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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. |