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RESPIRATORY
FAILURE
Dr. Hafsa Imtiaz (DPT)
Definition
 When pulmonary gas exchange fails to maintain
normal oxygen and carbon dioxide levels is referred to
as respiratory failure.
 Hypoxia= reduced arterial concentration of Oxygen.
 Hypercapnia= increased arterial concentration of CO2.
Classification
 On the presence or absence of hypercapnia respiratory
failure is classified into two types:
 Type 1 or hypoxic and normocapnic respiratory failure
 Type 2 or hypercapnic respiratory failure
 Also classified as:
 Acute
 Chronic
Type 1 Or Hypoxic And Normocapnic
Respiratory Failure
 Is defined as “ when arterial oxygen concentration
(PaO) is lower then 60mmHg and carbon dioxides
level remains same or decreases (PaCO2). “
 This is the most common type
 Occur in almost all acute lung diseases affecting unit or
part of lungs.
Causes Of type 1 Respiratory failure
ACUTE CHRONIC
Acute asthma COPD
Pulmonary edema Lung Fibrosis
Pneumonia Lymphangitic carcinomatosis
Lobar collapse Right to left shunts
pneumothorax
Pulmonary embolus
ARDS (acute respiratory distress
syndrome)
Pathophysiology
 When lung disease i.e. pneumonia or asthma affects any part of lung,
impairs ventilation through that part.
 blood entering to these regions of lungs, become hypoxic and carbon
dioxide laden.
 Ventilation of lungs in normal regions increases to remove excess
carbon dioxide leading to normocapnia
 But unable to restore normal oxygen level because the hemoglobin
passing through normal lung areas is already saturated with oxygen
leading to hypoxia
 Admixture of blood from normally ventilated and under ventilated
regions of lungs leads to type 1 respiratory failure “hypoxia with
normocapnia”
Blood Gas Abnormalities In Type 1
Respiratory Failure
 Hypoxia (PaO2 <8.0 kPa (60mmHg))
 Normal or low PaCO2 (≤6 kPa (45mmHg))
 H+ remains normal
 Bicarbonate level remains normal
TYPE II respiratory failure
 Hypoxia i.e. <60mmHg
 Hypercapnic i.e. CO2 level >45mmHg
 Seen in conditions causing generalized lung damage
 Leading to severe ventilation perfusion mismatch
 Leaving insufficient normal lung to correct PaCO2.
 Occur due to any disease that reduces total ventilation either
of lungs itself or any part of neuromuscular mechanism of
ventilation.
Causes Of Type II Respiratory Failure
Acute Chronic
Acute severe asthma COPD
Acute exacerbation of COPD Sleep apnea
Upper airway obstruction kyphoscoliosis
Acute neuropathies/ paralysis Myopathies/muscular dystrophy
Narcotic Drugs Ankylosing spondylitis
Primary alveolar
hyperventilation
Flail chest injury
Pathophysiology
 Any condition which impairs large area of lungs or
affecting neuromuscular system of ventilation such as
Guillain–Barré syndrome
 Leaving insufficient area to compensate ventilation
perfusion mismatch
 Leading to increased PaCO2 and decreased PaO2 due
to impaired ventilation
Blood Gas Abnormalities In Type II
Respiratory Failure
 Hypoxia (PaO2 <8.0kPa (60mmHg))
 Hypercapnia PaCO2 (>6kPa (45mmHg))
 H+ level
 Acute= Increased
 Chronic= normal or increased
 Bicarbonate
 Acute= normal (kidney compensate)
 Chronic= increased
Acute Respiratory Failure
 Acute respiratory failure is characterized by life-
threatening derangements in arterial blood gases and
acid-base status
 Acute hypercapnic respiratory failure develops over
minutes to hours; therefore, ph is less than 7.3.
Causes Of Acute respiratory Failure
Type I Type II
Acute asthma Acute severe asthma
Pulmonary edema Acute exacerbation of COPD
Pneumonia Upper airway obstruction
Lobar collapse Acute neuropathies/ paralysis
pneumothorax Narcotic Drugs
Pulmonary embolus Primary alveolar
hyperventilation
ARDS (acute respiratory distress
syndrome)
Flail chest injury
Chronic Respiratory Failure
 Chronic respiratory failure is a condition that results in the inability
to effectively exchange carbon dioxide and oxygen, and
induces chronically low oxygen levels or chronically high carbon
dioxide levels.
 manifestations of chronic respiratory failure are less dramatic and
may not be as readily apparent.
