all about home niv. respiratory mechanics spontaneous breathing
TRANSCRIPT
What is spontaneous ventilation?What is spontaneous ventilation? Purpose of ventilation
‐ Supply fresh gas to the lungs, to be exchanged at the alveolar-capillary level
through blood circulation
‐ Provide cells with adequate 02 (Oxygenation)
‐ get rid of CO2 (Alveolar ventilation)
‐ Maintain normal acid base balance
Arterial Blood Arterial Blood GGasesasesNormal valuesNormal values
‐ ABGs: Arterial Blood Gases
• Pa02 and PaC02
‐ Oxygenation assessment
• Pa02 80-100 mmHg
• Sa02: 92% to 100%
‐ Ventilation assessment
• PaC02: 35-45 mmHg
‐ Acid base status• pH:7,35-7,45
Some Some DDefinitionsefinitions
Tidal Volume (Vt)‐ Quantity of air in the lungs in 1 inspiration
Minute Ventilation‐ Quantity of air in the lungs in 1 min (= Vt x respiratory
rate) Hypoxemia
‐ state in which Pa02<60 mmHg (in the blood)
‐ Sa02<92% (Oxygen saturation)
Hypoxia
‐ state in which there is inadequate 02 at the tissue level
Some Some DDefinitionsefinitions
Hypercapnia
‐ when PaC02 >45mmHg
Hypocapnia
‐ when PaC02<35mmHg
Acidosis:‐ pH<7,35
Alkalosis:‐ pH>7,45
Spontaneous breathingSpontaneous breathing
On Inspiration: Active phenomena
Muscles Contract
Pressure Changes
Air Flows Into
Lungs
Spontaneous breathingSpontaneous breathing
On Expiration: passive phenomena
Muscles Contract
Pressure Changes
Air Flows out
Lungs
Spontaneous breathingSpontaneous breathing
End Expiration: Intrinsic PEEP
Extra work is needed to generate the following inspiration
Resistance creates a residual pressure at the end of expiration
Spontaneous breathingSpontaneous breathing
Opposing Forces to Ventilation
Elastic recoil Resistance
of the lungs to airflow
Work of Breathing
Opposing Forces to VentilationOpposing Forces to Ventilation
Tendency of the Lungs to Resist Inflation
Pressure / Volume = Elastance
Resistance to Air Movement in the Airways
Pressure / Flow rate = Airways Resistance
Breathing with Lung DiseaseBreathing with Lung Disease
Decreased Elastance Increased Resistance
Stronger Muscle Contractions Required
Larger Patient Effort
Excessive Work of Breathing
Respiratory Failure
Breathing with Lung DiseaseBreathing with Lung Disease
Flow and/or Volume
Normal
Disease
Patient Effort
Consequences of Respiratory FailureConsequences of Respiratory Failure
Excessive Work of Breathing
Respiratory Muscle Dysfunction
Inadequate Alveolar Ventilation
Severe Hypoxia
Goals of Ventilatory SupportGoals of Ventilatory Support
Improve Alveolar Minute Ventilation
Decrease the Work of Breathing
Correct Gas Exchange Abnormalities
Types of Ventilatory Types of Ventilatory SSupportupport
Invasive‐ endotracheal tube‐ tracheostomy
Noninvasive‐ mask
Home NIV ObjectivesHome NIV Objectives
Correct hypoventilation and associated syndromes (like OSA):‐ Despite the leaks‐ Ensuring a good comfort‐ Preserving a good quality of sleep
Provide a comfortable ventilation to ensure a good patient compliance‐ May prefer comfortable parameters (IPAP, EPAP, RR) with a
higher CO2 level
‐ Adapt the patient to his therapy takes time: if it has already failed once then it is even more difficult the second time!
Expected ResultsExpected Results
Restrictive pathologies Obstructive pathologies
Short Term
• Symptoms relief• Reduce desaturations
• Symptoms relief• Reduce desaturations and increase ventilation (overcome oxygen side effect)
Long Term
• Reduce Pa C02• Improve survival• Reduce decompensation episodes
• Reduce Pa CO2• Improve quality of life• Reduce decompensations episodes risks (or at least severity)
What is CRF?What is CRF?
Chronic respiratory failure (CRF) may result from different pathologies, which make the body inept to bring oxygen and/or wash out its CO2.
