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Surgery > Critical Care Author Information
Introduction
Rate this Article Clinical
Differentials
Respiratory Failure Email to a Colleague Workup
Treatment
Last Updated: January 22, 2003 Medication
Synonyms and related keywords: hypoxemic respiratory failure, Follow-up
Miscellaneous
hypercapnic respiratory failure, type I respiratory failure, type II respiratory Pictures
failure, chronic obstructive pulmonary disease, COPD Bibliography
AUTHOR INFORMATION Section 1 of 11
Click for related
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow- images.
up Miscellaneous Pictures Bibliography
Author: Sat Sharma, MD, FRCPC, FCCP, DABSM, Program

Related Articles
Director, Associate Professor, Department of Internal Medicine,
Divisions of Pulmonary and Critical Care Medicine, University of Acute Respiratory
Manitoba; Site Coordinator of Respiratory Medicine, St Boniface Distress Syndrome
General Hospital Apnea, Sleep
Sat Sharma, MD, FRCPC, FCCP, DABSM, is a member of the
following medical societies: American Academy of Sleep Asthma
Medicine, American College of Chest Physicians, American College
of Physicians-American Society of Internal Medicine, American Atelectasis
Thoracic Society, Canadian Medical Association, Royal College of
Cardiogenic Shock
Physicians and Surgeons of Canada, Royal Society of
Medicine, Society of Critical Care Medicine, and World Medical Cardiomyopathy,
Association Diabetic
Editor(s): Cory Franklin, MD, Director, Professor, Department of
Medicine, Division of Critical Care Medicine, Cook County Hospital, Cardiomyopathy,
Finch University of Health Science/Chicago Medical Dilated
School; Francisco Talavera, PharmD, PhD, Senior Pharmacy
Cardiomyopathy,
Editor, Pharmacy, eMedicine; Harold L Manning, MD, Associate Hypertrophic
Professor, Departments of Medicine, Anesthesiology, and Physio,
Section of Pulmonary and Critical Care Medicine, Dartmouth Medical Cor Pulmonale
School; Timothy D Rice, MD, Associate Professor, Departments of
Internal Medicine and Pediatrics and Adolescent Medicine, Saint Cyanosis
Louis University School of Medicine; and Zab Mohsenifar, MD,
Director, Division of Pulmonary/Critical Care Medicine, Department of Diaphragmatic
Medicine, Cedars-Sinai Medical Center; Professor, Department of Paralysis
Internal Medicine, University of California at Los Angeles School of
Medicine Emphysema
INTRODUCTION Section 2 of 11 Myocardial

Infarction
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-
Myocardial
Ischemia
Background: Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas exchange functions: Pneumonia,
oxygenation and carbon dioxide elimination. In practice, respiratory Aspiration
failure is defined as a PaO2 value of less than 60 mm Hg while
breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, Pneumonia,
Bacterial
respiratory failure may be acute or chronic. While acute respiratory
failure is characterized by life-threatening derangements in arterial Pneumonia,
blood gases and acid-base status, the manifestations of chronic Community-
respiratory failure are less dramatic and may not be as readily Acquired
apparent.
Pneumonia, Viral
Classification of respiratory failure
Pneumothorax
Respiratory failure may be classified as hypoxemic or hypercapnic Pulmonary Edema,
and may be either acute or chronic. Cardiogenic
Hypoxemic respiratory failure (type I) is characterized by a PaO 2 of Pulmonary Edema,

less than 60 mm Hg with a normal or low PaCO2. This is the most Neurogenic
common form of respiratory failure, and it can be associated with
Pulmonary
virtually all acute diseases of the lung, which generally involve fluid Embolism
filling or collapse of alveolar units. Some examples of type I
respiratory failure are cardiogenic or noncardiogenic pulmonary Pulmonary Fibrosis,
edema, pneumonia, and pulmonary hemorrhage. Idiopathic
Hypercapnic respiratory failure (type II) is characterized by a Pulmonary Fibrosis,

Interstitial
PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients
(Nonidiopathic)
with hypercapnic respiratory failure who are breathing room air. The
pH depends on the level of bicarbonate, which, in turn, is dependent Pulmonary
on the duration of hypercapnia. Common etiologies include drug Hypertension,
overdose, neuromuscular disease, chest wall abnormalities, and Primary
severe airway disorders (eg, asthma, chronic obstructive pulmonary
disease [COPD]). Pulmonary
Hypertension,
Secondary
Distinctions between acute and chronic respiratory failure
Respiratory
Acute hypercapnic respiratory failure develops over minutes to hours; Acidosis
therefore, pH is less than 7.3. Chronic respiratory failure develops
over several days or longer, allowing time for renal compensation and Restrictive Lung
an increase in bicarbonate concentration. Therefore, the pH usually is Disease
only slightly decreased.
Shock, Distributive
The distinction between acute and chronic hypoxemic respiratory Ventilation,
failure cannot readily be made on the basis of arterial blood gases. Mechanical
The clinical markers of chronic hypoxemia, such as polycythemia or
cor pulmonale, suggest a long-standing disorder. Ventilation,
Noninvasive
Pathophysiology: Respiratory failure can arise from an abnormality
in any of the components of the respiratory system, including the
airways, alveoli, CNS, peripheral nervous system, respiratory Continuing
muscles, and chest wall. Patients who have hypoperfusion secondary Education
to cardiogenic, hypovolemic, or septic shock often present with CME available for
respiratory failure. this topic.
Click here to take
Hypoxemic respiratory failure: The pathophysiologic mechanisms that this CME.
account for the hypoxemia observed in a wide variety of diseases are
ventilation-perfusion (V/Q) mismatch and shunt. These 2 Patient Education
mechanisms lead to widening of the alveolar-arterial oxygen Click here for
difference, which normally is less than 15 mm Hg. With V/Q patient education.
mismatch, the areas of low ventilation relative to perfusion (low V/Q
units) contribute to hypoxemia. An intrapulmonary or intracardiac
shunt causes mixed venous (deoxygenated) blood to bypass
ventilated alveoli and results in venous admixture. The distinction
between V/Q mismatch and shunt can be made by assessing the
response to oxygen supplementation or calculating the shunt fraction
following inhalation of 100% oxygen. In most patients with hypoxemic
respiratory failure, these 2 mechanisms coexist.
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
A decrease in alveolar ventilation can result from a reduction in

overall (minute) ventilation or an increase in the proportion of dead
space ventilation. A reduction in minute ventilation is observed
primarily in the setting of neuromuscular disorders and CNS
depression. In pure hypercapnic respiratory failure, the hypoxemia is
easily corrected with oxygen therapy.
Ventilatory capacity versus demand
Ventilatory capacity is the maximal spontaneous ventilation that can

be maintained without development of respiratory muscle fatigue.
Ventilatory demand is the spontaneous minute ventilation that results
in a stable PaCO2. Normally, ventilatory capacity greatly exceeds
ventilatory demand. Respiratory failure may result from either a
reduction in ventilatory capacity or an increase in ventilatory demand
(or both). Ventilatory capacity can be decreased by a disease process
involving any of the functional components of the respiratory system
and its controller. Ventilatory demand is augmented by an increase in
minute ventilation and/or an increase in the work of breathing.
Pathophysiologic Mechanisms in Acute Respiratory

