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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).

Arterial Blood Gases Made Easy Pdf

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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.

If CO2 production is altered, we adjust our breathing to exhale more or less CO2, as necessary, to maintain Paco2 within normal limits. The bulk of the acid produced by our bodies is in the form of CO2, so it is our lungs that excrete the vast majority of the acid load. Renal metabolic mechanisms The kidneys are responsible for excreting metabolic acids.

However, the kidneys do not just regulate acid—base balance; they must also maintain stable concentrations of the major electrolytes e. The need to perform these other tasks can sometimes interfere with pH regulation — either driving disturbances of acid—base balance or preventing their correction. Thus, a change in CO2 will not lead to a change in pH if it is balanced by a change in HCO3 that preserves the ratio and vice versa.

Because CO2 is controlled by respiration and HCO3 by renal excretion, this explains how compensation can prevent changes in blood pH. If it is due to a rise in Paco2, it is called a respiratory acidosis; if it is due to any other cause, then HCO3 is reduced and it is called a metabolic acidosis.

An alkalosis is any process that acts to increase blood pH.

If it is due to a fall in Paco2, it is called a respiratory alkalosis; if it is due to any other cause, then HCO3 is raised and it is called a metabolic alkalosis.

If one system is overwhelmed, leading to a change in blood pH, the other usually adjusts, automatically, to limit the disturbance e. This is known as compensation. Acid—base disturbances can therefore be considered as a set of scales. Normal acid—base balance When acid—base balance is entirely normal, with no alkalotic or acidotic pressures, it is like having a set of scales with no weights on it Figure Uncompensated acid—base disturbance When an acidosis or alkalosis develops, the scales become unbalanced, leading to acidaemia or alkalaemia, respectively.

In Figure 12, there is a primary respiratory acidosis with no opposing metabolic process. Importantly, compensatory changes in respiration happen over minutes to hours, whereas metabolic responses take days to develop.

Figures 13 and 14 represent two scenarios in which the lungs have responded to a primary metabolic acidosis by increasing alveolar ventilation to eliminate more CO2 compensatory respiratory alkalosis. In Figure 13, an acidaemia persists despite compensation partial compensation ; in Figure 14, blood pH has returned to the normal range full compensation.

When faced with such an ABG, how can we tell which is the primary disturbance and which is the compensatory process? The irst rule to remember is that overcompensation does not occur. The midpoint of the acid—base scales lies at a pH of 7.

The second rule is that the patient is more important than the ABG. When considering an ABG, one must always take account of the clinical context. For example, if the patient in Figure 14 were a diabetic, with high levels of ketones in the urine, it would be obvious that the metabolic acidosis was a primary process diabetic ketoacidosis.

If these two processes oppose each other, the pattern will be similar to a compensated acid—base disturbance Figure 14 and the resulting pH derangement will be minimised. A good example is salicylate poisoning, where primary hyperventilation respiratory alkalosis and metabolic acidosis salicylate is acidic occur independently.

By contrast, if the two processes cause pH to move in the same direction metabolic acidosis and respiratory acidosis or metabolic alkalosis and respiratory alkalosis , a profound acidaemia or alkalaemia may result Figure If the plotted point lies outside the designated areas, this implies a mixed disturbance. A note on … predicting compensatory responses It is not always easy to distinguish two primary opposing processes from a compensated disturbance.

A more precise method than that described earlier involves calculating the expected compensatory response for any given primary disturbance. However, these calculations are usually unnecessary and are not required for the case scenarios in Part 2. Metabolic acidosis may be caused by accumulation of metabolic acids excess ingestion, increased production or reduced renal excretion or by excessive loss of base HCO3. When renal measures are insuficient to prevent a fall in HCO3, there is normally a compensatory increase in alveolar ventilation to lower Paco2.

If this respiratory compensation is then overwhelmed, an acidaemia will result. The severity of a metabolic acidosis should be judged according to both the underlying process and the resulting acidaemia.

The dominant symptom in metabolic acidosis is often hyperventilation Kussmaul respiration owing to the respiratory compensation. Other signs are fairly non-speciic or related to the underlying cause. Metabolic acidosis with a high anion gap is usually caused by ingestion of an exogenous acid or increased production of an endogenous acid. In high anion gap acidosis, the size of the gap is usually proportionate to the severity of the acidosis. Lactic acidosis and diabetic ketoacidosis DKA — two common and clinically important causes of high anion gap metabolic acidosis — are discussed on the following pages.

Other speciic causes of metabolic acidosis are covered in the relevant cases in Part 2. When the supply of O2 to tissues is inadequate to support normal aerobic metabolism, cells become dependent on anaerobic metabolism — a form of energy generation that does not require O2 but generates lactic acid as a by-product.

This can occur due to a problem with local blood supply e. The extent of lactic acidosis is an indicator of disease severity. In particular, the initial serum lactate concentration is a powerful predictor of death in patients with sepsis. Rarely, lactic acidosis may, instead, be caused by drug toxicity metformin , malignant tumours or mitochondrial dysfunction. It is usually but not always associated with low blood pressure. Inadequate perfusion of tissues can be detected through changes in skin e.

