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1 week into placement, I have taken the lead on a patient who is nearing discharge. I visited the patient to attempt to do a stairs assessment earlier that day, and deemed it not safe to do so until I had consulted the medical team, since his blood pressure was around 178/52. When it came time for the MDT meeting, I was the only member of the physiotherapy team present, so brought up the issue of the patient's BP. His consultant said that this was fine and that I should continue with the stairs assessment. I wanted to specify that I'd like the doctor to document this before I saw the patient, so that I could evidence having consulted the medical team in case anything went wrong, however I was nervous confronting the consultant about this and worried I was holding up the meeting.

I realised later that day that the consultant had not documented this confirmation. And, whilst I wasn't surprised, this was frustrating and meant that I had to reprioritise my afternoon and the afternoon of the band 5 physio accompanying me for the session.

I later found out that the original consultant had gone home, so I went to speak to another doctor, who was now managing my patient. This time, I specified that I needed written confirmation that she was happy for me to continue with this patient, and she agreed. I went to see another patient, giving this consultant another half hour or so to document our conversation in case she was busy. However, when I returned, there was still no note on the patient's records. I went back into this doctor's office and reiterated my request for documentation, and eventually she wrote a medical note on the patient’s record. I was then able to proceed with the stairs assessment, which has led to the patient's imminent discharge.

Waiting around for documentation led to a significant waste of my time and that of the physiotherapist supervising me, and potentially led to a later discharge for the patient. This could have been avoided if my communication was clearer.

If I had expressed my specific needs in the MDT meeting to begin with. The consultant could have documented our discussion much sooner, saving everyone time.

If I had been clearer with the second consultant that I wasn't comfortable seeing the patient without her documentation, she may have done it the first time I asked rather than me having to try again later and wait.

In the future, I will try to be more concise and specific with my communication within the MDT.

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https://open.spotify.com/episode/7LAWM6WvJsKuqk8RMQv5Go?si=SF8bPRsnT2SmVSre-_3pMg

‘Dr. Matt and Mike’s medical podcast’ - Delirium.

Professor Andy Teodorczuk

Delirium is described here as an acute brain failure.

Prof. Teodorczuk discusses the need for clearer diagnosis of delirium, factors leading to ‘incident’ vs ‘prevalent’ delirium, and ways in which we might prevent and treat it.

Cognitive reserve is described as space in a cup. When the cup fills up and spills over, we see delirium.

Neurodegenerative diseases such as dementia can be masked in their severity by the patient having a high cognitive reserve or high baseline cognition.

Factors that may pre-dispose people to delirium:

Age

Neurodegenerative disease such as dementia

Sensory impairment eg. hearing loss, vision loss

Frailty

Acute causes (PINCH ME):

Pain -

Infection - such as UTI's are a common cause of delirium. Pts may be at higher risk of infection due to certain medications.

Nutrition -

Constipation -

Hydration -

Medication - Perhaps the most common cause of incident delirium in the hospital setting.

Environment - Hospital environment contains a lot of new stimuli which may be confusing for a patient. Patients also frequently don't sleep well in hospital.

25% of ED patients will experience delirium.

Preventing incident delirium:

familiar pictures

family visits

reducing/ minimising/ reviewing medication

Appropriate pain management

Further reading:

Stress-Vulnerability model

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Listen to this episode from Dr. Matt and Dr. Mike's Medical Podcast on Spotify. This episode was an eye opener! Delirium is poorly understood and very common. Luckily, Professor Andy Teodorczuk is here to help us understand what Delirium is and how it is treated. Want to support us?

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Functional Ax reflection

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Schreier AM. Nursing care, delirium, and pain management for the hospitalized older adult. Pain Management Nursing. 2010;11(3):177–185.

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Schreier AM. Nursing care, delirium, and pain management for the hospitalized older adult. Pain Management Nursing. 2010;11(3):177–185.

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Patients who received opioid pain relief were more likely to develop mild rather than moderate or severe delirium.

Generally worse pain management seems to cause more severe delirium, regardless of any effects of the pain medication itself, whether that is directly causing delirium or indirectly such as by causing constipation.

One of the reasons older pts are not prescribed opiate medication in the ED is because of the risk of delirium, this study may suggest that pain carries more weight in causing this phenomenon and therefore should be treated as a priority (Nassisi D, Korc B, Hahn S, Bruns J, Jagoda A. The evaluation and management of the acutely agitated elderly patient. Mount Sinai Journal of Medicine. 2006;73(7):976–984 also supports this).