Failure
The act of respiration engages 3 processes: (1) transfer of oxygen

across the alveolus, (2) transport of oxygen to the tissues, and (3)
removal of carbon dioxide from blood into the alveolus and then into
the environment. Respiratory failure may occur from malfunctioning of
any of these processes. In order to understand the pathophysiologic
basis of acute respiratory failure, an understanding of pulmonary gas
exchange is essential.
Physiology of gas exchange
Respiration primarily occurs at the alveolar capillary units of the

lungs, where exchange of oxygen and carbon dioxide between
alveolar gas and blood takes place. Following diffusion into the blood,
the oxygen molecules reversibly bind to the hemoglobin. Each
molecule of hemoglobin contains 4 sites for combination with
molecular oxygen, 1 g of hemoglobin combines with a maximum of
1.36 mL of oxygen. The quantity of oxygen combined with
hemoglobin depends on the level of blood PaO 2. This relationship,
expressed as the oxygen hemoglobin dissociation curve, is not linear,
but has a sigmoid-shaped curve with a steep slope between a
PaO2 of 10 and 50 mm Hg and a flat portion above a PaO 2 of 70 mm
Hg. The carbon dioxide is transported in 3 main forms: (1) in simple
solution, (2) as bicarbonate, and (3) combined with protein of
hemoglobin as a carbamino compound.
During ideal gas exchange, blood flow and ventilation would perfectly
match each other, resulting in no alveolar-arterial PO 2 difference.
However, even in normal lungs, not all alveoli are ventilated and
perfused perfectly. For a given perfusion, some alveoli are
underventilated while others are overventilated. Similarly, for known
alveolar ventilation, some units are underperfused while others are
overperfused. The optimally ventilated alveoli that are not perfused
well are called high V/Q units (acting like dead space), and alveoli
that are optimally perfused but not adequately ventilated are called
low V/Q units (acting like a shunt).
Alveolar ventilation
At steady state, the rate of carbon dioxide production by the tissues is

constant and equals the rate of carbon dioxide elimination by the
lung. This relationship is expressed as PaCO 2 = VCO2 x 0.862/Va.
This relationship signifies whether the alveolar ventilation is adequate
for metabolic needs of the body.
The efficiency of lungs at carrying out of respiration can be further

evaluated by measuring alveolar-to-arterial PaO 2 difference. This
difference is calculated by the following equation:
PaO2 = FIO2 x (PB ?PH2O) ?PaCO2/R
For the above equation, PaO2 = alveolar PO2, FIO2 = fractional

concentration of oxygen in inspired gas, PB = barometric pressure,
PH2O = water vapor pressure at 37 , PaCO2 = alveolar PCO2,
assumed to be equal to arterial PCO 2, and R = respiratory exchange
ratio. R depends on oxygen consumption and carbon dioxide
production. At rest, VCO2/VO2 is approximately 0.8.
Even normal lungs have some degree of V/Q mismatching and a

small quantity of right-to-left shunt, alveolar PO2 is slightly higher than
arterial PO2. However, an increase in alveolar-to-arterial PO2above
15-20 mm Hg indicates pulmonary disease as the cause of
hypoxemia.
Pathophysiologic causes of acute respiratory failure
Hypoventilation, V/Q mismatch, and shunt are the most common

pathophysiologic causes of acute respiratory failure. These are
described in the following paragraphs.
Hypoventilation is an uncommon cause of respiratory failure and

usually occurs from depression of the CNS from drugs or
neuromuscular diseases affecting respiratory muscles.
Hypoventilation is characterized by hypercapnia and hypoxemia. The
relationship between PaCO2 and alveolar ventilation is hyperbolic. As
ventilation decreases below 4-6 L/min, PaCO 2 rises precipitously.
Hypoventilation can be differentiated from other causes of hypoxemia
by the presence of a normal alveolar-arterial PO 2 gradient.
V/Q mismatch is the most common cause of hypoxemia. V/Q units

may vary from low to high ratios in the presence of a disease
process. The low V/Q units contribute to hypoxemia and hypercapnia
in contrast to high V/Q units, which waste ventilation but do not affect
gas exchange unless quite severe. The low V/Q ratio may occur
either from a decrease in ventilation secondary to airway or interstitial
lung disease or from overperfusion in the presence of normal
ventilation. The overperfusion may occur in case of pulmonary
embolism, where the blood is diverted to normally ventilated units
from regions of lungs that have blood flow obstruction secondary to
embolism. Administration of 100% oxygen eliminates all of the low
V/Q units, thus leading to correction of hypoxemia. As hypoxemia
increases the minute ventilation by chemoreceptor stimulation, the
PaCO2 level generally is not affected.
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. 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.
Anatomical shunt exists in normal lungs because of the bronchial and

thebesian circulations, accounting for 2-3% of shunt. A normal right-
to-left shunt may occur from atrial septal defect, ventricular septal
defect, patent ductus arteriosus, or arteriovenous malformation in the
lung. Shunt as a cause of hypoxemia is observed primarily in
pneumonia, atelectasis, and severe pulmonary edema of either
cardiac or noncardiac origin. Hypercapnia generally does not develop
unless the shunt is excessive (>60%). When compared to V/Q
mismatch, hypoxemia produced by shunt is difficult to correct by
oxygen administration.
Frequency:
In the US: Respiratory failure is a syndrome rather than a

single disease process, and the overall frequency of
respiratory failure is not well known. The estimates for
individual diseases mentioned here can be found in the
appropriate eMedicine article.
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.
CLINICAL Section 3 of 11
History: The diagnosis of acute or chronic respiratory failure begins

with clinical suspicion of its presence. Confirmation of the diagnosis is
based on arterial blood gas analysis. Evaluation of an underlying
cause must be initiated early, frequently in the presence of concurrent
treatment for acute respiratory failure.
The cause of respiratory failure often is evident after a careful

history and physical examination.
o Cardiogenic pulmonary edema usually develops in the

context of a history of left ventricular dysfunction or
valvular heart disease.
o A history of previous cardiac disease, recent symptoms

of chest pain, paroxysmal nocturnal dyspnea, and
orthopnea suggest cardiogenic pulmonary edema.
o Noncardiogenic edema (eg, acute respiratory distress

syndrome [ARDS]) occurs in typical clinical contexts
such as sepsis, trauma, aspiration, pneumonia,
pancreatitis, drug toxicity, and multiple transfusions.
Physical: The signs and symptoms of acute respiratory failure reflect

the underlying disease process and the associated hypoxemia or
hypercapnia. Localized pulmonary findings reflecting the acute cause
of hypoxemia, such as pneumonia, pulmonary edema, asthma, or
COPD, may be readily apparent. In patients with ARDS, the
manifestations may be remote from the thorax, such as abdominal
pain or long-bone fracture. Neurological manifestations include
restlessness, anxiety, confusion, seizures, or coma.
Asterixis may be observed with severe hypercapnia.

Tachycardia and a variety of arrhythmias may result from
hypoxemia and acidosis.
Once respiratory failure is suspected on clinical grounds,

arterial blood gas analysis should be performed to confirm the
diagnosis and to assist in the distinction between acute and
chronic forms. This helps assess the severity of respiratory
failure and also helps guide management.
Cyanosis, a bluish color of skin and mucous membranes,

indicates hypoxemia. Visible cyanosis typically is present when
the concentration of deoxygenated hemoglobin in the
capillaries or tissues is at least 5 g/dL.
Dyspnea, an uncomfortable sensation of breathing, often

accompanies respiratory failure. Excessive respiratory effort,
vagal receptors, and chemical stimuli (hypoxemia and/or
hypercapnia) all may contribute to the sensation of dyspnea.
Both confusion and somnolence may occur in respiratory

failure. Myoclonus and seizures may occur with severe
hypoxemia. Polycythemia is a complication of long-standing
hypoxemia.
Pulmonary hypertension frequently is present in chronic

respiratory failure. Alveolar hypoxemia potentiated by
hypercapnia causes pulmonary arteriolar constriction. If
chronic, this is accompanied by hypertrophy and hyperplasia
of the affected smooth muscles and narrowing of the
pulmonary arterial bed. The increased pulmonary vascular
resistance increases afterload of the right ventricle, which may
induce right ventricular failure. This, in turn, causes
enlargement of the liver and peripheral edema. The entire
sequence is known as cor pulmonale.
Criteria for the diagnosis of acute respiratory distress

syndrome
o Clinical presentation - Tachypnea and dyspnea;
crackles upon auscultation
o Clinical setting - Direct insult (aspiration) or systemic

process causing lung injury (sepsis)
o Radiologic appearance - Three-quadrant or 4-quadrant

alveolar flooding
o Lung mechanics - Diminished compliance (<40 mL/cm

water)
o Gas exchange - Severe hypoxia refractory to oxygen

therapy (PaO2/FIO2 <200)
o Normal pulmonary vascular properties - Pulmonary

capillary wedge pressure <18 mm Hg
Causes: These diseases can be grouped according to the primary

abnormality and the individual components of the respiratory system,
as follows:
Central nervous system disorders
o A variety of pharmacological, structural, and metabolic

disorders of the CNS are characterized by depression
of the neural drive to breathe.
o This may lead to acute or chronic hypoventilation and

hypercapnia.
o 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.
Disorders of the peripheral nervous system, respiratory

muscles, and chest wall
o These disorders lead to an inability to maintain a level

of minute ventilation appropriate for the rate of carbon
dioxide production.
o Concomitant hypoxemia and hypercapnia occur.

