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Related Subjects: Asthma |Acute Severe Asthma |Respiratory Failure |

Thoracic anatomy

• Chest wall is composed of sternum, 12 ribs, intercostal spaces and the thoracic vertebra
• First seven ribs articulate at the sternum.
• Ribs 8,9,10 articulate with manubriosternal cartilage.
• Ribs 11 and 12 are free floating and do not articulate anteriorly
• Inferiorly lies the dome shaped diaphragm

Physiology

• Basics
  • Get atmospheric or medically supplied oxygen to all of the cells of the body and their mitochondria.
  • Mitochondrial oxidative phosphorylation will cease when PO2 falls below 1 mmHg (0.13 Kpa)
  • This will allow the process of oxidative phosphorylation and krebs cycle with oxygen transport system
  • The end product of combining oxygen and glucose is ATP and CO₂ and H₂0 which need excreted
  • Normal respiration rate is 15/minute. Time for Inspiration to Expiration is 1:2
  • The ease at which a lung expands is the compliance - LOW with LVF, ARDS, Pneumonia
  • Airway resistance = pressure gradient from mouth to alveolus divided by rate of flow - HIGH with Asthma, COPD
• Air is sucked in due to a negative intrathoracic pressure due to
  • Contraction of the diaphragm downwards becoming flatter (phrenic nerve C3/4/5)
  • Contraction of external intercostals pulling ribs up and outwards
  • Occasional use of Accessory muscles - scalenes, sternocleidomastoids, pectoralis major, trapezius
  • Expiration is largely passive using relaxation of diaphragm and elasticity of lung tissue
  • Active expiration can be aided by internal oblique, external oblique,rectus abdominis, transversus abdominis
• Both actions
  • Increase thoracic volume which creates negative intrathoracic pressure.
  • Air moves along pressure gradient inward, enters through both nostrils
  • Air enters the nose where the rich vascular supply warms it and is humidified and filtered.
  • Air then passes via nasopharynx down across the larynx and into the trachea
• Except when positive pressure ventilated
  • Air is pushed against a pressure gradient into the lungs as respiratory muscles paralysed
  • Through an endotracheal tube or with non Invasive ventilation - a tight fitting face mask/nose
  • This creates a positive intrathoracic pressure which may be continuous or intermittent
  • Positive airways pressure can increase risk of lung trauma and pneumothorax
• Negative pressure ventilation
  • Historical interest - The "Iron lung" invented mainly to manage patients with polio related chest muscle weakness
  • Patient lay inside sealed compartment. Driven often by medical students.
  • Stimulated the whole development of ITU medicine and ventilation

Pulmonary perfusion

• Lung has a dual blood supply
  • Bronchial vessels - 120/80 mmHg
  • Pulmonary vessels - 25/10 mmHg
  • Pulmonary circulation is low resistance network
  • Less power needed so RV is thin walled
• Hypoxia
  • Causes localised hypoxic vasoconstriction
  • Areas of low pO₂ have low pulmonary blood flow
  • Blood diverted to areas of higher pO₂
• The lungs vascular system acts to
  • Oxygenate blood
  • Excrete CO₂
  • Filter out microthrombi eturning from systemic circulation
  • Convert Angiotensin I to angiotensin II
  • Acts as a blood reservoir - increased with inspiration
• Oxygenated blood returning to the heart in the pulmonary vein also gets some deoxygenated bronchial vein blood.
• The Left ventricle receives deoxygenated coronary blood via the thebesian veins
• Shunting
  • Successful oxygenation requires matching ventilation with perfusion.
  • If areas are perfused but get no oxygen this is a shunt and leads to deoxygenated blood entering the left atrium.
  • No matter how much additional oxygen is given it will not restore full oxygenation with a shunt.
  • This may be seen in pneumonia and consolidation or atelectasis or cyanotic congenital heart diseases.
• In pulmonary embolism there is oxygenation but not perfusion.