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Delirium is an acute, transient, usually reversible, fluctuating disturbance in attention, cognition, and consciousness level. Causes include almost any disorder or drug. Diagnosis is clinical, with laboratory and usually imaging tests to identify the cause. Treatment is correction of the cause and supportive measures.

Delirium may occur at any age but is more common among older people. At least 10% of older patients who are admitted to the hospital have delirium; 15 to 50% experience delirium at some time during hospitalization. Delirium is also common after surgery and among nursing home residents and intensive care unit (ICU) patients. When delirium occurs in younger people, it is usually due to use of a drug (recreational drug or medication) or a life-threatening systemic disorder.

Delirium is sometimes called acute confusional state or toxic or metabolic encephalopathy.

Delirium affects mainly attention, is typically caused by acute illness or drug toxicity (sometimes life threatening), and is often reversible.

Dementia affects mainly memory, is typically caused by anatomic changes in the brain, has slower onset, and is generally irreversible.

1. Fong TG, Inouye SK:The inter-relationship between delirium and dementia: The importance of delirium prevention. Nat Rev Neurol 18 (10):579-596, 2022. doi: 10.1038/s41582-022-00698-7

The most common causes of delirium are the following:

Many other conditions can cause delirium (see table ). In about 10 to 20% of patients, no cause is identified.

Predisposing factors include brain disorders (eg, dementia, stroke Overview of Stroke Strokes are a heterogeneous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurologic deficit. Strokes can be Ischemic (80%), typically resulting... read more , Parkinson disease), advanced age, sensory impairment (eg, impaired vision or hearing), alcohol intoxication, and multiple coexisting disorders.

Precipitating factors include use of drugs (particularly ≥ 3 new medications), infection, dehydration, shock, hypoxia, anemia, immobility, undernutrition, use of bladder catheters (whether urinary retention is present or not), hospitalization, pain, sleep deprivation, and emotional stress. Unrecognized liver or kidney failure may cause medication toxicity and delirium by impairing the metabolism and reducing the clearance of a previously well-tolerated medication.

Recent exposure to anesthesia also increases risk, especially if exposure is prolonged and if anticholinergics are given during surgery. After surgery, pain and the use of opioid analgesics can also contribute to delirium. Decreased sensory stimuli at night may trigger delirium in at-risk patients.

Mechanisms are not fully understood but may involve

Stress of any kind upregulates sympathetic tone and downregulates parasympathetic tone, impairing cholinergic function and thus contributing to delirium. Older people are particularly vulnerable to reduced cholinergic transmission, increasing their risk of delirium.

Regardless of the cause, the cerebral hemispheres or arousal mechanisms of the thalamus and brain stem reticular activating system become impaired.

Symptoms and Signs of Delirium

Delirium is characterized primarily by

Consciousness level fluctuates; patients are disoriented to time and sometimes place or person. They may have hallucinations, delusions, and paranoia. Confusion regarding day-to-day events and daily routines is common, as are changes in personality and affect. Thinking becomes disorganized, and speech is often disordered, with prominent slurring, rapidity, neologisms, aphasic errors, or chaotic patterns.

Symptoms of delirium fluctuate over minutes to hours; they may lessen during the day and worsen at night.

Other symptoms may include inappropriate behavior, fearfulness, and paranoia. Patients may become irritable, agitated, hyperactive, and hyperalert, or, conversely, they may become quiet, withdrawn, and lethargic. Very old people with delirium tend to become quiet and withdrawn-changes that may be mistaken for depression. Some patients alternate between the two.

Usually, patterns of sleeping and eating are grossly distorted.

Because of the many cognitive disturbances, insight is poor, and judgment is impaired.

Other symptoms and signs depend on the cause.

Delirium, particularly in older patients, is often overlooked by clinicians. Clinicians should consider delirium (and dementia) in any older patient who presents with impairment in memory or attention.

Correcting the cause (eg, treating infection, giving fluids and electrolytes for dehydration) and removing aggravating factors (eg, stopping medications or drugs) may result in resolution of delirium. Nutritional deficiencies (eg, of thiamin or vitamin B12) should be corrected, and good nutrition and hydration should be provided.

