Download Respiratory Failure File

Respiratory failure update
Dr Ahmed Elmasry
MD, chest diseases, Ain Shams University
PhD, respiratory medicine, Uppsala University
Acute Respiratory Failure
• Failure in one or both gas exchange
functions: oxygenation and carbon dioxide
elimination
• In practice:
PaO2<60mmHg or PaCO2>46mmHg
• Derangements in ABGs and acid-base status
HYPERCAPNIC RESPIRATORY FAILURE
At a constant rate of carbon dioxide
production, PaCO2 is determined by the
level of alveolar ventilation (Va), where
VCO2 is ventilation of carbon dioxide and K
is a constant value (0.863).
Va = (K x VCO2)/PaCO2
ALVEOLAR-ARTERIAL OXYGEN
DIFFERENCE
The efficiency of lungs at carrying out of
respiration can be further evaluated by
measuring alveolar-to-arterial PaO2
difference.
This difference is calculated by the
following equation:
ALVEOLAR –ARTERIAL OXYGEN
DIFFERENCE
PaO2 = FIO2 x (PB – PH2 O) – PaCO2/R
For the above equation, PaO2 = alveolar PO2, FIO2 =
fractional concentration of oxygen in inspired gas,
PB = barometric pressure, PH2 O = water vapor
pressure at 37°C, PaCO2 = alveolar PCO2, assumed to
be equal to arterial PCO2, and R = respiratory
exchange ratio. R depends on oxygen consumption
and carbon dioxide production. At rest, VCO2/VO2 is
approximately 0.8.
SHUNT EFFECT
Shunt is defined as the persistence of
hypoxemia despite 100% oxygen inhalation.
The deoxygenated blood (mixed venous
blood) bypasses the ventilated alveoli and
mixes with oxygenated blood that has flowed
through the ventilated alveoli, consequently
leading to a reduction in arterial blood
content.
SHUNT EFFECT
The shunt is calculated by the following equation:
QS/QT = (CCO2 – CaO2)/CCO2 – CVO2)
QS/QT is the shunt fraction, CCO2 (capillary oxygen
content) is calculated from ideal alveolar PO2, CaO2
(arterial oxygen content) is derived from PaO2 using the
oxygen dissociation curve, and CVO2 (mixed venous
oxygen content) can be assumed or measured by
drawing mixed venous blood from pulmonary arterial
catheter.
SHUNT EFFECT
Even normal lungs have some degree of V/Q
mismatching and a small quantity of right-toleft shunt, alveolar PO2 is slightly higher than
arterial PO2. However, an increase in alveolarto-arterial PO2 above 15-20 mm Hg indicates
pulmonary disease as the cause of hypoxemia.
Mortality/Morbidity
The mortality rate associated with respiratory
failure varies according to the etiology. For
acute respiratory distress syndrome, the
mortality rate is approximately 50% in most
studies. Acute exacerbation of COPD carries a
mortality rate of approximately 30%. The
mortality rates for other causative disease
processes have not been well described.
Criteria for the diagnosis of ARDS
• Clinical presentation - Tachypnea and dyspnea;
crackles upon auscultation
• Clinical setting - Direct insult (aspiration) or systemic
process causing lung injury (sepsis)
• Radiologic appearance - Three-quadrant or 4quadrant alveolar flooding
• Lung mechanics - Diminished compliance ( <40
mL/cm water)
• Gas exchange - Severe hypoxia refractory to oxygen
therapy (PaO2/FIO2 <200)
• Normal pulmonary vascular properties - Pulmonary
capillary wedge pressure <18 mm Hg
CAUSES
Central nervous system disorders
• A variety of pharmacological, structural, and
metabolic disorders of the CNS are characterized
by depression of the neural drive to breathe.
• This may lead to acute or chronic hypoventilation
and hypercapnia.
