Case 6 physiology Flashcards
Relative composition of inspired air
Oxygen- 20.71 %
Carbon dioxide- 0.04%
Water vapour- 1.25%
Nitrogen- 78%
Relative composition of expired air
Oxygen- 14.6%
Carbon dioxide- 3.8%
Water vapour- 6.2%
Nitrogen- 75.4%
Relative composition of alveolar air
Oxygen- 13.2%
Carbon dioxide- 5%
Water vapour- 6.2%
Nitrogen- 75.6%
How much oxygen does the body use
It uses 25% of the oxygen which is delivered to the tissues.
Oxygen saturation of venous and arteriole blood
Venous blood has an oxygen saturation of 75% whilst arteriole saturation is 98%
Factors which affect the oxygen cascade
- Permeability of the cells and lung wall
- Surface area of the cells and lung wall
- The Conc./pressure gradient of the cells and lung wall
Oxygen delivery equation (DO2)
DO2= (SaO2 x Hb x CO x 1.34) + (PaO2 x 0.003)
• DO2: oxygen delivery, works out to a 1000 ml/min
• SaO2: oxygen saturation (Hb and O binding)
• Hb: haemoglobin concentration (g/l)
• PaO: dissolved oxygen (kPa)
• Hufner’s constant: 1.34 ml/g
• Oxygen solubility coefficient: 0.003
What is oxygen consumption dependent on
The amount of aerobic respiration in the tissues
Oxygen consumption (VO2) equation
VO2 = CO x Hb x 1.34(SaO2 – SvO2)
• VO2= volume of oxygen consumed (250ml/min)
• SaO2- arterial saturation of oxygen
• SvO2- venous saturation of oxygen
Simplified oxygen consumption (VO2) equation
VO2= CO x (CaO2 – CvO2)
The amount of oxygen consumed is dependent on the difference between the arterial saturation of oxygen and the venous saturation
What is the emergency medication used in asthma
Prednisolone
Why does the composition of alveolar gas stay relatively constant
The alveoli do not change in size or volume during respiration. The ‘bulk flow’ effect of ventilation- expanding the thoracic cavity to create a negative pressure, ends at the respiratory bronchioles. So gas composition is mostly determined by random diffusion. The inputs and outputs of CO2 and O2 mostly balance out meaning the alveolar gas stays relatively constant
The layers of the diffusion barrier
Alveolar epithelium, tissue fluid, capillary endothelium, plasma and red blood cell membrane.
Right-left shunt (venous admixture)
Allows the blood to flow from the venous side of circulation and enter the arterial side without passing into functional respiratory epithelium. Meaning that normal gas exchange does not occur
An example of a right-left shunt
Bronchial circulation= The bronchial artery is supplying oxygen to the bronchial, the deoxygenated blood then flows out and mixes directly with the oxygenated blood in the pulmonary vein. So the oxygenated blood which returns in the pulmonary vein will contain a very small amount of deoxygenated blood
Pathologies which can cause a R-L shunt and the problem with it
Pneumonia or anatomical variations (Truncus arteriosis, patent foramen ovale and transposition of the great vessels). The problem with these pathologies is that they can not be treated by giving the subject 100% O2 because the shunted blood bypasses the ventilated alveoli and is not exposed to gaseous exchange.
Effects of Hypoventilation (reduced alveolar ventilation
- Causes a decreases PAO2 leading to less oxygen in the arterioles– Hypoxia.
- Increases PACO2 which increases the amount of CO2 in the arterioles- Hypercapnia.
- Hypoxaemia= decrease in arterial O2 levels which causes a decrease in the oxygen carrying capacity of the blood, this can be independent of hypoventilation.
Causes of Hypoventilation
Increased airway resistance i.e. asthma and COPD, drugs such as morphine or barbiturates. As well as paralysis of respiratory muscles
V/Q ratio at rest
V/Q = Alveolar ventilation / Cardiac output
The resting alveolar ventilation (4L/min) and the resting cardiac output (5L/min). So, the resting V/Q ratio of the lungs is 4/5=0.8
Alveolar ventilation equation
Alveolar ventilation= (Tidal volume- Dead space) x Respiratory rate
Ideal V/Q
The ideal value is 1, this is where ventilation and perfusion are matched, however, this doesnt happen in real life, it is normally 0.8. Gas in this alveolus contains a normal percentage of O2 and CO2. There will be 13.7 kPa of O2 and 5.2 kPa of CO2.
