The document provides an extensive overview of acute respiratory failure, including its definition, classification into hypoxemic and hypercapnic types, and underlying causes such as hypoventilation and ventilation-perfusion mismatch. It also outlines clinical manifestations, diagnostic methods, and treatment options for the different types of respiratory failure. Key clinical features include dyspnea, confusion, and tachypnea, with management strategies ranging from addressing underlying conditions to mechanical ventilation when necessary.

1. Acute Respiratory Failure
Deanship of Graduate Studies &
Scientific Research, 21 September
University of Medical & Applied
Sciences.
Presented by: Mosa Alfageh BS, MsRC Student
Supervised by: Prof: Ahmed
Fad dahmesh BS, MsRC Student

2. 11/23/2024 2
MsRC
⇰Introduction
⇰Defination
⇰Classification
⇰Pathophysiology
⇰Clinical manifestation
Outline

4. Introduction
• The body depends on the coordinated functioning of the central nervous
system, pulmonary system, heart, and vascular system to achieve effective
respiration. Respiratory failure arises when one or more of these systems or
organs fail to maintain optimal functioning. If respiratory failure occurs rapidly,
such that compensatory mechanisms cannot accommodate, or if these
compensatory mechanisms are overwhelmed, acute respiratory failure
develops.

5. Definition
11/23/2024 MsRC 5
Failure in one or both gas exchange functions: oxygenation and
carbon dioxide elimination
In practice
Pao2 <60mmhg or PaCO2>50mmhg
Respiratory failure is a syndrome of inadequate gas exchange due to
dysfunction of one or more essential components of the respiratory
system

6. Types of respiratory failure
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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.

7. TYPE 3 (PERI-OPERATIVE):
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Residual anesthesia effects, post-operative pain, and abnormal abdominal
mechanics contribute to decreasing FRC and progressive collapse of
dependant lung units.
Causes of post-operative atelectasis include;
• Decreased FRC
• Supine/ obese/ ascites
• Anesthesia
• Upper abdominal incision
• Airway secretions

8. TYPE 4 (SHOCK):
11/23/2024 MsRC 8
Describes patients who are intubated and ventilated in the
process of resuscitation for shock
• cardiogenic
• hypovolemic
• septic

9. 11/23/2024 MsRC 9

10. 11/23/2024 MsRC 10

11. 11/23/2024 MsRC 11

12. ARF is classified as:
Hypoxemic Respiratory
Failure
• PaO2 < 60 mmHg
• PaCO2 Normal or Low
• PA-aO2 Increased
Hypercapnic
Respiratory Failure
• Pao2 decreased
• PaCO2 > 50 mmHg
• PA-aO2 Normal
• PH decreased

16. Hypoxemic Respiratory
Failure TYPE 1
• Definition: Hypoxemic respiratory failure is a subtype of acute respiratory failure
characterized by inadequate oxygenation of the blood. (hypoxemia) without an
increased level of carbon dioxide in the blood (hypercapnia), and indeed the PaCO2 may be
normal or low.
• Key Indicator: Low levels of oxygen (PaO2) in arterial blood, typically defined as
PaO2 less than 60 mmHg.
PaCO2normal or decreased (<50 mmHg) ,PA-aO2increased
• Impaired Gas Exchange: The condition is marked by the failure of the lungs to
efficiently transfer oxygen from the air into the bloodstream.

17. Etiology and Pathophysiology
1.Decreased O2 Delivery:(e.g. at high altitude)
2.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
3.V/Q Mismatch:(parts of the lung receive oxygen but not
enough blood to absorb it, e.g. pulmonary embolism)
4.Shunt:(oxygenated blood mixes with non-oxygenated blood
from the venous system, e.g. right-to-left shunt)
5.Decreased Diffusion:(oxygen cannot enter the capillaries due
to parenchymal disease, e.g. in pneumonia or ARDS)

18. 1.Decreased O2 Delivery:
Examples-
• A decrease in barometric pressure [e.g. breathing at high
altitude].
• A decrease in FIO2 – accidental [e.g. anesthetist does not
supply enough oxygen or improper installation of oxygen
supply lines or a leak in the breathing circuit].
• P(A-a)O2 normal
• PaCO2 is decreased. This reduction in PaCO2 (hypocapnia) is
due to hyperventilation in response to hypoxemia.
• Peripheral chemoreceptors sense the low arterial PO2 and
initiate an increase in ventilation through their input to the
medullary respiratory centre
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Etiology and Pathophysiology

19. Etiology and Pathophysiology
2.Hypoventilation:
• Mechanisms:
• CNS depression: Drugs (opiates, sedatives), medical conditions (strokes, brain
tumors)
• Neuromuscular disorders: ALS, spinal cord injury, Guillain-Barre, myasthenia
gravis
• Chest wall or pleural issues: Ankylosing Spondylitis, pleural effusions,
pneumothorax, obesity
• Airway obstruction: Asthma, COPD, foreign body aspiration
• Note :this form can also cause type 2 respiratory failure if severe

20. Etiology and Pathophysiology
3.V/Q Mismatch:
• Mechanisms:
• Ventilation-perfusion mismatch: Airflow (V) doesn't reach areas
with blood flow (Q), or vice versa.
• Dead space ventilation: Ventilation to areas without blood flow
(e.g., collapsed alveoli).
• Shunting within the lung: Blood flow bypassing alveoli (e.g.,
pneumonia, emboli).

