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Neuromuscular
Respiratory Failure
Dr. Muhammad Asim Rana
MBBS, MRCP, EDIC, SF-CCM, FCCP
Department of Critical Care Medicine
Introduction
•
•
•
•

Respiratory Failure… definition
Types…. I & II
Why this distinction is important?
Causes & Classification

– Pulmonary
– Non pulmonary
• Nonpulmonary causes of respiratory failure
include diverse group of disorders….
• Pathophysiologic hallmark….. Hypoventilation
• Approx 20% cases of respiratory failure
Introduction
• Hypoventilation
• Theoretical definition:
– Deviation from the usual state of ventilatory
control resulting in decreased minute ventilation
relative to metabolic requirements

• Operational definition:
– Hypoventilation exists when alveolar or arterial
PaCO2 exceeds normal upper limit (44 mmHg)
Single compartment lung model

PaCO2= VCO2/VE (1-VD/VT)
PAO2= FiO2(Patm-P H2O)-1.2(PaCO2)
–
–
–
–

VCO2= CO2 elimination rate
VE= minute ventilation
VD= dead space
VT= tidal volume
EtiologicalClassification
Plum & Leigh & Phillipson
Nonpulmonary causes of respiratory failure

Ventilatory control

Neuromuscular Disorders

↓Peripheral
Chemosensitivity

Anterior horn cells

Brain stem neurons

Phrenic neuropathies

Spinal Cord pathways

NMJ disorders
Respiratory muscles
In all these conditions the lungs are normal !!!!

Chest wall & Other
disorders
Obesity-hypovent
Syndrome
Kyphoscoliosis
Fibrothorax
Thoracoplasty
Ankylosing
spondylitis
Flail chest
Metabolic alkalosis
Primary disorders of ventilatory control

↓Peripheral
Chemosensitivity

Carotid body
surgery
Prolonged hypoxia
Metabolik alkalosis

Brain stem neurons

Bulbar polio
Syringobulbia
Encephalitis
Infarction
Neoplasm
Demyelinating
disorders
Drugs
Neoplasms

Spinal Cord pathways

Trauma
Bilateral high
cervical cordotomy
Anterior spinal
cord surgery
Transverse myelitis
Encephalomyelitis
Neuromuscular disorders

Anterior horn cells

Amyotrophic
lateral sclerosis
Spinal muscular
atrophies
Poliomyelitis

Phrenic neuropathies

GBS
Porphyria
Neuralgic
amyotrophy
Surgical (cardiac
hypothermia)
Paraneoplastic
Critical illness
polyneuropathies

Respiratory muscles
NMJ disorders

Myasthenia gravis
Eaton-lambert
Muscular
dystrophies
Drugs
Myotonic
Toxins
dystrophies
Tetanus
Mitochondrial
Electrolyte
abnormalities
myopathies
Rhabdomyolysis
Prolonged
neuromuscular
Scleroderma
blockade
Recognizing Neuromuscular
Respiratory Failure
When to Suspect
Neurogenic Respiratory Failure
• Definition
– Respiratory failure due to difficulties with
•
•
•
•

Cortical, Brainstem respiratory centers
Motor neurons (Cell bodies)
Axons
Neuromuscular junction
– Pre synaptic
– Post synaptic

• Muscle

– Not due to primary pulmonary problems
Clinical Recognition
Signs and Symptoms
• The initial manifestation of respiratory failure & the
age at presentation can vary….
• Primary disorders of ventilatory control
–
–
–
–

Excessive day time somnolence
Pulmonary HTN
Corpulmonale
Severe respiratory failure following sedatives

• Neuromuscular disorders
–
–
–
–

Unexplained hypercapnia
Dyspnea
Sleep disruption
Recurrent pneumonia
Manifestation of Respiratory Muscles Involvement
• Tachypnea …. (expression of muscle fatigue)
• Signs of diaphragmatic weakness
–
–
–
–

Orthopnea
Paradoxical abdominal wall movement
Respiratory alternans
REM associated hypoventilation