• Examples include tumors or vascular
abnormalities involving the brain stem, an
overdose of a narcotic or sedative, and metabolic
disorders such as myxedema or chronic metabolic
alkalosis.
CAUSES
Disorders of the peripheral nervous system,
respiratory muscles, and chest wall
• These disorders lead to an inability to maintain a level
of minute ventilation appropriate for the rate of carbon
dioxide production.
• Concomitant hypoxemia and hypercapnia occur.
• Examples include Guillain-Barré syndrome, muscular
dystrophy, myasthenia gravis, severe kyphoscoliosis,
and morbid obesity.
CAUSES
Abnormalities of the airways
• Severe airway obstruction is a common cause of
acute and chronic hypercapnia.
• Examples of upper airway disorders are acute
epiglottitis and tumors involving the trachea;
lower airway disorders include COPD, asthma, and
cystic fibrosis.
CAUSES
Abnormalities of the alveoli
• The diseases are characterized by diffuse alveolar
filling, frequently resulting in hypoxemic respiratory
failure, although hypercapnia may complicate the
clinical picture.
• Common examples are cardiogenic and
noncardiogenic pulmonary edema, aspiration
pneumonia, or extensive pulmonary hemorrhage.
These disorders are associated with intrapulmonary
shunt and an increased work of breathing.
Common causes of type I (hypoxemic) respiratory failure
Chronic bronchitis and emphysema (COPD)
Pneumonia
Pulmonary edema
Pulmonary fibrosis
Asthma
Pneumothorax
Pulmonary embolism
Pulmonary arterial hypertension
Pneumoconiosis
Granulomatous lung diseases
Cyanotic congenital heart disease
Bronchiectasis
Adult respiratory distress syndrome
Fat embolism syndrome
Kyphoscoliosis
Obesity
Common causes of type II (hypercapnic) respiratory failure
Chronic bronchitis and emphysema (COPD)
Severe asthma
Drug overdose
Poisonings
Myasthenia gravis
Polyneuropathy
Poliomyelitis
Primary muscle disorders
Porphyria
Cervical cordotomy
Head and cervical cord injury
Primary alveolar hypoventilation
Obesity hypoventilation syndrome
Pulmonary edema
Adult respiratory distress syndrome
Myxedema
Tetanus
Laboratory Studies
• Arterial blood gases in all patients who are seriously ill
or in whom respiratory failure is suspected.
• A complete blood count; anemia can contribute to
tissue hypoxia, whereas polycythemia may indicate
chronic hypoxemic respiratory failure.
• Abnormalities in renal and hepatic function may either
provide clues to the etiology of respiratory failure or
alert the clinician to complications associated with
respiratory failure.
• Abnormalities in electrolytes such as potassium,
magnesium, and phosphate may aggravate respiratory
failure.
Laboratory studies
• Measuring serum creatine kinase with fractionation
and troponin I helps exclude recent myocardial
infarction in a patient with respiratory failure.
• An elevated creatine kinase with a normal troponin I
may indicate myositis, which occasionally can cause
respiratory failure.
• In chronic hypercapnic respiratory failure, serum
thyroid-stimulating hormone should be measured to
evaluate the possibility of hypothyroidism, a potentially
reversible cause of respiratory failure.
Imaging Studies
Chest radiograph
• Chest radiography is essential because it frequently
reveals the cause of respiratory failure. However,
distinguishing between cardiogenic and
noncardiogenic pulmonary edema often is difficult.
• Increased heart size, vascular redistribution,
peribronchial cuffing, pleural effusions, septal lines,
and perihilar bat-wing distribution of infiltrates
suggest hydrostatic edema; the lack of these findings
suggests ARDS.
Imaging studies
Echocardiography
• Echocardiography need not be performed routinely in all
patients with respiratory failure. However, it is a useful test
when a cardiac cause of acute respiratory failure is
suspected.
• The findings of left ventricular dilatation, regional or global
wall motion abnormalities, or severe mitral regurgitation
support the diagnosis of cardiogenic pulmonary edema.
