Respiratory failure Flashcards
Whats resp failure?
What 2 things can cause it?
Common medical emergency in A&E with non specific sx, eg mild confusion or agitation.
Oximeter: o2 sats from finger or earlobe- falsy reassuaring - not good when :1. pt is on oxygen. They will not detect alveolar hypoventilation, producing high levels of pCO2.
All unconscious patients should have ABGs taken.
Causes: 1. Resp pump failure 2. I trinsic lung disease
What happens in respiratoty pump failure?
Arterial pCO2 is ⬆️.
- Severe airflow limitation. Eg COPD
- Neurological depression- coma, sedatives, overdose.
- Chest wall problem: flail chest, pneumothorax.
- Neuromuscular prob- Guillain Barre, old poliomyelitis.
What happens in intrinsic lung disease?
(Apart from COPD)- Hypoxaemia is often combined with a reduced PaCO2.
Hypoxaemia arises from V/Q miscmatch. - ventilation perfusion in the pulmonary alveolar bed.
Hypoxic stimulation of ventilation coupled with abnormal respiratoty sensation–> leads to a reduced arterial pCO2 (alveolar hyperventilation).
⬆️ PaCO2 indicated impending resp arrest as it suggests:
1. Either a reductiom in ventilatory effort or
2. A Failure of the respiratory pump.
What should we consider in hypoxia and reduced PaCO2?
- ie HYPERVENTILATION- breathing fast to clear that CO2 out, but no right time to fill lungs with oxygen.
Infection- eg pneumonia
Shock- eg sepsis, hypovolaemia, acute lung injury .
Asthma
Cardiac disease: eg LVF, pulmonary HTN.
Pulmonary embolism
Why are ABGs necessary in resp failure?
Asses severity
Identify type, alveolar hypo and hyperventilation
Any compensation? Chronicity of problem
A coexisting metabolic acidosis- Base excess.
In ABGS essential to note FiO2- inspiratory o2 concentration.
Respiratory acisosis- what happens?
- CO2 clearance is reduced.
- There is alveolar hypoventilation.
- PaCO2 + (H+) rise.
- Examples: COPD, flail chest, Guillain -Barre syndrome.
What happens in resp alkalosis?
- Alveolar hyperventilation and both PaCO2 + H+ are ⬇️.
- HCO3 slightly ⬇️.
- Examples: Asthma, anxiety attack.
What hapoens in metabolic acidosis?
- Disturbance of bicarbonate regulation(drops) or H+ production.(goes up?)
- HCO3 ⬇️
Sooooo 3. PaCO2 falls due to resp compensation.- trying to create balance. - Examples: DKA, Renal failure, shock.
Metabolic alkalosis: what hapoens?
- HCO3 ⬆️. +
- Relative hypoventilation–> smaller compensatory increase in PaCO2.
- Examples: Xs vomitting, profound hypokalaemia.
What are the common ABG values?
FiO2- 21%. pH~7.4 PaO2->10 kPa PaCO2- 4.5-6 kPa HCO3- 24-28mmol/L
To convert from kPa to mmHg- multiply by 7.5.
The pH changes by 0.1 per 1kPa change in PaCO2.
What are some common ABG abnormalities?
- Life threatening asthma
- Acute or chronic respiratory F in Pts w/ COPD
- Severe pneumonia.
What happens in life threatening asthma attacks?
pH: 7.2 PaO2- 15.4 PaCO2: 6 HCO3: 16.2 BE: -7.3
Note high O2.. Supplemental O2 provided. Metabolic acidosis- pH and BE. As a result of metabolic demands exceeding O2 delivery and producing a lactic acidosis. Airflow limitation limits the normal respiratory compensation to this profound acidosis.
What happens in Resp F in COPD pts?
pH: 7.3 PaO2: 25.2 PaCO2: 12.6 HCO3:42.1- renal compensation BE: +4.3
Acute or chronic respiratory acidosis exacerbated by a high FiO2 using masks. (40-60% O2)
Patient changed to 28%.
As high oxygen will stop resp drive, letting CO2 to accumulate.
What happens in severe pneumonia? (FiO2 60%)
pH: 7.15 PaO2: 4.8 PaCO2: 3.5 HCO3: 12.5 BE: -9.3
Despite a high FiO2- pt hypoxaemic cz of ventilation perfusion mismatch. This profound hypozaemia-
Need for urgent intubation and IPPV and are a reflection of circulatory failure resulting from septic shock.
How so we manage resp F?
🔸CXR,
🔹Call anaesthetist?
🔸Semi-elective intubation preferred to resp arrest; performed in ward, b4 ICU transfer.
How do we recognise resp arrest?
🔹Tachycardia >120
🔸Tachypnoea, RR >30
🔹Hypotension
🔸Sympathetic activation: pale and sweaty, agitation, confusion
🔹Progressive increase in PaCO2 or fall in PaO2
🔸Rapid desaturation on disconnection from O2- eg when drinking or coughing.
Evaluation: end of bed- is pt tired?
Treating the cause
♦️Tension Pneumothorax- intercostal drain- or large pleural effusion.
🔹Neurological coma: intubation necessary for airway protectiom or to manage ⬆️ICP by hyperventilation.
🔶Drug induced resp F- can be confired by a theraputic trial pf specific antidote- i.e bolus injection naloxone for opiates and flumazanil for benzodiazepines.
🔷Oxygen supplementation- via fixed performance mask in COPD.
What are coarse crackles an indication for?
Retained secretions eg in COPD.
65 Y Male with advanced COPD ADMITTED WITH HX OF COUGH AND PURULENT SPUTUM. his RR was 35, BP 170/90, sweaty, O2 sats 72%, PaO2:5.8, paCO2: 8.1, HCO3: 28.
What do these gases mean?
Hypoxaemia withn mild acute resp acidosis. No evidence of chronic resp F with chronically elevated PCO2 as HCO3 is normal. Ie no compensation.
Initial tx at A+E
- Nebulised bronchodilators- salbutamol 5mg nebulised. + ipatropium bromide 500mikrograms.
- 28% O2 by Venturi mask- controlled mask.
- IV amoxicillin( erythromycin if pt pen allergic)
- IV steroids- hydrocortisone 100mikrog x3 daily.
- Encourage to clear secretions- sit pt up attend physiotherapist.
- CXR to exclude pneumothorax or demonstrate assc pneumonia.
What do we mean by controlled mask?
Venturi mask- leads to intermittent therapy- not tolerated well by agitated or confused breathless patients.
Nasal prongs oxygen at 1/2L/min is more effective and continuous but not controlled.
What is non invasive ventilatory support?
BiPap with tight fitting facial mask
“Spontaenous pressure support or time breaths” (pressure controlled ventilation.
An exhalation valve reduces re-brreathing.
NIV is succesful in~ 70% of pts with Resp F from COPD.
SHOULD NOT PROCEED if intubation more appropriate.
What are some CI of NIV?
Unconsious/ uncooperative Vomiting Large amount of resp secretions Cardiovascularly unstable (beware hypotension) Recent facial or upper airway surgery Recent Upper GI surgery Inability to protect airway by reflexes.
Whats mechanical ventilation?
What are the aims of intubation and mechanical ventilation?
Why is hypotension after intubation very common?
In an unstable situation- essential to maintain oxygentation.
Refer to ITU for hard intubation pts.
aims of intubation and mechanical ventilation:
- Immediat correction of hypoxaemia
- Slower correction of hypercapnia
- Allow effective suctioning of resp secretions.
Hypotension:
- Vasodilation caused by sedatives.
- High airway pressures limiting venous return and causing a fall in CO.
- A fall in sympathetic tone.
