Ventilatory support - Indications

1. Ventilatory support - Indications Acute ventilatory insufficiency Defined by an acute rise in PaCO2 and respiratory acidosis (pH<7.2). PaCO2 is directly proportional to the body‘s CO2 production and inversely proportional to alveolar ventilation (minute ventilation minus dead space ventilation). May be caused by : • Respiratory centre depression, e.g. by depressant drugs or intracranial pathology • Peripheral neuromuscular disease, e.g. Guillain – Barre’ syndrome, myasthenia gravis or spinal cord pathology • Therapeutic muscle paralysis, e.g. as part of balanced anaesthesia, tetanus or status epilepticus

2. Loss of chest wall integrity, e.g. chest trauma, diaphragmatic rupture • High CO2 production, e.g. burns, sepsis or severe agitation • Reduced alveolar ventilation, e.g. airways obstruction (asthma, acute bronchitis, foreign body), atelectasis, pneumonia, pulmonary oedema (ARDS, cardiac failure), pleural pathology, fibrotic lung disease, obesity. • Pulmonary vascular disease (pulmonary embolus, cardiac failure, ARDS)

3. Oxygenation failure Hypoxaemia is defined by PaO2<11kPa on fIO2>0.4. May be due to : • Ventilation / perfusion mismatching (reduced ventilation in or preferential perfusion of some lung areas), e.g. penumonia, pulmonary oedema, pulmonary vascular disease, extremely high cardiac output • Shunt (normal perfusion but absent ventilation in some lung zones) e.g. pneumonia, pulmonary oedema • Diffusion limitation (reduced alveolar surface area with normal ventilation), e.g. emphysema; reduced inspired oxygen tension, e.g. altitude, suffocation • Acute ventilatory insufficiency (as above)

4. To reduce intracranial pressure Reduction of PaCO2 to approximately 4kPa causes cerebral vasoconstriction and therefore reduces intracranial pressure after brain injury. Recent studies suggest this effect is transient and may impair an already critical cerebral blood flow.

5. To reduce work of breathing Controlled ventilation + sedation and muscle relaxation reduces respiratory muscle activity and therefore work of breathing. In cardiac failure or non-cardiogenic pulmonary oedema the resulting reduction in myocardial oxygen demand is easier matched to oxygen supply.

6. Indications for ventilatory support Ventilatory support should be considered if : • Respiratory rate > 30/min • Vital capacity <10-15ml/min • PaO2 <11kPa on FIO2 > 0.4 • PaCO2 high with repiratory acidosis (pH<7.2) • VD/VT >60% • QS/QT >15-20% • Exhaustion • Confusion • Severe shock • Severe LVF • Raised ICP

7. IPPV – description of ventilators Classification of mechanical ventilators • Mechanical ventilators may be classified according to the method of cycling from inspiration to expiration. • This may be when a pre-set time has elapsed (time-cycled), when a pre set pressure has been reached (pressure-cycled) or when a pre-set volume has been delivered (volume-cycled). • Although the method of cycling is classified according to a single constant, modern ventilators allow a greater degree of control. • In volume cycled mode with pressure limit the upper pressure alarm limit is set or the maximum inspiratory pressure is controlled.

8. The ventilator delivers a pre-set tidal volume (VT) unless lungs are non complaint or airway resistance is high. • This is useful to avoid high peak airway pressures. • In volume cycled mode with time limit inspiratory flow is reduced; the ventilator delivers the pre-set VT unless impossible at the set respiratory rate. • If pressure limitation is unless impossible at the set respiratory rate. • If pressure limitation is not available this is useful to limit peak airway pressure. • In time cycled mode with pressure control, pre-set pressure is delivered throughout inspirtion (unlike pressure-cycled ventilation), cycling being determined by time. • VT is dependent on respiratory compliance and airway resistance and high peak airway pressures can be avoided.

9. Setting up the mechanical ventilator Tidal volume • Normally 7-10ml/kg but may require 10-12ml/kg in acute respiratory failure. In Severe airflow limitation (i.g. asthma, acute bronchits) smaller VT and minute volume may be needed to allow prolonged expiration. Respiratory rate • Usually set in accordance with VT to provide minute ventilation of 85-100ml/kg/min. In time cycled or time limited modes the set respiratory rate determines the timing of ventilator cycles.

