Respiratory Anatomy and Physiology Michaela Dixon Clinical Development Nurse PICU BRHFC Respiratory Anatomy Function of the Respiratory System - In conjunction with the cardiovascular system, to supply oxygen to the cells of the body and remove by-products of cellular metabolism (carbon dioxide) Additionally the lungs play a major role in Maintaining homeostasis Mounting a host defence response to potentially threatening organisms Development of the Respiratory System The development of the respiratory system in the foetus is divided into five distinct phases Embryonic period Pseudoglandular period Canalicular period Saccular period Alveolar period 1
Development of the Respiratory System Embryonic Period Ventral out-pouching from the foregut occurs between days 26 and 52 Foregut divides to form the oesophagus and trachea Lung buds appear from the trachea Primary bronchial buds split to form the main bronchi and the lung lobes Blood supply from the Pulmonary Artery Development of the Respiratory System Pseudoglandular Period Occurs from day 56 week 16 of gestation All major conducting airways including the terminal bronchioles are formed Arterial blood supply increases Diaphragm is derived from the fusion of pleuro-peritoneal fields (normally between 8-10 weeks) Development of the Respiratory System Canalicular Period Occurs week 16 26 of gestation Development of the respiratory bronchioles each of which ends in a small dilated bulge (primitive alveoli) Continued development of the pulmonary vascular beds 2
Development of the Respiratory System Saccular Period Occurs week 24 38 of gestation Lung vascularisation intensifies Development of elastic fibres Close contact between air spaces and capillaries develops True alveoli present by week 34 of gestation Gas exchange is possible throughout this period but not optimal Development of the Respiratory System Alveolar Period Occurs week 36 onwards (to term) Further refinement of terminal sacs and walls of true alveoli Development of columnar cells into two types Type One alveolar surface area Type Two surfactant production 3
Pressure changes associated with respiration Before inspiration (diaphragm relaxed) Atmospheric pressure = Alveolar pressure 760mmHg = 760mmHg No air movement Inspiration (diaphragm contracting) Atmospheric pressure > Alveolar pressure 760mmHg > 758mmHg Air moves into the lungs Pressure changes associated with respiration: Inspiration (diaphragm contracting) Atmospheric pressure > Alveolar pressure 760mmHg > 758mmHg Air moves into the lungs Expiration (diaphragm relaxing) Atmospheric pressure < Alveolar pressure 760mmHg < 762mmHg Air is expelled by the lungs Pulmonary Volumes and Capacities Tidal Volume (TV or Vt) The volume of air entering and leaving the lungs in a single breath in the resting state Tidal volume is constant throughout life at between 6 8mls/kg Infant of 3kgs: TV = 18-24mls (6 / 8 x 3) Adult of 70kgs: TV = 420 560mls (6 /8 x 70) 4
Pulmonary Volumes and Capacities Inspiratory Reserve Volume (IRV) The amount of air that can be inspired over and above the resting tidal volume Expiratory Reserve Volume (ERV) The volume of air remaining in the lungs at the end of normal expiration which may be exhaled by active contraction of the expiratory muscles Pulmonary Volumes and Capacities Residual Volume (RV) The amount of air remaining in the lungs after maximal expiration presence of this prevents the lungs from emptying completely Vital Capacity (VC) The sum of normal tidal volume, inspiratory reserve volume and expiratory reserve volume Infants: 33 40ml/kg Adults: 52ml/kg Pulmonary Volumes and Capacities Functional Residual Capacity (FRC) The amount of air remaining in the lungs at the end of normal expiration In the presence of atelectasis FRC falls as the number of alveoli participating in gas exchange decreases SO WHAT? Airway closure (complete collapse) occurs in areas of the lungs that have low volumes this is known as the closing volume or capacity 5
Pulmonary Volumes and Capacities Importance In adults closing capacity is usually at residual volume (amount of air remaining in the lungs after maximal expiration) In infants closing capacity is at FRC due to the reduced elasticity of lung tissue, therefore closing capacity may be present during normal tidal breathing Pulmonary Volumes and Capacities Functional Residual Capacity (2) Any pulmonary disease which affects the relationship between tidal volume, FRC and closing capacity will contribute significantly to ventilation perfusion mismatching and hypoxia Chronic Lung Disease (infants) Cystic Fibrosis Asthma Bronchiolitis Pneumonia Pulmonary Volumes and Capacities Dead Space Anatomic dead space the volume of conducting air that fills the nose, mouth, pharynx, larynx, trachea, bronchi and distal bronchial branches which does not participate in gas exchange Normal anatomic dead space is 2ml/kg 6