 Chronic respiratory failure develops over several days or longer,
allowing time for renal compensation and an increase in
bicarbonate concentration. Therefore, the pH usually is only
slightly decreased
Cont.
 Most common cause of chronic type II respiratory
failure is severe COPD
 PaCO2 are persistently raised but there is no persisting
acidemia because kidney retain bicarbonate correcting
arterial PH to normal.
Causes Of Chronic Respiratory
Failure
Type I Type II
COPD COPD
Lung Fibrosis Sleep apnea
Lymphangitic carcinomatosis kyphoscoliosis
Right to left shunts Myopathies/muscular dystrophy
Ankylosing spondylitis
Sign And Symptoms
 Respiratory failure is accompanied by a number of symptoms
including:
 Bluish coloration of the skin or mucous membranes (Cyanosis)
 restlessness, anxiety, confusion, seizures, or coma
 Fainting or change in level of consciousness or lethargy
 Fatigue
 Tachycardia or variety of arrythmias result from hypoxemia and acidosis.
 Tachyapnea
 Dyspnea due to Excessive respiratory effort, vagal receptors, and chemical
stimuli (hypoxemia and/or hypercapnia)
 Asterixis may be observed with severe hypercapnia
DIAGNOSIS
 Careful history taking
 ABG analysis
 Chest radiography
 Pulmonary functions tests (PFTs)
 Electrocardiography (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
Cont.
 A complete blood cell (CBC) count may indicate anemia, which
can contribute to tissue hypoxia, whereas polycythemia may
indicate chronic hypoxemic respiratory failure.
 Renal and hepatic function testing
 Measuring serum creatine kinase with fractionation and troponin I
helps exclude recent myocardial infarction in a patient with
respiratory failure
 In chronic hypercapnic respiratory failure, serum levels of thyroid-
stimulating hormone (TSH) should be measured to evaluate the
possibility of hypothyroidism, a potentially reversible cause of
respiratory failure.
Radiography
 Chest radiography is essential in the evaluation of respiratory failure
because it frequently reveals the cause
 Increased heart size, vascular redistribution, peribronchial cuffing, pleural
effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest
hydrostatic edema; the lack of these findings suggests acute respiratory distress
syndrome (ARDS).
Pulmonary function test
 Patients with acute respiratory failure generally are unable to
perform PFTs; however, these tests are useful in the evaluation of
chronic respiratory failure.
 Normal values for forced expiratory volume in 1 second (FEV1)
and forced vital capacity (FVC) suggest a disturbance in
respiratory control. A decrease in the FEV1 -to-FVC ratio
(FEV1/FVC) indicates airflow obstruction, whereas a reduction in
both FEV1 and FVC and maintenance of FEV1/FVC suggest
restrictive lung disease.
 Respiratory failure is uncommon in obstructive diseases when
FEV1 is greater than 1 L and in restrictive diseases when FVC is
greater than 1 L
Management
 For Acute Respiratory failure:
 Type 1:
 40-60% oxygen by mask relieves hypoxia
 Mechanical ventilation may be used in patients with severe
pneumonia affecting several lobes
 Humidified oxygen should be given to those who requires
high conc. Of oxygen for more than few hours
Cont.
 Type II:
 Those with high ventilatory drive but unable to move sufficient air and if
inspiratory stridor is present indicates acute upper airway obstruction from
foreign body inhalation or laryngeal obstruction. Life saving management
includes.
 Heimlich maneuver (first-aid procedure for dislodging an obstruction from a
windpipe in which a sudden strong pressure is applied on abdomen, between the
navel and the ribcage.)
 immediate intubation or
 tracheostomy
Cont.
 In case of tension pneumothorax air should be aspirated and chest
drain inserted
 Patient with history of Asthma and COPD salbutamol 2.5mg
nebulised with oxygen should be given until bronchospasm is
relieved
 Underlying cause should be treated appropraitely.
