Вы находитесь на странице: 1из 49
Basics for beginners
Basics for beginners

Basics for beginners

Basics for beginners

Mechanical Ventilation


It is a method to mechanically assist or replace spontaneous breathing when patients can not do so on their own.

General Considerations

Mechanical ventilation has resulted in profoundly improved survival from acute and chronic respiratory failure.

Mechanical ventilation in the intensive care unit (ICU) is delivered under positive pressure in contrast to normal human breathing in which inspiration induces negative pressure in the thorax. This makes the complications of barotrauma and hypotension predictable. To achieve ventilation, rate, tidal volume (VT), fraction of inspired oxygen (FIO 2 ), and positive end-expiratory pressure (PEEP) are selected. It is useful to track the product of VT and rate, the minute ventilation ( E), to assess for complications and readiness to wean. A normal E is less then 10 L/min.

and readiness to wean. A normal E is less then 10 L/min. Pressures in ventilators: There
and readiness to wean. A normal E is less then 10 L/min. Pressures in ventilators: There

Pressures in ventilators: There are two types of pressures used in ventilators.

a. Negative pressure ventilators: The best example is “iron lung” that creates a negative pressure environment around the patient’s chest, thus sucking air into the lungs. This is a large elongated tank, which encases the patient up to the neck. The neck is sealed with a rubber gasket so that the petient’s face and airway are exposed to the room air. This was largely used to treat patients with respiratory paralysis due to poliomyelitis

largely used to treat patients with respiratory paralysis due to poliomyelitis triplehelix 3 Mechanical Ventilation

b. Poistive pressure ventilators: This is the main form of ventilators currently used. These ventilators work by increasing the pressure in the patient’s airway, and thus forcing additional air into the lungs.

The fundamental difference between positive pressure and negative pressure is, in positive pressure ventilation, air is introduced into the lungs forcefully creating positive pressure, but in negative pressure ventilation, negative pressure is created outside of the lungs that sucks the chest to inflate, and creates negative pressure within lungs, as a result air flows into the lungs.

Ventilation: Invasive Vs non-invasive:

The difference is just use of a tube (i.e. endotracheal tube, tracheostomy tube). If you use endotracheal tube, it is invasive ventilation. If you do not use, it is non-invasive ventilation.

Non-invasive ventilation can be delivered with the use either of:

a. Negative pressure ventilators (e.g. Iron lung)

b. Positive pressure assistance to the airway by mask (using NIPPV). Non Invasive Positive Pressure Ventilation (NIPPV) can be delivered by several appliances, including face masks, nasal masks, nasal pillows etc

by several appliances, including face masks, nasal masks, nasal pillows etc triplehelix 4 Mechanical Ventilation

Bi-PAP setting:

Bi-PAP setting: triplehelix 5 Mechanical Ventilation

Nasal/face mask:

Nasal/face mask: triplehelix 6 Mechanical Ventilation
triplehelix 7 Mechanical Ventilation
triplehelix 8 Mechanical Ventilation
Nasotracheal intubation: triplehelix 9 Mechanical Ventilation

Positive pressure machines:

Positive pressure machines: triplehelix 10 Mechanical Ventilation

Negative-pressure ventilation

Ü Negative-pressure ventilators support ventilation by lowering the pressure surrounding the chest wall during inspiration and reversing the pressure to atmospheric level during expiration. These devices augment the tidal volume by generating negative extrathoracic pressure.

Ü Several of these devices, such as body ventilators and iron lungs, are available and either cover the whole body below the neck or apply negative pressure to the thorax and abdomen.

Noninvasive positive-pressure ventilation (NPPV)

Ü NPPV is delivered by a nasal or face mask, therefore eliminating the need for intubation or tracheostomy. NPPV can be given by a volume ventilator, a pressure-controlled ventilator, a bilevel positive airway pressure (BIPAP or bilevel ventilator) device, or a continuous positive airway pressure (CPAP) device. Volume ventilators are often not tolerated because they generate high inspiratory pressures that result in discomfort and mouth leaks.

Ü NPPV delivers a set pressure for each breath (with a bilevel or standard ventilator in the pressure-support mode). Although positive-pressure support is usually well tolerated by patients, mouth leaks or other difficulties are sometimes encountered. BIPAP ventilators provide continuous high-flow positive airway pressure that cycles between a high positive pressure and a lower positive pressure.

Ü NPPV may be used as an intermittent mode of assistance depending on patients' clinical situations. Instantaneous and continuous support is given to the patients in acute respiratory distress. As the underlying condition improves, ventilator-free periods are increased as tolerated, and support is discontinued when the patient is deemed stable. In most studies, the duration of NPPV use in patients with acute on chronic respiratory failure averages 6-18 hours.

Ü The total duration of ventilator use varies with the underlying disease; approximately 6 hours is used for acute pulmonary edema and more than 2 days is used for COPD exacerbation.

Mechanisms of action

Ü NPPV decreases the work of breathing and thereby improves alveolar ventilation while simultaneously resting the respiratory musculature. The improvement in gas exchange with BIPAP occurs because of an increase in alveolar ventilation.

Ü Externally applied expiratory pressure (eg, positive end-expiratory pressure [PEEP]) decreases the work of breathing by partially overcoming the auto-PEEP, which is frequently present in these patients. The patients generate a less negative inspiratory force to initiate a breathing cycle.

Inhalation and exhalation:

Ü In spontaneous mode, upon detection of inspiration, higher pressure is delivered until the flow rate falls below the threshold level. The expiratory pressure with bilevel pressure support is equivalent to the PEEP, and the inspiratory pressure is equivalent to the sum of the PEEP and the level of pressure support.

Ü In timed mode, biphasic positive airway pressure ventilation alternates between the inspiratory and expiratory pressures at fixed time intervals, which allows unrestricted breathing at both pressures. This differs from the spontaneous mode of BIPAP, which cycles on the basis of the flow rates of the patient's own breathing.

Ü Supplemental oxygen can be connected to the device, but a higher flow of oxygen therapy is usually required.

Ü NPPV is more effective in a relaxed patient and is not optimal in an anxious uncooperative patient or a patient fighting the ventilator. Patients must be adequately prepared with properly fitting masks, and the increase of the inspiratory and the expiratory pressures should occur gradually.

Ü Effectiveness should be determined clinically by improved respiratory distress, decreased patient discomfort, and improved results from arterial blood gas determinations.

BIPAP ventilator versus conventional ventilator

The conventional ventilator offers a number of advantages, such as the delivery of precise oxygen concentrations and separate inspiratory and expiratory tubing that minimizes carbon dioxide rebreathing. Patient disconnection can be readily detected because monitoring and alarm features are more sophisticated in conventional ventilators than in bilevel systems.

Nasal mask versus face mask

No randomized trials have compared nasal masks to full face masks in NPPV. Most patients in acute respiratory failure are mouth breathers; therefore, a facial mask may be preferable in some patients. These patients should be carefully observed because of the risk of aspiration.

Neurally Adjusted Ventilatory Assist (NAVA)

Ü NAVA is a new positive pressure mode of mechanical ventilation, where the ventilator is controlled directly by the patient's own neural control of breathing.

Ü The neural control signal of respiration originates in the respiratory center, and are transmitted through the phrenic nerve to excite the diaphragm. These signals are monitored by means of electrodes mounted on a nasogastric feeding tube and positioned in the esophagus at the level of the diaphragm. As respiration increases and the respiratory center requires the diaphragm for more effort, the degree of ventilatory support needed is immediately provided.