Pulmonary Volumes and Capacities Dead Space Alveolar dead space the volume of gas which fills alveoli whose perfusion is either reduced or absent Contributing Factors: Hypotension Compression of the alveolar capillary bed Pulmonary embolism Pulmonary Volumes and Capacities Physiologic Dead Space The sum of both anatomic and alveolar dead space Dead Space Ventilation The amount of gas ventilating physiologic dead space per minute. It is expressed as a fraction of TV Normal ratio is 0.3 (30%) which means that 30% of the volume of each breath does not participate in gas exchange Surfactant Pulmonary surfactant is a mixture of Phospholipids produced by - Type II alveolar Pneumocytes Function of surfactant is to Lower surface tension Increase compliance 7
Surfactant: How does it work? Each alveoli is lined with a water containing fluid film Due to the polarity of the water molecules they act as weak magnets, pulling towards each other. This force also pulls the alveoli walls inwards causing them to collapse increasing the surface tension The presence of surfactant acts as a barrier against these forces preventing the collapse of the alveoli (Smaller alveoli generate greater forces clinical implication for infants) Gas Laws 8
The total pressure of a gas is the sum of all the partial pressure of the gases within the mixture - Normal atmospheric air consists of: Oxygen Nitrogen Carbon Dioxide Water Atmospheric pressure is 760mmHg Gas Laws Boyles Law The volume of a gas varies inversely with pressure assuming constant temperature In order for inspiration to occur the lungs expand, reducing the pressure within this facilitates the movement of gas along the pressure gradient When expiration occurs the lungs recoil, increasing pressure within - consequently reducing the volume of air present Gas Laws Charles Law The volume of a gas is directly proportional to temperature assuming pressure is constant When a gas is heated, the molecules move faster the force exerted by the molecules causes expansion of the gas volume When gases enter the warmer lungs, gases expand increasing lung volumes 9
Gas Laws Henrys Law The quantity of a gas that will dissolve in a liquid is proportional to the partial pressure and its solubility coefficient (physical attraction to water) when temperature is constant The higher the partial pressure of a gas over a liquid the more gas will stay in solution Gas Laws Henrys Law Example: 78% of room air is Nitrogen but little dissolves in the plasma because it has a low solubility coefficient In compressed air used by divers, nitrogen dissolves in plasma because of altered partial pressures - if a diver returns to the surface too quickly nitrogen bubbles remain in the blood stream causing the Bends Gas Laws Henrys Law Clinical Application Solubility co-efficient of CO 2 is high but O 2 is low and N 2 is very low therefore a reduction in haemoglobin will significantly impact on oxygen carrying capacity and delivery as there is no real alternative transport system 10
Gas Laws Ficks Law Diffusion through tissue is proportional to the partial pressure of the gas and the difference in the partial pressures on the two sides It is inversely proportional to the thickness of the tissue Gas Laws Ficks Law Clinical Application Children with chronic lung conditions such as CF or CLD post prematurity will have decreased capacity for effective gas exchange if they have developed fibrotic changes in their lung parenchyma. These children are at greater risk of respiratory failure secondary to infection than those with normal healthy lungs Gas Exchange 11
Gas Exchange All organ systems depend to varying degrees on the delivery of oxygen to maintain normal cellular metabolism The primary function of the respiratory system is to move O 2 from the air to the blood and CO 2 from the blood to the air Gas Exchange This process of gas exchange involves three stages Pulmonary ventilation External respiration Internal respiration 12
