Initiating Ventilatory Support
description
Transcript of Initiating Ventilatory Support
Ventilator Monitoring
Initiating Ventilatory Support215a
ObjectivesList the indications for ventilatory supportList the factors analyzed to determine initial ventilator modes and settingsDefine the current modes of ventilation, listing The advantages and disadvantages of eachBasic intro to settings
First a Review of Ventilation formulashttp://www.youtube.com/watch?v=mF4OvuzlfXc&feature=related
Ve, VA, ComplianceIndications for Ventilatory SupportRespiratory failure (type I or II)Exacerbation of COPDNeuromuscular diseaseComa
The volume of carbon dioxide eliminated per minute (which in a steady state is equal to that produced by the body (V'CO2) is dependent on the concentration of carbon dioxide in alveolar gas and n V'A. V'CO2=V'A alveolar CO2 concentration or alveolar CO2 concentration=V'CO2/V'A. HypoxemiaThe condition of hypoxemia refers to the low partial pressure of oxygen in the arterial blood. Hypoxemia is often confused with either anoxia, asphyxia, hypoxia or anemia. Although, these are in some way related to reduction in the levels of oxygen in the body, these are distinct medical conditions. Anoxia is the absence of oxygen supply in the body. This implies extremely low levels of oxygen in the body.Asphyxia is the absence of oxygen along with the accumulation of carbon dioxide.Hypoxia is the deficiency of oxygen in some specific part of the body.Anemia refers to a condition when oxygen content in the arterial blood is low and the partial pressures in the arterial blood are high.Hypoxemia refers to refers to a condition when oxygen content in the arterial blood is low as also the partial pressures in the arterial blood.http://www.youtube.com/watch?v=f8zIVc9yTMgArterial Oxygen Content (CaO2)The arterial oxygen content can be given by the following equation:
Arterial Oxygen Content = (Hgb x 1.34 x SaO2) + (0.0031 x PaO2) where,
Hgb is the hemoglobinSaO2 is the percentage of hemoglobin saturated with oxygen PaO2 is the partial pressure of arterial oxygen
Clinical Manifestations of Type I Respiratory FailureClinical signs of hypoxemiaDyspneaTachycardiaTachypneaUse of accessory muscles of ventilationNasal flaringCyanosis peripheral and centralCentral nervous system dysfunction irritability, confusion, coma
Symptoms of Hypoxemia(The symptoms of hypoxemia depend on the severity i.e. the amount by which the partial pressure has reduced.)
Symptoms of mild hypoxemia:
RestlessnessAnxietyDisorientation, confusion, lassitude and listlessnessHeadaches
Symptoms of HypoxemiaSymptoms of acute hypoxemia:
Cyanosis (Skin appearing bluish due to insufficient oxygen)Cheyne-Stokes respiration (irregular pattern of breathing)Increased blood pressureApnea (temporary cessation of breathing)Tachycardia (increased rate of heartbeats, more than 100 per min)Hypotension (abnormally low blood pressure, below 100 diastolic and 40 systolic. Here, as an effect of an initial increase in cardiac output and rapid decrease later.)Ventricular fibrillation (irregular and uncoordinated contractions of the ventricles)Asystole (severe form of cardiac arrest, heart stops beating)Polycythemia (abnormal increase in RBCs. The bone marrow may be stimulated to produce excessive RBCs in case of patients suffering from chronic hypoxemia)Coma
Clinical Manifestations of Acute Ventilatory Failure
Clinical Manifestations of Type I Respiratory FailureAuscultationWheezing indicates bronchospasm (asthma?)Diminished (COPD?)Unilateral wheezing endobronchial lesion, FBAOUnilaterally diminished or absent atelectasis, infection, effusion
Clinical Manifestations of Type I Respiratory FailureRadiologic FindingsBlack radiograph Hyperinflated lungs (COPD) V/Q mismatchWhite radiograph Occlusion of alveoli shunt
Clinical Manifestations of Type II Respiratory FailureDecreased respiratory drive
Bradypnea leading to apneaClinical signs of decrease in respiratory driveRespiratory rate < 12 bpmAltered state of consciousness (increase CO2, amonia, blood sugar, ICB)Rapid, shallow breathing pattern (obesity, neuromuscular)Evidence of trauma (brain injury)Fatigue (hypothyroidism, sleep apnea)Radiologic findings atelectasis secondary to hypoventilationClinical Manifestations of Type II Respiratory FailureNeurological disease
Drooling, dysarthria (unable to speak), weak cough (ALS)Unable to swallow (Dysphagia)Muscle wastingDiaphragmatic weaknessSupine paradoxical breathing (ALS)Lower extremity weakness, progressing superiorly (Guillain-Barre)Ocular muscle weakness (myasthenia gravis)