Ü This means that the patient's respiratory center is in direct control of the mechanical support required on a breath-by-breath basis, and any variation in the neural respiratory demand is responded to by the appropriate corresponding change in ventilatory assistance.

Choosing amongst ventilator modes

Ü Assist-control mode minimizes patient effort by providing full mechanical support with every breath. This is often the initial mode chosen for adults because it provides the greatest degree of support.

Ü In patients with less severe respiratory failure, other modes such as SIMV may be appropriate.

Ü Assist-control mode should not be used in those patients with a potential for respiratory alkalosis, in which the patient has an increased respiratory drive. Such hyperventilation and hypocapnia (decreased systemic carbon dioxide due to hyperventilation) usually occurs in patients with end-stage liver disease, hyperventilatory sepsis, and head trauma. Respiratory alkalosis will be evident from the initial arterial blood gas obtained, and the mode of ventilation can then be changed if so desired.

Ü Positive End Expiratory Pressure may or may not be employed to prevent atelectasis in adult patients. It is almost always used for pediatric and neonatal patients due to their increased tendency for atelectasis.

Ü High frequency oscillation is used most frequently in neonates, but is also used as an alternative mode in adults with severe ARDS.

Ü Pressure Regulated Volume Control is another option.

Guidelines for the use of NPPV in patients with acute respiratory failure

Ü Blood gas findings


Partial pressure of carbon dioxide in arterial gas (PaCO 2 ) greater than 45




pH less than 7.35 but more than 7.10



2 and fraction of inspired oxygen (FIO 2 ) less than 200

Ü Clinical inclusion criteria


Signs or symptoms of acute respiratory distress


Moderate-to-severe dyspnea, increased over usual


Respiratory rate greater than 24 breaths per minute


Accessory muscle use


Abdominal paradox





PaCO 2 greater than 45 mm Hg and pH less than 7.35


PaCO 2 -to-FIO 2 ratio less than 200 mm Hg

Ü Diagnosis



COPD exacerbation


Acute pulmonary edema



Ü Contraindications


Respiratory arrest


Inability to use mask because of trauma or surgery


Excessive secretions


Hemodynamic instability or life-threatening arrhythmia


High risk of aspiration


Impaired mental status


Uncooperative or agitated patient


Life-threatening refractory hypoxemia (alveolar-arterial difference in partial pressure of oxygen [PaO 2 ] <60 mm Hg with FIO 2 of 1)

Ü Factors predictive of success


Younger age


Lower acuity of illness (ie, acute physiology and chronic health evaluation [APACHE] score)


Patient able to cooperate


Ability to coordinate breathing with ventilator


Moderate hypercapnia (PaCO 2 >45 mm Hg but <92 mm Hg)


Moderate acidemia (pH >7.10 but <7.35)


Improvement in gas exchange and heart and respiratory rates within first 2


Protocol for Initiation of NPPV in patients with acute respiratory failure

Ü Position the head of the bed at a 45° angle.

Ü Choose the correct size of mask and initiate ventilator at CPAP (expiratory positive airway pressure or EPAP) of 0 cm water with a pressure support of 10 cm water.

Ü Hold the mask gently on the patient's face until the patient is comfortable and in full synchrony with the ventilator.

Ü Apply wound care dressing on the patient's nasal bridge and other pressure points.

Ü Secure the mask with head straps, but avoid a tight fit.

Ü Slowly increase CPAP to more than 5 cm water.

Ü Increase pressure support (ie, inspired positive airway pressure or IPAP, 10-20 cm water) to achieve maximal exhaled tidal volume (10-15 mL/kg).

Ü Evaluate that ventilatory support is adequate, which is indicated by an improvement in dyspnea, a decreased respiratory rate, achievement of desired tidal volume, and good comfort for the patient.

Ü Oxygen supplementation is achieved through NPPV machine-to-machine oxygen saturation of greater than 90%.

Ü A backup rate may be provided in the event the patient becomes apneic.

Ü In patients with hypoxemia, increase CPAP in increments of 2-3 cm water until FiO 2 is less than 0.6.

Ü Set the ventilator alarms and backup apnea parameters.

Ü Ask the patient to call for needs, and provide reassurance and encouragement.

Ü Monitor with oximetry, and adjust ventilator settings after obtaining arterial blood gas results.

Benefits of NPPV

In acute respiratory failure, NPPV offers a number of potential advantages over invasive PPV. These advantages include the avoidance of intubation-related trauma, a decreased incidence of nosocomial pneumonia, enhanced patient comfort, a shorter duration of ventilator use, a reduction in hospital stay, and ultimately, reduced cost.

Guidelines for use of NPPV in chronic respiratory failure resulting from restrictive processes



Blood gas and clinical criteria



PaCO 2 greater than 45 mm Hg


Nocturnal hypoventilation and symptoms (eg, hypersomnolence, morning headache)


Appropriate diagnosis



Neuromuscular diseases


Thoracic deformity


Obesity hypoventilation syndrome


Obstructive sleep apnea unresponsive to CPAP




Inability to clear secretions


Moderate-to-severe bulbar involvement


Uncooperative patients


Patients who need continuous ventilatory support

Indication of mechanical ventilation:

Ü Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to maintain life.

Ü It is also indicated as prophylaxis for imminent collapse of other physiologic functions, or ineffective gas exchange in the lungs.

Ü Because mechanical ventilation only serves to provide assistance for breathing and does not cure a disease, the patient's underlying condition should be correctable and should resolve over time.

Ü In addition, other factors must be taken into consideration because mechanical ventilation is not without its complications

Common medical indications for use include:

Ü Acute lung injury (including ARDS, trauma)

Ü Apnea with respiratory arrest, including cases from intoxication

Ü Acute respiratory acidosis with partial pressure of carbon dioxide (pCO 2 ) > 50 mmHg and pH < 7.25, which may be due to paralysis of the diaphragm due to Guillain-Barré syndrome, Myasthenia Gravis, spinal cord injury, or the effect of anaesthetic and muscle relaxant drugs

Ü Increased work of breathing as evidenced by significant tachypnea, retractions, and other physical signs of respiratory distress

Ü Hypoxemia with arterial partial pressure of oxygen (PaO 2 ) with supplemental fraction of inspired oxygen (FiO 2 ) < 55 mm Hg

Note: Mechanical ventilation does not mandate endotracheal intubation, nor does intubation require mechanical ventilation. For example, endotracheal intubation may be life saving in a case of impending upper airway obstruction or high risk for aspiration, without need for a ventilator.

Types of ventilators:

Ventilation can be delivered via:

A. Hand-controlled ventilation such as:

Ü Continuous-flow or Anaesthesia (or T-piece) bag

B. A mechanical ventilator.

Types of mechanical ventilators include:

Ü Transport ventilators. These ventilators are small, more rugged, and can be powered pneumatically or via AC or DC power sources.

Ü ICU ventilators. These ventilators are larger and usually run on AC power (though virtually all contain a battery to facilitate intra-facility transport and as a back-up in the event of a power failure). This style of ventilator often provides greater control of a wide variety of ventilation parameters (such as inspiratory rise time). Many ICU ventilators also incorporate graphics to provide visual feedback of each breath.

Ü PAP ventilators. These ventilators are specifically designed for non- invasive ventilation. This includes ventilators for use at home, in order to treat sleep apnea.

Modes of mechanical ventilation:

A "mode" of mechanical ventilation refers to the program by which the ventilator interacts with the patient, the relationship between the possible types of breaths allowed by the ventilator, and the variables that define inspiration.

