L26/27 Disorders of Ventilatory Control and the Respiratory Pump

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jknell
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L26/27 Disorders of Ventilatory Control and the Respiratory Pump
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2013-02-21 22:35:12
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Pulmonary II
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  1. Components and Functions of the respiratory pump
    • Components:
    • 1. Chest wall
    •      -rib cage
    •      -upper abdomen
    • 2. Muscles of respiration
    • 3. Central respiratory control

    • Functions:
    • 1. Move air in and out of lungs
    •      -tidal breathing
    •      -forced inhalation
    •      -forced exhalation
    •      -tidal exhalation (passive)
    • 2. Venous blood return to heart
  2. Muscles of Respiration
    • Inhalation
    • -diaphragm
    • -external intercostal
    • -accessory muscles (scalene, SCM, trapezii)

    • Exhalation-Passive
    • -recoil of lungs
    • -recoil of thoracic cage

    • Forced Exhalation
    • -internal intercostals
    • -abdominal muscles
  3. Control of Ventilation
    • 1. Central Chemoreceptors (ventral pons and medulla)
    • -mostly PCO2 and pH

    • 2. Peripheral Chemoreceptors (carotid body, aortic arch)
    • -PO2 and pH

    3. Lung parenchyma and thoracic stretch receptors

    4. Voluntary control
  4. Hyperventilation
    • Increased minute ventilation due to:
    • -tachypnea
    • -increased tidal volume

    • Leads to hypocapnia
    • -low PCO2
    • -respiratory alkalosis

    • Causes:
    • 1. CNS disease
    • -infections
    • -CVA
    • -trauma
    • 2. Liver failure
    • -central chemoR stimulatns (progesterone, glutamate, ammonia)
    • 3. Lung disease
    • -asthma
    • -PE
    • -infection
    • -interstitial lung disease
  5. Hypoventilation
    • Decreased minute ventilation due to:
    • -bradypnea
    • -low tidal volume

    • Leads to hypercapnia
    • -high PCO2
    • -respiratory acidosis

    • Causes:
    • 1. Primary or Idiopathic
    • -congenital
    • -Ondine's curse (when sleeping)
    • 2. Obesity hypoventilation syndrome
    • 3. COPD
    • 4. Neuromuscular disease
  6. COPD Type A
    • Type A:
    • -pure emphysema
    • -pink puffer
    • -tachypnea, dyspnea
    • -PCO2 may be low
    • -SaO2 normal
    • -only late do they become hypoxic and hypercapnic
    • -barrel chest
    • -severe hyperinflation (barrel chest, flat diaphragm)

  7. COPD Type B
    • Type B:
    • -bradypnea
    • -hypoventilation
    • -NOT DYPSNEIC (resetting of central Rs)
    • -PCO2 always high
    • -SaO2 always low
    • *can get Cor Pulmonale (hypoxia)
  8. Lung Volume Patterns
  9. Neuromuscular Diseases that lead to hypoventilation
    • 1. Spinal Cord Lesions
    • -MS
    • -disc compression
    • -hemorrhage
    • -infarction

    • 2. Motor Neuron Disease
    • -ALS (progressive)
    • -spondlyosis
    • -poliomyelitis
    • -GBS (completely Reversible)
    • -lymphoma
    • -sarcoidosis

    • 3. Disorders of the NMJ
    • -Botulism
    • -hypermagnesemia
    • -lambert eaton
    • -myasthenia gravis (reversible with tx)
    • -meds

    • 4. Muscle Diseases
    • -metabolic abnormalities
    • -malnutrition
    • -muscular dystrophy (progressive)
    • -polymyositis/dermatomyositis
  10. Clinical Manifestations of Neuromuscular Disease
    • Insufficient Ventilation
    • -dyspnea
    • -orthopnea
    • -rapid shallow breathing
    • -use of accessory muscles
    • -paradoxical breathing
    • -hypercapnea/hypoxemia

    • Nocturnal Hypoventilation
    • -choking
    • -insomnia
    • -daytime sleepiness
    • -morning HA-fatigue
    • -impaired cognition

    • Bulbar Dysfunction
    • -difficulty swallowing
    • -dysarthria
    • -dysphagia
    • -weak mastication
    • -facial weakness
    • -nasal speech
    • -protruding tongue

    • Ineffective Cough
    • -aspiration
    • -retention of secretions
    • -pneumonia
  11. Management of pulmonary complications of neuromuscular disease
    • 1. Nutritional Evaluation
    • -both obesity and malnutrition are deleterious
    • -evaluate swallowing/PEG tube

    • 2. Early Screening for Sleep Disordered Breathing
    • -sleep hypoventilation
    • -OSA
    • -polysomnogram
    • -early use of NIV

    • 3. Treatment of Pump Failure
    • -progesterone
    • -phrenic nerve stimulation (invasive)
    • -NIV, PPV
    • -management of secretion

    • 4. Management of Secretions
    • -may be due to ineffective cough
    • -measure MEP (>60 is ok)
    • -assisted coughing (manual or mechanical)
    • -chesty physiotherapy
  12. NIV during the day
    • Use when:
    • -PCO2 > 50
    • -SpO2 < 92%

