Neurological & Vascular Aspects of Respiratory Medicine Flashcards
explain the process that controls breathing
Central chemoreceptors are located on the ventral side of the medulla oblongata.
They detect changes in PaCO2, through detecting change in CO2 content of CSF.
Peripheral chemoreceptors are located in the carotid and aortic arches.
They sense changes in PaO2 and blood pH (measure of CO2).
These chemoreceptors send sensory information to the brainstem respiratory centre.
The brain stem then sends appropriate impulses to the muscles of breathing (diaphragm and intercostals).
These then speed up or slow breathing - changes in alveolar ventilation - changes in PaCO2, PaO2 and blood pH.
explain the process that allows breathing to change during exercise
During exercise metabolism is increased.
This results in a build-up of carbon dioxide and a reduction in the supply of oxygen.
These changes are detected by chemoreceptors (both centrally and peripherally) and impulses are sent to the respiratory control centre in the brainstem.
Signals are sent to the diaphragm and intercostal muscles to increase the rate of ventilation (this process in involuntary).
As the ventilation rate increases, CO2 levels in the blood will drop –> restoring blood pH.
O2 levels will also rise.
what effect would brain injury have on chemoreceptors?
Injury to the brain is more likely to affect respiratory function if the breathing centres in brainstem are affected.
A brainstem lesion (e.g.tumour) in the medulla will compress chemoreceptors –> slowing down of breathing.
Eventually chemoreceptors will be blocked off stopping you from breathing –> respiratory arrest –> unconscious
You can look out for cranial nerve signs to locate where the lesion is.
Lesions are difficult to see on CT scans, better on MRI
On the MRI (right) you can see white plaque areas on the brain stem.
These are areas of demyelination (multiple sclerosis) which then affect how you breathe.
how is the brain stem effected during brain injury?
The brainstem may also be affected by large lesions in the cortex above it pushing it downwards.
The brain stem is pushed down against the foramen magnum.
The results in compression of chemoreceptors –> slow breathing down –> respiratory arrest.
Lesions in the cortex include:
Haemorrhage: [blue]
An Ischaemia event will result in swelling and oedema in the brain [red]
what effect do drugs have on the brain stem?
Drugs can also disrupt the brain stem:
Sedative drugs:
Decrease respiratory drive –> decrease effort of respiratory muscles –> decreased ventilation
Patients are given sedatives in Post-surgery
Patients can also overdose on sedatives.
Common sedative drugs:
Benzodiazepines
Morphine + other opiates
what neuromuscular disease (NMD) effect ventilation?
Examples of NMD that effect ventilation:
- Motor neurone disease (MND)
- Duchenne’s muscular dystrophy
They usually cause a chronic deterioration of respiratory function
what tests can you do to dentify NMD?
Spirometry –> low FVC
Transcutaneous CO2 monitoring overnight
Arterial blood gases –> abnormally high PaCO2 –> Type 2 respiratory failure
If you have chronic reduction in alveolar ventilation –> build of PaCO2.
what is a motor neurone disease (MND)?
what does it result in?
is it progressive?
MND: Degeneration of ventral horns in spinal cord where the UMN meets the LMN
As a result, you get a mixture of UMN and LMN pathology.
Symptoms usually start in the limbs or in the bulbar muscles (muscles of mouth/throat –> swallowing and speech)
This can result in:
Diaphragmatic weakness –> respiratory failure
Poor swallowing –> recurrent aspirations
MND is Progressive (fatal 2-5 years form diagnosis):
1 in 5 survive 5 years
1 in 10 survive 10 years
how do you manage respiratory failure in NMD?
No cures for NMD.
You also can’t reverse damages.
Treatment: support breathing via non-invasive ventilation (air through face/nasal mask)
Treatment will:
Reduces CO2 levels
Extends life
Improves QOL
describe the physiology of our breathing when we sleep
Relevant anatomy:
When we breathe in air needs to pass across a number of structures to get into the trachea.
