Session 7 - Lecture 1 - Hypoxia & Respiratory Failure Flashcards
1 - Dr Sita Nanayakkara
Hypoxaemia and respiratory failure
“clear up concepts, e.g. ventilation mismatch in Session 4, covering that in a bit more detail, so be quite clear”
2 - Hypoxia & Hypoxaemia
Hypoxia & Hypoxaemia
• Hypoxaemia - low pO2
in blood
• Hypoxia - O2 deficiency at tissue level
Tissues can be hypoxic without hypoxaemia (eg anaemia, poor circulation)
However, generally, the term hypoxia is used to include hypoxaemia as well
Normal ranges
• O2
saturation 94 -98% Anything below LLN is hypoxaemia
• pO2 9.3 – 13.3 kPa (UHL)
Tissue damage most likely when
• O2 saturation < 90%
• pO2 < 8 kPa
• These levels used to diagnose Respiratory failure
“So to start, I just want to make the distinction between hypoxaemia which is a low O2 contained in blood, low pO2 in blood and low O2 sat in blood; whereas term hypoxaemia means O2 def at tissue level, so tissues can be hypoxic w/o hypoxaemia e.g. if you had a thrombus or embolus occluding the femoral artery now that leg is going through tissues in leg become hypoxic, but ABG on that pt the pO2 in blood will be normal, lugns oxygemated will happen normally, so can have tissue hypoxia due to conditions like poor circulation or anaemia, w/o having a problem with blood gases or low pO2 in blood – so first concept to get head round. And then, just to define what you mean by hypoxaemia – normal ranges based on what we used in UHL currently, anything below lower limit of normal (LLN) is called hypoxaemia, but the body can cope with mild degrees of hypoxia, tissue dmg becomes most likely when O2 sat <90% and pO2 <8 kPa, so those lvls are used to define resp failure, so then we would say that would be resp failure. “
3 - Respiratory failure
Respiratory failure
Impairment in gas exchange causing hypoxia with or without hypercapnia
• Type 1 Respiratory failure
• low pO2 < 8 kPa or O2 saturation <90% breathing room air at sea level
• pCO2 normal or low
• Type 2 respiratory failure
• low pO2 + high pCO2
“Okay, so, resp failure is basically where there is an impairment in gas exchange causing hypoxia with or w/o hypercapnia – going to do in this lecture will consider what diseases will give you which – and which ones will affect both gases, if only 1 parameter affected then type 1 – easy to remember, type 1 = 1 of the gases which is always hypoxia. On the other hand, sometimes others will cause a drop in O2 and a rise in Co2, in that situation, we say that person has type 2 resp failure – both gases are affected. Okay, so what I’m going to do now is”
4 - Hypoxia may caused by
Hypoxia may caused by
- Low inspired pO2-
- Hypoventilation – (respiratory pump failure)
- Ventilation/Perfusion mismatch
- Diffusion defect – problems of the alveolar capillary membrane
- Right to left shunt (eg. Cyanotic heart disease)
“just look at how we maintain or how hypoxia mainly may arise, so if we just think about the steps by which the blood acquires O2 and gets rid of CO2, we need to breathe in air, and air we breathe should be having normal amounts of O2 in atmosphere, so if we were inspiring air v thin such as top of mountain, then have low inspired pO2, which can cause hypoxia. Secondly, so that’s a v more environmental problem rather than problems with lungs – red are conditions where lungs are involved. Let’s say we are all here in sea lvl, breathing in and out, resp muscles and chest wall generate/stretch lungs. If mechanism is not working, e.g. resp muscles weak; chest wall deformed, then you have hyperventilation, then giving rise to hypoxia + hypercapnia (explained shortly). So air then moves to lungs, but that air then has to meet blood, so match up ventilation to perfusion, so if that is not happening, then we have a ventilation/perfusion mismatch, and can cause hypoxia, and finally assuming we have air and blood diffusion meeting at interface, if problems in alveolar capillary membrane, can again cause hypoxia – main conditions that can cause hypoxia involving lung and cause resp failure. Can still have hypoxia if R to L shunt even if lungs perfectly normal e.g. cyanotic heart disease e.g. Tetralogy of Fallot – R to L side, entirely bypassing lung, clearly that will also give you hypoxia. But today we are only going to talk about these 3 conditions, bc our brief is to talk about resp – conditions that affect the lungs.”
