Physiology of Respiration

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A short and concise presentation on the physiology of respiration

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By: damaziotembo (18 month(s) ago)

its straight forward.

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PHYSIOLOGY OF VENTILATION & OXYGENATION Dr Deepa C MD

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VENTILATION Mechanical process that moves air in and out of the lungs EXTERNAL RESPIRATION Gas exchange between air in lungs and blood Transport of O₂ and CO₂ in the blood INTERNAL RESPIRATION Gas exchange between the blood and tissues O₂ utilisation & CO ₂ production RESPIRATION

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RESPIRATORY SYSTEM Ventilating pump - Respiratory control centres in the brain - Connecting tracts and nerves - Chest wall and respiratory muscles Gas-exchange system - Lungs

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RESPIRATORY TRACT UPPER Nose, pharynx & assoc. structures LOWER Larynx, tracheobronchial tree

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CONDUCTING ZONE Trachea, bronchi , bronchioles & terminal bronchioles 16 generations RESPIRATORY ZONE Respiratory bronchioles, alveolar ducts and alveoli Rest 7 generations TRACHEOBRONCHIAL TREE

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TOTAL CROSS-SECTIONAL AREA Trachea – 2.5 cm² Alveoli – 11,800 cm²

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300 MILLION ALVEOLI Total area of alveolar walls in contact with capillaries in both lungs – 70 m²

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ALVEOLOCAPILLARY MEMBRANE Pulmonary epithelium Capillary endothelium Fused basement membranes PAMs, APUD cells, plasma cells

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ALVEOLOCAPILLARY MEMBRANE

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ALVEOLAR SURFACE TENSION & SURFACTANT Dipalmitoylphosphatidylcholine Type II pneumocytes Increases lung compliance Reduces lung’s tendency to recoil Makes work of breathing easier Prevents alveolar collapse Prevents pulmonary edema

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MECHANICS OF VENTILATION

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Pump handle motion increases the AP dimension of rib cage Bucket handle motion increases lateral dimension of rib cage

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Intrapleural -10 cm H₂O Intrapleural -2.5 cm H₂O

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END OF EXPIRATION DURING INSPIRATION

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END OF INSPIRATION DURING EXPIRATION

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LUNG VOLUMES & CAPACITIES

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TIDAL VOLUME (TV) – the volume of gas inspired or expired in an unforced respiratory cycle (approximately 500 ml) INSPIRATORY RESERVE VOLUME (IRV) – the max. vol. of air that can be inspired during forced breathing in addn. to TV (2100–3200 ml) EXPIRATORY RESERVE VOLUME (ERV) – the max. vol. of air that can be exspired during forced breathing in addn. to TV (1000–1200 ml) RESIDUAL VOLUME (RV) – the vol. of air remaining in the lungs after maximal forced expiration (1200 ml) LUNG VOLUMES

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LUNG CAPACITIES INSPIRATORY CAPACITY (IC) – the max. amount of air that can be inspired after a tidal expiration (IRV + TV) FUNCTIONAL RESIDUAL CAPACITY (FRC) – amount of air remaining in the lungs after a tidal expiration (RV + ERV) VITAL CAPACITY (VC) – the max. amount of air that can be expired after a max. inspiration(TV + IRV + ERV) TOTAL LUNG CAPACITY (TLC) – the total amount of air in the lungs after a max. inspiration

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CLOSING VOLUME The lung volume above residual volume at which airways in the lower, dependent parts begin to close off CLOSING CAPACITY = CV + RV Old age and infants – CC > FRC

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AIRWAY RESISTANCE : 0.6 – 2.4 cm H₂O/L/sec Inversely proportional to R⁴ TOTAL COMPLIANCE = ∆V/∆P  150ml/cm H₂O (STATIC) 100ml/cm H₂O (DYNAMIC) ↓compliance  ↑ work of breathing WORK OF BREATHING - work performed by the respiratory muscles in stretching the elastic tissues of the chest wall and lungs (elastic work – 65%), moving inelastic tissues(7%) and moving air through the respiratory passages(28%) 0.3 -0.8 kg-m/min

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PRESSURE-VOLUME & DISTRIBUTION OF VENTILATION The pressure volume curve varies between apex and base of the lung. At the base the lungs are slightly compressed by the diaphragm so upon inspiration have greater scope to expand. The volume change is greater for a given change in pressure. Dependent alveoli are more compliant than the non-dependent ones. Hence alveolar ventilation declines with height from base to apex.