Inspiration is defined by three variables:

Ü trigger

Ü limit

Ü cycle

Trigger is the change detected by the ventilator that causes inspiration to begin;

Limit is the value that cannot be exceeded during inspiration (volume, pressure, or flow)

Cycle is the value that when reached, terminates inspiration.

Using these definitions, three breath types are possible:

Ü Full ventilator control (mandatory), the ventilator controls the breathing

Ü Partial ventilator control (assisted), ventilator assist with patient’s breathing

Ü Full patient control (spontaneous), patient controls the breathing completely.

The most commonly used modes in adults are volume limited.

In controlled mechanical ventilation (CMV), there is no patient triggering; rather, all breaths are ventilator triggered, limited, and cycled. CMV is used in patients who make no respiratory effort, such as those with neuromuscular paralysis.

In assist/control ventilation (ACV), by contrast, the clinician sets a minimum rate and tidal volume. The patient can trigger the ventilator at a more rapid rate, and will receive the set volume each time.

In intermittent mandatory ventilation (IMV), ventilator-limited (ie, volume or pressure) breaths are similarly delivered at a set (minimum) rate, but the patient can breathe spontaneously by triggering a demand valve between machine-limited breaths.

In current ventilators IMV is modified to synchronized IMV (SIMV), in which the ventilator synchronizes machine breaths with patient effort.

In the patient who does not trigger the ventilator, CMV, ACV, and SIMV are qualitatively identical. In assist control, there is a greater potential for respiratory alkalosis and intrinsic PEEP (PEEP i ), or "autoPEEP,"

What is auto-PEEP (PEEPi):

This is persistent positive alveolar pressure at end of expiration, often with associated hyperinflation, due to delivery of full machine breaths for all patient efforts. The hyperinflation results from insufficient time for the lungs to empty. This causes gas trapping, and builds up of positive pressure in the lungs.

Is the patient gas trapping? – Expiratory flow does not return to baseline before inspiration commences (i.e. gas is trapped in the airways at end-expiration).

inspiration commences (i.e. gas is trapped in the airways at end-expiration). triplehelix 19 Mechanical Ventilation
inspiration commences (i.e. gas is trapped in the airways at end-expiration). triplehelix 19 Mechanical Ventilation
inspiration commences (i.e. gas is trapped in the airways at end-expiration). triplehelix 19 Mechanical Ventilation
In principle, machine breaths in the assist/control or IMV modes can be defined by a

In principle, machine breaths in the assist/control or IMV modes can be defined by a set volume or pressure.

If volume control is selected, the tidal volume is fixed, and airway pressure varies with the resistance and compliance of the patient's lungs and chest wall.

If pressure control is selected, a fixed inspiratory pressure level is maintained for a set inspiratory time or inspiration:expiration (I:E) ratio, and tidal volume and flow vary with patient effort and mechanics.

Two additional common modes of ventilation are continuous positive airway pressure (CPAP) and pressure support ventilation (PSV).

triplehelix 21 Mechanical Ventilation
triplehelix 21 Mechanical Ventilation
triplehelix 21 Mechanical Ventilation

CPAP is spontaneous breathing with no mandatory or assisted breaths; a constant level of pressure is applied to the airway throughout the respiratory cycle. The mode CPAP is similar to PEEP, which is not a mode but is the addition of baseline positive pressure during mechanical ventilation.

In PSV, breaths are patient triggered, pressure limited, and flow cycled. That is, with no machine backup rate, the ventilator assists the patient's inspiratory effort with a preset pressure. Patients determine their own respiratory rate, inspiratory time, and tidal volume.

own respiratory rate, inspiratory time, and tidal volume. PSV can be combined with other modes, such

PSV can be combined with other modes, such as SIMV, to assist patient efforts between the set machine breaths.

Although the ventilator performs the full work of breathing in CMV and the patient performs the full work of breathing in CPAP, two important points should be emphasized.

Ü First, the ideal work of breathing for the mechanically ventilated patient remains unclear (ie, the ideal amount that prevents muscle atrophy, yet permits rest).

Ü Second, patient work of breathing is not necessarily less in ACV or SIMV than in PSV, particularly if patient–ventilator synchrony is optimized in PSV

Several newer "alternative" ventilatory modes have been developed in recent years in an attempt to combine attractive features of pressure and volume ventilation into a single mode that will deliver the minimum necessary ventilator pressure for a tidal volume goal. Modes including mandatory minute ventilation (MMV) "automatically" titrate the amount of ventilator assistance to changing patient mechanics and breathing drive. These modes have not yet been shown to improve clinical end points in prospective trials, but are increasingly encountered in general practice.

Ventilator Settings:

The major variables to set for the volume-controlled modes, ACV and SIMV are

¬ respiratory rate,

¬ tidal volume,

¬ flow rate and pattern,

¬ FIO 2 , (fraction of inspired oxygen) and

¬ PEEP level.

Respiratory rate:

Ü Although a rate of 10–20 breaths/min is generally appropriate for most patients with respiratory failure, patients with airflow limitation who are at risk for developing PEEP i may benefit from lower rates and patients with a need for high minute ventilation due to metabolic acidosis need higher rates.

Ü In SIMV, it is best to initially deliver at least 80% of minute ventilation with machine breaths.

Ü In ACV, setting the rate about 4 breaths/min below the patient rate ensures that the patient and not the machine is dictating minute ventilation, and yet provides adequate backup if the patient becomes apneic.

Tidal Volume:

Ü Although tidal volumes as high as 10 mL/kg (and perhaps higher) may be appropriate for patients without lung disease, lower volumes are otherwise indicated.

Ü In acute respiratory distress syndrome (ARDS), the use of a tidal volume of 6 mL/kg (ideal body weight) was associated with improved mortality compared with 12 mL/kg, and should be considered the standard of care.

Ü A tidal volume of 6–8 mL/kg is often used in obstructive lung disease (asthma, COPD) to avoid high airway pressures and development of PEEP i .

Ü In fact, studies of asthma and ARDS suggest that a lung protective ventilatory strategy, termed "permissive hypercapnia," may lead to improved outcomes. This strategy reduces tidal volumes and/or rate and allows a respiratory acidosis to a pH as low as 7.15–7.20.

Ü Generally, when increased ventilation is needed, it is more effective to adjust minute ventilation by changes in rate rather than tidal volume, because increases in tidal volume occasionally have the paradoxical effect of slowing respiratory rate.

Ü Frequent arterial blood sampling to check CO 2 tension in the stable patient can be avoided by noting the minute ventilation needed to achieve a given level of PaCO 2 .

Flow rate and pattern:

Ü The peak flow rate determines the maximal inspiratory flow delivered by the ventilator during inspiration. Although 60 L/min is a common initial peak flow setting, higher flows, with subsequent higher peak inspiratory pressure are commonly needed for high ventilatory demand or underlying airway obstruction.

Ü Flow is delivered during the inspiratory period via one of three waveforms:

¬ constant (square wave),

¬ decelerating (ramp wave), or

¬ sinusoidal.

What is the difference between constant, decelerating and sinusoidal flow waveforms? Flow of gas is
What is the difference between constant, decelerating and sinusoidal flow waveforms? Flow of gas is
Flow of gas is calculated in liters per minute. Flow commences at the beginning of a
breath and stops at the end of the breath. Gas flows into the lungs in inspiration and
out of the lungs in expiration. The pattern of expiratory flow is more or less the same
for different modes of ventilation, as long as the expiratory phase is long enough to
prevent gas trapping.
The normal flow pattern of gas moving in and out of the lungs is sinusoidal.
In volume control ventilation a variety of different wave patterns can be used.
In clinical practice, constant and decelerating flow patterns are used; the latter is
preferred. In constant, decelerating and sinusoidal flow patterns, the inspiratory flow
rate is equal to the peak flow rate, but the mean flow rate is higher in constant flow
patterns rather than the other two. This suggests that this pattern will cause more
shearing injury to the lung parenchyma. Therefore a decelerating flow pattern is
probably the most effective flow pattern – it ensures peak flow early in inspiration,
while simultaneously minimizing flow during the phase of the inspiratory cycle in
which the patient is least likely to need it.