Clinical Manifestations of Type II Respiratory FailureIncreased work of breathingIncreasingly rapid, but shallow breathing (exacerbation of COPD)Diminished breath soundsIrritability, confusion
Chronic Respiratory FailureDevelopment of respiratory failure in patients with chronic respiratory conditions over an extended period of time, as much as yearsAllows compensatory mechanisms to adapt to the disease stateMost commonly Type II failure with compensatory metabolic alkalosis (COPD)Compensation for Type I is polycythemia (Fibrosis/COPD)May be complicated by superimposed acute respiratory failure
Chronic Respiratory Failure With Superimposed Acute RFPrecipitating factorsBacterial or viral infectionsCongestive heart failure http://www.youtube.com/watch?v=JJAMYHAwCMs&feature=relatedPulmonary embolismChest wall dysfunctionNon-compliance with medical ordersNormal blood gases for these patients may be outside normal limits
Chronic Respiratory Failure With Superimposed Acute RFGoals of therapy
Normalization of pHElevation of SaO2Improvement of airflowTreatment of infectionsMaintain fluid status
Indications for Ventilatory SupportAcute respiratory failurePost-Operative respiratory failure (over sedation, complications)Sepsis (sudden increase in VO2 and CO2 production)Cardiac failure (MI, CHF)
Indications for Ventilatory SupportAcute respiratory failureARDS (from PN, Sepsis)Trauma (blood loss, head trauma)Pneumonia (causing plugs)
Indications for Ventilatory SupportApnea (sedation, drug OD)Impending respiratory failureInability to oxygenate
Clinical Manifestations of Acute Ventilatory FailureRapid, shallow respiratory pattern frequently have pleural space disease (pleural effusion, hemothorax, pneumothorax).
Clinical Manifestations of Acute Ventilatory FailurePatients with end-expiratory effort and wheezes on chest auscultation frequently have small airway obstructive disease (asthma). Patients with deep, labored chest movements frequently have pulmonary parenchymal disease (pulmonary edema, pulmonary contusions, space-occupying masses). Patients with obvious stridor, minimal air movement at the nares or mouth, and marked inspiratory effort typically have upper airway obstruction (laryngeal edema or paralysis, foreign body aspiration). These patterns are hardly exclusive: Often patients have multiple problems, and some patients may have serious underlying respiratory problems and yet clinically appear normal.What nonrespiratory conditions can mimic acute respiratory distress?Numerous disorders cause tachypnea, orthopnea, and other signs referable to the respiratory system in the absence of true respiratory disease. These disorders can confuse the clinician. Disorders such as hyperthermia, shock, metabolic acidosis and alkalosis, hyperthyroidism, fear or anxiety, pericardial tamponade, anemia, abdominal organ enlargement or ascites, and abnormalities with central control of respiration from drugs and metabolic or organic central nervous system disease are all causes of signs that may mimic true respiratory distress.
Clinical Manifestations of Acute Ventilatory FailureCardiovascular symptomsTachycardia; when severe bradycardiaHypertension; when severe, hypotensionVasodilation
Clinical Manifestations of Acute Ventilatory FailureNeurologic symptomsHeadacheDrowsiness; when severe non-responsivenessConvulsionsBiots/Cheyne stokes breathingClinical Manifestations of Acute Ventilatory FailureOther signsSweatingRedness of the skin
Goals of Ventilatory SupportMaintenance of adequate alveolar ventilation and oxygen deliveryRestore acid-base balance
Goals of Ventilatory SupportReduce the work of breathingReduce myocardial work secondary to hypoxemia And increased work of breathing
Considerations When Initiating Ventilatory SupportType of airway: endotracheal tube vs. tracheostomy tubePressure-controlled vs. volume-controlled ventilation- depends on if patient has pre-existing congestion, loss of compliance, known lung problemshttp://www.youtube.com/watch?v=4O4vGPqM2RM