• A normal heart size and normal systolic and diastolic
function in a patient with pulmonary edema would suggest
ARDS.
• Echocardiography provides an estimate of right ventricular
function and pulmonary artery pressure in patients with
chronic hypercapnic respiratory failure.
Pulmonary function tests
Patients with acute respiratory failure generally are unable to
perform pulmonary function tests (PFTs). However, PFTs are
useful in the evaluation of chronic respiratory failure.
• Normal values of forced expiratory volume in one second
(FEV1) and forced vital capacity (FVC) suggest a disturbance
in respiratory control.
• A decrease in FEV1 -to-FVC ratio indicates airflow
obstruction, whereas a reduction in both the FEV1 and FVC
and maintenance of the FEV1 -to-FVC ratio suggest
restrictive lung disease.
• Respiratory failure is uncommon in obstructive diseases
when the FEV1 is greater than 1 L and in restrictive diseases
when the FVC is more than 1 L.
ECG
An ECG should be performed to evaluate the
possibility of a cardiovascular cause of
respiratory failure; it also may detect
dysrhythmias resulting from severe hypoxemia
and/or acidosis.
Right heart catheterization
• This remains a controversial issue in the management of
critically ill patients.
• Invasive monitoring probably is not routinely needed in
patients with acute hypoxemic respiratory failure, but
when significant uncertainty about cardiac function,
adequacy of volume resuscitation, and systemic oxygen
delivery remain, right heart catheterization should be
considered.
• Measurement of pulmonary capillary wedge pressure
may be helpful in distinguishing cardiogenic from
noncardiogenic edema.
• The pulmonary capillary wedge pressure should be
interpreted in the context of serum oncotic pressure and
cardiac function.
MEDICAL CARE
• A patient with acute respiratory failure
generally should be admitted to a respiratory
care or intensive care unit.
• Most patients with chronic respiratory failure
can be treated at home with oxygen
supplementation and/or ventilatory assist
devices along with therapy for their underlying
disease.
MEDICAL CARE
Airway management
• Assurance of an adequate airway is vital in a
patient with acute respiratory distress.
• The most common indication for endotracheal
intubation (ETT) is respiratory failure.
• ETT serves as an interface between the patient
and the ventilator.
• Another indication for ETT is airway protection in
patients with altered mental status.
MEDICAL CARE
Correction of hypoxemia
• After securing an airway, attention must turn to
correcting the underlying hypoxemia, the most lifethreatening facet of acute respiratory failure.
• The goal is to assure adequate oxygen delivery to
tissues, generally achieved with a PaO2 of 60 mm Hg or
an arterial oxygen saturation (SaO2) of greater than
90%.
• Supplemental oxygen is administered via nasal prongs
or face mask; however, in patients with severe
hypoxemia, intubation and mechanical ventilation
often are required.
MEDICAL CARE
Coexistent hypercapnia and respiratory acidosis may
need to be addressed. This is done by correcting the
underlying cause or providing ventilatory assistance.
• Mechanical ventilation is used for 2 essential
reasons: (1) to increase PaO2 and (2) to lower PaCO2.
• Mechanical ventilation also rests the respiratory
muscles and is an appropriate therapy for respiratory
muscle fatigue.
MEDICAL CARE
Overview of mechanical ventilation
• Positive-pressure versus negative-pressure
ventilation
• Controlled versus patient-initiated (ie, assisted)
• Pressure-targeted versus volume-targeted:
MEDICAL CARE
Interface between patient and ventilator
(mask vs endotracheal intubation)
• Mechanical ventilation requires an interface between the patient and the
ventilator. In the past, this invariably occurred through an endotracheal or
tracheostomy tube, but in recent years, an increasing trend has occurred towards
noninvasive ventilation, which can be accomplished by the use of either a full face
mask or a nasal mask.
