3/2/2008 ธ รกร ธ รก ตต ก ล พบ.

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1 Ventilator care and weaning in neurosurgical patients ธ รกร ธ รก ตต ก ล พบ. หน วยโรคระบบการหายใจ เวชบ าบ ดว กฤต และภ ม แพ ภาคว ชาอาย รศาสตร คณะแพทยศาสตร มหาว ทยาล ยเช ยงใหม Respiratory Management in the Neurological patient Neuroanatomy of respiration Respiratory patterns Brainstem lesions Cervical cord lesions Acute airway management in patients with possible intracranial hypertension Ventilator issues specific to the Neurological patient Occurs in the ventral pons and medulla Reciprocal innervation impulses in descending pathways both excite and relax antagonistic muscles of respiration different than spinal mediated reflexes Two medullary centers Cluster of neural cell bodies that discharge with inspiration - I neurons Cluster of neural cell bodies that discharge with expiration - E neurons ( only during active ventilation ) Medullary respiratory center - I neurons Apneustic Center Dorsal group - rhythmic discharges to the contralateral phrenic nerve and also projects to a Ventral group efferents Cranial division - nucleus ambiguus innervates the ipsilateral accessory muscles through the vagus nerve Caudal division - retroambigualis innervates crossed intercostal muscles 1

2 Medullary Respiratory center - I neurons Afferent input Stretch receptors from the lung- inhibitory influence via the vagus nerve ( Herring - Bruer reflex ) Cortical component influence Respiration directly through influence on the medullary center and a pathway that directly effects the respiratory muscles ( cortical component of respiration) Pneumotaxic center - located in the pons has tonic and variable discharges that terminate or limit inspiration Afferent input Chemoreceptors Carotid bodies Aortic bodies - have afferents to cell bodies in the medulla that directly stimulate the respiratory center Adjusted to maintain alveolar P CO2 The link between metabolism and respiration is affected by CO 2 not O 2. This is maintained by carbon dioxides effect on hydrogen ion concentration Neural Control of Respiration Summary Respiration is driven by a group of inspiratory neurons in the ventral medulla How, Why these fire is unknown no intrinsic pacemaker or leaky neuronal cell bodies like in the SA node in the heart I neurons inhibit E neurons but Expiration is passive I neurons are cortically and chemically modulated I neurons are shut off by a pontine pneumotaxic center There is no known active off center. Cortex has both a direct and indirect effect on respiration 2

3 Neurogenic Patterns of Respiration Cheynes - Stokes respiration Periodic breathing pattern with hypernea alternates with apnea ( hypernea > apnea ) found in prolonged circulation times with poor Cardiac output, CHF, Pulmonary edema, Metabolic causes, Sleep. ABG - mildly decreased CO 2, O 2. Pathogenesis Anatomic - represents bilateral damage to descending forebrain cortical pathways to the respiratory center anywhere from cortex to the pons Functional - any metabolic consequence that does the same. Neurogenic Patterns of Respiration Cheynes - Stokes Respiration Represents a deafferentation of the cortical damping effects on the medullary respiratory centers. Thus these inspiratory neuronal pools of cells are disproportionately affected by the chemoreceptors adjacent to them. Increased CO 2 leads to hyperpnea followed by apnea until CO 2 levels rise. Typically not an unstable respiratory pattern by itself Neurogenic Patterns of Respiration Central Neurogenic Hyperventilation represents a dysfunction of the brain involving the rostral brainstem pathologically damage is between the lower 1/3 of the midbrain and the middle third of the pons. Typically there is damage to the PPRF ventral to the aqueduct. Persists during sleep ABG - increased ph and PaO 2, slightly decreased pco 2. R/O CHF, stimulant drugs, or direct stimulation of the carotid or aortic bodies. Variable effect of chemoreceptors on respiration ( i.e. avoid assist control ventilation ) Neurogenic Patterns of Respiration Apneustic breathing prolonged inspiratory cramp or pause after full inspiration localizing value to midpontine level ( dorsolateral tegmentum )? Pneumotaxic center in man Found in basilar occlusion, pontine hemorrhage, herniation Ataxic breathing irregular deep and shallow respiration typically localizes to the dorsolateral medulla represents a disruption of the normal medullary control of respiration Found in medullary compressive or posterior fossa lesions Breathing patterns in spinal cord injury high cervical lesions C 3-5 phrenic nerve innervates the diaphragm which provides 80% of respiratory effort. Intercostals provide additional inspiratory force but also allow splinting of the diaphragm High cervical lesions only neck accessory muscles are available for respiratory effort. Patients must be sat upright to allow for maximal accessory muscle utility unstable respiratory pattern. Most will need intubation. 3

