Respiratory acidosis Flashcards
What is respiratory acidosis?
- Is defined as pH less than 7.35 (acidaemia) and PaCO₂ more than 45.
- It is a primary acid-base disorder in which arterial levels of PCO₂ rise to higher than expected levels.
What are the stages of respiratory acidosis?
- Acute: < 24 hours. The body’s initial compensatory response is limited during this phase.
- Chronic: > 24 hours. As the body’s renal compensatory response increases over the next few days, the pH returns towards the normal value.
Explain the mechanisms involved in maintenance of normal values of PaCO₂ in the plasma.
- There is a balance in between the CO₂ that is produced by the body and the CO₂ that is eliminated by alveolar ventilation, to maintain the plasma CO₂ levels at around 40 mmHg.
- So paCO₂ = VCO₂ / VA
- paCO₂ is proportional to CO₂ production by the body, meaning an ↑ in the production (VCO₂) will equal to an ↑ paCO₂.
- There is an inverse relationship between paCO₂ and alveolar ventilation (VA). The rise of VA will ↓ paCO₂ and vice-versa.
- An adult at rest produces about 200mls of CO2 per minute: this is excreted via the lungs and the arterial pCO2 remains constant.
- An increased production of CO2 would lead to a respiratory acidosis if ventilation remained constant.
- The chemosensitive areas of the respiratory center in the medulla (brainstem/tronco cerebral) sense cerebral interstitial changes in pH.
- Peripheral chemoreceptors in the carotid and aortic bodies sense the changes in PaO₂,
- PaCO₂ and pH in the blood.
- PaCO₂ is the major stimulus to respiration, as very minute changes in PaCO₂ can induce changes in minute ventilation;
- A rise in PaCO₂ of 1 mmHg can increase minute ventilation by 1 to 4 L.
- This contrasts with the response to hypoxemia in that minute ventilation may not increase significantly until Pao2 is less than 60 mmHg.
Describe the mechanisms of how PaCO₂ ↑ can occur.
An increase of pCO₂ can occur in the following ways:
1. Presence of CO₂ on inspired gas (CO₂ gas can be added to the inspired gas or it may be present because of rebreathing. In these situations, hypercapnia can be induced even in the presence of normal alveolar ventilation and normal carbon dioxide production by the body.)
2. ↑ CO₂ production by the body.
3. ↓ VA.
These are also the classification of the causes of Respiratory Acidosis by Mechanism
Name ALL the causes of respiratory acidosis.
The causes of respiratory acidosis can be divided into 3 main groups:
- Inadequate alveolar ventilation;
- Over-production of CO₂;
- Increased Intake of CO₂ / CO₂ present on inspired gas.
Each main group can be further subdivided into specific causes:
A. Inadequate alveolar ventilation:
* Central Respiratory Depression & Other CNS Problems
1. Respiratory depression due to drugs (opiates, sedatives, anaesthetics);
2. CNS trauma, infarct, haemorrhage, or tumor;
3. Cervical cord trauma or lesion (at or above C4);
4. High central neural blockade / Central neuraxial blocks;
5. Cardiac arrest with cerebral hypoxia;
6. Hypoventilation of obesity (eg Pickwickian syndrome);
7. Polyomielitis;
8. Tetanus.
-
Lung / Chest wall / Parenchymal defects
1. Acute exacerbation of COPD;
2. Acute respiratory distress syndrome (ARDS)
3. Chest trauma (contusion, flail chest, haemothorax);
4. Pneumothorax;
5. Pulmonary oedema;
6. Restrictive lung disease (fibrosis);
7. Aspiration;
8. Diaphragmatic paralysis or splinting (due to damage of the phrenic nerve). -
Airway disorders
1. Upper airway obstruction;
2. Laryngospasm;
3. Bronchospasm / Asthma. -
Nerve or Muscle Disorders
1. Guillain-Barré syndrome;
2. Myastenia gravis;
3. Muscle relaxant drugs;
4. Toxins (eg organophosphates, snake venom);
5. Other myopathies [muscular dystrophies (duchenne and becker)]. -
External factors
1. Inadequate mechanical ventilation.
B - Increased production of CO₂
* Hypercatabolic Disorders
1. Malignant hyperthermia (It is only in situations where ventilation is fixed that increased production will cause respiratory acidosis. Examples of this would be a ventilated patient who develops acute malignant hyperthermia: the arterial pCO2 will rise unless the alveolar ventilation is substantially increased).
2. Sepsis [Patients who are paralysed and on controlled ventilation cannot increase their alveolar ventilation to excrete any increased amounts of CO₂ produced by the body (eg in hypercatabolic states such as sepsis or MH)]
C - Presence of CO₂ / Increased Intake of CO₂
- Rebreathing of expired (expiração/inspiração) gas containing CO₂ (Various circuit misconnections & malfunctions, or soda lime exhaustion);
- Addition of CO₂ to inspired gas;
- Insufflation of CO₂ into body cavities (laparascopic surgeries).
In clinical practice, nearly all cases are due to inadequate alveolar ventilation.
What are the effects that hypercapnia can cause in the body?
- Stimulation of ventilation via both central and peripheral chemoreceptors;
- Cerebral vasodilatation ➜ ↑blood flow ➜ ↑ intracranial pressure;
- Central depression at very high levels of PaCO₂ (>100mmHg);
- Stimulation of the sympathetic nervous system ➜ tachycardia, peripheral vasoconstriction and sweating;
- Peripheral vasodilation by direct effect on vessels.
What are the effects of hypercapnia on CNS?
- Stimulation of ventilation via both central and peripheral chemorecptors (can lead to dyspnoea);
- Cerebral vasodilation ➜ ↑ blood flow ➜ ↑ ICP (disorientation, acute confusion, headache, mental obtundation or even focal neurologic signs).