• Signs of abdominal muscle weakness
– Decreased cough effort

• Signs of bulbar muscle weakness
–
–
–
–
–

Dysarthria
Dysphonia
Dysphagia
Aspiration
Obstructive sleep apnea
Functional Assessment
Disorders of ventilatory control

Chronic neuromuscular disorders

•
•
•
•
•
•

• Lung mechanics & muscles

Lung mechanics
Respiratory muscle strength
Gas exchange
Arterial PaCO2
Central apneas
Response to exogenous
hypoxia
• Polycythemia & ↑ HCO3
• Voluntary breath-holding
• Response to elastic & resistive
load..(Borg scale of dyspnea)

– Restricted lung volumes
– Decline in vital capacity
– PI max & PE max (
– Electromyography

• Gas exchange
– Mild hypoxemia
– Normal diffusion capacity

• Contribution of additional
factors
– Microatelactasis
– Alteration in surfactant
– Progressive deformity of thorax
Laboratory Values in Monitoring
Acute Neuromuscular Failure
Normal
value

Measurement

Procedure

Vital capacity

Max exhalation

45-70 mL/kg

Maximal Inspiratory
pressure (PI max)

Max inhalation

M >-100 cm H2O

F >-70 cm H2O
Maximal expiratory pressure
(PE max)

Max blowing out

M >200 cm H2
F >140 cm H2O
Respiratory weakness
•
•
•
•
•
•

Normal – 45--70 ml/kg
Weak cough – 30 ml/kg
Atelectasis – 20--25 ml/kg
Sigh lost, atelectasis and shunting 15 ml/kg
Hypoventilation – 10 ml/kg
Hypercapnia – 5-10 ml/kg
Respiratory weakness
• Arterial blood gases
– Initial changes
• Subtle drop in oxygen levels with the development of
atelectasis

– Later changes
• Mild hypercapnia with normal ph
• Rapid deterioration with apnea
Respiratory weakness
• Respiratory parameters
– Forced vital capacity
• Generally intubate if <10 ml/kg
• May be underestimated by respiratory technician
• Similar flow volume loops as COPD
– Prolonged tail due to extended exhalation time

• Count to 30 on one breath
– Cheap but effective way to estimate VC
– Approximately 2 Liters

• Neck flexors and proximal muscle strength correlate
best with respiratory strength
Guillain-Barre Disease
(Acute Inflammatory demyelinating polyneuropathy)
• Autoimmune process
– Effects myelin sheath of
peripheral nerves
– Humoral attack may be
induced by viruses,
vaccinations
– Demyelination slows
conduction along nerves
• Leads to progressive
weakness
– Axonal variant
MGH Series
Retrospective Series
n=169
Upper
respiratory
tract infection
36%

No prior
illness
38%

Prospective Series
n=120
Upper respiratory
tract infection
49%
No prior
illness
27%

Diarrhea
10%

Diarrhea
8%
Malaise
6%

Surgery
6%

Ropper, Wijdicks, Truax, 1991

EBV
5%

Pregnancy
1%

Hodgkin’s
disease,
surgery, SLE,
vaccination
3%

CMV
Malaise 3%
3%

EBV
3%

Pneumonia
2%

CP1142597-8
Diagnostic Criteria for GBS
• Strongly supportive features
–
–
–
–

Progression of symptoms over 4 weeks
Symmetric legs greater than arms weakness
Mild sensory symptoms
Cranial nerve involvement especially bilateral facial
weakness
– High protein content in the CSF with < 10 cells
– EMG/ NCV: Conduction block, increased F waves and distal
latencies
Treatment for GBS
• Supportive
– Respiratory
• Intubate Early
• No role for BiPap in GBS

– Treat dysautonomia
• Deafferented cardiac and baroreceptors
• Pseudoobstruction
• DVT prophylaxis
• Plasma Exchange
• IVIG
• Steroids not helpful
– Evaluate for CIDP
Plasma Exchange Trials in GBS
North American study