Ü Although important differences in clinical outcome have not been demonstrated for particular flow patterns, decelerating flow is most commonly used because it may achieve better gas exchange (ie, lower alveolar–arterial oxygen gradient and lower dead space) as well as lower peak inspiratory pressure, despite higher mean airway pressure.

Ü To improve oxygenation in ARDS, mean airway pressure is increased. To do this in volume-controlled modes, the peak inspiratory flow rate is decreased. In pressure control ventilation, inspiratory time is increased (pressure control) to

reach an I:E ratio greater than 1, a practice termed inverse ratio ventilation (IRV).

Ü IRV is uncomfortable for the patient, often requiring deep sedation or even paralysis, and carries the risk of gas trapping, it should be used selectively and by experienced clinicians.

Fraction of inspired osygen (FIO2):

Ü The FIO 2 is typically started at 1.0 (100% oxygen).

Ü Although the literature does not stipulate a cutoff for a safe level of inspired oxygen in humans, concerns over oxygen radical-mediated lung injury have led to the common practice of decreasing the FIO 2 below 0.5–0.6 as soon as feasible.

Ü Pulse oximetry may be used to titrate FIO 2 , with one study suggesting that a threshold of 92% in light-skinned patients and 95% in darker-skinned patients ensures adequate oxygenation.

Ü Measurement of partial pressure of arterial oxygen by arterial blood gas (PaO 2 >55–60 mm Hg is typically acceptable) is recommended at the start of ventilation to verify accuracy of pulse oximetry for each patient.

Positive End Expiratory Pressure (PEEP):

Ü PEEP is selected to improve oxygenation.

Ü It can also be used to improve work of breathing and inspiratory triggering in patients with PEEP i .

Ü Potential adverse effects of PEEP include elevation of intracranial pressure and hemodynamic compromise/hypotension.

Ü PEEP improves oxygenation mostly by "recruiting" lung units.

Ü Paradoxically, PEEP may sometimes worsen oxygenation by

¬ decreasing cardiac output and thereby the oxygen saturation of mixed venous blood returning to the lungs,

¬ directing pulmonary blood flow to more consolidated airspaces by compressing alveolar capillaries in nondiseased, more compliant airspaces, or

¬ promoting right-to-left interatrial shunting. Because high levels of PEEP reduce cardiac output and impair oxygen delivery to tissues, measurement of the effect of PEEP on oxygen delivery, termed a "best PEEP trial," may be helpful.

Ü In patients with airflow limitation (eg, COPD), PEEP i increases the work of breathing by increasing the inspiratory effort needed to initiate ventilator flow. In such patients with dynamic airflow limitation and expiratory airway collapse,

addition of ventilator PEEP up to 85% of the PEEP i level may improve inspiratory triggering and work of breathing. However, given the potential for worsening of hyperinflation, particularly for patients with asthma, PEEP for this purpose should be used cautiously. A stable inspiratory plateau pressure (Pplat) after addition of ventilator PEEP suggests absence of worsened hyperinflation

PEEP is an adjuvant to the mode of ventilation used to help maintain functional residual capacity (FRC). At the end of expiration, the PEEP exerts pressure to oppose passive emptying of the lung and to keep the airway pressure above the atmospheric pressure. The presence of PEEP opens up collapsed or unstable alveoli and increases the FRC and surface area for gas exchange, thus reducing the size of the shunt. For example, if a large shunt is found to exist based on the estimation from 100% FiO 2 , then PEEP can be considered and the FiO 2 can be lowered (< 60%) in order to maintain an adequate PaO 2 , thus reducing the risk of oxygen toxicity.

In addition to treating a shunt, PEEP may also be useful to decrease the work of breathing. In pulmonary physiology, compliance is a measure of the "stiffness" of the lung and chest wall. The mathematical formula for compliance (C) = change in volume / change in pressure. The higher the compliance, the more easily the lungs will inflate in response to positive pressure. An underinflated lung will have low compliance and PEEP will improve this initially by increasing the FRC, since the partially inflated lung takes less energy to inflate further. Excessive PEEP can however produce overinflation, which will again decrease compliance. Therefore it is important to maintain an adequate, but not excessive FRC.


PEEP can cause significant haemodynamic consequences through decreasing venous return to the right heart and decreasing right ventricular function. As such, it should be judiciously used and is indicated for adults in two circumstances.

If a PaO 2 of 60 mmHg cannot be achieved with a FiO 2 of 60%

If the initial shunt estimation is greater than 25%

If used, PEEP is usually set with the minimal positive pressure to maintain an adequate

PaO 2 with a safe FiO 2 . As PEEP increases intrathoracic pressure, there can be a resulting decrease in venous return and decrease in cardiac output. A PEEP of less than 10 cmH 2 O is usually safe in adults if intravascular volume depletion is absent. Lower

levels are used for pediatric patients. Older literature recommended routine placement of

a Swan-Ganz catheter if the amount of PEEP used is greater than 10 cmH 2 for

hemodynamic monitoring. More recent literature has failed to find outcome benefits with

routine PA catheterisation when compared to simple central venous pressure monitoring ] If cardiac output measurement is required, minimally invasive techniques, such as oesophageal doppler monitoring or arterial waveform contour monitoring may be sufficient alternatives. PEEP should be withdrawn from a patient until adequate PaO 2 can be maintained with a FiO 2 < 40%. When withdrawing, it is decreased through 1-2 cmH 2 O decrements while monitoring haemoglobin-oxygen saturations. Any unacceptable haemoglobin-oxygen saturation should prompt reinstitution of the last PEEP level that maintained good saturation.


Prone (face down) positioning has been used in patients with ARDS and severe hypoxemia. It improves FRC, drainage of secretions, and ventilation-perfusion matching (efficiency of gas exchange). It may improve oxygenation in > 50% of patients, but no survival benefit has been documented.


Most intubated patients receive sedation through a continuous infusion or scheduled dosing to help with anxiety or psychological stress. Daily interruption of sedation is commonly helpful to the patient for reorientation and appropriate weaning.


To protect against ventilator-associated pneumonia, patients' bed is often elevated to about 30°.

Deep vein thrombosis prophylaxis with heparin or sequential compression device is important in older children and adults.

A histamine receptor (H2) blocker or proton-pump inhibitor may be used to prevent gastrointestinal bleeding, which has been associated with mechanical ventilation

Modification of settings

Ü In adults when 100% FiO 2 is used initially, it is easy to calculate the next FiO 2 to be used and easy to estimate the shunt fraction. The estimated shunt fraction refers to the amount of oxygen not being absorbed into the circulation. In normal physiology, gas exchange (oxygen/carbon dioxide) occurs at the level of the alveoli in the lungs. The existence of a shunt refers to any process that hinders this gas exchange, leading to wasted oxygen inspired and the flow of un-oxygenated blood back to the left heart (which ultimately supplies the rest of the body with unoxygenated blood).