Morbidity and mortality rates are high in patients who have delirium and are admitted to the hospital or who develop delirium during hospitalization; 35 to 40% of hospitalized patients with delirium die within 1 year. These rates may be high partly because such patients tend to be older and to have other serious disorders.

Because delirium greatly worsens prognosis for hospitalized patients, prevention should be emphasized. Hospital staff members should be trained to take measures to maintain orientation, mobility, and cognition and to ensure sleep, good nutrition and hydration, and sufficient pain relief, particularly in older patients. Family members can be encouraged to help with these strategies.

The number and doses of medications should be reduced if possible.

Delirium is more common among older people. About 15 to 50% of older patients experience delirium at some time during a hospital stay. For older patients in an ICU, risk of delirium (ICU psychosis) is particularly high.

Stress of any kind impairs cholinergic function, thus contributing to delirium. Older people are particularly vulnerable to reduced cholinergic transmission, increasing their risk of delirium. Anticholinergic medications can contribute.

Delirium is often the first sign of another, sometimes serious disorder in older people.

Causes of delirium in older people often include less severe conditions:

Certain age-related changes make older people more susceptible to developing delirium:

The most obvious symptom of delirium, confusion, may be harder to recognize in older people. Younger people with delirium may be agitated, but very old people tend to become quiet and withdrawn-changes that may be mistaken for depression. In such cases, recognizing delirium is even harder.

If a psychosis develops in an older person, it usually indicates delirium or dementia. Psychosis due to a psychiatric disorder rarely begins during old age.

Memory impairment and inattention may also be the initial symptoms of delirium in older people.

In older people, delirium tends to last longer, and recovery may be slow (days to even weeks or months), resulting in longer hospital stays, increased risk and severity of complications, increased costs, and long-term disability. Some patients never fully recover from delirium.

Because older patients are more likely to have dementia, delirium is often overlooked by clinicians. Clinicians should consider delirium in any older patient who presents with impairment in memory or attention.

NOTE: This is the Professional Version. CONSUMERS: View Consumer Version

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Delirium - Neurologic Disorders - MSD Manual Professional Edition

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Delirium - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - Medical Professional Version.

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NICE guidelines for delirium

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Delirium: prevention, diagnosis and management in hospital and long-term care

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This guideline covers diagnosing and treating delirium in people aged 18 and over in hospital and in long-term residential care or a nursing home. It also covers identifying people at risk of developing delirium in these settings and preventing onset.

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Today was a busy day for me. Leading on all my patients and seeing around half of them independently, therefore also having to write most of the notes, make several phone calls and liaise with the MDT.

Though I managed to see all of my patients for the day, I ran out of time to finish documenting all of their notes. Furthermore, these notes were more difficult to write as I left them all until the end of the day, when the details of my sessions were not fresh in my memory.

In the future, I will aim to ensure I complete all of these notes so that they don’t spill into the next day’s workload. I will achieve this by:

- discussing with coworkers that I see patients with and splitting these notes evenly after sessions.

- completing notes sooner following each session before moving on to other patients. Eg. Not seeing more than 2 different patients without completing the first note.

(This will ensure that I don’t forget details of my sessions so that documentation is as accurate as possible and will also mean that I have a better idea by the afternoon of how much time I will need/ if I require any help).

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My time management was much better today. I had a similar-sized caseload but was able to manage it well and get all my notes done by delegating and completing notes sooner after completion of a session.

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Will mentioned something today which I wasn't familiar with. It explained the symptoms one of my patients was presenting with and why I was having trouble getting her to engage with physiotherapy, so thought id make a note.

Following seizure(s), patients may experience neurological deficits or psychiatric symptoms. This period between the end of the seizure and the pt returning to baseline is called the postictal period. It can last from less than an hour to days.

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Wanted to learn more about assessment and management of fear of falling. Got a difficult patient at the moment who has very good strength and balance but is++anxious about falls when completing certain tasks. It has resulted in readmission and is a risk to the patient’s well-being, so I’m hoping to find out more about how I can better manage her condition.

Notes:

look for cautious gait, flat feet, like walking on ice

Falls efficacy scale or Icon FES (more Americanised but more detailed)

Frequency important: ideally 3x per week

Exercise programmes need to include resistance training, and exercising in standing, making the point that although chair based programmes have their place that falls prevention can’t be achieved by this alone.

Graded exposure as part of CBT: “out of 10 how confident would you be doing this without falling” -> add and remove levels of support accordingly and re-Ax.