o Examples include Guillain-Barr?syndrome, muscular
dystrophy, myasthenia gravis, severe kyphoscoliosis,
and morbid obesity.
Abnormalities of the airways
o Severe airway obstruction is a common cause of acute

and chronic hypercapnia.
o Examples of upper airway disorders are acute

epiglottitis and tumors involving the trachea; lower
airway disorders include COPD, asthma, and cystic
fibrosis.
Abnormalities of the alveoli
o The diseases are characterized by diffuse alveolar

filling, frequently resulting in hypoxemic respiratory
failure, although hypercapnia may complicate the
clinical picture.
o 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
o Chronic bronchitis and emphysema (COPD)
o Pneumonia
o Pulmonary edema
o Pulmonary fibrosis
o Asthma
o Pneumothorax
o Pulmonary embolism
o Pulmonary arterial hypertension

o Pneumoconiosis
o Granulomatous lung diseases
o Cyanotic congenital heart disease
o Bronchiectasis
o Adult respiratory distress syndrome
o Fat embolism syndrome
o Kyphoscoliosis
o Obesity
Common causes of type II (hypercapnic) respiratory failure
o Chronic bronchitis and emphysema (COPD)
o Severe asthma
o Drug overdose
o Poisonings
o Myasthenia gravis
o Polyneuropathy
o Poliomyelitis
o Primary muscle disorders
o Porphyria
o Cervical cordotomy
o Head and cervical cord injury
o Primary alveolar hypoventilation
o Obesity hypoventilation syndrome

o Pulmonary edema
o Adult respiratory distress syndrome
o Myxedema
o Tetanus
DIFFERENTIALS Section 4 of 11
Acute Respiratory Distress Syndrome

Apnea, Sleep
Asthma
Atelectasis
Cardiogenic Shock
Cardiomyopathy, Diabetic
Cardiomyopathy, Dilated
Cardiomyopathy, Hypertrophic
Cor Pulmonale
Cyanosis
Diaphragmatic Paralysis
Emphysema
Myocardial Infarction
Myocardial Ischemia
Pneumonia, Aspiration
Pneumonia, Bacterial
Pneumonia, Community-Acquired
Pneumonia, Viral
Pneumothorax
Pulmonary Edema, Cardiogenic
Pulmonary Edema, Neurogenic
Pulmonary Embolism
Pulmonary Fibrosis, Idiopathic
Pulmonary Fibrosis, Interstitial (Nonidiopathic)
Pulmonary Hypertension, Primary
Pulmonary Hypertension, Secondary
Respiratory Acidosis
Restrictive Lung Disease
Shock, Distributive
Ventilation, Mechanical
Ventilation, Noninvasive
WORKUP Section 5 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
Lab Studies:
Respiratory failure may be associated with a variety of clinical manifestations.

However, these are nonspecific, and very significant respiratory failure may be
present without dramatic signs or symptoms. This emphasizes the importance of
measuring arterial blood gases in all patients who are seriously ill or in whom
respiratory failure is suspected.
A complete blood count may indicate anemia, which can contribute to tissue
hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory
failure.
A chemistry panel may be helpful in the evaluation and management of a patient

in 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 and other organ function.
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
o Chest radiography is essential because it frequently reveals the cause of

respiratory failure. However, distinguishing between cardiogenic and
noncardiogenic pulmonary edema often is difficult.
o 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.
Echocardiography
o 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.
o The findings of left ventricular dilatation, regional or global wall motion

abnormalities, or severe mitral regurgitation support the diagnosis of
cardiogenic pulmonary edema.
o A normal heart size and normal systolic and diastolic function in a patient
with pulmonary edema would suggest ARDS.
o Echocardiography provides an estimate of right ventricular function and

pulmonary artery pressure in patients with chronic hypercapnic respiratory
failure.
Other 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.
o Normal values of forced expiratory volume in one second (FEV 1) and

forced vital capacity (FVC) suggest a disturbance in respiratory control.
o A decrease in FEV1-to-FVC ratio indicates airflow obstruction, whereas a

reduction in both the FEV1 and FVC and maintenance of the FEV 1-to-FVC
ratio suggest restrictive lung disease.
o Respiratory failure is uncommon in obstructive diseases when the FEV 1 is

greater than 1 L and in restrictive diseases when the FVC is more than 1
L.
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.
Procedures:
Right heart catheterization

o This remains a controversial issue in the management of critically ill
patients.
o 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.
o Measurement of pulmonary capillary wedge pressure may be helpful in

distinguishing cardiogenic from noncardiogenic edema.
o The pulmonary capillary wedge pressure should be interpreted in the

context of serum oncotic pressure and cardiac function.
TREATMENT Section 6 of 11
Medical Care: Hypoxemia is the major immediate threat to organ function. Therefore,
the first objective in the management of respiratory failure is to reverse and/or prevent
tissue hypoxia. Hypercapnia unaccompanied by hypoxemia generally is well tolerated
and probably is not a threat to organ function unless accompanied by severe acidosis.
Many experts believe that hypercapnia should be tolerated until the arterial blood pH
falls below 7.2. Appropriate management of the underlying disease obviously is an
important component in the management of respiratory failure.
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.
Airway management
o Assurance of an adequate airway is vital in a patient with acute respiratory

distress.
o The most common indication for endotracheal intubation (ETT) is

o ETT serves as an interface between the patient and the ventilator.
o Another indication for ETT is airway protection in patients with altered

mental status.
Correction of hypoxemia
o After securing an airway, attention must turn to correcting the underlying

hypoxemia, the most life-threatening facet of acute respiratory failure.
o 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%.
o Supplemental oxygen is administered via nasal prongs or face mask;

however, in patients with severe hypoxemia, intubation and mechanical
ventilation often are required.
Coexistent hypercapnia and respiratory acidosis may need to be addressed. This

is done by correcting the underlying cause or providing ventilatory assistance.
o 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.
Ventilator management
o The use of mechanical ventilation during the polio epidemics of the 1950s
was the impetus that led to the development of the discipline of critical
care medicine.
o Prior to the mid 1950s, negative-pressure ventilation with the use of iron
lungs was the predominant method of ventilatory support.
o Currently, virtually all mechanical ventilatory support for acute respiratory

failure is provided by positive-pressure ventilation. Nevertheless, negative-
pressure ventilation still is used occasionally in patients with chronic
o Over the years, mechanical ventilators have evolved from simple

pressure-cycled machines to sophisticated microprocessor-controlled
systems. A brief review of mechanical ventilation is presented as follows.
Overview of mechanical ventilation
o Positive-pressure versus negative-pressure ventilation: In order for air to

enter the lungs, a pressure gradient must exist between the airway and
alveoli. This can be accomplished either by raising pressure at the airway
(positive-pressure ventilation) or by lowering pressure at the level of the
alveolus (negative-pressure ventilation). The iron lung or tank ventilator is
the most common type of negative-pressure ventilator used in the past.
These ventilators work by creating subatmospheric pressure around the
chest, thereby lowering pleural and alveolar pressure, and thus facilitating
flow of air into the patient's lungs. These ventilators are bulky, poorly
tolerated, and are not suitable for use in modern critical care units.
Positive-pressure ventilation can be achieved by an endotracheal or
tracheostomy tube or noninvasively through a nasal mask or face mask.
o Controlled versus patient-initiated (ie, assisted): Ventilatory assistance can

be controlled (AC) or patient-initiated. In controlled modes of ventilation,
the ventilator delivers assistance independent of the patient' s own
spontaneous inspiratory efforts. In contrast, during patient-initiated modes
of ventilation, the ventilator delivers assistance in response to the patient'
s own inspiratory efforts. The patient' s inspiratory efforts can be sensed
either by pressure or flow-triggering mechanisms (see Triggering
mechanism).
o Pressure-targeted versus volume-targeted: During positive-pressure

ventilation, either pressure or volume may be set as the independent
variable. In volume-targeted (or volume preset) ventilation, tidal volume is
the independent variable set by the physician and/or respiratory therapist,
and airway pressure is the dependent variable. In volume-targeted
ventilation, airway pressure is a function of the set tidal volume and
inspiratory flow rate, the patient' s respiratory mechanics (compliance and
resistance), and the patient' s respiratory muscle activity. In pressure-
targeted (or pressure preset) ventilation, airway pressure is the
independent variable and tidal volume is the dependent variable. The tidal
volume during pressure-targeted ventilation is a complex function of
inspiratory time, the patient' s respiratory mechanics, and the patient' s
own respiratory muscle activity.
Interface between patient and ventilator (mask vs endotracheal intubation)
o 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 (covering both the nose and mouth) or a nasal
mask (see Noninvasive ventilatory support).
o Care of an endotracheal tube includes correct placement of the tube,

