8. Definition
*Failure in one or both gas exchange functions:
oxygenation and carbon dioxide elimination
*In practice:
PaO2<60mmHg or PaCO2>50mmHg
*Derangements in ABGs and acid-base status
9. Definition
Respiratory failure is a syndrome of
inadequate gas exchange due to
dysfunction of one or more essential
components of the respiratory system
10. Types of Respiratory Failure
Type 1 (Hypoxemic ): * PO2 < 60 mmHg on room air.
Type 2 (Hypercapnic / Ventilatory): *PCO2 > 50
mmHg
Type 3 (Peri-operative): *This is generally a subset of
type 1 failure but is sometimes considered
separately because it is so common.
Type 4 (Shock): * secondary to cardiovascular
instability.
15. Type 4 (Shock)
Type IV describes patients who are intubated and
ventilated in the process of resuscitation for
shock
• Goal of ventilation is to stabilize gas
exchange and to unload the respiratory
muscles, lowering their oxygen consumption
*cardiogenic
*hypovolemic
*septic
16. Hypoxemic Respiratory Failure (Type 1)
Causes of Hypoxemia
1. Low FiO2 (high altitude)
2. Hypoventilation
3. V/Q mismatch (low V/Q)
4. Shunt (Qs/Qt)
5. Diffusion abnormality
6. low mixed venous oxygen due to cardiac
desaturation with one of above mentioned
factors.
17. Physiologic Causes of
Hypoxemia
Low FiO2 is the primary cause
of ARF at high altitude and
toxic gas inhalation
Hypoxemic Respiratory Failure (Type 1)
18. Physiologic Causes of Hypoxemia
However, the two most common causes of
hypoxemic respiratory failure in the ICU are
V/Q mismatch and shunt. These can be
distinguished from each other by their
response to oxygen. V/Q mismatch
responds very readily to oxygen whereas
shunt is very oxygen insensitive.
Hypoxemic Respiratory Failure (Type 1)
19. V/Q: possibilities
0
1
∞
V/Q =1 is “normal” or “ideal”
V/Q =0 defines “shunt”
V/Q =∞ defines “dead space” or “wasted ventilation”
21. Why does “V/Q mismatch” cause
hypoxemia?
Low V/Q units contribute to
hypoxemia
High V/Q units cannot compensate
for the low V/Q units
Reason being the shape of the
oxygen dissociation curve which is
not linear
22. Hypoxic respiratory failure
Gas exchange failure
Respiratory drive responds
Increased drive to breathe
– Increased respiratory rate
– Altered Vd /Vt (increased dead space etc)
– Often stiff lungs (oedema, pneumonia etc)
Increased load on the respiratory pump which
can push it into fatigue and precipitate
secondary pump failure and hypercapnia
25. Causes of increased dead space ventilation
*Pulmonary embolism
*Hypovolemia
*Poor cardiac output, and
*Alveolar over distension.
26. 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.
27. 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.
28. Components of Respiratory System
*CNS or Brain Stem *Nerves
*Chest wall (including pleura, diaphragm)
* Airways * Alveolar–capillary units
*Pulmonary circulation
29. Type 2 ( Ventilatory /Hypercapnic
Respiratory Failure)
Causes of Hypercapnia
1. Increased CO2 production (fever,
sepsis, burns, overfeeding)
2. Decreased alveolar ventilation
decreased RR
decreased tidal volume (Vt)
increased dead space (Vd)
31. Why does “V/Q mismatch” cause
hypoxemia?
• Low V/Q units contribute to
hypoxemia
• High V/Q units cannot compensate
for the low V/Q units
• Reason being the shape of the
oxygen dissociation curve which is
not linear
32. Hypoxic respiratory failure
• Gas exchange failure
• Respiratory drive responds
• Increased drive to breathe
– Increased respiratory rate
– Altered Vd /Vt (increased dead space etc)
– Often stiff lungs (oedema, pneumonia etc)
Increased load on the respiratory pump which can
push it into fatigue and precipitate secondary
pump failure and hypercapnia
35. Causes of increased dead space
ventilation
*Pulmonary embolism
*Hypovolemia
*Poor cardiac output, and
*Alveolar over distension.
36. 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.
37. 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.
38. Components of Respiratory System
*CNS or Brain Stem *Nerves
*Chest wall (including pleura, diaphragm)
* Airways * Alveolar–capillary units
*Pulmonary circulation
39. Type 2 ( Ventilatory /Hypercapnic
Respiratory Failure)
Causes of Hypercapnia
1. Increased CO2 production (fever,
sepsis, burns, overfeeding)
2. Decreased alveolar ventilation
• decreased RR
• decreased tidal volume (Vt)
• increased dead space (Vd)
43. NIF (negative inspiratory force). This is a measure
of the patient's respiratory system muscle
strength.
It is obtained by having the patient fully exhale.
Occluding the patient's airway or endotracheal
tube for 20 seconds, then measuring the maximal
pressure the patient can generate upon
inspiration.
NIF's less than -20 to -25 cm H2O suggest that the
patient does not have adequate respiratory muscle
strength to support ventilation on his own.
Evaluation of Hypercapnia
44. P0.1 max. is an estimate of the patient's
respiratory drive.
This measurement of the degree of pressure drop
during the first 100 milliseconds of a patient
initiated breath. A low P0.1 max suggests that the
patient has a low drive and a central
hypoventilation syndrome.
Central hypoventilation vs. Neuro-
muscular weakness
central = low P0.1 with normal NIF
Neuromuscular weakness = normal P0.1 with low
NIF
Evaluation of Hypercapnia
45. n The P (A—a)O2 ranges from 10 mm Hg in young
patients to approximately 25mm Hg in the elderly while
breathing room air.
n P (A-a)O2 if greater than >300 on 100% =
Shunt < 300 = V/Q mismatch
• RULE OF THUMB
The mean alveolar-to-arterial difference [P(A—a)o2]
increases slightly with age and can be estimated ~ by the
following equation:
Mean age-specific P(A—a)O2 age/4 + 4
A-a Gradient
46. Increased Work of Breathing
Work of breathing is due to physiological work and
imposed work.
Physiological work involves overcoming the elastic forces during
inspiration and overcoming the resistance of the airways and lung
tissue
Imposed Work of Breathing
In intubated patients, sources of imposed work of breathing include:
n the endotracheal tube,
n ventilator Circuit
n auto-PEEP due to dynamic hyperinflation with airflow obstruction, as is
commonly seen in the patient with COPD.
Increased Work of Breathing
n Tachypnea is the cardinal sign of increased work of breathing
n Overall workload is reflected in the minute volume needed to maintain
normocapnia.
47. Rationale for ventilatory assistance
Respiratoryload
Respiratorymuscles
capacity
Alveolar hypoventilation
PaO2 and PaCO2
Abnormal
ventilatorydrive