10. Inspiratory flow • Usually set between 40-80L/min. A higher flow rate is more comfortable for alert patients and also allows for longer expiration in patients with severe airflow limitation. • However, it is also associated with higher peak airway pressures. In addition, the flow pattern may be adjusted on most ventilators. • A square wave is common but decelerating flow, by reducing the average flow rate at a set peak flow rate, may reduce peak airways pressure.

11. I.E ratio • A function of respiratory rate, VT, inspiratory flow and inspiratory time. • Prolonged expiration is useful in severe airflow limitation and a prolonged inspiratory time is used in ARDS to allow slow reacting alveoli time to fill. • Alert patients are more comfortable with shorter inspiratory times and high inspiratory flow rates. FIO2 • Set according to arterial blood gases. • Usual to start at FIO2=0.6-1. Airway pressure • In pressure controlled or pressure limited modes the peak airway pressure (circuit rather than alveolar pressure) can be set (usually <40 cm H2O). PEEP can be used to maintain FRC when respiratory compliance is low.

12. Initial ventilator set-up • Check for leaks • Check oxygen on • FIO2 0.6-1 • VT 7-12ml/kg • Rate 10-15/min • I:E ratio 1:2 • Peak Pressure <40cm H2O • PEEP 0-5cm H2O

13. Ventilator adjustments in response to blood gas measurements • Low PaO2 • Increase FIO2 • Increase PEEP (may increase peak airways pressure or reduce CO) • Increase I:E ratio • Review VT and respiratory rate • Consider CMV, increased sedation + muscle relaxants • High PaO2 • Decrease PEEP (usually to 5cm H2O before reducing FIO2) Decrease FIO2 • Decrease I:E ratio • High PaCO2 • Increase VT (if peak airway pressure will allow) • Increase respiratory rate • Consider reducing respiratory rate if to high (to reduce intrinsic PEEP) • Consider reducing dead space • Consider CMV, increased sedation + muscle relaxants • Consider tolerating (Permissive hypercapnia) • Low PaCO2 • Decrease respiratory rate (to 10-12/min) • Decrease VT (to <7ml/kg)

14. IPPV – modes of ventilation Controlled mechanical ventilation (CMV) • A per-set number of breaths are delivered to supply all the patient’s ventilatory requirements. These breaths may be at a pre-set VT (volume controlled) or at a pre-set inspiratory pressure (pressure controlled) Assist – control mechanical ventilation (ACMV) • Patients can trigger the ventilator to determine the reparatory rate but, as with CMV, a pre-set number of breaths are delivered if the spontaneous respiratory rate falls below the pre-set level.

15. Intermittent mandatory ventilation (IMV) • A pre-set mandatory rate is set but patients are free to breathe spontaneously between set ventilator breaths. • Mandatory breaths may be synchronized with a patient’s spontaneous efforts (SIMV) to avoid mandatory breaths occurring during a spontaneous breath. • This effect, known as ‘stacking’ may lead to excessive tidal volumes, high airway pressure, incomplete exhalation and air trapping. • Pressure support may be added to spontaneous breaths to overcome the work of breathing associated with opening the ventilator demand valve.

16. Pressure support ventilation (PSV) • A pre-set inspiratory pressure is added to the ventilator circuit during inspiration in spontaneously breathing patients. The pre-set pressure should be adjusted to ensure adequate VT. Choosing the appropriate mode • Pressure controlled ventilation avoids the dangers associated with high peak airway pressures, although it may result in marked changes in VT if compliance alters. • Allowing the patient to make some spontaneous respiratory effort may reduce sedation requirements, re-train respiratory muscles and reduce mean airway pressures.

17. Apnoeic patient • Use of IMV or ACMV in patients who are totally apnoeic provides the total minute volume requirement if the pre-set rate is high enough (this is effectively CMV) but allows spontaneous respiratory effort on recovery. Patient taking limited spontaneous breaths • A guaranteed minimum minute volume is assured with both ACMV and IMV depending on the pre-set rate. • The work of spontaneous breathing is reduced by supplying the pre-set VT for spontaneously triggered breaths with ACMV, or by adding pressure support to spontaneous breaths with IMV. • With ACMV the spontaneous tidal volume is guaranteed whereas with IMV and pressure support is that gradual reduction of pre-set rate, as spontaneous effort increases, allows a smooth transition to pressure support ventilation. • Subsequent weaning is by reduction of pressure support level.