AMCS

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Respiratory Failure:

Type 1: hypoxaemia (<75mmHg) with normocapnia (35-45 mmHg)

Type 2: Hypoxaemia (<75mmHg) with Hypercapnia (>45mmHg)

Type 1: Pulmonary-vascular disease

Type 2: due to ventilation

Arterial blood gases:

pH is the most important factor

If pO2 increases, pCO2 should decrease and vice versa

Describe activity in 2 systems: respiratory and metabolic:

If one system is disturbed, the other compensates to restore balance

resp system is quick responding (sec/mins) but metabolic system is slower (hours/days)

1. is it alkalotic or acidotic? (7.35-7.45)

2. Look at pCO2. If its acidosis and CO2 is low, the resp system has tried to compensate (increasing resp rate) and therefore the problem is metabolic: metabolic acidosis.

3. If paCO2 is low during an alkalosis, it is contributing rather than compensating, therefore it is respiratory.

4. sHCO3 (bicarb) will be high in alkalosis and low in acidosis.

5. sHCO3 can tell us about duration of a problem, for example in respiratory acidosis with pH outside normal values, if the bicarb is normal, it (the metabolic system) likely hasn't had time to respond, therefore this is an acute respiratory acidosis.

6. If we have a normal-low pH, but bicarb is high, the metabolic system has had time to compensate, therefore it is a chronic respiratory acidosis.

7. We cannot live long with a pH outside normal range, therefore nomatter the other values, if the pH is outside 7.35-7.45, there is an acute problem.

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Key points

Most doctors struggle with arterial blood gas (ABG) interpretation

ABG interpretation is easy

The first priority for the respiratory system is pH

If partial pressure of carbon dioxide (pCO2) goes down, partial pressure of oxygen (pO2) should go up

Mistakes in arterial blood gas (ABG) interpretation are common in clinical practice. The following is a simplified explanation of ABGs, including a practical method for interpreting results. It is simple, perhaps simplistic, but it will hopefully arm the reader with the tools (and confidence) to make better sense of ABG results in future. This is not for the dedicated physiologist. Overly complex explanations can be a barrier to a working understanding of the basics.

On acute medical take, ABGs are used to determine the nature as well as the severity of a problem. The results often have a direct bearing on management. Yet most doctors struggle with interpretation of this common test.

Arterial blood gas measurements

Unlike other 'blood tests', which are either 'high or low', ABGs present the doctor with six numbers that need to be interpreted as 'one result'. Given that this can be difficult, there is a need for a simple algorithm for systematically handling each of the numbers in turn, as discussed below. However, I begin with a few basic points to understand.

Respiratory and metabolic systems - in balance

ABGs tell us about activity in two systems; the respiratory system and the 'metabolic' system. If one system is disturbed, the other tries to restore balance. Both systems are primarily concerned with keeping blood pH in the normal range. Even for the respiratory system, pH (rather than oxygen) is the priority.

The respiratory system - oxygenation vs pH

In health, we are driven to take our next breath by the arterial partial pressure of carbon dioxide (P aCO ₂), which is intimately linked to pH. Although there is an additional receptor (the hypoxic centre) in the brain stem that monitors P aO ₂, it spends most of it time 'asleep' and is rather unconcerned about minor fluctuations in the level of oxygenation. This is because individuals generally live at a level of oxygenation well above that which is required to sustain life. This 'margin of oxygen safety' enables the respiratory system to focus on pH and to adjust ventilation (to 'blow off' or retain CO ₂) without the fall in oxygenation that underventilation would bring causing any difficulties. Therefore, if, for example, a metabolic alkalosis were to develop, ventilation would fall (at the expense of a small reduction in oxygenation) to retain CO ₂ and, thus, return pH to the normal range. Only when hypoxia is more severe (approximately P aO ₂ <8 kPa) does the hypoxic centre 'wake up' and take note. Only then, will it drive ventilation to prevent harmful levels of hypoxia.

Respiratory and metabolic systems - the speed of response

The respiratory system can respond quickly to a metabolic derangement, with changes occurring to the blood gases within seconds to minutes. However, the metabolic system (largely regulated by the kidneys excreting or retaining acid or bicarbonate) is much slower and changes can take hours to days.

