A basic overview of respiratory failure: the clinical presentation, workup Approach, treatment & Management, medication & guidelines

1. Respiratory
failure

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

3. Introduction
Background, pathophysiology and etiology
3

4. Definition
▸ 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, it may be classified as
either hypoxemic or hypercapnic
4

5. Hypoxemic
respiratory
failure
(type I)
▸ 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
▸ Example:
▹ cardiogenic or noncardiogenic pulmonary
edema
▹ Pneumonia
▹ pulmonary hemorrhage
5

6. Hypoxemic
respiratory
failure
(type I)
▸ Type 1 respiratory failure is defined as a low
level of oxygen in the blood
(hypoxemia) without an increased level
of carbon dioxide in the blood (hypercapnia),
and indeed the PaCO2 may be normal or low.
▸ It is typically caused by a ventilation/
perfusion (V/Q) mismatch; the volume of air
flowing in and out of the lungs is not
matched with the flow of blood to the lungs.
6

7. Hypoxemic
respiratory
failure
(type I)
This type of respiratory failure is caused by conditions
that affect oxygenation such as:
▸ 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 if severe
▸ Diffusion problem (oxygen cannot enter the capillaries
due to parenchymal disease, e.g. in pneumonia or ARDS)
▸ Shunt (oxygenated blood mixes with non-oxygenated
blood from the venous system, e.g. right to left shunt)
7

8. Hypercapnic
respiratory
failure
(type II)
▸ Type II is characterized by a PaCO2
>50 mm Hg
▸ Hypoxemia is common in patients
with hypercapnic respiratory failure
who are breathing room air
▸ The pH depends on the level of
bicarbonate, which, in turn, is
dependent on the duration of
hypercapnia
8

9. Hypercapnic
respiratory
failure
(type II)
▸ Type 2 respiratory failure is caused by
inadequate alveolar ventilation; both
oxygen and carbon dioxide are affected
▸ Defined as the buildup of carbon dioxide
levels (PaCO2) that has been generated by
the body but cannot be eliminated
▸ Common etiologies of type II:
▹ drug overdose
▹ neuromuscular disease
▹ chest wall abnormalities
▹ severe airway disorders (eg, asthma and COPD)
9

10. Hypercapnic
respiratory
failure
(type II)
The underlying causes include:
▸ Increased airways resistance (COPD, asthma,
suffocation)
▸ Reduced breathing effort (drug effects, brain
stem lesion, extreme obesity)
▸ A decrease in the area of the lung available for
gas exchange (such as in chronic bronchitis)
▸ Neuromuscular problems (Guillain–Barré
syndrome, motor neuron disease)
▸ Deformed (kyphoscoliosis), rigid (ankylosing
spondylitis), or flail chest.
10

11. Prognosis
The mortality associated with respiratory
failure varies according to the etiology
▸ ARDS, mortality is approximately 40-45%
▸ Younger patients (<60 y) have better survival rates
than older patients
▸ For patients with COPD and acute respiratory
failure, the overall mortality has declined from
approximately 26% to 10%
▸ Acute exacerbation of COPD carries a mortality of
approximately 30%
11

12. Clinical
presentation
History and physical examination findings
12

13. 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 is often
evident after a careful history and physical
examination
13

14. Physical
Examination
▸ Localized pulmonary findings reflecting the
acute cause of hypoxemia (eg, pneumonia,
pulmonary edema, asthma, or COPD)
▸ Neurologic 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
14

15. Physical
Examination
▸ Cyanosis, a bluish color of skin and mucous
membranes, indicates hypoxemia
▸ Dyspnea, an uncomfortable sensation of
breathing, often accompanies respiratory
failure
▸ Pulmonary hypertension frequently is
present in chronic respiratory failure.
Alveolar hypoxemia potentiated by
hypercapnia causes pulmonary arteriolar
constriction
15

16. Criteria for
diagnosis of
ARDS
16

17. Criteria for
diagnosis of
ARDS
▸ Clinical presentation - Tachypnea and
dyspnea; crackles upon auscultation
▸ Clinical setting - Direct insult (aspiration) or
systemic process causing lung injury
(sepsis)
▸ Radiologic appearance - 3-quadrant or 4-
quadrant alveolar flooding
17

18. Criteria for
diagnosis of
ARDS
▸ Lung mechanics - Diminished compliance
(<40 mL/cm water)
▸ Gas exchange - Severe hypoxia refractory to
oxygen therapy (ratio of arterial oxygen
tension to fractional concentration of oxygen
in inspired gas [PaO 2/FiO 2] <200)
▸ Normal pulmonary vascular properties -
Pulmonary capillary wedge pressure <18
mm Hg
18

