Diagnosis of Pulmonary Failure in Surgical Patients
Most causes of pulmonary failure in the surgical patient can
be ascribed to one or more of nine causes: the pulmonary failure of shock, trauma, and sepsis; mechanical failure caused by deranged respiratory system mechanics; atelectasis; aspiration; pulmonary contusion; pneumonia; pulmonary embolism; cardiogenic pulmonary edema; and, rarely, neurogenic pulmonary edema.
The pulmonary failure of shock, trauma, and sepsis arises from
extrapulmonary trauma, infection, or ischemia-reperfusion in the
setting of shock. Products of coagulation and inflammation are washed
out from the damaged tissues and carried to the lungs (or to the
liver, in the case of the splanchnic circulation, and from there
to the lungs), where they set up an acute inflammatory reaction. The
extrapulmonary causes are many and range from necrotizing infections
to noninfective inflammatory responses (such as pancreatitis) to
reperfusion of ischemic limbs to soft tissue injury to broken bones
(and embolism of fat and clot from the bone marrow—the
so-called fat embolism syndrome, now an outdated term). Nothing
is gained by making a distinction between it and the more general concept
of pulmonary failure of shock and trauma.
The concept of pulmonary failure secondary to extrapulmonary
ischemia-reperfusion, coagulation, and inflammation, which is common
in surgical patients, can be subsumed into a broader category of
pulmonary failure, known as the acute respiratory distress
syndrome (ARDS). ARDS is defined by the sudden onset of hypoxemia
with bilateral infiltrates, a Pao2:Fio2 less than 200 and the absence of left atrial hypertension (a pulmonary
arterial wedge pressure < 18 if measured). A less severe form,
acute lung injury (ALI) requires a Pao2:Fio2 less than 300 with the other criteria.
The causes of ARDS include those that are responsible for pulmonary
failure of shock, trauma, and sepsis and also include severe pneumonia
and aspiration. The end result in all of these conditions is activation
of macrophages and other inflammatory cells in the lungs. The mediators
disrupt the microvascular endothelium, and plasma extravasates into
the interstitium and, in the case of the lungs, into the alveoli.
The resultant pulmonary edema impairs both ventilation and oxygenation;
the microembolization to the lungs impairs perfusion. Arterial oxygen
saturation decreases and carbon dioxide content increases—assuming
that no compensatory mechanisms come into play. Lastly, to make things
worse, the inflammatory process in the lungs releases mediators
into the systemic circulation that can lead to inflammation and
dysfunction in the liver, gut, and kidneys.
A number of different mediators of coagulation and inflammation
have been implicated as causes of the increased permeability. Proteases,
kinins, complement, oxygen radicals, prostaglandins, thromboxanes,
leukotrienes, lysosomal enzymes, and other mediators are released
from aggregates of platelets and white cells or from the endothelium or
plasma as a consequence of the interaction between the aggregates
and the vessel wall. Some of these substances are chemoattractants
of more platelets and white blood cells, and a vicious cycle of inflammation develops that worsens the disruption of the vascular endothelium.
Pathologically, ARDS (and the pulmonary failure of shock, trauma,
and sepsis) is characterized by diffuse alveolar damage and a nonspecific
inflammatory reaction, with the loss of alveolar epithelium and
hyaline membrane formation. Monocytes and neutrophils invade the interstitium.
Edema appears within a few hours, alveolar flooding is florid within
1 day, and fibrosis begins in 1–2 weeks. If the process
is unchecked, the lungs become sodden and resemble liver tissue
on gross inspection; scar tissue appears within a week, and function-limiting
fibrosis begins to develop within 2 weeks. If early treatment is
effective, the lungs return to normal, both grossly and microscopically.
Mechanical failure can arise from chest wall trauma,
pain and weakness after surgery and anesthesia, debility caused by
the catabolic metabolism of long-term illness, or bronchopleural
fistula. Massive trauma to the chest with multiple fractures of
multiple ribs or bilateral disruption of the costochondral junctions
can result in a free-floating segment of chest wall known as a flail
chest. Expansion and relaxation of the chest wall during spontaneous
breathing results in paradoxic motion of the free segment in response
to changes in intrathoracic pressure; ventilation becomes compromised;
and the partial pressure of arterial carbon dioxide (Paco2)
increases. In addition, hypoventilation leads to progressive atelectasis
and hypoxemia. Lesser degrees of chest wall injury can lead to hypoventilation
secondary to pain with similar results. Prolonged mechanical ventilation
with loss of muscle mass and power in the diaphragm and the accessory
muscles of respiration can require ventilatory support until muscle
function returns to normal. A bronchopleural fistula—a communication
from the airway to the pleural cavity to the atmosphere, either through a chest tube or through a hole in the chest wall—can develop after pulmonary surgery, trauma, or infection. Large air leaks can compromise ventilation to the uninvolved lung as well as to the diseased side because insufflated air preferentially goes to the side with the fistula.