maintenance of proper cuff pressure, and suctioning to maintain a patent
airway.
o Following intubation, the position of the tube in the airway (rather than
esophagus) 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). Confirming proper placement of the
endotracheal tube with a chest radiograph is recommended.
o The tube should be secured to prevent accidental extubation or migration

into the mainstem bronchus, and the endotracheal tube cuff pressure
should be monitored periodically. The pressure in the cuff generally should
not exceed 25 mm Hg.
o Endotracheal suctioning can be accomplished by either open-circuit or

closed-circuit suction catheters. Routine suctioning is not recommended
because suctioning may be associated with a variety of complications,
including desaturation, arrhythmias, bronchospasm, severe coughing, and
introduction of secretions into the lower respiratory tract.
Specific modes of ventilatory support
o Pressure support ventilation (PSV): PSV can be categorized as patient-

initiated, pressure-targeted ventilation. With PSV, ventilatory assistance
occurs only in response to the patient' s spontaneous inspiratory efforts.
With each inspiratory effort, the ventilator raises airway pressure by a
preset amount. When the inspiratory flow rate decays to a minimal level or
to a percentage of initial inspiratory flow (eg, 25% of peak flow), inspiration
is terminated. During PSV, the patients are free to choose their own
respiratory rate; inspiratory time, inspiratory flow rate, and tidal volume are
determined, in part, by the patient' s respiratory efforts. This mode of
ventilation should not be used in patients with unstable ventilatory drive,
and care must be exercised when the patient's respiratory mechanics are
changing because of bronchospasm, secretions, or varying levels of auto
ositive end-expiratory pressure (auto-PEEP).
o Intermittent mandatory ventilation (IMV): IMV is a mode whereby

mandatory breaths are delivered at a set frequency, tidal volume, and
inspiratory flow rate. However, the patient can breathe spontaneously
between the machine-delivered breaths. Most modern ventilators have
synchronized IMV (SIMV), whereby the ventilator attempts to deliver the
mandatory breaths in synchrony with the patient's own inspiratory efforts.
In essence, the ventilator allows the patient an opportunity to breathe. If
the patient makes an inspiratory effort during a window of time determined
by the IMV rate, the ventilator delivers a mandatory breath in response to
the patient' s inspiratory effort. However, if no inspiratory effort is detected
by the ventilator, a time-triggered breath is delivered. Compared to IMV,
SIMV may improve patient comfort and may limit dynamic hyperinflation,
which may occur when a preset breath is delivered immediately after the
patient' s spontaneous inspiratory effort (ie, prior to exhalation).
o Assist-control ventilation: In assist-control ventilation, patients receive a

fixed tidal volume and inspiratory flow rate with each inspiratory effort,
regardless of their respiratory rate. However, a ack-up rate" is selected
that guarantees that the patient receives a minimum number of breaths
per minute. If the patient' s respiratory rate falls below the back-up rate,
the ventilator delivers the number of breaths necessary to reach the back-
up rate; such breaths are delivered independently of any inspiratory effort
by the patient.
o Volume-control: In this mode, respiratory rate, tidal volume, and inspiratory

flow rate (or inspiratory time) are fixed. This mode is used most often in
heavily sedated or paralyzed patients.
o Pressure-control: In contrast to volume control, in pressure-control mode,

airway pressure is raised by a set amount at a fixed number of times per
minute. The physician or respiratory therapist also sets the inspiratory-to-
expiratory (I:E) ratio or the inspiratory time. This mode is used most often
in heavily sedated or paralyzed patients.
o Pressure-control inverse-ratio ventilation (PCIRV): PCIRV is a variation of

simple pressure-control ventilation. In this mode, inspiration is set to be
longer than expiration. The I:E ratio should rarely, if ever, exceed 3:1.
Triggering mechanism: pressure versus flow triggering
o In patient-initiated (assisted) ventilation, the ventilator must sense the

patient' s inspiratory effort in order to deliver assistance. Ventilator
triggering may be based on either a pressure or a flow change.
o With pressure-triggering, the ventilator is set to detect a certain change in

pressure. The ventilator is triggered whenever airway pressure drops by
the set amount. For example, in a patient on no positive end-expiratory
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.
o In flow-triggering, a continuous flow of gas is sent through the ventilator

circuit. In some ventilators, this continuous flow rate may be set by the
physician or respiratory therapist, whereas in other ventilators, the
continuous flow rate is fixed. A flow sensitivity is selected, and the
ventilator senses the patient' s inspiratory efforts by detecting a change in
flow. When the patient makes an inspiratory effort, some of the gas that
was previously flowing continuously through the circuit is diverted to the
patient. 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.
Positive end-expiratory pressure
o By maintaining airway (and hence alveolar) pressure greater than zero,

PEEP may recruit atelectatic alveoli and prevent their collapse during the
succeeding expiration. PEEP also 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.
o In patients with disorders such as ARDS or acute lung injury, PEEP is

applied to recruit atelectatic alveoli, thereby improving oxygenation and
allowing a reduction in FiO2 to nontoxic levels (FiO2 <0.6). Applying PEEP
of 3-5 cm water to prevent a decrease in functional residual capacity in
patients with normal lungs is a common practice.
o PEEP causes an increase in intrathoracic pressure, which may decrease

venous return and cardiac output, particularly in patients with
hypovolemia.
Inspiratory flow
o 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.
o 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.
o 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.
Determinants of ventilator-associated lung injury
o Mechanical ventilation is associated with a variety of insults to the lung.
o 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. For example, the earliest sign of
pneumothorax in supine patients may be the deep-sulcus sign or a
collection of air anteriorly along cardiophrenic angle.
o More recently, lung damage indistinguishable from ARDS has been

recognized to possibly be caused by certain patterns of ventilatory
support. Early experiments in animals showed that mechanical ventilation
employing high peak airway pressures and high tidal volume led to the
formation of pulmonary edema. 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 ventilator-associated lung
injury.
o 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.
Mechanical ventilation in specific diseases
o 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.
o 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.
o Acute respiratory distress syndrome
The primary objective is to accomplish adequate gas exchange

while avoiding excessive inspired oxygen concentrations and
alveolar overdistension.
The traditional ventilatory strategy of delivering high tidal volumes

leads to high end-inspiratory alveolar pressures (ie, plateau
pressure).
Many investigators currently believe that repeated cycles of

opening and collapsing of inflamed and atelectatic alveoli are
detrimental to the lung. Failure to maintain a certain minimum
alveolar volume may further accentuate the lung damage.
Furthermore, transalveolar pressure (reflected by plateau pressure)
exceeding 25-30 cm water is considered to be an important risk
factor for stretch injury to the lungs.
Patients with ARDS should be targeted to receive a tidal volume of

6 mL/kg. Importantly, remember that 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.
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.
o 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 (because of decreased
venous return) 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 and its associated adverse consequences.
Following the initiation of mechanical ventilation, patients with

status asthmaticus frequently develop severe dynamic
hyperinflation, which often is associated with adverse
hemodynamic effects. The development of dynamic hyperinflation
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.
In the absence of hypoxia, hypercapnia generally is well tolerated in

most patients. Even marked levels of hypercapnia are preferable to
attempts 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.
If a decision is made to measure trapped-gas volume (VEI), as

recommended by some investigators, an attempt should be made
to keep it below 20 mL/kg. The routine measurement of VEI is not
recommended because measurement of plateau pressure and
auto-PEEP provide similar information and are much easier to
perform.
Patients with COPD have expiratory flow limitation and are prone to
the development of dynamic hyperinflation. Here again, the 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. Care must be exercised to avoid causing further
hyperinflation, and the set level of PEEP should always be less
than the level of auto-PEEP.
Facilitating patient-ventilator synchrony
o During mechanical ventilation, many patients sometimes 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.
o In order 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 espiratory
clock" switches to expiration. Asynchronous interactions, commonly
referred to as ighting 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.
o Patient-ventilator asynchrony should be minimized, and a variety of ways

is available to achieve this. Modern ventilators are equipped with
significantly better valve characteristics compared to older-generation
ventilators. Flow-triggering (with a continuous flow rate) appears to be
more sensitive and more responsive to patients' spontaneous inspiratory
efforts.
o Patient-ventilator asynchrony often occurs in the presence of auto-PEEP.

