History. 2. What is the Oxygenation status. 3. What is the pH? Acidemia or Alkalemia? 4. What is the primary disorder present? 5. Is there appropriate. sO2. 70 - 75%. ABG EASY AS 1,2,3. NORMAL VALUES & DEFINITIONS 3 STEPS TO ABG INTERPRETATION made no attempt to help normalise the pH. Key points. Most doctors struggle with arterial blood gas (ABG) interpretation. ABG interpretation is easy. Break it down into steps. The first priority for the.
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Mistakes in arterial blood gas (ABG) interpretation are common in clinical practice. The following is a simplified explanation of ABGs, including a practical. The principles of oxygen transport and ventilation are core concepts for critical care nurses to understand in managing acutely and critically ill patients. Nurses. ARTERIAL BLOOD GASES MADE EASY i This page intentionally left blank Arterial Blood Gases Made Easy Second Edition Iain A M Hennessey MBChB ( Hons).
The most likely cause of chronic type 2 respiratory impairment in this case is severe obesity. Isla T. Part 1 of this book is designed to answer these questions. When faced with such an ABG, how can we tell which is the primary disturbance and which is the compensatory process? This patient has type 1 respiratory impairment and will not rely on hypoxic drive. All rights reserved.
Examination He is lucid, alert and mildly distressed. He is using accessory muscles of respiration and breathing through pursed lips. Chest examination reveals features of hyperinlation, generally diminished breath sounds and scattered rhonchi wheeze. Hamish R. Which one of the following ABG values is most likely to have changed signiicantly in the past 24 h: Which two of the above ABG values indicate the need for caution when providing O2 therapy?
His oxygen saturations improve signiicantly, but when he is reviewed 1 h later, his condition has deteriorated and he is unable to provide a history.
Examination He is drowsy and barely rousable. Chest examination results are unchanged. What has been the cause of his deterioration? She has a history of asthma, with two previous exacerbations requiring hospital admission. She now feels very breathless and is obtaining no relief from her salbutamol inhaler. Auscultation of her chest reveals widespread polyphonic wheeze. Jessica G. Which of the above ABG value gives the greatest cause for concern?
How would you classify the severity of this asthma attack? While being examined by the emergency department doctor she becomes extremely agitated and upset. Despite a normal ankle X-ray and extensive reassurance by the emergency department staff, she refuses to believe that her ankle is not broken and starts crying. While leaving the department, she develops a clutching sensation in her chest, shortness of breath and a tingling sensation in her hands and around her mouth.
She reports that she feels unable to take a deep breath. Examination The patient appears frightened and extremely distressed. Other than tachypnoea and a mild sinus tachycardia, cardiorespiratory examination is unremarkable. Electrocardiogram, chest X-ray and peak low measurements are all normal. Trinny F. Are there any other abnormalities?
What is the likely diagnosis? The paramedics estimate he is likely to have been trapped in a smoke-illed room for up to 20 minutes before rescue. Examination The patient is heavily contaminated with soot and smells strongly of smoke. Fortunately, he has not sustained any thermal injuries. He appears to be confused and has just vomited. Robert J. Which of the values provided is falsely high: Po2, So2 or Hb? He was discharged from hospital 4 weeks before after sustaining a large myocardial infarction.
Since then he has had no chest pain but has reported gradually worsening breathlessness associated with progressive swelling of the ankles. Examination He is in severe respiratory distress and using accessory muscles of respiration. The jugular venous pressure JVP is elevated to the earlobe and he has bilateral lower limb oedema to the knees.
There are bilateral crackles to the mid zones. His chest X-ray is shown below. Keegan C. What is the cause of the metabolic acid—base disturbance?
What factors are driving it? After 30 minutes, his Spo2 has improved but he remains very breathless and appears extremely tired. A repeat blood gas is performed. What is the most concerning ABG result? What treatments should be considered now? The tumour was discovered at colonoscopy after she presented to her doctor with a 6-month history of rectal bleeding. On admission, she appears to be severely short of breath and extremely tired.
Further questioning reveals that her rectal blood loss has been no greater than usual. Ethel S. What is the most likely cause of her breathlessness? What would be the most effective way of improving O2 delivery to her tissues?