• Following intubation, the position of the tube in the airway should be confirmed
by auscultation of the chest and, ideally, by a carbon dioxide detector. As a general
rule, the endotracheal tube should be inserted to an average depth of 23 cm in
men and 21 cm in women (measured at the incisor). Confirm proper placement
with a chest radiograph.
• The tube should be secured. The pressure in the cuff generally should not exceed
25 mm Hg.
• Endotracheal suctioning can be accomplished by either open-circuit or closedcircuit suction catheters.
MEDICAL CARE
Specific modes of ventilatory support
• Pressure support ventilation (PSV)
• Intermittent mandatory ventilation (IMV) (SIMV)
• Assist-control ventilation
• Volume-control ventilation.
• Pressure-control ventilation
• Pressure-control inverse-ratio ventilation (PCIRV)
MEDICAL CARE
Triggering mechanism: pressure versus flow triggering
• In patient- assisted ventilation, the ventilator must sense the
patient's inspiratory effort in order to deliver assistance.
• With pressure-triggering, in a patient on no positive endexpiratory pressure (PEEP) with a trigger sensitivity set at 1 cm
water, a breath is triggered whenever airway pressure falls below
-1 cm water. In a patient on 5-cm water PEEP with the same
trigger sensitivity, a breath is triggered whenever airway pressure
falls below +4 cm water.
• In flow-triggering, a flow sensitivity is selected. When the
patient makes an inspiratory effort, the ventilator senses the
decrease in flow returning through the circuit, and a breath is
triggered. One problem with flow-triggering is that autotriggering
sometimes results from leaks in the ventilator circuit.
MEDICAL CARE
Positive end-expiratory pressure
• PEEP may recruit atelectatic alveoli and prevent their
collapse
• PEEP shifts lung water from the alveoli into the
perivascular interstitial space and helps with
recruitment of alveoli.
• However, it does not decrease the total amount of
extravascular lung water.
• In patients with ARDS or ALI, PEEP is applied to
recruit atelectatic alveoli, improving oxygenation and
allowing a reduction in FiO2 to nontoxic levels (FiO2
<0.6).
MEDICAL CARE
Positive end-expiratory pressure
•PEEP of 3-5 cm water to prevent a decrease in functional
residual capacity in patients with normal lungs is a common
practice.
• Higher PEEP produces better oxygenation and lung
compliance but no benefit to survival, time on ventilator, or
nonpulmonary organ dysfunction.
• Ideal PEEP helps to achieve adequate oxygenation and
decrease the requirement for high FiO2 without causing
harmful effects of PEEP.
• Current evidence does not support routine application of high
PEEP strategy in people with ALI or ARDS.
• PEEP causes an increase in intrathoracic pressure, which may
decrease venous return and cardiac output, particularly in
patients with hypovolemia.
MEDICAL CARE
Inspiratory flow
• In volume-targeted ventilation, inspiratory flow is a
variable that is set by the physician or respiratory
therapist. The inspiratory flow rate is selected on the basis
of a number of factors, including the patient's inspiratory
drive and the underlying disease.
Two flow patterns are used commonly: (1) a constant-flow
(ie, square-wave) pattern and (2) a decelerating-flow
pattern. With a constant-flow pattern, inspiratory flow is
held constant throughout the breath, whereas with a
decelerating-flow pattern, flow rises quickly to a maximal
value and then decreases progressively throughout the
breath.
MEDICAL CARE
Inspiratory flow
•In pressure-targeted ventilation, the inspiratory flow rate
is a dependent variable that varies as a function of the
preset pressure and the patient's own inspiratory effort.
Because airway pressure is held constant while alveolar
pressure rises during inspiration, the pressure difference
between airway and alveoli decreases, leading to a
decelerating pattern of inspiratory flow.
MEDICAL CARE
Determinants of ventilator-associated lung injury
•Mechanical ventilation is associated with a variety of
insults to the lung.