Lots of these structures can get in the way. E.g, soft palate, tonsils, tongue, epiglottis.
what is sleep apnoea?
what stage of sleep does it happen?
Sleep apnoea: when breathing stops and starts during sleep
When we sleep we cycle between the Non-REM sleep and REM sleep
During the REM sleep:
- Decreased muscle tone
- Increases sympathetic NS activity
- This means in the REM sleep the muscles (tongue muscles, muscles the around neck, soft palate) relax.
- If these structures are abnormally large, they can close off airway –> Obstructive sleep apnoea
what is the difference between Hypopneas and Apnoea?
Hypopneas: abnormally slow or shallow breathing,
Apnoea : no breathing
Either can occur, depending on severity
This results in the reduction of O2 levels in the night.
what tests are done to diagnose sleep apnoea?
To diagnose obstructive sleep apnoea we do overnight sleep studies:
We measure, heart rate, air flow, how the abdomen and thorax are moving and O2 saturations.
When the airway obstructs:
- Airflow drops/stops
- Increase in thoracic effort
- You get paradoxical breathing: abdomen does not breathe synchronously the with thorax
- These results in decrease in O2 levels.
- A drop of more than 3% - defined as apnoea.
- This effect causes you to wake up and start breathing again.
describe the night time traces
what is the difference between the normal trace and obstructive sleep aponea trace?
Red: Oxygen staturation
Blue: Pulse Rate
Normal Trace:
- O2 satruation is maintained at 97%
- Pulse rate status steady througout the night
Obstructive Sleep Aponea:
- Lots of episodes where greater than 3% decrease in O2 saturation
- More than 30 3% dips –> OSA
- When this happens, you get an increase in SympaNS stimulation –> tachycardia
what are the clinical features of OSA?
Characteristics:
- Snoring
- ‘Choking’ during the night
- Daytime sleepiness (Never get a deep sleep as you are constantly being woken up)
- This can be very dangerous if patient drives around (fall asleep behind the wheel)
- Patients with OSA must advise the DVLA
- Morning headaches: hypoventilation at night –> CO2 rises –> Headache. When you wake up you breathe normally –> clear CO2 –> no more headaches.
what conditions is OSA associated with?
- Obesity
- Craniofacial abnormalities (large tongue, inset mandible etc.)
- Downs syndrome (due to cranio-facial abnormalities)
- Tumour in soft palate
- Acromegaly –> enlargement of soft tissue and mandible.
- Treacher-Collins syndrome –>small jaw (micrognathia) - require Surgical correction
what does PE look like on CXR?
- Often normal
- Subtle anomalies
- Basal atelectasis: little bits of lung collapsed on themselves
- Hampton’s hump: Pleural based wedge shape of increased opacity
- Westermark’s sign: hypovolaemia (due to interrupted blood flow)
- Looks darker than the normal side
- Small effusion in costophrenic angles
- Rarely you may see infarction with cavitation
what is a CT pulmonary angiogram?
what does it show?
It is the Gold standard for PE diagnosis
It consists of a CT scan of chest with contrast to identify pulmonary arteries and vessels
Clot shows up grey (whereas contrast (white) cannot reach)
Clot in main pulmonary artery causes back pressure on heart meaning on the CT the right heart looks bigger than left (left supposed to be bigger)
when is a VQ scan used?
- Used in pregnancy or breast cancer (avoid radiation)
- Inject radio isotope and inhale radio isotope –> used to see V/Q mismatch
- In PE you can see a V/Q mismatch
- Lack of perfusion to areas but adequate ventilation.
what is the Aetiology (causes) of PAH?
- Thromboembolic disease (clots)
- Chronic lung disease (COPD)
- Hypoxia: Hypoxia causes vasoconstriction within pulmonary arterial system which leads to pulmonary hypertension.
- Idiopathic: problem in vascular bed itself for which we do not know the cause.
- Left sided heart disease (coronary heart disease) causes back pressure on right heart –> pulmonary hypertension
