Acid-Base Abnormalities Part II Case File

Acid-Base Abnormalities Part II Case File

Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 25

A 44-year-old man who was diagnosed with cryptogenic cirrhosis 2 years ago is now being hospitalized for a fractured left hip sustained after a  car accident. also has a pulmonary emboli, is in respiratory distress, and is admitted to the ICU for monitoring. He is currently on the waiting list for a  liver transplant. He has a 25-pack-year smoking history  but does not drink alcoholic beverages and has not  used illicit drugs for the past 10 years. His  current medications include aspirin spironolactone, lactulose, propranolol, and furosemide. On physical examination, his temperature is 36°C (96.8° F), heart rate is 92 beats/minute, respiration rate is 28 breaths/minute, and blood pressure is 98/55 mm Hg. He is cachectic and has scleral icterus and palmar erythema. His mentation appears normal, and a sterixis are absent. The cardiac examination reveals no heart murmurs or rubs, and his lungs are clear. The abdomen is distended but is not tender. Peripheral edema is present in both lower extremities. The laboratory reports the following values: sodium 134 mEq/L, potassium 3.3 mEq/L, chloride 107 mEq/L, bicarbonate 18 mEq/L. Arterial blood gas studies (on room air) show a pH 7.48, a PACO2 of 25 mm Hg and a PAO2 of 92 mm Hg, bicarbonate level of 18 mEq/L.

⯈What is this patient's acid-base disorder?

⯈What is the best treatment for this patient?

ANSWER TO CASE

Acid-Base Abnormalities Part II

Summary: This is a 44-year-old man with a history of cryptogenic cirrhosis who underwent a motor vehicle accident and developed a pulmonary embolism. He is noted to have an arterial pH of 7.48, PACO2 of 25 mm Hg, PAO2 of 92 mm Hg, and bicarbonate level of 18 mEq/L.

• Acid-base disorder: Respiratory alkalosis with appropriate partial metabolic compensation
• Treatment options: Adequate pain control avoiding respiratory depression. BiPAP may be indicated to address the respiratory distress. If the ascites is under tension, a high-volume paracentesis may be performed to alleviate the pressure on the diaphragms. This increased respiratory drive is due to restriction imposed on the lungs by the diaphragm elevation. Pleural effusions secondary to the ascites further exacerbate the situation. The ascitic fluid should be sent for a CBC and culture in search for spontaneous bacterial peritonitis, which is commonly seen in patients with ascites.

ANALYSIS

Objectives

1. To use a common stepwise approach to acid-base evaluation.
2. To understand the respiratory effects on acid-base disorders.
3. To understand the most common causes of respiratory disorders, related to an acid-base imbalance.

Considerations

This patient has end-stage liver disease. Respiratory alkalosis often develops in patients with end-stage liver disease, and the partial metabolic acidosis compensation (decreased bicarbonate level) speaks for a chronic respiratory alkalosis. This likely is due to an increased minute ventilation (VE). One speculated mechanism is that diminished hepatic steroid metabolism leads to elevated serum progesterone levels, which stimulate respiratory drive. Additionally, the patient has acute pulmonary embolism, which leads to a VQ mismatch, stimulating an acute increase in minute ventilation.

Approach To:

Acid- Base Disorders II

Introduction

Acid-base status can be diagnosed by answering a series of questions (see Case 24): In respiratory disorders, PACO2 and HCO3 move in the same direction. If the PACO2 decreases, so does the HCO3; and if the PACO2 falls, the HCO3 also falls (Table 24-1). This correlation exists, since the respiratory and metabolic parameters compensate for changes in the other. In pure metabolic disorders, the pH,

PACO2 and HCO3 all point in the same direction. When the PACO2 or HCO3 move in the opposite direction of the pH, a mixed respiratory and metabolic component is responsible for the disorder.

For example, if the primary respiratory disorder is acute in nature, then the measured HCO3 should change in coordination with the change in PACO2. For every 10 mm Hg decrease in PACO2, there should be a 2 mEq/L decrease in HCO3 (normal HCO3 of 24 mEq/L) in the acute condition, and a fall of 4 mEq/L from the normal HCO3 in the chronic condition. If the change in HCO3 is less than expected, then a metabolic acidosis accompanies the respiratory alkalosis. If the HCO3 is greater than expected, then a concomitant metabolic alkalosis is present.

Respiratory Acidosis

Respiratory acidosis is due to a primary increase in arterial PACO2, which accumulates when the ventilation is inadequate. Hypoventilation can result from neurological disorders (stroke) or medications (narcotics) that affect the respiratory center of the CNS, respiratory muscle weakness (eg, myasthenia gravis or Guillain-Barre syndrome), chest wall deformities (severe kyphoscoliosis), obstruction of airways (COPD), or pulmonary venous thromboembolism. Treatment of respiratory acidosis should focus on addressing the underlying disorder. In patients with acute respiratory acidosis and hypoxemia, supplemental O2 may be administered carefully, keeping the O2sat around 90% to avoid further hypercapnia. Aerosolized bronchodilators should be delivered under controlled FIO2 or compressed ambient air (FIO2 21 %). To increase the effective alveolar ventilation, BiPAP on NIV or endotracheal intubation and mechanical ventilation may be needed.