 Patient with COPD and type II respiratory failure become sensitized
to increased level of CO2
 Their ventilatory drive depends on increased levels of CO2
 So low level of oxygen that is 24-28% by venturi mask should be
given to avoid respiratory depression
Lung Transplantation
 Is a treatment choice for patients who are
unresponsive to medical treatment
 Single lung transplantation may be used for
patients with advanced emphysema or lung
fibrosis
 Both lungs are transplanted in patients with
conditions causing infections such as cystic
fibrosis or bronchiectasis
 heart lung transplantation is indicated in
patients with congenital heart diseases
Respiratory failure

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Respiratory failure

  • 2. Definition  When pulmonary gas exchange fails to maintain normal oxygen and carbon dioxide levels is referred to as respiratory failure.  Hypoxia= reduced arterial concentration of Oxygen.  Hypercapnia= increased arterial concentration of CO2.
  • 3. Classification  On the presence or absence of hypercapnia respiratory failure is classified into two types:  Type 1 or hypoxic and normocapnic respiratory failure  Type 2 or hypercapnic respiratory failure  Also classified as:  Acute  Chronic
  • 4. Type 1 Or Hypoxic And Normocapnic Respiratory Failure  Is defined as “ when arterial oxygen concentration (PaO) is lower then 60mmHg and carbon dioxides level remains same or decreases (PaCO2). “  This is the most common type  Occur in almost all acute lung diseases affecting unit or part of lungs.
  • 5. Causes Of type 1 Respiratory failure ACUTE CHRONIC Acute asthma COPD Pulmonary edema Lung Fibrosis Pneumonia Lymphangitic carcinomatosis Lobar collapse Right to left shunts pneumothorax Pulmonary embolus ARDS (acute respiratory distress syndrome)
  • 6. Pathophysiology  When lung disease i.e. pneumonia or asthma affects any part of lung, impairs ventilation through that part.  blood entering to these regions of lungs, become hypoxic and carbon dioxide laden.  Ventilation of lungs in normal regions increases to remove excess carbon dioxide leading to normocapnia  But unable to restore normal oxygen level because the hemoglobin passing through normal lung areas is already saturated with oxygen leading to hypoxia  Admixture of blood from normally ventilated and under ventilated regions of lungs leads to type 1 respiratory failure “hypoxia with normocapnia”
  • 7. Blood Gas Abnormalities In Type 1 Respiratory Failure  Hypoxia (PaO2 <8.0 kPa (60mmHg))  Normal or low PaCO2 (≤6 kPa (45mmHg))  H+ remains normal  Bicarbonate level remains normal
  • 8. TYPE II respiratory failure  Hypoxia i.e. <60mmHg  Hypercapnic i.e. CO2 level >45mmHg  Seen in conditions causing generalized lung damage  Leading to severe ventilation perfusion mismatch  Leaving insufficient normal lung to correct PaCO2.  Occur due to any disease that reduces total ventilation either of lungs itself or any part of neuromuscular mechanism of ventilation.
  • 9. Causes Of Type II Respiratory Failure Acute Chronic Acute severe asthma COPD Acute exacerbation of COPD Sleep apnea Upper airway obstruction kyphoscoliosis Acute neuropathies/ paralysis Myopathies/muscular dystrophy Narcotic Drugs Ankylosing spondylitis Primary alveolar hyperventilation Flail chest injury
  • 10. Pathophysiology  Any condition which impairs large area of lungs or affecting neuromuscular system of ventilation such as Guillain–Barré syndrome  Leaving insufficient area to compensate ventilation perfusion mismatch  Leading to increased PaCO2 and decreased PaO2 due to impaired ventilation
  • 11. Blood Gas Abnormalities In Type II Respiratory Failure  Hypoxia (PaO2 <8.0kPa (60mmHg))  Hypercapnia PaCO2 (>6kPa (45mmHg))  H+ level  Acute= Increased  Chronic= normal or increased  Bicarbonate  Acute= normal (kidney compensate)  Chronic= increased
  • 12. Acute Respiratory Failure  Acute respiratory failure is characterized by life- threatening derangements in arterial blood gases and acid-base status  Acute hypercapnic respiratory failure develops over minutes to hours; therefore, ph is less than 7.3.