Arterial Blood Gases Made Easy

It tends to occur in patients with type 1 diabetes who are either presenting for the irst time or have not been taking their usual insulin therapy. In the absence of insulin, the body cannot metabolise glucose and, therefore, increases metabolism of fats. The breakdown of fats produces ketones — small organic acids that provide an alternative source of energy but can accumulate, leading to acidosis.

DKA is therefore characterised by the triad of: A high anion gap metabolic acidosis 2. An elevated plasma glucose hyperglycaemia 3. The presence of ketones detectable in blood or urine The severity of DKA is graded according to a variety of factors, including the severity of both the acidotic process and the resultant acidaemia see Box 1.

Patients are often profoundly dehydrated, with altered mental status. Ketones can also be excreted as salts of sodium or potassium: Increased production of ketones can also occur in the setting of severe alcohol excess or starvation. In the former, there may be a profound acidosis, whereas ketoacidosis due to prolonged fasting is usually mild e. The absence of hyperglycaemia is often an important clue to these alternative causes. As a consequence, primary metabolic alkalosis is frequently accompanied by alkalaemia.

By contrast, metabolic compensation for chronic respiratory acidosis chronic type 2 respiratory failure — a common cause of metabolic alkalosis in clinical practice — does not, by itself, result in alkalaemia. Additional factors that impair this response are therefore also necessary. Normally, lungs are able to increase ventilation to maintain a normal Paco2 — even in conditions of increased CO2 production e.

Thus, respiratory acidosis always implies a degree of reduced alveolar ventilation. This may occur from any cause of type 2 respiratory impairment see Section 1. Primary causes are pain, anxiety hyperventilation syndrome , fever, breathlessness and hypoxaemia. It may also occur to counteract a metabolic acidosis.

It leads to profound acidaemia as there are two simultaneous acidotic processes with no compensation. In clinical practice it is often due to severe ventilatory failure, in which the rising Paco2 respiratory acidosis is accompanied by a low Pao2, resulting in tissue hypoxia and consequent lactic acidosis.

Indeed, an opposing metabolic alkalosis suggests that a respiratory acidosis must have been present for some time. In other words, the presence of metabolic compensation distinguishes chronic from acute type 2 ventilatory failure see Section 1. The following steps should be used as a guide see also video on www. Routine sampling should, initially, be attempted from the radial artery of the non-dominant arm. Greater extension of the wrist may impede arterial low.

Most ABG syringes will then ill under arterial pressure see info box on page On the safety of radial artery cannulation. Anaesthesiology ; If the colour returns to the hand within 10 s this indicates C adequate circulation Figure 20 Modified Allen test.

Any sample with more than very ine bubbles should be discarded. Venous or arterial blood? It also identiies the presence of metabolic acidosis and alkalosis.

Other indications are listed in Box 1. In respiratory distress, rising PaCO2 often signiies exhaustion and is an ominous sign. Patients require urgent reversal of the process, leading to ventilatory failure or assisted ventilation.

It is essential for titrating O2 therapy in patients with chronic type 2 respiratory failure and for optimising ventilator settings. Venous blood gas VBG analysis can yield clinically useful information and has become increasingly popular as an alternative to ABG in some clinical settings, especially within emergency departments. In some situations, analysis of venous blood can provide enough information to assist in clinical decisions; for example, VBG is now deemed adequate for both the diagnosis and the monitoring of diabetic ketoacidosis in the latest UK guidelines Box 1.

However, it is also important to recognise the limitations of VBG in relation to arterial analysis. The following is therefore a rough guide to the use of VBG: Therefore, VBG cannot be used to assess oxygenation.

By contrast, a venous PCO2 less than 45 mmHg makes signiicant arterial hypercapnia unlikely and, therefore, may avert the need for arterial puncture in some patients. VBG may, therefore, be useful to screen for overall acid—base status.

The interpretation of arterial blood gases

However, a normal venous lactate level makes lactic acidosis unlikely. Po2 is not a measure of O2 content but it does determine the extent to which haemoglobin is saturated with O2. Pao2 refers speciically to the partial pressure of O2 in arterial blood. PCO2 4. Paco2 refers speciically to the partial pressure of CO2 in arterial blood. Sao2 refers speciically to the O2 saturation of arterial blood. High bicarbonate levels signify a metabolic alkalosis and low levels signify a metabolic acidosis.

The authors recommend using this measurement of bicarbonate in ABG analysis. A positive BE indicates that there is more base than normal metabolic alkalosis and a negative BE indicates that there is less base than normal metabolic acidosis. Lactate 0. Glucose 3. PaO2 SaO2 Mild 8— High FiO2 requirements it is chronic or acute, then assess severity of hypercapnia to maintain adequate PaO2 and hypoxaemia Table 1. The presence of exhaustion is also an ominous sign.