Plasma
exchange
n=122

Conventional
n=123

Days to reach grade 2 (median)

53

85

Patient improved at least 1 grade at 6 months (%)

97

87

Patients walking independently at 6 months (%)

82

71

French study
Days to onset motor recovery (median)

n=111

n=109

6

13

Days weaning (median)

18

31

Days to recover walking without
assistance (median)

70

111
CP1142597-47
Prognosis GBS
• Depends upon degree and extent of Axonal
damage
– Demyelination alone will recover within days to
weeks
– Axonal damage with intact myelin sheaths will
recover within months
– Most patients will make a complete recovery
• Psychological support
• GBS Support groups
Patient Management
Acute Respiratory Failure
Chronic Respiratory Failure
Respiratory weakness
• Clinical findings
(Not all patients will have)

– Dyspnea
• VC is half of predicted

– Brow sweating
– Accessory muscle use
• INTUBATION SHOULD NOT BE BASED
UPON THE CLINICAL PRESENTATION
ALONE BUT ON THE RATE OF
RESPIRATORY DECLINE, AND
PULMONARY FUNCTION TESTS
Acute Respiratory Failure
• Inspiratory and expiratory muscles
involvement is variable
• Inspiratory muscle fatigue occurs because….
• Work of breathing is increased because….
• Blood flow to respiratory muscles is
compromised because….
• Inspiratory muscles weakness → atelactasis
Acute Respiratory Failure
• Risk of respiratory failure increases when VC falls
below 15 mL/kg
• Watch the trend….. Serial measurements
• The question of when to start ventilatory
support….
• An anticipatory approach avoids risks associated
with emergent intubation and minimizes
complications
• The mode of ventilation..
• Supportive care is important
Chronic Respiratory Failure
• Prolonged mechanical ventilation is defined by
the Centers for Medicare and Medicaid Services
in the United States as greater than 21 days of
mechanical ventilation for at least 6 hours per
day.
• Most patients requiring prolonged mechanical
ventilation will have a tracheostomy placed to
facilitate comfort, communication, and chronic
ventilator facility or home ventilation placement.
Chronic Respiratory Failure
• Common problems among patients undergoing
prolonged mechanical ventilation
– Infections (e.g., pneumonia,line sepsis, Clostridium difficile
colitis
– Ileus
– Renal failure
– Pneumothorax
– Seizures
– Tracheal bleeding
– Laryngeal edema
– Development of tracheal granulation tissue
– Tracheoesophageal fistula formation
– Loss of airway patency because of unplanned extubation
or decannulation
Chronic Respiratory Assist Devices
(Mode of Ventilation)
• Abdominal displacement
– Pneumobelt
– Rocking Bed

• Negative Pressure Ventilation
– Pneumosuit
– Chest Cuirass
– Iron lung

• Positive Pressure Ventilation
– Volume Cycled
– Pressure Cycled
Chronic Respiratory Assist Devices
Pneumobelt
Chronic Respiratory Assist Devices
Rocking Bed
Chronic Respiratory Assist Devices
Pneumosuit and Iron Lung
Chronic Respiratory Assist Devices
Iron Lung
Chronic Respiratory Assist Devices
Diaphargm Pacing
Conclusions
• A normal P(A - a)O2 difference should not be
required as a diagnostic criterion for
nonpulmonary causes of respiratory failure.
• The etiologic classification of nonpulmonary
disorders causing respiratory failure consists
of the following broad categories:
– disorders of ventilatory control,
– neuromuscular disorders
– disorders of the chest wall, and upper airway
obstruction.
Conclusions
• Clinical recognition of these disorders depends on
familiarity with the physiologic consequences of
chronic hypoxia and hypercapnia, the signs and
symptoms of respiratory muscle weakness, and their
effects on pulmonary function tests.
• The approach to the management of acute
respiratory failure does not differ in principle from
the approach used in lung diseases.
• Noninvasive nocturnal ventilatory support has gained
acceptance as a means of controlling diurnal
hypercapnia and providing respiratory muscle rest.
Questions and Remarks
If NO Thank you very much
Neuromuscular Respiratory Failure

