Flashcards in Anaesthetics - Oxygen therapy Deck (31)
What are the causes of tissue hypoxia?
Tissue hypoxia occurs within 4 minutes of cardiorespiratory arrest because blood, lung and tissue reserves are small. Causes of tissue hypoxia can be divided into those resulting in: (a) arterial hypoxaemia and (b) failure of oxygen-haemolgobin transport systems without arterial hypoxaemia.
What 6 mechanisms cause hypoxaemia?
Hypoxaemia is a low partial pressure of oxygen in the blood and is can cause, but is not the same as, hypoxia (which is a low tissue tension of oxygen). 6 main causes of hypoxaemia are:
1) Low inspired PO2
2) Hypoventilation (alveolar gas equation)
4) Ventilation perfusion inequality
5) Impaired diffusion
6) Venous saturation
What is the alveolar arterial (A-a gradient)?
This is the difference between alveolar oxygen tension and arterial oxygen tension. A normal A-a gradient is approximately 5mmHg. PaO2 can be obtained from blood gas measurements and PAO2 is determined from the alveolar gas equation. The simplified equation is:
PAO2 = PiO2 - (1.25 x PaCO2)
[PiO2 = FiO2 x (barometric - water vapour pressure),
breathing air, PiO2 = 0.21 x (101-6.2) = 19.9kPa]
The A-a gradient exists in a healthy person because a fraction of venous blood mixes with oxygenated blood. This mixing of unoxygenated and oxygenated blood is called the venous admixture. Two physiologic causes of venous admixture are the result of small anatomical shunt (e.g. bronchial circulation, thebesian veins) and regional variations in V/Q ratio. Approximately half of the normal A-a gradient is caused by bronchial circulation and half is caused by regional variations in V/Q ratio. An A-a ratio of greater than 15mmHg is considered abnormal and usually leads to hypoxaemia.
When can a low inspired PO2 cause hypoxaemia?
Low inspired oxygen partial pressure occurs at high altitude due to reduced barometric pressure, during fires due to O2 combustion and after toxic fume inhalation.
What is the most common cause of hypoxaemia?
Ventilation/ perfusion (V/Q) mismatch is the most frequent cause of hypoxaemia even in diseases like pulmonary fibrosis where diffusion limitation might expect to predominate.
Why does V/Q inequality cause hypoxaemia?
Normal V/Q ratio is 0.8 (i.e. minute ventilation and cardiac output are almost matched). When a partially obstructed airway occurs (low V/Q ratio), a fraction of the blood that passes through the capillary bed of the obstructed airway does not get fully oxygenated, resulting in an increase in venous admixture. Only a small amount of venous admixture is required to lower systemic arterial PO2 as a result of the nature of the oxygen dissociation curve. Because of the non linear shape of the dissociation curve, a low V/Q ratio causes both a drop in PO2 and O2 content. Patients who have abnormally low V/Q ratios have a high A-a gradient, low PO2 and a low O2 content, but usually a normal or slightly elevated PaCO2. PaCO2 does not change much because the carbon dioxide equilibrium curve is nearly linear, which allows excess CO2 to be removed from the blood by the lungs.
Lung units with a large V/Q ratio (i.e. ventilated but not perfused, due to PE) contribute to deadspace but not hypoxaemia. Cardiac output is redirected to other parts of the lung resulting in overperfusion, but this does not compensate the O2 content.
What is a shunt?
Shunt refers to venous blood that bypasses lung gas exchange and passes directly into the systemic arterial system. These could either be an anatomical right-to-left shunt or an absolute intrapulmonary shunt. The latter occurs when an airway is totally occluded (e.g. by a foreign body or mucus plug). Patients with hypoxaemia from a shunt have a high A-a gradient, low PO2, low O2 content, and a normal or slightly elevated PaCO2.
What can be done to prove that a shunt is the cause of a patients hypoxaemia?
It is difficult to distinguish shunt from hypoxaemia caused by low V/Q ratios is to have the patient breath 100% oxygen for 15 minutes. If the PaO2is greater than 13kPa the cause is a low V/Q ratio. If the PaO2 is less than 13kPa then the cause is a shunt. Strictly speaking, shunts cannot be treated with 100% oxygen unless the shunt fraction is >30%. The patient with regional hypoventilation who breathes 100% oxygen compensates for the low V/Q ratio, and because all of the blood leaving the pulmonary capillary is now fully saturated, the venous admixture is eliminated. But the low arterial PO2 does not get corrected by breathing 100% O2 in a patient with a shunt because enriched oxygen mixture never comes into contact with the shunt. Alveolar recruitment techniques are better.
What effect does generalised hypoventilation have on the A-a gradient?