She describes the pain as being colicky with no particular radiation. She does not complain of any alteration in her bowel habit and has not vomited. Her only medical history is that of atrial ibrillation, for which she takes aspirin and digoxin. Examination On examination, the patient is haemodynamically stable with warm, well-perfused peripheries. Despite severe abdominal discomfort, abdominal examination is relatively unremarkable: No hernias or aneurysms are palpable and rectal examination is unremarkable.
An abdominal and erect chest X-ray are taken and found to be normal. During the course of the examination, her clinical condition deteriorates and she is moved to the resuscitation area. Susan U. Following a discussion with her partner it emerges she has not been eating for the past few days due to a vomiting illness and, as a precaution, has also been omitting her insulin.
Examination On examination, she appears drowsy and peripherally shutdown, with very dry mucous membranes. Her breath smells of acetone and her respirations are deep and sighing. Isla T. Calculate the anion gap. He was found near a bottle of vodka and a half-empty bottle of what appears to be methanol. It is unclear if he has drunk any of the contents.
There are no apparent focal neurological abnormalities. Gary S. What is the anion gap? Is the acid—base status consistent with methanol ingestion? He also complains of mild fatigue and lethargy. There is no history of gastrointestinal disturbance and he is not on any regular medications.
Examination The patient is well and clinical examination reveals no abnormalities. As part of the investigations, an ABG is obtained. Roger P.
She complains of nausea and a high-pitched noise in her ears. Examination On examination, she is mildly confused. Her respirations are increased in both rate and depth. Examination is otherwise unremarkable. Libby F. What substance is she most likely to have taken? Examination She appears lushed and sweaty, with a pyrexia of Her observation chart and ABG results are shown below.
Sonia K. What is the cause of the acid—base abnormality? Which ABG value carries the greatest signiicance for prognosis and treatment in this context? They report that he has no history of signiicant medical illness but has recently been undergoing tests for progressive fatigue and weight loss.
Over the last few days, he has become increasingly weak and lethargic and has also complained of muscle cramps. They became alarmed today when he appeared drowsy and disoriented. Examination The patient appears listless and confused. He has cool peripheries and poor capillary reill. He is afebrile and there is no rash, lymphadenopathy or meningism.
Abdominal examination is unremarkable and there are no focal chest or neurological signs. Rufus W. Are there any other abnormalities on the ABG? What speciic treatment does this patient require? Cardiopulmonary resuscitation was commenced promptly, as no pulse or respiratory effort was detected, and has now been in progress for 12 minutes.
He has a medical history of ischaemic heart disease, dementia and chronic renal failure. Examination The patient has a Glasgow Coma Scale score of 3 and appears pale and mottled. The cardiac monitor reveals an agonal rhythm as shown below. No pulses are palpable and there is no respiratory effort. David K. What is his prognosis? He now also feels very breathless. He admits to drinking up to units of alcohol per week for the past few weeks.
Examination The patient is in evident distress and appears very unwell. There is marked epigastric tenderness. A chest X-ray on admission is shown below.
Daniel C. What is his approximate Fio2? She continues to vomit profusely for another 3 days. Examination of her luid balance chart reveals that she is failing to keep up with her luid losses but has not been prescribed intravenous luids. Examination The patient appears dehydrated, with reduced skin turgor and dry mucous membranes. Abdominal examination is unremarkable.
Jenny A. What electrolyte abnormalities are present? What treatment will correct the acid—base abnormality? The parents report that he had an uncomplicated delivery with no postpartum complications. He initially fed well, appeared to be thriving and gave no cause for concern but has deteriorated markedly over the past 2 weeks, vomiting all of his meals and now losing weight.
Examination The child is agitated, crying and malnourished. His mucous membranes are dry, and on examination of his abdomen, a small mass is found in the epigastrium. Richard B. What is the underlying diagnosis? There has been no recent change in breathlessness or sputum production. Examination She has evidence of chest hyperinlation and globally diminished breath sounds. Her JVP is markedly elevated and there is extensive peripheral oedema with ascites.