19. Respiratory
Failure Workup
19

20. Approach
Consideration
▸ 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
20

21. Laboratory
Studies
1. ABG analysis should be performed
to confirm the diagnosis and to
assist in the distinction between
acute and chronic forms
2. CBC may indicate anemia, which
can contribute to tissue hypoxia,
whereas polycythemia may indicate
chronic hypoxemic respiratory
failure
21

22. Laboratory
Studies
3. Abnormalities in renal and hepatic
function may either provide clues to
the etiology of respiratory failure or
alert the clinician to complications
4. Abnormalities in electrolytes such
as K+, Mg, and phosphate may
aggravate respiratory failure and
other organ function
22

23. Laboratory
Studies
5. Measuring serum creatine kinase
with fractionation and troponin I
helps exclude recent MI in a patient
with respiratory failure
6. In chronic hypercapnic respiratory
failure, serum levels of TSH should
be measured to evaluate the
possibility of hypothyroidism
(a potentially reversible cause of respiratory failure)
23

24. Chest X-ray
Chest radiography frequently reveals the cause
24

25. Bilateral airspace infiltrates on chest radiograph film secondary to acute
respiratory distress syndrome that resulted in respiratory failure
25

26. Extensive left-lung pneumonia caused respiratory failure; the mechanism of
hypoxia is intrapulmonary shunting
26

27. 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
27

28. This patient developed acute respiratory failure that turned out to be the initial
presentation of SLE. The lung pathology evidence of diffuse alveolar damage is the
characteristic lesion of acute lupus pneumonitis
28

29. This patient developed acute respiratory failure that turned out to be the initial
presentation of SLE. The lung pathology evidence of diffuse alveolar damage is the
characteristic lesion of acute lupus pneumonitis
29

30. Treatment &
Management
30

31. Approach
Consideration
▸ Correction of Hypoxemia
▸ Principles of Mechanical Ventilation
▸ Ventilation Approaches for Specific
Diseases
▸ Noninvasive Ventilatory Support
▸ Weaning From Ventilator
▸ Long-Term Monitoring
31

32. Correction
of
Hypoxemia
▸ The first objective in the
management of respiratory failure is
to reverse and/or prevent tissue
hypoxia
▸ Many experts believe that
hypercapnia should be tolerated until
the arterial blood pH falls < 7.2
32

33. Correction
of
Hypoxemia
▸ Patient with acute respiratory failure
generally should be admitted to ICU
▸ 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
33

34. Correction
of
Hypoxemia
34
Extracorporeal membrane oxygenation (ECMO) may be more
effective than conventional management for patients with severe
but potentially reversible respiratory failure

35. Correction
of
Hypoxemia
▸ Once the airway is secured, attention is
turned toward correcting the underlying
hypoxemia
▸ The goal is to assure adequate oxygen
delivery to tissues, generally achieved with
an PaO2 of 60 mm Hg or an SaO2 >90%
▸ Supplemental oxygen is administered via
nasal prongs or face mask
▸ In patients with severe hypoxemia, intubation
and mechanical ventilation are often
required
35

36. Mechanical
Ventilation
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
36

37. Ventilation
Approaches
for Specific
Diseases
▸ The mode of ventilation should be
suited to the needs of the patient
▸ After the initiation of mechanical
ventilation, ventilator settings should
be adjusted on the basis of:
▹ the patient’s lung mechanics
▹ underlying disease process
▹ gas exchange
▹ response to mechanical ventilation.
37

38. Ventilation
Approaches
for Specific
Diseases
▸ SIMV and assist control ventilation are often
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
▸ The lowest FiO2 that produces an SaO2
>90% and a PaO2 >60 mm Hg generally is
recommended
▸ The prolonged use of an FiO2 <0.6 is unlikely
to cause pulmonary oxygen toxicity
38
SIMV: Synchronized Intermittent Mechanical Ventilation
PSV: Pressure support ventilation

39. Acute respiratory
distress
syndrome
Ventilation Approach
39

40. Acute
respiratory
distress
syndrome
▸ In ARDS, the primary objective of
mechanical ventilation is to
accomplish adequate gas exchange
while avoiding excessive inspired
oxygen concentrations and alveolar
over distention
▸ Patients with ARDS should be
targeted to receive a tidal volume of
6 mL/kg.
40

41. Acute
respiratory
distress
syndrome
▸ It is important to 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
▸ A lung-protective strategy in which the
PaCO2 is allowed to rise (permissive
hypercapnia) may reduce barotrauma and
enhance survival
41

42. Obstructive
airway diseases
Ventilation Approach
42

43. Obstructive
airway
diseases
▸ In patients with COPD or asthma,
initiation of mechanical ventilation
may worsen dynamic hyperinflation
(auto-PEEP or intrinsic PEEP)
▸ The goals of mechanical ventilation
in obstructive airway diseases are:
▹ to unload the respiratory muscles
▹ achieve adequate oxygenation
▹ minimize the development of dynamic
hyperinflation and its associated adverse
consequences
43

