Assisted ventilation in Neurosurgery:


Dr. A. Vincent Thamburaj,

Neurosurgeon, Apollo Hospitals,  Chennai , India.

Assisted ventilation plays a key role in the management of critically ill patients. It improves gas exchange, decreases the work of breathing, thereby decreasing the oxygen demand and allowing the patient to rest. 

In neurosurgical practice artificial ventilation is employed in

a)      Trauma- (flail chest, pulmonary contusions etc.)

b)      Postoperative – to reduce the work of breathing and allow a period for haemostability to be established following a major surgery.

c)      Control of ICP. 

Neurosurgeons should be aware of the principles of assisted ventilation and related physiology.

Types of ventilation:

There are essentially three types:

a)      Positive-pressure- The simplest form is mouth to mouth resuscitation or with a self-inflating bag and face mask (ambu bag). Endotracheal tube and a ventilator allow this process for an indefinite period.

b)      Negative-pressure-This is more physiological in that air is drawn into the lungs by creating sealed unit around the body or chest. There is no need for intubation. They are for patients with neuromuscular disorders who require nocturnal ventilation. This is not in use these days.

c)   High frequency ventilation may be divided into three subtypes:

-High-frequency positive pressure ventilation (HFPPV) using 60-100 100cycles(breaths)/minute; 

-High-frequency jet ventilation using rates of 150-500 cycles/minute.

-High-frequency oscillatory ventilation using rates of 400-2400 cycles/minute. 

High frequency ventilation is a last resort to improve the gas exchange in the severely lung injured and require a special ventilator; it is not in use these days, except during rigid bronchoscopy.



There are a large number of different ventilators of different categories depending on how they function.

All are designed to squeeze air into the lungs. 

Flow generators produce a predetermined flow of gas irrespective of the resistance it meets, but sometimes at the price of high airway pressure. It is difficult for the patient to take a spontaneous breath while connected; it is also difficult to monitor. 

Pressure generators produce a pre-set pressure waveform. Changes in airway resistance (eg: bronchospasm) and lung compliance (eg: pulmonary edema) will alter impedance and tidal volume resulting in hypoxia and CO2 retention which may be counter productive in neuro intensive care. 

Cycling is switching from expiration to inspiration. It may be controlled by time, pressure or volume. For volume-cycled ventilators the duration of inspiration is determined by the inspiratory flow rate. Pressure-cycled ventilators cycle once a preset pressure is a reached irrespective of the tidal volume delivered. Time-cycled ventilators is self-explanatory. 

Expiration occurs passively due to the elastic recoil of the lungs. It is essential to maintain a low resistance expiratory pathway.

Types of intermittent positive-pressure ventilation (IPPV): 

Controlled mechanical ventilation (CMV): The ventilator delivers a preset number of breadths and tidal volume, and makes no allowance for any effort by the patient. This is used in heavily sedated and paralyzed or deeply unconscious patients. Any respiratory attempt by the patient may lead to fighting the ventilator, resulting in hemodynamic instability, coughing, restlessness and raised ICP due to cerebral venous congestion..

The advantage is its ability to deliver adequate alveolar ventilation.

The disadvantages are many. The airway will be exposed to a large number of positive pressure breadths. Additionally, a high mean airway pressure will develop resulting in an increase in pulmonary barotrauma and reduction in cardiac output due to reduction in preload. The hyperventilation may result in respiratory alkalosis and hypocapnia, which may result in bronchospasm. 

Assist-controlled ventilation: Here the ventilator senses the patient’s respiratory effort. After the initiation of a spontaneous effort, the ventilator cycles on and delivers a predetermined tidal volume to the patient. The number of these positive pressure breaths will vary, depending on the patient’s efforts. These breadths are in addition to the previously determined number of controlled positive pressure breaths. Both will deliver the same tidal volume.

The advantage is some respiratory muscle tone is maintained. The disadvantage is the resultant hypocapnia due to the greater number of positive pressure breaths, which may necessitate sedation with or without muscle relaxants. 

Intermittent mandatory ventilation (IMV): The patient takes spontaneous breaths from a parallel low resistance circuit attached to the ventilator and also continues to receive pre-set breaths of known tidal volume. The mandatory breaths are not synchronized. The ventilator delivers a mandatory breath before the patient has finished exhaling a spontaneous breath, thus leading to hyperinflation of the lungs, which is detrimental in the head injured.

This mode has been largely replaced by synchronized mandatory ventilation. 

Synchronized intermittent mandatory ventilation (SIMV): This is similar to IMV, but the ventilator can sense the patient’s effort allowing the mandatory breath to be synchronized. The sensor can detect the gas flow or a fall in pressure generated by the patient thereby avoiding the patient fighting the ventilator. This is a weaning mode. 

