ACUTE RESPIRATORY FAILURE

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ACUTE RESPIRATORY FAILURE

• Dr. Neha Gupta

University College of Medical Sciences GTB
Hospital, Delhi
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• Respiratory failure is inability to maintain
  either normal delivery of O2 to the tissues or
  the normal removal of CO2 from the tissues
  ( Egans- 9th edition)
• or
• Failure of gas exchange due to inadequate
  function of one or more essential components of
  respiratory system
• (Harrisons principles of internal medicine-
  16th edition)
• The condition results from imbalance between
  respiratory workload and ventilatory strength or
  endurance

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• Respiratory Failure
• PaO2 lt60, and/or
• PaCO2 gt50
• Pathophysiology
• Acute Chronic
• Hypoxemic (Type I) Hypercapnic (Type II)

By Campbell (1965)
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Physiology

• Normal respiration requires five separate
  components-
• Nervous system- dorsal and ventral nuclei of
  respiratory control group, their afferent and
  efferent nuclei
• Musculature- diaphragm, accessory msls and chest
  wall
• Airways- up to the terminal bronchiole
• Alveolar units
• Vasculature

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V/Q ratio
Condition V/Q ratio Consequences
V/Q match 1 Normal PaO2
Dead space ventilation gt1 ?PaO2 ?PaCO2
Intrapulmonary shunting lt1 ?PaO2 ?PaCO2
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Intrapulmonary shunts

• PaO2 falls progressively as shunt fraction
  increases but PaCO2 remaining constant unless
  shunt fraction exceeds 50
• The shunt fraction also determines the influence
  of inhaled oxygen on PaO2

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• Hypoxemic respiratory failure (type I)
• V/Q mismatch
• Shunt
• Alveolar hypoventilation
• Diffusion impairment
• P/D impairment
• ? FiO2
• Venous admixture

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• 1. V/Q mismatch
• Even in normal lungs ? areas present where V/Q
• mismatching is present
• ? ,ie, V/Q - ? at apex
• - ? at bases
• ?
• but overall a balance is maintained to
  achieve a steady ratio of 0.8 for the
  whole lung (in healthy lungs)
• In certain pathological states, the imbalance
  occurs leading to hypoxemia and V/Q mismatching

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• Pathophysiology
• Obstruction
• Fluid filled alveoli
• Atelectasis,
• e.g.
• Obstructive lung disease
• Bronchospasm
• Mucous plugging
• Inflammation
• Premature airway closure ? asthmatic exacerbation
• Infection
• CHF
• Inhalational injury
• ARDS

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• Clinical features
• Hypoxia
• Dyspnea, TC, tachypnea
• Use of accessory muscle (nasal flaring)
• Cyanosis peripheral or central
• Irritability
• Confusion / coma
• Other signs Specific to disease process
• Radiologically V/Q mismatch
• Black hyperinflated lungs, e.g. COPD
• White in c/o occluded alveoli

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• Shunt
• Extreme version of V/Q mismatch in which there is
  no ventilation to match perfusion (V/Q 0)
• Normal anatomical shunt
• 2-3
• bronchial and thebesian veins
• Pathological anatomical shunt
• R ? L blood flow through cardiac openings (e.g.
  ASD/VSD) or in pulm A-V malformations
• Physiological shunt
• Atelectasis, pulmonary edema, or pneumonia ? does
  not generally respond to O2 supplementation as
  the gas exchange units are completely closed /
  collapsed (the alveolus)

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• 2. Diffusion impairment
• Diffusion is movement of gas across the
  alveolar capillary membrane d/t pressure
  gradient.
• Any impairment in diffusion leads to inability
  of O2 to pass to the arterial blood, thereby
  lowering the arterial PaO2. e.g.,
• ILD, emphysema, pulm vascular abnormality,
  anemia, pulm HTN

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• Clinical features
• Rarely present as acute hypoxemia
• ILD
• Dry cough
• Crackles (fine, basilar)
• Clubbing of nailbeds
• Rheumatological manifestations
• Raynauds disease
• S/o PHTN

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• 3. Perfusion diffusion impairment
• Rare cause with liver disease complicated by
  hepatopulmonary syndrome
• R ? L intracardiac shunts
• Dilated pulm capillaries
• Thus, normal partial pressure of O2 are
  insufficient to drive O2 molecule through
  dilated pulm capillary
• ?
• Supplemental O2

Impaired gas exchange
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• 4. ? PiO2
• ? barometric pressure (high altitude)
• 5. ? Mixed venous oxygen saturation
• The oxygen content in arterial blood
  represents the sum of oxygen in mixed venous
  blood and O2 added from alveolar air.
• Normal gas exchange- PAO2 is major determinant of
  PaO2
• Impaired gas exchange- PvO2 determines PaO2
• Thus a fall in mixed venous oxygen saturation can
  aggravate hypoxemia caused by V/Q abnormality.

