LO G O

Respiratory Failure

Jiang sheng-hua
 O2 CO2

CO2

External Internal
circulation
respiration respiration
The act of respiration engages 3
processes:

 (1) transfer of oxygen across the alveolus,

 (2) transport of oxygen to the tissues,
 (3) removal of carbon dioxide from blood into the
alveolus and then into the environment.
 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.
 The quantity of oxygen combined with
hemoglobin depends on the level of blood PaO2.
 This relationship, expressed as the oxygen
hemoglobin dissociation curve, is not linear,
 has a sigmoid-shaped curve with a steep slope
between a PaO2 of 10 and 50 mm Hg and a flat
portion above a PaO2 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.
 in normal lungs, not all alveoli are ventilated and
perfused perfectly
 some units are underperfused while others are
overperfused.
 The optimally ventilated alveoli that are not
perfused well are called high V/Q ：
（ ventilation/perfusion ratio ） units (acting like
dead space),
 alveoli that are optimally perfused but not
adequately ventilated are called low V/Q units
(acting like a shunt).
Alveolar ventilation
 the rate of carbon dioxide production by the
tissues is constant and equals the rate of carbon
dioxide elimination by the lung
 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 PO2 above 15-20 mm Hg indicates
pulmonary disease as the cause of hypoxemia
What is respiratory failur
 Respiratory failure develops when the rate of
gas exchange between the atmosphere and
blood is unable to match the body's metabolic
demands.
 It is diagnosed when the patient loses the ability
to provide sufficient oxygen to the blood and
develops hypoxemia or when the patient is
unable to adequately ventilate and develops
hypercarbia and hypoxemia.
 Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas
exchange functions: oxygenation and carbon
dioxide elimination.
 In practice, respiratory 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. （ mmHg=millimeter hydrargyrum ）
 2 ． Classification
（ 1 ） According to PaCO2
■ （ Type I ） respiratory failure （ Hypoxemic respiratory
failure ）
a PaO2 of less than 60 mm Hg with a normal or low PaCO2.
Cause of ： Edema, Vascular disease, Chest Wall &
Pleural disease.
■ （ TypeⅡ ） respiratory failure （ Hypercapnic
respiratory failure ）
a PaO2 low 60 mm Hg and PaCO2 of more than 50
mm Hg. Cause of ： Airway obstruction,
Neuromuscular disease.
 examples of type I respiratory failure are
cardiogenic or noncardiogenic pulmonary
edema, pneumonia, and pulmonary hemorrhage

 Common etiologies of type II include drug

overdose, neuromuscular disease, chest wall
abnormalities, and severe airway disorders (eg,
asthma, chronic obstructive pulmonary disease
[COPD]).
acutely or chronically
 In acute respiratoryfailure, a sudden,
catastrophic event leads to life-threatening
respiratory insufficiency.

 In chronic respiratory failure, gradual worsening

of respiratory function leads to progressive
impairment of gas exchange, the metabolic
effects of which are partially compensated by
adaptations in other systems
 chronic respiratory insufficiency
 In patients with long-standing respiratory
disease, resulting in a state in which patients do
not have true respiratory failure but have little or
no functional respiratory reserve.
 acute on chronic respiratory failure
a mild insult to the respiratory system
Distinctions between acute and chronic respiratory
failure
 Acute hypercapnic respiratory failure develops
over minutes to hours; therefore, pH is less than
7.3.
 Chronic respiratory failure develops over
several days or longer, allowing time for renal
compensation and an increase in bicarbonate
concentration. Therefore, the pH usually is only
slightly decreased.
 The distinction between acute and chronic
hypoxemic respiratory failure cannot readily be
made on the basis of arterial blood gases.

 The clinical markers of chronic hypoxemia, such

as polycythemia or cor pulmonale, suggest a
long-standing disorder
 EPIDEMIOLOGY
 Respiratory failure is a common diagnosis
among patients in medical intensive care units
(ICUs) and is associated with a poor prognosis.