Atelectasis—localized collapse of alveoli—can develop with prolonged immobilization, as during anesthesia or in association with
bed rest. The problem is usually full blown within a few hours after
the initiating event. Only mechanical failure (to which it is related),
aspiration, cardiogenic pulmonary edema, and pulmonary embolism
can produce equivalent levels of hypoxemia so soon, and no other cause
of hypoxemia can respond so quickly to therapy. The diagnosis is
supported by auscultation of bronchial breath sounds at dependent
portions of the lung and occasionally, if severe enough, by x-ray
confirmation of platelike collapse of pulmonary parenchyma. The most
reliable confirmation of the diagnosis, however, comes with response
to therapy, which can include encouragement of deep breathing and
coughing, ambulation, bronchoscopy, and intubation and mechanical
ventilation. Atelectasis should respond within a few hours.
Aspiration of gastric contents or blood can occur
in any patient who cannot protect the airway. Shock, severe brain
injury, or pharmacologic depression (anesthesia, narcotics, or benzodiazepines)
can result in a depressed level of consciousness and loss of airway
protective reflexes. Gastric acid or particulate matter in the airways
leads to disruption of the alveolar and microvascular membranes,
causing interstitial and alveolar edema. The resultant hypoxemia
is usually evident within a few hours and is associated with a localized
infiltrate on x-ray. Recovery of gastric contents by suctioning
from the endotracheal tree confirms the diagnosis.
Pulmonary contusion arises from direct trauma to
the chest wall and the underlying lung parenchyma. Hypoxemia associated
with a localized infiltrate on x-ray develops over 24 hours as the
injured lung becomes edematous.
Pneumonia can arise primarily or may be superimposed
on aspiration, pulmonary contusion, or the pulmonary failure of
shock, trauma, and sepsis. The diagnosis is made by recovery of
bacteria and purulent material from the endotracheal tree, hypoxemia,
signs of systemic inflammation, and a localized infiltrate on x-ray. The
Clinical Pulmonary Infection Score (CPIS), which is derived from
these parameters, can be used to quantify the clinical, radiographic,
and laboratory findings of pneumonia. It is useful both for diagnosis
and for determining length of treatment. Bronchoalveolar lavage
and quantitative culture may occasionally be used to assist in distinguishing
pneumonia from ARDS and other causes of pulmonary inflammation.
Pulmonary embolism typically presents with sudden
deterioration of pulmonary function 3 days or more after an event—such
as an operation, injury, or the beginning of immobilization—that
can stimulate deposition of clot in a large systemic vein. Patients with
cancer are at particularly high risk, and in any patient the greater
the magnitude of operation or injury, the greater the chance of
venous thrombosis and embolization. Clot emboli must be organized
to be clinically significant; embolism to the lung of fresh soft
clot rarely causes any difficulty. The pulmonary endothelium contains
potent fibrinolysins that can break up any poorly organized embolus.
Sudden deterioration in pulmonary function sooner than 3 days after
an event that stimulates clot formation is unlikely to be caused
by an embolus; the deterioration is more likely to be caused by
mechanical failure, atelectasis, aspiration, or pneumonia.
The chest film is usually nonspecific. A fairly definite diagnosis
can often be made by high-definition contrast enhanced computed
tomograms of the pulmonary vasculature. The study requires transfer
to the radiology suite and the use of large amounts of radiographic
contrast material. Pulmonary arteriography carries the same risks—transfer
to the radiology suite and use of contrast—and requires right-heart catheterization, but it does have advantages. It gives a definitive diagnosis with one test. At the end of the diagnostic
study, an indwelling catheter can be placed proximal to the clot and used for infusion of lytic agents. If needed, a filter can be placed in the inferior vena at the end of the study, before the patient
leaves the angiography suite.
Cardiogenic pulmonary edema arises from high left
atrial and pulmonary microvascular hydrostatic pressures. Patients
who have suffered an acute myocardial infarction can present this
way, as can patients with underlying myocardial or coronary artery
disease when faced with fluid shifts and surgical stress. Occasionally,
the rapid administration of intravenous fluid—especially
in elderly patients with poor myocardial performance—will
outstrip the heart’s ability to pump, and pulmonary edema
will result. Acute valvular disease, though rare after injury or
cardiac surgery, is another possible cause of inability of the left
heart to pump effectively.
The diagnosis is made on the basis of hypoxemia, rales, a third
heart sound, perihilar infiltrates, Kerley lines, and cephalization
of blood flow on x-ray along with elevated pulmonary arterial wedge
pressures on pulmonary arterial catheterization. A wedge (or left
atrial) pressure of 24 mm Hg can produce cardiogenic pulmonary edema
even in the presence of an intact endothelium in the pulmonary microvasculature.
Pulmonary arterial wedge pressures less than 24 mm Hg will generally
not produce edema if the pulmonary vascular endothelium is intact;
pressures exceeding 16 mm Hg can worsen the edema associated with increased
permeability (such as ARDS). The goal for the wedge pressure in
a patient with uncomplicated cardiogenic pulmonary edema in the
absence of an inflammatory process in the lungs should be 20 mm
Hg or less; the goal in a patient with an inflammatory process should
be 12–16 mm Hg.
Neurogenic pulmonary edema is associated both experimentally
and clinically with head injury and increased intracranial pressure.