Auto-PEEP creates an inspiratory threshold load and thereby decreases
the effective trigger sensitivity. This may be partially offset by the
application of external PEEP.
o Sometimes, additional sedation may be necessary to achieve adequate

patient-ventilator synchrony.
Noninvasive ventilatory support
o The application of ventilatory support through a nasal or full face mask in

lieu of ETT is being used increasingly for patients with acute or chronic
o Noninvasive ventilation should be considered in patients with mild-to-

moderate acute respiratory failure. The patient should have an intact
airway, airway-protective reflexes, and be alert enough to follow
commands.
o In clinical trials, noninvasive positive-pressure ventilation (NPPV) has

proven beneficial in acute exacerbations of COPD and asthma,
decompensated CHF with mild-to-moderate pulmonary edema, and
pulmonary edema from hypervolemia. Reports conflict regarding its
efficacy in acute hypoxemia due to other causes (eg, pneumonia). A
variety of methods and systems are available for delivering noninvasive
ventilatory support.
o The benefits of NPPV depend on the underlying cause of respiratory

failure. 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.
o In a large randomized trial (Brochard 1995) comparing NPPV with a

standard ICU approach, 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%).
o Plant and colleagues recently published the largest prospective

randomized study comparing NPPV to standard treatment in patients with
COPD exacerbation. NPPV was administered on the ward; the nurses
were trained for 8 hours in the preceding 3 months. Treatment failed in
significantly more patients in the control group (27% vs 15%), and in-
hospital mortality rates were significantly reduced by NPPV (20% to 10%).
o In addition, 3 Italian cohort studies with historical or matched control

groups have suggested that long-term outcome of patients treated with
NPPV is better than that of patients treated with medical therapy and/or
endotracheal intubation.
o In acute hypoxemic respiratory failure, NPPV also helps maintain an

adequate PaO2 until the patient improves.
o In cardiogenic pulmonary edema, NPPV improves oxygenation, reduces

work of breathing, and may increase cardiac output.
o 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.
o Patients with obesity-hypoventilation syndrome benefit from NPPV by

reversal of the alveolar hypoventilation and upper airway obstruction.
o Most studies have used NPPV as an intermittent rather than continuous

mode of support. 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
o 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. In patients who required more prolonged respiratory
therapy, the process of liberating the patient from ventilatory support may
take much longer.
o 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.
o 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.
o 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.
o 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.
o SIMV appears to result in less rapid weaning than PSV or trials of

spontaneous breathing.
o Patient-ventilator desynchrony is an important component in a carefully

designed weaning protocol.
o Attention must be directed towards patient comfort, avoidance of fatigue,

adequate nutrition, and prevention and treatment of medical complications
during the weaning period.
o 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.
Monitoring of patients with acute respiratory failure
o A patient with respiratory failure requires repeated assessments, which

may range from bedside observations to the use of invasive monitoring.
o 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.
o Cardiac monitoring, blood pressure, pulse oximetry, SaO 2, 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 FiO 2 to a value less
than 0.6, and the PaCO2 guides adjustments of minute ventilation.
Treatment of underlying cause
o 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.
o The specific treatment depends on the etiology of respiratory failure.
o In Medications, a brief discussion of medications used to treat common

causes of respiratory failure, such as cardiogenic pulmonary edema,
chronic obstructive pulmonary disease, and asthma, is provided.
o The reader is recommended to review the article specific to the disease

for the workup and management of the various disorders, all of which
progress by different means but ultimately converge on a final common
pathway of respiratory failure.
Consultations:
Consultation with a pulmonary specialist and an intensivist often are required.
Patients with acute respiratory failure or exacerbations of chronic respiratory

failure need to be admitted to the intensive care unit for ventilatory support.
Activity:
Patients generally are prescribed bed rest during early phases of respiratory
failure management. However, ambulation as soon possible helps ventilate
atelectatic areas of the lung.
MEDICATION Section 7 of 11
The pharmacotherapy of cardiogenic pulmonary edema and acute exacerbations of

COPD are discussed here. The goal of therapy in cardiogenic pulmonary edema is to
achieve a pulmonary capillary wedge pressure of 15-18 mm Hg and a cardiac index
greater than 2.2 L/min/m2, while maintaining adequate blood pressure and organ
perfusion. These goals may need to be modified for some patients. Diuretics, nitrates,
analgesics, and inotropic agents are used in the treatment of acute pulmonary edema.
Drug Category: Diuretics -- First-line therapy generally includes a loop diuretic such
as furosemide, which inhibits sodium chloride reabsorption in the ascending loop of
Henle.
Furosemide (Lasix) -- Administer loop diuretics
IV because this allows for both superior potency
Drug Name and a higher peak concentration despite increased
incidence of adverse effects, particularly
ototoxicity.
10-20 mg IV for patients symptomatic with CHF
not already using diuretics
40-80 mg IV for patients already using diuretics
80-120 mg IV for patients whose symptoms are
Adult Dose refractory to initial dose after 1 h of
administration or who have significant renal
insufficiency
Higher doses and more rapid redosing may be
appropriate for patients in severe distress
Pediatric Dose Not established
Documented hypersensitivity, hepatic coma,
Contraindications
anuria, state of severe electrolyte depletion
Metformin decreases concentrations; conversely,
furosemide interferes with the hypoglycemic
effect of antidiabetic agents; also antagonizes
muscle-relaxing effect of tubocurarine
Auditory toxicity appears to be increased with
Interactions concurrent use of aminoglycoside and furosemide;
hearing loss of varying degrees may occur
Anticoagulant activity of warfarin may be
enhanced when taken concurrently
Increased plasma lithium levels and toxicity are
possible when taken concurrently
C - Safety for use during pregnancy has not been
Pregnancy
established.
Monitor for electrolyte imbalance; caution with
Precautions
coadministration of nephrotoxic drugs
Metolazone (Mykrox, Zaroxolyn) -- Metolazone
has been used as adjunctive therapy in patients
initially refractory to furosemide. It has been
demonstrated to be synergistic with loop diuretics
in treating refractory patients and causes a greater
Drug Name
loss of potassium. Potent loop diuretic that
sometimes is used in combination with Lasix for
more aggressive diuresis. Also used in patients
with a degree of renal dysfunction for initiating
diuresis.
Adult Dose 5-10 mg PO before redosing with furosemide
Documented hypersensitivity, hepatic coma,
Contraindications
encephalopathy, anuria
Thiazides may decrease effect of anticoagulants,
sulfonylureas, and gout medications;
anticholinergics and amphotericin B may increase
toxicity of thiazides; effects of thiazides may
decrease when used concurrently with bile acid
Interactions sequestrants, NSAIDs, and methenamine
When coadministered, thiazides increase toxicity
of anesthetics, diazoxide, digitoxin, lithium, loop
diuretics, antineoplastics, allopurinol, calcium
salts, vitamin D, and nondepolarizing muscle
relaxants
Pregnancy D - Unsafe in pregnancy
Exercise caution with hepatic and renal disease,
Precautions diabetes mellitus, gout, and systemic lupus
erythematosus
Drug Category: Nitrates -- These agents reduce myocardial oxygen demand by

lowering preload and afterload. In severely hypertensive patients, nitroprusside causes
more arterial dilatation than nitroglycerin. Nevertheless, due to the possibility of
thiocyanate toxicity and the coronary steal phenomenon associated with nitroprusside,
IV nitroglycerin may be the initial therapy of choice for afterload reduction.
Nitroglycerin (Nitro-Bid, Nitrol) -- SL

