Transport in animals Flashcards
(30 cards)
The cardiac cycle
Ventricles relax, atria contract
ventricles contract, atria relax
ventricles relax, atria relax
The cardiac cycle 1
Ventricles relax, atria contract- atria contract decreasing volume and increasing pressure
This pushes blood into ventricles through AV valves
slight increase in ventricular pressure and volume as they receive blood from atria
The cardiac cycle 2
Ventricles contract, atria relax- ventricles contract decreasing vol and increasing pressure
Pressure in ventricles becomes higher than atria which forces AV valves shut
pressure in ventricles also higher than pulmonary artery and aorta which forces Semi lunar valves open and blood forced into arteries
The cardiac cycle 3
Ventricles relax, atria relax- both relax and higher pressure in arteries close SL vlaves
blood returns to heart and atria fill again due to higher pressure in vena cava and pulmonary vein
This starts to increase atria pressure as venticles continue to relax pressure falls below that of atria so AV valves open
blood flows passively into ventricles
Atria contract and process repeats
Sino-atrial node
sends regular waves of electrical activity over atrial walls
Causes right and left atria to contracts at same time
band of non-conducting collagen tissue prevents waves being passed directly to ventricles
instead passed to AVN
Atrioventricular node
AVN passes waves of electrical activity on to bundle of his
Slight delay before AVN reacts to make sure ventricle doesnt contract until after atria fully emptied
Bundle of His
group of muscle fibres that conduct waves to finer muscle fibres in right and left ventricle walls called purkyne tissue
Purkyne tissue
Carries waves into muscular walls of right and left ventricles causing them to contract simultaneously from bottom up
ECG (electrocardiogram)- P waves
caused by contraction (depolarisation) of atria
ECG (electrocardiogram)- QRS complex
caused by contraction (depolarisation) of ventricles
ECG (electrocardiogram)- T wave
due to relaxation (repolarisation) of ventricles
Heart rate=
60/time taken for one heartbeat
ECG (electrocardiogram)- Tachycardia
heartbeat is too fast (around 120bpm)- heart isnt pumping blood efficiently
ECG (electrocardiogram)- Bradycardia
Heartbeat is too slow (around 50bpm)- can indicate a problem w electrical activity of heart
ECG (electrocardiogram)- Ectopic heartbeat
an extra heartbeat that interrupts regular rhythm
Can be caused by early contraction of atria or early contraction of ventricles
ECG (electrocardiogram)- Fibrillation
irregular heartbeat- atria or ventricles completely lose rhythm and stop contracting properly
Affinity for oxygen and pO2 in lungs
Alveoli has high oxygen conc, high pO2, high affinity so oxygen loads (associates)
Respiring tissue has low oxygen conc, low pO2, low affinity so oxygen unloads (dissociates)
Fetal haemoglobin
Andult and fetal have different affinities for oxygen (fetal higher)
When mothers blood reaches placenta, oxygen saturation has decreased (some used by mother)
Placenta has low pO2 so adult oxyhaemoglobin will unload (dissociate) its oxygen
Fetal haemoglobin becomes more saturated in lower pO2
The Bohr effect
when cells respire they produce CO2 which increases rate of oxyegn unloading- dissociation curve shifts right
Saturation of blood w oxygen is lower for a given pO2 so more oxygen released
The Bohr effect explanation
CO2 in RBC reacts w water producing carbonic acid (CO2+H2O-H2CO3)
Carbonic anhydrase speeds it up
HCO3- diffuses out RBC
H+ react w haemoglobin to form haemoglobinic acid (HbO2-HHb+O2)
Causes rapid dissociation of O2
Decreased affinity for oxygen
Reversible
CO2 can directly bind w haemoglobin- carbaminohaemoglobin
The chloride shift
HCO3- diffuses out RBC into plasma, charge maintained by influx of chloride ions (Cl-)
Haemoglobin
Conjugated protein- protein part and prosthetic group
Quaternary structure- 4 polypeptide chains called globin
2 sorts- alpha and beta
Each polypeptide has own non-protein group attached w iron ion where oxygen binds
Pressure filtration
At capillary bed nearest arteries hydrostatic pressure is higher than that of tissue fluid
This forces fluid out capillaries into space around cells forming tissue fluid
Reduces hydrostatic pressure in capillary- lower at end nearest venules
As water leaves conc of plasma proteins in capillary increases whch generate oncotic pressure so high oncotic pressure at venule end and low wp
wp in capillary lower than tissue fluid water re-enter capillary by osmosis
Lymph vessels
extra fluid gets returned to blood by lymphatic system
smallest lymph vessels are lymph capillaries
excess tissue fluid passes into lymph vessels now called lymph
Valves in lymph vessels stop lymph going backwards
Lymph moves towards main lymph vessel in thorax and is returned to blood near heart