The exact mechanism by which this occurs is unknown, but it is probably
related to sympathetic discharge with postmicrovascular vasoconstriction
in the lungs and a resultant increase in pulmonary microvascular hydrostatic
pressure. This form of pulmonary edema and oxygenation defect is rare.
In the great majority of patients with a head injury and pulmonary edema, the edema will be caused by some other mechanism, such as ARDS.
Indications for Intubation & Use of Mechanical Ventilation
The indications for intubation and mechanical ventilation are
related but often assessed separately. Patients who have primary
airway compromise—caused by stridor, maxillofacial trauma, facial
and airway burns with edema, or a depressed mental status—may
need intubation to protect the airway. In these cases, early intervention
is the rule as rapid clinical deterioration can convert a semiurgent
procedure into an emergency. In some cases, intubation should be
performed before the patient shows evidence of airway compromise.
In severe cases, such as massive facial edema, early cricothyroidostomy
should be performed.
Intubation of the airway is also indicated if mechanical ventilation
is needed for the treatment of established pulmonary failure or
for prophylaxis against potential failure or for pulmonary toilet
in the face of aspiration. The decision to intubate and initiate
mechanical ventilation should be made on the basis of clinical criteria.
A respiratory rate exceeding 36 breaths/min, labored ventilation,
use of accessory muscles of ventilation, and tachycardia are all
indications for intervention. Finally, intubation and mechanical
ventilation should be performed in anticipation of treatment that
can compromise the airway or worsen the pulmonary status. These
include the need for excessive sedation or narcotics, massive fluid
resuscitation, and the manipulation of fractures.
Arterial blood gas (ABG) measurements are of no value in making
decisions about intubation and mechanical ventilation in patients
in extremis. These patients should be intubated regardless of the
blood gas results. ABG measurements, however, can assist in the
decision to intubate less severely stressed patients. In the setting
of hypoxemia, intubation should be considered if the Pao2 is
less than 60 mm Hg and the patient’s supplemental oxygen
exceeds an O2 concentration of 50%. For hypercapneic patients,
a Paco2 greater than 45 mm Hg in the setting
of acidemia should prompt intubation, especially if serial measurements
demonstrate a worsening respiratory acidosis. Regardless of the
laboratory values, these guidelines should always be put in the
clinical context. A Paco2 of 40 mm Hg in
a patient breathing 40 breaths/min is as alarming as a
Paco2 of 60 mm Hg in a patient with a respiratory
rate of 10 breaths/min. A Pao2 of
60 mm Hg on room air in a patient with chronic lung disease may
be acceptable; the same value in a patient who is tensing the sternocleidomastoid
and intercostal muscles with each breath, making excessive or dyscoordinated
use of the abdominal musculature, and who seems to be struggling
to draw in enough air, mandates immediate intubation.
The indications for intubation should be more liberal for a surgical
patient than for a medical patient. The medical patient with an
exacerbation of chronic obstructive lung disease can be poorly served by
placement of a foreign body in the trachea. Airway resistance increases, coughing
becomes less effective, and opportunistic organisms obtain a foothold on
and near the tube. The benefit from intubation may be minimal and
noninvasive ventilation techniques, such as bilevel positive airway
pressure (BiPAP), may be all that is needed. This support can be
given simultaneously with other treatments—such as administration
of bronchodilators, antibiotics, and diuretics—in order
to avoid intubation and its potential complications.
Circumstances for the seriously ill surgical patient are usually
different. The patient who has multiple injuries, for example, can
temporarily tolerate the increased airway resistance, loss of cough,
and increased likelihood of tracheobronchial infection. What cannot
be tolerated is respiratory arrest during trauma resuscitation or
during preparation for an operation.
The indications for intubation in the patient with a suspected
or known injury to the cervical spine are the same as those in patients
with no likelihood of injury. Under no circumstances should concern
about the cervical spine lead to procrastination about securing
the airway. The consequences of respiratory arrest and anoxic brain
damage are as tragic as those of exacerbating a cervical spine injury.
The trachea can be intubated via the mouth, the nose, the cricothyroid
membrane (cricothyroidostomy), or directly (tracheostomy). The tubes
used for intubation come with either of two different types of cuffs.
Tubes with high-pressure, low-volume cuffs are easy to insert and are
useful for short-term intubation and ventilation. The high cuff
pressure, however, can interfere with tracheal blood supply and
lead to tracheomalacia, erosion into the innominate artery (tracheoinnominate
fistula), erosion into the esophagus (tracheoesophageal fistula), or
airway stenosis. Tubes with low-pressure, high-volume cuffs are
more difficult to insert but should be used for intubation if the
intubation is expected to be longer than 24 hours.
Of the four methods available for intubation, the orotracheal
route is usually the easiest. Nasotracheal intubation requires the
presence of spontaneous ventilation in order to guide tube placement;
cricothyroidostomy and tracheostomy require surgical exposure. Orotracheal
intubation allows for passage of a larger tube than the nasotracheal
route and avoids the problems of sinusitis and necrosis of the nares,
which can occur with nasotracheal intubation. On the other hand, nasotracheal
intubation can be accomplished in the awake patient with minimal sedation,
and some patients seem to find long-term presence of a nasotracheal tube
more comfortable than that of an orotracheal tube. Neither nasotracheal nor
orotracheal intubation requires neck flexion or axial rotation. Either approach can be used in patients with suspected injuries to the cervical spine, assuming that axial traction is maintained
during the intubation.
