The document provides a comprehensive overview of respiratory failure, including its types (hypoxemic and hypercapnic), causes, clinical presentation, workup, and treatment approaches. It details diagnostic strategies, symptoms associated with both forms of respiratory failure, and the role of various medical interventions, including supplemental oxygen and mechanical ventilation. Emphasis is placed on early diagnosis and addressing underlying causes to effectively manage the condition.

1. Respiratory
failure
PREPARED BY : ABDULAZIZ MUSLIM SHAHBAZ
SUPERVISED BY : Dr. ABDULAZEEZ SULIMAN SAVO

2. ▸ Background &
introduction
▸ Clinical Presentation
▸ Workup Approach
▸ Treatment & Management
▸ Medication & guidelines
Content

3. Introduction
Background, pathophysiology and etiology
3

4. ▸ Respiratory failure is a syndrome in
which the respiratory systemfails in
one or both of its gas exchange
functions:
▹oxygenation
▹and carbon dioxide elimination
▸ In practice, it may be classified as
either
 hypoxemic PaO2 <60 mmHg ( < 8,0 kPa)
or
 Hypercapnic PaCO2 >50 mmHg ( > 6,7
kPa)
4
Definition

5. ▸ Type I is characterized by an
arterial oxygen tension (PaO2) <60
mm Hg with a normal or low
arterial carbon dioxide tension
(PaCO2)
▸This is the most common form
of respiratory failure
▸ causes of hypoxemia classified as:
▹V/Q missmatch
▹Impaired diffusion
▹Rt to Lt shunt
5
Hypoxemic
respiratory
failure
(type I)

6. 6
Hypoxemic
respiratory
failure
(type I)
causes
1. Pulmonary
oedema
2. Pulmonary
embolism
3. Lung collapse
4. Pneumothorax
5. ARDS
acute chronic
1. Lung fibrosis
2. (idiopathic
pulmonary
fibrosis)
3. Rt to Lf cardiac
shunt
4. Recurrent or
chronic
pulmonary
embolism

7. This type of respiratory failure is caused by conditions
that affect oxygenation suchas:
▸ Low ambient oxygen (e.g. at high altitude)
▸ Ventilation-perfusion mismatch (parts of the lung
receive
oxygen but not enough blood to absorb it,e.g. pulmonary
embolism)
▸ Alveolar hypoventilation (decreased minute volume
due to reduced respiratory muscle activity, e.g. in acute
neuromuscular disease); this form can also cause type 2
respiratory failure ifsevere
▸ Diffusion problem (oxygen cannot enter the capillaries
due to parenchymal disease, e.g. in pneumonia or ARDS)
7
Hypoxemic
respiratory
failure
(type I)

8.  shunt is an abnormal communication between the right
and left sides of the heart or between the systemic and
pulmonary vessels, allowing blood to flow directly from
one circulatory system to the other.
 Causes of shunt:
Intracardiac
• Right to left shunt
 Fallot’s tetralogy
 Eisenmenger’s syndrome
Pulmonary
• A/V malformation(Arteriovenous malformation)
• Pneumonia
• Pulmonary edema
• Atelectasis/collapse
8
Hypoxemic
respiratory
failure
(type I)

9. ▸ Type II is characterized by a
PaCO2
>50 mm Hg
9
Hypercapnic
respiratory
failure
(type II)
Types 2 RF
1. Hypoxemia (PaO2 < 60
mmHg))
2. Hypercapnoea (PaCO2
> 50 mmHg))
3. Acidosis (pH <7.35)
1. Hypoxemia (PaO2 < 60
mmHg))
2. Hypercapnoea (PaCO2
> 50 mmHg))
3. pH normal (7.35-
7.45)
acute chronic

10. 10
Hypercapnic
respiratory
failure
(type II)
Causes: Type 2 RF
• Brain stem lesion
• CVA
• sedative & narcotic drug
over dose
• Spinal cord injuries
• Guillain – Barre disease
• Myasthenia Gravis
• motor neuron disease
• poliomyelitis
• Flail chest injury
• Acute severe asthma
• Acute epiglottitis
• COPD
• Chronic severe bronchial
asthma
• Kyphoscoliosis
• Ankylosing spondyliltis
• Sleep apnoea syndrome
• obesity
acute chronic
acute chronic

11. Clinical
manifestations
History and physical examination findings
1
1

12. ▸ The diagnosis of acute or chronic
respiratory failure begins with
clinical suspicion of its presence
▸ Confirmation of the diagnosis is basedon
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 is often
evident after a careful history and physical
examination
1
2
History

13. 13
Clinical
manifestations
Symptoms of Hypoxemia and Hypoxia
• Dyspnea, tachypnea. Hyperventilation
• Cyanosis
• Impaired mental performance drowsiness,
confusion, convulsion and coma
• Tachycardia and arrhythmias
• Lactic acidosis
The consequences of untreated chronic hypoxaemia include:
• pulmonary hypertension, right ventricular hypertrophy
& cor pulmonal
• polycythaemia ( increase erythropoietin synthesis)

14. 14
Clinical
manifestations
Symptoms of hypercapnia:
• The patient is a drowsy confused,
somnolense (increase tendensy to sleep)
• Convulsion & coma
• Headache
• Asterixis (flaping tremor)
• Warm extremities, collapsing pulse
• Papilloedema
• Acidosis (respiratory, and metabolic)
↓pH, ↑ lactic acid

