LOS ANGELES VALLEY COLLEGE. RESPIRATORY THERAPY 4 SYLLABUS Fall 2016 CLINICAL APPLICATIONS Ventilator Management Module

Transcription

1 LOS ANGELES VALLEY COLLEGE RESPIRATORY THERAPY 4 SYLLABUS Fall 2016 CLINICAL APPLICATIONS Ventilator Management Module Goal: To provide the respiratory therapy student with advanced study, training and clinical experience in clinical assessment & delivery of mechanical ventilation. Texts: Cairo, J.M. and Pilbeam, S.P., Respiratory Care Equipment. Saint Louis, current edition, Mosby, Inc. Los Angeles Valley College Respiratory Therapy Syllabus, edited by Morrison G.S. and Sinsheimer, F. A. Scanlan, C. L. et al, Egan's Fundamentals of Respiratory Therapy and Study Guide. Saint Louis, current edition, Mosby-Yearbook, Inc.. Course Requirements all of the following must be completed passing = 75% 2 Quizzes (5 points ea) 10 points Mid Term Exam 44 points 10 Patient Profiles - 20 points Final Exam - 76 points Total = 140 points must have passing grade 75% on final exam & complete all lab activities and clinical objectives to successfully Complete RT 4 All Lab assignments all labs, tasks, & self study / training modules due on final exam Clinical Evaluation Student must have an acceptable clinical evaluation & meet clinical objectives and competencies including critical thinking and verbal communication. Student must complete all required Clinical forms including physician interaction and attendance records RT 4 Student Learning Outcomes Respiratory Therapy, 4, Applications of Respiratory Therapy & Clinical Experience II RT 4 Course Objectives List and explain the effects of positive pressure on the pulmonary and cardiovascular systems. Demonstrate clinical thinking skills by performing a bedside ventilator patient assessment and make recommendations for the appropriate parameter adjustments to address the patient s oxygen, ventilation, work of breathing, or airway protection problems. Demonstrate teamwork skills in the clinical setting by communicating and collaborating with Respiratory therapists, nurses, doctors and other health care professionals to make recommendations in the management of the patient. List and explain the indications, risks, and contraindications for each mechanical ventilator mode and parameter. List and explain the risks and benefit of each ventilator support and weaning strategy. Demonstrate how to perform, document, and communicate a ventilator weaning assessment. RT 4 Student learning Outcome Students can apply ventilator management and assessment, skills in the clinical setting. SLO Measurement Activity Student Clinical performance - each clinical rotation the students will demonstrate how well they applied course objectives in actual patient care setting. The evaluation includes competency, critical thinking, teamwork, interpersonal, and communication skills using a rubric of 0 2 fails, meets, or exceeds expectations 1

2 Clinical and Lab objectives: RT 4 Ventilator management List & describe the indications for mechanical Ventilation Describe & assess patients for Respiratory Failure type 1 ( hypoxic) & type II ( Hypercapnic) Define terminology applied to respiratory failure & mechanical ventilation Assess, monitor, & document ventilator patients Explain physiologic effects of mechanical Ventilation List & explain the common modes & parameters of mechanical ventilation Describe & apply advanced modes of ventilation Trace the flow of a ventilator & ventilator circuit Explain indications & rational for appropriate ventilator mode & parameter adjustments List & explain hazards / precautions of mechanical ventilation Explain how each ventilator parameter effects oxygenation and or ventilation Describe indications for non invasive ventilation Describe current strategies for Critical Care management of Ventilator patients List & explain current methods for administering inline aerosol medication therapy Explain how Positive Pressure effects the patient s hemodynamics List & describe ventilator weaning assessment, parameters & strategies List & explain BIPAP & CPAP parameters Assess patient for appropriate Mask for BIPAP Describe use & purpose of Ventilator waveforms & graphics Describe effects & relationships of Pressure, Flow, & Volume Setup & Calibrate Ventilators Describe strategies to minimize hazards of mechanical ventilation Course Requirements all of the following must be completed to successfully complete RT4 Digital Literacy All students are required to acquire and maintain a student address and have computer access to download any course information or files from either the LAVC Portal mylavc.edu or Haiku Educational Portal. You will be invited via by Gregory Morrison to join the Haiku Learning class RT 4 - Clinical Experience II 2

3 Accommodation / Access If you are a student with a disability requiring classroom accommodations, and have not contacted SSD, do so in a timely manner. SSD is located in the Student Services Annex, Room 175 or call SSD at (818) or TTD (818) to meet with a SSD counselor. If SSD has already sent the memo to instructor confirming accommodations required by student for this class, please meet with me to discuss arrangements. Financial Aid Financial Aid is available! Call (818) Go to the Financial Aid Office in the Student Services Center, first floor. For more info: Academic Dishonesty / Plagiarism and Student Conduct Plagiarism is the use of others words and/or ideas without clearly acknowledging their source. When you incorporate those words and ideas into your own work, you must give credit where credit is due. Plagiarism, intentional or unintentional, is considered academic dishonesty and is not tolerated. Anyone found to be plagiarizing or cheating on assignments (e.g., copying or giving answers, using crib sheets, etc.) will (1) receive a zero (fail) on the assignment, and (2) be referred to the Vice President of Student Services for further disciplinary action, following due process. For further information on plagiarism, go to the Writing Center website ( and refer to the STANDARDS OF STUDENT CONDUCT AND DISCIPLINARY ACTION in the current Schedule of Classes and Catalog Office Hours Professor Morrison Mondays 1-3:00 AHS 309 Tuesdays 11-1:30 Wednedsdays and Thursdays after 2:00 by appointment morrisgs@lacv.edu cell Cheryl Pearson Mondays 9:00 11:00 & 2:00 4:00 Tuesdays -Thursdays buy appointment pearsoch@lavc.edu Office

4 LOS ANGELES VALLEY COLLEGE Fall Semester, 2016 RESPIRATORY THERAPY 4 - Lab (Monday ) Instructors: Professors Gregory Morrison morrisgs@lavc.edu and Cheryl Pearson pearsoch@lavc.edu Lab Schedule Monday Lab 8:00 a.m. - 11:15 AHS 331 Wens Vent Competency labs ( 1 st 4 weeks ) 8/ :00 1:00 AHS WEEK Clinic Schedule Starts 9/28 ends 12/08 Wednesday Clinic Day Shift 7:00-3:30 TBA based on Clinic shift hours Thursday Clinic Day Shift 7:00-3:30 TBA based on Clinic shift hours 16 clinic hours TBA 4 12 hr shifts (in place of 8hrs) or 2 extra 8 hour shifts Week # Day / Date Topic Chapters 1 Monday 9:15 - Review RT 3 Final Exam; Physiologic effects of lab mechanical Ventilation, Course and student evals Wens 9 1:00 Monday Wen 9:00 1:00 Monday 9:15- Wen 9:00 1:00 Monday 9:15-12:30 Wen 9:00 1:00 Monday 9:15 W/Thu 9/28 &29 Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 Wens Clinic Monday 9:15 W/Thu Clinic Monday 9:15 W/Thu Clinic Monday 9:15 Thu 12/17 final Ventilator competency Lab 1 Labor day holiday No lab Ventilator competency Lab 2 Indications for Mechanical Ventilation Ventilator competency Lab 3 Ventilator management & Weaning Strategies Ventilator competency Lab 4 - Quiz # 1Ventilator Skills Lab - Clinic Starts Wednesday 9/28 Ventilator Graphics & Monitoring RT 4 Mid Term exam Mid Term Review - Pressure Control & Advanced modes of Ventilation Pressure Control & Advanced modes of Ventilation Chapter 10, Chapter 44 Chapter 47 Egan Chapter 42,43, & 44 Non Invasive Ventilation Chapter 45 Quiz # 2 Ventilator Bundles & Critical Care Strategies Pressure control and Non invasive Pressure Control and Non Invasive skills Lab Thanksgiving Holiday Th no clinic Pressure Control and Non Invasive skills Lab Pressure Control and Non Invasive skills Lab last day of clinic Final Exam review open lab Thursday Final Exam 12:00-16;00 RT 5 starts Mon. Jan 09 clinic Jan 11 W,Th 12 hour shifts ( except CHLA tues-thurs 8 hours) Chapter 46 4

5 Module One: RT 4 Mechanical Ventilator Terminology 5

6 Mechanical Ventilator & ABG fundamentals Outline The provider will be able to: 1. List & describe the major modes of ventilation 2. List & describe what ventilator parameters effect Co2 3. List & describe what ventilator parameters effect oxygenation 4. List & describe the functions of the ventilator alarms 5. List & describe the oxygenation parameters of a blood gas 6. List & describe the ventilation / respiratory components of a blood gas 7. List & describe the metabolic components of a blood gas 8. Evaluate the metabolic & respiratory acid base balance of a blood gas Basic Modes of mechanical Ventilation What are the 3 basic Modes? Assist / Control (or CMV) All breaths are mechanical ( or Mandatory) Delivers the most support for the patient Assisted Breath = patient initiated (by Flow triggering or Negative Pressure triggering sensitivity) Mechanical Breath = Actual rate will be greater than set rate Control Breath = Ventilator ( time triggered using set rate as a minimum) How can you tell if the patient triggered the breath or the ventilator? 6

7 Spontaneous mode (also called CPAP or Pressure Support) = all spontaneous breaths. All breaths are triggered by the patient All breaths inspiration is cycled by the patient Most comfortable breath for active breathing patients Uses an APNEA alarm and back up to trigger mechanical breaths only if patient has apnea longer than the Apnea alarm delay. Invasive Ventilation Spontaneous Terminology CPAP = expiratory pressure Similar to PEEP increased FRC Pressure Support = Pressure applied during Inspiration in addition to CPAP increased Spontaneous VT CPAP + PSV = PIP Non Invasive Ventilation Terminology BiPAP or NIPPV CPAP = EPAP = increases FRC IPAP = PIP IPAP EPAP = PSV = increased VT 7