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High High High VENTILATION & PERFUSION Zone I P A > Ppa Zone II Ppa >P A > Ppv Zone III Ppa > Ppv >P A

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ZONES

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DEAD SPACE & SHUNT DEAD SPACE – wasted ventilation ( no gas exchange due to absent perfusion) eg.; pulmonary embolism SHUNT – wasted perfusion (eg.; atelectatic segment, one-lung ventilation) Alveolar Ventilation = (V T - V D ) x RR V D /V T = (PaCO₂ – P E CO₂) / PaCO₂ Q S /Q T = (CćO₂ – CaO₂) / (CćO₂ – CvO₂)

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Ventilation in the alveoli is matched to perfusion through pulmonary capillaries. If ventilation decreases in a group of alveoli, P CO 2 increases and P O 2 decreases. Blood flowing past these alveoli does not get oxygenated. Decreased tissue P O 2 around under-ventilated alveoli constricts their arteries (mediated by O₂-sensitive K⁺ channels) and diverts blood to better ventilated alveoli LOCAL CONTROL OF VENTILATION & PERFUSION

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ADJUSTMENTS IN VENTILATION AND PERFUSION

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GAS EXCHANGE LUNGS TISSUES

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GAS LAWS CHARLES’ LAW - The volume occupied by a gas is directly related to the absolute temperature ( V α T ) HENRY’S LAW - The amount of gas dissolved in a liquid is determined by the pressure of the gas and it’s solubility in the liquid. DALTON’S LAW - The total pressure of a gas mixture is the sum of the pressures of the individual gases. BOYLE’S LAW - The pressure exerted by a gas is inversely proportional to its volume ( P α 1/V )

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ALVEOLAR GAS EQUATION P A O₂ = [F I O₂ (P B - P H₂O )] - [PaCO₂/R]

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DIFFUSION ACROSS THE ALVEOLOCAPILLARY MEMBRANE The diffusing capacity of the lung for a given gas is directly proportional to the surface area of the alveolocapillary membrane inversely proportional to its thickness The diffusing capacity for CO (DLCO) is measured as an index of diffusing capacity At rest -- 25ml/min/mmHg DLO₂ - 25ml/min/mmHg

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OXYGEN TRANSPORT Oxygen is transported by hemoglobin (98.5%) and is dissolved in plasma (1.5%) Oxygen content = [ 1.34 x Hb x SpO₂] + [0.003 x PO₂] Arterial blood – 19.8 ml O₂/dL Venous blood – 15.2 ml O₂/dL

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OXYGEN-Hb DISSOCIATION CURVE AT pH 7.40 & TEMPERATURE 38⁰C

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FACTORS AFFECTING Hb AFFINITY FOR OXYGEN pH [Bohr effect] Temperature pCO₂ 2,3-DPG

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P₅₀ is the PO₂ at which Hb is 50% saturated with O₂ Normal P₅₀ is 25 mm Hg The higher the P₅₀ , the lower the affinity of Hb for O₂ SHIFT OF O₂- Hb DISSOCIATION CURVE TO RIGHT ↓ affinity for O ₂…..↑ O ₂ release ↓pH ↑Temperature ↑ PCO ₂ ↑ 2,3 - DPG

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HbF – SHIFT OF CURVE TO LEFT

