215a Objectives List the indications for ventilatory support List the factors analyzed to determine initial ventilator modes and settings Define the current modes of ventilation, listing The advantages and disadvantages of each Basic intro to settings First a Review of Ventilation formulas… http://www.youtube.com/watch?v=mF4OvuzlfXc&fea ture=related Ve, VA, Compliance Indications for Ventilatory Support Respiratory failure (type I or II) Exacerbation of COPD Neuromuscular disease Coma 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 οn V'A. V'CO2=V'A× alveolar CO2 concentration or alveolar CO2 concentration=V'CO2/V'A. Hypoxemia The 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=f8zIVc9yTMg Arterial 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 hemoglobin SaO2 is the percentage of hemoglobin saturated with oxygen PaO2 is the partial pressure of arterial oxygen Clinical Manifestations of Type I Respiratory Failure Clinical signs of hypoxemia Dyspnea Tachycardia Tachypnea Use of accessory muscles of ventilation Nasal flaring Cyanosis – peripheral and central Central 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: Restlessness Anxiety Disorientation, confusion, lassitude and listlessness Headaches Symptoms of Hypoxemia Symptoms of acute hypoxemia: Cyanosis (Skin appearing bluish due to insufficient oxygen) Cheyne-Stokes respiration (irregular pattern of breathing) Increased blood pressure Apnea (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 Failure Auscultation Wheezing indicates bronchospasm (asthma?) Diminished (COPD?) Unilateral wheezing – endobronchial lesion, FBAO Unilaterally diminished or absent – atelectasis, infection, effusion Clinical Manifestations of Type I Respiratory Failure Radiologic Findings “Black” radiograph Hyperinflated lungs (COPD) – V/Q mismatch “White” radiograph Occlusion of alveoli – shunt Clinical Manifestations of Type II Respiratory Failure Decreased respiratory drive Bradypnea leading to apnea Clinical signs of decrease in respiratory drive Respiratory rate < 12 bpm Altered 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 hypoventilation Clinical Manifestations of Type II Respiratory Failure Neurological disease Drooling, dysarthria (unable to speak), weak cough (ALS) Unable to swallow (Dysphagia) Muscle wasting Diaphragmatic weakness Supine paradoxical breathing (ALS) Lower extremity weakness, progressing superiorly (Guillain-Barre) Ocular muscle weakness (myasthenia gravis) Clinical Manifestations of Type II Respiratory Failure Increased work of breathing Increasingly rapid, but shallow breathing (exacerbation of COPD) Diminished breath sounds Irritability, confusion Chronic Respiratory Failure Development of respiratory failure in patients with chronic respiratory conditions over an extended period of time, as much as years Allows compensatory mechanisms to adapt to the disease state Most 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 RF Precipitating factors Bacterial or viral infections Congestive heart failure http://www.youtube.com/watch?v=JJAMYHAwCMs&feature=related Pulmonary embolism Chest wall dysfunction Non-compliance with medical orders “Normal” blood gases for these patients may be outside normal limits Chronic Respiratory Failure With Superimposed Acute RF Goals of therapy Normalization of pH Elevation of SaO2 Improvement of airflow Treatment of infections Maintain fluid status Indications for Ventilatory Support Acute respiratory failure Post-Operative respiratory failure (over sedation, complications) Sepsis (sudden increase in VO2 and CO2 production) Cardiac failure (MI, CHF…) Indications for Ventilatory Support Acute respiratory failure ARDS (from PN, Sepsis…) Trauma (blood loss, head trauma…) Pneumonia (causing plugs…) Indications for Ventilatory Support Apnea (sedation, drug OD…) Impending respiratory failure Inability to oxygenate Clinical Manifestations of Acute Ventilatory Failure Rapid, shallow respiratory pattern frequently have pleural space disease (pleural effusion, hemothorax, pneumothorax). Clinical Manifestations of Acute Ventilatory Failure Patients 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 Failure Cardiovascular symptoms Tachycardia; when severe bradycardia Hypertension; when severe, hypotension Vasodilation Clinical Manifestations of Acute Ventilatory Failure Neurologic symptoms Headache Drowsiness; when severe non-responsiveness Convulsions Biots/Cheyne stokes breathing Clinical Manifestations of Acute Ventilatory Failure Other signs Sweating Redness of the skin Goals of Ventilatory Support Maintenance of adequate alveolar ventilation and oxygen delivery Restore acid-base balance Goals of Ventilatory Support Reduce the work of breathing Reduce myocardial work secondary to hypoxemia And increased