8 SIMV Synchronized Intermittent Mandatory Ventilation Mechanical Breaths and Spontaneous Breaths ( PSV) Rate of Mechanical breaths is set triggered by Ventilator or the patient but will not exceed set rate All additional patient triggered breath are spontaneous ( PSV) Used for weaning and to minimize breath stacking or ventilator patient dysynchrony 8

9 Breath Types Mechanical VS. Spontaneous What is a Mechanical Breath? Mechanical Breath Types Triggered by ventilator (Control) or patient (assist) Volume Control (Vol. Cycled) set VT and Flow = Set I. time and PIP Variable can use Ramp or square flow pattern Pressure Control (Time Cycled) Set PCV (PC & PEEP + PIP) and set I. Time = VT variable and flow is always decelerating (RAMP) but adjusts breath to breath based on patient effort. Pressure CYCLE SET PIP and Flow VT and I Time vary What is Volume Control + or PRVC? What is Bi level or APRV? Spontaneous Breaths how are all spontaneous breaths cycled?) Pressure Support (PSV) Insp. Pressure added above CPAP during inspiration PIP is set Flow, I. time and VT are variable What are the 2 benefits of increasing PSV? What is Volume Support? What is Tubing Compensation? 9

10 What is Pressure Support Ventilation? From Wikipedia, the free encyclopedia Pressure support ventilation (PSV), also known as pressure support, is a spontaneous mode of ventilation. The patient initiates every breath and the ventilator delivers support with the preset pressure value. With support from the ventilator, the patient also regulates his own respiratory rate and tidal volume. [1] In Pressure Support, the set inspiratory pressure support level is kept constant and there is a decelerating flow. The patient triggers all breaths. If there is a change in the mechanical properties of the lung/thorax and patient effort, the delivered tidal volume will be affected. The user must then regulate the pressure support level to obtain desired ventilation. [2][3] Or the long version Pressure support is a method of assisting spontaneous breathing in a ventilated patient. It can be used as a partial or full support mode (1-3). The patient controls all parts of the breath except the pressure limit. The patient triggers the ventilator the ventilator delivers a flow up to a preset pressure limit (for example 10cmH2O) depending on the desired minute volume, the patient continues the breath for as long as they wish, and flow cycles off when a certain percentage of peak inspiratory flow (usually 25%) has been reached. Tidal volumes may vary, just as they do in normal breathing. The purpose of using CPAP (PEEP) is to restore functional Residual capacity to what is normal for the patient, when lung volumes are low: this reduces the workload of early inspiration. When lungs lose their compliance, higher intrapleural pressures are required to inflate the lungs to a normal tidal volume, even with CPAP. Consequently, pressure support can be added, to assist the patient up the volume pressure curve. Figure 1 is a simplified volume pressure curve for a normal lung. The lung rests at FRC, which is about 2litres, and inspiration is relatively easy, as the lungs are compliant. In the same patient with low lung volume and stiff non-compliant lungs (figure 2), there is a very high workload required just to bring the lung volume to the FRC level, above which the lung is reasonably compliant. This extra work, that which brings the lung to P1 on the diagram, may be enough to cause respiratory distress, muscle fatigue and failure to ventilate. There are two solutions to this problem. 10

11 The first is to return the resting volume to FRC by applying a pressure at end expiration (PEEP) and keeping it there (CPAP). If you look at figure 3, you can see that application of CPAP has returned the resting FRC to normal, but the work of breathing remains high due to the loss of lung compliance (P3 is required to achieve the target tidal volume in this patient of 500ml. The solution to this problem is to administer pressure support in inspiration, in order to reduce the workload of breathing, and achieve the targeted tidal volume, with lower intrapleural pressures (P4). The vast majority of patients in intensive care can be given ventilatory assistance in this way, and it is called pressure support ventilation (4). The presence of an endotracheal tube (as a minimum) increases the resistance to inspiration, add to this a lung injury and the patient incurs a high workload to breathing. Pressure support offsets this work it offloads the respiratory muscles in order to return the tidal volume to normal. A normal individual who is intubated and not attached to a ventilator will have a lower functional residual volume (FRC) the lungs tend to collapse inwards and a lower tidal volume. Positive end expiratory pressure (PEEP) re-recruits FRC and places the patient on the steep part (lower work required to inflate the lung) of the pressure volume curve. Pressure support overcomes the resistance to inspiration and reduces the workload of that part of the ventilatory cycle. The term pressure support ventilation describes the combination of pressure support and PEEP. Pressure support on mechanical ventilators is above PEEP, which is an incorrect term it is really the pressure above CPAP. Thus if a patient is on PEEP 5cmH2O and pressure support of 10cmH2O what is the peak/plateau pressure? 11

12 Pressure support is used to assist spontaneous breaths in SIMV ventilation. The patient can be easily weaned using this technique, as the backup rate is weaned initially, and then the pressure support Screen display of a patient on pressure support ventilation. The pressure support is set at 12cmH2O. Note the decelerating flow pattern and the termination of flow before the end of inspiration. The flat topped appearance of the pressure waveforms indicates a pressure controlled breath, and the slight variance in tidal volumes is typical of pressure support and, indeed, normal 12

13 13

14 14

15 Mechanical Ventilator Terminology arameter Definition Purpose 1. Modes: Volume vs. Pressure A/C. CPAP SIMV Assist control mode. All mechanical positive pressure breaths. Continuous positive airway pressure Synchronized Intermittent Mechanical Ventilation. Total ventilatory support Total spontaneous breathing with continuous airway pressure to keep lungs & airways open. No ventilatory support unless invasive PSV is used. Non Invasive CPAP = no PSV used for sleep apnea Combination of mechanical, spontaneous breathing. Patient vent support for weaning. PCV Pressure Control Ventilation Uses set pressure instead of set volume. Pressure is plateau constant with variable flow. Used on mechanical breaths in A/C or SIMV Modes. PSV Pressure Support Ventilation Set pressure to assist spontaneous breathing during CPAP & SIMV NIPPV (BIPAP) II. Set Parameters: Bipolar Intermittent Positive Airway Pressure Non invasive ventilation uses mask ventilation instead of intubation tube. Similar to PSV and CPAP. FiO2 Fractional Inspired Oxygen % of O2 in gas. Directly increases ventilation. % Vt Tidal Volume Volume of gas in 1 breath. Directly increases ventilation. Rate Set respiratory rate # of set mechanical breaths directly increases ventilation. PEEP Flow Positive End Expiratory Pressure Velocity of gas during mechanical inspiration Pressure at end of expiration, keeps lungs inflated at end expiration (FRC). Opens Alveoli, directly increased oxygenation, impedes venous return. Increases interthoracic pressures. Allows vent to meet patient s inspiratory demands. Puts vent and patient in synch adjusts inspiratory time. 15

16 III. Measured Parameters: Obs. Rate Observed Respiratory Rate Total Respiratory Rate. Set RR and patient triggered RR. Ve Minute Ventilation Amount of ventilation in one minute. Rate x Vt = Ve, directly determines pco2 PIP Peak Inspiratory Pressure Pressure to expand lungs indicates compliance stiffness of lungs and airway resistance. Plateau Press Plateau Pressure Pressure to hold lungs open. Indicates lung static compliance PIP Plat = airway resistance. Compliance Stiffness/ elasticity of lungs PIP/ VT = Compliance Opposite of elasticity. Static vs. Dynamic I. Time Inspiratory Time Amount of time to deliver mechanical breath. Directly effects oxygenation. I/E Ratio Inspiratory Expiratory Ratio Ratio of Inspiration to Expiration. Normal < ½ used to keep ventilator in sync with patient. NIF Negative Inspiratory Force Patient s inspiratory effort. Weaning effort > -20 cm. VC Vital Capacity RSB Rapid Shallow Breathing index Maximum volume patient can exhale. Weaning effort > 1.5 or ml /Kg Idm RR / VT ( liters) > 105 = poor weaning & increased WOB AUTOPEEP Intrinsic PEEP Air trapped inside lungs by ventilatory and airway collapse. Can not be seen on Press gauge. Hidden Hazard. Expiratory Pause used to measure this. MAP Mean Airway Pressure Average or total amount of press/time that lungs are exposed to. Directly increases oxygenation. MAP increases with Rate, Press or time. PEEP and I.Time have the greatest effects. 16

17 Ventilator Alarm Reasons for Alarm Corrective Action Low Pressure Tubing disconnect Leak in Patient Circuit Patient inspiratory needs exceeding Ventilator set flow rate Check patient and circuit for loose or disconnected tubing Increase Ventilator set flow rate ***Mandatory Alarm*** High Pressure Patient Coughing or obstruction secretions in airway or tubing Patient fighting or out of sync with vent breaths Pneumo-thorax or changes in lung stiffness Suction airway and oral pharynx Adjust flowrate to meet pt needs Sedation Auscultate check for equal breath sounds C-Xray Low Tidal Volume Leak in tubing Pt s spontaneous tidal volumes may be dropping due to sedation or depressed respiratory drive in SIMV or CPAP Pt taking very small spont breaths in between larger Mechanical breaths Check patient and circuit for leaks Observe pt s respiratory pattern consider stimulating patient or adjusting sedation Spont Tidal vol alarm may be set too high This alarm can be disabled for patients on SIMV Ventilator Inoperative Pt. tubing disconnected while PEEP is on causing a constant flow of gas and dema valve is open Power Failure - Reconnect Circuit to patient Contact RT immediately check vent parameters consider Low O2 Inlet Oxygen inlet line is disconnected Portable Oxygen is empty Check connections to wall Check cylinder valve and guage pressure 17

