The Nurse Reviews the Arterial Blood Gas Results of a Client and Notes the Following Ph 745

Indian J Crit Intendance Med. 2010 Apr-Jun; fourteen(2): 57–64.

Estimation of arterial blood gas

Pramod Sood

From: Disquisitional Care Division, Dayanand Medical College and Hospital, Ludhiana, Punjab, India

Gunchan Paul

From: Critical Intendance Partition, Dayanand Medical Higher and Hospital, Ludhiana, Punjab, India

Sandeep Puri

^aneDepartment of Medicine, Dayanand Medical College and Hospital, Ludhiana, Punjab, Republic of india

Abstruse

Disorders of acrid–base balance can lead to severe complications in many disease states, and occasionally the abnormality may exist so severe as to go a life-threatening run a risk factor. The procedure of assay and monitoring of arterial claret gas (ABG) is an essential part of diagnosing and managing the oxygenation status and acid–base residual of the high-gamble patients, equally well as in the care of critically sick patients in the Intensive Intendance Unit. Since both areas manifest sudden and life-threatening changes in all the systems concerned, a thorough understanding of acid–base residue is mandatory for any doctor, and the anesthesiologist is no exception. However, the understanding of ABGs and their interpretation can sometimes be very confusing and also an arduous chore. Many methods do be in literature to guide the interpretation of the ABGs. The discussion in this article does non include all those methods, such as analysis of base excess or Stewart's strong ion divergence, but a logical and systematic approach is presented to enable us to make a much easier estimation through them. The proper awarding of the concepts of acid–base balance will assist the healthcare provider not but to follow the progress of a patient, but also to evaluate the effectiveness of care being provided.

Keywords: Arterial blood gas estimation, ABG analysis, rules for rapid ABG assay, Anion gap, Approach to mixed disorders

Introduction

Arterial blood gas (ABG) analysis is an essential function of diagnosing and managing a patient'south oxygenation status and acid–base of operations rest. The usefulness of this diagnostic tool is dependent on being able to correctly interpret the results. Disorders of acid–base of operations residue tin create complications in many disease states, and occasionally the abnormality may be so astringent then as to get a life-threatening hazard cistron. A thorough agreement of acid–base balance is mandatory for any physician, and intensivist, and the anesthesiologist is no exception.

The iii widely used approaches to acid–base physiology are the HCO₃ ^- (in the context of pCO₂), standard base of operations excess (SBE), and strong ion departure (SID). It has been more than 20 years since the Stewart's concept of SID was introduced, which is defined as the absolute difference between completely dissociated anions and cations. According to the principle of electrical neutrality, this difference is balanced by the weak acids and CO₂. The SID is defined in terms of weak acids and CO₂ subsequently has been re-designated as effective SID (SID_eastward) which is identical to "buffer base of operations." Similarly, Stewart'southward original term for total weak acid concentration (A_TOT) is at present divers every bit the dissociated (A^-) plus undissociated (AH) weak acid forms. This is familiarly known every bit anion gap (AG), when normal concentration is actually acquired by A^-. Thus all the iii methods yield virtually identical results when they are used to quantify acid–base condition of a given blood sample.[i]

Why is it Necessary to Gild an ABG Analysis?

The utilization of an ABG analysis becomes necessary in view of the following advantages:

Aids in establishing diagnosis.
Guides treatment plan.
Aids in ventilator management.
Improvement in acid/base management; allows for optimal office of medications.
Acid/base of operations status may change electrolyte levels critical to a patient's status.

Accurate results for an ABG depend on the proper fashion of collecting, treatment, and analyzing the specimen. Clinically of import errors may occur at any of the above steps, only ABG measurements are peculiarly vulnerable to preanalytic errors. The most common problems that are encountered include nonarterial samples, air bubbles in the sample, inadequate or excessive anticoagulant in the sample, and delayed assay of a noncooled sample.

Potential Preanalytical Errors

Preanalytical errors are caused at the following stages:

During preparation prior to sampling

Missing or wrong patient/sample identification;
Use of the wrong type or amount of anticoagulant

- dilution due to use of liquid heparin;

- insufficient amount of heparin;

- binding of electrolytes to heparin;
Inadequate stabilization of the respiratory status of the patient; and
Inadequate removal of affluent solution in arterial lines prior to blood collection.