Ü When using 100% FiO 2 , the degree of shunting is estimated by subtracting the measured PaO 2 (from an arterial blood gas) from 700 mmHg. For each difference of 100 mmHg, the shunt is 5%. A shunt of more than 25% should prompt a search for the cause of this hypoxemia, such as mainstem intubation or pneumothorax, and should be treated accordingly. If such complications are not present, other causes must be sought after, and PEEP should be used to treat this intrapulmonary shunt. Other such causes of a shunt include:

¬ Alveolar collapse from major atelectasis

¬ Alveolar collection of material other than gas, such as pus from pneumonia, water and protein from acute respiratory distress syndrome, water from congestive heart failure, or blood from haemorrhage

Monitoring the Ventilated Patient

Managing a patient on the mechanical ventilator necessitates monitoring respiratory physiological variables. These variables track progression and resolution of disease, complications of mechanical ventilation, patient comfort, work of breathing, and likelihood of successful patient liberation from the ventilator.


Variables indicated on all mechanical ventilators include exhaled tidal volume and airway pressure. For the patient on volume-cycled ventilation for whom breath-to-breath volume is constant, airway pressure at any moment depends on:

Ü the impedance of the respiratory system to air delivery (ie, respiratory system compliance and airflow resistance),

Ü patient effort, and

Ü patient synchrony with the ventilator.

Respiratory system refers to the lung (parenchyma and airways) and its surrounding chest wall (pleura and thoracoabdominal cage). Although lung and chest wall mechanics may be distinguished with the use of invasive tools such as the esophageal balloon, this is rarely needed. Specifically, it is important to remember that pressures caused by changes in compliance of the chest wall, such as pneumothorax or even abdominal distention, are transmitted to the lung.

Pressure at the airway opening (Pao) will increase with any increase in PEEP, PEEP i , flow, resistance (eg, bronchospasm), or tidal volume, and with any decrease in compliance (eg, pneumothorax).

Pao increases progressively during inspiration with volume delivery by the ventilator until it reaches its peak, the peak inspiratory pressure (PIP), at the moment the full tidal volume is delivered.

Pao likewise normally decreases to atmospheric (or to PEEP, if PEEP is programmed into the ventilator) at the end of exhalation, as the respiratory system empties. The downstream pressure in the alveolar compartment (which includes PEEP and PEEP i ), reflecting respiratory system compliance, can be measured at the airway opening in isolation from the additional pressure generated in the airways by stopping flow (ie, making flow zero), and thereby making pressure generated by flow through the airways zero.

In practice, the maximum pressure of the alveolar compartment reached at completion of the tidal volume, or plateau pressure (Pplat), can be monitored by programming a 1.0-s end-inspiratory pause of zero flow. The PIP – Pplat difference equals the flow-resistive pressure (ie, the pressure generated by flow along the airways).

(ie, the pressure generated by flow along the airways). These measurements apply best to volume-controlled

These measurements apply best to volume-controlled ventilation, in which flow and tidal volume are programmed. By contrast, in pressure-controlled ventilation in which a constant pressure is applied to the airway opening for a prescribed inspiratory time, PIP is often equal to Pplat, as can be demonstrated by observing an end-inspiratory period of zero flow on the ventilator flow-time graph.

The monitoring variables of static compliance (Cstat), resistance to airflow (R), and intrinsic PEEP (PEEP i ) can be easily derived at the bedside. These variables are used to adjust the ventilator, follow disease progression, and monitor response to therapy.

Normally, at end exhalation (before the next delivered breath), the tidal volume in the alveolar compartment fully empties, and both expiratory airflow and alveolar pressure fall to zero. However, if elevated airflow resistance slows alveolar emptying beyond the available expiratory period, particularly in settings of decreased expiratory time (eg, elevated respiratory rate) and/or decreased alveolar driving pressure (eg, emphysema), positive alveolar pressure, or PEEP i , may persist at end exhalation. PEEP i is often initially detected by observing the flow graphic on the ventilator for persistent flow at end-expiration. PEEP i is measured by programming a 1.0-s end-expiratory pause of zero flow into the ventilator. PEEP i may cause hypoventilation, hypotension, or a false elevation in pulmonary capillary wedge pressure. Strategies to minimize PEEP i include decreasing the respiratory rate, use of bronchodilators, or addition of PEEP.


A useful approach to the ventilated patient who develops acute hypoxemia is depicted

below. By observing PIP and measuring Pplat, the problem can often be localized either

to the alveolar or the airways compartment, and an immediate differential diagnosis can

be generated. Specifically, elevation of PIP with an unchanged Pplat (ie, PIP–Pplat increased) may indicate mucus plugging or bronchospasm. Elevation of both PIP and Pplat in parallel (ie, PIP–Pplat unchanged) may indicate pneumothorax, pulmonary edema, or pneumonia. Alternatively, if neither is elevated, the possibility of a vascular event altering gas exchange should be considered (ie, pulmonary embolism).

event altering gas exchange should be considered (ie, pulmonary embolism). triplehelix 31 Mechanical Ventilation

What is the Peak inspiratory pressure (PIP) and Plateau Pressure (Pplat)?

The plateau pressure is the pressure applied (in positive pressure ventilation) to the small airways and alveoli. It is believed that control of the plateau pressure is important, as excessive stretch of alveoli has been implicated as the cause of ventilator induced lung injury.

The peak pressure is the pressure measured by the ventilator in the major airways, and it strongly reflects airways resistance. For example, in acute severe asthma, there is a large gradient between the peak pressure (high) and the plateau pressure (normal).

In pressure controlled ventilation, the pressure limit is (usually) the plateau pressure due to the dispersion of gas in inspiration. In volume control, the pressure measured (the PAW) by the ventilator is the peak airway pressure, which is really the pressure at the level of the major airways. To know the real airway pressure, the plateau pressure which is applied at alveolar level, the volume breath must be made to simulate a pressure breath.

An inspiratory hold (0.5 to 1 second) is applied, and the airway pressure, from the initial peak, drops down to a plateau. The hold represents a position of no flow.

peak, drops down to a plateau. The hold represents a position of no flow. triplehelix 32
triplehelix triplehelix 33 33 Mechanical Ventilation Mechanical Ventilation





Mechanical Ventilation

Mechanical Ventilation

What is permissive hypercapnia?

With acute respiratory distress syndrome (ARDS), a tidal volume of 6-8 mL/kg is used with a rate of 10-12/minute. This reduced tidal volume allows for minimal volutrauma but may result in an elevated pCO 2 (due to the relative decreased oxygen delivered) is called permissive hypercapnia, but this elevation does not need to be corrected.


Ü An adult patient breathing spontaneously will usually sigh about 6-8 times/hr to prevent microatelectasis, and this has led some to propose that ventilators should deliver 1.5-2 times the amount of the preset tidal volume 6-8 times/hr to account for the sighs. However, such high quantity of volume delivery requires very high peak pressure that predisposes to barotrauma.

Ü Currently, accounting for sighs is not recommended if the patient is receiving 10- 12 mL/kg or is on PEEP. If the tidal volume used is lower, the sigh adjustment can be used, as long as the peak and plateau pressures are acceptable.

Ü Sighs are not generally used with ventilation of infants and young children.

Connection to ventilators

There are various procedures and mechanical devices that provide protection against airway collapse, air leakage, and aspiration:

Ü Face mask - In resuscitation and for minor procedures under anaesthesia, a face mask is often sufficient to achieve a seal against air leakage. Airway patency of the unconscious patient is maintained either by manipulation of the jaw or by the use of nasopharyngeal or oropharyngeal airway. These are designed to provide a passage of air to the pharynx through the nose or mouth, respectively. Poorly fitted masks often cause nasal bridge ulcers, a problem for some patients. Face masks are also used for non-invasive ventilation in conscious patients. A full face mask does not, however, provide protection against aspiration.