18. IPPV – failure to tolerate ventilation • Agitation or fighting the ventilator’ may occur at any time. Poor tolerance during initial phase of ventilation • Immediately after initiating mechanical ventilation the most likely cause is a failure to match ventilator setting to the patient’s requirements. • Careful adjustment of VT, respiratory rate, inspiratory flow and trigger sensitivity may resolve the problem; alternatively, additional sedation + muscle relaxation may be required.

19. Poor tolerance after previous good tolerance • If agitation occurs in a patient who has previously tolerated mechanical ventilation, either the patient’s condition has deteriorated (e.g. tension pneumothorax) or there is a problem in the ventilator circuit (including artificial airway) or the ventilator itself. • The patient should be removed from the ventilator and placed on manual ventilation while the problem is resolved. Resorting to increased sedation + muscle relaxation in this circumstance is dangerous until the cause is resolved. • Check patency of the endotracheal tube (e.g. with a suction catheter) and re-intubate if in doubt.

20. Consider malposition of the endotracheal tube (e.g. cuff above vocal cords, tube tip at carina, tube in main bronchus) • Where patients are making spontaneous respiratory efforts it is often better to allow this with IMV and pressure support or, if ventilatory drive is adequate, with PSV alone, rather than increasing sedation. • If patients fail to sychronise with IMV by stacking spontaneous and mandatory breaths, increasing pressure support and reducing mandatory rate may help; alternatively, the use of PSV may be appropriate.

21. IPPV – Complications of ventilation Haemodynamic complications • Venous return is dependent on passive flow from central veins to right atrium. • As right atrial pressure increases secondary to the transmitted increase in intrathoracic pressure across complaint lungs there is a reduction in venous return. • This is less of a problem if lungs are stiff (e.g ARDS) although will be exacerbated by the use of inverse I:E ratio. • As lung volume is increased by IPPV the pulmonary vasculature is constricted, thus increasing pulmonary vascular resistance. • This increases the diastolic volume of the right ventricle and, by sepal shift, impedes filling of the left ventricle. • These effects all contribute to a reduced stroke volume. This reduction can be minimized by reducing airway pressures, avoiding prolonged inspiratory times and maintaining blood volume.

22. Ventilator trauma • The term barotrauma relates to gas escape into cavities and interstitial tissues occurring during IPPV. • The complication is a misnomer since it is probably the distending volume which is responsible rather than the pressure. It is most likely to occur with high VT and high PEEP. • It also occurs in IPPV and conditions associated with over inflation of the lungs (e.g. asthma). • Tension pneumothorax is life threatening and should be suspected in any patient on IPPV who becomes suddenly agitated, tachycardic, hypotensive or exhibits sudden deterioration in their blood gases. • An immediate chest drainage tube should be inserted if tension pneumothorax develops. Prevention of ventilator trauma relies on avoidance of high VT, high PEEP and high airway pressures.

23. Nosocomial infection • Endotracheal intubations bypasses normal defence mechanisms. • Ciliary activity and cellular morphology in the tracheobronchial tree are altered. • The requirement for endotracheal suction further increases susceptibility to infection. • In addition, the normal heat and moisture exchanging mechanisms are bypassed requiring artificial humidification of inspired gases. • Failure to provide adequate humidification increases the risk of sputum retention and infection.

24. Acid –base disturbance • Ventilating patients with chronic respiratory failure or hyperventilation may, by rapid correction of hypercapnia, cause respiratory alkalosis. • This reduces pulmonary blood flow and may contribute to hypoxaemia. • A respiratory acidosis due to hypercapnia may be due to inappropriate ventilator settings or may be desired in an attempt to avoid high VT and ventilator trauma.

25. Water retention • Vasopressin released from the anterior pituitary is increased due to a reduction in intrathoracic blood volume and psychological stress. • Reduced urine flow thus contributes to water retention. In addition, the use of PEEP reduces lymphatic flow with consequent peripheral oedema, especially affecting the upper body. Respiratory muscle wasting • Prolonged ventilation may lead to disuse atrophy of the respiratory muscles.