 The incidence of respiratory failure is 137 cases

per100,000 population, or 360,000 cases per
year in the United States,with 36% of these
individuals failing to survive the hospitalization.
 Therapeutic advances in both mechanical
ventilation and airwaymanagement have
improved the prognosis for patients with
respiratoryfailure over the past several decades.

 ventilator support systems

 Lung transplantation
PHYSIOLOGY
 Normal respiration requires the integrated
function of five separate components.
 1. Nervous system.
 2. Musculature (the pump).
 3. Airways (a complex conduit system for bulk
delivery of gases).
 4. Alveolar units (an efficient, distensible,
compact membrane system).
 5. Vasculature (a network of conduits capable of
transporting dissolved gases to and from the
functioning organs throughout the body).
 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve

Pleura

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure due to diseases that cause
dysfunction of the central control system can be
thought of as controller dysfunction, or central
apnea.
 Hypoventilation can be caused by disease at
any of the anatomical sites involved in
ventilation. Brainstem injury or disease may
result in impaired functioning of the respiratory
centre, which may also be suppressed by
depressant drugs
 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve

Pleura

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve
supplying respiratory
Pleura muscles

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve

Pleura

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Neuromuscular blockers or disease of the
neuromuscular junction (eg myasthenia gravis)
may impair transmission of nerve impulses to
respiratory muscles Or the problem may be in
the muscle itself.
 Respiratory muscle fatigue, disuse atrophy and
malnutrition are important causes of respiratory
muscle failure in the ICU
 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve

Pleura

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure involving diseases that
cause marked obstruction or dysfunction of the
air passages can be thought of as airway system
dysfunction
 Alternatively the problem may be a problem of
increased resistance to airflow. For example due
to obstruction of the upper airway or
bronchospasm
 Brainstem

Spinal
Airway cord root
Nerve

Lung Nerve

Pleura

Neuromuscular
Chest junction
wall
Respiratory
muscle

Sites at which disease may cause ventilatory disturbance

 Respiratory failure due to diseases that cause
ineffective function of the respiratory pump can
be thought of as pump dysfunction. Under
normal conditions, only elastic recoil is required
for expiration, but during respiratory failure
accessory muscles of expiration are required
 Alveolar units

 Respiratory failure as a result of diseases that

cause collapse, flooding, or injury to the
alveolar networkcan be thought of as alveolar
compartment dysfunction.
 O2

CO2

Alveolar epithelium Capillary

endotheliocyte
 Respiratory failure as a result of disease
involving the pulmonary vasculature can be
thought of as pulmonary vascular dysfunction.
Pathophysiology
 Failure of any one of these essential
components or significant dysfunction of more
than one essential component can lead to failure
of the integrated system and produce clinical
respiratory failure.

 including the airways, alveoli, CNS, peripheral

nervous system, respiratory muscles, and chest
wall. Patients who have hypoperfusion
secondary to cardiogenic, hypovolemic, or septic
shock often present with respiratory failure.
 Hypoxemic respiratory failure: The
pathophysiologic mechanisms that account for
the hypoxemia observed in a wide variety of
diseases are ventilation-perfusion (V/Q)
mismatch and shunt.
 These 2 mechanisms lead to widening of the
alveolar-arterial oxygen difference, which
normally is less than 15 mm Hg. With V/Q
mismatch, the areas of low ventilation relative to
perfusion (low V/Q units) contribute to
hypoxemia.
肺泡通气与血流比例失调（ Ventilation-perfusion-mismatching ）
（ 1 ） Type & cause of ventilation-perfusion-mismatching
■Decreased ratio of V·A/ Q·（部分肺泡通气不足）

支气管哮喘、慢性支气管炎、阻塞性肺气肿、肺纤维化、肺水肿
· ·
VA/ Q 比值↓ 部分病变严重的肺泡通
气↓
 · ·
■Increased ratio of VA/ Q （部分肺泡血流不足）
VA/ Q （部分肺泡血流不足）

肺动脉栓塞、肺内 DIC 、肺动脉炎、肺血管收缩 部分肺泡

血流↓ · ·
VA/Q↑ ＞ 60% 死腔样通气（ Dead space like
ventilation ）
功能死腔量（ Functional dead
呼衰 ， V ）
space
 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.
 Ventilatory capacity versus 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.
History
 Does the patient have factors that increase the
risk for respiratory failure? Factors may include
young age; history of prematurity;
immunodeficiency; and chronic pulmonary,
cardiac, or neuromuscular disease (eg,
cystic fibrosis, bronchopulmonary dysplasia,
unrepaired congenital heart disease, or spinal
muscular atrophy [SMA]).
 Does the patient have a cough, rhinorrhea, or
other symptoms of an
upper respiratory tract infection to define an
etiology?
 Does the patient have a fever or signs of sepsis?
Several infections can lead to respiratory failure
because of a systemic inflammatory response,
pulmonary edema, or
acute respiratory distress syndrome (ARDS) or
because it can produce a power-load imbalance
secondary to increased oxygen consumption
 How long have the symptoms been present?
The natural course of a respiratory illness
must be considered.
Respiratory syncytial virus (RSV) infections
frequently worsen over the initial 3-5 days
before improvement occurs.
 Does the patient have any pain? Pain can
suggest pleuritis or foreign-body aspiration.
 Does the patient have a possible or known
exposure to sedatives (eg, benzodiazepines,
tricyclic antidepressants, narcotics) or has
he or she recently undergone a procedure
that used general anesthesia? This could
suggest hypoventilation
 Does the patient have symptoms of
neuromuscular weakness or paralysis? What is
the distribution of weakness and duration of
symptoms to narrow the differential diagnosis?
Bulbar dysfunction suggests myasthenia
gravis.
Distal weakness that progresses upward
suggests Guillain-Barré syndrome.
Apnea associated with a traumatic injury
suggests a cervical spinal cord injury.
 Does the patient have a history suggestive of
a stroke or seizure?