Hypoventilation is a cause of arterial hypoxaemia. It occurs when alveolar ventilation is abnormally decreased. This can arise in COPD or respiratory depression (e.g. head injury, opiate OD). Because alveolar ventilation is depressed, there is also a significant increase in arterial PCO2, with a decrease in arterial pH. In generalised hypoventilation, total ventilation is insufficient to maintain normal systemic arterial PO2 and PCO2. But, there is a normal A-a gradient in hypoventilation, as a result of alveolar and arterial PO2 being lowered proportionately. If a patient has a low PO2 and a normal A-a gradient, the cause of hypoxaemia is entirely the result of generalised hypoventilation.
How should hypoventilation be treated?
The best corrective measure for generalized hypoventilation is to place the patient on a mechanical ventilator, breathing room air. This treatment will return both arterial PO2 and PCO2 to normal. Administering supplemental oxygen to a patient with generalized hypoventilation will correct hypoxaemia but not hypercapnia because ventilation is still depressed.
How does a diffusion block cause hypoxaemia?
This condition occurs when the diffusion difference across the alveolar capillary membrane is increased or the permeability of the alveolar capillary membrane is decreased. It is characterised by a low PaO2, a high A-a gradient and a high PaCO2. Pulmonary oedema is one of the major causes of diffusion block.
How does venous saturation cause hypoxaemia?
Venous blood with a very low SaO2 returning to the right heart usually has little effect on arterial PaO2, but in patients with impaired gas exchange or low CO it may reduce PaO2.
What are the clinical features of tissue hypoxia?
These are non specific (e.g. altered mental state, dyspnoea, hyperventilation, arrhythmias, hypotension). Central cyanosis is detected when deoxygenated haemoglobin is >1.5-5 g/dL. It is an unreliable sign of hypoxia because it can be absent in hypoxic, anaemic patients but apparent in normoxic polycythaemic patients.
What failures in oxygen-haemoglobin transport can cause hypoxia?
This is the second category of diseases that can cause tissue hypoxia. They include:
1) Inadequate organ perfusion
2) Low haemoglobin concentration (e.g. anaemia)
3) Reduced oxygen dissociation (e.g. haemoglobinopathies)
4) Failure of oxygen utilisation (e.g. sepsis, cyanide poisoning)
What methods can be used to monitor oxygenation?
1) Pulse oximetry and blood gas analysis
- Arterial PO2 is the tension driving oxygen into tissues
- Arterial SO2 reflects how much oxygen is being carried by haemoglobin molecules
- Pulse oximetry and blood gases can be NORMAL when tissue hypoxia is caused by low CO, anaemia or impaired oxygen utilisation. In these circumstances, mixed venous oxygen saturation <55-60% reflects inadequate oxygen delivery
2) A-a gradient determines efficiency of gas exchange
- A-a gradient is increased in shunt, V/Q mismatch and diffusion impairment
- normal value is 0.2-0.4kPa
What is respiratory failure?
Respiratory failure may be acute, chronic or acute on chronic. It is due to inadequate gas exchange and is defined as an arterial PaO2 <8kPa or arterial CO2 >6kPa.
What is type 1 respiratory failure?
Type 1 RF is due to a failure in oxygenation. It occurs when blood bypasses or is not fully oxygenated in the lungs causing hypoxaemia. PaCO2 is normal or low because ventilation is unchanged or increased due to breathlessness. Causes include V/Q mismatch (e.g. pneumonia), right to left shunts (e.g. heart defects), low FiO2 (altitude) and impaired diffusion (e.g. pneumonia, oedema, pulmonary fibrosis). PaO2 usually improves with oxygen therapy but re-expansion/ recruitment of collapsed alveoli and reduction of the V/Q mismatch may be equally effective - e.g. CPAP may improve oxygenation by recruiting collapsed lung.
What is type 2 respiratory failure?
Type 2 RF is due to failure in ventilation. Hypoventilation reduces CO2 clearance resulting in hypercapnia with, or very occasionally without, hypoxaemia. Hypoventilation is either due to inadequate respiratory drive or ineffective ventilation. Causes include neuromuscular weakness (e.g. MND), chest wall deformity (e.g. kyphoscoliosis), impaired respiratory drive (e.g. opiate overdose) and increased work of breathing due to primary lung disease (e.g. COPD). Ventilation is improved and WoB reduced by treating the precipitating cause, decreasing airway resistance (e.g. bronchodilation) and improving compliance (e.g. alveolar recruitment). If hypercapnia and acidosis persist, NIV is often effective.
What are the indications for mechanical ventilation in RF?
PaO2 <8kPa on >50% FiO2
Poor secretion clearance
Failure to improve after 1-4 hours on NIV
What are the indications for starting oxygen therapy?
1) Cardiac and respiratory arrest
2) Hypoxaemia (PaO2 <8kPa, SaO2 <90%)
3) Hypotension (systolic BP <100mmHg)
4) Low cardiac output
5) Metabolic acidosis (bicarbonate <18)
6) Respiratory distress (RR >24/min)
What are variable performance oxygen devices?
Oxygen can be administered by various devices. In variable performance devices, air is entrained during breathing whilst oxygen is delivered from a reservoir (i.e. mask, bag, nasopharynx).