As a result there is a decrease of the PaO2 (hypoxemia)
and/or an increase of the Pa CO2 (hypercapnia) noticed
during blood gases analysis
Chronic Respiratory Failure Chronic Respiratory Failure Patients ManagementPatients Management
« The management strategy is based on an individualized assessment of disease severity and response to various therapies. »
Source: Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary DiseaseGOLD scientific committee - NHLBI/WHO workshop summary - AJRCCM 2001GOLD scientific committee - NHLBI/WHO workshop summary - AJRCCM 2001
Therapy depends upon the patient’s Therapy depends upon the patient’s pathology type and severitypathology type and severity
COPD Patient COPD Patient Some definitionsSome definitions
COPD Chronic Obstructive Pulmonary Disease is the name given to
the progressive narrowing of the airways This narrowing may result from an obstruction of the airways
in patients with Chronic Bronchitis (scarring of the airways and sputum secretion) or emphysema
Emphysema Emphysema is brought about by cigarette smoking which results in
chemical changes that destroy lung tissue:‐ Loss of lung tissue: reduction of elasticity‐ Airways tend to close
COPD COPD
Chronic BronchitisEmphysema
Swollen airways
Narrowed airwaysPhlegm damages the tissue
Alveoli collapse
Pink pufferPink pufferEmphysema dominantEmphysema dominant
Blue bloaterBlue bloaterBronchitis dominantBronchitis dominant
COPDCOPD
COPD Patient COPD Patient TherapiesTherapies
Source: Global Strategy for the Diagnosis, Management, and Preventation of Chronic Obstructive Pulmonary DiseaseGOLD scientific committee - NHLBI/WHO workshop summary - AJRCCM 2001GOLD scientific committee - NHLBI/WHO workshop summary - AJRCCM 2001
<70% FEV1/FVC <30%
Drugs & Physiotherapy
Long Term Oxygen Therapy
Noninvasive Ventilation
Moderate stage
Worsening airflow limitation
Severe stage
Severe airflow limitation
Mild stage
Mild airflow limitation
« As the disease progresses, hypoxemia occurs and hypercapnia is seen in advanced disease »
COPD Patient COPD Patient Oxygen TherapyOxygen Therapy
LTOT (12-17hrs/day) has been shown to ‐ Increase survival‐ Decrease hospitalization rate
Adverse effects:
‐ Hypoventilation and CO2 retention
‐ Increased PaCO2 at night may contribute to arousals
‐ Sudden High PaCO2 deteriorate the gas balance and may lead to acidosis (exacerbation risks)
COPD PatientsCOPD PatientsHome NIVHome NIV Therapy Therapy
Conflicting results of studies COPD population likely to benefit from NIPPV :
‐ Substantial daytime CO2 retention‐ Severe airway obstruction‐ Nocturnal oxygen desaturation
Benefits:‐ Reduce nocturnal hypoventilation: allows respiratory centre to reset,
improves daytime hypercapnia. ‐ Improve sleep quality by reduced episodes of hypoventilation and
desaturations ‐ Resting chronically fatigued respiratory muscles, allowing recovery of
inspiratory muscle function‐ Decrease Decompensation episodes risks/severity
Benefits: improve patient quality of life
Source: Consensus conference : « Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD and Nocturnal hypoventilation » Chest 1999
COPD Patient & NonInvasive VentilationCOPD Patient & NonInvasive Ventilation
Gas exchange criteria
‐ Daytime PaCO2 > 55 mmHg or
‐ Nocturnal oxygen desaturation : SaO2 < 88% for > 5 min sustained while receiving oxygen therapy (<2l)
‐ PaCO2 of 50-54 mmHg and hospitalization related to recurrent episodes of hypercapnic respiratory failure (> 2 episodes in 1 year)
Source: Consensus conference - Chest 1999
Criteria usually followed in the daily practice:• Repeated decompensation episodes in the last 3 months• High CO2 level• Acceptation of the therapy (compliance: 8hrs ventilation at night)
Evidence Statements from NICEEvidence Statements from NICE
Addition of NIV to LTOT improved daytime PaCO2 during oxygen breathing
Resting dyspnoea improved in NIV+LTOT group, and was significantly better at month 24
After 2 years QOL was significantly improved Overall hospital admissions decreased by 45% in the NIV+LTOT
group compared with increase of 27% in LTOT (follow back period of 12 months)
http://thorax.bmjjournals.com/content/vol59/suppl_1/
NICE RecommendationNICE Recommendation
Adequately treated patients with chronic hypercapnic respiratory failure who have required assisted ventilation (whether invasive or non-invasive) during an exacerbation or who are hypercapnic or acidotic on LTOT should be referred to a specialist centre for consideration of long-term NIV.
Chronic Obstructive Pulmonary Disease: National clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and secondary care
Thorax 2004;59(suppl 1) 1-232
Restrictive PatientsRestrictive PatientsDifferent DiseasesDifferent Diseases
Obese Hypoventilation Chest wall deformities
‐ Kyphoscoliosis‐ Sequel of tuberculosis
Non progressive or slowly progressive neuromuscular disorders‐ Central hypoventilation‐ Spinal cord injury, spinal muscular dystrophy‐ Myopathies‐ Sequel of Poliomyelitis
Progressive neuromuscular disorders‐ Amyotrophic Lateral Sclerosis (ALS)‐ Duchenne muscular dystrophy
Restrictive PatientsRestrictive Patients Pathology ProgressionPathology Progression
Source: book “Assistance Ventilatoire à Domicile”D Robert, B.J. Make, P Léger, A. L. Goldberg, J. Paulus, T. Willig – 1994D Robert, B.J. Make, P Léger, A. L. Goldberg, J. Paulus, T. Willig – 1994Source: Consensus Conference - Chest 1999Consensus Conference - Chest 1999
<50% FVC <20%
Moderate stage Severe stageMild stage
Invasive ventilationNoninvasive Ventilation
Physiotherapy
Restrictive PatientsRestrictive Patients
“More recent reviews have cited the advantages of pressure targeted devices for comfort and their ability to compensate for leaks. Volume targeted equipment may be favorable for many patients simply because triggering mechanism are more adjustable and pressure targeted systems are not able to guarantee a minimum minute ventilation.”
Source: Consensus Conference - Chest 1999
10 years ago: Invasive ventilation/volume at the late stage of the disease Today:
‐ Start at the early stage in pressure support‐ Use security functions while patient becomes dependant‐ Ends up with invasive ventilation (< 5% of patients)