4 Breathing patterns in spinal cord injury Lower Cervical lesions Injury below C 5 will leave diaphragm intact but will affect intercostal breathing. Intercostals required for splinting of chest wall Pattern of breathing is abdominal protrusion with chest wall involution Patients feel better when lying flat where the diaphragm contracts more effectively. Respiratory pattern may be unstable needs close observation Improvement occurs after one week due to chest wall spasticity The balance between respiratory loads and demands determine the need for mechanical ventilatory support Endotracheal Intubation in the Neuro ICU Indications General Ventilatory failure - inability to exchange air and expire CO 2. Ph < 7.3, PCO 2 > 50 torr, PO 2 < 50 torr on 100% non rebreathing face mask. Airway maintenance most common cause of airway obstruction in the NICU is posterior displacement of the orophanyngeal soft tissues. Depressed LOC, neuromuscular failure, direct facial trauma Respiration becomes sonorous, chest involutes, trachea descends with respiratory effort Endotracheal Intubation in the NICU Treatment jaw thrust, swimmers position, oro or nasal pharyngeal airway Patients with GCS < 8 should have their airway protected Head trauma literature increased risk of aspiration and medical complications if not intubated 38% to 22% reduction in mortality Intubated in the 1 st hour after trauma 4

5 Endotracheal Intubation in the NICU All patients with diminished protective airway reflexes Cranial nerve deficits Skull base surgery Stroke Myasthenia gravis ALS SAH Endotracheal Intubation in the NICU Procedure typically uses rapid induction Succinyl choline 1.5 mg/kg ( not after seizures ) Increases ICP but Does not affect CBF Fentanyl 3-5ug/kg Thiopental 3-5 mg/kg May cause hypotension if volume depleted Propofol similar to Thiopental Etomidate 1-2 mg/kg * may be preferred agent Less CV depression No effect on CBF Fasiculations not seizures Lidocaine 1.5 mg/kg blunts increase in ICP with intubation cricoid pressure Endotracheal Intubation in the NICU Endotracheal Intubation in the NICU Head Trauma 10% associate Cervical spine injury Awake fiberoptic intubation preferred Often not practical Oral intubation In line traction and stabilization Cricothyroidotomy Cricothyroidotomy Major facial or airway trauma Complication rate 33% in ER, 6% in OR Oral intubation advantages used in emergency faster, easier disadvantages laryngoscopy is stressful uncomfortable less stable, migrates chewing gagging, needs bite block Nasotracheal intubation advantages comfort, less hemodynamic changes, more stable use in C -spine injuries disadvantages sinusitis, epistaxis avoid in facial or basilar skull fractures Mechanical Ventilation in the NICU The Effect of PEEP on ICP Physiological hypothesis : increases in PEEP will alter intrathoracic pressures to impede venous return Depends on both intracranial and pulmonary compliance patients with poor intracranial compliance can have significant increases in ICP due to transmitted increases in CVP. not a problem with normal intracranial compliance PEEP applied to patients with stiff lungs ( i.e ARDS ) does not increase ICP since intrathoracic pressure is poorly transmitted to CVP. PEEP > 12 to begin to show changes J Trauma 2005;58(3): Mechanical Ventilation in the NICU Effects of mechanical ventilation on ICP ICP also affected by mean alveolar pressure affected by peak airway pressures inspiration time Goals Goals keep airway pressures at a minimum ensure adequate oxygenation More likely to have cerebral vasodilation and ICP due to hypoxia or the cardiovascular effects of PEEP 5