Pulmonary ventilation Movement of air is between the lungs and the atmosphere is dependent on the existence of a pressure gradient and lung compliance Compliance is a measure which reflects the ease with which the lungs and thoracic wall expand Compliance is dependent upon elasticity (elastic recoil) and surface tension Decreased compliance = poor chest wall movement External Respiration Exchange of O 2 and CO 2 between the alveoli and the pulmonary capillaries Conversion of deoxygenated blood to oxygenated blood O 2 and CO 2 exchange occur through diffusion (Ficks Law applies) This process is aided by several anatomical features External Respiration Total thickness of the alveolar-capillary membrane is only 0.5 micrometres Lungs have an enormous surface area up to 70m 2 / 753ft 2 by adulthood Multiple capillaries lying over each alveoli allow 100ml of blood to participate in gas exchange at any one time Structure of the pulmonary capillaries is designed to give maximum exposure to facilitate gas exchange 13
Internal Respiration Oxygenated blood (transported by the circulatory system) leaves the lungs and is delivered to the tissue cells Exchange of O 2 and CO 2 occurs again at this point through diffusion and the presence of a concentration gradient At rest only 25% of available O 2 is extracted by the cells to meet their metabolic demands Ventilation Perfusion Mismatch Gas exchange becomes optimal when both ventilation and pulmonary blood flow are equally matched Under normal conditions the ventilation perfusion ratio (V/Q) is less than 1.0 This is because gravitational forces create regional differences in intra-pleural pressure and pulmonary pressures Ventilation Perfusion Mismatch Intrapulmonary shunting is the major cause of clinical hypoxaemia A shunt refers to venous blood that travels from the right to left side of the circulation without ever coming into contact with ventilated lung Anatomic shunt Capillary shunt - occurs when the alveolar-capillary blood flow comes into contact with non ventilating alveoli 14
Ventilation Perfusion Mismatch Venous blood passing non-functioning alveoli creates an admixture of venous and arterial blood which decreases the PaO 2 Venous admixture represents the ratio of shunted blood (Qs) to total pulmonary blood flow (Qt) Normal Qs/Qt is 3-7% Changes of more than 5% are considered significant Work of breathing significantly increases when the Qs/Qt is greater than 15% Oxygenation Index Oxygenation Index (OI) OI = Mean Airway Pressure x FiO2 (%) PaO 2 (mmhg) OI < 5 = Normal OI > 10 = Severe oxygenation problem OI > 20 = Extreme oxygenation problem Transportation of Gases 15
Oxygen Transportation Almost all of the oxygen transported in systemic arterial blood is chemically bound to haemoglobin - approx 98.5% (1.5% is dissolved in plasma) Normal haemoglobin consists of 4 O 2 binding sites Because so much oxygen is trapped inside red cells through binding, there are a number of factors which influence the ease with which it binds or dissociates from haemoglobin OXYHAEMOGLOBIN DISSOCIATION CURVE Reflects the relationship between the % saturation of haemoglobin and oxygen partial pressure The OHDC can move either to the right or to the left A right shift means that oxygen will be released by haemoglobin easily but it is more difficult for it to bind A left shift means that oxygen will bind easily with haemoglobin but it is more difficult for it to be released 16
Factors affecting Oxygen binding / release Partial pressure of oxygen Acidity (blood ph) Carbon Dioxide Temperature BPG (2,3 bisphosphoglycerate) The most important factor which determines how much O 2 binds to haemoglobin is the Partial Pressure of oxygen When PO 2 is high haemoglobin binds with large amounts of oxygen and is almost 100% saturated Therefore in the pulmonary capillaries where the PO 2 is high (because PO 2 in atmospheric air is higher) a lot of oxygen binds with haemoglobin In the tissue capillaries where PO 2 is lower haemoglobin does not hold as much oxygen therefore oxygen is released for use by the tissues through diffusion At a PO 2 of 40mmHg (5.4kPa) which is tissue capillary PO 2 haemoglobin is still 75% saturated WHY? 17
Acidity (Blood ph) As acidity increases the ph of blood will decrease As ph decreases the affinity of haemoglobin for O 2 decreases and more O 2 becomes available for the tissues This is reflected in a shift in the OHDC to the right and at any given PO 2 haemoglobin will be less saturated with O 2 known as the Bohr effect Acidity (Blood ph) Clinical Relevance: Haemoglobin can act as a buffer for acids (H + ions) in the blood to maintain blood ph within normal limits The process of binding hydrogen ions to the amino acids in haemoglobin causes a slight change in the structure of haemoglobin, decreasing its O 2 carrying capacity Carbon Dioxide Acts in a similar way to acidity as PCO 2 increases blood ph decreases and the OHDC shifts to the right Consequently O 2 is released by haemoglobin more easily 18