5 - Overview: Ventilation and Perfusion of the whole lung
Overview: Ventilation and Perfusion of the WHOLE lung VOLUMES - Tidal volume 500 ml - Anatomic dead space 150 ml - Alveolar gas 3000 ml - Pulmonary capillary blood 70 ml - Total ventilation 7500 ml/min Frequency 15/min - Alveolar ventilation 5250 ml/min / ~1 - Pulmonary blood flow 5000 ml/min From Respiratory Physiology THE ESSSENTIALS by John B West
6 - 1. Hypoventilation
- Hypoventilation
• When the ENTIRE LUNG is poorly ventilated
• Alveolar ventilation (minute volume) is reduced.
• Amount of O2 ENTERING BLOOD and CO2 entering alveolus per minute remains unchanged (since metabolic rate is the same)
• Alveolar pO2 falls arterial pO2 falls – hypoxaemia
• Alveolar pCO2 rises arterial pCO2 increases hypercapnia
“So hypoventilation, is a situation where the entire lung is poorly ventilated, so I want to maintain that this is the entire lung – not just part of lung – important distincting, this is where you’re not moving air into and out of lung. Min vol we calc will be reduced – however, perfusion will be 5L will be same, and blood going through lung picking up as much O2 as it could before and giving as much CO2 as it was before, bc metabolic rate hasn’t changed, so amount of O2 picked up in lungs depends how much O2 is being consumed, so stop ventilating, amount of CO2 being given up into lungs will remain constant, so what has changed, not shifting as much air in and out per min as previously, so alveolar pO2 will fall, so take away same amount of O2, but not moving as much O2 into lung as before. And the opposite will happen for CO2, so when the alveolar pO2 falls, the pO2 falls, so hypoxaemia and alveolar pCO2 rises so hypercapnia, so new eqm reaches, so high lower pCO2 or higher.”
7 - Hypoventilation - Important
Hypoventilation - Important
• Hypoventilation ALWAYS causes hypercapnia
• Therefore causes Type 2 respiratory failure
with both hypoxia + hypercapnia
“Now here’s a v v important point to remember about hypoventilation. Okay, it ALWAYS causes hypercapnia, so always with hypoventilation always causes pCO2 to be high, so do an ABG so see increased CO2 – should tell you that person is not moving enough air in and out of lungs – raise the q of whether we have to support his ventilation – do we need to assist him in breathing to get rid of CO2 to correct the situation, so 1 v important take away msg – when you see CO2 raised (and obvs O2 low) – not enough to just give O2, think about perhaps ventilation. So hypoventilation is always Type 2 (both hypoxia + hypercapnia)”
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Acute Hypoventilation • Need urgent treatment • +/- artificial ventilation E.g. • Opiate overdose • Head injury • Very severe acute asthma
Chronic Hypoventilation
• Chronic hypoxia and Chronic hypercapnia
• Slow onset and progression
• Time for compensation
• Therefore better tolerated
e.g. Severe COPD
• most common cause of chronic type 2 respiratory failure
• Acute exacerbations may occur due to LRT infection
“So now if you think about this situation, if it’s something that happens v quickly, supposing someone has like in the formative q – opiate OD, happens within mins, hav hypoxia & hypercapnia, and body doesn’t have much time to compensate for that, going to be q a big shift – pts will need urgent treatment, including perhaps artificial ventilation – maybe give antidote immediately (naloxone) may be able to ventilate immediately, but you have to be ready if not. But these are real emergencies that need ITU care. Now what if this comes on v gradually like COPD, CO2 increase v small and O2 drop v small, that allows amount of compensation to take place, therefore better tolerated – so you will have pts with type 2 chronic resp failure who are at home, they’re exercise tolerance will be impaired, symptomatic but able to carry on, so the condition you are most likely to encounter with chronic hypoventilation is severe COPD – v common condition, some group of COPD pts with chronic hypoventilation and therefore chronic type 2 failure. One thing to remember about these groups of pts is managing about these things if okay, example chest infection, might tip them over to acutely compensated – so q often these pts with chronic COPD get chest infection, pushes them onto acute-on-chronic resp failure, now there’s a lil worsening, acute-on-chronic resp failure, acute exacerbations may occur – when they have them, again they may mean urgent treatment, may need to support their ventilation. So, is everyone okay with that?”
