61 year old male with history of CHF transferred to medical ICU.
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.
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 ABC's of Blood Gas Application. These so-called ABC's are listed below. The clinician 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 insure the tissues and cells are receiving adequate oxygenation.
Our patient in this case is a 61 year old male with a 7 year history of CHF who enters the ED with severe cardiopulmonary distress culminating in a brief cardiac arrest. The patient is transferred to the ICU where arterial blood gases and electrolytes are drawn. His chest X-ray shows increased diffuse pulmonary congestion and hilar markings, A CVP is placed and is reading 15 mm Hg. The blood gas indicates a "Mixed Respiratory and Metabolic Acidosis with Mild Hypoxemia".
Arterial Blood Gases FIO2 0.60 sO2 85% pH 7.14 pCO2 55 mm Hg pO2 64 mm Hf cHCO3 18 mEq/L Vital Signs B/P 70/P mm Hg RR 26/min HR 108/min Temp 370C Electrolytes Na 143 mEq/L Cl 105 mEq/L K 5.3 mEq/L
Patients with single acid-base disturbances are said to have "simple acid-base problems". Patients with two or more acid-base disturbances are said to have "mixed acid-base disturbances". This individual presents to the ICU with a mixed respiratory and metabolic acidosis. When both respiratory and metabolic conditions are moving pH in the same direction, sometimes the term "combined acidosis" is used.
The respiratory acidosis is likely due to a combination of excessive ventilation perfusion mismatch (i.e. pulmonary shunting) secondary to the pulmonary fluid and exhaustion due to increased work of breathing. When either or both of these conditions are excessive, hypercapnia may ensue. There is also potential for hypoventilation secondary to the cardiac arrest and disease and diminished neurological circulation which may have occurred during the cardiac arrest.
The metabolic acidosis on the other hand is most likely secondary to tissue hypoxia and subsequent anaerobic metabolism and lactic acidosis. The cardiac arrest and mild hypoxemia may be contributing to this but the severe hypotension and likely low cardiac output is probably the primary cause.
The anion gap (Na - (HCO3 + Cl) is normally less than 16 mEq/L. An elevated anion gap is highly suggestive of an accumulation of fixed acids. In this case, the anion gap 20 mEq/L and suggests the accumulation of fixed acid consistent with lactic acidosis. An elevated lactate level would definitely confirm this cause of primary metabolic acidosis. Normal lactate should be less than 1.8 mMol/L.
Remember blood oxygenation looks at the efficiency of oxygen uptake in the lungs via the Oxygenation pO2/FlO2 (P/F) ratio. The very low P/F ratio of approximately 1.0 indicates severe pulmonary shunting. The shunting appears to be true or absolute since it is poorly responsive to oxygen therapy. The diffuse white out on the CXR supports the likelihood of pulmonary edema. The white out could indicate the development of acute lung injury or acute respiratory distress syndrome but the elevated CVP along with the hypotension and increase hilar markings is highly indicative of cardiogenic pulmonary edema secondary to CHF.
There appears to be little doubt that the patient's metabolic acidosis is a result of lactic acidosis secondary to cardiogenic pulmonary edema. The key factor in oxygen delivery to the tissues in CHF is usually the cardiac output. This type of hypoxia is often referred to as circulatory hypoxia or stagnant hypoxia. Decreased mixed venous (or CVP) oxygenation values would support this conclusion although they are not available in this patient. Normal mixed venous oxygen values are approximately 35-45 mm Hg pO2 (v)and sO2(v) less than 75%. The values may be slightly higher from a central venous line but lower values would be beneficial in confirming the diagnosis.
In CHF, the heart (pump) is often overloaded with venous return that it is incapable of pumping adequately. Starling's curve and law indicates that venous congestion impedes the ability of the heart to maximize cardiac output. Typically a reduction in venous return in these patients will improve cardiac output.
A variety of mechanisms may decrease venous return in these patients and improve cardiac function. Diuretics and digitalis is typically the mainstay of chronic management of CHF. Notwithstanding, PEEP (increased mean airway pressure) and positioning the patient in a sitting position may likewise prove beneficial and perhaps lifesaving. This is a simple therapeutic maneuver often overlooked by respiratory therapists which does not require a physician order.
The body also tries to compensate for diminished tissue oxygenation by releasing increased oxygen to the tissues. The low sO2 (less than 90%) despite a pO2 above 60 mm Hg suggests a right shift of the oxyhemoglobin curve. Typically, a right shift of this curve is beneficial as it results increased oxygen delivery to the cells. The hypercapnia and academia are responsible for this shift and the attempt of the body to improve tissue oxygenation. Nevertheless, this appears to be minor factor and the patient persists with tissue hypoxia.
Overall Assessment and Intervention
The patient appears to be suffering from acute cardiogenic pulmonary edema resulting in severe pulmonary shunting and hypercapnia. More importantly, the patient is in circulatory hypoxia secondary to diminished cardiac output. This seems apparent based on the hypotension, elevated CVP, and metabolic acidosis.
Therapy should be aimed at reducing venous return. This may be accomplished via decreased fluid management, pharmacologic intervention (e.g diuretics and inotropic agents), patient positioning, and application of positive pressure.
Intubation and mechanical ventilation is also indicated to reverse the acute hypercapnia (acute respiratory acidosis) and decrease venous return. Positive pressure may likewise prove useful in maintaining open alveoli and decreasing venous return and optimizing cardiac function.
The primary focus in this patient is normalization of acid-base, fluid and electrolyte status. Specifically, hypokalemia and metabolic alkalosis must be corrected. The patient should receive potassium, chloride and fluids in a carefully monitored manner. Pharmacological therapy, particularly diuretic and dosage should be reviewed. Cardiac and fluid status should be carefully monitored with vital signs and EKG and other clinical information.
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.
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 email@example.com.
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:||Sep 1, 2010|
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