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Neuromuscular Respiratory Failure

  • 1. Neuromuscular Respiratory Failure Dr. Muhammad Asim Rana MBBS, MRCP, EDIC, SF-CCM, FCCP Department of Critical Care Medicine
  • 2. Introduction • • • • Respiratory Failure… definition Types…. I & II Why this distinction is important? Causes & Classification – Pulmonary – Non pulmonary • Nonpulmonary causes of respiratory failure include diverse group of disorders…. • Pathophysiologic hallmark….. Hypoventilation • Approx 20% cases of respiratory failure
  • 3. Introduction • Hypoventilation • Theoretical definition: – Deviation from the usual state of ventilatory control resulting in decreased minute ventilation relative to metabolic requirements • Operational definition: – Hypoventilation exists when alveolar or arterial PaCO2 exceeds normal upper limit (44 mmHg)
  • 4. Single compartment lung model PaCO2= VCO2/VE (1-VD/VT) PAO2= FiO2(Patm-P H2O)-1.2(PaCO2) – – – – VCO2= CO2 elimination rate VE= minute ventilation VD= dead space VT= tidal volume
  • 5. EtiologicalClassification Plum & Leigh & Phillipson Nonpulmonary causes of respiratory failure Ventilatory control Neuromuscular Disorders ↓Peripheral Chemosensitivity Anterior horn cells Brain stem neurons Phrenic neuropathies Spinal Cord pathways NMJ disorders Respiratory muscles In all these conditions the lungs are normal !!!! Chest wall & Other disorders Obesity-hypovent Syndrome Kyphoscoliosis Fibrothorax Thoracoplasty Ankylosing spondylitis Flail chest Metabolic alkalosis
  • 6. Primary disorders of ventilatory control ↓Peripheral Chemosensitivity Carotid body surgery Prolonged hypoxia Metabolik alkalosis Brain stem neurons Bulbar polio Syringobulbia Encephalitis Infarction Neoplasm Demyelinating disorders Drugs Neoplasms Spinal Cord pathways Trauma Bilateral high cervical cordotomy Anterior spinal cord surgery Transverse myelitis Encephalomyelitis
  • 7. Neuromuscular disorders Anterior horn cells Amyotrophic lateral sclerosis Spinal muscular atrophies Poliomyelitis Phrenic neuropathies GBS Porphyria Neuralgic amyotrophy Surgical (cardiac hypothermia) Paraneoplastic Critical illness polyneuropathies Respiratory muscles NMJ disorders Myasthenia gravis Eaton-lambert Muscular dystrophies Drugs Myotonic Toxins dystrophies Tetanus Mitochondrial Electrolyte abnormalities myopathies Rhabdomyolysis Prolonged neuromuscular Scleroderma blockade
  • 9. Neurogenic Respiratory Failure • Definition – Respiratory failure due to difficulties with • • • • Cortical, Brainstem respiratory centers Motor neurons (Cell bodies) Axons Neuromuscular junction – Pre synaptic – Post synaptic • Muscle – Not due to primary pulmonary problems
  • 10. Clinical Recognition Signs and Symptoms • The initial manifestation of respiratory failure & the age at presentation can vary…. • Primary disorders of ventilatory control – – – – Excessive day time somnolence Pulmonary HTN Corpulmonale Severe respiratory failure following sedatives • Neuromuscular disorders – – – – Unexplained hypercapnia Dyspnea Sleep disruption Recurrent pneumonia
  • 11. Manifestation of Respiratory Muscles Involvement • Tachypnea …. (expression of muscle fatigue) • Signs of diaphragmatic weakness – – – – Orthopnea Paradoxical abdominal wall movement Respiratory alternans REM associated hypoventilation • Signs of abdominal muscle weakness – Decreased cough effort • Signs of bulbar muscle weakness – – – – – Dysarthria Dysphonia Dysphagia Aspiration Obstructive sleep apnea