Ventilation perfusion mismatching can be estimated by an increase in the Alveolar-arterial pO2 gradient which is normally < 2 KPa

Lung anatomy

• The trachea extends from cricoid cartilage to the bifurcation at the carina at the level of manubriosternal joint
• Trachea in cross section is composed of "C" shaped cartilage rings deficient posteriorly closely related to oesophagus.
• At the carina at the level of the sternal angle (T4/5) it bifurcates into right main bronchus and then left main bronchus.
• The right main bronchus is shorter, wider and more vertical than the left and so is the destination of aspirated material.
• There is repeated branching until terminal bronchioles and alveoli
• Pleura
  • Lungs are enveloped by visceral pleural and then a pleural space and then parietal pleura.
  • The pleura are continuous. The pleural space contains only a small amount of fluid and a virtual space.
  • Surface tension keeps the layers together and normal intrapleural pressure is between - 2 and - 5 cm H₂O.
  • Parietal pleura is innervated by the intercostal and phrenic nerves so pleuritic pain can go to the shoulder and to the chest wall.
• Lobes
  • The right lung is composed of 3 lobes Upper, Middle, Lower and has both transverse and oblique fissures.
  • The Left lung is composed of 2 lobes Upper (+ lingula) and lower separated by the oblique fissure
• Hila
  • Vessels, nerves and lymphatics all enter the lung medially at the lung hila.
• Lung segments
  • Lungs can be divided into separate surgically resectable bronchopulmonary segments
  • Each with their own segmental bronchus and artery and vein.
• Vascular supply
  • Airway branches below the terminal bronchioles receive their arterial supply from the bronchial arteries
  • These originate as an aortic branch

Airway levels

Alveolus/capillary/erythrocyte interface

• Surface area available for gas exchange is 90 m2.
• 300 million alveoli of less than 1/5th of a mm in diameter in two lungs
• The gases must traverse
  • alveolar epithelium
  • basement membrane of alveolus
  • basement membrane vascular endothelial cell
  • This works out at about 0.4 um.
• Oxygen passes from high oxygen tension alveoli to low oxygen tension venous blood.
• CO2 passes from high tension venous side to low tension alveolus side
• Both gases pass either way from alveolar air across alveolar epithelium basement membrane and capillary endothelium
• Oxygen binds erythrocyte Haemoglobin and a small volume of oxygen dissolves in blood but most is carried bound to Hb
• Haemoglobin bound oxygen carriage is determined by O2 dissociation curve.
• Type 1 pneumocytes
  • Line the alveoli forming a thin layer allowing gaseous exchange.
  • They are devoid of most organelles.
• Type 2 Pneumocytes
  • Secrete surfactant and some also become Type 1 pneumocytes
  • They have larger nuclei and microvilli and cytoplasm containing storage vesicles for surfactant release.
• Surfactant
  • Surfactant is composed of phospholipids including sphingomyelin and lecithin.
  • The molecules have a hydrophobic and hydrophilic end
  • Surfactant reduces alveolar collapse and improves alveolar stability.
  • Lines the alveoli and lowers surface tension
  • Allows easier inflation and deflation of the lungs
  • Loss of surfactant causes stiff lungs - neonates

• The curve is sigmoidal and not a straight line. At low oxygen tension binding is poor and Hb releases oxygen to surrounding hypoxic tissues - enhances oxygen delivery where it is needed.
• Hb is more "sticky" for oxygen when in high oxygen tension area and is good at binding oxygen when there is plenty such as in the lungs and giving it away when there is none. These properties are affected by certain environmental factors and changes also in Hb.
• The steep middle section means that when there is a small drop in local PaO₂ in the midzone there is a large release of oxygen

Oxygen delivery

• Room air contains 21% oxygen. Small increases in arterial pO₂ can cause significant improvements in oxygen carriage and delivery.
• Nasal cannula can deliver 24-40% depends on flow rate. Simple face masks variable FiO₂ depending on flow and respiratory rate
• Venturi mask - uses venturi effect to mix air and oxygen to a more accurate concentration. Recommended in COPD
• Non rebreather - used to give very high FiO₂ where COPD is not an issue

Haemoglobin

• Structure and function
  • Four subunits of Haem + globin each of which binds an O₂ molecule at differing strengths giving rise to the sigmoidal curve.
  • A process called Cooperative binding.
  • Anaemia makes the curve move vertically down and reduces oxygen delivery.
  • Polycythaemia makes the curve move vertically up improving O₂ delivery "altitude training"
• Anaemia becomes very significant in terms of oxygen delivery when Hb < 7g/dl
• Makes Hb hold onto to O₂ tighter "Collection" (Leftward shift)
  • Low PCO₂, Alkalosis, Low temperature, Reduced 2,3 DPG
  • Carbon monoxide binds to HbO₂ sites avidly forming COHb and actually increases O₂ affinity worsening tissue hypoxia
  • Fetal Hb - has to remove oxygen from maternal Hb
• Markers of metabolism makes Hb release O₂ more easily "Delivery" (Right shift)
  • Raised PCO₂, Acidosis, Raised temperature, Increased 2,3 DPG
  • Hb Kansas and some other abnormal Hb