6 Mechanical Ventilation in the NICU Hyperventilation as a therapy Decrease cerebral blood flow by around 1 to 2 ml per minute per 1 mm Hg drop of PaCO2 Drop in blood flow creates space within the intracranial compartment and decreases ICP Cerebral blood flow will fall to ischemia-inducing inducing levels? Only one prospective RCT in TBI : neurological outcome was worse in the hyperventilation group Hyperventilation is not recommended J Neurosurg 1991;75(5): Spinal cord injury Necessity for mechanical ventilation depend upon the level and extent of the lesion Lesions at C5 and above clearly require immediate and likely long-term ventilation because of complete paralysis of the phrenic and intercostal nerves Lesions at C6 and below may necessitate mechanical ventilation because of varying degrees of paralysis and extension of the lesion through edema and bleeding up to C5 and above Spinal cord injury Course of ventilatory failure. Initial insult to cervical cord results in an acute and severe respiratory decrease with vital capacity dropping to 30% or less various delayed declines in function fatigue, ineffective clearance of secretions, pneumonia,or atelectasis Spinal cord injury Patients with lower c-spine lesions who demonstrated no initial severe compromise in respiratory function. May has delayed and sudden apnea to undergo respiratory arrest often after seemingly normal function, commonly1 to 2 weeks after injury. Risk factors and warning signs for this delayed apnea diffuse and extensive cord lesions, transient respiratory distress, and bradycardia. more likely to occur in sleep Ventilator mode Volume preset Initiated Limited Cycled Control mode (CMV) Time Volume Volume/Time Assist-control mode (A/CMV) Pressure Volume Volume/Time Intermittent mandatory (IMV) Time Volume Volume/Time Synchronize (SIMV) Pressure Volume Volume/Time Volume variable Mechanical Ventilator Modes Pressure support (PSV) Pressure Pressure Flow Pressure control (PCV) Time Pressure Time Airway pressure release (APRV) Time Pressure Time CMV Continuous Mandatory Ventilation (CMV) : included Control mode (CMV), Assist-control mode (A/CMV) and Pressure control (PCV) Delivers : pre-set (Mandatory) Tidal volume (or pressure) Inspire : Expire duration (I:E) ratio minimum Respiratory Rate Patient can trigger additional breath with constant (set) volume (or pressure). Ventilator assumes the drop in pressure is due to patient s initiation of spontaneous breath (Sensitivity) If inadequate ventilation occur : Machine will overcome Backup or Control 6

7 CMV (Volume control : VCV) CMV (Pressure control : PCV) Pressure-Support Ventilation (PSV) Pressure-Support Ventilation (PSV) Spontaneous breathing mode Patient s effort augmented by pre-set pressure Clinician determine level of pressure for inspiration Patient set : Low level PSV Respiratory Rate used to overcome Inspiratory flow resistance Inspire : Expire duration (I:E) ratio through ET-tube Tidal Volume (TV) determined by : Level of pressure support Amount of patient effort Resistance and Compliance of respiratory system Intermittent Mandatory Ventilation (IMV) Control mode from ventilator Plus Allows for spontaneous breathing without increase resistance Control mode : required pre-set (Mandatory) Tidal volume (or pressure) Inspire : Expire duration (I:E) ratio Minimum respiratory rate Modern day ventilator : Usually Synchronized with patient s spontaneous breathing ( SIMV ) Ventilator breath Spontaneous breath Spontaneous pattern would have been without ventilator breath 7

8 Synchronize Intermittent Mandatory (SIMV) SIMV with PSV Continuous Positive Airway Pressure (CPAP) CPAP Spontaneous breathing mode Airway pressure set higher than atmospheric pressure. Low level CPAP used to overcome resistance through ET-tube. Evaluate ability to breathe spontaneously before extubation Factors affect Peak Inspiratory Pressure (PIP) in VCV Factors affect Tidal Volume (VT) in PCV Peak inspiratory flow setting : Higher flow setting increase PIP PEEP, Auto-PEEP : Increase PEEP, Auto-PEEP increase PIP Tidal volume : Increase TV increase PIP Resistance : Increase resistance result in higher PIP Compliance : Decrease compliance result in higher PIP Inspiratory flow pattern :Lower with Decelerating flow pattern Increase VT Increase PIP or PCV setting Increase Inspiratory time Decrease Resistance Greater patient inspiratory effort Decrease VT Increase Auto- PEEP Decrease compliance 8