Pressure-Controlled VentilationPressure support ventilation (PSV)Designed to augment spontaneous ventilation (increases Spontaneous tidal volume)Patient-triggered, pressure- limited, flow-cycled ventilationUsed to overcome RAW imposed by ETTMay be stand-alone mode or used with SIMV/CPAPhttp://www.youtube.com/watch?v=oLZ0fcJ9Rhw&NR=1Pressure-Controlled VentilationPressure control ventilation (PCV)Delivery of mandatory support breaths at a set inspiratory pressure (pressure limited/time cycled)May be used in assist-control mode or with SIMVSet pressure limit (PIP) and Inspiratory timeVolume and flow varyPressure-Controlled VentilationPressure control ventilation (PCV)Useful in limiting airway pressure and providing a decreasing flow, which may improve gas distribution and synchronyCan be set in any patient, however most often used for patients with low compliant lungs, especially if high PEEP levels will be usedVolume-Controlled VentilationUsed primarily to maintain constant tidal volumeUseful when lung mechanics are changing due to pathophysiologySet Tidal volume based on patients IBW in a range of 8-12 ml/kg and flow rateIBW= men 106 + 6 lbs for every inch over 60 inchesIBW=woman 105 + 5 lbs for ever inch over 60 inchesFor restrictive disease 5-7 ml/kg
Volume-Controlled VentilationVolume control is volume limited and flow cycledCan be set in AC or SIMV modesDirect control over VeI-time and pressure vary depending on patients lung compliancePressure-Regulated Volume Control (PRVC) Ventilation Offers pressure-controlled ventilation while guaranteeing a volumePressure and flow fluctuate to maintain a constant minimum TVMay not work well with restrictive lungsNon-Invasive (NPPV) vs. Invasive PPVAdvantages of NPPVAvoidance of intubationPreservation of natural airway defensesPatient comfort
Non-Invasive (NPPV) vs. Invasive PPVAdvantages of NPPVMaintenance of speech and swallowingIntermittent use
Non-Invasive (NPPV) vs. Invasive PPVDisadvantages of NPPVPatient cooperation essentialLimited access to airway during ventilationDiscomfort from mask
Non-Invasive (NPPV) vs. Invasive PPVDisadvantages of NPPVUlceration, face sores, eye irritation, rhinitis, dry noseStomach pain from gastric inflationLeak from improper fitAspiration risk
Non-Invasive (NPPV) vs. Invasive PPVDisadvantages of NPPVTransient hypoxemia from mask disconnectionBiPAP limited to maximum of 30 cmH2OTime consuming procedureDrying of secretions/plugs
Partial vs. Full Ventilatory SupportPartial ventilatory supportUse of ventilator settings requiring patient to provide portion of the ventilation
Modes of Partial VentilationSynchronized intermittent mandatory ventilation (SIMV)Pressure support ventilation (PSV)Volume support ventilation (VSV), PSV will fluctuate depending on set minimum VT
Modes of Partial VentilationAdaptive pressure ventilation (APV)Adaptive support ventilation (ASV)Mandatory minute volume ventilation (MMV)WE WILL TALK ABOUT THE ADAPTIVE MODES IN A SEPARATE LECTURE
Full Ventilatory SupportVentilator provides the full minute ventilation; no patient contributionAssist-control mode
Initial Ventilator SettingsChoice of mode (AC, IMV/SIMV, PCV, PRVC, APRV)Tidal volume (VT) 8 to 12 ml/kg IBWRate (f) typically backup rate of 8-12 breaths /min
Initial Ventilator SettingsTrigger sensitivity (either flow or pressure)Typically -0.5 to -2.o cmH2O to minimize effortMay need to be adjusted to avoid auto-cycling on some ventilatorsApplies only to patient triggered breathsInitial Ventilator SettingsTrigger sensitivityFlow triggering may have slightly less work than pressure triggering
Initial Ventilator SettingsInspiratory flow60 to 80 L/min. to achieve an inspiratory time of 1 second and an I:E ratio of 1:2 or betterMay require higher flows in patients with COPD to lengthen expiratory time, allowing improved gas exchange
Initial Ventilator SettingsFlow waveformDecelerating or decreasing flow waveform generally delivered in pressure ventilationDecelerating waveforms generally decrease peak inspiratory pressure, but increase mean airway pressure
Decelerating set in VC, automatic in PC
Constant Flow VC only
Increases MAP, decreased I-timeInitial Ventilator SettingsOxygen percentage (FIO2)If little is known concerning patient, begin with FIO2 of 1.0, decreasing to 0.4 to 0.5 as quickly as possiblePatients with known blood gas results should be given FIO2 consistent with the known data
Initial Ventilator SettingsPositive end-expiratory pressure (PEEP)PEEP of 5 cmH2O is advocated by some as physiologic PEEPShould be adjusted as necessary to allow FIO2 to be reduced to 0.4 as quickly as possible
58Initial Ventilator SettingsPressure limitStart at 50 cmH2OAdjust to 10 to 20 cmH2O above peak pressure when patient is stable