18 Apnea Patient is not taking spontaneous breath Check Apnea ventilation setting Ventilator will automatically give back up ventilation. Check Patient LOC and sedation Give manual Breaths 18

19 Arterial Blood Gases Parameter Description Ranges Oxygenation Parameters PaO2 SaO2 O2Hb SPO2 A a gradient Partial pressure of oxygen in arterial plasma Calculated % Oxygen Saturation of arterial hemoglobin Measured % Oxygen saturation of the hemoglobin % oxygen saturation measured by Pulse Oximeter Difference between the oxygen level in Alveoli and artery. Indicates level of oxygenation + diffusion problems mmhg = normal = mild hypoxemia = mod hypoxemia < 50 = severe hypoxemia = venous oxygenation % = normal % = mild hypoxemia % = mod hypoxemia. < 88 % = severe hypoxemia < 80 % = venous oxygenation What are the acceptable ranges for COPD ( documented Co2 retention) Typical Hospital Protocol AHA ER ischemic CVA or MI 20 mmhg = normal > 20 mmhg = oxygenation problem. ( 21% FiO2) Normal = FiO2 > 350 = hypoxic respiratory Failure type I a/ A ratio Ratio of Pa & PAo2 s esp. useful with vent pt s on high Fio2 s > 60% PCO2 HCO3 BE (Base Excess).90 = normal (90%) <.3 = severe hypoxemia Hypoxic Resp Failure Acid Base Parameters (Respiratory vs. Metabolic) Respiratory Component Partial pressure of CO2 in arterial plasma pco2 = ventilation. Metabolic Component Bicarbonate Buffer level in arterial blood Measurement of buffer level in blood, measures metabolic increases or decreases in HCO3 production mmhg = normal < 40 = hyperventilation + respiratory alkalosis > 40 = hypoventilation + respiratory acidosis 24 mmeq = normal (if pco2 in 40) > 24 = metabolic alkalosis (if pco2 = 40) >24 = metabolic acidosis ( if pco2 = 40) + or 2 = normal > 2 = alkalosis < -2 = acidemia 19

20 Rules of Respiratory /Metabolic Compensation H2O + CO2 < - > H2 CO3 < - > HCO3 + H (Water + CO2 = Carbonic Acid = Bicarbonate) Respiratory Compensation: 1. Increasing CO2 = increasing acid = respiratory acidosis 2. Decreasing CO2 = decreasing acid = respiratory alkalosis 3. Respiratory compensation is immediate and used for short term or acute problems, i.e. lactic acidosis, diabetic keto acidosis, etc 4. Respiratory compensation is never complete only partially compensates. Metabolic Compensation: 1. Increasing HCO3 and Base Excess levels = metabolic alkalosis. 2. Decreasing HCO3 and Base Excess levels = metabolic acidosis. 3. Metabolic compensation takes time and used for chronic problems, i.e.. COPD chronic CO2 retention 4. Metabolic compensation can be complete. Causative Agent vs. Compensating Factor (Who s to blame?) 1. Causative agent will usually match the ph. 2. Compensating factor will usually opposite of the ph. Evaluating ABG Results (Look at the Patient and the Numbers) Oxygenation: 1. Evaluate Oxygenation level. Oxygenation vs. oxygen delivery. What s the po2 + SaO2 compared to the FiO2. A a Gradient. 2. THb (total hemoglobin) How many trucks? COHb (Carbon monoxide) Carboxyhemoglobin: 5 7 % in smokers. MetHb (meth hemoglobin) Ventilation: 1. pco2 = ventilation pco2 < 40 = hyper ventilation (hypocarbia) vs. > 40 = hypoventilation ( hypercapnic). 2. How well are they moving air compared to the patient s effort /work of breathing (WOB), RR, Tidal volume + minute ventilation. Acid Base Balance: 1. ph - < 7.40 = acidemia vs. > 7.40 = alkalemia. 2. Evaluate respiratory component. PCO2 < 40 = resp. alkalosis vs. > 40 = resp. acidosis. 3. Evaluate metabolic component BE > + 2 = met alkalosis vs. BE < -2 = met acidosis. 4. Determine causative agent (which component matches the ph) 5. Determine compensating factor (which component opposes the ph) 6. Determine degree of compensation, i.e. complete vs. partial vs. uncompensated. Failure to compensate indicates a CRITICAL situation 20

21 Questions to Ask (Critical Thinking) Does the Patient: 1. Need more oxygen? (Delivery vs. demand). 2. Need to breathe more? (Ventilation). 3. Have normal ph or an acid base problem? 4. Have signs, symptoms, diagnosis, or medical history that apply to the ABG results? 5. Have to WORK to maintain these ABG results is he OK or tiring out? 6. Have a chronic disease like COPD? (What s normal for this patient?) Normal COPD ABG s 1. ph, (compensated resp. acidosis). 2. PCO2, (chronic CO2 retention). 3. PO2, (chronic hypoxemia). 4. HCO3, (metabolic compensation). 5. BE (metabolic compensation). 6. SaO2, % (chronic hypoxemia + reduced hypoxic drive). 7. THb, (chronic hypoxemia = polycythemia more trucks. 21

22 Module 2: RT 4 Mechanical Ventilator - Fundamental Principles of Mechanical Ventilation Ventilation gas (Co2) movement from Venous alveoli - atmosphere (Alveolar Ventilation - VA) Accomplished by creating pressure gradients during inspiration (expiration is passive) Transrespiratory Pressure Gradient Atmosphere Airways - Alveoli Transpulmonary Pressure Gradient Pleural space alveoli Normal Spontaneous Respiration creates a negative pleural space pressure Which Gas law explains this? Mechanical Ventilation creates a Positive Alveolar pressure ( PPV) What is the typical disadvantage of the PPV system? How do conventional mechanical Ventilators increase ventilation? What Arterial Blood Gas parameter reflects ventilation? Oxygenation: - transport of O2 from atmosphere to Alveoli to Arterial system. What are the 2 ways mechanical ventilators increase oxygenation? Increase inspired oxygen concentration FiO2. Increase Mean Airway Pressure MAP. What Arterial Blood Gas Parameters reflect oxygenation? PO2 SaO2 A-a gradient a/a ratio Fundamental Ventilator parameter relationships: (Egan Chapter 42 ) Pressure force per unit area i.e. Cm / H20 ( used to measure ventilator pressures) Volume amount of gas i.e. tidal volume measured in Liters Flow Velocity - movement through space measured in volume over time i.e. Liters / minute Time Duration i.e. I / E ratio Positive Pressure & Volume positive pressure increases Transpulmonary Pressure gradient Increasing Positive Pressure will cause typically cause lung Volume to increase Increasing Lung volume will typically cause positive Pressure to increase What forces must be overcome for this to happen? Airway resistance Chest & Lung elasticity What is the relation ship of Pressure / Volume called? 22

23 Pressure & Flow Increasing Flow increases Pressure ( until Pressure limit is reached) Increasing flow causes pressure limit to be reached sooner Why? Which Laws describe this? When Flow is Laminar Pressure increases linearly ( Poiseuille s Law). When Flow becomes turbulent (Reynold s number) pressure increases sharply. Resistance R = (P1 P2) V.(flow) What is a pneumotach? V. ( flow) = ( P1-P2) K ( resistance factor) What happens if a ventilator flow sensor gets wet or dirty? What factor has the greatest effect on airway resistance? What clinical factors can increase airway resistance for ventilator patients? Pressure & time: Increasing inspiratory time will generally increase pressure ( until Pressure limit is reached) Increasing I. time will increase distribution of Pressure Increasing Time & Increasing Pressure will increase MAP Volume & Flow: Increasing Flow will increase Volume (until volume limit is reached) Increasing Flow will cause Volume limit to be reached sooner Volume & Time: Increasing I. time increases Volume ( until volume limit is reached) Flow & Time: ( I. time) Increasing Flow will decrease I. time (unless I. time is set) What mode has a set I. Time? Decreasing Flow will Increase I. Time (unless I. time is set) Increasing flow will increase I/E ratio What effect will decreasing the I. Time have on the ventilator rate? ** adjusting one parameter will effect other parameters unless they are set or limited** 23

24 Types of Breath limits or cycling: what is set & what varies? (Egan Figure 42-5) What is the difference between an alarm & a limit? Do ventilator modes use more than one limit at a time? Pressure Limit Cycle: - inspiration ends when High or Pressure Limit is reached Pressure will remain constant Variable factors (unless they are limited) that increase as Pressure limit is increased Volume time What Pressure cycle modes does this happen? Flow Limit: - Inspiration ends when lower flow limit is reached? What Ventilator mode uses a flow limit & Pressure limit? What is the most physiologic type of flow pattern? Variable Factors: These will decrease as the flow limit is increased. Why? Volume Inspiratory time Time Limit: used to start or end inspiration Rate control controls when inspiration begins by controlling expiratory time Give one example of a ventilator that uses an expiratory timer to control rate? Time control controls duration of inspiration What mode uses an I. time control & a Pressure limit? Flow increases as I. time decreases to deliver a volume. What ventilator uses this? Volume decreases as I. time decreases Why? How can this be prevented? Volume limit: inspiration ends as Volume limit is reached Clinical Limits what happens when the limit is too low or too high? Pressure limit - Too low inadequate tidal volume = hypoventilation = increased WOB Too high ( > 35 cm H20 or Vt > 10 cc /Kg)= hyperexpansion- What are the 3 hazards of pressure? Barotrauma Decreased venous return Inflammatory response to alveoli Increase limit to meet patient demand Decrease limit minimize unnecessary volume & barotrauma risks Volume limit: Too low - inadequate tidal volume = hypoventilation = increased WOB Too high ( > 10 cc / Kg)= hyperexpansion 24