nitroglycerin and Nitrospray are particularly
useful in the patient who presents with acute
pulmonary edema with a systolic blood pressure
of at least 100 mm Hg. Similar to SL, onset of
Nitrospray is 1-3 min, with a half-life of 5 min.
Administration of Nitrospray may be easier, and it
can be stored for as long as 4 y. One study
demonstrated significant and rapid hemodynamic
Drug Name improvement in 20 patients with pulmonary
edema who were given Nitrospray. Topical nitrate
therapy is reasonable in a patient presenting with
class I-II CHF. However, in patients with more
severe signs of heart failure or pulmonary edema,
IV nitroglycerin is preferred because it is easier to
monitor hemodynamics and absorption,
particularly in patients with diaphoresis. Oral
nitrates, due to delayed absorption, play little role
in the management of acute pulmonary edema.
Adult Dose Nitrospray: 1 puff (0.4 mg) equivalent to a single
1/150 SL; may repeat q3-5min as hemodynamics
permit, not to exceed 1.2 mg
Ointment: Apply 1-2 inches of nitropaste to chest
wall
Injection: start at 20 mcg/min IV and titrate to
effect in 5- to 10-mcg increments q3-5min
Documented hypersensitivity, severe anemia,
Contraindications shock, postural hypotension, head trauma, closed-
angle glaucoma, cerebral hemorrhage
Aspirin may increase nitrate serum
concentrations; marked symptomatic orthostatic
Interactions hypotension may occur when coadministered with
calcium channel blockers, adjustment in dose of
either agent may be necessary
Pregnancy
established.
Caution in coronary artery disease and low
Precautions
systolic blood pressure
Nitroprusside sodium (Nitropress) -- Produces
vasodilation of venous and arterial circulation. At
Drug Name
higher dosages, may exacerbate myocardial
ischemia by increasing heart rate. Easily titratable.
10-15 mcg/min; titrate to effective dose range of
Adult Dose 30-50 mcg/min and a systolic blood pressure of at
least 90 mm Hg
Documented hypersensitivity, subaortic stenosis,
Contraindications optic atrophy, tobacco amblyopia, idiopathic
hypertrophic, atrial fibrillation or flutter
Patients receiving other hypertensive therapy may
Interactions
be more sensitive to sodium nitroprusside
Pregnancy
established.
Exercise caution with increased intracranial
pressure, hepatic failure, severe renal impairment,
and hypothyroidism.
In renal or hepatic insufficiency, levels may
Precautions
increase and can cause cyanide toxicity
Has potent effects on blood pressure (use only in
those patients with mean arterial pressures >70
mm Hg)
Drug Category: Analgesics -- Morphine IV is an excellent adjunct in the management

of acute pulmonary edema. In addition to being both an anxiolytic and an analgesic, its
most important effect is venodilation, which reduces preload. Also causes arterial
dilatation, which reduces systemic vascular resistance and may increase cardiac output.
Morphine sulfate (Duramorph, Astramorph, MS

Contin) -- DOC for narcotic analgesia due to
reliable and predictable effects, safety profile, and
Drug Name ease of reversibility with naloxone. Morphine
sulfate administered IV may be dosed in a number
of ways and commonly is titrated until desired
effect is obtained.
2-5 mg and repeated q10-15min unless respiratory
Adult Dose rate is <20 breaths per min or systolic blood
pressure is <100 mm Hg
Documented hypersensitivity, hypotension,
potentially compromised airway with uncertain
Contraindications
rapid airway control, respiratory depression,
nausea, emesis, constipation, urinary retention
Phenothiazine may antagonize analgesic effects of
opiate agonists; tricyclic antidepressants, MAOIs,
Interactions altered mental status, and other CNS depressants
may potentiate adverse effects of morphine when
used concurrently
Pregnancy
established.
Exercise caution with atrial flutter and other
supraventricular tachycardias; morphine has
vagolytic action and may increase the ventricular
Precautions
response rate; due to addictive nature, abuse also
is a possibility, although this is not a significant
concern in a critically ill patient
Drug Category: Inotropic agents -- Principal inotropic agents include dopamine,

dobutamine, inamrinone (formerly amrinone), milrinone, dopexamine, and digoxin. In
patients with hypotension presenting with CHF, dopamine and dobutamine usually are
employed. Inamrinone and milrinone inhibit phosphodiesterase, resulting in an increase
of intracellular cyclic AMP and alteration in calcium transport. As a result, they increase
cardiac contractility and reduce vascular tone by vasodilatation.
Drug Name Dopamine (Intropin) -- Stimulates both adrenergic

and dopaminergic receptors. Hemodynamic
effects depend on the dose. Lower doses stimulate
mainly dopaminergic receptors that produce renal
and mesenteric vasodilation. Cardiac stimulation
and renal vasodilation are produced by higher
doses. Positive inotropic agent at 2-10
mcg/kg/min that can lead to tachycardia,
ischemia, and dysrhythmias. Doses >10
mcg/kg/min cause vasoconstriction, which
increases afterload.
5 mcg/kg/min and increase at increments of 5
Adult Dose
mcg/kg/min to a dose of 20 mcg/kg/min
Documented hypersensitivity,
Contraindications
pheochromocytoma, ventricular fibrillation
Phenytoin, alpha- and beta-adrenergic blockers,
Interactions general anesthesia, and MAOIs increase and
prolong effects, thus, lower dosage
Pregnancy
established.
Closely monitor urine flow, cardiac output,
pulmonary wedge pressure, and blood pressure
during infusion; prior to infusion, correct
Precautions hypovolemia with either whole blood or plasma,
as indicated; monitoring of central venous
pressure or left ventricular filling pressure may be
helpful in detecting and treating hypovolemia
Dobutamine (Dobutrex) -- Produces vasodilation
and increases inotropic state. At higher dosages,
may cause increased heart rate, thus exacerbating
Drug Name
myocardial ischemia. Strong inotropic agent with
minimal chronotropic effect and no
vasoconstriction.
2.5 mcg/kg/min initially; generally therapeutic in
Adult Dose
the range of 10-40 mcg/kg/min
Documented hypersensitivity, idiopathic
Contraindications hypertrophic subaortic stenosis, atrial fibrillation
or flutter
Beta-adrenergic blockers antagonize effects of
Interactions nitroprusside; general anesthetics may increase
toxicity
Pregnancy
established.
Precautions Following an MI, use dobutamine with caution;
correct hypovolemia before using
Drug Category: Bronchodilators -- Bronchodilators are an important component of

treatment in respiratory failure caused by obstructive lung disease. These agents act to
decrease muscle tone in both small and large airways in the lungs. This category
includes beta-adrenergics, methylxanthines, and anticholinergics.
Terbutaline (Brethaire, Bricanyl) -- Acts directly

on beta2-receptors to relax bronchial smooth
Drug Name
muscle, relieving bronchospasm and reducing
airway resistance.
0.25 mg (0.25 cc of 1-mg/mL concentration) SC;
Adult Dose
not to exceed 0.5 mg SC q4h
Documented hypersensitivity, tachycardia
Contraindications
resulting from cardiac arrhythmias
Concomitant use with beta-blockers may inhibit
bronchodilatory, cardiac, and vasodilatory effects
of beta-agonists; coadministration of MAOIs with
beta-sympathomimetics may result in severe
hypertension, headache, and hyperpyrexia, which
Interactions may result in a hypertensive crisis
MAOIs also may potentiate activity of beta-
adrenergic agonists on vascular system
Coadministration of oxytocic drugs (eg,
ergonovine with terbutaline) may result in severe
hypotension
B - Usually safe but benefits must outweigh the
Pregnancy
risks.
Caution in coronary disease; through intracellular
shifts, may decrease serum potassium levels,
Precautions which can produce adverse cardiovascular effects;
however, decrease usually is transient and may
not require supplementation
Albuterol (Proventil) -- Beta-agonist useful in the
treatment of bronchospasm. Selectively stimulate
beta2-adrenergic receptors of the lungs.
Drug Name
Bronchodilation results from relaxation of
bronchial smooth muscle, which relieves
bronchospasm and reduces airway resistance.
5 mg/mL of solution for nebulization, usually
Adult Dose mixed as 0.5-1 cc with 2.5 cc of water and
nebulized prn in acute setting
Documented hypersensitivity to albuterol,
Contraindications
adrenergic amines, or related products
Beta-adrenergic blockers antagonize effects;
inhaled ipratropium may increase duration of
bronchodilation induced by albuterol;
Interactions cardiovascular effects may increase when
coadministered with MAOIs, inhaled anesthetics,
tricyclic antidepressants, and sympathomimetic
agents
Pregnancy
established.
Caution in hyperthyroidism, diabetes mellitus, or
Precautions
cardiovascular disorders
Theophylline (Theo-Dur, Slo-bid, Theo-24) -- Has
a number of physiological effects, including
increases in collateral ventilation, respiratory
muscle function, mucociliary clearance, and
central respiratory drive. Partially acts by
Drug Name
inhibiting phosphodiesterase, elevating cellular
cyclic AMP levels, or antagonizing adenosine
receptors in the bronchi, resulting in relaxation of
smooth muscle. However, clinical efficacy is
controversial, especially in the acute setting.
Target concentration: 10 mcg/mL
Dosing = (target concentration - current level) x
Adult Dose 0.5 (ideal body weight); alternatively, 1 mg/kg
results in approximately 2 mcg/mL increase in
serum levels
Documented hypersensitivity to theophylline,
Contraindications xanthines, or related products; uncontrolled
arrhythmias; hyperthyroidism
Aminoglutethimide, barbiturates, carbamazepine,
ketoconazole, loop diuretics, charcoal, hydantoins,
phenobarbital, phenytoin, rifampin, isoniazid, and
sympathomimetics may decrease effects; effects
may be increased by coadministration with
Interactions
allopurinol, beta-blockers, ciprofloxacin,
corticosteroids, disulfiram, quinolones, thyroid
hormones, ephedrine, carbamazepine, cimetidine,
erythromycin, macrolides, propranolol, and
interferon
Pregnancy
established.
Caution in tachyarrhythmias, hyperthyroidism,
and patients with compromised cardiac function;
do not inject IV solution faster than 25 mg/mm;
Precautions
patients diagnosed with pulmonary edema or liver
dysfunction are at greater risk of toxicity because
of reduced drug clearance
Ipratropium bromide (Atrovent) -- Anticholinergic
medication that appears to inhibit vagally
mediated reflexes by antagonizing action of
acetylcholine, specifically with the muscarinic
Drug Name receptor on bronchial smooth muscle. Vagal tone
can be significantly increased in COPD; therefore,
this can have a profound effect. Dose can be
combined with a beta-agonist because ipratropium
may require 20 min to begin having an effect.
Adult Dose 0.5 mg/nebulizer treatment
Contraindications Documented hypersensitivity
Albuterol and ipratropium together are more
efficacious than either one alone
Interactions
Drugs with anticholinergic properties (eg,
dronabinol) may increase toxicity
B - Usually safe but benefits must outweigh the
Pregnancy
risks.
Not indicated for initial treatment of acute
episodes of bronchospasm; caution in narrow-
Precautions
angle glaucoma, prostatic hypertrophy, and
bladder neck obstruction
Drug Category: Corticosteroids -- Have been shown to be effective in accelerating

