Mechanical Ventilation- Physiologic Goals
Normal physiologic goals
Targeting normal physiologic goals for the mechanically ventilated patient may not be the best choice. Trying to do so with little regard for the size of the tidal volumes, the pressures applied or the amount of oxygen used may be injurious to the patient. It could cause lung injury or release of inflammatory mediators.
Patients with abnormal lung mechanics are at risk such as the ARDS, asthmatic or COPD patient. Ventilation must be administered with due regard for their abnormal lungs.
Measurement of the patients end-inspiratory plateau pressure is an indirect measurement of their alveolar distending pressure.
To measure this a 0.5-2-second end inspiratory breath hold is applied. The plateau pressure should be less than 30cmH20. This usually results in tidal volumes of between 4-8 ml/kg and this has been shown to be lung protective.
The primary goal of ventilation is no longer to normalise blood gas values but rather maintaining adequate gas exchange while minimising the risks of mechanical ventilation. In order to do so sometimes we have to accept that the carbon dioxide levels are going to rise- a hypercapnia.
Hypercapnia may need to be tolerated with the ARDS patient for example. It has been shown that lower tidal volumes are important here as this reduces the stretching forces on the alveoli which can be damaging.
The patient in bronchospasm may be in a situation where the expiratory phase does not complete properly due to the narrowing of the airways, This generates an auto PEEP and the possibility of breath stacking where one breath comes on top of the previous.
Adjustments need to be made to the ventilator to allow a complete expiratory cycle such as increasing the inspiratory flow rate, decreasing the tidal volume or decreasing the respiratory rate.
Hypercapnia is associated with cerebral vasodilatation increasing cerebral blood flow. So those patients with a lesion, trauma oedema or any kind of inter cerebral bleed should have their CO2 levels kept within normal boundaries.
Also patients who are hypotensive should not be allowed to become hypercapnic as this will vasodilate them further dropping their blood pressure.
Physiologic effects of hypercapnia
- Pulmonary vasoconstriction
- Shift of the oxyheamoglobin dissociation curve to the right
- Central nervous system depression
- Decreased alveolar PO2
- Increased intercranial pressure
- Decreased renal blood flow
- Increased ventilatory drive
- Systemic vasodilatation
During permissive hypercapnia the pH may well worsen as this can be tolerated to as low as 7.2 in previously well patients.
To allow some renal compensation to occur it is important to make the rise in CO2 a gradual one where possible. Abrupt changes in the PCO2 are often poorly tolerated.
Ideally the oxygen should be no higher than 60%. In animal studies 100% oxygen has been shown to cause non-cardiogenic pulmonary oedema within 24-48 hours.
Whilst a higher plateau pressure is of greater concern in the ARDS patient where possible high oxygen requirements should also be monitored closely and if necessary there may have to be a tolerance of lower PaO2- permissive hypoxemia.
- Oxygenation- 10-13 Kpa however will need to adjust to lower targets in patients with ARDS or COPD
- Ventilation- normal PaCO2 is 4.5-6Kpa. If the risks of a high plateau pressure or tidal volumes are too great to achieve this then it can be allowed to rise to as high as 13Kpa providing there are no other contraindications as above.
- Acid base balance- if a rise in PaCO2 is gradual and renal and cardiovascular function are adequate a pH of 7.2-7.3 is usually well tolerated. Respiratory alkalosis should be avoided as this can lead to electrolyte disturbances, seizures and decreased oxygen unloading from heamoglobin.
Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome (ARDSNet) The Acute Respiratory Distress Syndrome Network*N Engl J Med 2000; 342:1301-1308
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