•In the past, physicians focused on barotrauma, including
pneumothorax, pneumomediastinum, and subcutaneous
and pulmonary interstitial emphysema. The manifestations
of barotrauma likely occur because of excessive alveolar
wall stress. Excessive airway pressure by itself does not
appear to cause barotrauma. In critically ill patients, the
manifestations of barotrauma can be subtle, the earliest
sign of pneumothorax in supine patients may be the deepsulcus sign or a collection of air anteriorly along
cardiophrenic angle.
MEDICAL CARE
Determinants of ventilator-associated lung injury
•More recently, lung damage indistinguishable from ARDS
has been recognized to possibly be caused by certain
patterns of ventilatory support. The mechanism was
thought to be due to direct parenchymal injury and altered
microvascular permeability secondary to high peak
alveolar pressures. Recently, other investigators have
shown that excessive tidal volumes resulting in alveolar
overdistension are the most important factor in ventilatorassociated lung injury.
•A strategy of using low tidal volumes in patients with
ARDS who are on mechanical ventilation has led to a
reduced incidence of barotrauma and improved survival
rates in recently published clinical trials.
MEDICAL CARE
Mechanical ventilation in specific diseases
General guidelines
• The mode of ventilation should be suited to the needs of the
patient. Following the initiation of mechanical ventilation, the
ventilator settings should be adjusted based on the patient's
lung mechanics, underlying disease process, gas exchange, and
response to mechanical ventilation.
• SIMV and assist-control ventilation often are used for the
initiation of mechanical ventilation.
• In patients with intact respiratory drive and mild-to-moderate
respiratory failure, PSV may be a good initial choice.
Supplemental oxygen
• The lowest FiO2 that produces an SaO2 greater than 90% and a
PaO2 greater than 60 mm Hg generally is recommended.
• The prolonged use of FiO2 less than 0.6 is unlikely to cause
pulmonary oxygen toxicity.
MEDICAL CARE
Acute respiratory distress syndrome
•The primary objective is to accomplish adequate gas exchange
while avoiding excessive inspired oxygen concentrations and
alveolar overdistension.
•Repeated cycles of opening and collapsing of inflamed and
atelectatic alveoli are detrimental to the lung. Failure to maintain
a minimum alveolar volume may further accentuate the lung
damage. Transalveolar pressure (reflected by plateau pressure)
exceeding 25-30 cm water is a risk factor for stretch injury to the
lungs.
•Patients with ARDS should receive a tidal volume of 6 mL/kg.
The set tidal volume should be based on ideal rather than actual
body weight. If the plateau pressure remains excessive (>30 cm
water), further reductions in tidal volume may be necessary. This
strategy may lead to respiratory acidosis, which requires either
high respiratory rates and or sodium bicarbonate infusion.
MEDICAL CARE
Acute respiratory distress syndrome
•Application of PEEP sufficient to raise the tidal volume above
the lower inflection point (Pflex) on the pressure-volume curve
may minimize alveolar wall stress and improve oxygenation. A
pressure-volume curve can be constructed for an individual
patient by measuring plateau pressures at different lung
volumes. Pflex is the point at which the slope of the curve
changes, indicating that the lung is operating at the most
compliant part of the curve.
•A lung-protective strategy where the PaCO2 is allowed to rise
(permissive hypercapnia) may reduce barotrauma and enhance
survival.
•In some patients with ARDS, the prone position may lead to
significant improvements in oxygenation; whether this translates
to improved outcome is unknown.
MEDICAL CARE
Obstructive airway diseases
•In patients with COPD or asthma, institution of mechanical
ventilation may worsen dynamic hyperinflation (auto-PEEP or
intrinsic PEEP [PEEPi]). The dangers of auto-PEEP include a
reduction in cardiac output and hypotension and barotrauma.
•The goals of mechanical ventilation in obstructive airway
diseases are to unload the respiratory muscles, achieve
adequate oxygenation, and minimize the development of
dynamic hyperinflation.