A step-by-step method for interpreting arterial blood gases

First - look at the pH

Decide whether this is an 'acidosis' or 'alkalosis' (if it is within the normal range, note whether it is sitting towards the 'acidotic' or 'alkalotic' end of that range). Fix that fact in your mind because it will not change, no matter what the other numbers are!

Second - look at the PaCO₂

Ask the question: is the P aCO ₂ contributing to, or attempting to compensate for, the problem. If, for example, the problem is an acidosis and the P aCO ₂ is low, then clearly the respiratory system is attempting to compensate. Thus, one can conclude that the problem is metabolic (similarly with other combinations). Therefore, after looking at only two numbers (pH and P aCO ₂), most of the interpretation is done.

The other numbers (actual bicarbonate [aHCO ₃], base excess [BE], P aO ₂ and so on) might do nothing more than confirm this conclusion. However, they can sometimes add information about time course or provide information on additional derangements, but they will not contradict the conclusion that has already been reached.

Third - look at the 'base picture'

Actual bicarbonate (aHCO ₃) vs standard bicarbonate (sHCO ₃) - what's the difference? What is perhaps surprising is that, after many years of looking at ABGs, those intelligent, enquiring minds have seemingly never once pondered that question.

aHCO ₃ is the actual measurement of bicarbonate in that actual blood sample (hence the name). The problem with this measurement is that it is markedly affected by P aCO ₂. If the P aCO ₂ is high, the aHCO ₃ is dragged higher and vice versa. What one would like to know is what the HCO ₃ would have been had the P aCO ₂ been normal. It is this value that would provide a direct handle on what the metabolic system is doing. One can calculate the value if aHCO ₃ and P aCO ₂ are known, although most blood gas machines do this automatically, known as the sHCO ₃.

What is the base excess?

Base excess (BE) measures all bases, not just bicarbonate. However, because bicarbonate is the greater part of the base buffer, for most practical interpretations, BE provides essentially the same information as bicarbonate. The major advantage of BE is that its normal range is really easy to remember. One could probably have guessed that the expected value of BE was zero (the clue is in the word: 'excess'). Therefore, a tight range around zero (−3 to +3) is normal. In simple terms, a high BE excess is the same as a high HCO ₃.

What does the base picture tell us?

If the pH and P aCO ₂ led to the conclusion that the problem was primarily metabolic, then sHCO ₃ (or BE) will do little more than confirm that; sHCO ₃ being high in an alkalosis, low in an acidosis. If one has established that problem is respiratory, then the BE can tell us something of the duration of the problem.

If, for example, in a respiratory acidosis, the sHCO ₃ has shown no sign of responding (still within the normal range), the probable explanation is that there has not yet been time to respond (ie the problem is an acute respiratory acidosis). In a respiratory 'acidosis' (perhaps with the pH in the lower half of the normal range), a high sHCO ₃ would indicate a longer time course (ie the problem is a chronic -respiratory acidosis). A respiratory acidosis with a low sHCO ₃ would indicate a combined respiratory and metabolic -acidosis.

Box 1. Example.

Remember that one cannot live for long with pH outside of the normal range. If the pH is outside the normal range, one should never fall into the trap of assuming the problem is 'probably all chronic' (no matter how high the bicarbonate). An abnormal pH means there has to be an acute component to the problem.

Finally, look at the oxygen

It is sometimes thought that type 2 respiratory failure is simply a more severe version of type 1. However, this is not the case. Type 1 and type 2 respiratory failures are due to entirely different mechanisms.

Type 2 respiratory failure is extremely an issue of ventilation, that is, the business of pumping air in and out of the lungs. When underventilation occurs, for what ever reason (eg muscular weakness or opiate overdose), the P aCO ₂ will increase (the definition of underventilation) and P a O2 must decrease (even if the lungs are perfectly healthy). Type 2 respiratory failure results from underventilation, which can occur even in the context of healthy lungs.

Lung (or pulmonary vascular) disease disturbs the delicate ventilation-perfusion (V/Q) matching system. In such circumstances, oxygen delivered to the lungs by ventilation is handled inefficiently and P aO ₂ falls. However, provided that overall ventilation is normal, P aCO ₂ is maintained. When P aO ₂ is low yet P aCO ₂ normal, type 1 respiratory failure is present, and such a result implies lung (or pulmonary -vascular) disease.