    • 1. Mouth piece with intermittent PPV
    • 2. Glossopharyngeal breathing
    • 3. Intermittent abdominal pressure ventilator (pneumo-belt)
    • 4. Negative pressure ventilation (rarely used)
    • 5. Intermittent BPAP
  13. Tracheostomy and Invasive Ventilation
    -if cannot tolerate NIV or have severe bulbar weakness

    • PROs:
    • -more secure airway
    • -easier to remove secretions
    • -24h ventilation

    • CONs:
    • -mucus plugging
    • -infection
    • -increased secretion
    • -inability to communicate

    *consider patient autonomy
  14. Guillain Barre Syndrome
    • Predisposing Factors:
    • -viral/bacterial infections
    • -stress
    • -no obvious cause

    • Sx:
    • -symmetrical ascending muscle weakness
    • -can lead to paralysis of diaphragm (1/3)
    • -dysesthesia
    • -may progress rapidly

    • Management:
    • -outcome depends on anticipation and management of ventilatory failure
    • -admit to ICU preemptively
  15. Poliomyelitis
    • Pathophys:
    • -polio virus attacks motor neurons of spinal cord and brainstem
    • -diaphragm and intercostal muscles can be affected
    • -can result in respiratory failure
    • -no bulbar involvement

    • Treatment:
    • -iron lung until recover
  16. ALS
    • Pathophys:
    • -rapidly progressive neurodegenerative disease
    • -affects UMN and LMN
    • -death due to respiratory failure in 2-3 years
  17. Abnormal Patterns of Breathing
    • Ataxic Breathing:
    • -stopping and starting
    • -varied depth
    • -CNS damage to medulla
    • -poor prognosis

    • Biot's
    • -clustered breathing
    • -periods of central apnea
    • -CNS damage
    • -opioid abuse

    • Kussmaul Breathing:
    • -not tachypnic
    • -deep breathing
    • -continuous
    • -Metabolic acidosis (DKA)

    • Apneustic Breathing:
    • -hold breath at top of inhalation
    • -CNS damage at pons/brainstem, severe
  18. Cheyne-Stokes Respiration
    • -waxing and waning of amplitude
    • -sometimes central apnea

    • Causes:
    • -transition from wake to sleep
    • -high altitude
    • -CHF
    • -severe CNS disease
    • -narcotics
    • -idiopathic
  19. Loop Gain
    • -ratio of the size of the response to the size of the disturbance
    • -delay btwn lung saturation and getting to peripheral receptors
    • -hyperresponsiveness to apneas --> perpetrates itself
  20. Diaphragmantic Fatigue
    • 1. Increased work of breathing
    • -COPD
    • -Asthma
    • -Pulmonary Fibrosis
    • -Thoracic bony abnormalities (ankylosis, kyphoscoliosis)

    • 2. Reduced Energy to Supply Diaphragm
    • -anemia
    • -hypoxemia
    • -heart failure

    • 3. Diaphragmatic biomechanical disadvantage
    • -hyperinflation (COPD, asthma)
  21. Testing Diaphragmatic Function
    • -Maximal inspiratory pressure (MIP)
    • -Spirometry (vital capacity)
    • -Sniff Test (fluoroscopy)
    • -Paradoxical breathing (abdominal collapse with rising of the chest while breathing supine)
  22. Unilateral Diaphragmatic Paralysis
    • Damages to the phrenic nerve
    • -neck surgery
    • -cardiac surgery
    • -malignancy

  23. Treatment of Diaphragmatic Failure
    • -total rest for 24-48 hours
    • -mechanical ventilation (BPAP or trache)
    • -improve energy supplies
    • -reduce hyperinflation
  24. Treatment of Hemidiaphragm Paralysis
    • 1. Conservative
    • -weight loss
    • -sleep semirecumbant
    • -physical and pulmonary rehab

    • 2. Surgical Therapy
    • -diaphragmatic plication (surgical flatten diaphragm)
    • -diaphragmatic pacing (requires intact phrenic nerve)

    3. Mechanical Ventilation
  25. Kyphoscoliosis and Ankylosing Spondylitis
    • -decrease chest wall compliance
    • -increased work of breathing
    • -reduced tidal volume
    • -increased respiratory frequency
    • -alveolar hypoventilation
    • -hypoventilation
    • -V/Q mismatch (hypoxia)

    • Clinical Consequences:
    • -asymptomatic early
    • -dyspnea on exertion
    • -restrictive pattern PFT
    • -hypercapnia
    • -hypoxemia
    • -pulmonary HTN
    • -cor pulmonale
  26. Respiratory Abnormalities in Obesity
    • -decreased chest wall compliance
    • -high diaphragm (decreased ERV and FRC)
    • -altered pattern of breathing (high RR, reduced TV)
    • -V/Q mismatch

    • 1. Obesity Hypoventilation Syndrome
    • -resetting of chemoreceptors
    • -low responsiveness to hypoxemia and hypercapnia
    • -moderate pulmonary HTN