Ü Laryngeal mask airway - The laryngeal mask airway (LMA) causes less pain and coughing than a tracheal tube. However, unlike tracheal tubes it does not seal

against aspiration, making careful individualised evaluation and patient selection mandatory.

Ü Tracheal intubation is often performed for mechanical ventilation of hours to weeks duration. A tube is inserted through the nose (nasotracheal intubation) or mouth (orotracheal intubation) and advanced into the trachea. In most cases tubes with inflatable cuffs are used for protection against leakage and aspiration. Intubation with a cuffed tube is thought to provide the best protection against aspiration. Tracheal tubes inevitably cause pain and coughing. Therefore, unless a patient is unconscious or anaesthetized for other reasons, sedative drugs are usually given to provide tolerance of the tube. Other disadvantages of tracheal intubation include damage to the mucosal lining of the nasopharynx or oropharynx and subglottic stenosis.

Ü Oesophageal obturator airway - commonly used by emergency medical technicians, if they are not authorized to intubate. It is a tube which is inserted into the oesophagus, past the epiglottis. Once it is inserted, a bladder at the tip of the airway is inflated, to block ("obturate") the oesophagus, and air or oxygen is delivered through a series of holes in the side of the tube.

Ü Cricothyrotomy - Patients who require emergency airway management, in whom

tracheal intubation has been unsuccessful, may require an airway inserted through

a surgical opening in the cricothyroid membrane. This is similar to a

tracheostomy but a cricothyrotomy is reserved for emergency access.

Ü Tracheostomy - When patients require mechanical ventilation for several weeks,

a tracheostomy may provide the most suitable access to the trachea. A

tracheostomy is a surgically created passage into the trachea. Tracheostomy tubes are well tolerated and often do not necessitate any use of sedative drugs.

Tracheostomy tubes may be inserted early during treatment in patients with pre- existing severe respiratory disease, or in any patient who is expected to be difficult to wean from mechanical ventilation, i.e., patients who have little muscular reserve.

Ü Mouthpiece - Less common interface. It does not provide protection against aspiration. There are lip seal mouthpieces with flanges to help hold them in place if patient is unable.

The other method of classifying mechanical ventilation is based on how to determine when to start giving a breath. Similar to the termination classification noted above, microprocessor control has resulted in a myriad of hybrid modes that combine features of the traditional classifications. Note that most of the timing initiation classifications below can be combined with any of the termination classifications listed above.

Ü Assist Control (AC). In this mode the ventilator provides a mechanical breath with either a pre- set tidal volume or peak pressure every time the patient initiates a breath. Traditional assist- control used only a pre-set tidal volume--when a preset peak pressure is used this is also sometimes termed Intermittent Positive Pressure Ventilation or IPPV. However, the initiation timing is the same--both provide a ventilator breath with every patient effort. In most ventilators a back-up minimum breath rate can be set in the event that the patient becomes apnoeic. Although a maximum rate is not usually set, an alarm can be set if the ventilator cycles too frequently. This can alert that the patient is tachypneic or that the ventilator may be auto-cycling (a problem that results when the ventilator interprets fluctuations in the circuit due to the last breath termination as a new breath initiation attempt).

Ü Synchronized Intermittent Mandatory Ventilation (SIMV). In this mode the ventilator provides a pre-set mechanical breath (pressure or volume limited) every specified number of seconds (determined by dividing the respiratory rate into 60 - thus a respiratory rate of 12 results in a 5 second cycle time). Within that cycle time the ventilator waits for the patient to initiate a breath using either a pressure or flow sensor. When the ventilator senses the first patient breathing attempt within the cycle, it delivers the preset ventilator breath. If the patient fails to initiate a breath, the ventilator delivers a mechanical breath at the end of the breath cycle. Additional spontaneous breaths after the first one within the breath cycle do not trigger another SIMV breath. However, SIMV may be combined with pressure support (see below). SIMV is frequently employed as a method of decreasing ventilatory support (weaning) by turning down the rate, which requires the patient to take additional breaths beyond the SIMV triggered breath.

Ü Controlled Mechanical Ventilation (CMV). In this mode the ventilator provides a mechanical breath on a preset timing. Patient respiratory efforts are ignored. This is generally uncomfortable for children and adults who are conscious and is usually only used in an unconscious patient. It may also be used in infants who often quickly adapt their breathing pattern to the ventilator timing.

Ü Pressure Support Ventilation (PSV). When a patient attempts to breath spontaneously through an endotracheal tube, the narrowed diameter of the airway results in higher resistance to airflow, and thus a higher work of breathing. PSV was developed as a method to decrease the work of breathing in-between ventilator mandated breaths by providing an elevated pressure triggered by spontaneous breathing that "supports" ventilation during inspiration. Thus, for example, SIMV might be combined with PSV so that additional breaths beyond the SIMV programmed breaths are supported. However, while the SIMV mandated breaths have a preset volume or peak pressure, the PSV breaths are designed to cut short when the inspiratory flow reaches a percentage of the peak inspiratory flow (e.g. 10-25%). Also, the peak pressure set for the PSV breaths is usually a lower pressure than that set for the full ventilator mandated breath. PSV can be also be used as an independent mode. However, since there is generally no back-up rate in PSV, appropriate apnoea alarms must be set on the ventilator.

Ü Continuous Positive Airway Pressure (CPAP). A continuous level of elevated pressure is provided through the patient circuit to maintain adequate oxygenation, decrease the work of breathing, and decrease the work of the heart (such as in left-sided heart failure - CHF). Note that no cycling of ventilator pressures occurs and the patient must initiate all breaths. In addition, no

additional pressure above the CPAP pressure is provided during those breaths. CPAP may be used invasively through an endotracheal tube or tracheostomy or non-invasively with a face mask or nasal prongs.

Ü Positive End Expiratory Pressure (PEEP) is functionally the same as CPAP, but refers to the use of an elevated pressure during the expiratory phase of the ventilatory cycle. After delivery of the set amount of breath by the ventilator, the patient then exhales passively. The volume of gas remaining in the lung after a normal expiration is termed the functional residual capacity (FRC). The FRC is primarily determined by the elastic qualities of the lung and the chest wall. In many lung diseases, the FRC is reduced due to collapse of the unstable alveoli, leading to a decreased surface area for gas exchange and intrapulmonary shunting, with wasted oxygen inspired. Adding PEEP can reduce the work of breathing (at low levels) and help preserve FRC.

Complications of Mechanical Ventilation

Multiple direct complications of mechanical ventilation have been described.

Other indirectly associated complications of mechanical ventilation include critical illness polyneuropathy, acalculous cholecystitis, and venous thromboembolism. Three of these, barotrauma, ventilator-induced lung injury, and altered hemodynamics, will be discussed below, as both direct and indirect complications have important practical implications.


Barotrauma (eg, pneumothorax, pneumomediastinum, systemic gas embolism, etc)

Ventilator-induced lung injury (ie, volutrauma, atelec-trauma, biotrauma)

Oxygen toxicity

Ventilator-associated pneumoni

Tracheal stenosis


Reduced cardiac output/hypotension

Right ventricular ischemia

Propagation of right-to-left interatrial shunt



Gastrointestinal hemorrhage


Fluid retention



Increased intracranial pressure


Ü Barotrauma is the term for the specific complications of extra-alveolar air such as pneumothorax or pneumomediastinum thought to occur from alveolar rupture into the adjacent bronchovascular interstitium.

Ü It is less common than in earlier days of positive pressure ventilation, likely because of attention to patient ventilator synchrony and high peak airway pressures.