Mandatory minute ventilation (MMV): The patient breathes spontaneously. If the minute volume falls below a preset value the ventilator gives a mandatory breath or breaths. 

Pressure support (PS): The ventilator supports the patient’s effort to breath by providing a predetermined pressure. This helps to reduce the work of breathing and increases the tidal volume. PS can be used in conjunction with SIMV, and CPAP, and not in CMV

Positive end-expiratory pressure (PEEP): This is generated by means of a valve on the expiratory limb of the circuit set at a pressure of 5-10cm H2O. This prevents airway collapse and increases the functional residual capacity (volume of gas in the lungs at the end of a normal expiration-FRC). This improves arterial oxygenation, but at times at the cost of reduced cardiac output and increased intrathoracic pressure and raise in ICP. The permissable PEEP without any adverse effect is upto 3cm H2O (physiological PEEP).

Continuous positive airway pressure (CPAP): This helps in spontaneously breathing patients by reducing the workload and prevents airway collapse. It can be applied by a close fitting nasal or a facemask or an endotracheal tube. This is a weaning mode from SIMV. 

Management of the ventilated patient: 

1) Airway:

Artificial ventilation for longer than few minutes requires an endotracheal tube. Intubation should be done with adequate sedation and paralyzing agents to prevent rise in ICP as well as to prevent laryngeal trauma. The tube cuff should be well inflated to provide airtight seal within the trachea to prevent gastric aspiration. 

An oral tube may be sufficient for a day or two. 

Nasal tube prevents tube biting and offers better fixation; but contraindicated in the presence of basal fracture with CSF fistulas, and also in faciomaxillary fractures. Tracheostomy is preferable in such situations.

Tracheostomy, either percutaneous or surgical, should be considered, if the ventilation is required for longer than a week. Tracheostomy  avoids laryngeal trauma, granuloma formation, tracheal stenosis and vocal cord palsy. It  also provides better mouth care. The anatomical dead space (the airway between the ventilator and alveolus) is reduced thereby lessening the workload.

A chest x-ray confirms tube position and provide a baseline for further radiological assessments.

A nasogastric tube should be inserted to decompress the stomach and for enteral feeding. 

2) Ventilation:


The following should be selected depending on the requirements:

1) Ventilatory mode, e.g. CMV or SIMV. 

2) Inspired oxygen concentration

3) Minute volume or inspiratory pressure for pressure-controlled ventilators (not advisable in the head injured as ventilation   and oxygenation may be compromised). It requires sedation and relaxants and continuous monitoring. 

4) Respiratory rate –usually 12-20/minute.

5) Tidal volume – 7-10ml/kg.

6) Inspiratory/expiratory ratio- 1:3 

In addition the relevant alarms should be activated. Humidification must be introduced in the circuit to prevent secretion retention and tube blockage. Bacterial filters to lesson the contamination should be used.

An alternative method of manually ventilating the patient (ambu’s) should be ready for use should ventilator fail or during physiotherapy. 

3) Monitoring:

Ventilation: Virtually all ventilators display airway pressure and expired minute volume measurement. The aim is to reduce the risk of barotraumas and to alert the staff to disconnection from the ventilator. More sophisticated ventilators identify patient spontaneous breaths and provide comprehensive data.

Patient: ECG and blood pressure monitoring and pulseoximeter to display peripheral oxygen saturation are the barest minimum required. An arterial line provides more accurate monitoring of blood pressure and allows serial blood gas studies. Capnography to measure end tidal CO2 saturation helps. 


Ideally, jugular venous bulb saturation should be used to ensure that oxygen delivery is not being compromised.

4) Sedation:


Most patients will not tolerate a tube and need to be sedated and if necessary, paralyzed. Drugs may be given as a continuous infusion or intermittent bolus. Ideal drug should be non-cumulative, free of side effects, and have short duration of action. There is no such ideal drug. Various drugs are used either alone or in combination.

Benzodiazepines- Midazolam is most often used; can accumulate if used for several days. Withdrawal may be complicated with hallucinations and agitation. Tolerance is common.

Opiates- Morphine and fentanyl are the commonest. They provide analgesia and sedation. Renal functions must be monitored. Naloxone may be used to antagonize if needed.

Anesthetic agents- Propofol is popular and short acting. Cardiovascular depression may be a problem. It is better to avoid this in children. Isoflurane was once popular; it is not widely accepted now.

Muscle relaxants- they have no analgesic or sedative properties whatsoever. They are used in patients who are adequately sedated, but still fighting the ventilator or those requiring hyperventilation to reduce ICP. Patients who are adequately paralyzed will not cough or respond to stimuli. Bolus doses need to be given periodically as continuous infusion run the risk of accumulation.