Cricothyroidostomy is indicated when an urgent surgical airway
is needed. Extensive maxillofacial trauma can make intubation by
the orotracheal or nasotracheal route impossible. Translaryngeal
intubation can also be difficult because of poor patient cooperation,
altered anatomy, or airway or laryngeal swelling. If the patient is
in extremis and respiratory collapse is imminent, attempts at orotracheal
or nasotracheal intubation should not be prolonged. As a rule, if
transpharyngeal intubation is not successful after one or two attempts,
cricothyroidostomy should be done. The cricothyroid membrane in the
midline is bounded superiorly by the lower border of the thyroid
cartilage. It is located by palpation and is incised by a stab incision.
After the hole has been enlarged with the knife handle, a No. 4
or No. 6 tracheostomy tube should be inserted into the trachea.
The patient can then be supported with mechanical ventilation and
supplemental oxygen as necessary. Cricothyroidostomies maintained for
longer than 2 or 3 days may produce glottic and subglottic stenosis;
tracheostomies are less likely to do so. Cricothyroidostomies should
be converted to tracheostomies as soon as is safe and practical,
assuming that continued intubation is needed.
Conversion to tracheostomy should be done under controlled conditions.
A transverse incision overlying the upper trachea is developed by
separating the strap muscles of the neck in the midline. Often the
thyroid isthmus must be either displaced or divided to allow for
adequate exposure of the anterior surface of the trachea. The tracheostomy
tube is placed through the second or third tracheal ring.
For long-term care, translaryngeal intubation has three major
advantages over a tracheostomy. First, a tube passed through the
larynx can be repositioned, distributing pressure on the tracheal mucosa
over a larger area, compared with the balloon on the end of a tracheostomy
tube, which is fixed in place. The result is a much lower incidence
of late tracheal stenosis and tracheoinnominate artery and tracheoesophageal
fistulas, compared with a tracheostomy. Second, because the opening
of a translaryngeal tube is well away from the neck and chest, intravenous
catheters in these areas can be kept sterile. Third, the cuffs on translaryngeal tubes usually lie in a more axial position in the trachea than those on a tracheostomy tube and are better able to
maintain a seal in patients with poor pulmonary compliance and high inspiratory pressures.
On the other hand, for long-term care, airway resistance with
a tracheostomy is lower, nursing care is simpler, suctioning is
more direct, and the tubes do not damage the vocal cords or larynx.
In addition and perhaps most importantly, accidental extubation
is less serious—a well-established tracheostomy tract can
be easily reintubated while the patient continues to breathe through
the stoma. Tracheostomy is also of benefit when weaning from mechanical
ventilation is slow and the patient has failed extubation on multiple
occasions. The presence of a tracheostomy allows for prolonged periods off
the ventilator without the need for reintubation. If the patient develops respiratory distress off the ventilator and a tracheostomy is present, the ventilator can simply be reconnected to the tracheostomy tube.
The timing of conversion from a translaryngeal intubation to
a tracheostomy is controversial. Recommendations as short as 3 days
have been made, but large numbers of patients have been intubated
for months by the orotracheal or nasotracheal route without serious sequelae.
Patients should be converted when airway protection, pulmonary toilet, or
any of the other indications outlined above are present. If, in addition, the need for more than 2–3 weeks of intubation is obvious, the threshold for performing tracheostomy should be
Modes of Mechanical Ventilation
Once the airway is controlled, the ventilator should be set up beginning with the mode of ventilation. There are three primary variables used to describe the mode of mechanical ventilation: trigger, limit, and cycle (see Table 12–2). The trigger can be patient or time triggered with the latter often referred to as “machine triggered.” This is the variable that determines when a patient receives a breath (starts inspiration). The second is the limit variable
and refers to the setting that, when reached, is maintained constant throughout the inspiratory cycle (ie, the “upper limit”). Limit variables are either pressure or flow. When flow is the limit
variable, the ventilator is said to be in volume control or volume limited because of the relationship flow × time = volume. Finally, the cycle variable is that which, once reached, terminates the inspiratory cycle and allows passive expiration. Using these three variables, different modes of ventilation have
been created. Some are mostly of historical interest, and others are newer, combination modes designed to maximize patient physiology, safety, and comfort.
