Respiratory Acidosis

Type

pCO₂ (mmHg)

Expected secondary response (compensation)

Expected serum [HCO₃ ⁻]

pH (calculated from Henderson equation)

Normal

–

7.40

Acute

70^a

For each mmHg increase in pCO₂, HCO₃ ⁻ increases by 0.1 mEq/L, ΔpCO₂ = 30 (70 – 40 = 30 × 0.1 = 3)

27 (24 + 3 = 27)

7.10

Chronic

70^a

For each mmHg increase in pCO₂, HCO₃ ⁻ increases by 0.4 mEq/L, ΔpCO₂ = 30 (70 – 40 = 30 × 0.4 = 12)

7.34

^aarbitrary value

Acute Respiratory Acidosis

Causes

There are several causes of acute respiratory acidosis, as shown in Table 32.2.

Table 32.2

Causes of acute respiratory acidosis

Depression of medullary respiratory center

Drugs: anesthetics, sedatives, opiates

Cerebral trauma or infarct

Central sleep apnea

Cardiac arrest

Failure of motor functions of respiratory muscles and chest wall

Drugs: succinylcholine, curare, aminoglycosides

High cervical cordotomy

Myasthenia crisis

Guillain–Barrè syndrome

Status epilepticus

Tetanus

Acute botulism poisoning

Familial hypokalemic periodic paralysis

Severe hypophosphatemia

Airway obstruction

Aspiration

Laryngospasm

Severe bronchospasm

Obstructive sleep apnea

Ventilatory defects

Flail chest

Pneumothorax

Hydrothorax

Adult respiratory distress syndrome

Acute pulmonary embolism

Acute pulmonary edema

Severe asthma

Severe pneumonia

Mechanical ventilation: increased production of CO₂ due to high carbohydrate feedings and fixed minute ventilation

Clinical Manifestations

As stated earlier, acute respiratory acidosis causes hypoxemia, resulting in several organ dysfunctions

CNS manifestations predominate and include the following:

Signs and symptoms: Nausea, vomiting, restlessness, headache, confusion, seizures, and coma

Cerebral blood flow: Increases acutely due to cerebral vasodilation of capillaries and venules. This cerebral vasodilation is mediated by nitric oxide

Intracranial pressure: Hypercapnia increases intracranial pressure due to increased blood volume and increased vascular pressure caused by vasodilation

Cardiac manifestations include an increase in blood pressure and heart rate secondary to increased sympathetic tone. Cardiac output increases. Also, coronary blood flow increases due to hypercapnia-induced vasodilation. Both peripheral vasodilation (due to hypercapnia) and vasoconstriction (due to increased sympathetic tone) occur in patients with acute respiratory acidosis. Arrhythmias are also common.

Renal effects include renal vasodilation with mild hypercapnia and vasoconstriction at pCO₂ > 70 mmHg. Renin–angiotensin II (AII)–aldosterone axis is stimulated by hypercapnia-induced sympathetic tone. Antidiuretic hormone (ADH) secretion is also increased.

Other effects include skeletal muscle contraction, particularly diaphragmatic movement is reduced.

Also, acute and chronic hypercapnias increase the production of gastric acid.

Diagnosis

History of cough, shortness of breath, fever, asthma, congestive heart failure (CHF), or trauma to head or back, drug use, and other medical conditions should be obtained
Physical examination should include vital signs, breathing pattern, body habitus, teeth (dentures, if any), mouth for any foreign material, chest exam for shape and accessory muscle use, auscultation of lungs for crackles, wheezing, tactile fremitus, movement of diaphragm, cardiac examination for an S₃ and an S₄, abdomen for muscle use, lower extremities for edema, upper extremities for clubbing, and a good neurologic examination
Laboratory results:

1.

Arterial blood gas (ABG): Low pH (< 7.25), slightly elevated serum HCO₃ ⁻ (< 30 mEq/L), and elevated pCO₂ (> 60 mmHg) characterize acute respiratory acidosis; pH, expected [HCO₃ ⁻], and pCO₂ shown in Table 32.1 distinguish acute respiratory acidosis from chronic respiratory acidosis

2.

Serum chemistry, including Ca²⁺, Mg²⁺, phosphate, and hemoglobin

3.

No change in serum Na⁺, K⁺, and Cl⁻

4.

Normal anion gap

5.

Acidic urine pH (< 5.5)

6.

Chest x-ray and electrocardiogram (EKG)

7.

Calculation of alveolar–arterial (A–a) gradient for gas exchange

Treatment

Correction of the underlying cause should be attempted whenever possible.

Immediate treatment should include the following:

Establishing a secure patent airway in both awake and obtunded patients

Hypercapnic encephalopathy may occur in patients with narcotic overdose and in those with chronic hypercapnia and superimposed acute respiratory acidosis

Administration of O₂ to improve hypoxemia. This is more important than lowering pCO₂ and raising pH. Assisted ventilation should be initiated promptly in severely obtunded, comatosed patients, or patients with pH < 7.10. If a patient is awake and hemodynamically stable, O₂ by nasal cannula or by high-flow Venturi face mask may be sufficient. The aim of O₂ therapy is to achieve pO₂ of 60–70 mmHg or an O₂ saturation > 88 %

Mechanical ventilation is indicated in apneic, obtunded, and hemodynamically unstable patients with pH < 7.10 and pCO₂ > 80 mmHg. Lowering pCO₂ may be sufficient to raise pH, but NaHCO₃ is needed in some patients

Loop diuretics may be needed in a patient with crackles

Antibiotics, β₂-agonists, and other bronchodilators, as well as corticosteroids, may be necessary in patients with infection and wheezing, to improve ventilation

Carbohydrate feedings in ventilator-dependent patients should be minimized to prevent excess CO₂ generation_. Calories from fat emulsions should be encouraged

Remember that clinical assessment and proper use of pharmacotherapy are extremely important in the management of acute respiratory acidosis .

Chronic Respiratory Acidosis

Steady-state hypercapnia is achieved in 3–5 days following secondary renal adaptive changes that increase serum [HCO₃ ⁻] by 0.4 mEq/L for each mmHg increase in pCO₂ above the normal level. Thus, the acid–base pattern of chronic acidosis is different from that of acute acidosis.

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