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Circulatory system - Coggle Diagram

- - - - impulse goes along vagus nerve to atria
      - no cell bodies in main spinal cord thoracic region
      - there is very little ventricular innervation from parasympathetic NS but this view may change
      - lowers heart rate, at rest heart rate is dominated by para
    - - cardiac sympathetic nerve to atria
      - they have a sympathetic pre ganglion neurone in the spinal cord and these determin ethe activity of the sympatetic nerve
      - increases heart rate
  - - - Increase in venous return means an increase in end diastolic volume
      - this means you pump more blood which creates a greater strength which gives a greater contraction so stroke volume increases
      - Frank-Starling law of heart states the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction
      - it is based on length-tension relationship of cardiac muscle (the more it is stretched th emore it contracts)
    - - sympathetic stimulation increases the contractibility of the heart and thereby increases stroke volume
      - the stronger the contraction means more blood ejected
      - increased Ca2+ triggered by noradrenaline and adrenaline
      - this shifts Frank-Sterling curve left, meaning for the same end diastolic volume, a larger stroke column is ejected on sympathetic stimulation as a result of increased contractibility of the heart
- - - - ventricles contract and ventricular pressure exceeds atrial pressure
      - AV valves close and semilunar valves closed as pressure not high enough to open, so no blood flowing in or out (isovolumetric contraction)
      - by the end of this phase the ventricle pressure is great enough to force open semilunar valves
      - aorta pressure continues to fall
    - - AV valves remain closed by pressure in ventricles
      - pulmonary and aortic valves open and blood moves into aorta and pulmonary pressure (aorta pressure rises and ventricular decreases)
      - Semilunar valves close ending ejection
      - aortic valves open, adn ejection from ventricle causes aortic pressure to quickly rise
      - Left ventricel creates condition of hypertrophic cardiomyopathy
  - - - it is the ration of ejected volume in one beat to volume contained in ventricle immediately prior to ejection
      - EF=ESV/EDV
  - - - P wave is atrial contraction
      - QRS is ventricular contraction
      - T wave is ventricular repolarises
      - PR segemetn is AV node delay
      - ST segment is ventricle completely depolarising and ventricles are contracted and emptying
      - TP segment is heart muscle completely reploarises
- - - - found in right atria, there resting potential is less negative than other cardiac muscle and are not stable; instead they gradually become even less negative until they reach threshold for AP
      - contains specialsed neurons, leaky to sodium
      - leaky channels means it slowly depolarises towards action potential, but as membrane becomes less negative Na+ channels close and T type Ca2+ channels open
      - eventually fires and action potential but major influx of Ca2+ generates the AP
      - Opening of K+ channels then allows K+ to exit and the cell repolarises
    - - receives excitation after wave of excitation goes across the atria
      - conducts at 0.5 m/s from SAN
      - it delays action potential by 0.1s it ensure blood can be squeezed into the ventricles
      - tendinous cords anchors valves and are responsible for stopping the backflow of blood
      - If SAN fails to fire then AVN can fire but at a slower rate, if conduction between atria and ventricles is blocked then atria beat at 70bpm and ventricles at 30bpm
    - - recieves signal from AVN
      - spreads throughout ventricular myocardium through left and right bundle branches that run to the tips of ventricles as Purkinje fibres
      - if AVN fails to fire then Bundle of His and Purkinje can fire at much slower rate
    - - these initiate action potentials without stimulation fromthe nervous system
      - they don't contract but generate rhythmic sequences of action potentials
  - - - sodium funny channels are open and slowly allow entry of sodium, the net movement moves the membrane potential to threshold
      - at the same time the potassium channels are closing
    - - sodium funny channels begin to close, decreasing permeability
      - transient calcium channels open as it moves towards the threshold
      - the calcium influx continues, but as it passes the threshold and reaches rising phase, transient channels close and long lasting channels open, these new channels drive towards firing action potential
      - at peak of action potential, the long lasting calcium channels close and potassium permeability increases potassium moves out the cell (membrane potential falls)
    - - potassium channels open at end of an precedding action poteintial
      - the potassium rate of efflux falls and there is a slow inward movement of sodium (since there are unique sodium channels to that open at these negative membrane potentials)
      - this causes a net drift to the threshold
  - - - resting potential at -90mV
      - membrane potential reversal due to increase in Na+ permeability and reaches +30mV
    - - Na+ permeability decreases
      - K+ channels open allowing fast limited efflux to give brief repolarisation
    - - Slow lang lasting calcium channels and voltage gated potassium channels open
      - resting potential restored and potassium channels close and leaky potasium channels open
    - - the long period prevents tetanus of cardiac muscle
      - the next action potential cannot be fired until excitable membrane has recovered from preceding action potential
      - the K+ channels are inactive becasue of membrane potential
      - protective cycle filling and emptying for normal function
- - - - barometric pressure decreases exponentially as altitude increases
      - proportion of atmospheric O2 is constant so a decrease in barometric pressure is paralleled by a decrease in ambient pO2 relatively
      - so arterial p)2 falls and causes hypoxic hypoxia
      - the decrease in alveolar and arterial pO2 is greater than decrease in ambient pO2
  - - - low altitude natives
      - they can go up the mountain and develop some changes and those that remain at the bottom
      - there are some reports of increased diffusing capacity in LAN that remain at altitude over several years but likely went up before puberty
    - - ventilation is higher than sea level people at sea level, but at altitude it is 20% less since acclimatised
      - so HAN are using less energy consuming methods to compensate for hypxic conditions like more efficient pulmoary gas exchange
      - if children are taken in early infancy to high altitude they develop adaptation of HAN
      - pulmonary diffusing capacity in HAN is greater at rest by 20-30% but there is no evidence of significant changes in pulmoary diffusing capacity in short term visitor
      - HAN have increase in alveolar SA, barrel shaped chest, increase lung volumes, more alveolar
    - - increase in uteine blood flow
      - increased vascularoty (large placenta)
      - smaller babies (slightly compromised)
  - - - sets in above 3km
      - if person is fit then only slightly
      - above 6km ventilation is 75% of sea level
      - it increases the amount of oxygen in alveoli and arteries but also increases expiration so increse loss of CO2 which leads to increase in pH (respiratory alkalosis)
    - - polycythaemia
        
        this is lots more red blood cells and is a long term chagne
        
        increased haematopoiesis is stimulated by erythropoietin in response to low blood pO2 (hormone released within 2 hours of exposure)
        
        rise in rbcs seen after 3-5 days and trend continues for several weeks
      - haemoglobin affinty
        
        in acclimitsed individuals there is a rightward shift to help get oxygen to cells
        
        this is likely because of an increase in 2,3-DPG concentration induced by respiratory alkalosis (and it favours the unstable forms)