work of breathing Considerations When Initiating Ventilatory Support Type of airway: endotracheal tube vs. tracheostomy tube Pressure-controlled vs. volume-controlled ventilation- depends on if patient has pre-existing congestion, loss of compliance, known lung problems http://www.youtube.com/watch?v=4O4vGPqM2RM Pressure-Controlled Ventilation Pressure support ventilation (PSV) Designed to augment spontaneous ventilation (increases Spontaneous tidal volume) Patient-triggered, pressure- limited, flow-cycled ventilation Used to overcome RAW imposed by ETT May be stand-alone mode or used with SIMV/CPAP http://www.youtube.com/watch?v=oLZ0fcJ9Rhw&NR=1 Pressure-Controlled Ventilation Pressure 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 SIMV Set pressure limit (PIP) and Inspiratory time Volume and flow vary Pressure-Controlled Ventilation Pressure control ventilation (PCV) Useful in limiting airway pressure and providing a decreasing flow, which may improve gas distribution and synchrony Can be set in any patient, however most often used for patients with low compliant lungs, especially if high PEEP levels will be used Volume-Controlled Ventilation Used primarily to maintain constant tidal volume Useful when lung mechanics are changing due to pathophysiology Set Tidal volume based on patient’s IBW in a range of 8-12 ml/kg and flow rate IBW= men 106 + 6 lbs for every inch over 60 inches IBW=woman 105 + 5 lbs for ever inch over 60 inches For restrictive disease 5-7 ml/kg Volume-Controlled Ventilation Volume control is volume limited and flow cycled Can be set in AC or SIMV modes Direct control over Ve I-time and pressure vary depending on patients lung compliance Pressure-Regulated Volume Control (PRVC) Ventilation Offers pressure-controlled ventilation while guaranteeing a volume Pressure and flow fluctuate to maintain a constant minimum TV May not work well with restrictive lungs Non-Invasive (NPPV) vs. Invasive PPV Advantages of NPPV Avoidance of intubation Preservation of natural airway defenses Patient comfort Non-Invasive (NPPV) vs. Invasive PPV Advantages of NPPV Maintenance of speech and swallowing Intermittent use Non-Invasive (NPPV) vs. Invasive PPV Disadvantages of NPPV Patient cooperation essential Limited access to airway during ventilation Discomfort from mask Non-Invasive (NPPV) vs. Invasive PPV Disadvantages of NPPV Ulceration, face sores, eye irritation, rhinitis, dry nose Stomach pain from gastric inflation Leak from improper fit Aspiration risk Non-Invasive (NPPV) vs. Invasive PPV Disadvantages of NPPV Transient hypoxemia from mask disconnection BiPAP limited to maximum of 30 cmH2O Time consuming procedure Drying of secretions/plugs Partial vs. Full Ventilatory Support Partial ventilatory support Use of ventilator settings requiring patient to provide portion of the ventilation Modes of Partial Ventilation Synchronized intermittent mandatory ventilation (SIMV) Pressure support ventilation (PSV) Volume support ventilation (VSV), PSV will fluctuate depending on set minimum VT Modes of Partial Ventilation Adaptive 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 Support Ventilator provides the full minute ventilation; no patient contribution Assist-control mode Initial Ventilator Settings Choice of mode (AC, IMV/SIMV, PCV, PRVC, APRV) Tidal volume (VT) – 8 to 12 ml/kg IBW Rate (f) – typically backup rate of 8-12 breaths /min Initial Ventilator Settings Trigger sensitivity (either flow or pressure) Typically -0.5 to -2.o cmH2O to minimize effort May need to be adjusted to avoid auto-cycling on some ventilators Applies only to patient triggered breaths Initial Ventilator Settings Trigger sensitivity Flow triggering may have slightly less work than pressure triggering Initial Ventilator Settings Inspiratory flow 60 to 80 L/min. to achieve an inspiratory time of 1 second and an I:E ratio of 1:2 or better May require higher flows in patients with COPD to lengthen expiratory time, allowing improved gas exchange Initial Ventilator Settings Flow waveform Decelerating or decreasing flow waveform generally delivered in pressure ventilation Decelerating 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-time Initial Ventilator Settings Oxygen percentage (FIO2) If little is known concerning patient, begin with FIO2 of 1.0, decreasing to 0.4 to 0.5 as quickly as possible Patients with known blood gas results should be given FIO2 consistent with the known data Initial Ventilator Settings Positive end-expiratory pressure (PEEP) PEEP of 5 cmH2O is advocated by some as “physiologic PEEP” Should be adjusted as necessary to allow FIO2 to be reduced to 0.4 as quickly as possible Initial Ventilator Settings Pressure limit Start at 50 cmH2O Adjust to 10 to 20 cmH2O above peak pressure when patient is stable