Is HCO3 high? Acidaemia Normal pH Alkalaemia pH less than 7. PaO2 is measured on arterial blood gas but PAO2 has to be calculated using the alveolar gas equation see box below. This means that: The normal range for PaO2 falls with age 2. Examination He is hot and lushed with a temperature of He does not appear distressed but is using accessory muscles of respiration.

There is diminished chest expansion on the left with dullness to percussion, bronchial breathing and coarse crackles in the left lower zone posteriorly. John S. Should the patient receive supplemental O2? Is pulse oximetry a suitable alternative to repeated ABG monitoring in this case? Apart from morbid obesity and type 2 diabetes, she is otherwise well and has no respiratory symptoms.

Marcella P. What is the most likely diagnosis? She lew to the UK from Australia the previous day and is very concerned she may have a pulmonary embolism. She has no pleuritic pain, haemoptysis or leg swelling, no history of lung disease or deep-vein thrombosis, and is a non-smoker.

Examination She appears anxious and distressed. Her respiratory rate is elevated but chest examination is unremarkable and there are no clinical signs of deep-vein thrombosis. A chest X-ray reveals no abnormalities. Jill R. A review of his charts reveals that he has received three 10 mg injections of morphine since returning to the ward, in addition to the morphine delivered by his patient-controlled analgesia device.

Examination The patient is unresponsive with shallow respirations and bilateral pinpoint pupils. Henry S. What treatment does this patient require? He is extremely short of breath and struggling to speak.

Following a conversation with his family, it emerges that he has a long history of chronic obstructive pulmonary disease. Over the last 3 days his breathing has worsened considerably and he has expectorated increased volumes of sputum.

Examination The patient is struggling for breath and appears extremely distressed. He exhibits signs of chest hyperinlation and is breathing through pursed lips. Breath sounds are generally diminished but there are no added sounds. Joseph S. Should you provide him with oxygen? Despite this, his Sao2 as measured by pulse oximetry increases only marginally and there is no improvement in his symptoms.

Examination Examination indings in the chest are unchanged but he now appears exhausted and slightly confused. Should his oxygen now be stopped? At outpatient review 3 months later, he remains dyspnoeic on mild exertion despite optimal therapy including smoking cessation. He has no features to suggest acute exacerbation. What treatment should now be considered? She is commenced on nasogastric feeding due to swallowing problems but has a large vomit 24 h later.

She initially appears well but over the next few hours develops worsening breathing dificulties. Examination She is agitated, distressed and pyrexial. A dull percussion note and coarse crackles are evident at both lung bases.

Other than acute confusion, neurological indings are unchanged from admission. Mary W. Is her condition mild, moderate or severe?

He is normally capable of walking around m but now has dificulty dressing and is breathless at rest. 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. The state of arterial blood oxygenation is determined by the PaO2.

This reflects gas exchange in the lungs and normally the PaO2 decreases with age. This is due to decreased elastic recoil in the lungs in the elderly, thereby yielding a greater ventilation-perfusion mismatch. Consequently, a PaO2 of 75 mmHg, which may be of concern in a young person, is usually unremarkable in an year-old.

PaO2 A PaO2 that is less than expected indicates hypoxaemia. This can result from hypoventilation or a mismatch of ventilation and perfusion. If alveolar ventilation is adequate that is, PaCO2 is normal , then the hypoxaemia is almost certainly caused by a ventilation-perfusion disturbance. Ask the question: If, for example, the problem is an acidosis and the P a CO 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 a CO 2 , most of the interpretation is done. The other numbers actual bicarbonate [aHCO 3 ], base excess [BE], P a O 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. What is perhaps surprising is that, after many years of looking at ABGs, those intelligent, enquiring minds have seemingly never once pondered that question. The problem with this measurement is that it is markedly affected by P a CO 2. It is this value that would provide a direct handle on what the metabolic system is doing.

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: 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. A respiratory acidosis with a low sHCO 3 would indicate a combined respiratory and metabolic -acidosis. Remember that one cannot live for long with pH outside of the normal range.

An abnormal pH means there has to be an acute component to the problem. 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 a CO 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.

In such circumstances, oxygen delivered to the lungs by ventilation is handled inefficiently and P a O 2 falls. However, provided that overall ventilation is normal, P a CO 2 is maintained. When P a O 2 is low yet P a CO 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.When underventilation occurs, for what ever reason eg muscular weakness or opiate overdose , the P a CO 2 will increase the definition of underventilation and P a O2 must decrease even if the lungs are perfectly healthy.

Bicarbonate should not be given if the pCO2 is elevated as the pH will not change according to the above formula, a metabolic acidosis is merely being replaced by a respiratory acidosis. External link. In fact, almost all O2 molecules in blood are bound to a protein called haemoglobin Hb; Figure 3.

However, there is an overall alkalaemia, indicating a primary metabolic alkalosis. However, because bicarbonate is the greater part of the base buffer, for most practical interpretations, BE provides essentially the same information as bicarbonate.

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