Example 1: A 47-year-old man with a history of severe COPD is admitted to the ICU for a COPD exacerbation and respiratory distress. He is evaluated because of weakness and dizziness and daytime hypersomnolence. Laboratory studies show serum sodium 140 mEq/L; potassium 5 mEq/L; chloride 100 mEq/L; and serum bicarbonate of 30 mEq/L. Arterial blood gas studies on room air reveal pH, 7.34; PACO2, 55 mm Hg; and bicarbonate, 38 mEq/L.

    What is the acid-base disorder?

• Is the patient acidemic or alkalemic? (pH = 7.34) Acidemic
• Is the acid-base disorder primarily metabolic or respiratory? Respiratory acidosis with appropriate compensation (chronic respiratory acidosis)
• What is the anion gap? 140 - (100 + 30) = 10 mEq/L (normal)
• If a metabolic/respiratory acidosis exists, is there appropriate metabolic/respiratory compensation? Yes, expected change = 1.5 X 4 = 6 + 24 (normal HCO) = 30 mEq/L (predicted compensated HCO3)
• If an anion-gap acidemia is present, is there a complicating metabolic disturbance? No

    Answer: Respiratory acidosis with partial metabolic alkalosis compensation.

Respiratory Alkalosis

Hyperventilation reduces the arterial PACO2, which increases the pH, causing respiratory alkalosis. Common causes of respiratory alkalosis can be sorted by conditions involving the pulmonary vasculature (eg, pulmonary hypertension and venous thromboembolism), pulmonary parenchyma (eg, pulmonary fibrosis, heart failure, and pneumonia), pulmonary airways (asthma) and conditions affecting ventilatory control (eg, anxiety, aspirin toxicity, sepsis, hypoxia, and pregnancy). The expected compensatory responses for acute and chronic respiratory alkalosis are shown in Table 40- 1. The underlying cause for respiratory alkalosis should be pursued. Patients with psychogenic hyperventilation ( anxiety) should be instructed to rebreathe air using a bag, which increases the systemic PACO2; these measures raise the PACO2 and pH, and also may help to reduce the pH in patients with mixed, severe life threatening alkalosis (pH > 7.70). The only acid-base disorder that can return back to a normal pH of 7.40 in the absence of a secondary acid-base disorder is chronic respiratory alkalosis.

Example 2: A 27-year-old woman presents with a 1-day history of severe anxiety and hysteria. She is being evaluated because of weakness and dizziness and an onset of paresthesias. She had a new onset of seizures that lasted 1 minute in which she had an episode of emesis. This led to her admission to the ICU for suspected aspiration pneumonia and treatment of possible rhabdomyolisis. Laboratory studies show serum sodium, 140 mEq/L; serum potassium, 5 mEq/L; serum chloride, 110 mEq/L, and serum bicarbonate of 21 mEq/L. Arterial blood gas studies on room air reveal pH, 7.54; PACO2 25 mm Hg, PAO2 77 mm Hg on 40% FIO2.

    What is the acid-base abnormality?

• Is the patient acidemic or alkalemic? (pH = 7.54) Alkalemic 
• Is the acid-base disorder primarily metabolic or respiratory? Respiratory 
• What is the anion gap? 140 - (110 + 21) = 9 
• If a metabolic/respiratory acidosis exists, is there appropriate metabolic/respiratory compensation? Yes. The change from the normal PACO2 of 40 mm Hg is 15 mm Hg so the expected compensation is 1.5 X 2 = 3 (normal HCO3 24 mEq/L) 24-3 = 21. The measured HCO3 is 21.

    Answer: This patient has an acute respiratory alkalosis with metabolic compensation.

Patients with restrictive lung diseases can only increase minute ventilation by increasing the respiratory rate. Some of these conditions include CHF, pneumonia, pulmonary fibrosis, obesity, ascites, chest bellows restriction, chest wall abnormalities, chest pain, trauma, contusions.

CLINICAL CASE CORRELATION

• See also Case 22 (Acute Liver Failure) and Case 24 (Acid-Base Abnormalities I).

COMPREHENSION QUESTIONS

25.1  A 68-year-old man is brought to the ICU after being dyspneic and tachypneic for 5 days. Axial CT scan diagnosed a pulmonary embolism. On physical examination, the patient's temperature is 36. 7°C (98°F), heart rate is 79 beats/minute, respiratory rate is 32 breaths/minute, and blood pressure is 156/80 mm Hg. He is lethargic and weak, in moderate respiratory distress, and oriented only to place and person. Laboratory studies revealed sodium 135 mEq/L, potassium 3.9 mEq/L, chloride 115 meEq/L, bicarbonate 11 mEq/L. Arterial blood gas studies (on room air) identified the following: pH 7.49, PACO2 15 mm Hg, and PAO2 67 mm Hg. Which of the following best characterizes the patient's

acid-base disorder?