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See IMGs
“Right so this is where I thought I’d talk you through the causes of hypoventilation by drawing a diagram, so, let’s just see, right, so, what I’ve drawn here, okay so that’s the cerebral cortex, here’s the brainstem, and this is where we have our resp centre. So the resp centre originates in centre which travel down the spinal cord, and having travelled down spinal cord will leave in various peripheral nerves, and then they will synapse on the nerve cell body of nerve, so for example, this may well be the phrenic nerve. Okay. And so this segment therefore will be somewhere between C3-C5, so cervical spine, so an UMN has come and given a message to the cell body of the phrenic nerve. So that then travels down phrenic nerve, and lower down, similar messages will be going to intercostal musclesa s well. Oh, is that okay? Right so here are the NMJs, and these are the muscles. So we can think of various conditions, and the easiest way to remember the conditions is to think about what can happen in the brainstem for instance. We already said narcotics. Strokes, and so on. And in the spinal cord, remember we are talking about the cervical spine (Cx spine) – can you hear me all right at theb ack there, Cx spine bc the phrenic nerve is the most important nerve it is important bc the diaphragm is the most impotant muscle of resp, the diaphragm is responsible for ~70% of chest expansion is from diaphragm, so we are interested, Cx spine is important bc roots of phrenic nerve are C3, C4 and C5. So if you have some kind of injury to Cx spinal cord – trauma, that can then cause acute hypoventilation bc those messages to resp centre are no longer getting down. Damage to cervical spine, road traffic accidents or something. So next I’m going to come down to phrenic nerve and IC nerve, affected by disorders that involve nerves – don’t know about this condition yet but you can read about it – it’s called Guillain-Barre syndrome, sorry move it up, okay, right, so that’s an acute polyneuropathy – acute meaning usdden onset – poly meaning many, neuropathy – disorder involving nerves – both the nerves, classic story start feeling weak in legs, then over next 2-3 days find weakness spreading upwards, can’t cough bc chest muscles and abdo muscles feel work, and then extend further out toward neck, then phrenic nerves. So good thing about it, just look after them to support them, and various other therapies used, usually make a full recovery. And can anyone thing of any injuries that involve the NMJ. What is the NT there – ACh (MG). Antibodies against ACh, remember someone said, MG, so some pts with MG can get an acute worsening and find they can’t breathe. Okayi n the morning, then as evening goes on, find it hard to breathe. So don’t know a lot about these conditions, just give framework to think about these causes. COnditions in muscle itself like myopathy. So in otoher words, all these conditoons we talked about are neuromuscular problems okay. So lugn itself, healthy, and its; really a pump problem, okay. Right, so so far so good. But we have to now move on and realise that’s not the only cause, so we can have problems, if the chest wall is abnormal. Okay, so for example, if v deformed, half of lung expand in muscles, expand, need a normal thoracic, if a person had morbid obesity for instance, if their spine was v curved, okay. So don’t bother with writing Iv’e got a massive list coming up I’m just talking you through – chest wall abnormalities, it’s not a massive list actually. And finally, problems with the lungs themselves – where lungs are v v stiff, get outstretched, or, let’s draw a lung then, or the air that enters has to reach the lung through alveolus, what if lung is severely narrowed, and v widespread, then again you can’t inflate the lung. All right so that’s just about the causes, let’s just go back now to our slides. Okay, erm, “
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