During sampling/handling

Mixture of venous and arterial blood during puncturing;
Air bubbles in the sample. Whatever air bubble in the sample must be expelled every bit soon as possible later on withdrawing the sample and before mixing with heparin or before any cooling of the sample has been washed. An air chimera whose relative volume is upwardly to 1% of the blood in the syringe is a potential source of significant error and may seriusly touch the pO₂ value.
Insufficient mixing with heparin.

During storage/transport

Wrong storage
Hemolysis of blood cells

General Storage Recommendation

Do not absurd the sample.[2]
Analyze inside thirty min. For samples with high paO₂ due east.g., shunt or with high leukocyte or platelet count also analyze inside 5 min.
When analysis is expected to be delayed for more than 30 minutes, employ of glass syringes and ice slurry is recommended.

During grooming prior to sample transfer

Visually audit the sample for clots.
Inadequate mixing of sample before assay.

Insufficient mixing tin cause coagulation of the sample. It is recommended to mix the blood sample thoroughly past inverting the syringe 10 times and rolling it betwixt the palms as shown in Figure one. This prevents stacking (such every bit coins or plates) of cherry-red blood cells.

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Correct method of mixing of the arterial sample with the anticoagulant in ii dimensions to preclude stacking of red blood cells.

During anticoagulation

Modern blood gas syringes and capillary tubes are coated with various types of heparin to prevent coagulation in the sampler and inside the blood gas analyzer:

Liquid nonbalanced heparin
Dry nonbalanced heparin
Dry electrolyte-balanced heparin (Na⁺, K⁺, Ca²⁺)
Dry out Caⁱⁱ⁺-counterbalanced heparin

Other anticoagulants, due east.g., citrate and EDTA are both slightly acidic which increase the risk of pH being falsely lowered.

Liquid heparin

The use of liquid heparin every bit the anticoagulant causes a dilution of the sample, i.e., dilutes the plasma, but not the contents of the blood cells. As a consequence, parameters such as pCO₂ and electrolytes are afflicted. Only 0.05 mL of heparin is required to anticoagulate one mL of blood. Expressionless space book of a standard 5 mL syringe with 1 inch 22 gauge needle is 0.two mL; filling the syringe dead space with heparin provides sufficient volume to anticoagulate a 4-mL blood sample. If smaller sample volumes are obtained or more liquid heparin is left in the syringe, so the dilution effect will be even greater. The dilution effect also depends on the hematocrit value. Plasma electrolytes decrease linearly with the dilution of the plasma along with pCO₂, cGlucose, and ctHb values. pH and pO₂ values are relatively unaffected by dilution. paO_two is simply equally little as 2% of the O₂ physically dissolved in the plasma, and so the oximetry parameters given in fractions (or %) will remain unaffected.[three]

Syringes for claret gas analysis tin can take a wide range of heparin amounts.[4] The units are typically given as IU/mL (international units of heparin per milliliter) blood drawn into the syringe. In order to obtain a sufficient final concentration of heparin in the sample, blood volume recommended on the syringe must be drawn. Example: a syringe stated to contain l IU/mL when filled with one.five mL of claret ways that the syringe contains a total 75 IU of dry heparin. If the user draws 2 mL of blood, and then the resulting heparin concentration volition be besides low and the sample may coagulate. If the user draws only 1 mL, then the resulting heparin concentration will be higher than that aimed for, which may lead to producing falsely low electrolyte results.

Heparin binds to positive ions such as Caⁱⁱ⁺, K⁺, and Na⁺. Electrolytes bound to heparin cannot be measured past ion-selective electrodes, and the final effect will be measurement offalsely low values. The binding issue and the resulting inaccuracy of results are particularly pregnant for corrected Caⁱⁱ⁺. The apply of electrolyte-balanced heparin significantly reduces the binding issue and the resulting inaccuracy.[5]

The following steps for rapid estimation of ABG are recommended:

Cheque for the consistency of ABG

While making an interpretation of an ABG e'er check for the consistency of the written report by the modified Henderson equation.

The hydrogen ion is calculated by subtracting the two digits later on the decimal betoken of pH from 80, due east.g., if the pH is 7.23 and so

[H⁺] = 80 - 23 = 57

[H⁺] = 10^(9-pH)

The hydrogen can be calculated from Table 1.