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Mixed venous oxygen saturation

• PvO2 k x DO2/VO2
• DO2- delivery of oxygen to tissues
• VO2- uptake of oxygen by the tissues
• E.g., CHF with low cardiac output
• low Hb
• ?O2 consumption

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Diagnostic evaluation of hypoxemic respiratory
failure
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• Hypercapnic respiratory failure (type II)
• (pump failure / ventilatory failure)
• Features
• Elevated PaCO2 creating an uncompensated
  respiratory acidosis
• PaCO2 1/? alveolar ventilation
• ? Vd / VT
• ? CO2 production
• Hypoxemia occurs d/t displacement of alveolar PO2
  by ? CO2

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• Causes
• 1. Alveolar hypoventilation
• ? ventilatory drive
• Neurologic disease impaired strength with
  failure of NM function in resp system
• 2.? Work of breathing
• 3. V/Q abnormality
• Shunt in late stages (edema, infiltrates)
• Dead space ventilation- Vd/Vt gt 50 (e.g.,
  advanced emphysema )
• 4. ? CO2 production , esp in patients with
  reduced ability to eliminate CO2.

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• Ventilatory drive
• Chemoreceptor
• Central (medullary)
• Peripheral (aortic carotid bodies) ? Respond
  to CO2 O2 tension
• The drive can be diminished by
• Drugs (overdose / sedation)
• Brainstem lesions
• Diseases of the CNS (multiple sclerosis,
  parkinsons)
• Trauma to the brainstem
• Hypothyroidism
• Obesity
• Sleep apnea
• Metabolic alkalosis
• Malnutrition
• ? ICP
• Metabolic encephalopathy

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• Neuromuscular disease
• CNS is stimulated but signal does not reach the
  goal
• Reduced strength (d/t impaired NM transmission),
  e.g.
• Spinal trauma
• Motor neuron disease (amyotrophic lateral
  sclerosis or poliomyelitis)
• MND (GBS)
• NMJ disorder (MG/botulinism)
• Respiratory muscle weakness
• Muscular disease (muscle dystrophy, myositis,
  critical care myopathy, metabolic disorders
  ,hypophosphatemia, hypomagnesemia)

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• ? Work of breathing
• Pathophysiologically
• Resistive load (bronchospasm)
• Loads d/t ? lung compliance (alveolar edema,
  atelectasis, auto PEEP)
• Loads d/t ? chest wall compliance (pneumothorax,
  PE, abd distension)
• Load d/t ? MV requirement (PE, sepsis)

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• Clinically
• ? airway resistance - COPD, asthma
• Thoracic abnormalities pneumothorax, rib H,
  pleural effusion, other RLD
• ? CO2 production as in hypermetabolic state, e.g.
  extensive burns

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Diagnostic evaluation of hypercapnic respiratory
failure
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• Type III resp failure
• d/t lung atelectasis
• Most commonly seen in periop period
  perioperative resp failure
• ? FRC ? collapse of dependent lung units
• Type IV resp failure
• Due to hypoperfusion of respiratory muscles in
  shock
• (Harrisons principles of internal medicine-
  16th edition)

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Diagnosis

• History
• e.g.,
• previous cardiac disease, VHD, recent symptom of
  orhopnea, chest pain
• Trauma
• Aspiration
• Sepsis
• Infection, etc

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Physical examination

• Signs of
• underlying disease process pneumonia, pulmonary
  edema, asthma, COPD, cor pulmonale etc
• Hypoxemia- restlessness, anxiety, confusion,
  somnolence, tachycardia, dyspnea, cyanosis, use
  of accessory muscles, arrhythmias, seizures etc
• Hypercapnia asterixis, tachycardia,
  hypertension etc

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Investigations

• Disease specific- Hb, LFT, KFT, S. Electrolytes,
  Thyroid profile
• ABG remains the confirmatory diagnostic tool-
  . PaO2
• PaCO2
• AaDO2
• pH
• HCO3
• O2 saturation
• Radiological tools- CXR, CT- chest, V/Q scan,
  ECHO
• Pulmonary function test- more useful in chronic
  resp failure

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Treatment

• Admission to respiratory care unit or ICU
• Hypoxemia
• Hypercapnia
• Underlying disease process