V/Q ratio in an obstructed alveoli
When ventilation is obstructed but blood flow is unchanged. The pO2 is 5.3kPa and the pCo2 is 6.1kPa, this causes the V/Q to get smaller and eventually hit zero. So, the PAO2 will fall and PACO2 will rise (alveolar). Less O2 will be taken up in the over perfused alveoli and the blood leaving these alveoli will be undersaturated and less CO2 will be removed. This is caused by airway limitation (asthma and COPD), lung collapse and loss of elastic tissue (emphysema).
V/Q ratio due to obstruction of blood flow
When perfusion is obstructed but ventilation remains unchanged. The pO2 is 20pKa whilst the pCo2 is zero, this causes the V/Q to get higher and higher till it reaches infinity. Some ventilation will be wasted and contribute to dead space. The PAO2 will rise and the PACO2 will fall (alveolar). No more O2 will be taken up by the overventilated alveoli as the haemoglobin is fully saturated and extra CO2 will be blown off. Can be caused by a pulmonary embolism, necrosis or fibrosis of the capillary bed.
V/Q ratio- emphysema
In emphysema you get destruction of alveoli and loss of capillaries. The destruction of alveoli leads to underventilation (low V/Q ratio) and the loss of capillaries leads to alveoli which are under perfused (high V/Q ratio). It therefore decreases the effectiveness of gas exchange as there will be areas of the lung with a low V/Q and other areas of the lung with a high V/Q ratio.
Hypoxic pulmonary vasoconstriction
Mechanism to reduce V/Q differences. Low alveolar pO2 due to reduced ventilation acts as a stimulus for pulmonary artery constriction, reducing blood flow. This restores the V/Q value back to normal so there is a more efficient gaseous exchange
Mechanism to reduce V/Q differences in low alveolar pCO2
Low alveolar pCo2 due to reduced blood flow causes constriction of the alveolar ducts. You therefore, reduce the ventilation and adjust the V/Q back to normal.
Mechanism to reduce V/Q differences= Last out first in principle
When there is an obstruction in the airways causing reduced ventilation. This will lead to a low V/Q with a low PO2 and a high PCO2. When breathing out air will preferentially leave the normal healthy alveolar first as there is no obstruction. So, there will be a lag before the air leaves the obstructed alveolus. This will cause a greater amount of air in the dead space from the obstructed alveolus. The dead space will have a low PO2 and a high PCo2. The air from this dead space will then go back into the unobstructed alveoli. The two airways will then have better match gas exchange as the air in the obstructed alveoli goes to the unobstructed alveoli
Regional differences in the V/Q ratio
Perfusion drops of at a much greater rate then ventilation, so perfusion is lower then ventilation at the apex. Whilst in the base perfusion is greater then ventilation. V/Q is higher in the apex but gets smaller as you go towards the base
Regional differences in perfusion and ventilation
Ventilation is greatest at the base due to gravity making it easier to ventilate alveoli as they open more. Perfusion is highest in the base because gravity helps blood flow as its going against low pressure, whilst at the apex the blood will have to work against gravity.
Importance of V/Q mismatch
Ventilation-perfusion inequality means that the lung is not able to transfer as much O2 and CO2 as a lung that is uniformly ventilated and perfused. The amount of O2 and CO2 being exchanged will change and will not be in line with the ideal amount.
How does O2 regulate pulmonary ventilation
At pO2 levels greater than 12.7kPa there is no significant change in ventilation, there is a significant drop in ventilation when the pO2 drops to 8kPa. So O2 does regulate ventilation but only when there are life threateningly low levels of O2
How does CO2 regulate pulmonary ventilation
An increase in pCO2 causes a steep increase in pulmonary ventilation, for a 1kPa increase in pCo2 there is an increase in 15L of ventilation. Pulmonary ventilation will continue to increase until it reaches about 15 kPa PCO2 with levels higher than this depressing ventilation causing a “Narcotic” effect. This is due to depression of brain function including areas that control ventilation. The patient will become unconscious. If levels of PCO2 are lowered below that of normal then ventilation is slightly decreased but quickly levels off with no further reduction in ventilation.