Type 1 and type 2 respiratory failure can occur simultaneously. Indeed, the combination is common in severe chronic obstructive pulmonary disease, for example. Given that the two conditions result from entirely different mechanisms, with implications for treatment, one should be able to distinguish between them. When the only derangement is P aO ₂, clearly the failure is type 1. However, when the P aCO ₂ is high, one has to work out whether the low P aO ₂ can be accounted for by underventilation alone or whether there is an additional type 1 problem (ie whether there is anything wrong with the lungs).

To do this, one needs to measure the alveolar-arterial gradient, that is, the difference between the alveolar partial pressure of oxygen (P AO ₂) and the P aO ₂. The P aO ₂ is measured in the ABG, the P A O2 has to be calculated using the alveolar gas equation:

where P IO ₂ is the partial pressure of oxygen in the inspired air (approximately 21 kPa when breathing room air, but 24 kPa when using a 24% Venturi mask and so on) and 0.8 is the 'respiratory quotient' (ie the ratio between the CO ₂ produced and the O ₂ utilised).

The alveolar-arterial gradient (P AO ₂-P aO ₂) can then be calculated. In healthy young adults, the difference should be less than 2 kPa. If the patient is older, breathing higher concentrations of O ₂ or over ventilating, then the gap can widen, although in healthy patients this would not usually be expected to be greater than 4 kPa. If the alveolar-arterial gradient is higher than it should be, then a type 1 respiratory failure is present. This implies a problem with V/Q matching (ie a problem with either the lungs or the pulmonary vasculature).

Remember!

ABG interpretation is not difficult. Break down the task into steps and do them in order.

For a more detailed review of arterial blood gas interpretation, see Ref 1. Box 1 provides an example of a patient presenting with breathlessness, where ABGs form an important diagnostic test.

Reference

1. Gibson GJ. London: Hodder Arnold; 2008. [ Clinical tests of respiratory function (3rd edn) Google Scholar]

Articles from Clinical Medicine are provided here courtesy of Royal College of Physicians

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Most doctors struggle with arterial blood gas (ABG) interpretation ABG interpretation is easy The first priority for the respiratory system is pH If partial pressure of carbon dioxide (pCO2) goes down, partial pressure of oxygen (pO2) should go up Mistakes in arterial blood gas (ABG) interpretation are common in clinical practice.

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Was unsure on differences and justification of THR vs uni- vs bi-polar hemiarthroplasty for NOF# patients so did some reading.

(RCT)

Bipolar hemi involves the addition of a secondary articular surface to the artificial femoral head. The acetabulum is not replaced as it is in a THR, but the addition of this secondary articulation reduces motion at the original femoroacetabular joint, theoretically reducing erosion of the acetabulum and perhaps reducing the prevalence of dislocations of the prosthesis.

no difference in complications or hip function directly following op between uni and bipolar.

But acetabular erosion 15% more prevalent in unipolar (20% vs 5%) at 1 year post-op.

Acetabular erosion was significantly less prevalent in patients with a lower BMI.

Bipolar is ~260USD more expensive

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Unipolar hemiarthroplasty versus bipolar hemiarthroplasty in the most elderly patients with displaced femoral neck fractures: a randomised, controlled trial

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Hemiarthroplasty (HA) is generally considered to be the treatment of choice in the most elderly patients with a displaced fracture of the femoral neck. However, there is inadequate evidence to support the choice between unipolar HA or bipolar HA.…

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Room air is ~21% O2

NC:

1L - 24%

2L - 28%

3L - 32%

4L - 36%

Simple face mask:

Max 40-60% on 15L but variable. Should not be used with flow rate of <5L.

Non-rebreathe:

60%-90% on 10-15L.

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Normal Values:

pH: 7.35 – 7.45

PaCO₂: 4.7 – 6.0 kPa || 35.2 – 45 mmHg

PaO₂: 11 – 13 kPa || 82.5 – 97.5 mmHg

HCO₃–: 22 – 26 mEq/L

Base excess (BE): -2 to +2 mmol/L

1. Are they hypoxic? Hypoxia is the most immediate threat to life, so best to check this first. (aim for above 10kPa on RA, or 10kPa less than %fiO2 if on oxygen therapy.

Type 1 resp failure: Hypoxic but normal CO2

Type 2 resp failure: hypoxic, with hypercapnia.

Have found it very useful to work through practice cases through this website: ABG Interpretation

Completed approximately 30 practice ABG analyses during CPD time.

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ABG analysis can be easy! Test your knowledge on the web's most interactive arterial blood gas learning tool.