External respiration=exchange of gases in lungs Internal respiration=exchange of gases at tissue level
Air passages Nose and sinuses Nasopharynx Larynx Trachea Bronchi Bronchioles Alveoli
Nose functions Respiratory passage AC of inspired air Protection of lower airway Lyzozyme,IgA , IgE , Sneeze reflex Vocal resonance-M/N/NG OLFACTION
Functions of pns Reduce weight of skull Humidification of air Resonance to voice Mucus traps dust particles
Composition of air Oxygen=21% Carbon dioxide=0.03% Nitrogen =78% Other=1% Expired air= oxygen-16% co2-4%
Respiratory movements inspiration Active process Primary muscles = diaphragm,external intercoastals Accessory muscles= scalene,scm,neck&back mucles Bucket handle movements-increase transverse dia &pump handle movements-increase AP dia expiration Passive process-recoil of lungs forced expiration=anterior abdominal wall msls,internal intercostals,
Pulmonary function tests Lung volumes Tidal volume-vol of air moving in with each inspiration=500ml Inspiratory reserve vol(IRV)=max air that can be inspired in excess of TV=3L Expiratory reserve vol(ERV)=max amount of air that can be expired after normal expiration=1L Residual volumeair left in lungs even after forceful expiration=1.2L
Pulmonary function tests Lung capacities Vital capacity=max amount of air that can be expired after max inspiration=4.5L VC=IRV+TV+ERV TOTAL LUNG CAPACITY=vol of air in lungs after deep inspiration=6L TLC=VC+RV INSPIRATORY CAPCITY= max amount of air that can be inspired from end expiratory position IC=IRV+TV
Pulmonary function tests Lung capacities FUNCTIONAL RESIDUAL CAPACITY(FRC)=amount of air presenr in lungs after normal expiration=2.3L FRC=RV+ERV TIMED VC= FEV1 FEV2 FEV3
ventilation Pulmonary ventilation=air inspired per minute=500ml*12=6L/min Alveolar ventilation=air that takes part in exchange of gases=350ml*12=4.2L Anatomical Dead space=nose till terminal bronchioles=150ml Physio dead space= “ + alveolar air not taking part in exchange In healthy people, anat dead space= physio dead space Ventilation-perfusion ratio=4.2/5=0.84
DIFUSSION CAPACITY=volume of air diffsing across resp memb per min for gradient of 1mmHg For oxygen, 21ml/min/mmHg For carbon dioxide,400ml/min/mmHg
Transport of oxygen pO2 at pulm capillary bed=40mmHg pO2 at alveolar air=104mmHg Therefore oxygen diffuses into capillary blood
Oxygen in blood 97% bound to Hb 3% dissolved in plasma Dissolved oxygen determines the partial pressure
Role of Hb in oxygen transport Each of four iron atoms combine with one molecule of oxygen 1 hb combines with 4 molecules of oxygen Binding of 1 st facilitates binding of next oxygen At 100mmHg pO2, Hb is 100% saturated with oxygen 1g of Hb combine with 1.34 ml of oxygen 15g of hb =20ml of oxygen/100ml blood=oxygen carrying capacity of blood 5ml given off to tissues
Oxygen hb dissociation curve Relationship between pO2 and saturation of Hb Sigmoid shape When O combines with Hb it assumes Rstate,favors binding When all 4 oxygen molecules combine, T state At 100mmHg ,1005 saturated with oxygen At 60mmHg , 90%satuarted
Left shift –loading of o2 Rise in pH Fall in temp Fall in 2,3-DPG HbF CO poisoning Right shift-unloading of o2 pH<7.4 ( bohr effect) Temp>38 Increase in 2,3-DPG
Transport of carbon dioxide 10% dissolved in plasma 80% as bicarbonate=HCO3- 10% as carbamino-Hb
Haldane effect deoxyHb rapidle combines with co2 as compared to oxyHb Binding of Hb tooxygen reduces its affinity for co2 This effect is necessary for exchange of gases at alveoli
Regulation of respiration Neural regulation Voluntary =motor cortex Involuntary= in pons and medulla Chemical regulation=central (medulla) and peripheral(carotid body) chemors =respond to fall in pH, rise in pCO2,fall in pO2 -stimulate respiration
pons Pneumataxic centre -limits inspiration by inhibiting apneustic centre,increase RR Apneustic centre -prolongs inspiration medulla Prebotzinger complex-pacemaker of respiration DRG-cause steady rise in TV VRG-control forced expiration
Initiation of respiration- prebotzinger > phrenic nerve> diaphatgm contraction>inspiration Maintainance of inspiration-apneustic centre >stimulate DRG>rise in TV during inspiration Termination of inspiration- pneumataxic centre ad vagal affernts from lung> inhinit apneustic centre >inhibit DRG
hypoxia Lack of oxygen at tissue level 4types Hypoxic hypoxia=low pO2 in blood High altitude,airway obs,pulm edema,asthma,heart ds Anemic hypoxia=pO2 normal but low oxygen carrying capacity Severe anemia , carbon monoxide poisoning Stagnant hypoxia=blood flow reduced>more oxygen extracted bytissues Shock,heart failure,local obstruction Histotoxic hypoxia=tissue cannot utilise oxygen due cytochrome oxidase inhibition eg -CN POISONING
CYANOSIS Bluish discoloration of skin and mucus membranesdue to excess deoxyHb (>5%) Central =heart ds,lung ds,HTN , Peripheral =circulatory shock,severe cold Severe anemia=cyanosis not evident