15. Respiratory
Failure Workup
15

16. ▸ Chest radiography is
essential.
▸ Pulmonary functions tests (PFTs), may
be helpful, although more useful in terms
of defining recovery potential
▸ ECG should be performed to evaluate
the possibility of a cardiovascular cause
of respiratory failure; it also may detect
dysrhythmias resulting from severe
hypoxemia or acidosis
▸ Right-sided heart catheterization
is controversial
16
Approach
Consideration

17. 1. ABG analysis should beperformed to confirm the diagnosis
and to assist in the distinction between acute and chronic
forms
Normal values of arterial blood gases:
-PH = 7.35 – 7.45 mmhg
-PCO2= 35 – 45 mmhg ( 4,7- 6,0 kPa)
-PO2 = 80 – 100 mmhg (10,6-13,3 kPa)
-HCO3 = 22 – 28 meq/L(Milliequivalents Per Litre)
2. CBC may indicate anemia,which can contribute to tissue
hypoxia, whereas polycythemia mayindicate chronic hypoxemic
respiratory failure
1
7
Laboratory
Studies

18. 3. Abnormalities in renal and hepatic
function mayeither provide clues to
the etiology of respiratory failure or
alert the clinician tocomplications
4. Abnormalities in electrolytes
such
as K+, Mg, and phosphate may
aggravate respiratory failure and
other organ function
18
Laboratory
Studies

19. 5. Measuring serum creatine kinase
with fractionation and troponin I
helps exclude recent MI in a patient
with respiratory failure
6. In chronic hypercapnicrespiratory
failure, serum levels of TSH
should be measured to evaluate
the
possibility of hypothyroidism
(a potentially reversible cause of respiratoryfailure)
19
Laboratory
Studies

20. Chest X-ray
Chest radiography frequently reveals the
cause
20

21. Bilateral airspace infiltrates on chest radiograph film secondary to acute
respiratory distress syndrome that resulted in respiratory failure
21

22. Extensive left-lung pneumonia caused respiratory failure; the mechanism of
hypoxia is intrapulmonaryshunting
22

23. Treatment &
Management
23

24. ▸ The aim to Maintain PaO2 at 55 to 60 mm Hg or
more and SaO2 at 90% or more at the lowest O2
concentration possible without increasing PaCO2 and
acidosis
▸ diagnosis and treatment of the
underlying causes:
• Tracheostomy for laryngeal obstruction
• nebulised bronchodilators in acute severe
asthma
• tube drainage for a tension pneumothorax
• antibiotic for pneumonia
• diuretic for cor pulmonale
2
4
Treatment of
respiratory
failure

25. ▸ Acute on chronic type 11 respiratory
failure:
• The further acute increase in PaCO2 results in acidaemia and
worsening hypercapnia, and may lead to drowsiness and
eventually to coma.
• Main cause is acute exacerbation of COPD
• Controlled oxygen therapy Start with 24% -28% by Venturi
mask is the most important treatment.
• Treating the precipitating condition .
• Frequent physiotherapy ± pharyngeal suction
• Nebulised bronchodilators
• Antibiotic
• If PaCO2 continues to rise or a safe PaO2 cannot be achieved
without severe hypercapnia and acidaemia, mechanical
ventilatory support may be required
25
Treatment
of type 11
RF

26. 26
Correction
of
Hypoxemia
O2 administration
High concentration Low concentration
• such as 40-60% oxygen
• via a high-flow mask
• useful in acute type I
respiratory failure
• pneumonia, asthma or
pulmonary oedema.
• If used for prolonged
periods should be
humidified by passing it
over warm water
• Venturi masks (24% or
28%)
• delivering controlled
oxygen therapy in type II
respiratory failure
• low concentrations of
oxygen (24-28%) may be
needed to avoid
precipitating worsening
respiratory depression
High concentration Low concentration

27.  Chronic oxygen delivery ( domicilliary home O2
therapy)
LONG-TERM OXYGEN THERAPY (LTOT)
oxygen is often given via a low-concentration mask or
nasal cannulae for > 15 hr /day 24% -28%
Portable oxygen may increase exercise tolerance in some
patients with chronic hypoxic lung disease
Indication
PaO2 ≤ 7.3 kPa (55 mmHg) irrespective of PaCO2 and
FEV1 ≤ 1.5 litres
PaO2 7.3-8 kPa (55-60 mmHg) plus pulmonary
hypertension, peripheral oedema or nocturnal
hypoxaemia
27
Correction
of
Hypoxemia

28. Adverse effects of O2 therapy:
1-High O2 is irritant & toxic if inhaled for more
than few hours.
2-Retro-lental fibroplasia & blindness in
pre mature infants.
3-Pulmonary oedema in adult if > 40% for
more than 24 hours continuously.
4-Loss of surfactant and atelectasis
5-Convulsion mainly in hyperbaric O2
28
Correction
of
Hypoxemia

29. Extracorporeal
membrane
oxygenation
29
Extracorporeal membrane oxygenation (ECMO) may be more
effective than conventional management for patients with severe
but potentially reversible respiratoryfailure

30. Mechanical Ventilation
 Mechanical Ventilation is ventilation of the lungs by artificial
means usually by a ventilator.
Indications for supported ventilation is::
• Failure to respond to initial treatment
• declining conscious level
• Worsening respiratory acidosis (H+ > 50 nmol/L (pH < 7.3),
• PaCO2 > 6.6 kPa (50 mmHg)) on blood gases
 Non- invasive ventillation
 invasive ventillation ( using endotracheal tube)
30
Mechanica
l
Ventilation

31. Mechanical ventilation is used for
two 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
31
Mechanical
Ventilation