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Respiratory Physiology -Part 2

Dr Swapnil Pawar January 12, 2021 493 5


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    Respiratory Physiology -Part 2
    Dr Swapnil Pawar

Written By – Dr Madhuri Anupindi

RESPIRATORY PHYSIOLOGY 2

How is ventilation controlled?

The control of ventilation can be thought of in terms of sensors, a central integrator and effectors.

The sensors consist of central chemoreceptors, peripheral chemoreceptors, mechanical receptors within the lung and other receptors.

Sensors:

  • Central chemoreceptors
    • These are located near on the ventrolateral surface of the medulla and surrounded by the extracellular fluid of the brain, the composition of which is mainly governed by the CSF.
    • The central chemoreceptors respond to changes in the concentration of hydrogen ions, an increase in hydrogen concentration results in increased ventilation. However, the blood-brain barrier is relatively impermeable to hydrogen and bicarbonate ions whereas CO2 can diffuse across it easily. Therefore, when the pco2 of blood rises, it diffuses into the CSF and decreases the pH resulting in increased ventilation.
  • Peripheral chemoreceptors
    • These are located in the carotid bodies, at the bifurcation of the common carotid arteries, and in the aortic bodies near the aortic arch. The carotid bodies have a very high rate of perfusion and consequently a very small arterial, venous po2 difference. This allows them to rapidly respond to changes in arterial blood gas tensions. The carotid bodies transmit signals to the medullary respiratory centre via the glossopharyngeal nerve while the aortic bodies transmit it via the vagus nerve.
    • The peripheral chemoreceptors are stimulated by:
      • A decrease in arterial po2: the firing rate is non-linear and there is very little response until the po2 is less than 100mmHg, after which the response increases dramatically. The carotid bodies are stimulated by a decreased partial pressure of oxygen, not by reduced oxygen content, therefore there is minimal stimulation in anaemia
      • Increase in paco2: the peripheral chemoreceptors respond to an increase in paco2 but to a much lesser extent than the central chemoreceptors
    • The carotid bodies but not the aortic bodies also are stimulated by:
      • The decrease in arterial pH: the carotid bodies respond to a fall in pH but the aortic bodies do not.
      • Increased temperature
      • Hypoperfusion of the peripheral chemoreceptors such as in profound shock
      • Metabolic changes: hypoglycemia, nicotine, acetylcholine, cyanide
  • Mechanical receptors
    • Pulmonary stretch receptors: are present within smooth muscle of the airways and are stimulated by increased distension of the lung. Increased stretch causes them to discharge, the impulses travel via the vagus nerve and result in a slowing of respiratory frequency. This is known as the Hering-Breuer inflation reflex
    • Noxious receptors are present between airway epithelial cells and are stimulated by dust, cold air and noxious gases. These impulses also travel via the vagus and result in bronchoconstriction and tachypnoea.
    • J receptors: are endings of nonmyelinated C fibres in alveolar walls and respond to chemicals within the pulmonary circulation causing rapid, shallow breathing
    • Bronchial C fibres: respond to chemicals in the bronchial circulation causing bronchoconstriction and tachypnoea.
  • Other receptors
    • Include upper airway receptors which respond to irritants by coughing and sneezing, joint and muscle receptors which are thought to be important in exercise-induced increased ventilatory drive, arterial baroreceptors which cause reflex hypoventilation when hypertension occurs, and pain and temperature receptors which cause hyperventilation.

Central integrator:

The normal automatic breathing pattern is generated within the respiratory centre in the medulla. There are two groups of neurons:

  • The dorsal respiratory group: which lies close to the nucleus tractus solitarius and is predominantly composed of inspiratory neurons with upper motor neurons passing to the contralateral inspiratory horn cells. The dorsal group is mainly concerned with the timing of the respiratory cycle.
  • The ventral respiratory group which is made up of:
    • Caudal ventral group: contains the nucleus retroambigualis which is mainly expiratory and has upper motor neuron axons passing to the contralateral expiratory muscles. It also contains the nucleus paraambigualis which has an inspiratory function. This has upper motor neuron axons passing to the contralateral inspiratory muscles and controls the force of contraction.
    • Rostral ventral respiratory group which is mainly composed of the nucleus ambiguous which is involved in airway dilatation of the larynx, pharynx and tongue.
    • Pre-Botzinger complex which is thought to be the location of the central pattern generator of the respiratory system
    • Botzinger complex which has expiratory functions.