Table 12–2. Characteristics of Five Commonly Used Modes of Mechanical Ventilation. |Favorite Table|Download (.pdf)
Table 12–2. Characteristics of Five Commonly Used Modes of Mechanical Ventilation.
|Intermittent Mandatory Ventilation (IMV)||Time (machine)||Flow (volume) or pressure||Time||Volume Control IMV|
|Pressure control IMV|
|Can be synchronized to patients effort (SIMV) and/or
used in conjunction with pressure support|
|Assist control (AC)||Patient and/or time||Flow (volume) or pressure||Time||Assist control volume control (AC VC)|
|Assist control pressure control (AC PC)|
|Pressure support (PS)||Patient||Pressure||Flow||Purely spontaneous mode and often referred to as a form of
continuous positive airway pressure (CPAP) on the ventilator controls|
|Inverse ratio||Time||Pressure||Time||PC IMV mode with prolonged inspiratory phase to increase
mean airway pressure and functional residual capacity|
|Pressure-regulated volume control||Patient and/or time||Pressure||Time||Variation of pressure control that limits pressure but adjusts
between breaths to ensure preset tidal volume|
Machine triggers are time functions based on the set rate, inspiratory
time, and inspiratory to expiratory ratio (I:E ratio). Two of the
three can be set, and the third is determined. A rate of 20 breaths/min
and an inspiratory time of 1 second results in an I:E ratio of 1:2
(1 s inspiration + 2 s expiration = 3 s for a complete
cycle; 20 cycles/min).
Patient triggers for delivery of an assisted breath can be either
pressure-based or “flow by” depending on the ventilator
model. A pressure trigger requires the patient to generate negative
pressure at the onset of inspiration—the pressure in the
ventilator tubing falls below a preset value and the ventilator
detects this fall in pressure and responds by delivering a breath.
The time involved in generating and delivering the breath to the patient,
however, can make this form of breathing uncomfortable for the patient. Modern
ventilators avoid this problem of triggering by using a flow-by
circuit. The ventilator delivers a constant flow of air through
the ventilator tubing during expiration, usually at a low level
of approximately 5 L/min. The ventilator compares the expiratory
and inspiratory flow rates. If the patient is making no inspiratory effort,
the flow rates will be the same. If the patient begins to take a
breath, the expiratory rate will fall below the inspiratory rate.
The ventilator is programmed to trigger a breath when the difference
in the flow rates reaches a preset value, usually around 2 L/min,
or when the expiratory flow rate falls to 3 L/min. The patient
is rewarded with the free flow of at least some air as soon as the
effort is initiated. The great majority of patients prefer flow-by
over pressure triggering.
Volume Control Ventilation
Volume control ventilation is most often used today in situations
in which the ventilation needs to be kept simple and the efforts
made by the patient need to be minimized, as in the acutely injured
or ill patient. The assist-control mode is the most commonly used
mode of volume ventilation. It is designed to assist any ventilatory
effort made by the patient by delivering a machine breath. Whenever the
patient begins to inspire, the ventilator is triggered and the preset
machine tidal volume is given. A machine backup rate is also set
to ensure a minimal number of machine breaths in the absence of spontaneous
Pressure Control Ventilation & Pressure Support Ventilation
In pressure control ventilation, the inspiratory
pressure, inspiratory time, and I:E ratio are selected, and the
ventilator automatically adjusts the gas flow rate to maintain a
constant pressure during inspiration. The main advantage of this
over volume control is that gas flow more closely matches the change
in lung compliance that occurs during inspiration. This has the
theoretical benefit of a more even distribution of inspired gas and
possibly a lower risk of regional alveolar overdistention. It is
also more comfortable for the awake patient. Although this can be
achieved through manipulating the flow pattern in more advanced volume
control ventilators, it is automatic in pressure control ventilation.
Physiologic inspiratory times and I:E ratios are usually chosen
to improve patient comfort. An inspiratory time of 1 second with an
expiratory time of 2 or 3 seconds is typical. Longer inspiratory
times with shorter expiratory times (inverse ratio ventilation)
can be used if the physiologic times prove inadequate to provide enough support. The long inspiratory times, along with the short expiratory times, result in air trapping and increase the mean airway pressure. The net result is an increase in functional residual capacity (FRC), similar to that accomplished with high positive end-expiratory pressure (PEEP) levels.
Pressure support ventilation is also a pressure-limited
form of ventilation and in most cases, can be considered a distinct mode of ventilation (see Table 12–2). It differs from pressure control in that it is always patient triggered and the inspiratory time is determined by the patient and not set
by the ventilator. As in pressure control ventilation, the ventilator adjusts
the flow to maintain a constant pressure during inspiration. The
inspiratory time, however, is determined by the interaction of the
gas flow with the patient’s inspiratory effort. To do this,
the ventilator measures the peak inspiratory flow rate during inspiration.
The flow rate usually reaches a maximum value early in the inspiration
and then tapers off as the patient’s inspiratory effort
decreases. When the flow rate decreases to a predetermined fraction
of the maximal flow (generally 25% of maximum), gas flow
is terminated, and the patient is allowed to exhale. Pressure support
can also be used in conjunction with the intermittent mandatory
ventilation mode (see next section).
The level of the pressure support is set so that the patient
breathes comfortably at a reasonable rate, usually less than 24 breaths/min.
The goal of the support is to ensure adequate oxygenation and a
pH greater than 7.30. The tidal volume generated under these circumstances
is generally unimportant.
