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Join date : 2014-11-03

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PostSubject: Arterial blood gas   Arterial blood gas EmptySun Dec 07, 2014 6:11 am

A 30-year -old female presents to an Emergency Department with acute breathlessness. The forced expiratory volume in one second (FEV1) is 3.00 (predicted 4.00) litres and forced vital capacity (FVC) is 3.75 (predicted 5.00) litres.

Arterial blood gases show:
pH = 7.47
: PaO2 = 95
PaCO2 = 32
HCO3 = 36 mEq/litre.
The most likely cause of the results is

A. pulmonary thromboembolism.
B. bulimia.
C. acute asthma.
D. salicylate overdosage.
E. hyperventilation syndrome

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PostSubject: Re: Arterial blood gas   Arterial blood gas EmptySun Dec 07, 2014 6:16 am

E is correct because the ABG shows respiratory alkalosis .
Readers are welcome to discuss their observations and share their comments.

6-step approach:
Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation:
[H+] = 24(PaCO2)
If the pH and the [H+] are inconsistent, the ABG is probably not valid.
pH Approximate [H+]
7.00 100
7.05 89
7.10 79
7.15 71
7.20 63
7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22
Step 2: Is there alkalemia or acidemia present?
pH < 7.35 acidemia
pH > 7.45 alkalemia
• This is usually the primary disorder
• Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 – 7.45)
• You will need to check the PaCO2, HCO3- and anion gap
Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction.
Acidosis Respiratory pH ↓ PaCO2 ↑
Acidosis Metabolic& pH ↓ PaCO2 ↓
Alkalosis Respiratory pH ↑ PaCO2 ↓
Alkalosis Metabolic pH ↑ PaCO2 ↑
Step 4: Is there appropriate compensation for the primary disturbance? Usually, compensation does not return the pH to normal (7.35 – 7.45).
Disorder Expected compensation Correction factor
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ± 2
Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10 ± 3
Chronic respiratory acidosis (3-5 days) Increase in [HCO3-]= 3.5(∆ PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)
If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present.
Step 5: Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] + [HCO3-] )-12 ± 2
• A normal anion gap is approximately 12 meq/L.
• In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.)
• If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations.
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure
• Toxic ingestion is suspected
OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8
• The OSM gap should be < 10
Step 6: If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO3-].
Assess the ratio of the change in the anion gap (∆AG ) to the change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]
This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis is present.
If this ratio falls outside of this range, then another metabolic disorder is present:
• If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be present.
• If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be present.
It is important to remember what the expected “normal” anion gap for your patient should be, by adjusting for hypoalbuminemia (see Step 5, above.)
Table 1: Characteristics of acid-base disturbances
Disorder pH Primary problem Compensation
Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2
Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2
Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]
Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]
Table 2: Selected etiologies of respiratory acidosis
• Airway obstruction
- Upper
- Lower
• asthma
• other obstructive lung disease
• CNS depression
• Sleep disordered breathing (OSA or OHS)
• Neuromuscular impairment
• Ventilatory restriction
• Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates
• Incorrect mechanical ventilation settings
Table 3: Selected etiologies of respiratory alkalosis
• CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection
• Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2
• Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus
• Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins
• Pregnancy, liver disease, sepsis, hyperthyroidism
• Incorrect mechanical ventilation settings
Table 4: Selected causes of metabolic alkalosis
• Hypovolemia with Cl- depletion
• GI loss of H+
• Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid
• Renal loss H+
• Loop and thiazide diuretics, post-hypercapnia (especially after institution of mechanical ventilation)
• Hypervolemia, Cl- expansion
• Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration
Table 5: Selected etiologies of metabolic acidosis
• Elevated anion gap:
• Methanol intoxication
• Uremia
• Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation ketoacidosis
• Paraldehyde toxicity
• Isoniazid
• Lactic acidosisa
• Type A: tissue ischemia
• Type B: Altered cellular metabolism
• Ethanolb or ethylene glycolb intoxication
• Salicylate intoxication
a Most common causes of metabolic acidosis with an elevated anion gap
b Frequently associated with an osmolal gap
• Normal anion gap: will have increase in [Cl-]
• GI loss of HCO3-
• Diarrhea, ileostomy, proximal colostomy, ureteral diversion
• Renal loss of HCO3-
• proximal RTA
• carbonic anhydrase inhibitor (acetazolamide)
• Renal tubular disease
• Chronic renal disease
• Distal RTA
• Aldosterone inhibitors or absence
• NaCl infusion, TPN, NH4+ administration
Table 6: Selected mixed and complex acid-base disturbances
Disorder Characteristics Selected situations
Respiratory acidosis with metabolic acidosis ↓in pH
↓ in HCO3
↑ in PaCO2
• Cardiac arrest
• Intoxications
• Multi-organ failure
Respiratory alkalosis with metabolic alkalosis ↑in pH
↑ in HCO3-
↓ in PaCO2
• Cirrhosis with diuretics
• Pregnancy with vomiting
• Over ventilation of COPD
Respiratory acidosis with metabolic alkalosis pH in normal range
↑ in PaCO2,
↑ in HCO3-
• COPD with diuretics, vomiting, NG suction
• Severe hypokalemia
Respiratory alkalosis with metabolic acidosis pH in normal range
↓ in PaCO2
↓ in HCO3
• Sepsis
• Salicylate toxicity
• Renal failure with CHF or pneumonia
• Advanced liver disease
Metabolic acidosis with metabolic alkalosis pH in normal range
HCO3- normal
• Uremia or ketoacidosis with vomiting, NG suction, diuretics, etc.
Suggested additional reading:
• Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders, 5th ed. New York: McGraw Hill Medical Publishing Division, c2001.
• Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256.
• Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—first of two parts. N Engl J Med 1998;338:26-34.
• Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—second of two parts. N Engl J Med 1998;338:107-111.
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