A. Mixed anion gap metabolic acidosis and respiratory acidosis

B. Mixed anion gap metabolic acidosis and respiratory alkalosis

C. Mixed metabolic alkalosis and respiratory alkalosis

D. Mixed non-anion gap metabolic acidosis and respiratory alkalosis

E. Chronic respiratory alkalosis with appropriate compensation

25.2  A 55 -year-old woman is admitted to the ICU with a urinary tract infection and septic shock. She is now intubated but is not on mechanical ventilation. Over the past 4 days, she has had increasing shortness of breath and fever. Her medications are limited to amlodipine and hydrochlorothiazide. On physical examination, her temperature is 38.8°C (101.8°F), heart rate is 110 beats/minute, respiration rate is 22 breaths/minute, and blood pressure is 85/50 mm Hg. Other than tachycardia, the cardiac examination is normal. On pulmonary examination, there are crackles over the bilateral lungs. Laboratory studies on admission: sodium 140 mEq/L, potassium 4.5 mEq/L, chloride 100 mEq/L, bicarbonate 14 mEq/L, ABG study (on 50% FIO2) showed: pH 6.94, PACO2 80 mm Hg, PAO2 58 mm Hg. Which of the following acid-base conditions is most likely present in this patient?

A. Anion gap metabolic acidosis

B. Mixed anion gap metabolic acidosis and respiratory acidosis

C. Mixed anion gap metabolic acidosis and respiratory alkalosis

D. Mixed non-anion gap metabolic acidosis and respiratory acidosis

E. Mixed non-anion gap metabolic acidosis and respiratory alkalosis

ANSWERS TO QUESTIONS

25.1  E. In a patient with a diagnosis of pulmonary emboli and a chronically high respiratory rate for 5 days, the presence of a chronic respiratory alkalosis is expected. This patient has a respiratory alkalosis with appropriate compensation. The presence of an alkaline pH with a decreased serum HCO3 level suggests a respiratory alkalosis with ongoing renal compensation or a metabolic acidosis with a respiratory alkalosis. A mixed disorder should be raised in a patient whose pH is above normal in the presence of a metabolic acidosis. To confirm the suspicion of a mixed disorder, Winter formula can be used to estimate the expected PCO2: Expected PCO2 = 1.5 x [HCO3^-] + 8 ± 2 = 24.5 ± 2 mm Hg. According to this formula, the expected PCO2 is approximately 22.5 to 26.5 mm Hg, but the measured PCO2 was 15 mm Hg, which confirms the presence of a respiratory alkalosis. The most likely cause of a mixed anion gap metabolic acidosis and respiratory alkalosis in this patient is salicylate toxicity.

25.2  B. A decrease in the pH and HCO3 level is consistent with an anion gap metabolic acidosis. There is also a primary respiratory acidosis. This patient has a mixed anion gap metabolic acidosis and respiratory acidosis. The pH < 7.38 indicates an acidosis. This anion gap metabolic acidosis is most likely due to septic shock-associated lactic acidosis. Winter formula can be used to estimate the expected PCO2 for the degree of acidosis: Expected PCO2 = 1.5 x [HCO3^-] + 8 ± 2 = 29 ± 2 mm Hg. According to this formula, this patient's PCO2 is significantly increased above the expected level, which indicates the presence of carbon dioxide retention and respiratory acidosis. This is due to ventilatory failure secondary to the patient's respiratory distress, likely due to ARDS.

CLINICAL PEARLS

⯈ The only acid-base disorder that returns to a normal pH without another acid-base cause being present is chronic respiratory alkalosis. 

⯈ The anion gap formula is [Na+] - ([CI^-] + [HCO3^-]}. The normal value is 12 +/- 2 (with an albumin of 4 g/L). It is the albumin that represents the anion gap. 

⯈ Each gram of albumin is responsible for 3 points of the normal anion gap of 12 +/- 2. Adjust the normal range of the anion gap accordingly. (Eg, Albumin of 2 g = 6 ± 2) 

⯈ Changes in PACO2 and HCO3 always move in the same direction. 

⯈ Acute respiratory alkalosis with significant elevation in pH can de-ionize calcium and induce a seizure  via a relative hypocalcemia. 

References

American College of Physicians and the Clerkship Directors in Internal Medicine. Internal Medicine Essentials for Clerkship Students. Philadelphia: ACP Press; 2007-2008. 

Loscalzo J. Harrison's Pulmonary and Critical Care Medicine, New York, NY: McGraw-Hill; 2011. 

Toy EC, Simon B, Takenaka K, Liu T, Rosh A, Case Files Emergency Medicine. 2nd ed, New York, NY: Lange Medical Books/McGraw-Hill; 2009.

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