21. Ventilation Perfusion ratio VA/Q
• The overall V/Q = 0.8 [ V=4Lper min, P=5L per min
• Ranges between 0.3 and 3.0
• Upper zone –nondependent area has higher ≥ 1
• Lowe zone – dependent area has lower ≤ 1
• VP ratio indicates overall respiratory functional status of
• lung
• V/Q = 0 means ,no ventilation-called SHUNT
• V/Q = ∞ means ,no perfusion – called DEAD SPACE
11/23/2024 MsRC 21

22. SHUNTS have different effects on arterial PCO2 (PaCO2 ) than on
arterial
PO2 (PaO2 ). Blood passing through under ventilated alveoli tends
to retain its CO2 and does not take up enough O2.
• Blood traversing over ventilated alveoli gives off an excessive
amount of
CO2, but cannot take up increased amount of O2 because of the
shape of the oxygen-hemoglobin (oxy-Hb) dissociation curve.
• from the over ventilated alveoli to compensate for the under
ventilated alveoli. Thus, with Shunt, PACO2 -to-PaCO2 gradients
are small, and PAO2 -to-PaO2 gradients are usually large.
11/23/2024 MsRC 22

23. VENTILATION PERFUSION INEQUALITY
• PaCO2 is normal
• P(A-a)O2 is elevated
• VA/Q inequality is the most common cause of
hypoxemia in
disease states
11/23/2024 MsRC 23

24. VENTILATION PERFUSION INEQUALITY
• The distribution of ventilation varies with common events,
such as changes in body posture, lung volumes, and age.
• Increasing age produces a gradual increase in the degree of
the
VA/Q inequality.
• Ventilation–perfusion imbalance exists even in the normal
lung, depending on the region, but remains fairly tightly
regulated when assessing normal lung aggregate function
11/23/2024 MsRC 24

25. 11/23/2024 MsRC 25

26. VENTILATION PERFUSION
INEQUALITY

27. In normal lungs, the volume of blood perfusing the lungs and the amount of gas reaching
the alveoli are almost identical. So, when you compare normal alveolar ventilation (4 to 6
L/min) to pulmonary blood flow (4 to 6 L/min), V/Q=1 (ventilation-perfusion
mismatch )-1ml of air for 1 ml of blood flow i.e.., 1:1
Condition that alter V/Q (V/Q mismatch )
• Increased secretion in airways-COPD
• Inc secretion in alveoli- pneumonia Limited airflow ventilation
• Bronchospasm- asthma but have no effect on blood flow
• Alveolar collapse- Atelectasis to the gas exchange units .
• Embolus.
PATHOPHYSIOLOGY-V/Q

28. REGIONAL V/Q DIFFERENCES IN THE NORMAL LUNG

29. Range of ventilation to perfusion (V/Q) relationships.

30. Etiology and
Pathophysiology
4.Shunt
• Types:
• Intracardiac: Blood flows directly from right to left side of heart without going through
lungs (congenital heart defects).
• Intrapulmonary: Blood bypasses alveoli within the lungs (pulmonary emboli, ARDS,
pneumonia with abscesses)

31. RIGHT TO LEFT SHUNT
• Shunt refers to the entry of blood into the systemic
arterial system without going through ventilated areas
of lung.
• Shunt may be anatomical or physiological.
• P(A-a)O2 is elevated.
• PaCO2 is normal.
11/23/2024 MsRC 31

32. RIGHT TO LEFT SHUNT
•Anatomic shunt: when a portion of blood bypasses the
lungs through an anatomic channel.
In healthy individuals
i) A portion of the bronchial circulation’s (blood supply to the
conducting zone of the airways) venous blood drains into the
pulmonary vein.
ii) A portion of the coronary circulation’s venous blood drains
through the thebesian veins into the left ventricle.
note: i & ii represent about 2% of the cardiac output and
account for 1/3 of the normal P(A-a)O2 observed in health.
11/23/2024 MsRC 32

33. RIGHT TO LEFT SHUNT
Congenital abnormalities
i) intra-cardiac shunt [e.g. Tetralogy of Fallot:
ventricular
septal defect + pulmonary artery stenosis]
ii) intra-pulmonary fistulas [direct communication
between a branch of the pulmonary artery and a
pulmonary vein].
11/23/2024 MsRC 33