There is a trend away from the use of relaxants and towards allowing the patients to breath spontaneously if possible. 

5) Hyperventilation as a treatment of increased ICP:  

Slow rates and large tidal volumes (12 breaths a minute and 10ml/kg of tidal volume) are recommended to ensure adequate venous drainage and re-expand atelectatic areas. 

PO2 must be maintained between 100-140 mmHg as higher pO2 induces cerebral vasoconstriction. A fall in pCO2 decreases cerebral blood flow and thus reduces ICP. 

The desired pCO2 should be consistent with the appropriate reduction of ICP. PCO2 in the range of 25 to 30 mmHg may be adequate. Further reduction can cause vasoconstriction and cerebral ischemia and should be avoided. It should be kept in mind that hypocapnia produces alkalaemia, which may cause cardiac irritability, decreased cardiac contractility, coronary vasospasm, hypocalcaemia (ionic calcium) and hypokalaemia, and a shift of oxygen dissociation curve to the left compromising oxygen delivery. 

Ideally, hyperventilation is employed in conjunction with regular arterial blood pressure, blood gas and ICP monitoring. There is no point in hyperventilating a patient with normal ICP. 


It is more important to maintain the cerebral perfusion pressure (CPP) of 70-100 mm Hg rather than merely reducing the ICP. This is dependent on ICP and MAP (CPP = MAP - ICP)

Continuous hyperventilation for more than a day or two becomes ineffective in controlling the raised ICP. However, more extreme degrees of hypocapnia temporarily, by hand bagging can lower an ICP even in patients who are refractory to milder reductions.

It is suggested that the patient should be maintained on normal range of PCO2.and hand bagging employed when the ICP goes above 25mm of Hg instead of continuous hyperventilation. 


Dehydration due to osmotherapy causes metabolic acidosis which may stimulate respiration in under sedated patients on a ventilator and reduce the pCO2  to less than desired to normalize the pH, which will compromise the CBF. Metabolic acidosis is the earliest sign of dehydration before it shows up in serum urea and creatinine levels. Dehydration must be avoided. 

6) Weaning:   

There are various criteria to assess suitability for weaning and vary depending on the mode of ventilation. 

The clinician should decide when weaning should commence. A spontaneous effort, which should generate an airway pressure of greater than –20 cm of H2O with a forced vital capacity of greater than 1liter indicates readiness for weaning. The mechanical breaths are discontinued and the patient is reattached to the ventilator after a short interval. This sequence is repeated, with the patient spending more time out of the ventilator. Blood gas analysis and clinical monitoring of the patient helps.

Weaning from assist-controlled ventilation involves removal of the controlled breaths and then may proceed as just described. 

Intermittent synchronous mandatory ventilation attempts to provide a smooth transition. Blood gas analysis help. PCO2 of 35to45mm Hg, pH of 7.35 and spontaneous respiratory rate of <30/minute are the widely accepted criteria. 

In neurology, weaning is an art; clinical examination is the best guidance, rather than the suggested criteria provided there is no pre-existing lung disease or multi organ failure. 

Blood gas analysis and clinical examination should continue for sometime after weaning. 

Complications of artificial ventilation: 

Normal breathing occurs at negative (sub atmospheric) pressure. IPPV applies positive pressure to the lungs in order to achieve gas flow. This decreases the venous return and thereby cardiac output, necessitating volume replacement. Due to decreased cardiac output, there is decreased urinary output leading to increased ADH and angiotensin and sodium and fluid retention. 

End inspiratory occlusion pressure is the best variable to assess the lung injury. High pressures (>35 cm H2O) are more detrimental than high oxygen. Pressure controlled ventilation may prevent this. Prolonged use of PEEP, neonates, patients with stiff, noncompliant lungs are at risk. Pneumothorax and hyperinflation are other possible complications. 

Prolonged use of O2 in high concentration damages the lungs. Due to nitrogen washout, there is alveolar collapse and further damage due to activation of complement cascade. Release of free radicals will lead to ‘shock lung’, i.e. acute respiratory distress syndrome (ARDS). 

During IPPV, there is ciliary dysfunction due to cold, dry gases; cough reflex is depressed due to sedation and there is retention of sputum and atelectasis. All these may lead onto infection.30% of the ventilated patients have pneumonia this increases by 1% per day. Prophylactic antibiotics are often ineffective. 

Patients are at risk of side effects from sedatives and paralyzing agents. Problems with tolerance, accumulation and withdrawal are commonly seen. 


Endotracheal tube related complications such as tube blockage, kinking, misplacement; accidental extubation and laryngeal trauma are other possible complications.

Punctured or insufficiently inflated cuff may lead to gastric aspiration.






















































































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