Table one

pH value and corresponding H+ ion concentration

pH	H+	pH	H+
half dozen.lxx	200	7.xl	xl
6.75	178	7.45	35
vi.lxxx	158	7.fifty	32
6.85	141	7.55	28
6.90	126	vii.60	25
6.95	112	7.65	22
7.00	100	7.lxx	20
seven.05	89	7.75	xviii
vii.x	79	7.fourscore	16
vii.15	71	7.85	14
7.20	63	seven.90	xiii
7.25	56	seven.95	11
7.xxx	50	8.00	x
7.35	45

Obtain a relevant clinical history

While making an interpretation of anABG, never comment on the ABG without obtaining a relevant clinical history of the patient, which gives a clue to the etiology of the given acid–base of operations disorder. For example, a patient with a history of hypotension, renal failure, uncontrolled diabetic condition, of handling with drugs such as metformin is likely to have metabolic acidosis; a patient, with a history of diuretic use, bicarbonate assistants, high-nasogastric aspirate, and vomiting, is probable to take metabolic alkalosis. Respiratory acidosis would occur in COPD, muscular weakness, postoperative cases, and opioid overdose, and respiratory alkalosis is likely to occur in sepsis, hepatic coma, and pregnancy.

Look at the oxygenation status of the patient

The oxygenation status of the patient is judged by the paO₂;however, never comment on the oxygenation status without knowing the corresponding FiO_ii. Calculate the expected paO_two (mostly five times the FiO₂).[6]

Based on the expected paO₂ classify as mild, moderate, and severe hypoxia.

Ventilatory status

Expect at paCO₂.

Acid–base of operations condition

Identify the primary disorder by looking at the pH

pH > 7.40–Alkalemia: – 7.forty-Acidemia

Then wait at paCO_ii which is a respiratory acid, whether it is increased, i.e., >forty (acidosis) or decreased <40 (alkalosis) and if this explains the alter of pH, so it is respiratory disorder; otherwise, see the trend of change of HCO₃ ^-(whether increased in alkalosis or decreased in acidosis)–if it explains the change of pH, and then it is a metabolic disorder.

In a normal ABG

pH and paCO₂ motion in contrary directions.
HCO₃ ^-and paCO₂ move in same direction.

When the pH and paCO_two alter in the same direction (which normally should not), the chief problem is metabolic; when pH and paCO_ii move in opposite directions and paCO_ii is normal, then the main problem is respiratory.
Mixed Disorder–if HCO₃ ^- and paCO₂ modify in contrary management (which they normally should not), then it is a mixed disorder: pH may be normal with abnormal paCO_two or aberrant pH and normal paCO₂).[7]

If the tendency of change in paCO₂ and HCO_iii ^- is the same, check the percent difference. The ane, with greater % departure, betwixt the ii is the one that is the dominant disorder.

e.g.: pH = 7.25 HCO_iii ^-=xvi paCO₂=60

Here, the pH is acidotic and both paCO_two and HCO₃ ^- explain its acidosis: so look at the % difference

HCO_three ^-% difference = (24 - xvi)/24 = 0.33

paCO₂% difference = (60 - 40)/40 = 0.5

Therefore, respiratory acidosis as the dominant disorder.

Respiratory disorders

After the primary disorder is established as respiratory, so the following points will assistance united states to approach further with regard to the respiratory disorder).[viii]

Ratio of rate of change in H⁺to alter in paCO₂
Alveolar arterial oxygen gradient
Bounty

Ratio of charge per unit of change in H⁺to change in paCO₂

The above ratio of charge per unit of change in H⁺to modify in paCO₂ helps in guiding us to conclude whether the respiratory disorder is acute, chronic, or acute on chronic. Equally we accept seen, the hydrogen can be calculated from Table 1 and the change in H⁺ is calculated by subtracting the normal H⁺ from the calculated H⁺ ion.[9]

>0.8–acute

0.3–0.viii–astute on chronic

Alveolar Arterial Oxygen Gradient

It is calculated as follows:

${PAO}_{ii} = {FiO}_{ii} (PB - {PH}_{ii} O) - \frac{{PaCO}_{ii}}{R}$

where PAO₂, alveolar fractional pressure of oxygen; PiO₂, partial pressure of inspired oxygen; FiO₂, fraction of inspired oxygen; PB, barometric pressure (760 mmHg at sea level); PH₂O, water vapor pressure (47 mm Hg), PaCO₂, fractional force per unit area of carbon dioxide in blood; R, respiratory quotient causeless to be 0.8.