What is the key regulator of ventilation
pCO2 at rest
How levels of H+ affect ventilation
There is no stimulation of ventilation until arterial pH is reduced by 0.1pH units and a fall in arterial pH of 0.4pH units which causes a 2-3 fold increase in ventilation.
Why is it dangerous to give oxygen to a patient in respiratory failure
In COPD the choroid plexus compensates by increasing the amount of bicarbonate to help buffer the excess CO2. The CSF pH may be close to normal due to this enhanced buffering effect. So, any increases in CO2 will have little effect on pH making the patient desensitised to CO2. The control of ventilation reliant on the peripheral chemoreceptors detecting hypoxia (oxygen levels). If O2 is then given as a treatment it could then result in removing the remaining drive for ventilation. Death may occur due to further hypoventilation caused by a failure to increase the ventilatory drive.
How does CO2 cause death
Leads to narcosis due to decreased ventilation, due to CO2’s narcotic effect as it depresses brain function.
Peripheral chemoreceptors
The carotid bodies are primarily sensitive to a decrease in pO2. They are located where the common carotid arteries divide and are above the aortic arch. Contain type 1 glomus cells which are chemo-sensitive and release neurotransmitters which regulate the rate of firing of the carotid bodies afferent fibres from the cranial nerve 9 (glossopharyngeal)
Blood supply to the carotid bodies
2L/min per 100g which is the highest blood flow to any tissue in the body per gram of tissue
Peripheral chemoreceptors (hypoxia)
In the presence of hypoxia the glomus cells become more sensitive to changes in CO2 and pH. If the carotid body was destroyed then ventilation would not increase at low pO2. So, glomus cells are the most important regulator of hypoxia.
Central chemoreceptors
Found on the ventral surface of the medulla. The neurons respond to an increase in CO2 by firing more. The blood is not in direct contact with the receptors, instead the blood brain barrier allows the CO2 to diffuse across it easily, it then diffuses into the CSF (cerebrospinal fluid) where it reacts with water to form carbonic acid. There is a decrease in the pH of the CSF, the bicarbonate will try to buffer it. The more CO2 there is the more reduced the pH is. The chemoreceptors then the detect the change in pH.
Describe the characteristics of the ventilatory responses to oxygen, carbon dioxide and acid.
In resting, healthy humans at sea level the main stimulus to ventilation is provided by arterial PCO2. CO2 is detected by central (80%) and peripheral (20%) chemoreceptors. Arterial PO2 and arterial pH are not important regulators under normal conditions, but may become so when significant changes occur. However, hypoxia and acidosis increase the effects of CO2 on ventilation. Hypoxia and acidosis are detected by peripheral chemoreceptors.
Respiratory centre
In the Pons and medulla, they regulate the respiratory muscles which control respiration
Importance of the medulla in breathing
Contains all the neuronal apparatus needed for inspiration and expiration, even when you remove any higher brain input and peripheral neuronal input. However, the breathing will be more like gasping. • Medullary regions can be divided into the Ventral Respiratory Group (VRG) and Dorsal Respiratory Group (DRG).
PRG (pontine respiratory group)
In the Pons region, influences pattern ventilation. They influence the basic rhythm of breathing. They have roles in phase switching i.e. switching off or inhibiting inspiration.
VRG
Contains both inspiratory and expiratory neurones. The control the amplitude (depth) of breathing. The pre-botzinger complex has roles in rhythm generation. Also contains the Botzinger complex
DRG
Is in the dorsal aspect of the medulla and contains lots of inspiratory neurons. The solitary tract integrates sensory information. It is a large fibre tract which carries afferent nerves from the periphery, through the medulla and into the higher centres of the brain. These afferent fibres are mainly from cranial nerves 9 and 10. Cranial nerve 9 (glossopharyngeal) also carries signals from the peripheral chemoreceptors (carotid bodies). Cranial nerve 10 (vagus) also carries mechanoreceptor information from the lung.
The 2 main theories about neuronal control of ventilation
- Pacemaker cells which fire and discharge rhythmically such as the cells in the pre-botzinger complex.
- Neuronal Network Theory- inspiratory neurons discharge which exert inhibitory control over the Expiratory neurons and vice versa.
