Pre-Eclampsia Dr Swapnil Pawar
The Role of Hyperventilation in ICP Control Dr Swapnil Pawar
ICU Primary Bedside Preparation Part 4 Dr Swapnil Pawar
Respiratory Physiology -Part 2
Dr Swapnil Pawar
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.
The normal automatic breathing pattern is generated within the respiratory centre in the medulla. There are two groups of neurons:
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.
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:
FRC is affected by:
A decreased FRC results in multiple effects
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
Consequences of increased closing capacity include
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.
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.