•Patients with status asthmaticus frequently develop severe
dynamic hyperinflation. This can be minimized by delivering the
lowest possible minute ventilation in the least possible time.
Therefore, the initial ventilatory strategy should involve the
delivery of relatively low tidal volumes (eg, 8-10 mL/kg) and
lower respiratory rates (eg, 8-12 breaths per min) with a high
inspiratory flow rate.
MEDICAL CARE
Obstructive airway diseases
•In the absence of hypoxia, even marked levels of hypercapnia are preferable
to normalize the PCO2, which could lead to dangerous levels of hyperinflation.
•Patients often require large amounts of sedation and occasionally paralysis
until the bronchoconstriction and airway inflammation have improved.
•To measure trapped-gas volume (VEI), as recommended by some
investigators, an attempt should be made to keep it below 20 mL/kg. The
measurement of plateau pressure and auto-PEEP provide similar information
and are much easier to perform.
•A goal of mechanical ventilation is to unload the respiratory muscles while
minimizing the degree of hyperinflation. The use of extrinsic PEEP may be
considered in spontaneously breathing patients in order to reduce the work
of breathing and to facilitate triggering of the ventilator. Avoid causing further
hyperinflation, level of PEEP should be less than the level of auto-PEEP.
MEDICAL CARE
Facilitating patient-ventilator synchrony
•Many patients experience asynchrony between their own spontaneous
respiratory efforts and the pattern of ventilation imposed by the ventilator. This
can occur with both controlled and patient-initiated modes of ventilation.
•To achieve synchrony, the ventilator must not only sense and respond quickly to
the onset of the patient's inspiratory efforts, it also must terminate the inspiratory
phase when the patient's "respiratory clock" switches to expiration. Asynchronous
interactions, commonly referred to as "fighting the ventilator," may occur when
ventilator breaths and patient efforts are out of phase. This may lead to excessive
work of breathing, increased respiratory muscle oxygen consumption, and
decreased patient comfort.
•Patient-ventilator asynchrony should be minimized. Modern ventilators are
equipped with significantly better valve characteristics. Flow-triggering (with a
continuous flow rate) appears to be more sensitive and more responsive to
patient's spontaneous inspiratory efforts.
•Patient-ventilator asynchrony often occurs in the presence of auto-PEEP. AutoPEEP creates an inspiratory threshold load and thereby decreases the effective
trigger sensitivity. This may be partially offset by the application of external PEEP.
•Sometimes, additional sedation may be necessary to achieve adequate patientventilator synchrony.
Noninvasive ventilatory support
•Noninvasive ventilation should be considered in patients with mildto-moderate acute respiratory failure. The patient should have an
intact airway, airway-protective reflexes, and be alert enough to
follow commands.
•NPPV has proven beneficial in acute exacerbations of COPD and
asthma, decompensated CHF with mild-to-moderate pulmonary
edema, and pulmonary edema from hypervolemia.
•In acute exacerbations of obstructive lung disease, NPPV decreases
PaCO2 by unloading the respiratory muscles and supplementing
alveolar ventilation. The results of several clinical trials support the
use of NPPV in this setting.
•The use of NPPV was shown to reduce complications, duration of
ICU stay, and mortality. In patients in whom NPPV failed, mortality
rates were similar to the intubated group (25% vs 30%). NPPV was
administered on the ward. Long-term outcome of patients treated
with NPPV is better.
Noninvasive ventilatory support
•NPPV also helps maintain an adequate PaO2 until the patient
improves.
•In cardiogenic pulmonary edema, NPPV improves oxygenation,
reduces work of breathing, and may increase cardiac output.
•When applied continuously to patients with chronic ventilatory
failure, NPPV provides sufficient oxygenation and/or carbon dioxide
elimination to sustain life by reversing or preventing atelectasis
and/or resting the respiratory muscles.
