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Respiratory Clinics

VENTILATORY MANAGEMENT IN A PATIENT WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A NEED FOR CAUTION  

R Khajotia MBBS (Bom), MD (Bom), MD (Vienna), FAMA (Vienna), FAMS (Vienna). International Medical University, Seremban, Malaysia

Address for correspondence: Dr. Rumi Khajotia, Associate Professor in Internal Medicine and Pulmonology,
International Medical University Clinical School, Seremban, Malaysia. Email:  rumi@imu.edu.my

Khajotia R. Ventilatory management in a patient with chronic obstructive pulmonary disease: a need for caution. Malaysian Family Physician. 2008;3(3):xx-xx

A 67 year old obese male patient, chronic smoker, is admitted to the Intensive Care Unit (ICU) with complaints of acute shortness of breath which has progressively increased over the past 10 days. He is a known case of paroxysmal breathlessness for the past 17 years and has been on treatment from his family physician with oral and inhaled bronchodilators. Since the patient’s condition progressively worsened in spite of home treatment, his family physician referred him to the hospital. On examination, the patient is drowsy and cyanosed with a very poor respiratory drive. His pulse rate is 86/min, regular and bounding. His BP is 156/92 mmHg. His chest examination reveals diminished air entry bilaterally over the chest, with prolonged expiration and scattered rhonchi. He is immediately transferred to the ICU and put on a volume-cycled ventilator (respirator) with assist-control (AC) mode, a high respiratory rate and FiO2 of 80%. Four hours later, the patient is found to have developed cardiac arrhythmias. His ECG shows ventricular premature contractions (VPC’s) with occasional supraventricular premature beats. The arterial blood gases (ABG) done on admission and 4 hours after ventilatory management, are as follows:

Question

1. What do the serial arterial blood gases (ABG) indicate?
2. What is the most likely cause behind the serial changes in the ABG readings and the cardiac arrhythmias?
3. What are the complications that may occur as a result of severe metabolic alkalosis?
4. What are the learning issues in this case report?

Answer

1. On admission, the ABG shows a moderate hypoxia with compensated  respiratory acidosis. However, following 4 hours of ventilatory management, the ABG shows predominant metabolic alkalosis.
2. The patient is a known case of chronic obstructive pulmonary disease (predominantly a blue-bloater), and therefore presented on admission with hypoxia, carbon dioxide retention, raised bicarbonate (HCO3) levels (as a  consequence of metabolic compensation) and respiratory failure. However, ventilatory management with an undulyhigh respiratory (ventilatory) rate led to a rapid washout of carbon dioxide from the blood within the spate of 4 hours, leaving no time for metabolic compensation to occur, resulting in the development of “post hypercapnoeic metabolic alkalosis”and the consequent cardiac arrhythmias.
3. Severe metabolic alkalosis causes diffuse arteriolar constriction with reduction in tissue perfusion. By decreasing cerebral blood flow, alkalosis may lead to tetany, seizures and obtundation. Metabolic alkalosis also decreases coronary blood flow and predisposes patients to refractory arrhythmias.  Metabolic alkalosis causes hypoventilation which may impair weaning from mechanical ventilation. It is almost always associated with hypokalemia, which can cause neuromuscular weakness and ventricular premature contractions.
4. This case report incorporates a very valuable learning issue. From here we learn that while ventilating a patient with chronic obstructive pulmonary disease, unduly high respiratory rates should be avoided. This is because the patient has chronically raised PaCO2 levels along with raised HCO3 levels, as a result of metabolic compensation. When an overzealous effort is made to rapidly bring down the carbon dioxide levels by increasing the ventilatory rate, the PaCO2 reduces rapidly leaving very little time for metabolic compensation to set in. Consequently, the patient develops severe post-hypercapnoeic metabolic alkalosis with potential complications. In conclusion, it must be emphasized that the PaCO2 levels in patients with chronic obstructive pulmonary disease should be gradually reduced, giving adequate time for metabolic compensation to set in, thereby preventing a severe metabolic alkalosis from occurring, along with its consequent complications.

References:

1. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. Jan 8 1998; 338 (2): 107-11.
2. Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and surgical patients. Southern Medical Journal. 1987; 80: 729-33.
3. Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Critical Care Medicine. 1980; 8: 725-28.

Recommended further reading:

1. 1.) Rose BD. Acid-base physiology and regulation of acid-base balance. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York: McGraw-Hill; 1994:274-339.
2. Rose BD. Metabolic alkalosis. In: Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th ed. New York: McGraw-Hill; 1994:515-35.
3. DuBose TD Jr. Metabolic alkalosis. In: Brenner and Rector's The Kidney. 6th ed. Philadelphia: WB Saunders; 2000:971-997.