34. RIGHT TO LEFT SHUNT
Physiologic shunt: In disease states, a portion of the
cardiac output goes through the regular pulmonary vasculature
but
does not come into contact with alveolar air due to filling of
the alveolar spaces with fluid [e.g. pneumonia, drowning,
pulmonary edema]
• An important diagnostic feature of a shunt
is that the arterial Po2 does not rise to the
normal level when the patient is given 100%
oxygen to breathe.
11/23/2024 MsRC 34

35. RIGHT TO LEFT SHUNT
Examples of intrapulmonary shunt.
(a) Collapsed and fluid filled alveoli are examples of intrapulmonary
shunt.
(b) Anomalous blood return of mixed
venous blood
bypasses the alveolus
and thereby
contributes to the
development of
intrapulmonary shunt
11/23/2024 MsRC 35

36. Etiology and Pathophysiology
• 5.Decreased Diffusion
• Mechanism:
• Oxygen can't easily cross from air sacs to the bloodstream due to:
• Thickened alveolar walls (scarring, protein buildup)
• Fluid in air sacs (edema, ARDS)
• Less membrane surface area (emphysema, lung collapse)
• Abnormal blood flow in capillaries (shunts, clots)

37. Clinical Manifestations
• 1. Dyspnea (Shortness of Breath)
• 2. Cyanosis
• 3. Tachypnea
• 4. Confusion or Altered Mental Status
• 5. Fatigue
• 6. Tachycardia
7. Use of Accessory Muscles

38. Diagnosis of Hypoxemic RF
• 1.Hypoventilation:
• Diagnosis:
• History and physical examination: Look for signs of respiratory distress,
decreased breath sounds.
• Chest X-ray: May reveal abnormalities like pneumonia or pleural effusions.
• ABG: Shows elevated CO2 levels and potentially low O2 levels.
• Pulmonary function tests: Measure lung function and identify airway obstruction.

39. Diagnosis of Hypoxemic RF
• 2.V/Q Mismatch
• Diagnosis:
• History and physical examination: Look for signs of respiratory distress and
underlying lung conditions.
• Chest X-ray and CT scan: May show abnormalities like pneumonia or emboli.
• ABG: May show low O2 levels and potentially elevated CO2 levels.
• V/Q scan: Helps identify areas of ventilation-perfusion mismatch.

40. Diagnosis of Hypoxemic RF
• 3.Shunt
• Diagnosis:
• History and physical examination: Look for signs of right heart strain or
pulmonary embolism.
• Chest X-ray and CT scan: May show enlarged heart or evidence of lung
abnormalities.
• Echocardiogram: To assess heart structure and function.
• V/Q scan: Helps identify areas of perfusion without ventilation (indicative of
shunt).

41. Diagnosis of Hypoxemic RF
• 4.Decreased Diffusion
• History and physical exam: Look for signs of respiratory distress, abnormal
breath sounds, and underlying lung conditions.
• Chest X-ray and CT scan: May show evidence of lung disease, fluid accumulation,
or structural abnormalities.
• Arterial blood gas (ABG): Shows low oxygen levels (PaO2) and potentially normal
or slightly elevated carbon dioxide levels (PaCO2).
• Pulmonary function tests: Can assess gas exchange efficiency and identify
ventilation-perfusion mismatch.

42. Treatment
1.Hypoventilation:
• Address the underlying cause: Reverse drug
effects, manage neurological disorders, treat
chest wall or airway issues.
• Non-invasive ventilation (BiPAP) or mechanical
ventilation may be needed in severe cases.
2. V/Q Mismatch:
• Address the underlying cause: Antibiotics for pneumonia, anticoagulation for emboli,
ventilation support for ARDS, bronchodilators for COPD.
• Oxygen therapy to improve oxygenation.
• Mechanical ventilation may be needed in severe cases.

43. Treatment
3.Shunt
• Depends on the type and cause of
shunt.
• Surgery for congenital heart defects.
• Anticoagulation for pulmonary emboli.
• Antibiotics for pneumonia with
abscesses.
• Mechanical ventilation for ARDS.
• 4.Decreased Diffusion
• Address the underlying cause:
• Treat lung disease with
medications or surgery
• Manage fluid accumulation with
diuretics or other therapies
• Anticoagulation for pulmonary
emboli
• Oxygen therapy to improve
oxygenation
• Mechanical ventilation may be
needed in severe cases

44. 11/23/2024 MsRC 44

45. Hypercapnic Respiratory Failure:TYPE 2
• Definition: (Hypoxemia with hypercapnia)
• Medical condition marked by elevated carbon dioxide (hypercapnia) and often concurrent low oxygen levels
(hypoxemia) in the blood.
• Key Indicators:
• Elevated levels of carbon dioxide (PaCO2) in arterial blood (typically >50 mmHg).
• Often accompanied by low levels of oxygen (PaO2), contributing to hypoxemia.
PaO2decreased (< 60 mmHg )
PaCO2increased (> 50 mmHg )
PA-aO2normal
Ph decreased
• Defined as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be
eliminated. The underlying causes include:
• Underlying Causes:
• Impaired ventilatory function or inadequate respiratory muscle activity.
• Commonly associated with chronic conditions like COPD exacerbation, neuromuscular diseases (e.g.,
myasthenia gravis), or chest wall disorders.