•Patients with obesity-hypoventilation syndrome benefit from NPPV
by reversal of the alveolar hypoventilation and upper airway
obstruction.
•Most trials have used inspiratory pressures of 12-20 cm water;
expiratory pressures of 0-6 cm water; and excluded patients with
hemodynamic instability, uncontrolled arrhythmia, or a high risk of
aspiration.
Weaning from mechanical ventilation
•Weaning or liberation from mechanical ventilation is initiated when the
underlying process that necessitated ventilatory support has improved. In some
patients, such as those recovering from uncomplicated major surgery or a toxic
ingestion, withdrawal of ventilator support may be done without weaning.
•A patient who has stable underlying respiratory status, adequate oxygenation
(eg, PaO2/FiO2 >200 on PEEP <10 cm water), intact respiratory drive, and stable
cardiovascular status should be considered for discontinuation of mechanical
ventilation.
•Over the years, many criteria have been used to predict success in weaning,
including a minute ventilation of less than 10 L/min, maximal inspiratory
pressure more than -25 cm water, vital capacity more than 10 mL/kg, absence of
dyspnea, absence of paradoxical respiratory muscle activity, and agitation or
tachycardia during the weaning trial. However, recent studies suggest that the
rapid-shallow breathing index, ie, the patient's tidal volume (in liters) divided by
the respiratory rate (breaths per min) during a period of spontaneous breathing,
may be a better predictor of successful extubation. In a recent study, a daily trial
of spontaneous breathing in patients with a rapid-shallow breathing index of less
than 105 resulted in a shorter duration of mechanical ventilation. A spontaneous
breathing trial of only 30 minutes appears adequate to identify patients in whom
successful extubation is likely.
Weaning from mechanical ventilation
•In patients who are not yet ready to be liberated from the ventilator, one should
focus on the cause of ventilator dependency, such as excessive secretions,
inadequate respiratory drive, impaired cardiac function, and ventilatory muscle
weakness, rather than the type of ventilator or the mode of assistance.
•The weaning protocol could be designed with assist-control ventilation, with
gradually increasing time spent in trials of spontaneous breathing or by gradually
reducing the level of PSV.
•SIMV appears to result in less rapid weaning than PSV or trials of spontaneous
breathing.
•Patient-ventilator desynchrony is an important component in a carefully designed
weaning protocol.
•Attention must be directed towards patient comfort, avoidance of fatigue,
adequate nutrition, and prevention and treatment of medical complications
during the weaning period.
•Ventilator monitoring: Peak inspiratory and plateau pressures should be assessed
frequently. Attempts should be made to limit the plateau pressure to less than 25
cm water. Expiratory volume is checked initially and periodically (continuously if
ventilator-capable) to assure that the set tidal volume is delivered. In patients
with severe airflow obstruction, auto-PEEP (PEEPi) should be monitored on a
regular basis.
MEDICAL CARE
Monitoring of patients with acute respiratory failure
•A patient with respiratory failure requires repeated
assessments, which may range from bedside observations
to the use of invasive monitoring.
•These patients should be admitted to a facility where close
observation can be provided. Most patients who require
mechanical ventilation are critically ill; therefore, constant
monitoring in a critical care setting is a must.
•Cardiac monitoring, blood pressure, pulse oximetry, SaO2,
and capnometry are recommended. An arterial blood gas
determination should be obtained 15-20 minutes after the
institution of mechanical ventilation. The pulse oximetry
readings direct efforts to reduce FiO2 to a value less than
0.6, and the PaCO2 guides adjustments of minute
ventilation.
MEDICAL CARE
Treatment of underlying cause
•After the patient's hypoxemia is corrected and the
ventilatory and hemodynamic status have stabilized, every
attempt should be made to identify and correct the
underlying pathophysiologic process that led to respiratory
failure in the first place.
•The specific treatment depends on the etiology of
respiratory failure.
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