Abg in the emergency room.
In addition, current blood gas machines also measure electrolytes, hemoglobin concentration and abnormal hemoglobin species, lactate, glucose, blood urea nitrogen (BUN) or creatinine. Thus, arterial blood gases, in conjunction with these additional analytes, provide a comprehensive view of the patient at a single point in time. Thus, the clinician can make a comprehensive assessment of the patient and often a differential diagnosis of acid-base and oxygenation disturbances.
A Systematic Approach
Effective blood gas interpretation and application requires the clinician to have an organized and systematic approach. The method I suggest can be referred to as the "ABCs of Blood Gas Application." These so-called ABC's are acid-base balance, blood oxygenation and cellular oxygenation. Clinicians should think through each of these areas discretely and completely.
Acid-base assessment also includes ventilation assessment as the PaCO2 is the primary indicator of respiratory acid-base disturbances and ventilation. Blood oxygenation looks at the effectiveness of the lungs in getting inspired oxygen into the pulmonary capillary blood. The simplest index of blood oxygenation is the P/F (PaO2/FIO2) ratio. Finally, cellular oxygenation assessment looks beyond the PaO2 or SpO2 (oxygen saturation as measured by pulse oximetry) in order to ensure the tissues and cells are receiving adequate oxygenation.
The patient in this case is a 56 year-old male presenting with nausea, vomiting, stomach pain and excessive urination. The patient was also breathing rapidly and deeply (gasping), although the cough was non-productive. The breath had a sweet fruity odor. The patient also complained of weakness, lethargy and increased thirst.
Arterial Blood Gases
SaO2 94% pH 7.07 PaCO2 9 mm Hg PaO2 107 mm Hg HCO3 7 mEq/L Electrolytes/Other Analytes Na 160 mEq/L Cl 131 mEq/L K 3.6 mEq/L G 1,023 mg/dL Lactate 2.5 mM/L BUN 36 mg/dL
The novice may easily see this patient and suspect some respiratory disorder responsible for the rapid, deep breathing. Indeed, nothing could be farther from the truth. The breathing is classic Kussmaul Breathing--compensatory hyperventilation in response to acute metabolic acidosis, particularly as seen in diabetic keto-acidosis.
In differential acid-base diagnosis, it is critical to determine the primary problem and not focus on compensatory responses. The blood gas acid-base classification is partially compensated metabolic acidosis. The acidosis is somewhat severe. The focus of acid-base diagnosis and treatment should be on the primary metabolic acidosis.
The first step in evaluation of primary metabolic acidosis is to calculate the anion gap (anion gap = Na+ - (Cl- + HCO3-). A normal anion gap is approximately (10 to 16 mEq/L). An increased anion gap is likely due to an accumulation of fixed acids, whereas a normal anion gap suggests the patient has lost base. The anion gap of 22 mEq/L in this patient clearly points toward an accumulation of fixed acids.
There are four classic causes of high anion gap acidosis: poisoning, renal failure, lactic acidosis and keto-acidosis.
Based on the extreme hyperglycemia (normal glucose approximately 125 mg/dL), the primary acid-base disturbance is clearly diabetic keto-acidosis (DKA). Often, glucose will not be this high, although, as seen, it can be far greater than 1,000 mg/dL. On average, glucose will typically be near 500 mg/dL in acute keto-acidosis. It is also common to see increased lactate in any patient with a pH < 7.1. The increased BUN in this patient is likely due to dehydration, and severe DKA can lead to acute renal failure.
As we know, in diabetes mellitus, the lack of insulin production prevents glucose from entering the cells and producing energy. When glucose cannot enter the cell, it accumulates in the plasma (hyperglycemia) and the urine (glycosuria). The hyperglycemia in the plasma leads to increased urine output secondary to hyperosmolar diuresis. The dehydration, in turn, may lead to dehydration, increased thirst, and potentially renal failure secondary to low perfusion. This is likely the reason for the mildly increased BUN.
Azotemia is the accumulation of nitrogenous wastes in the blood indicated by increased BUN or creatinine. In this case, the cause is likely pre-renal azotemia where hypovolemia leads to diminished renal perfusion. Uremia is the symptom complex (lethargy, weakness, etc.) associated with azotemia. Essentially, azotemic and uremic renal failure are the same entity.
In addition, the hypernatremia is likely a result of intracellular fluid depletion and hyperconcentration of electrolytes. Finally, plasma potassium, which often increases in metabolic acidosis, is likely depleted due to the loss of excessive GI fluids.
When glucose is not available within cells, fat metabolism increases. Fat metabolism results in the accumulation of beta-hydroxybutyric (B-OH) acid and acetoacetic acid. These two acids are the keto-acids. Similarly, ketone bodies accumulate in proportion to the keto-acids. The ketone bodies include acetoacetate, beta hydroxybutyrate, and acetone.
Ketone bodies will be seen in the blood and urine (ketonuria), and they are responsible for the sweet fruity breath odor. Interestingly, keto-acidosis may also be seen in starvation although the cause here is not lack of insulin but rather insufficient carbohydrate intake.
Typically, DKA will present with the biochemical triad: hyperglycemia, ketonuria/ketonemia and high anion gap metabolic acidosis.
Remember that blood oxygenation looks at the efficiency of oxygen uptake in the lungs via the PaO2/FIO2 (P/F) ratio. A PaO2 of greater than 100 mm Hg is often called hyperoxemia.
There are only two potential causes of hyperoxemia. The most common cause is exogenous oxygen therapy; however, this patient is breathing room air. Hyperventilation on room air as seen in Kussmaul breathing, may lead to PaO2s above 100 mm Hg, although PaO2 on room air rarely exceeds 120 mm Hg. There is no problem regarding oxygen uptake in the lungs in this patient despite the apparent shortness of breath.
It is also interesting to note that the SaO2 is only 94 percent despite a PaO2 greater than 100 mm Hg. This is due to the classic right shift of the oxyhemoglobin curve to the right. This right shift and decreased affinity of hemoglobin for oxygen is secondary to the severe acidosis.
The elevated lactate may suggest the presence of some hypoxia; however, the major concern regarding tissue oxygenation and energy production in this patient is insuring glucose can enter the cells and ensuring the patient is not hypovolemic. The primary focus in this patient is normalization of acid-base, fluid and electrolyte status.
Overall Assessment and Intervention
This patient is suffering from acute diabetic keto-acidosis. Insulin, glucose and fluid regulation should be the primary focus. Severe acidosis should be prevented. Severe acidosis may lead to arrhythmia, coma and death.
The American Diabetes Association (ADA) guidelines consider DKA under control when blood glucose is < 200 mg/dL, bicarbonate is greater than 18 mEq/L and pH is > 7.30. Sodium bicarbonate administered intravenously is the most common supportive treatment for metabolic acidosis.
Nevertheless, bicarbonate should be administered sparingly as these patients frequently may swing over to metabolic alkalosis following treatment. This occurs because base is produced endogenously as the ketone bodies are metabolized. Therefore, exogenous administration of bicarbonate in combination with endogenous production may overshoot the target of a normal pH. Generally, bicarbonate administration should be considered when pH falls below approximately 7.1.
William Malley, MS, RRT, CPFT, is Administrative Director of Respiratory/Pulmonary Services at The Western Pennsylvania Hospital in Pittsburgh, PA. Feel free to direct questions, comments, correspondence or additional cases to firstname.lastname@example.org.
by William Malley, MS, RRT, CPFT, FAARC
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|Title Annotation:||BLOOD GAS CASE STUDIES|
|Publication:||FOCUS: Journal for Respiratory Care & Sleep Medicine|
|Date:||May 1, 2010|
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