$= {FiO}_{two} (760 - 47) - \frac{{PaCO}_{2}}{0.8}$

Hypoxemic respiratory failure tin exist associated with normal (10–xv mmHg) or increasedalveolar arterial oxygen slope. Figure 2 shows the alogrithim for approach in a patient with hypoxemic respiratory failure. If this gradient is <20, then information technology indicates an extrapulmonary cause of respiratory failure.

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Flow diagram showing arroyo to hypoxemic respiratory failure

Differentials of extrapulmonary causes of respiratory failure:

Fundamental nervous system–Respiratory center depression due to causes such as drug overdose, principal alveolar hypoventilation, and myxedema.
Peripheral nervous system–Spinal string diseases, Guillain-Barré syndrome, Amyotrophic lateral sclerosis.
Respiratory muscles–Hypophosphatemia, muscle fatigue, myasthenia gravis, and polymyositis.
Chest wall diseases–Ankylosing spondylitis, flail chest, thoracoplasty.
Pleural diseases–Restrictive pleuritis
Upper air way obstruction–Tracheal Stenosis, song string tumor

Compensation

Rules of compensation

The compensatory response depends upon the proper performance of the organ system involved in the response (lungs or kidneys) and on the severity of acid–base disturbance. For example, the likelihood of complete compensation in chronic respiratory acidosis is <15% when paCO_two exceeds 60 mmHg.
Astute bounty occurs within vi–24 h and chronic within ane–four days. Respiratory compensation occurs faster than metabolic compensation.
In clinical practise, it is rare to see complete compensation. The maximum compensatory response in most cases is associated with only 50–75% return of pH to normal. Nevertheless, in chronic respiratory alkalosis, the pH may actually completely return to normalcy in some cases.

Respiratory acidosis

Acute: [HCO_three ^-] increase by one mEq/L for every 10 mmHg increase in paCO₂ above 40.

Chronic: [HCO_three ^-] increase by three.5 mEq/L for every x mmHg increment in paCO_two above 40.

Respiratory alkalosis

Astute: [HCO_three ^-] decrease past 2 mEq/Fifty for every 10 mmHg decrease in paCO₂ below 40.

Chronic: [HCO_iii ^-] decrease by 5 mEq/L for every ten mmHg decrease in paCO₂ beneath 40.

Metabolic disorders

In patients with metabolic acidosis, an backlog of acid or loss of base of operations is present. This causes the HCO₃ ^-:H₂CO₃ratio and pH to fall while no change occurs in pCO_two–uncompensated metabolic acidosis.

Equally a result of compensatory mechanisms, the lungs in the form of CO₂ excrete H₂CO₃ and the kidneys retain HCO₃ ^-. pCO₂ falls and HCO_three ^-: H₂CO₃ ratio and pH rise toward normal even though concentrations of HCO_iii ^-and H_iiCO₃ are less than normal. This is called compensated metabolic acidosis and the expected paCO₂ is calculated as paCO_ii = [1.5 × HCO₃+ eight] ± 2.

Anion gap

For more than than 40 years, the AG theory has been used by clinicians to exploit the concept of electroneutrality and has evolved as a major tool for evaluating the acid–base disorder. Anion gap is the divergence between the charges of plasma anions and cations, calculated from the difference between the routinely measured concentration of the serum cations (Na⁺ and K⁺) and anions (Cl^- and HCO_iii ^-). Because electroneutrality must exist maintained, the difference reflects the unmeasured ions. Commonly, this deviation or the gap is filled by the weak acids (A^-) principally albumin, and to a lesser extent phosphates, sulfates, and lactates.

When the AG is greater than that produced past the albumin and phosphate, other anions (eastward.g., lactates and ketones) must be nowadays in higher than normal concentration.

Anion gap = (Na⁺ + K⁺) - [Cl^- + HCO_iii ^-]

Because of its low and narrow extracellular concentration, K⁺ is often omitted from the adding The normal value ranges from 12 ± 4 when Thousand⁺ is considered, and 8 ± 4 when K⁺ is omitted. Figure 3 shows the alogrithm for the approach to patients with normal AG acidosis.