25 Flow Limit: The art of ventilator management meets patient demands Too low increased WOB doesn t meet patients inspiratory demand = flow starved Prolonged I. time I/E ratio < 1/2 = possible air trapping How could this appear if you ere observing the pressure manometer? Too high Increased pressure why? Increased WOB patient is blasted by high flow time decreased PIP limit is reached before complete VT is delivered Time Limit: - Control mode Expiratory time too long = decreased rate Doesn t meet patient demand waiting for the next breath Hypoventilation Expiratory time too short = increased rate = air trapping Inspiratory time too short Inadequate Vt Inspiratory time too long Excessive exposure to pressure Ventilator dysynchrony What is the risk if the patient is trying to exhale during the inspiratory cycle? 25

26 Respiratory Failure 3 Types Respiratory Failure 5 Reasons why we put people on mechanical Ventilators Type I Hypoxic Respiratory Failure - Documented severe hypoxia Oxygen Fraction Ratio PaO2/FiO2 < 200 normal = o <300 mmhg (40 kpa) = ALI; PaO2/FiO2 <200 mmhg (26.7 kpa)= ARDS. A-a gradient on 100 % Fio2 > 350 normal < 65 on 100% Fio2 a/a Ratio <.30 Failure to deliver adequate O2 (PO2 < 60 mmhg or Sp)2 < 90%) with FiO 2 > 60% Spo2 = 92 % on a Nonv rebreather? Is he Ok? Type II (2 types) Ventilatory Respiratory Failure or Unsustainable Work of Breathing (WOB) Ventilatory Respiratory Failure Pump failure with elevated Co2 & causing an uncompensated acidosis most common indicator for mechanical ventilation ph assessment determines if failure is chronic or acute Elevated PCo2 > 50 & without ph compensation ph < 7.30 COPD Normalize ABG s????? Increased WOB Respiratory Muscle Fatigue Indicators: Could these patients have normal ABG s? Clinical signs retractions & flaring increased accessory muscle use RR > 35 Vt < 5 ml / KG poor chest expansion ABG indicators hypercapnia ( increased PCo2 & acidosis) Airway Protection obstruction vs. ALOC Unable to handle Secretions Increased thick secretions Weak cough Requiring suctioning < q 2 hours Altered Level of Consciousness (ALOC) Unable to maintain airway and or respirations Underlying Causes (Non respiratory) Bleeding Post op support Severe acute hypotension Unstable Vital signs Septic shock Unstable cardiac status lethal arrhythmia s or decreased cardiac output Severe Metabolic acidosis why? 26

27 RT 4 Indications for Mechanical Ventilation Module 9 Egan table 41-3 Respiratory Failure: Failure to deliver adequate O2 (PO2 < 60 mmhg) Failure to remove adequate Co2 (PCO2 > 50 mm Hg) Hypoxic Respiratory Failure (Type I) Hypercapnic (ventilatory failure) Respiratory Failure (Type II) Acute Respiratory Failure (sudden) vs. Chronic Respiratory failure (exacerbated Chronic Disease) What is one example of a Chronic obstructive & a Chronic restrictive disease? Acute Hypoxic Respiratory Failure (Type I) Causes: List a typical disease or cause for each of the following: (Egan table 41-1) Ventilation / Perfusion mismatch Shunt severe V/Q mismatch (almost complete lack of ventilation) typically will not respond to supplemental oxygen Alveolar hypoventilation (indicates normal lung parenchyma) Diffusion impairment Perfusion / diffusion impairment: i.e. liver disorder causes hepatopulmonary syndrome Decreased inspired O2 concentration Which are the 3 main causes of type 1 failure? When is mechanical Ventilation necessary for Type 1 failure? What does refractory hypoxemia mean? Which of the type of type 1 failure typically causes refractory hypoxemia? How does a mechanical ventilator improve oxygen delivery? Can a patient have both type 1 & type 11 failure? Determining cause of Hypoxic failure (table 41-1) A a gradient PAO2 = FiO2 (PB H20) Paco2/R What is the normal A-a range for adults? Alveolar Hypoventilation corrected with improvement in ventilation V/Q mismatch some predictable response to increases in supplemental oxygen Shunt minimal response to increases in supplemental oxygen Acute Hypercapnic Respiratory Failure Type II Pump failure with elevated Co2 & causing an uncompensated acidosis most common indicator for mechanical ventilation PaCo2 = (0.863 VCo2) / VA Alveolar Ventilation ( VA) varies to PCo2 What does this mean? Dead-space Ratio VD/VT increases PCo2 Increased VCO2 = increased PCo2 27

28 Causes of Hypercapnic respiratory Failure Type II List a typical disease or cause for each of the following: (Egan table 41-1) Decreased Ventilatory Drive : = What would be the most common clinical sign? Inspiratory muscles innervation intercostals & phrenic nerves Co2 Drive Medullary ( central) & aortic ( peripheral) chemoreceptors What are the typical factors that can diminish this drive? Sedation Brainstem lesions cancer or trauma Obesity upper airway obstruction resulting in rapid shallow breathing pattern Decreased compliance Microatelectasis Increased WOB Hypothyroidism fatigue, hyporeflexia, myxedema coma Respiratory Muscle Fatigue or Failure: mini clinic 41-3 CNS signal interrupted ALS, Gulliane Barre Neuromuscular transmission abnormalities Myasthenia Gravis Muscle disease Muscular dystrophy muscle atrophy, muscle wasting Clinical signs hypercapnia Drooling failure to handle secretions Weak cough Which PFT parameter is the best indicator of respiratory effort / capacity? Increase Work of Breathing: unable to overcome imposed workload What are the two most common obstructive diseases that cause this? What are the 2 physiologic factors that cause WOB in these patients? Increased VD/VT Increase airway resistance Other factors/ causes: Intrinsic PEEP auto PEEP Thoracic abnormalities Pneumothorax Chest Trauma What is a flail chest? What problem does this cause? Increase Minute Ventilation requirements Increased metabolism = increased VCO2 i.e. burns or sepsis Clinical signs: When a patient should be hyperventilating but is not. Diminished BS Rapid shallow respirations with increased workload i.e. asthma / COPD exacerbations Irritability or confusion Tremors Cerebral Vasodilatation What clinical sign / symptom does this cause? 28

29 Chronic Respiratory Failure: Egan mini Clinic Causes (Acute on Chronic failure) Infections Heart Failure Kidney failure CVA Aspiration Pulmonary embolism Barotraumas Hemorrhage / shock Malnutrition Fluid overload / Pulmonary edema Chronic hypoxemia compensation for decreased PO2 Polycythemia HB shift acidosis release more oxygen to tissue Increased cerebral blood Flow cerebral vasodilation Chronic Ventilatory Failure compensation for elevated PCO2 Acid base balance maintained by excretion of HCO3 from kidneys = compensated acidosis Indications for Ventilatory Support (Egan Table 41-3) Do Ventilator preserve life or treat disease? What is the goal of mechanical Ventilation? support patient until the problem resolves Acute vs. Chronic Respiratory Failure Severity of changes in ph Acute ph changes with Increases in PCO2 ph decreases.08 for every 10 mm increase in PCO2 Chronic ph decreases.03 for every 10mmHg increase in pco2 29

30 Summary Typical indicators for mechanical Ventilation Severe refractory hypoxemia Oxygen Fraction Ratio PaO2/FiO2 < 200 normal = A-a gradient on 100 % Fio2 > 350 normal < 65 on 100% Fio2 Ventilatory failure ph assessment determines if failure is chronic or acute Elevated PCo2 > 50 & without ph compensation Respiratory Center not responding Signal is not getting through Lungs incapable of providing ventilation because of parenchymal disease weakness Increased VD/ VT % >.60 normal = Respiratory Muscle Fatigue Indicators: Could these patients have normal ABG s? MIP < -30 cm H20 esp. in neuromuscular FVC < 10 ml / KG - RR > 35 Vt < 5 ml / KG Spont VE / MVV > 60% Respiratory Alternans alternating tachypnea & bradypnea ABG indicators hypercapnia & acidosis Increased WOB Esophageal balloon / flow transducer = WOB Clinical signs retractions & flaring Auto PEEP present Tachypnea & increased VE Special Considerations Increased Intracranial Pressures Goal PCo to decrease ICP by cerebral vasoconstrictions Reduce PEEP Increased PEEP = Increased ICP Surgical anesthesia support COPD Normalize ABG s????? Hyperoxia effects 30

31 RT 4 Physiologic Effects of Mechanical Ventilation Pressure Changes & Gradients (Egan Table 43-1) Types of Ventilation Spontaneous Negative Pressure Positive Pressure Pressure Terminology Transpulmonary Pressure Alveolar pleural gradient ( PL=Palv PPL) Maintains alveolar inflation Ventilation into alveoli by increasing Pawo (airway opening pressure) or decreasing PPL Transthoracic Pressure Alveolar body surface gradient ( Ptt = Palv Pbs) Expands lung & chest wall Transairway Pressure Airway pressure alveoli ( Pta = Paw Palv) Airflow into alveoli from airways Results from airway resistance Transrespiratory Pressure Airway opening body surface area ( Ptr = Pawo P bs ) Spontaneous breathing Inspiration Muscles contract Volume increased P alv decreases Gas movement into alveoli Expiration Muscles stop contracting Palv gradient = 0 Elastic recoil of lungs & chest Gas movement out of lungs Volume of gas movement Volume = Pmuscles X Compliance (Resistance x Flow ) 31

