Respiratory Anatomy & Physiology PDF

STRUCTURE AND FUNCTION OF RESPIRATORY TRACT IN RELATION TO ANAESTHESIA  CONTENTS  Lung functions  Respiratory control system  Receptors in respiratory tract  Respiratory tract reflexes  Factors affecting respiration  Static characteristics of the lungs  Ventilation and perf...

STRUCTURE AND FUNCTION OF RESPIRATORY TRACT IN RELATION TO ANAESTHESIA  CONTENTS  Lung functions  Respiratory control system  Receptors in respiratory tract  Respiratory tract reflexes  Factors affecting respiration  Static characteristics of the lungs  Ventilation and perfusion  Lung volumes and capacities  Respiratory function during anaesthesia  LUNG FUNCTIONS  Provides large surface area for gas exchange  Moves air to and from the gas-exchange surfaces of lungs  Produces sounds permitting speech  Provides olfactory sensations to the CNS for sense of smell  Reservoir of blood available for circulatory compensation  Filter for circulation:  Thrombi, Microaggregates, etc. LUNG FUNCTIONS (Contd.)  Regulation of blood pH  Protects:  Respiratory surfaces from dehydration and temp changes  Provides nonspecific defenses against invading pathogens Secretory immunoglobulin's (IgA) Collectins (including Surfactant A and D) Defensins Peptides and Proteases Reactive oxygen species Activated epithelium release PGE 2 that protects epithelium Alveolar Macrophages - Chemotactic Antigen Processing Formation Of Granulocytes + Monocytes LUNG FUNCTIONS (Contd.) Metabolic and endocrine functions of the lungs  Biologically active Substances handled In Pulmonary Vascular Bed LUNG FUNCTIONS (Contd.) LUNG FUNCTIONS (Contd.)  Synthesis of Phospholipids(Surfactant)  Protein Synthesis  Elaboration of Mucopolysaccharides of Bronchial mucus CONTROL OF RESPIRATION  Basic elements of the respiratory control system are  Central controller  Strategically placed sensors  Respiratory muscles  CONTROL OF RESPIRATION  CENTRAL CONTROLLER: Controlled Mainly at the level of brainstem  Medullary respiratory centre:  Dorsal medullary respiratory neurones : Associated with Inspiration Neurons responsible for the basic rhythm of breathing Activates Reticulospinal tract in the spinal cord, phrenic and intercostal nerves and finally stimulate the respiratory muscles  Ventral medullary respiratory neurons Are associated with expiration. These neurons are silent during quite breathing Activated during forced expiration when the rate and the depth of the respiration is increased  CONTROL OF RESPIRATION  APNEUSTIC CENTRE :  Located in the lower pons  Exact role of this centre in the normal breathing is not known  Without constant influence of this centre respiration becomes shallow and irregular  PNEUMOTAXIC CENTRE:  Located in the upper pons.  Have an inhibitory effect on the both inspiratory and apneustic centres.  Responsible for the termination of inspiration by inhibiting the activity of the dorsal medullar neurones.  Regulates the volume and secondarily the rate of the respiration. CONTROL OF RESPIRATION CONTROL OF RESPIRATION  RESPIRATORY MUSCLES:  Diaphragm  Externalintercostals  Accessory ms. Inspiratory Scalene Sternomastoids Alae nasi  Abdominal ms. Expiratory  Internal intercostal ms. CONTROL OF RESPIRATION CONTROL OF RESPIRATION SENSORS  CENTRAL CHEMORECEPTORS  Located near the ventral surface of medulla  Bathed in brain ECF  Actually respond to changes in H+ concentration in these compartments  Increase in H+ stimulates chemoreceptors resulting in hyperventilation CONTROL OF RESPIRATION  CONTROL OF RESPIRATION  PERIPHERAL CHEMORECEPTORS  Located in – Bifurcation of Carotid artery Aortic arch  Connected to the respiratory centre In the medulla  Glossopharingeal nerve (carotid body)  Vagus nerve (aortic body)  Respond to ed arterial PO2 and ed PCo2 and H+  Rapidly responding CONTROL OF RESPIRATION Peripheral chemoreceptors are the only sensors detecting a fall in PO2  LUNG RECEPTORS  PULMONARY STRETCH RECEPTORS  Slow adapting  Lie in airway smooth muscles  Stimulated by distension of lung  Reflex action inhibits inspiratory activity & causes bronchodilatation  Determine rate & depth of breathing  Insensitive to "pathological" changes in the lungs such as Micro embolism Mild bronchoconstriction Inhalation of irritants and dust  Weakly sensitized by pulmonary congestion /edema due to LVF  LUNG RECEPTORS  IRRITANT RECEPTORS (Deflation or collapse receptors)  Rapidly adapting  Lie in airway epithelial cells  Stimulated by- noxious gases, cigarette smoke, inhaled dust & cold air  Cause bronchoconstriction , hyperpnea and hyperventilation  J (JUXTACAPILLARY) RECEPTORS  Ending of nonmyelinated C fibers  In alveolar wall close to capillaries  Stimulated by hyperinflation /Inhalation of strong irritant gases, including halothane  Cause tachypnea , rapid shallow breathing , bronchoconstriction , apnea (intense stimulation)  Role in rapid shallow breathing and dyspnea associated With LHF and ILD LUNG RECEPTORS  BRONCHIAL C FIBERS  Supplied by bronchial circulation  Stimulated by hyperinflation /chemicals injected into bronchial circulation  Cause rapid shallow breathing, bronchoconstriction & mucus secretion LUNG RECEPTORS  Two other types of respiratory receptor  Cough receptors in the tracheal epithelium  Pulmonary arterial baroreceptors. LUNG RECEPTORS COMPONENTS OF INVOLUNTARY CONTROL SYSTEM Central Muscle & Peripheral Lung stretch chemoreceptor joints Chemoreceptor receptors H+ receptors O2,CO2,H+ CN X Apneustic Pneumotaxic INSPIRATORY CENTRE centre centre Diaphragm SUMMARY:OVERALL CONTROL OF ACTIVITY OF RESPIRATORY CENTRE RESPIRATORY TRACT REFLEXES  HERING & BREUER INFLATION REFLEX  Inflation of the lungs inhibit further inspiratory ms. Activity  Mediated by pulmonary stretch receptors  Uncommon at quiet breathing  Barbiturate depress this reflex  DEFLATION REFLEX  Deflation of the lungs tends to initiate inspiratory activity RESPIRATORY TRACT REFLEXES  HEAD’S PARADOXICAL REFLEX  Paradoxically stimulates a deeper breath rather than inhibiting further inspiration  Responsible for  Deep Breath (Sighs)  First breaths of Infants FACTORS AFFECTING RESPIRATION  CO2 : Most imp. Stimulus  Most of the stimulus from central chemoreceptos but peripheral chemoreceptors also contribute  Magnified effect if PO2 is low  ed response – sleep, ing age, trained athletes, drugs  O2 : Hypoxia  Only peripheral chemo. Involved  Negligible control during normoxia  Imp. In high altitude & chronic hypoxia  FACTORS AFFECTING RESPIRATION  pH  Reduction stimulates ventilation  Site of action : peripheral chemoreceptors  EXERCISE  Ventilation increases  THEORIES  Passive movements increases ventilation  Increase in body temp.  Impulses from motor cortex  Oscillation in arterial Po2 , Pco2 FACTORS EFFECTING BREATHING STATIC CHARACTERISTICS OF THE LUNGS  COMPLIANCE Compliance - Effort needed to stretch lungs C T (L/cm H2O) = ΔV(L) ΔP (cmH2O) Normal : 0.2-0.3 L/cm H20  COMPLIANCE contd.  Reduced compliance  Pulmonary fibrosis  Alveolar edema  Atelectasis  Increased Compliance  Emphysema STATIC CHARACTERISTICS OF THE LUNGS  RESISTANCE Relationship between pressure gradient & rate of air flow  R(cmH2O/L/sec)= ΔP(cmH2O) ΔV(L/sec)  ΔP depends on – airway caliber, rate & pattern of airflow PATTERN OF AIRFLOW  Laminar flow – airway below main bronchi  Turbulent flow - trachea STATIC CHARACTERISTICS OF THE LUNGS  RESISTANCE contd.  Normal : 1 cm H20/ L/ sec.  