 Does the patient have a history of

headaches? With chronic hypercapnia,
headaches typically occur at nighttime or
upon the patient's awakening in the morning.
Physical
 During physical examination, clinicians should
avoid interfering with the patient's mechanisms
for compensation
General appearance

Does the patient appear well or sick?

Is the patient cyanotic?

Respiratory rate, quality, and effort
 Bradypnea is most often observed in central
control abnormalities. Slow and large tidal
volume breaths also minimize turbulence and
resistance in significant extrathoracic airway
obstruction (eg, epiglottitis).
Respiratory rate, quality, and effort
 The fast and shallow breathing of tachypnea
is most efficient in intrathoracic airway
obstruction. It decreases dynamic
compliance of the lung.
 Auscultation provides information about the
symmetry and quality of air movement.
Evaluate the patient for stridor, wheezing,
crackles, and decreased breath sounds (eg,
alveolar consolidation, pleural effusion).
Respiratory rate, quality, and effort
 Grunting is an expiratory sound made by
infants as they exhale against a closed
glottis. It is an attempt to increase functional
residual capacity and lung volume. This
attempt is made in order to raise functional
residual capacity above the critical closing
volume and to avoid alveolar collapse. This
is a concerning physical finding.
Respiratory rate, quality, and effort
 Assess for accessory muscle use and nasal
flaring. Suprasternal and intercostal
retractions are present when highly negative
pleural pressures are required to overcome
airway obstruction or stiff lungs.
Chest wall findings:
 Evaluate for paradoxical movement of the chest
wall. In the presence of abnormalities of the
pulmonary pump, paradoxical chest-wall
movement occurs because of instability of the
chest wall associated with absent intercostal
muscle use. As the diaphragm contracts and
pushes abdominal contents out, the chest wall
retracts inward instead of expanding normally.
Cardiovascular findings
 Tachycardia and hypertension may occur
secondary to increased circulatory
catecholamine levels.
 A gallop is suggestive of myocardial
dysfunction leading to respiratory failure.
 Peripheral vasoconstriction may develop
secondary to respiratory acidosis.
Neurologic findings
 Patients may be lethargic, irritable, anxious,
or unable to concentrate.
 The inability to breathe comfortably creates
anxiety, and superimposed hypoxemia and
hypercapnia accentuates any restlessness
and agitation. Increased agitation may
indicate a general worsening of the patient's
condition
 Respiratory Failure
Laboratory Testing

Arterial blood gas

PaO2
PaCO2
PH
Chest imaging
Chest x-ray
CT sacn
Ultrasound
pulmonary function tests
Laboratory Studies
 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
 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 肌炎 , 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.
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.
Echocardiography

 Echocardiography need not be performed

routinely in all patients with respiratory
failure. However, it is a useful test when a
card
 iac 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.
 Respiratory Failure
Laboratory Testing
Other tests
Hemoglobin
Electrolytes, blood urea nitrogen, creatinine
Creatinine phosphokinase, aldolase
Electromyography (EMG)
Nerve conduction study
Respiratory muscle pressures
MIP ( maximum inspiratory pressure)
MEP ( maximum expiratory pressure)
 Diagnosis

 According to history, clinical manifestations,

physical examination and blood gas analysis,
we can diagnose respiratory failure. Especially
arterial blood gas analysis may reveal
hypoxemia and hypercapnia.
 Diagnosis

 According to history, clinical manifestations,

physical examination and blood gas analysis,
we can diagnose respiratory failure. Especially
arterial blood gas analysis may reveal
hypoxemia and hypercapnia.
 Treatment
 The principle of treatment includes
 primary disease treatment
 airway maintenance
 correction of hypoxemia and hypercapnia
 management of symptoms caused by
hypoxemia and hypercapnia.
 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.
(1)Airway maintenance and enhance the
volume of ventilation