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• Guidelines for Standards of Care for Patients
  with Acute Respiratory Failure On Mechanical
  Ventilatory Support
• Task Force on Guidelines
• Society of Critical Care Medicine
• Crit Care Med 1991 Feb 19(2)275-278

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Treatment

• Airway management ETT if required
• Correction of hypoxemia- goal is to achieve a
  SaO2 of gt90, and a PaO2 of gt60 mm Hg
• -supplemental oxygen
• - NIPPV
• - intubation and mechanical vent

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Treatment

• Correction of coexistent hypercapnia and
  respiratory acidosis
• Ventilator management
• -non invasive
• -invasive

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Non-invasive ventilatory support

• The application of ventilatory support through a
  nasal prong or full face mask in lieu of ETT is
  being used increasingly for patients with
• acute or chronic mild to moderate respiratory
  failure
• Conscious
• Intact airway
• Intact airway reflexes
• The various modes by which NIPPV can be provided
  include volume assist control, pressure assist
  control, BiPAP, CPAP, etc

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Non-invasive ventilatory support

• Has proven beneficial in
• acute exacerbations of COPD and asthma,
• decompensated CHF with mild-to-moderate pulmonary
  edema,
• pulmonary edema from hypervolemia
• obesity hypoventilation syndrome
• Guidelines for noninvasive ventilation in acute
  respiratory failure. Indian J Crit Care Med
  200610117-47

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Invasive ventilatory support

• Useful when pt does not respond to non invasive
  methods of ventilation
• Indications for IPPV based on specific threshold
  values for PCO2 and pH or arterial oxygenation
  have not been validated by clinical evidence

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Invasive ventilatory support

• Indications-
• Apnea or bradypnea
• ALI ARDS
• Severe cardiogenic shock
• Traumatic brain injury
• Brain injury
• Indications for Invasive Mechanical Ventilation
  in Adults with Acute Respiratory Failure
  Conference proceedings- Respiratory Care 2002,
  47(3)

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Non-invasive vs invasive ventilatory support

• Guidelines for noninvasive ventilation in acute
  respiratory failure. Indian J Crit Care Med
  200610117-47
• Indications for Invasive Mechanical Ventilation
  in Adults with Acute Respiratory Failure
  Conference proceedings- Respiratory Care 2002,
  47(3)

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Non-invasive vs invasive ventilatory support

• NIV has been shown to be an effective treatment
  for acute hypercapnic respiratory failure (AHRF),
  particularly in chronic obstructive pulmonary
  disease (COPD). Facilities for NIV should be
  available 24 hours per day in all hospitals
  likely to admit such patients
• NIV should not be used as a substitute for
  tracheal intubation and invasive ventilation when
  the latter is clearly more appropriate
• Non-invasive ventilation in acute respiratory
  failure. Thorax 200257192211 (British Thoracic
  Society Standards of Care Committee)

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Follow up

• Complications
• Pulmonary embolism, barotrauma, fibrosis, cx
  secondary to use of mechanical devices, VILI,
  oxygen toxicity
• Cardiovascular- hypotension, reduced cardiac
  output, arrhythmia, pericarditis, and acute
  myocardial infarction.

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• Gastrointestinal- hemorrhage, gastric distention,
  ileus, diarrhea, and pneumoperitoneum.
• Infectious- pneumonia, urinary tract infections,
  and catheter-related sepsis
• Renal - Acute renal failure and abnormalities of
  electrolytes and acid-base homeostasis
• Nutritional malnutrition, hypoglycemia, abd
  distension, etc

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References

• Miller s anaesthesia- 7th edition
• Egans- Fundamentals of respiratory care-9th
  edition
• The ICU Book- Paul Marino 3rd edition
• Harrisons principles of internal medicine- 16th
  edition
• Emedicine from WebMD accessed from emedicine.com
• Guidelines for noninvasive ventilation in acute
  respiratory failure. Indian J Crit Care Med
  200610117-47
• Indications for Invasive Mechanical Ventilation
  in Adults with Acute Respiratory Failure
  Conference proceedings- Respiratory Care 2002,
  47(3)
• Non-invasive ventilation in acute respiratory
  failure Thorax 200257192211 (British Thoracic
  Society Standards of Care Committee)
• Treatment of Acute Exacerbations of Chronic
  Respiratory Failure Chest 2004125 2217-2223
• Guidelines for Standards of Care for Patients
  with Acute Respiratory Failure On Mechanical
  Ventilatory Support Crit Care Med 1991 Feb
  19(2)275-278

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Thank you.