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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.
Ventilators:
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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