 Assurance of an adequate airway is key in

the patient with respiratory failure.
correctly use of bronchodilators
 In severe cases intubation and mechanical
ventilation may be used.
Bronchodilators
 These agents 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 muscle, relieving
bronchospasm and reducing airway resistance
 Albuterol (Proventil)
Beta-agonist useful in the treatment of
bronchospasm. Selectively stimulate beta2-
adrenergic receptors of the lungs.
Bronchodilation results from relaxation of
bronchial smooth muscle, which relieves
bronchospasm and reduces airway resistance.
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 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.
Ipratropium bromide (Atrovent)
 Anticholinergic medication that appears to inhibit
vagally mediated reflexes by antagonizing action
of acetylcholine, specifically with the muscarinic
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.
 To most of the chronic respiratory failure,
correctly use of bronchodilators is very important.
Table 2.
Bronchodilators Route Dose
salbutamol MDI and spacer 400-600µg q1-4h
Aerosol solution 2.5-7.5mg q1-4h
Ipratropium MDI and spacer 80-120µg q4-6h
Aerosol solution
Theophylline IV 5.6mg/kg 0.3-0.6mg/kg/hr
oral
 Mechanical ventilation

The aim of mechanical ventilation is to improve hypoxemia and

to prevent hypercapnia. When do you select mechanical
ventilation? This is a question we always meet in our clinical
work.

1.progressive elevation in PaCO2>70-80mmHg

2.severe hypoxemia, after oxygen therapy, PaO2<40mmHg
3.respiratory rates>35 per minute or severe breathlessness
4.severe metabolic acidosis or pulmonary encephalopathy
 How to select artificial airway?
face mask or nasal noninvasive intermittent positive
pressure ventilation are delivered to augment alveolar
ventilation and reducing the work of breathing.
If hypoventilation can not be effectively reverses by
noninvasive methods, intubation must be adopted. When
artificial ventilation is required for more than 2 weeks, a
tracheotomy is often required.
Tracheotomy carries some risk of bleeding,
pneumothorax, and local infection and incidence of
aspiration.
 (2)Antiinfectious therapy
 Repeated bronchial and pulmonary infection is a major
cause of chronic respiratory failure.
 About 90% of COPD patients with respiratory failure is
caused by acute bronchial or pulmonary infection.
 Infection may also increase bronchial secretion and CO2
production.
 So antiinfectious therapy is an important method to treat
respiratory failure.
 Select effective antibiotics
According to sputum culture, we can select sensitive
antibiotics
 Using combined antibiotics
Because of multibacteria infection, it needs several
kind of antibiotics. For example, we may combine
second or third generation cephalosporin to
aminoglycoside or fluoroguinolone.
(3)Oxygen therapy

 The goal of oxygen therapy is to improve PaO2.

It makes PaO2>60mmHg.
In general, the lowest FiO2 achieving adequate
oxygenation. sometimes, arterial oxygen
saturation>90% should be used.
The methods of oxygen therapy:
nasal prongs 1-3L/min to chronic respiratory failure
venti mask 1-3L/min
For type 1 respiratory failure, we can elevate the percentage of
oxygen to maintain the PaO2.
We can use higher inspirated fration of oxygen in type 1
respiratory failure oxygen therapy. But in type 2 respiratory
failure we must select lower inspirated fration of oxygen .
 Oxygen Therapy

 Supplemental O2 therapy essential

 titration based on SaO2, PaO2 levels and PaCO2
 Goal is to prevent tissue hypoxia
 Tissue hypoxia occurs (normal Hb & C.O.)
- venous PaO2 < 20 mmHg or SaO2 < 40%
- arterial PaO2 < 38 mmHg or SaO2 <
70%
 Increase arterial PaO2 > 60 mmHg(SaO2 > 90%)
or venous SaO2 > 60%
 O2 dose either flow rate (L/min) or FiO2 (%)
 Risks of Oxygen Therapy
 O2 toxicity:
- very high levels(>1000 mmHg) CNS toxicity and
seizures -
lower levels (FiO2 > 60%) and longer exposure: - capillary
damage, leak and pulmonary fibrosis
- PaO2 >150 can cause retrolental fibroplasia
- FiO2 35 to 40% can be safely tolerated indefinitely
 CO2 narcosis: -
PaCO2 may increase severely to cause respiratory
acidosis, somnolence and coma
- PaCO2 increase secondary to combination of
a) abolition of hypoxic drive to breathe
b) increase in dead space
(4)Acid-base and electrolytes
disturbance

 There are many factors lead to acid-base and

electrolytes disturbance.
 These factors include severe pulmonary
infection, hypoxemia or (and) hypercapnia. So
airway maintenance, antibiotic therapy and use
of bronchodilators are beneficial to treat it.
The acid-base disorder types in
respiratory failure

 Usually the disorders are compound types.

