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Respiratory Failure Diagnosis and Management PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Respiratory failure: Diagnosis and management" by Dr Victor Duong.

This medical PowerPoint presentation talks about respiratory failure, a condition where the respiratory system is unable to maintain adequate oxygenation and/or carbon dioxide elimination in the body. It is a serious condition that requires immediate medical attention. This PowerPoint presentation discusses the diagnosis and management of respiratory failure.

Tags : respiratory failure, diagnosis of respiratory failure, management of respiratory failure, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 1919 | Downloads : 7

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Slide 1-

Respiratory failure:Diagnosis and management Dr Victor Duong Respiratory Registrar Slides provided by Dr Liam Hannan, Respiratory and Sleep Physician
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Overview Assessing respiratory failure Hypoxaemic respiratory failure Hypercapnic respiratory failure Bilevel PAP CPAP Cases and ABGs
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Respiratory failure Simplest method to differentiate – do an ABG Type I = hypoxaemic Type II = hypercapnic = ventilatory failure = respiratory acidosis
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Respiratory failure – Type I Hypoxaemic Alveolus
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Respiratory failure – Type I Differentials Alveolar problem – fluid, pus, destruction, collapse Circulation problem – V/Q mismatch, PE, shunt, destruction Interstitial problem – fibrosis, infiltration
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Respiratory failure – Type I By definition there is no problem with ventilation Options: High flow oxygen CPAP – for pulmonary oedema +/- atelectasis Bi-level – immunocompromised with LRTI (ICU) Invasive ventilation – where above fails (and failure can occur very quickly!)
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Evaluating ventilatory (type 2) failure Excess load or reduced capacity (=can’t breathe) Lung problem Chest wall problem Muscle problem Reduced drive (=won’t breathe) Drugs Central pathology Sleep problem (usually have load/capacity problem too)
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Ventilatory failure (T2RF) PaCO2>45mmHg Exacerbation of COPD Obesity hypoventilation syndrome Chest wall/neuromuscular – respiratory muscle weakness Progression of Type I cause (prior to respiratory arrest) Central – CNS depression/trauma/medications (opioid/BZDs)
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Respiratory failure – Type II Ventilatory failure → needs ventilation Exclude reversible causes (particularly drugs, oxygen) Ventilate – invasive vs non-invasive (Bi-level)
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Bi-level Limited (proven) indications COPD Neuromuscular disease Obesity hypoventilation Type I respiratory failure in immunocompromised patients with LRTI or pulmonary oedema Other uses are not proven
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Traps Asthma Classic temptation – evidence is generally lacking Elevated PaCO2 due to asthma precedes death by only a short period CO2 should generally be low in asthma exacerbation
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Traps Altered conscious state Chicken or egg scenario Contraindication to non-invasive therapy (no airway protection provided + theoretical aspiration risk from FFM) Exclusion of reversible causes and airway protection are the priority
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Settings, what settings? EPAP (and CPAP) = 1cmH2O for every 10kg of body weight 70kg male – 7cmH2O if over 100kg - start at 10cmH2O IPAP = start 4-6cmH2O above the EPAP Repeat the ABG (1-2hrs) and titrate settings: increase EPAP if oxygen requirements high increase PS (IPAP-EPAP) if CO2 high/pH low
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Continuous PAP Fixed pressure applied via face mask Provides a constant/continuous pressure throughout the respiratory cycle Does not provide ventilatory support Doesn’t offload respiratory muscles or lower PaCO2 What is CPAP?
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OSA Splints the upper airway during sleep APO increased intrathoracic pressure – decreased venous return decreased atelectasis and alveolar collapse does not affect ventilation/CO2 How does CPAP work?
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How to get CPAP or bilevel for your patient: Do an arterial blood gas Think carefully about the underlying diagnosis Speak to the respiratory registrar
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ABGs vs VBGs
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Why venous? Venous blood gases (VBG) have been considered as an alternative to arterial (ABG) to assess breathless patients Why? Safer? Better? Easier?
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Safer? For the patient Up-to-date data demonstrating harm from ABG just doesn’t exist Complication rate from arterial catheters 2.5% (which is why we do punctures) For the clinician Similar needlestick injury rates (both comprised 1% of all needlestick injuries in a 12 month period) Much safer than suturing (46% of injuries) or IM/SC injections (24% of injuries)
Slide 20-

Better? Correlation between PaCO2 and PvCO2 is good because they are physiologically linked (strength of relationship between two variables) Agreement between PaCO2 and PvCO2 is poor (relationship between two tests that attempt to measure the same thing) Limits of agreement are wide (-17 to +24mmHg in one review, more recent -10 to +3mmHg)
Slide 21-

VBG pH 7.32 PvCO2 50 PvO2 45 PvHCO3 30 95% confident that arterial pH is 7.35-7.36 95% confident that PaCO2 is between 40 and 53mmHg
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Easier? Yes VBGs are easier But that’s not really a justification for performing them
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Case 1 FiO2 0.21 pH 7.48 (7.35-7.45) pO2 45 (80-100) pCO2 37 (35-45) HCO3- 27.5 (22-32)
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Case 2 FiO2 0.21 pH 7.20 (7.35-7.45) pO2 62 (80-100) pCO2 90 (35-45) HCO3- 28.2 (22-32)
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Case 3 FiO2 0.21 pH 7.43 (7.35-7.45) pO2 49 (80-100) pCO2 54 (35-45) HCO3- 33.6 (22-32)
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Case 4 FiO2 0.21 pH 7.41 (7.35-7.45) pO2 60 (80-100) pCO2 50 (35-45) HCO3- 28.8 (22-32)
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Examples Drunk patient, SpO2 92% but comes up with oxygen ABG pH 7.15 CO2 63 What is the respiratory rate likely to be? Likely to be very low RR – 5-6bpm – and he may not be drunk as something is likely to be impairing his drive to breathe (drugs, CNS pathology)
Slide 31-

Examples Young asthmatic patient – RR 34, SpO2 93% ABG – PaCO2 47mmHg, pH 7.38 In trouble or doing OK? In BIG trouble – probably close to maximal respiratory effort but unable to keep CO2 down Needs ventilatory support ASAP
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Examples Elderly male with COPD – RR 28, SpO2 88% on oxygen therapy ABG pH 7.30 CO2 50 What evidenced-based, life saving treatment should he get? Bilevel PAP please don’t say CPAP!!
Slide 33-

Examples Elderly female, current smoker with clinically moderate AECOPD – SpO2 91% on 2LNP, RR=24 VBG pH 7.27 PvCO2 49 What should you do next? Do an ABG please! Might be an excellent candidate for bilevel
Slide 34-

Take home messages ABGs remain a vital component of the assessment of a breathless patient and reliably monitoring their response to therapy Differentiating hypoxaemic from hypercapnic respiratory failure is useful both for diagnostic and management purposes Evidence supports bilevel therapy predominantly for hypercapnic respiratory failure – except in immunocompromised and APO If you think your patient needs bilevel or CPAP, do an ABG and speak to the Respiratory registrar
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Questions?