32 Negative Pressure breathing Simulates spontaneous breathing by using a negative pressure ventilator in addition to respiratory muscles to decrease Pleural pressure & increase alveolar gradient. Few pulmonary complications Total body ventilator = Iron Lung Thoracic enclosed device = Portalung ( turtle shell) surrounds chest only Complications Restricts care, feeding, & access to patient Tank shock decreased venous return caused by negative pressure to entire body Positive Pressure breathing Pressure gradients are reversed by increasing airway & alveolar pressures Volume = P Vent + Pmuscles X Compliance (Resistance x Flow ) Use pressure of Vent & patient effort to over come what 2 forces? Elasticity of lungs & chest = inverse of compliance What are the 2 parameters that indicate compliance? Airway resistance = difference between inflating the lungs & holding the lung open What are the 2 ventilator parameters that reflect these pressures? Oxygenation effects of mechanical Ventilation Increased Inspired Concentration FiO2 = increased PAO2 Effectiveness of Increased Fio2 can indicate cause of hypoxemia Hypoventilation hypoxemia PaO2 Increases significantly with increased ventilation V/Q mismatch Pao2 increases with increases Fio2 Diffusion defect Pao2 increases with increased MAP using increased PEEP Shunt - PaO2increases with increased MAP using increased PEEP Fio2 is increased & there is a minimal increase in PaO2 what causes of hypoxia does that indicate? Which law describes Arterial oxygenation by diffusion? Fick s law of diffusion Diffusion = A X D ( P1 P2) T(membrane thickness) Pao2 increased by Increasing PAO2 using increased Fio2 Increasing alveolar Surface Area increase MAP by increasing PEEP to recruit & retain alveoli 32

33 What disease typically requires PEEP to increase oxygenation? What 2 types of hypoxia typically indicate the use of PEEP to increase oxygenation? High pressures that over distend alveoli can cause blood flow to redistribute to capillary beds surrounding poorly ventilated alveoli. What clinical conditions would result? Increasing Tissue oxygen delivery Pao2 is only part of the picture Oxygenation delivery Content of oxygen = Ca = PaO2, SaO2, & Hb concentration Delivery of oxygen = DO2 = Ca o2 X CO ( cardiac output) x10 PEEP effects & goals Increased PEEP = Increased Intrathoracic pressure = decreased Cardiac Output Goals of PEEP = Optimal PEEP Increased Pa02 > 60 mmhg Minimal effect on BP & Pulmonary hemodyamics Reduce FiO2 < 60 % Why????? What Lung Volume does PEEP increase? Mechanical Ventilator Effects on Ventilation Hyper capnia = ventilatory Failure PaCO2 = VC02 x VA VE = Vt X f VE total = VE vent + VE patient Tidal volume ranges Older Ranges - Normal Spontaneous tidal Volumes 5-7 ml / Kg Why are spontaneous volume ranges lower than mechanical? Mechanical Ventilator Tidal Volume ranges Normal Lungs 8 10 ml / KG ARDS 4-8 ml / KG (restrictive ALI) COPD 8-10 ml / KG (obstructive ) Severe Acute Asthma ( 4-8) to reduce PIP initially Neuromuscular disease Ml / Kg Ventilator Rate Normal / postoperative patients b / minute COPD = longer Expiratory times. Why? ARDS = shorter expiratory times & increased RR. Why? 33

34 Current Ranges for initiating VT and RR Egan Table 44-4 Patient Type Tidal Volume ml/kg Frequency Normal Neuromuscular/ Post Op (abnormal Lung mechanics) Restrictive / ALI/ARDS Obstructive / COPD Acute severe Asthma Children & Infant or 35 Neonates 5-7 > 30 34

35 Positive pressure ventilation effects on V/Q Spontaneous breathing effects Increased ventilation to dependent & peripheral lung fields Positive Pressure effects Increased Ventilation to non dependent lung fields Increases Blood flow to the dependent lung fields Result = minimal blood flow to areas where pressure is greatest Non dependent lung fields = increased Deadspace = increased V/Q ratio Dependent lung fields = increased shunt = decreased V/Q ratio Causes of increased PaCo2 Increased VCO2 Increased Deadspace VDS / VT List 2 clinical examples of this? Pulmonary embolism COPD - bullae Decreased VA ( or VE) What prevents these factors from increasing PaCo2? Increasing VA ( VT or f or both) What condition exists when PaCo2 increases & VA does not? What condition exists if VE increases but PaCo2 fails to decrease? 35

36 Acid Base changes Respiratory Acidemia = PCo2 > & ph < 7.35 Causes Inadequate VT Inadequate f Increased VD / VT What are some possible causes of increased VD / VT? o Volume loss due to tubing compliance with small VT s Complications of acidemia Cardiac hyperkalemia = cardiac arrhythmia goal ph > 7.25 Oxyhemoglobin right shift decreased Hb affinity = increased O2 delivery to tissues Increased Va ( respiratory compensation) = increased WOB What is the base deficit? When is it used? NaHco3 meq / L delivered = ¼ Kg x BD 2 Respiratory Alkalosis = hyperventilation = Pa Co2 < 35 mm Hg & ph > 7.45 Causes - Hypoxia Metabolic acidosis Pain Anxiety Excessive VT Excessive f Metabolic Alkalosis causes = Normal Co2 + ph > 7.45 & HCo3 > 26 meq /l or BE > 2 Hypochloremia or hypokalememia caused by GI loss ( NG tube or vomiting) Diuretics Steroids Complications of Alkalemia Cardiac hypokalemia = cardiac arrhythmia s goal ph < 7.50 Oxyhemoglobin left shift = increased affinity = decreased O2 tissue delivery Decrease Va ( resp compensation) = hypoventilation 36

37 Lung mechanic effects Inspiratory time normal spontaneous seconds 95-98% of alveoli inflated I. Time increases Increased Airway resistance Increased Compliance How would you adjust the I. time for an ARDS patient? Why? How you adjust the I. time for a COPD patient? Why? What ventilator parameters can be used to increase I. time? Pressure mechanics PIP = Peak airway Pressure = pressure to inflate lungs = dynamic pressure Pplat = plateau Pressure = pressure to inflate alveoli =static pressure = goal < 35 cmh20 why? Raw = airway resistance = PIP Pplat Vi ( insp flow) Compliance = Cstatic = VT (Pplat- PEEP) Mean Airway Pressure = Pressure over Time = amount of Positive pressure ( Egan Box 40-1) MAP can be increased by : Increasing mandatory breaths Increasing PIP Increasing I. time Increasing PEEP Decreasing E Time Changing Pressure or flow wave forms = increasing area Decreasing compliance Increasing Raw MAP effects Increased FRC Which MAP factor has the greatest effect? Intrinsic PEEP auto peep How is this measured? Decreased Venous Return Increased Air trapping & Barotrauma risks Deadspace = VD / VT Mechanical Ventilation Increases in VD Artificial airway Tubing between Y & patient How much VD in 6 of large bore tubing? Bronchodilator during inspiration Decreased perfusion to Area s lung with of Increased PPV 37

38 Alveolar Recruitment Maneuver (Egan Box 43-2) Indicated for Severe ARDS Sedate Patient to minimize Spontaneous Breaths and dysynchrony PRESSURE CONTOL PEEP = PCV set to KEEP PIP I.TIME 1-2 seconds Rate Duration 1-3 minutes Then PEEP 20 PC to keep VT 4-6 ml/kg Lower PEEP by 2 cm measure dynamic compliance PEEP goal based on best Oxygenation with Best Compliance What equipment should also be at the beside? What Vital signs should monitor closely? 38

39 Work Of Breathing Decreased WOB = Ventilator meets patient demand Increased WOB Inadequate Ventilation VT or f Inadequate Flow flow starved Ventilator / patient dysychrony What 3 parameters are typically adjusted to treat asynchronous ventilation? Flow Trigger sensitivity Mode Full mechanical support complete spontaneous What parameter is adjusted to reduce WOB in spontaneous breathing ventilator pt? Pressure Support How is WOB measured? Esophageal pressure balloon & airway pneumotach expensive & invasive RSBI rapid shallow breathing index RR/ VT ( liters) > 105 = poor weaning Cardiovascular effects of Mechanical Ventilation ( Egan figure 43-13) Which Ventilator parameter has the greatest effect on cardiopulmonary hemodynamics? How does decreased compliance effect cardiovascular effects of mechanical ventilation? Thoracic Pump & Venous return effects Increased Pleural Pressures Compression of intrathoracic veins Increased Central Venous pressures ( CVP) Increased Right Atrial Filling pressures Decreased Blood flow effects Decreased venous return Increased pooling of blood in abdominal vessels Blood volume removed from circulation Decreased left heart output Increased intercraninal blood pooling Increased ICP Decreased Cranial perfusion Possible cerebral ischemia & hypoxemia hey but the O2 sat is OK Healthy pt s can adjust effects are increased with compromised patients i.e. CVA patients Neurosurgical patients Head injuries 39

40 Normal physiologic compensation for decreased BP Increased HR Increased systemic & peripheral venous vascular resistance ( vasoconstriction) Shunting blood from kidneys & Lower extremities What factors increase these effects on venous return and decreased Cardiac output? What is the common factor? Excessive alveolar pressure impeding pulmonary blood flow & venous return Excessive PEEP = > optimal PEEP Excessive Tidal Volume Hypovolemia Hypotension Cardiac ischemia or infarction Possible PPV benefits to Increasing cardiac out put Left Ventricular failure patients ( may improve with PPV) PPV effects = Increased Cardiac Output caused by: Increased lf. ventricular ejection fraction ( ratio Stroke vol. / end diastolic vol.) Decreased left ventricular afterload ( increased afterload lowers CO in heart failure pt s) Endocardial blood flow ( coronary arteries) reduce with PPV Coronary Flow = systemic diastolic pressure Lf Vt. end diastolic pressure ( Wedge pressure) PPV effects on Cardiac Output & systemic Blood pressure usually compensated by Increased HR Increased Vascular resistance - vasoconstriction CO is compromised Excessive MAP causing excessive alveolar pressures Hypovolemia Usually CO compromise can be treated with fluid management & careful use of PEEP What is the most common cause for severe refractory hypotension with mechanically ventilated patients? Intercranial Pressures ( ICP) Intercranial perfusion = CPP = Gradient from Mean Arterial Pressure ( MAP) & ICP Increasing MAP = increased CPP Decreasing ICP = increased CPP PPV increases ICP & decreased MAP = decreased CPP Hyperventilation decreased PCo2 = cerebral vasoconstriction = decreased ICP = Increased CPP ( mild hyperventilation only avoid PCo2 < 3??? = restricted blood supply) Co2 is a cerebral vasodilator = alters ph of CSF effects can last 1 hour Why is hyperventilation a treatment for Traumatic Brain Injury ( TBI)? 40