  • 12. Functional Assessment Disorders of ventilatory control Chronic neuromuscular disorders • • • • • • • Lung mechanics & muscles Lung mechanics Respiratory muscle strength Gas exchange Arterial PaCO2 Central apneas Response to exogenous hypoxia • Polycythemia & ↑ HCO3 • Voluntary breath-holding • Response to elastic & resistive load..(Borg scale of dyspnea) – Restricted lung volumes – Decline in vital capacity – PI max & PE max ( – Electromyography • Gas exchange – Mild hypoxemia – Normal diffusion capacity • Contribution of additional factors – Microatelactasis – Alteration in surfactant – Progressive deformity of thorax
  • 13. Laboratory Values in Monitoring Acute Neuromuscular Failure Normal value Measurement Procedure Vital capacity Max exhalation 45-70 mL/kg Maximal Inspiratory pressure (PI max) Max inhalation M >-100 cm H2O F >-70 cm H2O Maximal expiratory pressure (PE max) Max blowing out M >200 cm H2 F >140 cm H2O
  • 14. Respiratory weakness • • • • • • Normal – 45--70 ml/kg Weak cough – 30 ml/kg Atelectasis – 20--25 ml/kg Sigh lost, atelectasis and shunting 15 ml/kg Hypoventilation – 10 ml/kg Hypercapnia – 5-10 ml/kg
  • 15. Respiratory weakness • Arterial blood gases – Initial changes • Subtle drop in oxygen levels with the development of atelectasis – Later changes • Mild hypercapnia with normal ph • Rapid deterioration with apnea
  • 16. Respiratory weakness • Respiratory parameters – Forced vital capacity • Generally intubate if <10 ml/kg • May be underestimated by respiratory technician • Similar flow volume loops as COPD – Prolonged tail due to extended exhalation time • Count to 30 on one breath – Cheap but effective way to estimate VC – Approximately 2 Liters • Neck flexors and proximal muscle strength correlate best with respiratory strength
  • 17. Guillain-Barre Disease (Acute Inflammatory demyelinating polyneuropathy) • Autoimmune process – Effects myelin sheath of peripheral nerves – Humoral attack may be induced by viruses, vaccinations – Demyelination slows conduction along nerves • Leads to progressive weakness – Axonal variant
  • 18. MGH Series Retrospective Series n=169 Upper respiratory tract infection 36% No prior illness 38% Prospective Series n=120 Upper respiratory tract infection 49% No prior illness 27% Diarrhea 10% Diarrhea 8% Malaise 6% Surgery 6% Ropper, Wijdicks, Truax, 1991 EBV 5% Pregnancy 1% Hodgkin’s disease, surgery, SLE, vaccination 3% CMV Malaise 3% 3% EBV 3% Pneumonia 2% CP1142597-8
  • 19. Diagnostic Criteria for GBS • Strongly supportive features – – – – Progression of symptoms over 4 weeks Symmetric legs greater than arms weakness Mild sensory symptoms Cranial nerve involvement especially bilateral facial weakness – High protein content in the CSF with < 10 cells – EMG/ NCV: Conduction block, increased F waves and distal latencies
  • 20. Treatment for GBS • Supportive – Respiratory • Intubate Early • No role for BiPap in GBS – Treat dysautonomia • Deafferented cardiac and baroreceptors • Pseudoobstruction • DVT prophylaxis • Plasma Exchange • IVIG • Steroids not helpful – Evaluate for CIDP
  • 21. Plasma Exchange Trials in GBS North American study Plasma exchange n=122 Conventional n=123 Days to reach grade 2 (median) 53 85 Patient improved at least 1 grade at 6 months (%) 97 87 Patients walking independently at 6 months (%) 82 71 French study Days to onset motor recovery (median) n=111 n=109 6 13 Days weaning (median) 18 31 Days to recover walking without assistance (median) 70 111 CP1142597-47
  • 22. Prognosis GBS • Depends upon degree and extent of Axonal damage – Demyelination alone will recover within days to weeks – Axonal damage with intact myelin sheaths will recover within months – Most patients will make a complete recovery • Psychological support • GBS Support groups
  • 23. Patient Management Acute Respiratory Failure Chronic Respiratory Failure
  • 24. Respiratory weakness • Clinical findings (Not all patients will have) – Dyspnea • VC is half of predicted – Brow sweating – Accessory muscle use • INTUBATION SHOULD NOT BE BASED UPON THE CLINICAL PRESENTATION ALONE BUT ON THE RATE OF RESPIRATORY DECLINE, AND PULMONARY FUNCTION TESTS
