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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The heart is a vital organ in the cardiovascular system, and it plays a crucial role in maintaining the overall health and function of the body. In summary, the heart is essential for the distribution of oxygen, nutrients, and hormones, as well as the removal of waste products, all of which are critical for the proper functioning and survival of the body's cells and organs. Without a functioning heart, the body's cells would not receive the necessary resources to sustain life, leading to organ failure and ultimately, death.

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