Ü In rare instances the air extravasates into blood vessels with resultant air emboli in the brain, heart, or skin causing changes in mental status, cardiac arrhythmias, and livedo reticularis.


Ü Intriguingly, although VILI is synergistic with preexistent lung injury, positive-pressure ventilation of even the normal lung can produce pathological hyaline membrane changes indistinguishable from ARDS. Studies in the early 1970s introduced the concept of "barotrauma," or pressure-induced lung injury,demonstrating that high inflation pressures injured the lung. Subsequent studies showed that the injurious variable was the transpulmonary pressure distending the lung rather than peak alveolar pressure (ie, alveolar pressure minus pleural pressure), or, more simply, end-inspiratory volume. This, in turn, led to the current VILI concept of volume-induced lung injury, or "volutrauma," with its implication that patients with decreased chest wall compliance from abdominal distention or other restrictive causes may be relatively "protected" from high airway pressures on the ventilator.

Ü A multicenter NIH-sponsored ARDS trial, which demonstrated improved mortality using a low (6 mL/kg ideal body weight) compared to a high tidal volume strategy (12 mL/kg ideal body weight), supports this volutrauma idea.

Ü The lung in patients with ARDS is heterogeneously affected, with the dependent, consolidated lung not participating in gas exchange. Only the relatively nondiseased, compliant portion of the lung is vulnerable to overdistention by the delivered tidal volume. This has led practitioners to theorize that pressure ventilation, with a uniform pressure ceiling in all lung units, is less injurious to the relatively normal lung than volume ventilation, which directs volume along the path of least resistance primarily to the nondiseased lung.

Ü Despite these claims, however, no well-designed, randomized, controlled trial has shown a difference in outcome between pressure- and volume-targeted ventilation in patients with ARDS.

Ü Finally, perhaps the most interesting recent concept of VILI is that of "biotrauma," the idea that VILI may lead to multiple organ dysfunction syndrome by "leakage" of both stretch-induced injurious lung cytokines and bacteria into the systemic circulation. Lower tidal volumes have been shown to generate fewer cytokines, and are associated with less extrapulmonary organ dysfunction.

Ü This phenomenon may explain why most patients with ARDS die of extrapulmonary complications rather than from respiratory failure itself.


Ü Positive-pressure ventilation and PEEP both cause hypotension by reducing cardiac output, with a blood pressure drop that is most dramatic immediately following endotracheal intubation.

Ü PEEP decreases venous return, and thus cardiac output, primarily by compressing the inferior vena cava. By increasing pulmonary vascular resistance and right ventricular afterload, high levels of PEEP may also:

¬ decrease right ventricular systolic function, particularly for patients with underlying right ventricular dysfunction or right coronary artery disease,

¬ aggravate right ventricular ischemia, and

¬ propagate right-to-left interatrial shunting through a patent foramen ovale. PEEP reduces left ventricular afterload, and thereby may occasionally lead to improved left ventricular function and cardiac output in patients with dilated cardiomyopathy.

Ü Because of this therapeutic effect of the ventilator, both occult left ventricular ischemia and left ventricular systolic dysfunction may occasionally complicate ventilator weaning.

When to Withdraw Mechanical Ventilation?

Ü Withdrawal from mechanical ventilation—also known as weaning—should not be delayed unnecessarily, nor should it be done prematurely. Patients should have their ventilation considered for withdrawal if they are able to support their own ventilation and oxygenation, and this should be assessed continuously.

Ü There are several objective parameters to look for when considering withdrawal, but there is no specific criteria that generalizes to all patients.

Ü The best measure of when a patient may be extubated is the Rapid Shallow Breathing Index (RSBI) (Tobin Index).

Ü This is calculated by dividing the respiratory rate by the tidal volume in liters(RR/TV). A rapid shallow breathing index of less than 100 is considered ideal for extubation. Certainly, other measures such as patient's mental status should be considered.



Ü First, most patients ( 75%) do not need to be "weaned" from the ventilator; a graduated reduction of support is unnecessary, particularly for postoperative patients.

Ü The majority can simply be extubated after their first successful attempt at spontaneous breathing. For patients who fail their initial attempts at spontaneous breathing, synchronized intermittent mandatory ventilation (SIMV) weaning appears to be inferior and may even prolong the duration of mechanical ventilation.

Ü Next, most of the long list of classic "weaning parameters" (eg, maximum inspiratory pressure, respiratory rate, vital capacity) are poorly predictive of successful liberation. The clinical gestalt of even experienced practitioners is often poorly predictive of successful liberation.

Ü Lastly, the duration of ventilation can be reduced by using validated clinical parameters, such as the rapid-shallow breathing index (RSBI), in a protocol- directed approach.

Ü Most experts agree that the process of liberation should involve an initial

0.5 andthat the process of liberation should involve an initial achievement of clinical criteria of readiness (eg,

achievement of clinical criteria of readiness (eg, SaO 2


arousable, some indication of improvement in the initial cause of respiratory failure, minute ventilation ideally <12–15 L/min), followed by some form of initial spontaneous breathing trial (SBT).

90% with FIO 2 2

initial spontaneous breathing trial (SBT). 90% with FIO 2 5 cm H 2 O, no or

5 cm H 2 O, no or low-dose vasopressors, mental status at least easily

Ü The initial trial may be by a T-piece (breathing without any assistance through the endotracheal tube with a flowing gas source), PSV, or CPAP (ie, PEEP without inspiratory pressure assistance).

Ü Initial SBT failure should be followed by reassessment and a more gradual weaning mode

Criteria for Assessing Tolerance of a Spontaneous Breathing Trial.


Ü Acceptable oxygenation: SaO 2

90% or PaO 2

90% or PaO 2

60 mm Hg on FIO 2

60 mm Hg on FIO 2

Ü Acceptable oxygenation: SaO 2 90% or PaO 2 60 mm Hg on FIO 2 0.5



Ü Acceptable ventilation: increase in PaCO 2

Ü Acceptable ventilation: increase in PaCO 2 10 mm Hg or pH decrease 0.10

10 mm Hg or pH decrease

Ü Acceptable ventilation: increase in PaCO 2 10 mm Hg or pH decrease 0.10


Ü Acceptable respiratory rate: respiratory rate in rate

35 breaths/min or < 50% increase

35 breaths/min or < 50% increase

Ü Acceptable hemodynamics: heart rate

140 beats/min or an increase

140 beats/min or an increase

20% of

20% of

baseline; systolic blood pressure 20% from baseline

80 mm Hg and

80 mm Hg and

80 mm Hg and

160 mm Hg, or change of <

Ü RSBI (rate/tidal volume) < 100 breaths/min/L


Ü No signs of elevated work of breathing, such as thoracoabdominal paradox or excessive use of accessory muscles

Ü No signs of distress, such as diaphoresis or agitation


Perhaps the best-validated and easiest index to assess readiness to wean is the RSBI, which is the respiratory rate divided by tidal volume in liters. When the RSBI is less than 100, as measured for 1 min on T-piece, the patient is likely to achieve successful extubation.

Ü For those patients who fail the initial SBT, three different methods for subsequent weaning are generally used: SIMV, PSV, and T-piece. The latter two have gained predominant support in the literature as effective weaning modes, and the former should be abandoned as a primary weaning strategy.

Ü SIMV involves a stepwise reduction of the mandatory respiratory rate (eg, a decrease by two breaths/min twice daily) until the patient can tolerate a minimal rate ( 4 breaths/min), with the remainder of breaths unassisted.

