Blood Gas and Acid-Base Disturbance in Respiratory Failure

Az Rifki

Spesialis Anestesiologi, Konsultan Intensive Care

RS Islam Siti Rahmah, Padang.

Introduction

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO₂ value of less than 60 mm Hg while breathing air or a PaCO₂ of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

Classification of respiratory failure

Respiratory failure may be classified as hypoxemic or hypercapnic and may be either acute or chronic and it is sub-classified into one of two types of respiratory failure based on the level of PaCO2 :

• Type 1 Hypoxemic respiratory failure:
• PaCO2 is normal or low
• PaO2 less than 60 mmHg

• Type 2 Hypercapnic respiratory failure:
• PaCO2 is greater than 50 mmHg
• PaO2 is less than 60 mmHg

Aetiology type 1 Hypoxemic respiratory failure

    

The causes of type 1 Hypoxemic respiratory failure :

• diseases that damage lung tissue
• conditions where there is a V/Q mismatch
• conditions where there is hypoxaemia due to right to left shunts

It may be acute or chronic.

Acute type 1 Hypoxemic respiratory failure

    

Acute type 1 respiratory failure may occur in conditions such as:

• asthma - in the acute phase the cause of respiratory failure in asthma is not the bronchoconstriction but rather the intense inflammation and oedema of the lungs which results in impaired oxygenation of the blood
• pulmonary embolus
• pulmonary oedema
• adult respiratory distress syndrome

Chronic type 1 Hypoxemic respiratory failure

Causes of chronic type 1 respiratory failure include:

• emphysema
• respiratory muscle disease, e.g. myasthenia gravis
• kyphoscoliosis
• thromboembolic pulmonary hypertension
• lymphangitis carcinomatosa
• pulmonary alveolar fibrosis

Aetiology of type 2 Hypercapnic respiratory failure

    

Type 2 Hypercapnic respiratory failure occurs in conditions which cause alveolar hypoventilation, for example, where there is:

• a reduced ventilatory effort
• increased dead space
• increased carbon dioxide production
• a combination of these

Type 2 Hypercapnic respiratory failure may be acute or chronic.

Acute type 2 Hypercapnic respiratory failure

    

Possible causes include:

• severe acute asthma - as the patient becomes exhausted type 2 hypercapnic respiratory failure occurs
• acute epiglottitis
• respiratory muscle paralysis; a number of aetiologies including Guillain-Barre syndrome

Chronic type 2 Hypercapnic respiratory failure

Possible causes include:

• chronic bronchitis
• primary alveolar hypoventilation
• motor neurone disease

Clinical features

Clinical features of respiratory failure may include:

• clinical features of the underlying cause of the respiratory failure
• hypoxia - restlessness, confusion and ultimately, coma
• hypercapnia causing:
• drowsiness
• flapping tremor
• warm peripheries
• headaches
• bounding pulse
• papilloedema

Investigations

    

Initial patient assessment:

·         assess the patient's previous disability

·         are there signs of deterioration?

Screening investigations:

·         chest radiology

·         blood gases

·         peak expiratory flow rate

·         ECG

·         full blood count

·         biochemistry

·         sputum and blood culture

·         store a blood sample for serology

Blood gases and acid-base disorders in respiratory failure

    

Type 1 Hypoxemic respiratory failure:

·         acute - PaO2 low, PaCO2 normal, pH normal, bicarbonate normal

·         chronic - PaO2 low, PaCO2 normal/low, pH normal/low, bicarbonate normal/low

Type 2 Hypercapnic respiratory failure:

·         acute - PaO2 low, PaCO2 high, pH low, bicarbonate normal

·         chronic - PaO2 low PaCO2 high, pH low/high, bicarbonate high

Blood gases

    

Blood gases are commonly measured, and with a logical, systematic approach they may be easily interpreted.

Blood gases provide information about:

·         ventilation

·         oxygenation and alveolar-arterial O2 gradient

·         acid-base status

Blood gases and oxygenation

    

The normal range for PaO2 is 80-100 mmHg. A partial pressure less than 60 mmHg defines respiratory failure.

Arterial hypoxaemia is commonly due to pulmonary disease:

·         poor gas transfer:

o   type I respiratory failure

o   PaCO2 is typically low

·         hypoventilation:

o   type II respiratory failure

o   PaCO2 is typically raised

Arterial hypoxaemia may occur when the lungs are normal :

·         low inspired partial pressure of oxygen e.g. altitude

·         ventilation-perfusion mismatch

·         right to left shunts:

o   congenital heart disease

o   arteriovenous malformation of the pulmonary vessels

The alveolar-arterial oxygen gradient

Measurement of the alveolar-arterial (A-a) gradient is useful in hypoxic patients and may help to distinguish hypoxaemia due to pulmonary disease from other causes of hypoxaemia.

The Alveolar : arterial oxygen gradient is an index of the efficiency of gas transfer across the alveolar membrane. It is the difference in oxygen tension across the alveolar membrane.

This difference is calculated by the following equation:

PaO₂ = FIO₂ x (PB – PH₂ O) – PaCO₂/R

For the above equation, PaO₂ = alveolar PO₂, FIO₂ = fractional concentration of oxygen in inspired gas, PB = barometric pressure, PH₂ O = water vapor pressure at 37°C, PaCO₂ = alveolar PCO₂, assumed to be equal to arterial PCO₂, and R = respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, VCO₂/VO₂ is approximately 0.8.

Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, alveolar PO₂ is slightly higher than arterial PO₂. However, an increase in alveolar-to-arterial PO₂ above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia.

Acid base balance

    

To ensure an acid-base balance the body has to deal with the following:

·         the daily fixed acid load of 50 to 100 mmoles

·         the daily carbon dioxide production of 13,000 to 15,000 mmoles

Homeostatic mechanisms maintain the following normal range of pH by regulation of the pCO2 and bicarbonate:

·         pH: 7.35 to 7.45

·         pCO2: 35 to 45 mmHg (regulated by ventilation)

·         bicarbonate: 22 to 24 mEq (regulated by the kidneys)

Blood gases and ventilatory efficiency

The arterial partial pressure of carbon dioxide, PaCO2 reflects alveolar ventilation and in most cases may be used as an index of ventilatory efficiency.

It is raised i.e. greater than 45 mmHg, with hypoventilation and decreased i.e. less than 35 mmHg, during hyperventilation.

Respiratory acidosis

This is characterised by a raised PaCO2, a normal or slightly elevated serum bicarbonate, and a low pH.

A respiratory acidosis may be pure, or it may be complicated by a metabolic derangement (i.e. a mixed acidosis). Measurement of the serum bicarbonate permits definitive diagnosis:

·         acute respiratory acidosis:

o   serum bicarbonate increases by 1 mmol/l for each 10 mmHg increase in PaCO2

·         chronic respiratory acidosis:

o   serum bicarbonate increases by 3.5 mmol/l for every 10 mmHg increase in PaCO2

·         if the bicarbonate is lower than expected then the condition is likely to be a mixed respiratory acidosis and metabolic acidosis

·         if the bicarbonate is higher than expected then the condition is likely to be a mixed respiratory acidosis and metabolic alkalosis

Metabolic acidosis

    

This is characterised by a primary decrease in serum bicarbonate and a slight decrease in paCO2. Serum pH may be reduced or normal.

Causes are distinguished on the basis of the anion gap. In acidosis with a normal anion gap, plasma chloride is increased in order to maintain electrical neutrality - hyperchloraemic acidosis.

Metabolic acidosis (increased anion gap)

·         diabetic ketoacidosis

·         starvation ketoacidosis

·         lactic acidosis (types A and B)

·         acidosis of renal failure

·         salicylate poisoning

·         methanol poisoning

·         ammonium chloride

Metabolic acidosis (normal anion gap)

Normal anion gap / hyperchloraemic acidosis:

·         bicarbonate loss in the gut, e.g. pancreatic fistula, diarrhoea, utero-enterostomy

·         renal tubular acidosis:

o   proximal - bicarbonate loss

o   distal - failure of acidification - proton pump failure

o   treatment with excessive carbonic anhydrase inhibitors

Features of a metabolic acidosis

    

The classical clinical finding in the patient with metabolic acidosis is the deep, sighing breathing pattern which is termed Kussmaul respiration.

The physiological consequences of metabolic acidosis include:

·         impaired myocardial contractility:

o   the effect is independent of hypoxia

o   cardiac failure may induce lactic acidosis

·         increased risk of ventricular fibrillation

·         pulmonary vasoconstriction

Anion gap

The anion gap is a method of assessing the contribution of unmeasured anions to acidosis. It is calculated as a difference between the total of sodium and potassium ion concentration, minus the total of chloride and bicarbonate concentration. Some people omit the potassium. Thus:

·         Anion Gap = [K+] + [Na+] - [Cl-] - [HCO3-] (plasma concentrations)

The normal range for the anion gap is 6 - 16 mmol/l. The anion gap provides a measure of the difference between unestimated anions - phosphate, acetate and ketones - and cations.

Reference:

1.    Joint Pathology Services Royal Liverpool & Broadgreen University Hospitals (September 2006)

2.    Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 1998. pp849-856

3.    Franco D’Alessio, et al.  Acute Respiratory Failure. Piccini & Nilsson: The Osler Medical Handbook, 2nd ed. Johns Hopkins University. 2006

4.    Sat Sharma, MD, FRCPC. Respiratory Failure. emedicine.medscape.com. Updated: Jun 29, 2006

5.    Richard M. Effros, M.D.   Jeffrey A. Wesson, M.D., Ph.D. Acid-Base Balance. Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed. 2005 Saunders, An Imprint of Elsevier

6.    Leonard D. Hudson, Arthur S. Slutsky. ACUTE RESPIRATORY FAILURE. Goldman: Cecil Medicine, 23rd ed. 2007 Saunders, An Imprint of Elsevier

7.    Kurt A. Wargo, PharmD, BCPS,* and Robert M. Centor, MD. ABCs of ABGs: A Guide to Interpreting Acid-Base Disorders. Hospital Pharmacy, Volume 43, Number 10, pp 808–815; 2008 Wolters Kluwer Health, Inc

8.    Dr. Praveen Kumar Neema. RESPIRATORY FAILURE. Indian J. Anaesth. 2003; 47 (5) : 360-366