41 Guidelines for Closed head injury patients reduce ICP < 20 mm Hg Current Guidelines prior to 2007 Old NBRC Guidelines Know em but don t use em! Hyperventilate Pco fist 3 days Hyperventilate during acute increases in ICP (plateau waves) 2007 based on outcome data showing improved mortality and recovery rates. Normalize PCo avoid respiratory alkalosis or Respiratory Acidosis Normal BP No Peep Hyperventilate immediate temporizing measure to decrease ICP ( PCo2 < 35 for 24 hours ) Avoid prolonged Hyperventilation ( PCo2 < 25 for > 24 hours) causes decreased perfusion & potential rebound tissue acidosis Avoid Hyperventilation 1 st 24 hours = decreased Cerebral Blood Flow ( CBF) Use increased BP and sedation to control BP Sedation Semi fowler s position Mannitol diuretic to decrease cerebral edema Minimize noxious stimuli ( i.e. noise, pain, suction) If primary methods fail to reduce ICP <20 then use mild hyperventilation 35 after 24 hours but no longer than 24 hours ( rebound vasodilation ) Minimize PEEP & PPV Hyperoxygenate PaO2 >100 What device is used to closely monitor Co2 levels in these patients? Minimize PEEP and PPV Maintain BP Avoid hyper oxygenation = increased ischemia 41

42 Renal Function effects PPV reduces ( redistribution) renal blood flow = decreased urinary output Long term PPV increases antidiuretic hormone levels Liver function effects PPV decreases hepatic blood flow = increased bilirubin levels Splanchnic perfusion effects PPV = decreased blood flow to mucosa Increased gastric mucosal ischemia Increased GI bleeds Increased stress ulcers Gastric distention Decreased intestinal motility = increased risk of infection bacteria & bleeding= translocation Malnutrition Increased metabolism Decreased absorption Decreased caloric intake What is TPN? 42

43 CNS effects PPV patients require sedation Disorientation Unable to communicate What are the basic sedation issues? Level of consciousness Pain Anxiety paralysis What are the common side effects of sedation? Hypotension Apnea / respiratory suppression Decreased compliance Addiction Decreased GI & organ perfusion General PPV hazards Artificial airway hazards. What are the general hazards with an ETT? ETT misplacement extubation vs. main stem intubation Nosocomial Infection control risks i.e., VAP Aspiration Bypassed defense mechanisms Humidification deficit Mucous plugging / obstructed airway Increased RAW ( length & diameter of tube) Damage / hemorrhage to airways, trachea, vocal cords, esophagus Pressure damage / barotraumas Alveolar over distention Pneumo thorax Alveolar inflammation ( P Plat > 35 cm h20) Pneumomedastinum Auto PEEP / Intrinsic PEEP common in Ventilator patients with obstructive disease Excessive FRC Air Trapping - incomplete exhalation Increased Barotrauma risks Increased volutrauma Increased WOB Increased asynchronous ventilation Increased use of sedation 43

44 How do you treat auto PEEP? Flow triggering Increase Exp. Time increase flow, decrease I. time, square flow wave, I/E > ½ Bronchodilator use PEEP adjustment SIMV with PSV Oxygen Toxicity lung tissue damage from high FiO2 s > 50% Fio2 s > 50 % for > hours Free Radicals HO2, OH-, & O2 form in high oxygen concentrations Free radicals detoxified by superoxide dismutase ( enzyme) A-C membrane increases permeability Decreases Type II cell surfactant production Direct injury with decreased surfactant = fluid filled alveoli = decreased compliance Effects determined by Fio2 (>50%) Exposure time Susceptibility pulmonary hx. Retinopathy of prematurity - ROP ( formerly RLF) Fibrous tissue behind lens occurring in premature infants with exposure to oxygen Bronchopulmonary Dysplasia (BPD) lung & pulmonary arterial scarring in neonates caused by PPV & Fio2 - Ventilator Acquired Pneumonia (VAP) shouldn t happen must be monitored Pneumonia is 2 nd most common nosocomial infection Typically caused by aspiration of colonized GI or upper airway secretions Most are gram neg MRSA? How do you prevent VAP? Respiratory Muscle atrophy Muscle atrophy Skin breakdown & lesions source of infection / sepsis Ventilator mechanical Failure Other than that nothing could go wrong as long as the O2 Sat is OK!!!!!!! 44

45 RT 4 Basic Ventilator Strategies Mechanical Ventilator Goals: - DO NO HARM 2 types of goals: support vs. weaning Ventilator support goals: Pressure goals: minimize barotraumas & hemodynamic risks & side effects Volume goals: avoid hypoventilation & hyper inflation (volutrauma) Oxygenation Goals: avoid hypoxia and oxygen toxicity Ventilation goals: avoid hypoventilation & hyperventilation normalize ph Work of Breathing goals: meet pt. demand, eliminate imposed WOB & minimize sedation I. Pressure goals: Minimize barotrauma risks Determine restrictive problems Determine lung compliance, dyn.(vt/pip) vs. static (Vt/Pplat) Minimize possible complications to healthy portions of lungs from PPV. = Plateau Pressure (Pplat)< 35 cm Protective Lung Strategy over distention = Open Lung Strategy o increased interstitial inflammation o decreased surfactant o decreased compliance o increased diffusion defect o increased Shunt o increased risk of pneumothorax Consider lower VT s, PCO2 < 55 (permissive hypercapnia), early PEEP, Pressure ventilation I:E pressure support or pressure control ventilation 45

46 Pressure Goals: minimize cardiovascular effects: Effects of PPV = mean pleural Pressure & cardiovascular status Mean pleural pressure measured with esophageal balloon Mean Airway Pressure best clinical indicator of mean pleural pressure Effects of PEEP on mean pleural pressures depends on patients lung compliance Increased Lung compliance = increased effects of PEEP on Pleural pressure & hemodynamics Increased Lung compliance = increased pressure transmitted from alveoli to pleural space Increased compliance ( i.e. COPD) = BP more sensitive to effects of PEEP Normal Compliance = BP less sensitive to effects of PEEP than High compliance pt s Low compliance = ( i.e. ARDS) BP less sensitive to effects of PEEP resultoften high levels of PEEP can be used on ARDS patients with less effects on hemodynamics. Decreased Chest compliance = increased effects of PEEP on hemodynamics & pleural pressures Stiff chest increased transmission of PEEP from Alveoli to pleural space What are 2 examples of decreased chest compliance? Pneumothorax Forced expiration during PPV inspiratory cycle Increased RAW = decreased effect of MAP/ PEEP = decreased pressure transmitted Normal Cardiovascular response to PPV PPV = decreased venous return What are the 2 Normal Cardiovascular responses to decreased venous return? Increased heart Rate Increased venous tone = vasoconstriction What are 2 types of cardiovascular conditions that could make a patient more sensitive to PEEP? Hypovolemic Decreased Venous / vascular tone response = i.e. shock Strategies to decrease PPV cardiovascular effects. 46

47 Decreased MAP Decreased PEEP. Greatest direct effect on MAP. How will this effect oxygenation? Decrease Vt = decreased PIP & Pplat. Which pressure reflects alveolar distention? Increase I / Ratio: Decreased I. time. How will this effect oxygenation? Increase E. time. How will this effect RR? SIMV mode = less mechanical breaths than A/C mode= < PPV Fluid balance = Increase Preload = increased Stroke volume. Which law defines this effect? Preload vol. in heart just before contraction Afterload vol. in heart after contraction Ejection Fraction - ratio of Stroke volume to end diastolic volume What are 3 ways cardiac output is decreased? Increased afterload Decreased contractility/ Strike volume ( caused by decreased pre load) Decreased heart rate Why do some ventilator patients require additional IV fluid? PPV causes a decreased venous return = relative hypovolemia in lungs Which types of patients are most likely to need additional IV fluid? Hypovolemic ( i.e. trauma or severe infection) Shock ( loss of vascular tone) Patients requiring high MAP & PEEP Which types of patients are most likely to be at risk from additional IV fluids? Left heart failure patients i.e. Pulmonary edema & CHF Pharmacological maintenance: Increased IV fluid is first line therapy Inotropic ( i.e. dopamine) increase contractility Vasodilators & diuretics control hypertension & decrease afterload & reduce fluid overload 47

48 II. Volume Goals: Tidal volume ranges ( 2008 ranges) Normal Spontaneous tidal Volumes 5-7 ml / Kg (2008) 4-8ml/kg (2012) Mechanical Ventilator Tidal Volume ranges Normal Lungs 8 10ml / KG ARDS 6-8 ml / KG (4-6 if P Plat >30) COPD 8-10 ml / KG Neuromuscular disease Ml / K Acute Asthma 4-6 ml / Kg if PIP > Ranges for initiating VT and RR Egan Table 44-4 Patient Type Tidal Volume ml/kg Frequency Normal Neuromuscular/ Post Op (abnormal Lung mechanics) Restrictive / ALI/ARDS Obstructive / COPD Acute severe Asthma Children & Infant or 35 Neonates 5-7 > 30 48