Maximum resistance in medium sized bronchi  Increases with Low lung volumes Increased gas density Decreased arterial PCO2 Cholinergic drugs SURFACE TENSION  S.T. is the molecular force present on the surface of a liquid that tends to make the exposed surface area as small as possible  Laplace law – pressure across a curved surface is equal to twice the surface tension at liquid interface divided by radius P = 2T / R SURFACE TENSION contd.  As alveoli ↓ in size during expiration, pressure tending to collapse them ↑ & a vicious cycle is established  Role of surfactant – conc. of surfactant ↑ on the surface of liquid as S.A ↓  Surfactant lower S.T at air liquid interface in the alveolus & prevent collapse at low lung volumes PULMONARY SURFACTANT  Reduces the surface tension of the alveolar lining layer  Produced by type II alveolar epithelial cells  Contains dipalmitoyl phosphatidylcholine  Absence results in reduced lung compliance, alveolar atelectasis, tendency to pulmonary edema FACTORS DECREASING SURFACTANT  Oxygen therapy  IPPV with high pressure  Pulmonary collapse  ↓ Pulmonary circulation - embolism  Anaesthetic agent  Patient with valve replacement procedure HUMIDIFICATION  Normal humidifying mechanism- nose & mouth  Bypassed – ETT - Tracheostomy  Benefits of humidification-  Protect drying of mucosa  Reduce heat loss  Reduce incidence of coughing & breath- holding during inhalational induction  DRY AIR ENTERING THE TRACHEA Inflammatory reaction Damage / Dried & tenacious inhibition of cilia secretions Difficult to remove cough out Loss of cilia & keratinization of tracheal epithelium HUMIDITY  Normally, air entering trachea is saturated with water vapour - humidity of 34 g /m3 i.e. fully saturated at 34ºC  Two methods of increasing humidity artificially  Humidifying the environment - in infant incubators  Humidifying the inspired gases- humidifiers SIZE OF DROPLETS  > 20 µm - form pool of water in tubing/upper resp. tract  5µm - fall in region of trachea  1µm - pass upto alveoli & get deposited  < 1µm - ideal  Extremely stable, can be  Inspired & expired again VENTILATION AND PERFUSION VARIATION OF VENTILATION WITH POSTURE  Upright posture - ventilation is more in the base of the lung than at the apex  Supine posture – Posterior areas better ventilated than the anterior ones Lateral position - dependent lung best ventilated NORMAL PHYSIOLOGY OF UPRIGHT POSITION  ‘WEST’ zones  Contraction of RV :  Propels blood into PA  Absolute pressure : Decreases 1 cm of H2O for each cm travelled vertically up the lung  DISTRIBUTION OF PULMONARY PERFUSION  Zone I -  PA> Ppa > Ppv  No blood flow  Wasted ventilation  Acts as alveolar dead space  Zone I increased in  Hypotension  Positive pressure ventilation  Zone II –  Blood flow is determined by : Ppa – PA  k/as – waterfall effect /Starling resistor / sluice / weir effect  Height of upstream river ~ Ppa  Height of Dam ~ PA  Mean driving pressure increases linearly down the lung zone  Zone III –  Blood flow is determined by : Ppa – Ppv  Transmural distending pressures increase down zone 3  Blood flow is continuous  Zone IV –  Vascular resistance of extra alveolar vessels increases  Pulmonary interstitial pressure > pulmonary venous pressure  Blood flow is determined by Ppa – Ppisf EFFECT OF PISF ON EXTRA ALVEOLAR VESSELS  Zone Four Increased in conditions of  Volume overload  Pulmonary embolism  Mitral stenosis DISTRIBUTION OF PULMONARY PERFUSION  Perfusion scanning:  Gravitational distribution + onion-like layering (reduced flow at the periphery of the lung than toward the hilum) DISTRIBUTION OF VENTILATION  Pleural pressure increases down the lung  Fourfold decrease in alveolar volume  Transpulmonary