The mode has many advantages. It is usually comfortable for the
patient. It overcomes resistance to inspiratory flow in the endotracheal
tube and in the ventilatory apparatus and decreases the work of
breathing. It makes it impossible for the ventilator to deliver
excessively high pressures. The flow is maintained for as long as
the patient continues to make an inspiratory effort, so the patient
can sigh at will. This minimizes the development of atelectasis.
It is also ideally suited for preparing the patient for weaning
Intermittent Mandatory Ventilation & Assist Control Ventilation
With intermittent mandatory ventilation (IMV), all
aspects of breathing are controlled including the rate, inspiratory
time, and expiratory time (and as a result, I:E ratio). The limit
variable can be either pressure (PC IMV) or volume (VC IMV). The
breaths are generally synchronized (SIMV) if the patient has spontaneous respiratory
effort. In this mode, any attempt to breathe at a greater frequency than
the set rate is unsupported unless additional pressure support is
added. In this case, the patient receives two different modes during
mechanical ventilation. The first is the mandatory, machine-triggered
breath at the set rate and inspiratory time. The second is a spontaneous, patient-triggered
breath at a rate equal to the total minus the set rate with an inspiratory time determined by the patient (see previous discussion of pressure support ventilation). These two breaths will have different waveform characteristics on the ventilator display.
Assist control mode was originally set up to “assist” the patient’s spontaneous effort with a completely supported mechanical breath. It can be used with a volume or pressure limit (VC or PC) and set
up with a backup rate when spontaneous effort is minimal or absent.
The main distinction from SIMV is that all of the patient’s
inspiratory efforts are completely supported (not just those at
the set rate). This has the small disadvantage of air trapping when the
patient’s respiratory rate is excessively high (> 30–35
breaths per minute) and should be used with caution in patients
at risk for hyperinflation (severe emphysema). There is no role
for pressure support ventilation in this mode as all breaths are
Over the past 15 years, it has become possible to ventilate patients with even more sophisticated hybrid modes. Some ventilators can be set up to deliver constant pressure during the inspiration in such a way that the tidal volume delivered falls in a preset range (pressure-regulated volume control, PRVC). Some ventilators can be set up to deliver
a preset tidal volume but without exceeding a preset pressure. Some ventilators can be set up with gradually decreasing ventilatory support with algorithms built into the system to minimize the need
for physician adjustment of the ventilator during weaning.
Setting Up the Ventilator
After choosing the mode (AC, SIMV, or PS; PC or VC), five parameters
remain to be determined: the backup ventilatory rate, the goal tidal
volume of the machine-delivered breaths, the inspiratory time, the
inspired oxygen concentration (Fio2), and
the PEEP level. The first two of these parameters determine ventilation; the
latter three are important in determining oxygenation.
Ventilation has three components: minute ventilation (VE),
alveolar ventilation (VA), and dead space ventilation (VD).
Although VA is most closely related to Paco2,
at steady state, the relationship with VE and VD is
roughly constant, and therefore, VE, which is easily quantified,
can be used as a surrogate. In patients with uncomplicated pulmonary
failure, the respiratory rate can be set at 12–15 breaths/min
and the tidal volume set to 7 mL/kg IBW. This produces
a VE of 6–7.5 L/min and a VA of
4–5 L/min (assuming VD of 33% in
a 70 kg patient). In the absence of significant pulmonary dysfunction,
this will result in a PaCO2 of approximately 40 mm Hg and
is a good starting point from which adjustments can be made.
If the Paco2 is elevated, increases in the respiratory rate
will often correct the problem. Although this is less efficient
than increasing the tidal volume (due to the increased dead space
ventilation that occurs with higher respiratory rates), it is a
reasonable first step when the respiratory rate is less than 25.
Excessively high respiratory rates (> 30 breaths/min) can result
in air trapping, especially in patients with expiratory air flow
obstruction (chronic obstructive pulmonary disease or severe asthma).
On the other hand, excessively high volumes may be associated with
elevated airway pressures and can result in barotrauma (pneumothorax),
volutrauma (alveolar overdistention), or both. Except in certain circumstances
(intracranial hypertension), it is better to accept a mild respiratory
acidosis than to ventilate the patient using excessively large tidal
volumes (greater than 10 mL/kg IBW) or excessively high
airway pressures (plateau pressure greater than 30 cm H2O).
When the pH is less than 7.20, very high rates or volumes may be
necessary until the pH can be brought into the normal range either
through renal compensatory mechanisms or administered bicarbonate.
Very high rates or volumes may also be necessary when a bronchopleural
fistula is present, to compensate for the volume lost through the fistula.
The inspired oxygen concentration should be kept high enough
so that, in most cases, the oxygen saturation of arterial blood
exceeds 92%. Patients with chronic obstructive pulmonary
disease and long-standing CO2 retention are an exception.
Such patients have lost the ability to increase their respiratory
drive in response to increases in Paco2 and
rely instead on their response to hypoxemia. Increasing the arterial oxygen saturation by adding exogenous oxygen takes away this hypoxic ventilatory stimulus and makes weaning from ventilatory support more difficult.