She does not appear in respiratory distress. Margaret M. What treatment might help to improve the acid—base abnormality? She has no other symptoms and no relevant medical history. Examination On examination, the patient is heavily pregnant but appears otherwise well. Examination of her chest reveals no abnormalities. Julie D. What is the most likely explanation for the low Po2? She underwent elective knee replacement surgery 4 days before and has been immobile in bed since the operation.
She is otherwise well with no relevant medical history. Examination The patient appears well but slightly short of breath. Other than mild tachycardia and tachypnoea, examination of the cardiovascular and respiratory systems yields no positive indings, and there is no clinical evidence of deep-vein thrombosis. A chest X-ray reveals no abnormalities and an electrocardiogram shows only sinus tachycardia.
Jill A. What is the A — a gradient? Does she require any further investigation? Yes 3. Yes This patient has moderate type 1 respiratory impairment. Although hyperventilation is an appropriate response to the hypoxaemia and sensation of dyspnoea, it has resulted in a mild alkalaemia remember that metabolic compensation does not occur in response to acute respiratory acid—base disturbance. The correct management for his condition is supplemental oxygen to correct the hypoxaemia and appropriate antibiotics to treat the infection.
In a patient such as this, with moderate hypoxaemia and no ventilatory impairment, monitoring by pulse oximetry is more appropriate than repeated ABG sampling. Indications for further ABG analysis would include signs of exhaustion or hypercapnia p. Chronic type 2 respiratory impairment due to morbid obesity At irst glance, it may be dificult to determine whether this ABG represents respiratory acidosis with metabolic compensation or metabolic alkalosis with respiratory compensation, as both give a high HCO3 and a high Paco2 level.
This would represent overcompensation for an alkalosis and, therefore, suggests an acidosis as the primary abnormality overcompensation does not occur. The mildly impaired oxygenation is consistent with the degree of hypoventilation. The most likely cause of chronic type 2 respiratory impairment in this case is severe obesity. Pulmonary embolism This patient is a young, it, non-smoker with no history of lung problems but, despite hyperventilating low Paco2 , has a Pao2 below the normal range, indicating impaired oxygenation.
Given the recent long-haul light and absence of clinical and X-ray abnormalities, the most likely cause of her breathlessness and impaired oxygenation is pulmonary embolism, and she must be investigated accordingly. This is one of the clinical situations where calculation of the A—a gradient can be helpful more so when the Pao2 is just within the normal range. Opioid toxicity 3.
Opioid antagonist Opioids have a depressant effect on respiration and may lead to acute ventilatory failure type 2 respiratory failure. This elderly man has received a large amount of morphine in a short period and exhibits pinpoint pupils, making opioid toxicity by far the most likely cause of his severe ventilatory failure.
Because metabolic compensation takes several days to occur, the acute respiratory acidosis has produced a severe acidaemia. In addition to basic life-support measures, he should be administered an opioid antagonist e. This patient has type 1 respiratory impairment and will not rely on hypoxic drive. Although this patient is likely to have a chronically low Pao2, the acute deterioration in both his symptoms and exercise tolerance suggests a further recent decline from his normal baseline.
Importantly, even a small drop in Pao2 around this level [steep part of the O2—haemoglobin Hb curve] may cause a marked reduction in Sao2, compromising O2 delivery to tissues. Thus, O2 is required both to alleviate symptoms and to prevent the development of tissue hypoxia, and should not be withheld for fear of precipitating hypoventilation.
This patient with an acute exacerbation of COPD has been struggling to overcome severe obstruction to airlow over a period of hours to days and is now exhausted from the increased work of breathing.
As a result, his alveolar ventilation is declining, leading to acute type 2 respiratory failure. This may complicate type 1 respiratory failure from any cause, not just from COPD. The rising Paco2 is, therefore, not due to diminished hypoxic drive and removing his oxygen will not correct it.
Indeed, his Fio2 should probably be increased in addition to other treatment as he remains signiicantly hypoxaemic. Remember that, with acute respiratory acidosis, there is no time for metabolic compensation to develop and a dangerous acidaemia develops rapidly.
Adequate ventilation must be restored, as a matter of urgency, to correct the Paco2. Possible measures, in this case, include a respiratory stimulant e. If these fail, intubation and mechanical ventilation may be required, if considered appropriate. It should be offered to patients who, despite being clinically stable and on optimal medical therapy, have a Pao2 less than 7. Ideally, the Pao2 should be conirmed on two separate ABGs taken at least 3 weeks apart.