The pons also contains a pontine respiratory group which is thought to influence the medullary respiratory neurons and help control the respiratory rhythm.

The cerebral cortex is also important for behavioural and volitional control of respiration such as during speaking and singing.

Effectors

  • These are the muscles of respiration including the diaphragm, intercostal muscles, abdominal muscles and accessory muscles.

Describe the structure and effects of surfactant.

Surfactant is a lipoprotein complex produced by Type 2 alveolar cells in the lung which is responsible for lowering the surface tension of the alveoli air-liquid interface. It is comprised mainly of phospholipids of which the majority is dipalmitoyl phosphatidyl choline. The remainder of surfactant is composed of proteins and a small amount of neutral lipids. The phospholipids form a monolayer and have hydrophobic ends which project into the alveoli and hydrophilic ends which lie within the alveolar lining fluid. There are four types of surfactant protein (SP A, B, C and D). SP-A and D are hydrophilic while SP-B and C are hydrophobic. SP-A and D are collectins which are a family of innate immune proteins and activate alveolar neutrophils and macrophages. SP-B enhances the surface tension reducing properties of surfactant and SP-C is thought to stabilise the phospholipid later.

Surface tension is the cohesive force exerted upon the surface molecules of a liquid by the bulk liquid beneath which makes the liquid assume the shape having the least surface area. The Law of Laplace states that transmural pressure = 2 x surface tension divided by radius. Therefore, increasing surface tension or decreasing radius will increase the transmural pressure and increase the likelihood alveolar collapse. Surfactant reduces the surface tension at the alveoli air interface by reducing the cohesion of the liquid molecules. This reduces work of breathing and prevents alveolar collapse. Furthermore, as alveoli decrease in size, the surfactant molecules are brought closer together and exert more of an effect on surface tension. Surfactant also has an important role in the innate immune system and modulation of the immune response.

What is the functional residual capacity?

Functional residual capacity is the volume of gas remaining in the lung following a normal, passive expiration. It is composed of the residual volume plus the expiratory reserve volume and is normally approximately 30-35ml/kg. The functional residual capacity also represents the point where the elastic recoil of the lung tissue is in equilibrium with the chest wall outward expansion.

The FRC is important because:

  • It is the point where pulmonary vascular resistance is at its lowest
  • It is representative of compliance: a decrease in compliance will decrease FRC
  • It represents the point where work of breathing required to inflate the lung is at its lowest – that is optimal compliance
  • It provides an oxygen reserve – therefore gas exchange can continue during the whole respiratory cycle
  • It prevents collapse of small airways thus minimising atelectasis

FRC is affected by:

  • Changes to inward recoil of lung or lung compliance
    • FRC increased in conditions such as emphysema due to alveolar destruction
    • FRC decreased in ARDS due to decreased lung compliance
  • Changes to outward expansion of lung or chest wall compliance
    • Decreased FRC with conditions such as kyphoscoliosis, severe burns due to decreased chest wall compliance
    • This is also the case for pregnancy, obesity or increased abdominal pressure which increases pressure on the diaphragm, decreases chest wall compliance and reduces FRC
    • Anaesthesia reduces diaphragm tone and decreases FRC
    • Position: FRC is greatest when upright and decreases by about 20% when supine
  • Lung size
    • Height: taller people have generally larger lung volumes and FRC
    • Gender: men generally have larger FRC
  • FRC slightly increases with age

A decreased FRC results in multiple effects

  • Decreases lung compliance and increases airway resistance thus resulting in increases work of breathing
  • Decreases oxygen reserve
  • Increases atelectasis which may result in increased shunt
  • Increased pulmonary vascular resistance which may cause an increase in right ventricular afterload

Define closing capacity and outline the factors that alter it, its clinical significance and one method of measuring it.