All of the nonoxygen volume of ventilator gas is made up of nitrogen,
which, unlike oxygen, is not absorbed from alveoli. Nitrogen can
be of great value in stenting open the alveoli. When it is replaced
by increasing concentrations of oxygen, increased atelectasis caused
by oxygen absorption can occur. In addition, high concentrations
of oxygen can cause chronic pulmonary fibrosis. Ideally, the inspired
oxygen concentration should be kept at 0.50 or less.
Keeping the inspired oxygen levels at acceptably low levels is
frequently facilitated by the use of PEEP. The pressure is generated
by closure of a valve in the expiratory circuit of the ventilator
to keep the airway pressure above a preset level during expiration
and to minimize alveolar collapse. Placement of an endotracheal
tube bypasses the normal physiologic PEEP present during spontaneous
ventilation from closure of the glottis at the end of expiration.
In addition, supine patients may have a lower functional residual
capacity due to increased intra-abdominal pressure and cephalad displacement
of the diaphragm into the chest. This can be overcome through the use
of low levels of “physiologic” PEEP (5 cm H2O).
Increasing the PEEP should be considered when the respiratory system compliance
is low or when adequate oxygenation requires an Fio2 that
Low levels of PEEP (< 10 cm H2O) are well tolerated
by most patients. The consequences of excessive PEEP are barotrauma
and decreased cardiac output. First, the high pressure can compress
the superior and inferior vena cava and the pulmonary veins, compromising diastolic
filling of the ventricles (in contrast with a spontaneous inspiration, which
augments filling). Second, the high pressures can compress the thin-walled atria
and right ventricle, further compromising end-diastolic volumes
(also in contrast with a spontaneous inspiration). Finally, the
high pressures can compress the pulmonary microvasculature, making it
difficult for the right ventricle to push blood through the pulmonary
vasculature. The remedy for the decreased cardiac output is usually
fluid infusion. The potential problem with this remedy is worsening
of the pulmonary failure that prompted the use of the PEEP in the
first place. Accounting for all of these factors, PEEP levels greater
than 10–12 cm H2O should generally be used with
a pulmonary arterial catheter in place. Titrating to the optimal
oxygen delivery, and not arterial Pao2,
will ensure a balance between the risks and benefits of high PEEP
levels. Monitoring the mixed venous oxygen saturation serves as
a reasonable method to achieve this goal. Even with invasive monitoring,
PEEP levels greater than 15–20 cm H2O are rarely
Ventilator Safety & Alarms
As can be inferred, modern ventilators are complex, and they
should, in general, be used only in the setting of continuous cardiopulmonary
monitoring to include electrocardiography and pulse oximetry. In
addition, the ventilators themselves have alarms for early warning
of apnea, changes in tidal volume or minute ventilation, and excessive
inspiratory pressures. These should be individualized to each patient
so that nurses, respiratory therapists, and physicians are notified
early in the course of the physiologic derangement. In many cases,
the ventilator alarm will precede changes in the pulse oximeter
or electrocardiogram. All personnel taking care of the patient should
be knowledgeable with both the equipment and the mode of ventilation.
Discontinuing Mechanical Ventilation
Patients who seem to be doing well and who have required mechanical
ventilation for less than 24 hours can frequently be extubated quickly
after undergoing a trial of spontaneous ventilation. Patients must
be able to maintain their own airway, and their acute illness should
be resolving. They should be able to maintain adequate oxygenation
with an inspired oxygen concentration of 0.40 or less and with a
PEEP of 8 cm water or less.
The majority of ventilated patients are most effectively weaned
with daily spontaneous breathing trials. The breathing trial can
be given with T-piece ventilation in which the endotracheal tube
is attached to a length of tubing connected to a blow-by oxygen
source. Alternatively, the trial can be accomplished with a low
level (typically 5 cm of water) of pressure support with PEEP or
with PEEP alone. In either case, the patient is asked to support
his or her own breathing for 30 minutes. If the patient is breathing
comfortably at the end of the trial, the patient can be extubated.
If a question arises as to the degree of comfort, arterial blood
should be drawn for gases, and the patient should be put back on
the ventilator while waiting for the results of the blood gas analysis.
If the patient was reasonably comfortable at the end of the 30-minute
trial and if the pH comes back at a normal value, the patient can
be extubated. Note that at the conclusion of the 30-minute trial,
full ventilator support should be resumed pending the laboratory
results. The patient needs to be well rested when the endotracheal
tube is removed. If the patient fails the 30 minute trial, full
support is resumed for the remainder of the day, and the trial is
repeated the following day.
Weaning from mechanical ventilation can also be achieved with
IMV. Although generally inferior to the once-daily spontaneous breathing
trial, patients who are severely debilitated and have required mechanical
ventilation for prolonged periods (> 2–3 weeks) can be
successfully weaned using this technique when combined with a gradual
reduction in pressure support. The IMV rate is gradually decreased,
requiring the patient to contribute increasingly to the maintenance
of adequate minute ventilation. The patient’s overall clinical
status, respiratory rate, and arterial Pco2 are
used as guidelines to determine the rate of weaning. When an IMV
of 4/min or less is well tolerated for long periods, the
patient is placed on pressure support, which is weaned daily until
mechanical support is no longer needed. Patients who repeatedly
fail extubation or are severely deconditioned benefit from a more
deliberate and gradual weaning of the ventilator. Frequently, these
patients benefit from tracheostomy and optimization of nutritional
status as adjuncts to weaning. Factors that increase the work of
breathing—such as reactive airway disease, large pleural effusions,
and chest wall or visceral edema—should be treated and
The decision to extubate the patient depends both on the assessment
for the need for airway protection as well as the need for mechanical
ventilation. As mentioned previously, the latter can be determined
based on the result of a 30-minute trial of spontaneous breathing.