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Approach to a patient with normal anion gap acidosis

The master trouble with AG is its reliance on the use of the normal range produced by the albumin and to a lesser extent phosphate, the level of which may be grossly abnormal in critically ill patients. Because these anions are non potent anions, their charges volition be altered by changes in pH.[x,11]

Serum protein and phosphate

Normal AG = ii{albumin(gm/50)} + 0.5 {phosphate (mg/dL)}

Acid–base status

In Acidemic state - Anion gap decreases by ane-3

In Alkalemic state - Anion gap increases by 2-5

Major clinical uses of the anion gap

For signaling, the presence of a metabolic acidosis and confirm other findings.
Helping to differentiate between causes of metabolic acidosis: High AG versus normal AG metabolic acidosis. In an inorganic metabolic acidosis (e.g., due to HCl infusion), the infused Cl^- replaces HCO₃ ^-, and the AG remains normal. In an organic acidosis, the lost bicarbonate is replaced by the acid anion which is not usually measured. This means that the AG is increased.
Providing help in assessing the biochemical severity of the acidosis and follow the response to treatment.

Disorders that are associated with a low or negative serum AG are listed in Table ii.

Table 2

Disorders associated with low serum anion gap

Cause	Comments
Laboratory fault	Most frequent cause of depression anion gap
Hypoalbuminemia	2d virtually common cause of low serum anion gap
Multiple myeloma	Level of anion gap correlates with serum concentration of paraprotein
Halide intoxication	Anion gap depends on serum halide concentration
(bromide, lithium, iodide)	(depression anion gap with lithium ≥4 mEq/Fifty)
Hypercalcemia	more than likely in hypercalcemia associated with 10 hyperparathyroidism
Hypermagnesemia	Theoretical crusade just not documented in literature
Polymyxin B	Anion gap depends on serum level; occurs with preparation with chloride
Underestimation of serum sodium	Well-nigh frequent with hypernatremia or hypertriglyceridemia
Overestimation of serum chloride	Rare with ion selective electrodes
Overestimation of serum bicarbonate	Spurious ⁭in serum HCO₃ if cells not separated from sera

Table 3 elaborates the species of the unaccounted anions along with their sources of origin and diagnostic adjunts in case of loftier AG metabolic acidosis.

Tabular array iii

Description of the species of unmeasured anions, source of origin, and diagnostic adjuncts in case of high anion gap metabolic acidosis

Cause	Loftier serum anion gap
	Comments
	Species	Origin	Diagnostic adjuncts
Renal failure	Phosphates, sulphates	Protein metabolism	BUN/creatinine
Ketocidosis	Ketoacids	Fatty acid metabolism	Serum/urine ketones
Diabetic	β Hydroxybutyrate
Alcoholic
Starvation	Acetoacetate
Lactic acidosis	Lactate		Lactate levels
Exogenous poisoning	Salicylate	Salicylate	Concomitant
	Lactate	Respiratory and metabolic alkalosis
	ketoacids

In the patients with metabolic alkalosis, there is an excess of base or a loss of acid which causes the HCO₃ ^-:H₂CO₃ ratio and pH to rise, only with no change occurring in pCO_ii, which is called uncompensated metabolic alkalosis. However, the kidney has a large capacity to excrete backlog bicarbonate and so, for sustaining the metabolic alkalosis, the elevated HCO₃ ^-concentration must be maintained through an abnormal renal retention of HCO_iii ^-.

Compensatory respiratory acidosis may be and so marked that pCO₂ may rise higher than 55 mmHg. Expected paCO₂is calculated as paCO_ii = [0.seven × HCO₃ ^-+ 21] ± 2 or 40 + [0.7 ΔHCO₃]. This is chosen compensated metabolic alkalosis.

Most of the patients with metabolic alkalosis can be treated with chloride ions in the form of NaCl (saline responsive) rather than KCl (which is preferable). When NaCl is given, Cl^-ions are supplied, and then the blood volume increases and the secretion of aldosterone in excess decreases. Thus, excessive urinary loss of M⁺and excessive reabsorption of HCO₃ ^- stops. When metabolic alkalosis is due to the effects of excessive aldosterone or other mineralocorticoids, the patient does not respond to NaCl (saline resistant) and requires KCl.