 It is difficult to judge the type of disorder
according to the clinical symptoms and signs.
Arterial blood gas analysis is the major method
to judge the type of disorder.
How to judge the acid-base disorder
 PH
 PaCO2
the acid-base index.
 HCO3-
the index of respiratory

the metabolism
Treatment of acid-base
disorders

 looking for the etiology of the disorder

is the most important .
 Respiratory acidosis
 It is most commonly encountered in clinical practice of
respiratory diseases.(COPD)
 It is essential to improve alveolar ventilation, while
alkaline supplement is not necessary.
 For example: PH:7.32;PCO276mmHg;
PO276mmHg SO2%94%
BE13.9 HCO3- 41mmol/L
 Respiratory acidosis complicated with
metabolic acidosis
 First of all, the cause of metabolic acidosis should be
clarified and treated, such as severe hypoxia may lead to
increase in lactic acid or it is due to renal dysfunction or
diabetic ketoacidosis.
 If the level of PH is less than 7.2, alkaline drugs should
be treated.
 5%NaHCO3(ml)=[normal HCO3-(mmol/L)-actual HCO3-
(mmol/L)] ×0.2×weight(Kg)
Respiratory acidosis complicated with
metabolic acidosis

 Arterial gas analysis:

PH:7.20;PCO276mmHg;
PO256mmHg SO2%86%
BE-7; HCO3- 20mmol/L
(5)Use of respiratory stimulant

 Nikethamide

 Lobeline

 Doxapram
(6)Corticosteroids

 Methyprednisone is usually used to reduce the

airway inflammation, and to improve FEV!. The
treatment is recommended in all patients but it is
not used for a longer time.
(7)Gastrointestinal bleeding treatment
Because of hypoxemia, hypercapnia and by using
corticosteroids, gastrointestinal bleeding always
be happened.
The treatment mathod include correct hypoxemia
and hypercapnia, use of H2-blocker and some
block bleeding drugs.
(8)Nutritional support therapy
Tracheal intubation–Indications

 Hypoxemia which is not quickly reversed

by supplemental oxygen
 Airway obstruction
 Impaired airway protection
 Inadequate handling of secretions
 Facilitation of mechanical ventilation
Trach eal in tubation
Mechanical ventilation–Indications
 Apnea
 Acute hypercapnia that is not quickly
reversed by appropriate specific therapy
 Severe hypoxemia
 Progressive patient fatigue despite
appropriate treatment
 Mechanical ventilation is used for 2 essential
reasons:
 (1) to increase PaO2
 (2) to lower PaCO2.
 (3) Mechanical ventilation also rests the
respiratory muscles and is an appropriate
therapy for respiratory muscle fatigue.
Ventilator management
 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.

 Prior to the mid 1950s, negative-pressure

ventilation with the use of iron lungs was the
predominant method of ventilatory support.
 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 respiratory failure.

 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
Mechanical ventilation–Modes
 Assisted mechanical ventilation (AMV) or
assist/control (A/C)
 Synchronized intermittent mandatory
ventilation (SIMV)
 Pressure support ventilation (PSV)
 Mechanical ventilation–Modes

 Pressure control ventilation (PCV)

 Continuous positive airway pressure
(CPAP)
 Positive end-expiratory pressure (PEEP)
Mechanical ventilation–Complications

 Atelectasis of the centrolateral lung and

overdistention of the intubated lung
 Barotrauma, manifested by subcutaneous
emphysema, pneumomediastinum,
subpleural air cysts, pneumothorax, or
systemic gas embolism
Mechanical ventilation–Complications

 Subtle parenchymal lung injury

 Acute respiratory alkalosis
 Hypotension
 Ventilator-associated pneumonia,
mortality rate of this disorder is about 50–
60%
Bilateral airspace infiltrates on chest x-ray film secondary to acute

respiratory distress syndrome that resulted in respiratory failure

Extensive left-lung pneumonia caused respiratory failure;

the mechanism of hypoxia is intrapulmonary shunting

LO G O

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