Closing capacity is the maximal lung volume at which airway closure can be detected in the dependent parts of the lung. It is composed of the residual volume plus the closing volume. Small airway closure occurs when the elastic recoil of the lung overcomes the negative intrapleural pressure that keeps the airway open. This is more likely to occur in dependent regions of the lung where the airways are smaller. Normally, closing capacity is less than FRC but it increases with age. At approximately 44 years old it equals FRC in the supine position and at age 66 it equals FRC in the upright position.

Factors which increase closing capacity

  • Age: closing capacity increases with age but is also increased in neonates due to their decreased lung compliance, very compliant chest wall and decreased ability to maintain negative intrathoracic pressures
  • Obstructive airways disease such as COPD
  • Increased expiratory airflow and effort
  • Increased pulmonary blood volume e.g. in left ventricular failure due to increased pressure on dependent lung
  • Decreased pulmonary surfactant
  • Pulmonary parenchymal disease: conditions that cause loss of radial traction of the small airways increase closing capacity
  • Increased intra-abdominal pressure

Consequences of increased closing capacity include

  • Increased atelectasis which may result in shunt and hypoxia
  • Cyclic atelectasis causing injury to alveoli and bronchioles
  • Gas trapping
  • Reduced lung compliance
  • Injury to alveoli and bronchioles

Closing capacity can be measured by inspiration of a tracer gas such as xenon at the beginning of inspiration from residual volume. This is when airways are closed in the dependent part of the lungs so the tracer gas will preferentially be distributed to the upper parts of the lung. After a maximal inspiration to total lung capacity the patient slowly exhales while the concentration of the tracer gas is measured at the mouth. Initially dead space gas will come out and the concentration of tracer gas will not rise. Following this the tracer gas concentration will increase and then plateau. When closing capacity is reached, the dependent airways will close and the tracer concentration measured at the mouth will once again rise as only the upper alveoli which contain more of the tracer gas will still be open. This method technically measures closing volume. Residual volume cannot be measured directly but can be calculated by measuring the FRC with body plethysmography, helium dilution or nitrogen washout. The expiratory reserve volume can be measured with spirometry. As FRC = ERV + RV, by subtracting ERV from FRC we can obtain a value for residual volume. This can then be added to the closing volume previously measured to calculate the closing capacity.

Define mixed venous po2. Briefly describe the factors that influence the oxygen content in mixed venous blood.

Mixed venous p02 is the partial pressure of oxygen in the pulmonary artery. This contains blood mixed in the right ventricle and is a representation of the venous blood and therefore the oxygen extraction, from the rest of the body. The normal value is 35 – 40mmHg.

Oxygen content of the blood is dependent on the amount of haemoglobin, the saturation of haemoglobin and the partial pressure of oxygen where oxygen content = (1.34 x hb x sats) + 0.003 x po2. The po2 of mixed venous blood helps determine the saturation of haemoglobin via the oxygen-haemoglobin dissociation curve. This curve is slightly right shifted for mixed venous blood compared to arterial blood due to the Bohr effect.

Factors influencing the mixed venous oxygen content include factors which impact on oxygen delivery and oxygen consumption.

  • Oxygen delivery
    • Cardiac output
    • Haemoglobin concentration
    • Haemoglobin saturation
    • Pao2
  • Oxygen consumption

Factors that decrease oxygen delivery such as low cardiac output states or increase oxygen consumption such as fever will decrease mixed venous oxygen content. Factors which increase oxygen delivery such as high pao2 or decrease oxygen consumption such as impaired tissue uptake in cyanide toxicity will increase mixed venous oxygen content.

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