The former should be based on several factors, including the patient’s
level of consciousness, the presence of airway injury or edema,
the need for ongoing endotracheal suctioning, and the possible need for
further operative procedures within the next 24 hours. Finally,
a subjective determination of a patient’s ability to tolerate
extubation and spontaneous ventilation should be made. An alert
and communicative patient who can lift her head off the pillow is
a good candidate for extubation; a lethargic, diaphoretic patient
is not. For patients who require continued airway protection but
no longer require mechanical ventilatory support, a tracheostomy
should be considered.
Adjuvant Diagnostic & Therapeutic Measures
Chest x-rays should be obtained daily in patients being treated
with mechanical ventilation. A review of the film should confirm
the placement of all lines and tubes, including the endotracheal
tube, central venous catheters, pleural tubes (thoracostomies),
and nasogastric or nasoenteric tubes. A search for specific pulmonary
and pleural processes should be performed. Local infiltrates such
as pneumonia or patchy/diffuse processes such as the acute
respiratory distress syndrome should be identified.
In addition to a daily chest radiograph, a stat chest x-ray should
be obtained whenever a patient’s cardiopulmonary status
rapidly deteriorates. Tubes or lines might be displaced; new problems with
a reversible etiology—such a pneumothorax, a lobar collapse,
or a new infiltrate suggesting aspiration—might be identified.
Sedation & Muscle Relaxants
Mechanically ventilated patients frequently require sedatives and/or
analgesia to ameliorate the agitation and pain associated with their
disease and treatment. Narcotic analgesia in the form of intermittent
or continuous opiate infusion may be sufficient. Narcotics, however,
should not be used to treat agitation and anxiety that is thought
to be caused by the ventilator. Sedating agents, including propofol
and benzodiazepines, should be used instead. In addition, haloperidol
and risperidone may be useful adjuncts, either alone or in combination
with benzodiazepines. As a general rule, intermittent dosing is
preferred to continuous infusions. When the latter is used, the
agent should be stopped at least once daily—giving the
patient a so-called sedation holiday—to assess neurologic status
and determine the need for continuing sedation.
Neuromuscular blocking agents add an additional level of patient
control and can greatly simplify ventilatory management in patients
with severe pulmonary insufficiency. These agents should be reserved for
severe patient-ventilator dyssynchrony, a situation in which the
patient’s spontaneous respiratory efforts result in dyscoordinated
and inadequate ventilation by the mechanical ventilator. This may
have the untoward effect of life-threatening hypoxemia in a patient
with little physiologic reserve.
Nonphysiologic ventilatory methods, such as inverse ratio or
high-frequency oscillatory ventilation, may also require the use
of neuromuscular blocking agents. Major side effects include a potential
increased risk of ventilator-associated pneumonia (VAP), through loss
of cough mechanism, and an association with late polyneuromyopathy
of critical illness. As a result, they should be used only when
absolutely necessary and for the shortest possible time.
VAP is the most common nosocomial infection in the intensive
care unit. The risk of acquiring VAP is directly related to the
duration of mechanical ventilation. There is no gold standard for
VAP diagnosis. Possible criteria include a new or progressive infiltrate
on chest radiograph, worsening hypoxemia, increased sputum quantity,
new onset of purulent sputum associated with abundant white cells
and organisms on Gram-stained smears, or positive sputum cultures
with known pathogenic organisms. Signs of systemic sepsis with increased temperature,
leukocytosis, increasing fluid requirements, and glucose intolerance
are also common findings in VAP.
If all of these are present, antibiotics should be started. If only
one or two are present, antibiotics are probably best withheld to
avoid overgrowth of resistant organisms that could later cause fatal
pneumonia. Exceptions to this approach include older, severely debilitated
patients, immunocompromised patients, and those who are critically
ill in whom delayed antibiotic therapy might result in irretrievable
deterioration. Thus, an 80-year-old patient with flail chest and
a new infiltrate should probably be given antibiotics early; a 20-year-old
patient who was hospitalized for a gunshot wound involving the colon
and who develops questionable pneumonia 2 weeks later is more likely
to tolerate a delay in the initiation of antibiotics until the diagnosis
is more definite. In addition, the latter patient may have an alternative
explanation for his fever and leukocytosis, such as an intra-abdominal
abscess. In this case, the wrong diagnosis might delay appropriate
source control (abscess drainage). The CPIS can be useful to guide
the diagnosis. The goal is to avoid overtreatment with the risk of
antimicrobial resistance and superinfection. Antibiotics can safely
be discontinued in patients empirically started on antibiotics for
suspected pneumonia who have a CPIS value of 6 or less at 72 hours.
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