Ü PSV typically involves the stepwise reduction in PS level (eg, by 2 cm H 2 O twice daily) until a minimal PS level is reached (eg, 5 cm H 2 O). This low pressure is thought to approximate the work of breathing off the ventilator by "overcoming" the additional work of breathing imposed by the endotracheal tube. PSV was the most effective mode when compared to SIMV and T-piece in a large randomized trial, and is used in many centers.

Ü T-piece involves unassisted spontaneous breathing by disconnection of the endotracheal tube from the ventilator circuit and reconnection to a flowing, oxygen-enriched source of gas. It was the most effective weaning mode in a second large randomized controlled trial. Although progressive increases in T-

piece trial duration and daily number (eg, increasing from a few minutes twice a day to two or more hours several times daily) are commonly used, and, in fact, may be necessary in chronically ventilator-dependent patients, once-daily T-piece trials have been shown to be as effective as multiple daily trials for patients without complications.

Ü In sum, for the patient who fails an initial attempt at spontaneous breathing, several strategies, all using SBTs, are available for progressive withdrawal from the ventilator: daily SBTs (T-piece, CPAP, or PS); T-piece, CPAP, or PS trials of increasing duration; or gradual decreases in PS level. In certain cases an argument can be made for the superiority of one of these methods. For example, patients with COPD may occasionally have difficulty tolerating PSV. Second, because patients with congestive heart failure (CHF) may derive enough assistance in cardiac performance from positive pressure ventilation, it is arguably most predictive to perform their SBTs on T-piece.


Ü Failure to wean commonly reflects an imbalance of excessive respiratory workload and insufficient respiratory muscle strength or endurance, with a typical pattern of tachypnea and shallow tidal volumes.

Ü Depending on the clinical scenario, occult coronary ischemia, occult left ventricular dysfunction/pulmonary edema, PEEP i , concretions narrowing the endotracheal tube, and critical illness myopathy/polyneuropathy should be considered.

Ü Most patients, particularly those with diaphragmatic dysfunction, congestive heart failure, emphysema, morbid obesity, or abdominal distention, should be positioned upright during weaning.

Ü Electrolytes affecting muscle function, including potassium, magnesium, and phosphate, should be repleted, and correction of metabolic acidosis should be considered, particularly if excessive minute ventilation persists.

Ü Lastly, in patients with COPD exacerbation who fail SBTs, extubation straight to noninvasive positive pressure ventilation [ie, bilevel positive airway pressure (BiPAP)] can be tried. In such patients, studies show improved weaning rates, less nosocomial pneumonia, and decreased mortality.

Causes of Failure to Wean from Mechanical Ventilation.

Respiratory muscle weakness

Electrolyte depletion (eg, hypokalemia, hypomagnesemia), malnutrition

Critical illness polyneuropathy

Inadequate rest

Prolonged paralysis or myopathy (eg, neuromuscular agents, corticosteroids, aminoglycosides)

Decreased ventilatory drive


Excessive administration of sedatives or opiates

Increased ventilatory load

Increased resistance: bronchospasm, secretions, plugged endotracheal tube

Decreased lung compliance: pulmonary edema, ARDS

Decreased chest wall compliance: pleural effusions, abdominal distention, and obesity

Increased minute ventilation: elevated dead space ventilation, fever, and overfeeding

Intrinsic PEEP

Cardiac problems

Left ventricular dysfunction

Coronary ischemia

Daily evaluation: (Do NOT wean if any one is present)

Ü Dopamine infusion >5mcg/kg/min

Ü Systolic BP <90 mmHg

Ü HR <50 or > 130 bpm

Ü Temperature >100.4’F

Ü FiO2 >50% or PEEP >8 cm H20

Weaning assessment (Do NOT wean if any one is present):

Ü RR >35 breaths/min

Ü Spontaneous tidal volume <0.3 L

Ü Rapid Shallow Breathing Index >100

Ü O2 saturation <90%

Ü HR <50 or >130 bpm, or increase from baseline >20 bpm

Ü Prominent accessory muscle use

A System for Analyzing Ventilator Waveforms

Step 1: -determine the CPAP level

This is the baseline position from which there is a downward deflection on, at least, beginning of inspiration, and to which the airway pressure returns at the end of expiration.

which the airway pressure returns at the end of expiration. Step 2: Is the patient triggering?

Step 2: Is the patient triggering?

There will be a negative deflection into the CPAP line just before inspiration.

There will be a negative deflection into the CPAP line just before inspiration . triplehelix 45

Step 3: What is the shape of the pressure wave?

If the curve has a flat top, then the breath is pressure limited, if it has a triangular or shark’s fin top, then it is not pressure limited and is a volume breath

top, then it is not pressure limited and is a volume breath Step 4: What is

Step 4: What is the flow pattern?

If it is constant flow (square shaped) this must be volume controlled, if decelerating, it can be any mode.

be volume controlled, if decelerating, it can be any mode. Step 5: Is the patient gas

Step 5: Is the patient gas trapping?

Expiratory flow does not return to baseline before inspiration commences (i.e. gas is trapped in the airways at end-expiration). This indicates auto-PEEP.

Step 6 : The patient is triggering – is this a pressure supported or SIMV

Step 6 : The patient is triggering – is this a pressure supported or SIMV or VAC breath?

This is easy, the pressure supported breath looks completely differently than the volume control or synchronized breath: the PS breath has a decelerating flow pattern, and has a flat topped airway pressure wave. The synchronized breath has a triangular shaped pressure wave.

pressure wave. The synchronized breath has a triangular shaped pressure wave. triplehelix 47 Mechanical Ventilation

Step 7: The patient is triggering – is this pressure support or pressure control?

The fundamental difference between pressure support and pressure control is the length of the breath – in PC, the ventilator determined this (the inspired time) and all breaths have an equal “i” time. In PS, the patient determined the duration of inspiration, and this varies from breath to breath.

determined the duration of inspiration, and this varies from breath to breath. triplehelix 48 Mechanical Ventilation
determined the duration of inspiration, and this varies from breath to breath. triplehelix 48 Mechanical Ventilation

Step 8: Is the patient synchronizing with the ventilator?

Each time the ventilator is triggered a breath should be delivered. If the number of triggering episodes is greater than the number of breaths, the patient is asynchronous with the ventilator. Further, if the peak flow rate of the ventilator is inadequate, then the inspiratory flow will be "scooped" inwards, and the patient appears to be fighting the ventilator.

inwards, and the patient appears to be fighting the ventilator. triplehelix 49 Mechanical Ventilation
inwards, and the patient appears to be fighting the ventilator. triplehelix 49 Mechanical Ventilation

Patient-Ventilator Dysynchrony

Ü Dysynchrony is a term which describes a patient fighting the ventilator. If we assume that this is not because the patient is undersedated and is rebelling against the endotracheal tube, in the majority of cases failure to synchronize is due to inadequate flow delivery from the ventilator.

Ü If the flow of gas is inadequate, the patient attempts to suck gas out of the ventilator – which is extremely unpleasant. This only occurs in volume control modes.

Ü In pressure control, flow is unlimited – the reason is that flow is related to the pressure gradient between the upper and lower airway – a deeper attempted inspiration makes the pressure in the alveoli more negative in relation to the upper airway (this is true also in normal individuals, how else would you take a deep breath!), and the pressure gradient is larger – and the flow greater.

Ü In volume limited ventilation, this flexibility (which is physiological) does not exist. Of course, as with most problems in critical care, a number of technological solutions have been developed. the first was pressure augmentation.

of technological solutions have been developed. the first was pressure augmentation. triplehelix 50 Mechanical Ventilation



Mechanical Ventilation