BPG (2,3 bisphosphoglycerate) Decreases the affinity of haemoglobin for O 2 therefore making it more available to the tissues BPG is produced by the red cells when they metabolise glucose to produce ATP (energy) Increased energy demands from cells cause an increase in BPG levels OHDC shifts to the right Temperature As temperature increases the OHDC moves to the right and more oxygen is released to the tissues Heat is a by-product of the metabolic activity in the cells the heat of contracting muscle fibres tends to raise body temperature Metabolically active cells require more O 2 to maintain anaerobic metabolism a by-product of increased metabolism is the production of acids Control of Respiration 19
Breathing is an involuntary process that is controlled by the medulla and pons of the brain stem. The frequency of normal, involuntary breathing is controlled by three groups of neurons or brain stem centres; the medullary respiratory centre the apneustic centre the pneumotaxic centre Central Chemoreceptors The central chemoreceptors located in the brain stem, are the most important for the minute-to-minute control of respiration These chemoreceptors are located on the ventral surface of the medulla, near the point of exit of the Glossopharyngeal and Vagus nerves and only a short distance from the medullary inspiratory centre Central chemoreceptors communicate directly with the inspiratory centre 20
The brain stem chemoreceptors are exquisitely sensitive to changes in the Ph of cerebrospinal fluid (CSF) Decreases in the ph of CSF produce increases in respiratory rate (hyperventilation) Increases in the ph of CSF produce decreases in respiratory rate (hypoventilation) Peripheral Chemoreceptors There are peripheral chemoreceptors for O 2, CO 2 and H + in the carotid bodies located at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch Information about PaO 2 / PaCO 2 and ph is relayed to the medullary inspiratory centre which orchestrates an appropriate change in breathing rate Peripheral Chemoreceptors Decreases in PaO 2 are the most important responsibility of the peripheral chemoreceptors BUT Peripheral chemoreceptors are relatively insensitive to changes until PaO 2 reaches 60mmHg or less (< 8kPa) Once in this range of PaO 2 the chemoreceptors are exquisitely sensitive to O 2 21
Peripheral Chemoreceptors Decreases in arterial ph cause an increase in ventilation mediated by peripheral chemoreceptors for H + This effect is independent of changes in the PaCO 2 and is mediated only by chemoreceptors in the carotid bodies (not by those in the aortic bodies) Thus, in metabolic acidosis, in which there is decreased arterial ph, the peripheral chemoreceptors are stimulated directly to increase the ventilation rate Peripheral Chemoreceptors The peripheral chemoreceptors also detect increases in PaCO 2 but the effect is less important than their response to decreases in PaO 2 Detection of changes in PaCO 2 by the peripheral chemoreceptor is also less important than detection of changes in PaCO 2 by the central chemoreceptors Lung stretch receptors Mechanoreceptors are present in the smooth muscle of the airways. When stimulated by distention of the lungs and airways, mechanoreceptors initiate a reflex decrease in breathing rate called the Hering-Breuer reflex. The reflex decreases breathing rate by prolonging expiratory time Joint and muscle receptors Mechanoreceptors located in the joints and muscles detect the movement of limbs and instruct the inspiratory centre to increase the breathing rate. Information from the joints and muscles is important in the early (anticipatory) ventilatory response to exercise 22
Irritant receptors Irritant receptors for noxious chemicals and particles are located between epithelial cells lining the airways. Information from these receptors travels to the medulla and causes a reflex constriction of bronchial smooth muscle and an increase in breathing rate J receptors Juxtacapillary (J) receptors are located in the alveolar walls and therefore, are near the capillaries. Engorgement of pulmonary capillaries with blood and increases in interstitial fluid volume may activate these receptors and produce an increase in the breathing rate 23