  • 13. Causes Of Acute respiratory Failure Type I Type II Acute asthma Acute severe asthma Pulmonary edema Acute exacerbation of COPD Pneumonia Upper airway obstruction Lobar collapse Acute neuropathies/ paralysis pneumothorax Narcotic Drugs Pulmonary embolus Primary alveolar hyperventilation ARDS (acute respiratory distress syndrome) Flail chest injury
  • 14. Chronic Respiratory Failure  Chronic respiratory failure is a condition that results in the inability to effectively exchange carbon dioxide and oxygen, and induces chronically low oxygen levels or chronically high carbon dioxide levels.  manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.  Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased
  • 15. Cont.  Most common cause of chronic type II respiratory failure is severe COPD  PaCO2 are persistently raised but there is no persisting acidemia because kidney retain bicarbonate correcting arterial PH to normal.
  • 16. Causes Of Chronic Respiratory Failure Type I Type II COPD COPD Lung Fibrosis Sleep apnea Lymphangitic carcinomatosis kyphoscoliosis Right to left shunts Myopathies/muscular dystrophy Ankylosing spondylitis
  • 17. Sign And Symptoms  Respiratory failure is accompanied by a number of symptoms including:  Bluish coloration of the skin or mucous membranes (Cyanosis)  restlessness, anxiety, confusion, seizures, or coma  Fainting or change in level of consciousness or lethargy  Fatigue  Tachycardia or variety of arrythmias result from hypoxemia and acidosis.  Tachyapnea  Dyspnea due to Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia)  Asterixis may be observed with severe hypercapnia
  • 18. DIAGNOSIS  Careful history taking  ABG analysis  Chest radiography  Pulmonary functions tests (PFTs)  Electrocardiography (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
  • 19. Cont.  A complete blood cell (CBC) count may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure.  Renal and hepatic function testing  Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure  In chronic hypercapnic respiratory failure, serum levels of thyroid- stimulating hormone (TSH) should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure.
  • 20. Radiography  Chest radiography is essential in the evaluation of respiratory failure because it frequently reveals the cause  Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS).
  • 21. Pulmonary function test  Patients with acute respiratory failure generally are unable to perform PFTs; however, these tests are useful in the evaluation of chronic respiratory failure.  Normal values for forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) suggest a disturbance in respiratory control. A decrease in the FEV1 -to-FVC ratio (FEV1/FVC) indicates airflow obstruction, whereas a reduction in both FEV1 and FVC and maintenance of FEV1/FVC suggest restrictive lung disease.  Respiratory failure is uncommon in obstructive diseases when FEV1 is greater than 1 L and in restrictive diseases when FVC is greater than 1 L
  • 22. Management  For Acute Respiratory failure:  Type 1:  40-60% oxygen by mask relieves hypoxia  Mechanical ventilation may be used in patients with severe pneumonia affecting several lobes  Humidified oxygen should be given to those who requires high conc. Of oxygen for more than few hours
  • 23. Cont.  Type II:  Those with high ventilatory drive but unable to move sufficient air and if inspiratory stridor is present indicates acute upper airway obstruction from foreign body inhalation or laryngeal obstruction. Life saving management includes.  Heimlich maneuver (first-aid procedure for dislodging an obstruction from a windpipe in which a sudden strong pressure is applied on abdomen, between the navel and the ribcage.)  immediate intubation or  tracheostomy
  • 24. Cont.  In case of tension pneumothorax air should be aspirated and chest drain inserted  Patient with history of Asthma and COPD salbutamol 2.5mg nebulised with oxygen should be given until bronchospasm is relieved  Underlying cause should be treated appropraitely.  Patient with COPD and type II respiratory failure become sensitized to increased level of CO2  Their ventilatory drive depends on increased levels of CO2  So low level of oxygen that is 24-28% by venturi mask should be given to avoid respiratory depression
  • 25. Lung Transplantation  Is a treatment choice for patients who are unresponsive to medical treatment  Single lung transplantation may be used for patients with advanced emphysema or lung fibrosis  Both lungs are transplanted in patients with conditions causing infections such as cystic fibrosis or bronchiectasis  heart lung transplantation is indicated in patients with congenital heart diseases