Importantly, the FiO2 delivered to the lungs depends on the oxygen flow rate, the patients inspiratory flow, respiratory rate and the amount of air entrained.
E.g. O2 flow rate in a Hudson mask (or low flow face mask) is 2-10L/min and is supplemented by air drawn into the mask. The FiO2 achieved depends on ventilation
Ventilation = 5L/min
O2 flow = 2L/min; Air (21% O2) flow = 3L/min
FiO2 = ( 2+ 0.21 x 3)/5 x 100 = 53%
The main point is that the higher the ventilatory rate the lower the percentage of oxygen is inspired. These devices cannot be used if accurate control of FiO2 is desirable, e.g. COPD with hypercapnia. Examples of variable performance devices are low flow face masks, nasal cannulae and non rebreathing face masks with reservoir bags.
What is a low flow face mask? What oxygen flow rates can be used with this mask?
This is a variable performance device (remember that this means the FiO2 changes with the pattern of breathing).O2 flows at 2-15L/min into the mask and is supplemented by air drawn into the mask. Flow rate must be >5L/ min to prevent CO2 rebreathing. FiO2 can reach 60% with oxygen flow rates up to 15L/min.
What oxygen flow rates can be used with nasal cannulae?
Oxygen flow rates up to 4L/min. High rates dry out mucosa. FiO2 is between 24-35%.
The oxygen flow is constant so FiO2 varies with ventilatory volume. More comfortable and not removed during eating or coughing.
What are non-rebreathe masks?
Oxygen flows into the bag during expiration. When the patient breathes they breath oxygen from the bag and with some mixed air. One way valve prevents expired gas going into the bag. High flow rates (10-15L/min) provide high FiO2 >60% and up to 100%. A one way valve stops exhaled air entering reservoir bag.
What is a fixed performance oxygen device?
These are independent of the patients breathing pattern and inspiratory volume. Fixed oxygen through a Venturi mask entrains the correct proportion of air to achieve the required O2 concentration. This system delivers more gas than is inspired. Consequently, FiO2 is less affected by breathing pattern. The resulting masks are high flow, low concentration and fixed performance.
What oxygen saturations should one aim for in normal patients?
Normal patients are those at low risk of hypercapnic respiratory failure (HCRF), so aim to achieve saturations of 94-98% if <70 years old and 92-98% if >70 years old. These ranges ensure Hb is fully saturated (i.e. on the plateau of the dissociation curve). Consequently, increasing PaO2 further has no impact on oxygen delivery because little oxygen is dissolved in plasma.
How should oxygen therapy be given to those patients at risk of HCRF?
These patients (e.g. neuromuscular disease, COPD) the target SaO2 should be 88-92% pending ABG analysis. A higher SaO2 has few advantages but results in hypoventilation, hypercapnia and respiratory acidosis in patients dependent on hypoxaemic respiratory drive.
In what groups of patients is oxygen therapy of little benefit?
Oxygen therapy is of little benefit in "normoxic" patients because haemoglobin is fully saturated and oxygen solubility is low even at high PaO2. Early restoration of tissue blood flow is often more important in these cases. Oxygen therapy is of little value in myocardial infarction, drug overdoses, metabolic disorders, hyperventilation or non hypoxic pregnant women in labour. It may be harmful in normoxic patients with strokes, paraquat poisoning, bleomycin lung injury, or acid inhalation and to the foetus in normoxic obstetric emergencies. However, in CO poisoning high dose oxygen is essential, despite a normal PaO2, to reduce carboxyhaemoglobin half life.
What dangers are associated with oxygen therapy?
1) Carbon dioxide retention
- 10% of breathless patients, mainly COPD, have type II respiratory failure; 40-50% of COPD patients are at high risk of type II RF
2) Rebound hypoxaemia
- occurs if oxygen is suddenly withdrawn in type II failure
3) Absorption collapse
- oxygen in poorly ventilated alveoli is rapidly absorbed causing collapse; whereas nitrogen absorption is slow
4) Pulmonary oxygen toxicity
- FiO2 >60% may damage alveolar membranes causing ARDS if inhaled for >24-48 hours. Hyperoxia can cause coronary and cerebral vasospasm
6) Paul-Bert effect
- Hyperbaric oxygen can cause cerebral vasoconstriction and epileptic fits
How should patients on oxygen therapy be monitored? When can oxygen therapy be stopped?
SaO2 should be measured regularly in all breathless patients and recorded on the observation chart with the oxygen dosage. SaO2 is observed for 5 minutes after starting or changing oxygen dose and adjusted to achieve the target SaO2. If possible, an ABG is measured before and within 1 hour of starting oxygen therapy, especially in those at risk of HCRF, and then at intervals.
Stop oxygen therapy when the patient is clinically stable on low dose oxygen (1-2L/min) and SaO2 is within the desired range on two consecutive occasions. Monitor SaO2 5 minutes after stopping O2 and then 1 hour later.