have large cross sectional area

Inversely proportional relationship between blood flow speed and vessel size due to pressure drop

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The Three Circulations


  • Low pressure - gaseous exchange occuring
  • Right ventricle -> lung -> left atria


  • High pressure to pump blood far from heart
  • Left ventricle -> capillary beds -> right atria


  • High pressure
  • Left atria -> aorta through cardiac muscle -> right atria

Same volume through each segment of circulation each minute

Blood velocity inversly proportional to vascular coss sectional area

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Capillary Beds

  • Hydrostatic pressure from ECF
  • Fluid lost is returned by lymphatic system
  • Blood in capillaries from ~1-3s - diffusional equillibrium
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Cardiac Blood Supply

  • Aaorta supplies cornary arteries with blood
  • Vital to oxygenate heart - heart attack
  • Pressure in cornary capillaries from muscle contraction
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Venous Return

  • Requires muscular activity
  • Contraction decreases vein volume - massages veins = low pressure flow
  • Valves prevent blood backflow
  • Artery pulsation - degree of force
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Frank-Starling Law

Stroke volume - blood volume ejected by left ventricle on contraction

Frank-Starling Law - ventricular filling determines stroke volume

Altered overlap of actin-myosin leads to greater contraction force

Preload - volume of blood in vena cava reaching the ventricle and stretching it

Only up to a certain point otherwise muscle splits/rips

After-load - effect of aortic pressure on cardiac output (significant in hypertension - aorta resists contraction = heart failure)

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Perfusion (Blood Pressure) Controls

Capillary Bed Perfusion

  • Regulated by smooth muscle contraction of precapillary sphincters surrounding arterioles
  • Relaxed - blood enters capillary bed
  • Contracted - blood bypasses capillary bed 
  • Poiselle's law - small arteriole radius changes produce large flow changes

Nervous System Control - Vasomotor centre - Medulla Oblongata (brain)

  • Baroreceptors - detect changes in blood pressure (strech w/in walls)
    • High blood pressure = increase vagal inhibition = slow hear (parasympathetic)
    • Low blood pressure - pressor response - produces higher blood pressure by stimulating vessel constriction (exercise, stress, loss of blood)
  • Chemoreceptors - detect CO2 changes (pH - carbonic acid dissociation into H+)

Sympathetic innervation:

  • Systemic arteriole constiction - increases peripheral resistence
  • Constriction of major veins - compensate for blood/fluid loss
  • Stimulation of heart
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Giraffe Circulatory System

  • Big hearts - x2 normal blood pressure to brain against gravity
  • Upper neck = complex pressure regulation system - rete mirable
    • Prevents excess brain blood flow - collecting extra blood
    • :Prevents brain damage during head lowering
  • Lower leg blood vessels - high hydrostatic pressure
    • Extra vasation (fluid leakage) reduced by tight sheath of thick skin = high extravascular pressure - surgical stockings
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Giraffe Circulatory System

  • Big hearts - x2 normal blood pressure to brain against gravity
  • Upper neck = complex pressure regulation system - rete mirable
    • Prevents excess brain blood flow - collecting extra blood
    • :Prevents brain damage during head lowering
  • Lower leg blood vessels - high hydrostatic pressure
    • Extra vasation (fluid leakage) reduced by tight sheath of thick skin = high extravascular pressure - surgical stockings
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ECG Trace


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