recovery from acute COPD exacerbations and are an important anti-inflammatory
therapy in asthma. While they may not make a clinical difference in the ED, they have
some effect 6-8 h into therapy; therefore, early dosing is critical.
Methylprednisolone (Solu-Medrol, Depo-Medrol)

-- Usually given IV in ED for initiation of
Drug Name
corticosteroid therapy, although PO should
theoretically be equally efficacious.
The optimal dosage is uncertain
Adult Dose 125 mg IV q6h often administered for the first 24-
48 hours of therapy
Contraindications Documented hypersensitivity; viral, fungal, or
tubercular skin infections
Clearance may decrease when coadministered
with estrogens; when coadministered with
digoxin, may increase digitalis toxicity secondary
to hypokalemia; phenobarbital, phenytoin, and
Interactions
rifampin also may increase metabolism of
glucocorticoids; therefore, consider increasing
maintenance dose; monitor patients for
hypokalemia with concurrent use of diuretics
Pregnancy
established.
Hyperglycemia, edema, osteonecrosis, peptic
ulcer disease, hypokalemia, osteoporosis,
Precautions euphoria, psychosis, growth suppression,
myopathy, and infections are possible
complications of glucocorticoid use
FOLLOW-UP Section 8 of 11
Complications:
Pulmonary
o Common pulmonary complications of acute respiratory failure include

pulmonary embolism, barotrauma, pulmonary fibrosis, and complications
secondary to the use of mechanical devices.
o Patients also are prone to develop nosocomial pneumonia.
o Regular assessment should be performed by periodic radiographic chest

monitoring.
o Pulmonary fibrosis may follow acute lung injury associated with ARDS.
o High oxygen concentrations and the use of large tidal volumes may
worsen acute lung injury.
Cardiovascular
o Common cardiovascular complications in patients with acute respiratory

failure include hypotension, reduced cardiac output, arrhythmia,
pericarditis, and acute myocardial infarction.
o These complications may be related to the underlying disease process,

mechanical ventilation, or the use of pulmonary artery catheters.
Gastrointestinal
o The major gastrointestinal complications associated with acute respiratory

failure are hemorrhage, gastric distention, ileus, diarrhea, and
pneumoperitoneum.
o Stress ulceration is common in patients with acute respiratory failure; the

incidence can be reduced by routine use of antisecretory agents or
mucosal protectants.
Infectious
o Nosocomial infections, such as pneumonia, urinary tract infections, and

catheter-related sepsis, are frequent complications of acute respiratory
failure.
o These usually occur with the use of mechanical devices.
o The incidence of nosocomial pneumonia is high and associated with

significant mortality.
Renal
o Acute renal failure and abnormalities of electrolytes and acid-base

homeostasis are common in critically ill patients with respiratory failure.
o The development of acute renal failure in a patient with acute respiratory

failure carries a poor prognosis and high mortality. The most common
mechanisms of renal failure in this setting are renal hypoperfusion and the
use of nephrotoxic drugs (including radiographic contrast material).
Nutritional
o These include malnutrition and its effects on respiratory performance and

complications related to administration of enteral or parenteral nutrition.
o Complications associated with nasogastric tubes, such as abdominal

distention and diarrhea, also may occur.
o Complications of parenteral nutrition may be mechanical due to catheter

insertion, infectious, or metabolic (eg, hypoglycemia, electrolyte
imbalance).
Prognosis:
The mortality rate for ARDS is approximately 40%. Younger patients (<60 y) have
better survival rates than older patients. Approximately two thirds of patients who
survive an episode of ARDS manifest some impairment of pulmonary function 1
or more years after recovery.
Significant mortality also occurs in patients admitted with hypercapnic respiratory

failure. This is because these patients have a chronic respiratory disorder and
other comorbidities such as cardiopulmonary, renal, hepatic, or neurologic
disease. These patients also may have poor nutritional status. For patients with
COPD and acute respiratory failure, the overall mortality rate has declined from
approximately 26% to 10%.
MISCELLANEOUS Section 9 of 11
Medical/Legal Pitfalls:
Risks of oxygen therapy are oxygen toxicity and carbon dioxide narcosis.
Pulmonary oxygen toxicity rarely occurs when an FiO2 of less than 0.6 is used;
therefore, an attempt to lower the inspired oxygen concentration to this level
should be made in critically ill patients.
Carbon dioxide narcosis occasionally occurs when some patients with

hypercapnia are given oxygen to breathe. PaCO 2 increases sharply and
progressively with severe respiratory acidosis, somnolence, and coma. The
mechanism primarily is the reversal of pulmonary vasoconstriction and the
increase in dead space ventilation.
Respiratory failure is a common and a life-threatening condition that demands

prompt diagnosis and assessment and appropriate management.
Failure to visualize an obvious abnormality on chest x-ray in hypoxemic

respiratory failure suggests the possibility of right-to-left shunting.
The vast majority of patients in acute respiratory failure due to cardiogenic

pulmonary edema respond to measures to reduce preload and afterload.
Those with ARDS require early elective intubation because the duration of
respiratory failure is longer.
Hypercapnic respiratory failure occurs secondary to a variety of causes, including
an increased respiratory muscle load, impaired neuromuscular function, or
decreased respiratory drive caused by CNS depression.
PICTURES Section 10 of 11
Caption: Picture 1. Bilateral airspace infiltrates on chest x-ray film secondary to acute
respiratory distress syndrome that resulted in respiratory failure.
View Full Size Image
eMedicine Zoom View

(Interactive!)
Picture Type: X-RAY

Caption: Picture 2. Extensive left-lung pneumonia caused respiratory failure; the
mechanism of hypoxia is intrapulmonary shunting.
eMedicine Zoom View (Interactive!)
Picture Type: X-RAY

Caption: Picture 3. A 44-year-old woman developed acute respiratory failure and diffuse
bilateral infiltrates. She met the clinical criteria for the diagnosis of acute respiratory distress
syndrome. In this case, the likely cause was urosepsis.
eMedicine Zoom View

(Interactive!)
Picture Type: X-RAY
Caption: Picture 4. A clear chest x-ray film suggests either a CNS cause of respiratory
failure or airway disease (asthma or chronic obstructive pulmonary disease).
eMedicine Zoom View

(Interactive!)
Picture Type: X-RAY
Caption: Picture 5. This patient developed acute respiratory failure that turned out to be the
initial presentation of systemic lupus erythematosus. The lung pathology evidence of diffuse
alveolar damage is the characteristic lesion of acute lupus pneumonitis.
eMedicine Zoom View

(Interactive!)
Picture Type: X-RAY

Caption: Picture 6. A Bilevel positive airway pressure support machine is shown here. This
could be used in spontaneous mode or timed mode (backup rate could be set).
eMedicine Zoom View

(Interactive!)
Picture Type: Photo
Caption: Picture 7. Headgear and full face mask commonly are used as the interface for
noninvasive ventilatory support.

