Respiratory failure occurs when the lungs cannot effectively exchange oxygen and carbon dioxide, resulting in hypoxemia (low blood oxygen) and hypercapnia (high blood carbon dioxide). Acute respiratory failure develops suddenly in patients without preexisting lung disease, while chronic respiratory failure is caused by conditions like COPD. Treatment involves oxygen therapy, ventilation if needed, treating the underlying cause, and monitoring vital signs.

1. PULMONARY FAILURE

2. Respiratory Failure
 Exists whenever the exchange of oxygen for
carbon dioxide in the lungs cannot keep up
with the rate of oxygen consumption &
carbon dioxide production in the cells of the
body.
 This results in a fall in arterial oxygen tension
(Hypoxemia)
 And a rise in arterial carbon dioxide tension
(hypercapnia)

3. Acute Respiratory
Failure
Respiratory failure (lung failure) is a
condition in which the level of oxygen in
the blood becomes dangerously low or
the level of carbon dioxide becomes
dangerously high.

4. Difference between acute &
chronic
Acute respiratory failure
Chronic respiratory failure
 Appears in patient whose
lung was structurally &
functionally normal before
the onset of present illness.
 After acute attack, the lung
usually returns to normal.
 Respiratory failure seen in
patients with chronic lung
diseases such as chronic
bronchitis, emphysema, &
black lung disease (coal
miner’s disease)
 Patients develop tolerance
to gradually worsening
hypoxia & hypercapnia.
 Structural damage is
irreversible

5.  Chronic, or long-term, respiratory failure is
commonly caused by chronic obstructive
pulmonary disease (COPD), neuromuscular
disease, or even morbid obesity.

6.  Chronic Obstructive Pulmonary Disease
(COPD)
 Breathing is effortless and unconscious for most
people.
 Hundreds of times each day you breathe in
oxygen and exhale carbon dioxide while gas
exchange takes place in your lungs.
 Fresh, inhaled oxygen is absorbed into the blood
circulating through your lungs.
 Oxygen-rich blood then travels from the lungs to
the heart and is pumped into the arteries to be
distributed throughout your body.

7.  At the same time, carbon dioxide (a waste product
produced by your cells) travels to your heart through
your veins.
 It is then pumped into your lungs to be released as you
exhale.
 For people with chronic obstructive pulmonary disease
(COPD), breathing is not this easy.
 Damage to the lung’s airways and air sacs, typically
caused by smoking, environmental exposure or
genetics, makes it physically difficult to breathe in and
out.
 Inflammation of the airways blocks the movement of
air, and it becomes difficult to get oxygen into the
body.
 Breathlessness may occur during exercise, during very
little activity or even at rest depending on the severity
of COPD.

8. Causes of Acute Respiratory
Failure
 Respiratory failure results from inadequate
ventilation:
 Causes are:
 Upper airway obstruction
 Central nervous system depression
 Postoperative period ( major thoracic or upper abdominal
surgery)
 Pleural effusion, hemothorax, and pneumothorax
 Trauma caused by motor vehicle accidents
 Acute diseases like
 pneumonia,
 chemical pneumonitis,
 bronchial asthma,
 atelectasis,
 pulmonary embolism, &
 pulmonary edema

9.  Atelectasis
 is the collapse of part or all of a lung by blockage
of the air passages (bronchus or bronchioles), or
by very shallow breathing.

10.  Pulmonary Embolism
 blockage in an artery in the lungs caused by an
embolus (a free-floating blood clot) that travels
through the blood vessels (usually from a vein in a
leg or in the pelvic area) to the lungs.
 Pulmonary embolism causes damage to lung
tissue, disrupts the proper functioning of the
damaged lung, and can cause death

11. CNS Depression
 The respiratory center, which controls every
breath, lies in the lower part of the brain stem
(pons & medulla).
 Drug overdose, anesthesia, head injury, stroke,
brain tumors, encephalitis, meningitis, hypoxia, &
hypercapnia are all capable of depressing the
respiratory center.
 In these patients, respiration becomes slow
& shallow & respiratory arrest may occur in
severe cases.

12.  Any disease of the nerves, spinal cord, muscles,
or neuromuscular junction involved in
respiration will seriously affect ventilation.
 Examples:
 Polyneuritis
 Myasthenia gravis
 Damage to the cervical segment of spinal cord
 Large acute lesions of multiple sclerosis in the brain
stem
 poliomyelitis
 The impulse arising in the respiratory center
travel through nerves that extend from the brain
stem down the spinal cord to receptors in the
muscles of respiration.

13. Post operative period
 Effects of anesthetic drugs, analgesics, &
sedatives (pentobarbital & morphine)
 Pain in thoracic & abdominal area interferes
with deep breathing & coughing
 Muscle relaxants, some patients may have
difficulty in metabolizing or excreting these
drugs, so their effects last longer than usual,
making patients weak in postop period.