44. Obstructive
airway
diseases:
ASTHMA
▸ After the initiation of mechanical ventilation,
patients with status asthmaticus frequently
develop severe dynamic hyperinflation
▸ Can be minimized by delivering the lowest
possible minute ventilation in the least
possible time.
▸ Initial ventilatory strategy: delivery of
relatively low tidal volumes (eg, 6 mL/kg) and
lower respiratory rates (eg, 8-12 breaths/min)
with a high inspiratory flow rate.
44

45. Obstructive
airway
diseases:
COPD
▸ Patients with COPD have expiratory flow
limitation and are prone to the development
of dynamic 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
45

46. Noninvasive
Ventilatory
Support
46

47. Noninvasive
Ventilatory
Support
▸ Ventilatory support via a nasal or full-face
mask rather than via an endotracheal tube
is increasingly being employed for patients
with acute or chronic respiratory failure
▸ 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
47

48. Respiratory
Failure
Medication
Pharmacotherapy for cardiogenic pulmonary edema and
acute exacerbations of COPD
48

49. Diuretics
▸ First-line therapy generally includes
a loop diuretic such as furosemide,
which inhibits sodium chloride
reabsorption in the ascending loop
of Henle
▸ Administer loop diuretics such as
furosemide intravenously (IV)
because this allows both superior
potency and a higher peak
concentration despite an increased
incidence of adverse effects
49

50. Nitrates
▸ Nitrates reduce myocardial oxygen
demand by lowering preload and
afterload
▸ Sublingual nitroglycerin tablets and
spray are particularly useful in the
patient who presents with acute
pulmonary edema with a systolic
blood pressure of at least 100 mm
Hg
50

51. Opioid
Analgesics
▸ Morphine IV is an excellent adjunct
in the management of acute
pulmonary edema
▸ In addition to anxiolysis and
analgesia, its most important effect
is venodilation, which reduces
preload
▸ It also causes arterial dilatation,
which reduces systemic vascular
resistance and may increase cardiac
output
51

52. Inotropic
Agents
▸ The principal inotropic agents are
dopamine, dobutamine, inamrinone
(formerly amrinone), milrinone,
dopexamine, and digoxin
▸ In patients with hypotension who
present with CHF, dopamine and
dobutamine usually are employed
52

53. Beta2
Agonists
▸ 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
53

54. Xanthine
Derivatives
▸ Theophylline has a number of physiologic
effects, including increases in collateral
ventilation, respiratory muscle function,
mucociliary clearance, and central
respiratory drive
▸ It partially acts by inhibiting
phosphodiesterase, elevating cellular cAMP
levels, or antagonizing adenosine receptors
in the bronchi, resulting in relaxation of
smooth muscle
54

55. Cortico-
steroids
▸ Corticosteroids have been shown to be
effective in accelerating recovery from
acute COPD exacerbations and are an
important anti-inflammatory therapy in
asthma
▸ Although they may not make a clinical
difference in the emergency department,
they have some effect 6-8 hours into
therapy; therefore, early dosing is critical.
55

56. Summary of
guidelines
56

57. Summary
of
guidelines
Bilevel noninvasive mechanical ventilation
(NIV) may be considered in COPD patients with
an acute exacerbation in the following three
clinical settings:
1. To prevent acute respiratory acidosis (ie, when PaCO
2 is normal or elevated but pH is normal)
2. To prevent endotracheal intubation and invasive
mechanical ventilation in patients with mild-to
moderate acidosis and respiratory distress
3. As an alternative to invasive ventilation in patients
with severe acidosis and more severe respiratory
distress
57

58. Bilevel
NIV
▸ Bilevel NIV also may be used as the only
method for providing ventilatory support in
patients who are not candidates for or
decline invasive mechanical ventilation
▸ Bilevel NIV is recommended as follows:
▹ Patients with ARF leading to acute or acute-on-
chronic respiratory acidosis (pH ≤7.35) due to COPD
exacerbation
▹ Patients considered to require endotracheal
intubation and mechanical ventilation, unless the
▹ patient is immediately deteriorating
58

59. Summary
of
guidelines
▸ Either bilevel NIV or continuous positive
airway pressure (CPAP) is recommended
for patients with ARF due to cardiogenic
pulmonary edema
▸ CPAP or bilevel NIV is suggested for
patients with ARF due to cardiogenic
pulmonary edema in the prehospital setting
▸ Early NIV is suggested for
immunocompromised patients with ARF
59

60. Summary
of
guidelines
NIV use is suggested as follows:
▹ For patients with postoperative ARF
▹ Can be offered to dyspneic patients for palliation in the
setting of terminal cancer or other terminal conditions
▹ For the prevention of post-extubation respiratory
failure in high-risk patients; not suggested to prevent
post-extubation respiratory failure in non–high-risk
patients
▹ To facilitate weaning from mechanical ventilation in
patients with hypercapnic respiratory failure
60