49 What are the 3 effects if the Tidal volume is too low? Increased WOB demand not met Hypoventilation Increased Vd/VT What is Volutrauma? Over distention of alveoli Results in o Pulmonary edema interstitial edema Decreased surfactant o Loss in compliance What is the best way to detect over distention during volume cycled PPV? Pressure / volume graphics beaking III. Oxygenation Goals: we always treat severe hypoxia = Pao2 < 50 Oxygenation Monitoring PaO2 > 50 SpO2 > 92% A-a gradient a/a ratio Oxygen index What are the 2 ways oxygenation is increased by a mechanical ventilator? Oxygen toxicity risks avoid FiO2 s > 50 % for prolonged periods hrs ROP risk in premature neonates PaO2 s & minimizes Fio2 fluctuations COPD hypoxic drive PPHN risk in newborn full term infants keep PaO2 > for first hours 49

50 IV. Ventilation goals: Effects of Hypoventilation Increased WOB Respiratory acidosis Hypoxemia Effects of hyperventilation Respiratory alkalosis Unnecessary PPV, MAP, or VT s = increased barotruama, volutrauma, or CV compromise What is the greatest risk to the patient from severe acidemia or severe alkalemia? Ventilation Goals: PCo with normalized ph ( > < 7.45 ) COPD pt s baseline PCo2 may be higher determined by ph Permissive hypercapnia pco2 < 55 with ph > 7.30 to lower PPV risks by using lower VT s ( 5-7cc KG) Intercranial Patients pco to lower ICP & improve CCP 50

51 V. Work of Breathing Goals: the ultimate goal. What is the most common reason that ventilator patients ( with FiO2 s < 40%) fail weaning? What are 2 methods for decreasing the WOB for spontaneous breathing patients on SIMV? Increase # of mechanical breaths Increase PSV Minimize W. O. B. = Decrease patient effort to trigger ventilator. Determine presence of AUTO PEEP. Adjust flow-rate to meet patient demand (vent / pt. synchrony) consider Pressure ventilation mode with variable flow-rates (pt controlled flow rate) Consider flow triggering and waveforms, Low Level PEEP (aprox.5 cm H20 ) = maintain patent airway Determine obstructive problems Determine Inspiratory airway resistance (PIP PLAT press > 10cm) ABG s CO2 retention vs. minute ventilation Consider bronchodilators, I: E ratios > ½ Where can auto PEEP be best detected? What are methods for minimizing Auto PEEP? (Egan box 44-11) Increase ETT diameter Flow triggering Increased PEEP setting to meet Auto PEEP level Increase flow = decreased I. time = increased E time = I/ E ratio > ½ Rise Time %? Pressure Cycled breaths with variable flow rates i.e. PSV or PCV Square wave in volume cycled A/C? Bronchodilators? What inline aerosol method will deliver the most effective dose of bronchodilator w/ PPV? What are the typical signs of WOB for a ventilator patient? RSB > 100 ( RR/ Vt liters) Increased accessory muscle use Auto PEEP Increased HR & BP RR > 20 ( RR > 30 = impending Resp. failure) Vt < 300 ml Ventilator / patient dysychrony i.e. fighting the vent -What is indicated after all ventilator adjustments have been made and WOB is still not relieved? 51

52 RT 4 VENTILATOR WEANING PROTOCOL STRATEGIES Initial Ventilation: Total Vent Support: Goal = Stabilize Patient Oxygenation O2 Saturation monitoring, ABG s, FiO2, PEEP Minimize W. O. B. = Decrease patient effort to trigger ventilator. Determine presence of AUTO PEEP. Adjust flow-rate to meet patient demand (vent / pt. synchrony) consider Pressure ventilation mode with variable flow-rates (pt controlled flow rate) Consider flow triggering and waveforms, Low Level PEEP 3-5 cm H20 (maintain patent airway) Determine obstructive problems Vt 8-10 cc s / Kg IBW ( Old ) 6-8 ( New ) Determine Inspiratory airway resistance (PIP PLAT press > 10cm) ABG s CO2 retention vs. minute ventilation Consider bronchodilators, I: E ratios > ½ Determine restrictive problems Vt 6-8 cc / Kg IBW Determine lung compliance, dyn. vs. static Oxygenation FiO2, A-a GRAD, PEEP Minimize possible complications to healthy portions of lungs from pos. press. = Plateau Pressure < 35 cm Protective Lung Strategy Consider lower VT s, PCO2 < 55 (permissive hypercapnia), early PEEP, Pressure ventilation I:E pressure support or pressure control ventilation. Consider underlying diagnosis and general patient condition Hemodynamics, vital signs, L.O.C., sedation, neuromuscular status, secretions, Chest x-ray, & nutrition. Determine weaning potential: Typical criteria for attempting weaning. 1. Consider underlying diagnosis and general patient condition LOC, hemodynamic, Chest x-ray 2. PaO2 > 60mmhg with FiO2 < 50% +PEEP < 8 cm H2O 3. ph > 7.3 with PCO2 < 45. (May need to re-evaluate if patient has history of CO2 retention). 4. Negative inspiratory force (NIF) > 20 30cm H2O. 5. VC > ml/kg ideal body weight. O < 1.5 L for adults 52

53 6. Rapid shallow breathing index frequency/ VT ratio. RR / VT (liters) >105 = ponegative indicator for weaning 7. Spontaneous respiratory rate < 35 per minute. Consider dynamic compliance > 22, static compliance > 33, A-a gradient, minute ventilation < 15 liters per minute, L.O.C., secretions vs. mucokinesis, VD/ VT and hemodynamic stability.. 53

54 Routine CPAP Weaning Procedure Action A. Determine weaning potential: CPAP trials may be initiated if the Ventilator patient meets the following criteria. Criteria for attempting weaning: 1. Patient does NOT require suctioning for excessive secretions or hemoptysis more than q 1 hour RATIONAL/PRECAUTIONS 1. Establish consistent minimum goals to avoid stressing or exacerbating a patient that is not yet ready to wean from significant ventilator support. 2. Sp02 >92% or PaO2 > 60mmhg with FiO2 < 50% +PEEP < 7cm H2O. 2. Minimize unnecessary delays in routine weaning attempts. 3. ph > 7.3 with PCO2 < 50. (May need to reevaluate if patient has history of CO2 retention). 3. Establish safe guidelines for determining appropriate patients for weaning 4. Spont Vt. > 5cc s per Kg as above #3 5. Spontaneous respiratory rate < 25 per minute. 6. Total Minute Ventilation < 15 l/min.. 7. MAAS score 2-4 with minimal sedation 8. Consider: dynamic compliance > 22, static compliance > 33, A-a gradient, secretions vs. mucokinesis, VD/ VT and hemodynamic stability. 9. Consider: underlying diagnosis and general patient condition. B. CPAP WEANING PROTOCOL / Procedure 1. CPAP MODE A. Respiratory Therapist to CPAP FiO2 or 10% higher than the ventilator FiO2. B. Ventilator Mode Changes to CPAP C. FIOz2 set 10% higher than current ventilator setting D. CPAP setting adjusted to 5 E. PSV set to 8 cm H20 F. T-tube weaning can be used in place of routine CPAP trials only with a direct order by the MD 1. Minimize potential hypoxia caused by decreased vent support PSV 8 to compensate for WOB imposed by ETT airway resistance 2. Continuous oximetry in place. 2. Titrate FiO2 to prevent 54

55 hypoxia. 55

56 3. Patient is to be directly observed at first for 5 15 minutes off ventilator breathing while on CPAP. Monitor W.O.B., respiratory rate, accessory muscle use, SaO2 (adjust FiO2 to maintain SPO2), mucokinesis, cardiac, hemodynamic status, and vital signs. 3. Patient is at highest risk of increased WOB & respiratory failure in first 5-15 minutes of vent removal. 4. Patient should be returned back to the ventilator as soon as there are marked changes in vital signs, sp02 < 92 % w / increased Fi02 or increased W.O.B., I:E, respiratory rate, diaphoresis, increase accessory muscle use or paradoxical respiration s. 4.Avoid significant or prolonged increased WOB or hypoxia. 5. CPAP trials should be done once daily but may be done more frequently if patient tolerates it. 5. Verify CPAP trial or accommodate changes in pt. 6. Weaning Parameters will be measured following 1 hour CPAP trial RSB & NIF 7. After Weaning parameters patient Pt is returned to original ventilator setting until the MD is contacted with weaning assessment results. The MD can then assess & make additional changes / orders such as ABG extubation, continued CPAP or T-tube weaning, or ventilator parameter / support changes. 6. Rapid shallow breathing index frequency/ VT ratio. RR / VT (liters) <100 = positive indicator for weaning Negative inspiratory force (NIF) > - 20cm H2O. = positive indicator for weaning 7. Patient comfort and validate pt. tolerance. 8. Consider discontinuing ventilation after patient tolerated using CPAP for 4 5 hours at a time. 8. Avoid needless risks of mech. Ventilation. 9. Ventilation can only be discontinued or patient extubation after a written physician s order. 9. Verify min. underlying clinical conditions, contraindications or risks. 56

57 10. Respiratory Therapist will document all CPAP weaning & or T-tube trials on Ventilator flow sheet, online vent assessment & online T-tube procedure 10. Document trends & outcomes. 57