- Anaesthetic effects of very high arterial pCO2 (eg > 100mmHg) (coma);
- Arterial hypoxaemia
The rise in intracranial pressure due to hypercapnia may be particularly marked in patients with intracranial pathology (eg tumours, head injury) as the usual compensatory mechanism of CSF translocation may be readily exhausted. Any associated hypoxaemia will contribute to an adverse outcome.
Explain the acute compensation mechanism in respiratory acidosis?
- ↑ in HCO₃- levels
The compensation mechanism of RA has 2 parts:
* Acute setting:
1. CO₂ + H₂O ⟷ H₂CO₃ ⟷ H⁺ + HCO₃⁻
2. An ↑ of PaCO₂ concentration, causes the shift of the equation to the right.
3. The compensation mechanism of RA is exclusively / limited to intracellular buffering.
4. CO₂ enters the deoxyhaemoglobin and reacts with water.
5. H⁺ are buffered by haemoglobin and resulting in an increased HCO₃⁻ production.
6. The HCO₃⁻ exchanges with Cl⁻ and exits the cell, ↑ slightly plasma levels of HCO₃⁻.
7. The plasma ↑ of HCO₃⁻ only partially returns the extracellular pH towards normal.
Predicted value for HCO₃⁻ in acute RA
- In acute settings HCO₃⁻ rises by 1 mmol/l (from reference value of 24) for every 10mmHg increase in PaCO₂ (from reference value of 40).
-
Chronic setting
1. With continuation of the acidosis (with high levels of PaCO₂) , the kidneys respond by retaining HCO₃⁻.
2. Thus the HCO₃⁻ plasma level ↑ to higher levels, due to renal retention;
3. This comoensation reaches its maximal effect in 3-4 days.
Predicted value for HCO₃⁻ in chronic RA
- HCO₃⁻ ↑ 4 mmol/L (from reference value of 24) for every 10 mmHg ↑ of PaCO₂ (reference value of 40).
In summary, the compensation for hypercapnia is:
* Acute: Buffering only and predominantly intracellular (99%).
* Chronic: Renal retention of bicarbonate (in addition to buffering).
Based on the Henderson-Hasselbalch equation, an ↑ [HCO3-] will counteract the effect (on the pH) of an ↑ pCO2.
What is the general rule for compensation in all acid-base disorders?
- The general rule for all acid-base disorders is that the body’s compensatory response is almost never sufficient to return the plasma pH to normal.
- If the pH is normal then it suggests that a second, compensating acid-base disorder is present.
Describe the treatment for RA.
➜ The treatment is directioned at resolving the primary cause of RA;
- In severe cases, intubation and mechanical ventilation will be necessary to restore adequate alveolar ventilation.
What are the issues that arise from correcting the PaCO₂ too quickly in a patient with chronic RA?
The patient can deteriorate following intubation and ventilation if the RA is chronic.
* Hypercapnia causes stimulation of the sympathetic nervous system ➜ tachycardia, peripheral vasoconstriction and sweating;
* Thus patients exposed to hypercapnia for chronic periods, will more likely be vasoconstricted and volume depleted.
* When correcting the PaCO₂ too quickly, these patients will develop hypotension;
* These patients might require significant fluid loading;
* Patients might develop post hypercapnic alkalosis.
What is post hypercapnic alkalosis
- It occurs when the PaCO₂ of a chronic RA is corrected quickly (eg. on a intubated and ventilated patient), but the HCO₃⁻ levels remain high due to slow renal excretion.
Main causes for maintenance of HCO₃⁻ levels high after PaCO₂ are:
* Cl⁻ depletion;
* K⁺ depletion;
* ECF depletion;
* ↓ GFR;
* Use od diuretics (Cl⁻ depletion;
* Loss of GI acidic secretions (nasogastric drainage ➜ Cl⁻ depletion);
* Use of H2-blockers (ranitidine).
➜ These patients are often avidly retaining sodium in the kidneys and in the presence of low chloride levels, this is associated with high levels of bicarbonate reabsorption.
➜ In general, bicarbonate levels in this situation are in the 30 to 45 mmol/l range.
➜ Correction of fluid and chloride depletion leads to a fall in plasma bicarbonate levels.
Assesment of other acid-base disorders in RA
Calculate expected PaCO₂
Expected PaCO₂ = [(1.5 x HCO₃⁻) + 8 ]
Detail the management and prevention of RA?
- Inadequate alveolar ventilation is the underlying problem in nearly all patients so any patient who could have impaired ventilation is at risk of developing respiratory acidosis. So recognise these at-risk situations.
- Inadequate ventilation will also necessarily affect arterial oxygenation so steps to avoid, recognise and/or treat arterial hypoxaemia are very important. The simple measure of providing supplemental oxygen by face mask to patients can often correct or prevent hypoxaemia.
Some particular medical situations where prevention can be utilised are:
* Better airway care and attention to safe positioning of cerebrally obtunded patients (ie prevent airway obstruction);
* Increased care in patients using drugs (such as CNS sedatives or opiate drugs) which can depress ventilation;
* Increased attention to the care of patients at risk of aspiration (eg unconscious patients);
* Ensuring adequate reversal of neuromuscular relaxants.
The end-tidal pCO2 is typically lower than the arterial pCO2 due to alveolar dead space. So if the end-tidal pCO2 is elevated then the arterial pCO2 is usually even more elevated.
Breaking down some concepts
Name the 3 main causes of respiratory acidosis.
- Inadequate alveolar ventilation;
- ⬆︎ production of CO₂ by the body;
- Presence of CO₂ / ⬆︎intake of CO₂.
In clinical practice, nearly all cases are due to inadequate alveolar ventilation.