  • 25. Acute Respiratory Failure • Inspiratory and expiratory muscles involvement is variable • Inspiratory muscle fatigue occurs because…. • Work of breathing is increased because…. • Blood flow to respiratory muscles is compromised because…. • Inspiratory muscles weakness → atelactasis
  • 26. Acute Respiratory Failure • Risk of respiratory failure increases when VC falls below 15 mL/kg • Watch the trend….. Serial measurements • The question of when to start ventilatory support…. • An anticipatory approach avoids risks associated with emergent intubation and minimizes complications • The mode of ventilation.. • Supportive care is important
  • 27. Chronic Respiratory Failure • Prolonged mechanical ventilation is defined by the Centers for Medicare and Medicaid Services in the United States as greater than 21 days of mechanical ventilation for at least 6 hours per day. • Most patients requiring prolonged mechanical ventilation will have a tracheostomy placed to facilitate comfort, communication, and chronic ventilator facility or home ventilation placement.
  • 28. Chronic Respiratory Failure • Common problems among patients undergoing prolonged mechanical ventilation – Infections (e.g., pneumonia,line sepsis, Clostridium difficile colitis – Ileus – Renal failure – Pneumothorax – Seizures – Tracheal bleeding – Laryngeal edema – Development of tracheal granulation tissue – Tracheoesophageal fistula formation – Loss of airway patency because of unplanned extubation or decannulation
  • 29. Chronic Respiratory Assist Devices (Mode of Ventilation) • Abdominal displacement – Pneumobelt – Rocking Bed • Negative Pressure Ventilation – Pneumosuit – Chest Cuirass – Iron lung • Positive Pressure Ventilation – Volume Cycled – Pressure Cycled
  • 30. Chronic Respiratory Assist Devices Pneumobelt
  • 31. Chronic Respiratory Assist Devices Rocking Bed
  • 32. Chronic Respiratory Assist Devices Pneumosuit and Iron Lung
  • 33. Chronic Respiratory Assist Devices Iron Lung
  • 34. Chronic Respiratory Assist Devices Diaphargm Pacing
  • 35. Conclusions • A normal P(A - a)O2 difference should not be required as a diagnostic criterion for nonpulmonary causes of respiratory failure. • The etiologic classification of nonpulmonary disorders causing respiratory failure consists of the following broad categories: – disorders of ventilatory control, – neuromuscular disorders – disorders of the chest wall, and upper airway obstruction.
  • 36. Conclusions • Clinical recognition of these disorders depends on familiarity with the physiologic consequences of chronic hypoxia and hypercapnia, the signs and symptoms of respiratory muscle weakness, and their effects on pulmonary function tests. • The approach to the management of acute respiratory failure does not differ in principle from the approach used in lung diseases. • Noninvasive nocturnal ventilatory support has gained acceptance as a means of controlling diurnal hypercapnia and providing respiratory muscle rest.
  • 37. Questions and Remarks If NO Thank you very much

Notas do Editor

  1. Resp failure def from 3rd ed. Introductory line from 2nd ed. First paragraph.
  2. Any given patient may have more than one process leading to respiratory failure. Example hypothyroidism… poliomyelitis… muscular dystrophies…A series of responsis is elicited by chronic hypoxemia and hypercapnia….
  3. Now as a physician you should have a wide index of suspicion, awareness of the possible involvement of muscles of respiration in particular the diaphragm and the ability to recognize its clinical expression areoften the most important elements in the diagnosis.