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TRANSPORT OF CARBONDIOXIDE Carbon dioxide is transported as bicarbonate ions (70%) in combination with blood proteins (23%) and in solution with plasma (7%) [solubility 20 times more] CO₂ content Arterial blood – 49 ml/dL Venous blood – 53 ml/dL

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CHLORIDE SHIFT Mediated by Band 3 protein

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Insert fig. 16.39 REVERSE CHLORIDE SHIFT IN LUNGS HALDANE EFFECT – binding of O₂ to Hb reduces the affinity of Hb for CO₂

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TRANSPORT OF O₂ AND CO₂

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O₂ consumption = Cardiac output x C(a-v) O₂ = 250 ml/min CO₂ production = 200 ml/min RESPIRATORY QUOTIENT = V CO₂ /V O₂ = 0.8 . .

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Neural Chemical Non-chemical REGULATION OF RESPIRATION NEURAL CONTROL VOLUNTARY CONTROL -- Cerebral cortex  CS tracts  Resp. motor neurons AUTOMATIC CONTROL -- Medullary pacemaker cells in the pre-Botzinger complex

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INSPIRATORY AREA (DORSAL RESP. GROUP) determines basic rhythm of breathing causes contraction of diaphragm and external intercostals EXPIRATORY AREA (VENTRAL RESP. GROUP) Inactive during normal quiet breathing Activated by inspiratory area during forceful breathing Causes contraction of internal intercostals and abdominal muscles

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Switching between inhalation and exhalation controlled by: PNEUMOTAXIC CENTER located in pons inhibits inspiratory area of medulla to stop inhalation APNEUSTIC AREA located in pons stimulates inspiratory area of medulla to prolong inhalation

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CENTRAL CHEMORECEPTOR When Pa CO 2 increases carbon dioxide crosses the BBB, but not H + Central chemoreceptors monitor the P CO 2 indirectly in the CSF. The bicarbonate and H+ are formed and the receptors respond to the H + Feedback via the respiratory control centre increases ventilation in response to increased Pa CO 2 Decreased Pa CO 2 slows ventilation rate.

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PERIPHERAL CHEMORECEPTORS Carotid and aortic bodies Detect changes in arterial PO 2 and [H+] Cause reflex stimulation of ventilation following significant fall in arterial PO 2 or a rise in [H+] Respond to arterial PO 2 not oxygen content Increased [H+] usually accompanies a rise in arterial PCO 2 CO 2 + H 2 O  H 2 CO 3  H 2 CO 3 - + H + Transduction mechanism

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NON-CHEMICAL CONTROL Afferents from proprioceptors Afferents from pons, hypothalamus and limbic system Afferents from baroreceptors: arterial, atrial, ventricular, pulmonary Vagal afferents from the receptors in the airways and lungs

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Rhythm of ventilation is also modified by: TEMPERATURE  temp =  ventilation (and vice versa) sudden cold stimulus may cause apnea PAIN Sudden severe pain can cause apnea Prolonged somatic pain increases respiratory rate Visceral pain may slow respiratory rate IRRITATION OF AIRWAYS

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RECEPTORS IN LUNG AND AIRWAY VAGAL - myelinated and unmyelinated (C ) fibers MYELINATED  Slowly adapting & rapidly adapting SLOWLY ADAPTING RECEPTORS (among airway sm. m) Stimulus – Lung inflation Response – Hering-Breuer inflation and deflation reflexes, bronchodilation, tachycardia RAPIDLY ADAPTING RECEPTORS (among airway ep. cells) Stimulus – Lung hyperinflation, exogenous & endogenous substances Response – Hyperpnea, cough, bronchoconstriction, mucus secretion

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UNMYELINATED C FIBERS -- J RECEPTORS Located close to pulmonary blood vessels Stimulus – Lung hyperinflation, exogenous & endogenous substances Response – Apnea folld. by rapid breathing, bronchoconstriction, bradycardia, hypotension, mucus secretion (PULMONARY CHEMOREFLEX) Occurs in pathological states such as pulmonary congestion or embolization

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THANK YOU