Because of the signiicant risk of ire hazard, home oxygen therapy is usually not offered to patients who continue to smoke. Aspiration pneumonia 3. Severe This patient has mild to moderate hypoxaemia despite receiving a high Fio2, and therefore, has severe impairment of oxygenation.
The slightly low Paco2 indicates that ventilation is adequate, so this is type 1 respiratory impairment. The probable explanation for the mild metabolic acidosis is lactic acidosis resulting from tissue hypoxia. The history, examination indings and chest X-ray all suggest a diagnosis of aspiration pneumonia.
This patient is severely unwell and any further decline in her Pao2 could be catastrophic on the steep part of the O2—Hb saturation curve. PO2 3. Even in chronic type 2 impairment, a further acute rise in PaCO2 would lead to an acidaemia. The pH here is normal, so the PaCO2 has not changed appreciably in the last few days i. His PaO2 is likely to have dropped, leading to the increased breathlessness and marked decline in exercise capacity: As this patient has chronic hypercapnia, he may rely on hypoxic drive as a stimulus to ventilation.
The goal is to ensure adequate oxygenation we must not ignore his hypoxaemia without depressing ventilatory drive. Excessive supplemental O2 Care must be taken when prescribing supplemental O2 to patients with chronic type 2 respiratory failure. The aim is to reverse any recent worsening of hypoxaemia and allow adequate tissue oxygenation, without depressing ventilatory drive through an excessive rise in Pao2.
The response to therapy must be closely monitored, with frequent clinical assessment and repeated ABG measurement. Note that pulse oximetry is not an adequate substitute for ABG in these circumstances, as knowledge of the Sao2 alone does not permit assessment of ventilatory adequacy.
The latter point is well illustrated in this case as the patient now has life-threatening acute-on-chronic respiratory failure despite a normal Sao2. The rising Paco2 must be rapidly checked and reversed through improving ventilation.
Potential strategies include reducing inspired O2 concentration, respiratory stimulants or assisted ventilation. The PaCO2 high end of normal range 3. Life-threatening attack This patient has several features of a severe asthma attack but it is the high—normal Paco2 that is the most worrying aspect of her presentation and makes it a life-threatening attack.
Consequently, her Paco2 signals a life-threatening attack. The intensive care unit should be informed immediately of any patient with acute severe asthma and life-threatening features. Patients must receive intensive treatment and monitoring, including repeated ABG measurements to assess response and identify the need for intubation. Low ionised calcium 3. Psychogenic hyperventilation This is a classic clinical picture of psychogenic hyperventilation.
Note that the HCO3 and base excess is normal, as there has been insuficient time for metabolic compensation to occur. Consequently, the reduction in Paco2 has caused a marked alkalaemia. This is the most likely cause of the numbness and tingling. Care must be taken in ruling out other cardiovascular and respiratory pathologies before ascribing symptoms of chest pain and shortness of breath to psychogenic hyperventilation.
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Skip to content. Search for books, journals or webpages All Webpages Books Journals. Iain Hennessey Alan Japp. Paperback ISBN: Published Date: 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. 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. National Center for Biotechnology Information , U.
Journal List Clin Med Lond v. Clin Med Lond. Graham P Burns , consultant respiratory physician A. Author information Article notes Copyright and License information Disclaimer. Address for correspondence: Arterial blood gases, physiology, oxygen, carbon dioxide, pH. This article has been cited by other articles in PMC. Key points Most doctors struggle with arterial blood gas ABG interpretation ABG interpretation is easy Break it down into steps 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.
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 a CO 2 , which is intimately linked to pH. 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.
Second — look at the P a CO 2 Ask the question: What is the base excess? What does the base picture tell us? Box 1. Open in a separate window.
Finally, look at the oxygen It is sometimes thought that type 2 respiratory failure is simply a more severe version of type 1. Reference 1. Gibson GJ. Hodder Arnold; Clinical tests of respiratory function 3rd edn [ Google Scholar ]. Support Center Support Center.