Respiratory control

• Central chemoreceptors in ventral medulla
  • Responds to increasing pCO2 indirectly by detecting increased CSF [H+]
  • Stimulates inspiratory centre - increased rate and depth of respiration
  • Affected by sedation, drugs, sleep, alcohol
• Peripheral chemoreceptors in Carotid body (IX cranial nerve) and Aortic arch (X cranial nerve)
  • Detect low pO₂ primarily but also raised pCO₂ and [H+]
  • Stimulates inspiratory centre - increased rate and depth of respiration
• Senation of Dyspnoea comes from
  • Afferent receptors in respiratory muscles
  • Juxtacapillary J receptors in lung sense interstitial oedema
  • Chemoreceptors sensing hypoxia and hypercarbia
• Feedback
  • Normally pCO₂ is the main gas that determines resp rate and depth
  • Under hypoxia (PO₂ < 8Kpa) hypoxia along with hypercarbia and acidosis drives the response
  • In those with COPD hypoxia can become the main regulator normally "hypoxic drive"

Causes of hypoxia

• Lung gets 4-6 L/min of air and 5L/min blood. Ventilation/perfusion ratio = 0.8 (4/5)
• Lung apices V > Q so ratio > 0.8. Lung bases V < Q so ration < 0.8
• Pulmonary embolism Q falls . V >> Q and so there is a VQ mismatch as aerated lung is under perfused "dead space"
• Asthma/Pneumonia V falls. V < Q and there is a VQ mismatch as perfused lung is not aerated "shunt"

Physics of Respiration

• Dalton's law - for 2 individual unreactive gases the total pressure exerted is the pressure of the first plus the second
• Normal atmospheric pressure at sea level is 760 mmHg = 101 kPa. Air contains 21% oxygen and 78% nitrogen and 1% inert gases
• Partial pressure of oxygen at sea level - Fraction in inspired air x atmospheric pressure = 0.21 x 760 = 159 mmHg = 21.2 Kpa
• Partial pressure of oxygen On summit of Everest - Fraction in inspired air x atmospheric pressure = 0.21 x 252 = 52 mmHg = 6.9 Kpa so high FiO2 must be given

Spirometry

• Spirometry involves blowing out as fast as possible into a special piece of equipment called a Spirometer. When the maximal blow is performed together with a maximal suck this test is sometimes referred to as a 'Flow Volume Loop'.
• The test will be performed with you seated and your nose may be sealed with a nose clip. You will be asked to breathe normally into a mouthpiece and instructed to take a deep breath in and then to blow out as fast as possible and try and keep blowing until your lungs are empty. This will be performed a minimum of three times, but you will be given adequate rest between each blow.
• This test measures the volumes and speed of the air you can blow out from your lungs and will give the doctor an indication of how clear the airways are in your lungs. For example, the airways may be narrower in conditions such as COPD or Asthma.
• Spirometry may then be repeated after you have been given an inhaler or nebuliser. This will be to see if there is any improvement in your airways as a result of taking this medication.

Forced expiratory volume in 1 second (FEV1)

• The FEV1 (forced expiratory volume 1) is the volume of air forcefully exhaled in 1 second

Forced Vital Capacity (FVC)

• The FVC is the volume of air that can be maximally forcefully exhaled - and therefore contains the FEV1 within it.
• If the FEV1/FVC ratio is <80%, it indicates that an obstructive defect is present.

Summary of lung volumes

• TV (Tidal volume) is the volume that flows in or out of the lungs with each breath during quiet breathing. (Normally about 7 cm3/kg)
• IRV (Inspiratory reserve volume) is the maximum amount of air that can be inspired in excess of the tidal volume. (Normally approximately 3.3 dm3 in men and 1.9 dm3 in women)
• ERV (Expiratory reserve volume) is the maximum amount of air that can be expired in excess of the tidal volume. (Normally approximately 1.0 dm3 in men and 0.7 dm3 in women).
• RV (Residual volume) is the volume left in the lungs after maximum expiration. (Normally approximately 1.2 dm3 in men and 1.1 dm3 in women). advanced applied science: ? IC (Inspiratory capacity) is IRV + TVFRC (Functional residual capacity) is ERV + RV ie volume remaining in the lungs at the end of a normal expiration.
• TLC (Total lung capacity) is IRV + TV + ERV + RV or SVC + RV. It is typically about 3 - 5 dm3. TLC increases when elasticity of the lungs is lost, e.g. in COPD, due to emphysema.
• VC or SVC (Vital capacity) is IRV + TV + ERV and is the maximum breath volume.