9 Advantage and Disadvantage of VCV and PCV Type Volume Control Ventilation (VCV) Pressure Control Ventilation (PCV) Advantage Constance VT with change in resistance and compliance Familiar to most clinician Reduce risk of overdistension with changes in compliance Variable flow improves synchrony Disadvantage Increase plateau pressure (P plat ) with decrease compliance Fixed inspiratory flow may cause dyssyncrony Changes VT with changes in resistance and compliance Clinician less familiar Weaning Parameters-Extubation criteria MICU VC VC cc/kg 15cc/kg TV > 4cc/kg MVV < 10L NIF cm/h 2 0 RR < 35 / min Gas exchange PaO 2 > 80 torr on < 60% FiO 2 PCO2 < 45 torr A-a gradient 300 on 100% NICU NICU Awake ( consistently ) follows commands frequency of suctioning > q 2 hrs control of secretions good swallow good cough intact lower cranial nerve function McMaster University Evidence-Based Medicine Group eight parameters useful in predicting outcome from ventilation discontinuation 1. assessments on the ventilator minute volume, maximum inspiratory pressure, airway occlusion pressure 0.1 second after the onset of inspiratory effort 2. Index involving compliance, respiratory rate, oxygenation, and pressure McMaster University Evidence-Based Medicine Group 3. Assessments off ventilation respiratory rate, tidal volume and a ratio of these parameters. 4. The most valuable assessment is a well-controlled spontaneous breathing trial (SBT) When an SBT is part of a formal protocol, it has been demonstrated to reduce the number of weaning days and total ICU stay. Chest 2001;120(6 Suppl): ):375S 95S Chest 2001;120(6 Suppl): ):438S 44S Implications of Extubation Delay in Brain Injured Patients Meeting Standard Weaning Criteria Prospective observational cohort study of practice of physicians treating brain injured patients at Harborview medical center. Inclusion criteria TBI, SAH, ICH, SE, Strokes, Encephalitis. Extubation delay Associated with increased risk of pneumonia RR 1.8 CI ( ) Longer ICU and Hospital LOS and subsequent increased cost $34, Increased mortality RR 2.2 CI ( ) Implications of Extubation Delay in Patients with Brain Injury Conclusions Timely extubation appears to be safe Patients who met spontaneous ventilatory parameters had adequate gas exchange and were cardiovascular and neurologically stable were able to be extubated without increased risk of Reintubation Pneumonia Death Delayed extubation was associated with increased LOS, Cost of hospitalization, and possibly increased morbidity and mortality Am J Respir Crit Care Med 2000;161:

10 Diagrams of the dead-space volume of the upper airway (A), a tracheostomy tube (B), and an oral endotracheal tube (C). Arch Surg 1999;134(1): Arch Surg 1999;134(1): SUCCESSFUL EXTUBATION FOR NEUROLOGIC AND RESPIRATORY PREDICTORS Patients were assigned randomly to Control or Intervention groups after informed consent was obtained by study physicians not involved in their routine care. Study physicians recorded demographic and laboratory data, initial ventilator settings, minute entilation (E), respiratoryrate (f), fraction of inspired oxygen (FIO2), static compliance, set tidal volume (VT), spontaneous VT, peak pressure, plateau pressure, endotracheal tube size, acute lung injury (ALI) score, and Acute Physiology and Chronic Health Evaluation (APACHE) II score. Vital signs, including Glasgow Coma Scale (GCS) score,were recorded prospectively by ICU nurses. Am J Respir Crit Care Med Vol 163. pp , 664, 2001 Am J Respir Crit Care Med Vol 163. pp , 2001 Potential Obstacles to Successful Clinical Studies on Tracheostomy and Weaning Inability to blind investigators (and clinicians) as to groupings Bias of clinicians managing patients Inability to predict which patients will require prolonged ventilatory support Varying weaning protocols Varying criteria for weaning success and failure Funding and reimbursement factors Varying specialties performing procedure Varying levels of training and experience among operators Ventilatory management is a diverse subject involving the complex interplay of physiology and technology. The nature of neurosurgical patients are unique subpopulation that demands careful consideration with respect to multiple aspects of ventilatory support. Mechanical ventilation can be used as a therapy, as opposed to being simply supportive in this setting. The evidence looking specifically at neurosurgical patients is limited. The growing emergence of specialist neurological ICUs, however, offers growing opportunity to investigate optimal management of this challenging group of patients. 10

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