Why the pacemaker cells are not soley in control of ventilation
They don’t account for metabolic changes, how would it integrate with other functions like speach?
Where do the Medulla and Pons send their signals to
When the Medulla and Pons send out signals the phrenic nerve innervates the diaphragm and synapses on the spinal neuron in C5. The external intercostals receive innervation from T5/T6 and the lateral internal intercostals from T11/T12.
How the Pons and Medulla affect inspiration and expiration
The neuronal signal is not an instantaneous burst of action potentials, instead it begins weakly and increases steadily in a ‘ramp like’ manner for about 2 seconds in normal respiration. This allows for a steady increase in volume instead of sudden short inspiratory gasps. It then stops for three seconds to allow for expiration. There is still activity at the beginning of expiration, this is known as post-inspiratory activity. This slows down expiration by working against the elastic recoil of the lungs.
The factors which affect the respiratory centre
Chemical input- i.e. changes in CO2 and O2 which are detected by peripheral and central chemoreceptors, this can increase/decrease ventilation.
Neurogenic input- neural reflexes or input from the brain and medulla.
Cortical factors
In the cerebral cortex within the higher brain centre. This is in charge of voluntary control of breathing, such as holding your breath. The limbic system and hypothalamus in the brain can alter the pattern of breathing as seen in emotional states such as fear or anger.
Reflexes from the lung
1) Irritant receptors
2) C-fibre receptors
3) Hering-Breuer inflation reflex (stretch receptors)
4) J- receptor reflexes
Irritant and C-fibre reflexes
Involved in the autonomic control of the airway. Irritant receptors are located between the airway epithelial cells and respond to both mechanical and chemical stimuli such as dust and smoke.
Hering-Breuer reflex
Within the lung. Contains two types of stretch receptors, slowly adapting and rapidly adapting. Following stimulation, signals travel via afferents from the vagus nerve up the solitary tract to the dorsal ventilatory group for integration. These receptors stop ventilation preventing over-inflation of the lung.
Juxta-pulmonary capillary receptors (J receptors)
Found in the alveolar walls close to the capillaries. They are stimulated by increased pressure in the pulmonary capillaries, this increases the interstitial fluid volume, which is pushed out into the space between the cells causing the layers of cells to separate, this activates the J receptors. This causes rapid, shallow breathing.
Aortic and Carotid sinus baroreceptors
An increase in arterial blood pressure can cause reflux hypoventilation through stimulation of the aortic and carotid sinus baroreceptors. Increasing ventilation will decrease intrapleural pressure this encourages venous return to the heart increasing cardiac output.
Chemosensitive neurons
Within the muscles are joints, cause the sudden increase in ventilation at the onset of exercise before any changes in pO2 or pCO2 have been detected
Pain afferent nerves- ventilation
Stimulation of pain afferent nerves may cause a period of apnea (stopping breathing) followed by hyperventilation. Heating of the skin may also stimulate hyperventilation.
Overriding respiratory reflexes- Laryngeal reflex and swallowing
The larynx moves forward during swallowing in order to occlude the trachea and therefore preventing food from entering the lungs.
Overriding respiratory reflexes- coughing
Protects the lower airways from irritants, requires a rapid inspiration of air followed by closure of the glottis. Contraction of expiratory muscles and the abdomen cause pressure to increase, the glottis to open and an explosive expulsion of air.
Overriding respiratory reflex- sneezing
Removes particles from the upper airways. This is the sudden expiratory blast through the nose produced by irritation of the nasal mucosa and stimulation of the nasal branches of the maxillary nerve.
Overriding respiratory reflex- speech
A controlled rapid inspiration and a prolonged expiration
Overriding respiratory reflex- Sigh
A larger then normal breath that occurs automatically due to the counteract collapse of the alveoli. A yawn is an exaggerated sigh.
Overriding respiratory reflex- Gasping
Can be due to cold water, causes hyperventilation
Overriding respiratory reflex- Hiccups
The repeated spasmodic contraction of the diaphragm and the external intercostals where the glottis close suddenly so no more air can enter the chest
The integration of chemical and neural control systems
Chemical reflexes are of primary importance in adjusting ventilation to the body’s metabolic needs. Neural reflexes are of secondary importance and tend to modify the pattern of ventilation rather than regulate the overall level of ventilation.