Based on the urinary chloride, metabolic alkalosis is divided into:

Chloride responsive or extracellular book depletion (urinary chloride < 20)

Vomiting
Diuretic
Post hypercapnic
Chronic diarrhea
Chloride resistant (urinary chloride > xx)
Severe potassium depletion
Mineralocorticoid excess–Primary hypealdosteronism, Cushing's Syndrome, Ectopic ACTH
Secondary hypereldosteronism–Renovascular disease, malignant hypertension, CHF, cirrhosis

Aproach to mixed disorder

Mixed metabolic disturbances (due east.g., loftier AG from diabetic ketoacidosis plus normal AG from diarrhea) tin can exist identified using the relationship betwixt AG and HCO₃ ^-, which is called the gap–gap ratio. Information technology is the ratio of change in anion gap (ΔAG) to change in HCO₃ ^- (ΔHCO₃ ^-). When hydrogen ions accumulate in blood, the decrease in serum HCO₃ ^- is equivalent to the increase in AG and the increase in AG backlog/HCO₃ ^- deficit ratio is unity, i.e., pure increase in AG metabolic acidosis. When a normal AG acidosis is present, the ratio approaches zero. When a mixed acidosis is present (high AG + normal AG), the gap–gap ratio indicates the relative contribution of each type to the acidosis. If information technology is <1, then it suggests that at that place is a normal AG metabolic acidosis associated with it and if >2 information technology suggests that there is associated metabolic acidosis.

Rules for rapid clinical estimation of ABG

When required to brand a proper approach towards the evaluation of blood gas and acid–base disturbances in the torso, the post-obit scheme is suggested:

Look at pH - < 7.40 - Acidosis; > 7.40 - Alkalosis
If pH indicates acidosis, then look at paCO₂and HCO₃ ^-
If paCO₂is ↑, then information technology is primary respiratory acidosis
1. To determine whether it is acute or chronic
  
  ΔH⁺ / ΔpaCO_ii <0.3–chronic
  
  >0.8–acute
  
  0.3-0.viii–acute on chronic
2. Calculate compensation by the respective methods
  
  Acute: [HCO₃ ^-] ↑ by i mEq/L for every 10 mmHg ↑ in paCO2 above 40.
  
  Chronic: [HCO₃ ^-] ↑ by iii.5 mEq/Fifty for every ten mmHg ↑ in paCO2 above 4
If paCO₂↓ and HCO_iii ^- is also ↓→ primary metabolic acidosis

Summate expected paCO_iias follows:

paCO₂ = [1.v × HCO_three+ viii] ± two metabolic acidosis simply

paCO₂ < expected paCO₂→ concomitant respiratory alkalosis.

paCO₂ > expected paCO_ii→ concomitant respiratory acidosis
If HCO₃ ^-is ↓, then AG should be examined.
If AG is unchanged → and then information technology is hyperchloremic metabolic acidosis.
If AG is ↑ → so it is wide AG acidosis.
Check gap-gap ratio

ΔAG/Δ HCO3^- = 1, pure increased AG metabolic acidosis

<one normal anion gap metabolic acidosis

>2 associated metabolic acidosis.
If pH indicates alkalosis, and then look at HCO₃ ^- and paCO_ii.
If paCO₂is ↓ → then information technology is main respiratory alkalosis.
1. Whether it is acute or chronic (with the aforementioned formula every bit to a higher place)
2. Calculate compensation by the respective methods:
  
  Acute: [HCO₃ ^-]↓ by two mEq/L for every 10 mmHg
  
  ↓ in paCO₂below twoscore.
  
  Chronic: [HCO₃ ^-] ↓ past five mEq/L for every
  
  10mmHg ↓ in paCO_ii beneath 40.
If paCO₂ ↑ and HCO₃ ^- also ↑ → and then it is primary metabolic alkalosis.

Calculate the expected paCO_ii

paCO₂ = [0.7 × HCO3^-+ 21] ± 2 Or 40 + [0.7 ΔHCO3] → metabolic alkalosis only

paCO₂ < expected paCO2 → concomitant respiratory alkalosis.

paCO_two > expected paCO2 → concomitant respiratory acidosis
Check urinary chloride

if urinary chloride < xx → chloride responsive or ECV depletion

if urinary chloride > 20→ chloride resistant
If pH is normal ABG may be normal or mixed disorder
1. ↑paCO₂ and ↓HCO₃ ^-→ respiratory and metabolic acidosis
2. (b) ↓paCO_ii and↑ HCO₃ ^-→ respiratory and metabolic alkalosis.
  
  Calculate % difference (ΔHCO₃ ^-/HCO_iii ^-and ΔpaCO_ii/paCO₂) to run across which is dominant disorder.

Footnotes

Source of Support: Nothing

Disharmonize of Interest: None declared.

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