46. Etiology and pathophysiology
• Hypoventilation: This is the most common cause of hypercapnic
respiratory failure and occurs when the body is not taking in enough
breaths or the breaths are not deep enough. This can be due to a
variety of reasons, including:
• CNS depression: This can be caused by medications like opioids, sedatives, or
anesthesia, or by conditions like stroke, brain tumors, or metabolic imbalances.
• Neuromuscular disorders: These disorders affect the nerves or muscles that
control breathing, such as ALS, Guillain-Barre syndrome, or myasthenia gravis.
• Chest wall or pleural disease: Conditions that restrict the movement of the
chest wall or lungs, such as Ankylosing Spondylitis, pleural effusions, or
pneumothorax, can make it difficult to take deep breaths.
• Obesity: Severe obesity can restrict the movement of the diaphragm and make
it difficult to breathe deeply.
• Airway obstruction: Blockage of the upper or lower airways can make it
difficult to get enough air into the lungs.

47. CAUSE OF HYPO VENTILATION

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51. Clinical Features
• Respiratory:
• Tachypnea: Increased breathing rate, often in an attempt to compensate for the lack of oxygen.
• Shallow breaths: Patients may take shallow breaths due to fatigue or muscle weakness.
• Apnea: In severe cases, patients may stop breathing altogether for short periods.
• Wheezing: This may be present if there is also an underlying airway obstruction.
• Crackles: These are abnormal sounds heard during lung auscultation, which can indicate fluid
in the lungs.
• Neurological:
• Confusion: Patients may be confused or disoriented due to the buildup of carbon
dioxide in the blood.
• Somnolence: Patients may feel drowsy or sleepy.
• Headache: This is a common symptom of hypercapnia.
• Coma: In severe cases, patients may lapse into a coma

52. Diagnosis
1. ABG
2.Chest X-ray
3.Pulmonary Function Tests (PFTs)
4.Neuromuscular Studies
5.Capnography
6.Continuous Oxygen Saturation
Monitoring

53. Treatments
• Bronchodilators
• Oxygen Therapy
• Non-Invasive Ventilation (NIV): BiPAP and
CPAP
• Corticosteroids
• Mechanical Ventilation

54. • Shunt versus Dead space
• • Anatomic shunt cause deoxygenated blood to
• transfer into the systemic circulation without
passing
• through the pulmonary circulation:
• • Bronchial and Thebesian Veins
• • Accounts for 75% of the difference between
alveolar
• O2 and arterial O2.
11/23/2024 MsRC 56

57. 59
DEAD SPACE
Not all inspired gas participating in alveolar
gas exchange
DEAD SPACE – VD
Some gas remains in the non respiratory
airways
ANATOMIC DEAD SPACE
Some gas in the non per fused /low per fused
alveoli
PHYSIOLOGIC DEAD SPACE

58. 60
DEAD SPACE
Means – Wasted Ventilation
Dead Space estimated as ratio Vd/Vt
Dead space expressed as a fraction of total tidal volume Vd/Vt
Vd = PACO2-PECO2
Vt PACO2
Normal dead space ratio < 33%
Q
V
V/Q= ∞

59. • 3. ALVEOLAR – ARTERIAL O2 GRADIENT : PAO2-PaO2
• Varies with FiO2 & age
• 7-14 to 31-56mm Hg
• 4. ARTERIAL – ALVEOLAR RATIO : PaO2/PAO2
• FiO2 independent
• >0.75 -normal
• 0.40-0.75-acceptable
• 0.20-0.40– poor
• < 0.20 –very poor
11/23/2024 MsRC 61

60. • The Alveolar–arterial gradient ( A–a gradient
• is a measure of the difference between
• the alveolar concentration (A) of oxygen and
• the arterial (a) concentration of oxygen.
• It is used in diagnosing the source of hypoxemia.
• It helps to assess the integrity of alveolar capillary unit.
• For example, in high altitude, the arterial oxygen [[PaO2]]
• is low but only because the alveolar oxygen (PAO2) is also
• low. However, in states of ventilation perfusion
• mismatch, such as pulmonary embolism or right-to-left
• shunt, oxygen is not effectively transferred from
• the alveoli to the blood which results in elevated A-a
• gradient
11/23/2024 MsRC 62