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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
11/23/2024 2 MsRC ⇰Introduction ⇰Defination ⇰Classification ⇰Pathophysiology ⇰Clinical manifestation Outline
‏‏RF - نس خة.pptx
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.
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
Types of respiratory failure 11/23/2024 MsRC 6 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.
TYPE 3 (PERI-OPERATIVE): 11/23/2024 MsRC 7 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
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
11/23/2024 MsRC 9
11/23/2024 MsRC 10
11/23/2024 MsRC 11
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
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
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.
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)
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 11/23/2024 MsRC 18 Etiology and Pathophysiology
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
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).
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
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
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
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
11/23/2024 MsRC 25
VENTILATION PERFUSION INEQUALITY
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
REGIONAL V/Q DIFFERENCES IN THE NORMAL LUNG
Range of ventilation to perfusion (V/Q) relationships.
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)
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
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
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
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
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
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)
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
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.
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.
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).
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.
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.
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
11/23/2024 MsRC 44
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.
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.
CAUSE OF HYPO VENTILATION
11/23/2024 48
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
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
Diagnosis 1. ABG 2.Chest X-ray 3.Pulmonary Function Tests (PFTs) 4.Neuromuscular Studies 5.Capnography 6.Continuous Oxygen Saturation Monitoring
Treatments • Bronchodilators • Oxygen Therapy • Non-Invasive Ventilation (NIV): BiPAP and CPAP • Corticosteroids • Mechanical Ventilation
• 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
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
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
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= ∞
• 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
• 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
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx
‏‏RF - نس خة.pptx

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‏‏RF - نس خة.pptx

  • 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
  • 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 11/23/2024 MsRC 6 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): 11/23/2024 MsRC 7 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
  • 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 11/23/2024 MsRC 18 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
  • 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
  • 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
  • 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

Editor's Notes

  • #2: ABCDEF bundle Element A (Assess, Prevent, and Manage Pain) Element B (Both SATs and SBTs) Element C (Choice of Analgesia and Sedation) Element D (Delirium Assess and Manage) Element E (Early Mobility and Exercise) Element F (Family Engagement/Empowerment)
  • #4: Ventilation Perfusion Diffusion
  • #30: 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.  2 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.
  • #45: HYPOVENTILATION • Hypoventilation is used here to refer to conditions in which alveolar ventilation is abnormally low in relation to oxygen uptake or carbon dioxide output. • Alveolar ventilation is the volume of fresh inspired gas going to the alveoli (i.e. Non–dead space ventilation). • Hypoventilation occurs when the alveolar ventilation is reduced and the alveolar Po2 therefore settles out at a lower level than normal. For the same reason, the alveolar Pco2, and therefore arterial Pco2, are also raised
  • #46: Increased airways resistance (chronic obstructive pulmonary disease, 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.
  • #47: HYPOVENTILATION • P(A-a)O2 is normal. • PaCO2 is elevated (hypercapnia) • Increasing the fraction of inspired oxygen (FIO2) can alleviate the hypoxemia and the hypercapnia can be corrected by mechanically ventilating the patient to eliminate CO2.