    • 2. Obstructive Sleep Apnea
    • -strongly associated with obesity (70%)
    • -intermediate responsiveness to hypoxemia and hypercapnia
  27. Treatment of chronic hypoxemia in the setting of chronic hypercapnia
    • -50/50 club (COPD pt)
    • -too much O2 may worsen hypercapnia

    • 1. Blocks hypoxic ventilatory drive
    • -minor role

    • 2. Increased V/Q mismatching
    • -O2 releases hypoxic vasoconstriction
    • -major mechanism for rise in PCO2

    • 3. Haldane Effect
    • -release of CO2 from Hb with supplemental O2
    • -also minor effect

    • Take Home:
    • -avoid excessive supplemental O2
    • -raise SpO2 to 88-90%
  28. Obstructive Sleep Apnea Definition (apnea, hypopnea)
    • -pauses in breathing during sleep (apneas)
    • -followed by loud snoring/gasping when breathing starts
    • -results in arousals
    • -excessive daytime sleepiness

    No flow but persistence of effort

    • Apnea
    • -cessation of airflow for > 10s

    • Hypopnea
    • -reduction in airflow amplitude of > 30% for > 10 sec associated with a >4% desat
  29. Apnea-Hypopnea Index (AHI)
    -number of evens per hour of sleep

    • Normal < 5/hr
    • Mild 5-14/hr
    • Moderate 15-29/hr
    • Severe > 30/hr
  30. Obstructive Apnea
    • NO FLOW, PERSISTENT EFFORT

    • -Complete cessation of airflow
    • -Gradual increase in effort until patient starts gasping
    • -Paradoxical breathing
  31. Central Apnea
    • -NO FLOW, NO EFFORT
    • -Esp associated with Cheynes Stokes Ventilation (HF)
  32. Mixed Apneas
    • -starts as central (no effort, no flow)
    • -in the middle of the apneic event becomes obstructive (patient starts making effort)

    -Ea event associated with desat --> CV sequelae
  33. Hypopnea
    • CONTINUED SNORING DURING THE EVENT (vs apneas)

    • -decremental airflow (30-50%)
    • -paradoxical effort
    • -desat not as severe as apneas
  34. OSA Associations
    • -Obesity
    • -CV disease
    • -Diabetes
    • -Stroke
    • -Metabolic syndrome
    • -Cognitive Impairment
    • -Depression
    • -Normal Pressure Glaucoma
    • -Erectile Dysfunction

    • ***25-30% of OSA are thin

    • "You're welcome Jordan :)"
    • Note appropriate use of winky face!
  35. OSA Prevalence
    • 24% of men
    • 9% of women

    Increasing prevalence

    More common in specific populations (ie: chronic renal failure up to 80%)
  36. OSA Syndrome Clinical Features
    • -loud chronic snoring
    • -excessive daytime sleepiness
    • -snoring interrupted by periods of apnea
    • -frequent nocturnal awakenings
    • -waking up to urinate several times a night
    • -wake up with a HA
    • -poor concentration/memory/judgement
    • -changes in personality
    • -auto accidents

    • Cardiovascular Disease

  37. Cardiovascular Disease and OSA
    • -Hypertension
    • -arrhythmias (PVCs)
    • -angina
    • -stroke
    • -pulmonary HTN
    • -heart failure
    • -death

    BP rises and falls with ea apnea
  38. Pathophysiology of OSA
    • 1. Abnormal anatomy
    • -reduced upper airway caliber (obesity)

    2. Macroglossia (scalloping of tongue, permanent indentation of teeth)

    • 3. Mallampati Score
    • -how well you can see structures of upper airway (classes)
    • -kissing tonsils

    • 4. Severe Retrognathia
    • -bird beak syndrome
    • -sets tongue back

    • 5. Narrowing of hard palate
    • -makes mouth cavity small
    • -thin and have long face

    • 6. Upper airway function during sleep
    • -lose cough reflex, swallowing during sleep
  39. Upper Airway Neuromuscular Tone in OSA
    OSA shows basal increase in neuromuscular tone to compensate for physical abnormalities

    Compensation decreases significantly during sleep

  40. OSA and Gender
    • Premenopause ratio = 3 male:1 female
    • Postmenopause ratio = 1:1

    Testosterone may cause or aggravate OSA

    Estrogen replacement increased genioglossus tone
  41. High Loop Gain has a tendency for Mixed Apnea
  42. Therapy for OSA
    1. Weight Loss

    • 2. CPAP
    • -most effective therapy for OSA
    • -corrects airway narrowing
    • -decreases loop gain

    • 3. Sleeping on side
    • -tape tennis ball to back

    • 4. Mandibular advancement device
    • -can be effective in mild to moderate OSA
    • -can result in TMJ and teeth malocclusion

    • 5. Uvulopalatopharyngoplasty
    • -remove tissue of soft palate
    • -effective only in very select cases

    • 6. Maxillomandibular advancement surgery
    • -best for severe retrognathia

    • 7. Improved Fitness
    • -exercise independent of weight loss can be beneficial

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