Picture Type: Photo
Caption: Picture 8. Bilevel positive airway pressure (BiPAP) and inspiratory positive airway
pressure (IPAP) settings are shown. IPAP or expiratory positive airway pressure (EPAP) and
frequency can be preset.
eMedicine Zoom View

(Interactive!)
Picture Type: Photo

Caption: Picture 9. Noninvasive ventilation with bilevel positive airway pressure for acute
respiratory failure secondary to exacerbation of chronic obstructive pulmonary disease.
eMedicine Zoom View

(Interactive!)
Picture Type: Photo

Caption: Picture 10. Wave forms of a volume-targeted ventilator: Pressure, flow, and
volume waveforms are shown with square-wave flow pattern. A is baseline, B is increase in
tidal volume, C is reduced lung compliance, and D is increase in flow rate. All 3 settings lead
to increase in peak airway pressures. Adapted from Spearman CB et al.
eMedicine Zoom View

(Interactive!)
Picture Type: Graph
Caption: Picture 11. The cause of respiratory failure may be suggested by spirometry.
Picture Type: Photo

Caption: Picture 12. A 65-year-old man developed chronic respiratory failure secondary to
usual interstitial pneumonitis. Loss of normal architecture is seen upon biopsy. Also seen are
varying degrees of inflammation and fibrosis.
eMedicine Zoom View

(Interactive!)
Picture Type: Image

Caption: Picture 13. Lung biopsy from a 32-year-old woman who developed fever, diffuse
infiltrates seen on chest x-ray film, and acute respiratory failure. The lung biopsy shows
acute eosinophilic pneumonitis; bronchoscopy with bronchoalveolar lavage also may have
helped reveal the diagnosis.
eMedicine Zoom View

(Interactive!)
Picture Type: Image
Caption: Picture 14. Lung biopsy on this patient with acute respiratory failure and diffuse
pulmonary infiltrates helped yield the diagnosis of pulmonary edema. Therefore, cardiogenic
pulmonary edema should be excluded as the cause of respiratory failure prior to considering
lung biopsy.
eMedicine Zoom View

(Interactive!)
Picture Type: Photo

Caption: Picture 15. Pressure-volume curve of a patient with acute respiratory distress
syndrome (ARDS) on mechanical ventilation can be constructed. The lower and the upper
ends of the curve are flat, and the central portion is straight (where the lungs are most
compliant). For optimal mechanical ventilation, patients with ARDS should be kept between
the inflection and the deflection point.
eMedicine Zoom View

(Interactive!)
Picture Type: Photo

Caption: Picture 16. Surgical lung biopsy was performed in the patient described in Image
3. The histology shows features of diffuse alveolar damage, including epithelial injury,
hyperplastic type II pneumocytes, and hyaline membranes.
eMedicine Zoom View

(Interactive!)
Picture Type: Image
Caption: Picture 17. A Power Point presentation of respiratory failure.
Picture Type: Presentation

BIBLIOGRAPHY Section 11 of 11
Albert RK, Martin TR, Lewis SW: Controlled clinical trial of methylprednisolone in
patients with chronic bronchitis and acute respiratory insufficiency. Ann Intern
Med 1980 Jun; 92(6): 753-8[Medline].
Brochard L, Mancebo J, Wysocki M: Noninvasive ventilation for acute

exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995 Sep
28; 333(13): 817-22[Medline].
Connors AF Jr, Dawson NV, Thomas C: Outcomes following acute exacerbation

of severe chronic obstructive lung disease. The SUPPORT investigators (Study
to Understand Prognoses and Preferences for Outcomes and Risks of
Treatments) [published erratum appears in Am J Respir Crit Care Med 19. Am J
Respir Crit Care Med 1996 Oct; 154(4 Pt 1): 959-67[Medline].
Keenan SP, Kernerman PD, Cook DJ: Effect of noninvasive positive pressure
ventilation on mortality in patients admitted with acute respiratory failure: a meta-
analysis. Crit Care Med 1997 Oct; 25(10): 1685-92[Medline].
Kramer N, Meyer TJ, Meharg J: Randomized, prospective trial of noninvasive

positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care
Med 1995 Jun; 151(6): 1799-806[Medline].
Spearman CB, Egan DF, Egan J: Fundamentals of respiratory therapy. 4th ed.
St. Louis, Mo: Mosby; 1982.
NOTE:
Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies
daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate
and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing
and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do
not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the
results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all
drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER
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Author: Sat Sharma, MD, FRCPC, FCCP, DABSM, Program

INTRODUCTION Section 2 of 11 Myocardial

Hypoxemic respiratory failure (type I) is characterized by a PaO 2 of Pulmonary Edema,

Hypercapnic respiratory failure (type II) is characterized by a Pulmonary Fibrosis,

Hypercapnic respiratory failure: At a constant rate of carbon dioxide

A decrease in alveolar ventilation can result from a reduction in

Ventilatory capacity is the maximal spontaneous ventilation that can

Pathophysiologic Mechanisms in Acute Respiratory

The act of respiration engages 3 processes: (1) transfer of oxygen

Physiology of gas exchange

Respiration primarily occurs at the alveolar capillary units of the

At steady state, the rate of carbon dioxide production by the tissues is

The efficiency of lungs at carrying out of respiration can be further

PaO2 = FIO2 x (PB ?PH2O) ?PaCO2/R

For the above equation, PaO2 = alveolar PO2, FIO2 = fractional

Even normal lungs have some degree of V/Q mismatching and a

Pathophysiologic causes of acute respiratory failure

Hypoventilation, V/Q mismatch, and shunt are the most common

Hypoventilation is an uncommon cause of respiratory failure and

V/Q mismatch is the most common cause of hypoxemia. V/Q units

Shunt is defined as the persistence of hypoxemia despite 100%

QS/QT = (CCO2 ?CaO2)/CCO2 ?CVO2)

QS/QT is the shunt fraction, CCO2 (capillary oxygen content) is

Anatomical shunt exists in normal lungs because of the bronchial and

In the US: Respiratory failure is a syndrome rather than a

Mortality/Morbidity: The mortality rate associated with respiratory

History: The diagnosis of acute or chronic respiratory failure begins

The cause of respiratory failure often is evident after a careful

o Cardiogenic pulmonary edema usually develops in the

o A history of previous cardiac disease, recent symptoms

o Noncardiogenic edema (eg, acute respiratory distress

Physical: The signs and symptoms of acute respiratory failure reflect

Asterixis may be observed with severe hypercapnia.

Once respiratory failure is suspected on clinical grounds,

Cyanosis, a bluish color of skin and mucous membranes,

Dyspnea, an uncomfortable sensation of breathing, often

Both confusion and somnolence may occur in respiratory

Pulmonary hypertension frequently is present in chronic

Criteria for the diagnosis of acute respiratory distress

o Clinical setting - Direct insult (aspiration) or systemic

o Radiologic appearance - Three-quadrant or 4-quadrant

o Lung mechanics - Diminished compliance (<40 mL/cm

o Gas exchange - Severe hypoxia refractory to oxygen

o Normal pulmonary vascular properties - Pulmonary

Causes: These diseases can be grouped according to the primary

Central nervous system disorders

o A variety of pharmacological, structural, and metabolic

o This may lead to acute or chronic hypoventilation and

o Examples include tumors or vascular abnormalities

Disorders of the peripheral nervous system, respiratory

o These disorders lead to an inability to maintain a level

o Concomitant hypoxemia and hypercapnia occur.

Abnormalities of the airways

o Severe airway obstruction is a common cause of acute

o Examples of upper airway disorders are acute

Abnormalities of the alveoli

o The diseases are characterized by diffuse alveolar

o Common examples are cardiogenic and noncardiogenic

Common causes of type I (hypoxemic) respiratory failure

o Chronic bronchitis and emphysema (COPD)

o Pulmonary arterial hypertension