Ventilatory Failure and Oxygen Therapy Flashcards
What is the difference between respiratory and ventilatory failure?
Respiratory Failure (RF) is the inability to maintain normal arterial gas tensions. Defined through blood results. This can be split into type 1 and type 2 respiratory failure.
Ventilatory Failure (VF): A pathological reduction in alveolar ventilation below the level required for the maintenance of normal alveolar gas tensions.
Ventilatory failure causes a type 2 respiratory failure
Type 1: Hypoxia with a normal PaCO2
Type 2: Hypoxia with hypercapnia
What is the relationship between PaCO2 and alveolar ventilation?
PaCO2 is inversely proprtional to alveolar ventilation
What happens to PaCO2 during exercise?
Although VCO2 rises, the PaCO2 actually decreases.
This is explained by the increase in alveolar ventilation to not only make up for the VCO2 but also for the lactic acid increase (respiratory compensation for a metabolic acidosis).
What is the normal VCO2 (rate of CO2 production)?
200ml/min
What happens to PaCO2 levels during hyperventilation?
They will drop up until a certain point.
There is a large body reservoir of CO2 – approximately 120L (100x that of oxygen). These stores buffer any rapid changes in CO2 levels.
This also explains why the rate of rise and fall of PCO2 with ventilation is not mirrored
Use an anatimical approach?
What are the 10 different causes of ventilatory failure?
A = Respiratory Centre may be depressed causing inadequate ventilatory drive. May be caused by hypercarbia, severe hypoxia, drugs, brain lesions
B = Upper motor neurones may be damaged through trauma or pathological tumours, syringomyelia, demyelination, brainstem strokes and AVMs. Phrenic nerve needs to remain intact C3,4,5.
C = Anterior Horn cells damaged in poliomyelitis.
D = Lower motor neurones affected in phrenic nerve injury, motor neurone disease, Guillain-
Barre
E = Neuromuscular junction may be affected with toxins/poisons i.e. botulinum, ACh inhibition with organophosphorus compounds. Also affected in autoimmune disorders such as myasthenia gravis and Eton Lambert syndrome.
F = Respiratory muscles affected with mechanical splinting of the diaphragm, disuse atrophy and other muscular diseases
G = Lungs/chest wall with anything that affects the elasticity or structural integrity.
H= Increased small airway resistance i.e. asthma/COPD
I= Upper airway obstruction
J = Increased dead space ((Alveolar minute ventilation = TV- Dead space volume) x RR))
What is the best acute indicator of ventilatory insufficiency and what is the best long term indicator?
The best long term indicator of inadequacy in ventilation is PaCO2. PaCO2 takes time to rise so would not be noted to rise much in a short space of time.
Oxygen falls in a much shorter space of time therefore in the acute setting PaO2 is of much more use.
During IPPV what happens to the gas flow in fast vs slow inspiration?
- Fast inspiration: preferential gas flow to lung areas with short time constants
- Slow inspiration: Gas flow according to compliance
In IPPV is expiration an active or passive process?
Expiration remains a passive process where airway pressure falls back to ambient pressure + PEEP
What are the respiratory effects of IPPV?
- FRC and lung compliance falls;
- Intrapleural pressure changes much more than with spontaneous ventilation (from approximately -5 cm H2O in expiration up to +5 cm H2O in inspiration) this increases the risk of PTX.
- Risk of barotrauma
- Atelectasis may occur in dependent lung tissue causing increased dead space and A-a gradient. (PEEP is used to counteract the atelectasis)
What are the cardivascular effects of IPPV?
All effects arise from an increased intrathoracic pressure which can cause:
* Increased pulmonary vascular resistance
* Reduced preload due to reduced venous return and subsequent drop in cardiac output
* Reduced compliance of L ventricle causingfurther reduction in R ventricular filling and preload
* Raised CVP –> reduced drainage of head and neck –>Raised ICP
What are the potential renal complications of IPPV?
- Reduction in renal arterial BP and increased venous pressure
- Reduced renal perfusion
- Reduced GFR which stimulates the Renin Angiotensin System
- Vasopressin secretion
- Reduced ANP secretion.
- Urine output can drop up to 40% with sodium retention
Note: Ileus is also common with prolonged IPPV
What are the neurological consequences of oxygen toxicity?
Exposure to oxygen at a partial pressure > 2atm may result in convulsions and may be seen in hyperbaric oxygen therapy. Divers must be aware of this. Correlates with the decreased concentration of GABA levels state induced by oxygen in the brain.
What are the pulmonary consequence of oxygen toxicity?
12-24 hours of 100% oxygen:
* Substantial discomfort and tracheobronchial irritation
24-36h hours: (think lung trying to get rid of oxygen)
* Reduced compliance, vital capacity and diffusing capacity
* Increased dead space and arteriovenous shunt
Changes or damage after 24-36 hours:
* Reduced mucous clearance
* Endothelial damage with infiltration of macrophages and neutrophils
* Potential decrease in surfactant and increase in capillary permeability
What is a safe level of oxygen and why are some anaesthetists reluctant to pre-oxygenate prior to extubation?
FiO2 of 50% is safe over any period of time and to reduce risk of oxygen toxicity, the lowest FiO2 should be used.
Absorption Collapse: Due to the high inspired concentration of oxygen, the nitrogen in the alveoli will be displaced and oxygen will diffuse out of the alveoli leaving it with no gas to keep it splinted open causing alveolar collapse (this is also known as absorption atelectasis)