14. Pleural effusion,
hemothorax, & pneumothorax
 Interfere with ventilation by preventing
expansion of the lungs.
 Pleural Effusions
 is an accumulation of fluid between the layers of
the membrane that lines the lungs and chest
cavity.

15. Respiratory Failure
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.
 Normal Values:
pH: 7.35-7.45
PO2: 80-100 mm Hg
PCO2: 35-45 mm Hg
% of O2 saturation: 95-100%

16. Signs and symptoms:
Anxious
 eyes are closed
 the accessory muscles of ventilation are fully used
Position, sitting forward with drooling secretions
 Hypoxia and hypercarbia produce characteristic
effects on the CNS and cardiovascular system
(CVS).

17. 1 Hypoxia:
 CNS - Uncooperative, confused, drunken-like state
 CVS - Bradycardia, variable blood pressure,
cyanosis
2 Hypercarbia:
 CNS - Tremor and overt flap
 CVS - Raised pulse rate, peripheral vasodilation with
pink peripheries, blood pressure changes are
variable

18. Diagnostic Test
ABG analysis
CXR
ECG
Pulse oximetry
CBC
Serum electrolytes
Pulmonary artery
catheterization

19. Treatment and drugs:
Cautious oxygen therapy (nasal prongs or Venturi mask)
If Respiratory Acidosis persist, Mechanical ventilation
with an Edotracheal is attached or Tracheostomy
Antibiotics
Bronchodilators
Corticosteroids
 If cor pulmonale and cardiac output decreased
administer Inotropic agents,vasopresors, and diuretics
may ordered

20. Cor pulmonale
 disease of the heart:
 enlargement and failure of the right ventricle of
the heart, caused by disease of the lungs or
pulmonary blood vessels.

21. Management:
(a) Establish an airway
This applies particularly to the unconscious
patient, e.g. due to overdose, general
anaesthesia, CNS trauma and so on.
The patient is placed on the side with the
head down, and lower jaw pulled forward to
prevent the tongue falling back and obstructing
the upper airway.
 At this stage it may become obvious that the
obstruction is due primarily to foreign bodies or
vomit, so this must be cleared, if possible.

22.  Indications for artificial airways
 (1) Oropharyngeal: this is useful where it is
expected that the patient will soon recover
consciousness, e.g. post-operatively, or where there
is lack of expertise in endotracheal intubation. A
laryngeal mask may be used as an alternative in this
situation
 (2) Endotracheal tube (ETt): If unconsciousness is
expected to last for more than a matter of minutes,
as in drug overdose, then an ETT must be used both
to ensure and to protect the airway (e.g. from
aspiration of gastric contents). If ventilation is
depressed or inadequate due to trauma or disease,
than mechanical ventilation will be required.

23. (3) Cricothyrotomy and
tracheostomy obstruction above the cords due
to disease or infection may make intubation
impossible. Cricothyrotomy or tracheostomy is
then necessary to restore the airway.
(4) Bronchoscopy may also be required for
bronchial toilet, removing viscid mucous and
obtaining specimens for microscopy and culture

24. cricothyrotomy
 Tracheotomy by incision through the skin &
cricothyroid membrane esp. as an emergency
procedure for relief of an obstructed airway.

25.  (b) Administer oxygen to ensure adequate
tissue oxygenation
 It is of paramount importance to maintain
a PaO2 sufficient to give an arterial Hb
saturation of at least 85% (i.e. 8-9 kPa
(kilopascal) or 60-70 mmHg).
 Hyperoxia should be avoided, particularly
in the bronchitic who is a CO2 retainer and
dependent on hypoxic ventilatory drive.

26. (c) Maintain alveolar ventilation and treat
underlying cause
These two are inextricably linked. The causes of
ARF (acute respiratory failure) are many and
varied as are the requisite therapies. If treatment of
the underlying cause is not successful (i.e. steroids,
bronchodilators in asthma; physiotherapy,
antibiotics, mucolytics, bronchodilators in acute or
chronic bronchitis), then the carbon dioxide
tension will begin to rise, necessitating
intermittent positive pressure ventilation
(IPPV).

27.  There is little place for respiratory stimulants,
except perhaps narcotic antagonists in opiate
overdose. NB Infection is a cause of
exacerbation of ARF in bronchitics in less than
50% of cases. Other causes such as heart
failure, dysrthymias and pneumothorax must
be excluded and treated where necessary.
 In ARF due to chronic obstructive pulmonary
disease (COPD), muscle fatigue is a major
contributory factor to continuing hypoxia and
hypercarbia. Non-invasive methods of
ventilation (e.g. nasal mask) as well as
endotracheal intubation and IPPV may be
needed

28. NURSING MANAGEMENT:
> Orient the patient to the treatment unit to prevent anxiety
> To reverse hypoxemia, administer oxygen as ordered
> Maintain patent airway
> Monitor BP, RR and PR
> Place patient in semi-fowlers position

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