pressure decrease from top to bottom of lung  Dependent alveoli are more compliant (steep slope)  Non dependent alveoli are relatively non complaint (flat slope)  Basal regions are more ventilated DISTRIBUTION OF VENTILATION VENTILATION PERFUSION MISMATCH  V/Q RATIO AND REGIONAL COMPOSITION OF ALVEOLAR GAS  Alveoli ( Bottom ) Retain CO2 Does not take enough O2  Alveoli ( Top ) Gives off excessive CO2 Cannot take up enough O2 (Due to flatness of ODC curve in this region) PACO2 – PaCO2 : GRADIENT SMALL PAO2 – PaO2 : GRADIENT LARGE Final Composition : Which Zone occupies the Major lung portion ? SHUNT – VENOUS ADMIXTURE  Venous admixture is said to occur when blood passes through the lung without being properly oxygenated  Anatomic Shunt- portion of CO that bypasses pulmonary capillaries (2% of CO) - bronchial, pleural, thebesian, anterior cardiac veins  Capillary Shunt- portion of CO that perfuses nonventilated alveoli - atelectasis, pulmonary edema, consolidated pneumonia  Hypoxemia ( not responsive to increased FiO2) LUNG VOLUMES AND CAPACITIES 4 VOLUMES:  Tidal volume  Inspiratory reserve volume  Expiratory reserve volume  Residual volume 2 or more volumes comprise a capacity 4 CAPACITIES:  Vital capacity  Inspiratory capacity  Functional residual capacity  Total lung capacity LUNG VOLUMES  Tidal Volume (TV): vol. of air inhaled or exhaled with each breath during quiet breathing. N – 500ml  Inspiratory Reserve Volume (IRV): maximum volume of air inhaled from the end- inspiratory tidal position. N ~3000ml  Expiratory Reserve Volume (ERV): maximum volume of air that can be exhaled from resting end-expiratory tidal position. N ~1100ml LUNG VOLUMES  Residual Volume (RV):  Volume of air remaining in lungs after maximum exhalation. N ~1200ml  Indirectly measured (FRC-ERV) not by spirometry N ~1100ml LUNG CAPACITIES  Total Lung Capacity (TLC): - volume of air in lungs after maximum inspiration - Sum of all volume compartments  Vital Capacity (VC): maximum volume of air exhaled from maximal inspiratory level VC = TLC - RV  Inspiratory Capacity (IC): maximum volume of air that can be inhaled from the end- expiratory tidal position IC = IRV + TV LUNG CAPACITIES Functional Residual Capacity (FRC):  Volume of air in the lungs at end-expiratory tidal position  FRC = RV + ERV  TLC, FRC, RV measured by:  Helium dilution  Body plethysmography RESP. FUNCTION DURING ANAESTHESIA  Anesthesia causes impairment in pulmonary function, whether pt. is breathing spontaneously or is ventilated mechanically  Impaired oxygenation of blood occurs during anaesthesia, hence FiO2 is maintained at 0.3-0.4  Clinically significant pulmonary complications is seen 1-2 % after minor surgery & upto 20% after upper abdominal & thoracic surgeries. LUNG VOLUME & RESP. MECHANICS DURING ANESTHESIA  FRC is decreased around 20% of awake. Loss of respiratory muscle tone. Cranial shift of diaphragm in transverse diameter of thorax  Lung compliance is reduced ed ventilation vol.  Resistance is increased. ed airway dimensions  ATELECTASIS DURING ANAESTHESIA  Seen in 90% of anaesthetized pts.  Both in spontaneous breathing & after muscle paralysis.  Development depends on preoxygenation, FiO2 during surgery, PEEP, postanaesthesia O2, BMI.  Obese pt. - larger atelectasis  Independent of age  PREVENTION OF ATELECTASIS  Application of PEEP  Recruitment maneuvers  Minimizing gas resorption- use of Low FiO2 during anaesthesia  Use of low FiO2 in postanesthetic oxygenation. Hypoxic pulmonary vasoconstriction (HPV) Physiological mechanism that optimizes V-P matching and pulmonary gas exchange by diverting blood flow from poorly ventilated areas of lung Inhaled anaesthetics inhibit HPV Thank you