Resp 7 - Breathlessness and control of breathing (awake) Flashcards
Name 5 functions of the respiratory muscles
- Maintain arterial pO2, pCO2, and pH (pH most important)
- Defence of airways
- Exercise
- Speech
- Control of intrathoracic and infra-abdominal pressures
Does arterial pCO2 change at all during life?
What about arterial pO2?
Arterial pCO2 doesn’t change.
Arterial pO2 is lower neonatally and in old age than years between.
What does minute ventilation equal?
VE = VT x f
What is TTOT?
Duration of single respiratory cycle
Can be split into Inspiratory (TI) and Expiratory (TE)
What nerve supplies the diaphragm?
Phrenic Nerve
What is normal ventilation rate?
6L / min
What is normal tidal volume?
0.5L
What does adding dead space do ?
It increases neural drive.
VT/TI (neural drive) increases to clear the extra space.
What happens in patients with chronic bronchitis and emphysema?
Shorter VTs and TTOTS but similar gradients to normal people
- These patients struggle more on expiration.
- They have higher residual volume than normal people - increasing chest stiffness and the work of breathing.
- They have much shorter TTOTs - shallower and faster breathing
- VT/TI is roughly similar - so these patients don’t breathe harder
- Exercising increases neural drive and ventilation. It also halves TTOT (doubling frequency)
What is the difference between people with COPD and normal people when exercising, with regard to TI/TTOT.
Normal = longer TI/TTOT - more time for inspiration
COPD = shorter TI/TTOT - gives more time for expiration
People with obstructive disease have difficulty expiring
T. This is key
Where is the involuntary centre which controls breathing (aka metabolic centre)
What about the voluntary centre (aka behavioural centre)
Medulla = involuntary/metabolic
Motor area of cerebral cortex = voluntary/behavioural
Name involuntarily controlled parts of the cortex which influence metabolic centre
Emotional responses
Name an influencer of the metabolic centre.
Sleep via reticular formation
What happens to pCO2 during sleep?
It rises a little
What does the metabolic centre respond to?
Metabolic demands for CO2 production (VCO2), and also determines the set point of CO2 (usually measured as PaCO2)
Name 3 things that may influence the metabolic centre.
- Limbic system (survival)
- Frontal cortex (emotions)
- Sensory inputs (pain)
Where is the metabolic centre of the brain?
In the brainstem - automatic bulbopontine region
Describe how the metabolic controller works.
- H+ ion receptor in metabolic controller.
- It regulates the phrenic nerves - activates muscles in chest wall and lungs
- Chemoreceptors in carotid bodies in the neck sense H+ levels in the blood and feedback to controller.
- The controller itself has H+ receptors too.
- Information (secondary) also received from lungs and respiratory muscles.
- Upper airway muscles also controlled by controller.
Where does the (peripheral) carotid body chemoreceptor lie?
At the junction of the internal and external carotid arteries.
This is the fast response as it is hyperperfused
Unlike the heart, breathing has many pacemakers that are close together in the brain stem and are inaccessible. How many groups of nerves are there and where are they located?
10 groups and in the medulla - near the nuclei of cranial nerves 9 and 10.
What is special about the pre-Botzinger complex?
Essential for generating respiratory rhythm - aka the “gasping centre”.
The pre-botzinger complex must be coordinated with other controllers to convert gasping into an orderly rhythm.
Disease affecting control centres in the brain are rare.
What is the important role of pharyngeal and laryngeal muscles?
They open up the airways and act as a brake in breathing
Which 3 nerves regulate reflex control of breathing (sneezing, coughing, etc)
5th nerve - afferent from nose and face (irritant)
9th nerve - from pharynx and larynx (irritant)
10th nerve - from bronchi and bronchioles (irritant and stretch)
Hering-Breur reflex is a cut off signal. How?
Pulmonary stretch receptors that lie in airway smooth muscle are activated by lung inflation and inhibit medullary inspiratory neurons.
For every 1kPa rise in arterial pCO2, what is the rise in minute ventilation?
30 L/min
What does hypoxic breathing do to the acute CO2 response?
It increases the sensitivity
What happens during sleep?
Ventilation drops to 0, but continuing CO2 production means that arterial pCO2 rises above apnoeic point which restarts breathing.
What could be a cause of reduction in sensitivity to arterial pCO2?
Respiratory muscle weakness
For every 7kPa decrease in arterial pO2, there is a 30 L/min rise in minute ventilation.
What conclusion can be drawn?
The system is much more sensitive to pCO2 than pO2.
Which is better defended: oxygen saturation or arterial pO2.
Oxygen saturation (due to oxygen binding to Hb and ODC)
How does a fall in ventilation get corrected.
- Fall in ventilation = fall in pO2 = rise in pCO2.
- Fall in pO2 increases sensitivity of carotid body to pCO2 and H+.
- Ventilation therefore increases and pO2 increases.
- pCO2 falls by negative feedback.
Why is the human not so well equipped for fall in pO2 caused by altitude?
- Hypoxic hyperventilation lowers pCO2. This inhibits the ventilatory response.
- Therefore, several days of acclimatisation are required to adjust to a lower pO2 set point.
What are the 2 responders to acid-base problems?
Lung (fast responder) and kidney (slow responder)
What are the 2 types of acidosis and alkalosis?
- Metabolic
2. Respiratory
Describe metabolic acidosis.
When source of H+ comes from metabolism rather than ventilation.
Causes = diabetic ketoacidosis, salicylate overdose, renal tubular defects.
What are the compensatory mechanisms for metabolic ketoacidosis?
- Ventilation to lower pCO2 and H+
- Renal excretion of weak acids
- Renal retention of chloride - reduces strong ion difference
Describe metabolic alkalosis.
- Loss of H+ leads to excess HCO3-.
2. Causes = vomiting, diuretics, dehydration
What are the compensatory mechanisms for metabolic alkalosis?
- Hypoventilation raises pCO2 and H+
- Renal retention of weak acids
- Renal excretion of chloride to increase strong ion difference
Describe respiratory acidosis
Lungs fail to excrete CO2 produced by metabolic processes (hypoventilation)
What determines the H+ ion concentration in the blood?
The pCO2:bicarbonate ratio
What are central hypoventilation conditions?
Acute - metabolic centre poisoning
Chronic - vascular or neoplastic disease of metabolic centre, Obesity Hypoventilation syndrome, etc
What are peripheral hypoventilation conditions?
Acute - muscle relaxant drugs
Chronic - Neuromuscular with respiratory muscle weakness
What is respiratory alkalosis?
Ventilation in excess of metabolic needs
Causes = chronic hyperaemia, excess H+, pulmonary vascular disease, chronic anxiety
What is the difference between dyspnea at rest and exercise?
Rest - implies difficulty in expiration or inspiration
Exercise - excessive breathing for the task
What are the 3 types of breathlessness?
- Tightness - difficulty inspiring due to airway narrowing
- Increased work and effort - breathing normally/high minute ventilation but HIGH lung volume (or against inspiratory/expiratory resistance)
- Air hunger - sensation of a powerful urge to breathe (worst)
Mismatch between VE demand and VE achieved in air hunger. What 2 inputs does the cerebral cortex compare?
Demand and output
How can breathlessness be scored?
BORG scale (out of 10).
What does Breath Holding Time do?
Tests strength of behavioural vs metabolic controller.
Breakpoint can be prolonged by increasing lung volume, lowering pCO2, taking an isoxic/isocapnic breath near break point.