58 C. Advantages T-tube verses CPAP without PSV Weaning methods 1. Patient has no artificially induced increased W.O.B. caused by breathing through a ventilator circuit and having to create a negative pressure (-2cm or as high as 6 or 8cm if auto PEEP present) to open the ventilator demand valve. 2. Most direct method to observe patient breathing without any ventilator support. 3. Psychological advantage for staff and patient by observing patient breathing successfully without the ventilator. 1. Decreased WOB imposed by Ventilator. 2. Verifies no artificial vent support. 3. As above. 4. Simple to set up and assess. 4. Efficient & cost effective. D. Disadvantage T-tube vs. CPAP without PSV 1. No CPAP inflation. 1. Potential decreased FRC & hypoxia. 2. No ventilator monitors to measure VT, respiratory rate, or detect apnea. 2. Increased risk of resp failure 3. No Pressure Support Ventilation 3. Increased WOB risk. 4. Cardio-respiratory monitor with HR, RR (apnea), and SP02 are the only safety alarms in the event of apnea. 4. No direct monitoring of spont resp Vt. 5. No Automatic Apnea Back up Ventilation 5. Safety risk to patient - potential severe hypoxia & hypoventilation possible cardiac or respiratory arrest 58

59 SIMV WEANING PROTOCOL WITH PRESSURE SUPPORT 1. Change patient to SIMV mode. 2. Set back up SIMV rate (order by MD.) Recommend 4 6 breaths per minute. 3. Determine appropriate minimum spontaneous VT (order by MD.) Recommend 5 8 ml/kg ideal body weight. 4. Set PSV at minimum 6cm H2O (eliminates W.O.B. caused by ETT and vent. Demand valve) then increase PSV until patient s spontaneous VT is approximate at the patient s minimum spontaneous VT. 5. ABG s should be drawn approximately 30 minutes to one hour after patient s minute ventilation, respiratory rate, VT, W.O.B., and vital signs stabilize. 6. PSV should be weaned by small increments (1 2cm) rather than larger changes. Changes can be made hourly or daily as patient tolerates. 7. If patient is still meeting weaning protocol criteria on SIMV 4 6 with PSV 6 10cm, PEEP <7cm, FiO2 < 50% daily T-tube trials should be started. 8. Consider changing patient back to A/C or increased SIMV at night to allow patient to recover or if patient deteriorates during weaning attempts (order by MD). 9. Respiratory Therapist will update ventilator orders at end of shift or daily I:E, FiO2 weaned to 50%, PSV weaned to 15cm per weaning protocol. 10. Daily ABG s, weaning parameters and continuous oximetry for all patients ordered for weaning protocol. 11. MD will specify acceptable ABG and SaO2 ranges, minute ventilation, respiratory rate, VT, for each patient. Advantage for SIMV with PSV 1. Patient ventilator synchrony patient control flowrates, inspiratory time, respiratory rate, and VT. = More comfortable breathing. 2. Controls ventilating pressure (PIP) to prevent over distention and minimize possible pressure effects. 3. Minimizes W.O.B. and patient effort to trigger ventilator by overcoming resistance of ventilator circuit and ETT. (Approximate 6cm H2O). 4. Minimized accessory muscle use and therefore lowers CO2 production and O2 consumption, which allows patient to rest respiratory muscles until the patient is ready for weaning. Disadvantages Minute ventilation, respiratory rate, and VT can drop if patient has apnea or sedated or lung compliance decreases. 2. SIMV with Low Back up rates (i.e. < 8 b/min or < ½ of total VE) can increase WOB 3. PSV < 10 can cause WOB imposed by Ventilator & Airway 4. Prolonged WOB can overwork accessory muscles & prevent weaning 59

60 T-TUBE WEANING PROTOCOL 1. Respiratory Therapist to set up T-tube aerosol at same FiO2 or 10% higher than the ventilator FiO2. 2. Continuous oximetry in place. 3. Patient is to be observed at first for 5 15 minutes off ventilator breathing through T-tube. Monitor W.O.B., respiratory rate, accessory muscle use, SaO2 (adjust FiO2 to maintain SaO2), mucokinesis, cardiac, hemodynamic status, and vital signs. 4. Patient should be returned back to the ventilator as soon as there are marked changes in vital signs or increased W.O.B., I:E, respiratory rate, diaphoresis, increase accessory muscle use or paradoxical respiration s. 5. T-tube trials should be done once daily but may be done more frequently if patient tolerates it. 6. ABG s should be drawn after patient is able to tolerate T-tube trial for one hour. 7. After first T-tube ABG patient may be left on T-tube during day as much as tolerated and returned to assisted ventilation at night. 8. Consider discontinuing ventilation after patient tolerated using T-tube for 4 5 hours at a time. 9. Ventilation can only be discontinued after a written physician s order. 10. Respiratory Therapist will document all weaning and T-tube trials. Advantages T-tube verses CPAP without PSV. 1. Patient has no artificially induced increased W.O.B. caused by breathing through a ventilator circuit and having to create a negative pressure (-2cm or as high as 6 or 8cm if auto PEEP present) to open the ventilator demand valve. 2. Most direct method to observe patient breathing without any ventilator support. 3. Psychological advantage for staff and patient by observing patient breathing successfully without the ventilator. 4. Simple to set up and assess. Disadvantage T-tube vs. CPAP without PSV 1. No CPAP inflation. 2. No ventilator monitors to measure VT, respiratory rate, or detect apnea. 3. No back up APNEA ventilation mode 60

61 Basic Weaning Plan Post Op Rapid Weaning Assess weaning criteria Oxygenation - Po2 > 60 on <50% & < PEEP 8 LOC pt is alert & follows commands Hemodynamically Stable BP > 100 without Pressors Minimal Bleeding / Chest tube drainage Ventilation pco Assess for metabolic acidosis Procedure MD orders rapid weaning Assess pt weaning criteria Decrease Patient to SIMV 6 & PEEP 5 Obtain ABG Change to Spontaneous Breathing -CPAP 5 with PSV 8 Obtain ABG Positive ABG and assessment = extubation Basic Ventilator Weaning plan for patient s hours mechanical ventilation Assess for criteria for attempting weaning. Consider underlying diagnosis and general patient condition Reason for initiating Mechanical Ventilation resolved? Level of consciousness- Withdrawal of sedation Trial required every AM. Fomerly Sedation Vacation Goal = Alert & follows commands hemodynamics - BP & BP support required Goa bp > 100 without Pressors Chest xray always compare this with required oxygenation & source of hypoxia AM ABG s acceptable on current mechanical ventilation Assess Ventilation, WOB & Oxygenation goals Spontaneous respiratory rate < 35 per minute. Consider dynamic compliance > 22, static compliance > 33, A-a gradient, minute ventilation < 15 liters per minute, L.O.C., secretions vs. mucokinesis, VD/ VT and hemodynamic stability.. PaO2 > 60mmhg with FiO2 < 50% +PEEP < 8 cm H2O ph > 7.3 with PCO2 < 45. (May need to re-evaluate if patient has history of CO2 retention). Negative inspiratory force (NIF) > 20 30cm H2O. VC > ml/kg ideal body weight. O < 1.5 L for adults 61

62 Spontaneous Breathing Trial CPAP 5 PSV 8 Assess at bedside for Apnea or clinical deterioration (at least 5 minutes at bedside) Assess Weaning Parameters ( minutes after initiating SBT) Rapid shallow breathing index frequency/ VT ratio. RR / VT (liters) >105 = negative indicator Goals min + max ranges for ABG s, Sp02, RR, spont Vt Obtain Weaning parameters Negative inspiratory force (NIF) > 20 30cm H2O. VC > ml/kg ideal body weight. O < 1.5 L for adults VD /ratios Assess response to SBT Document Response If they failed Why? Decrease SPo2 Increased Agitation Increased WOB resp rate, spont VT, Accessory muscle use Overwhelming secretions suction large amounts every 2 hours Poor cough effort ( when off sedation) Apnea Cardiac / hemodynamics HR, arrhythmias, & BP Direct communication RT assume responsibility for calling ABG s & Po2/ FiO2 ratio RT seeks out MD when MD is making rounds RN & RT communicate Vent plan, Pt vital signs, Hemodynamics, Sedation Plan RT identifies the patients respiratory problems oxygen, ventilation, WOB, protect airway. RT attends multidisciplinary rounds Reassess weaning plan recommendations to improve weaning outcomes Agitation conscious sedation anti-anxiety vs. delirium vs. pain management Progressive weaning SIMV Aggressive weaning - Tube Everybody speaks same language RT asks for weaning goals Where do you want the pt instead of where do you want the vent settings What else do you want???? What s the plan????? 62

63 Suggestions for Modifying breathing tx s on vent patients MDI s on vent pt s remove routine standard dose inline neb tx s due to medication loss in tubing MDI s x 10 puff s for routine inline bronchodilator tx s or increase neb dosage or ferquency Continuous neb tx s mgm per hour for severe bronchospasm Inline neb tx s if mucolytics (mucomyst) are required. New Ultrasonic / psioelectric nebulizers improve medication delivery and minimize changes to ventilator pressure, FiO2, volumes and flow. Goals Everybody on the same page -= we got a plan When MD makes rounds the pt should be Weaned as far as tolerated within ordered ranges Resting as well as possible within ordered ranges 63

64 Flow Patterns SQUARE FLOW WAVE DECELERATING FLOW WAVE Flow Characteristics Flow constant cycled Used for patients with high flow demand spontaneous Flow Characteristics Flow decelerates volume cycled set ramp wave Press. Limited pt. demand/ flow More physiologic mimics resp. pattern Used in transport ventilators Used in patients with RR < 20 Used with patients that require short I. Time Used in PCV & PSV Increased RAW Decreased RAW Pressure effects Higher PIP Short I. time Increased 1/E ratio Decreased MAP Pressure effects lower PIP longer I. time decreased I / E ratio increased MAP 64

65 Flow, I/E ratio, & Rate Calculations Respiratory rate & time 60 sec / rate = amount of time for each breath i.e. 60 / 15 = 4 seconds per breath I. time & E time calculations Breath time I. time = E. time i.e. 4 seconds 1.0 ( I. Time) = 3.0 Seconds E. time I/E ratio Calculations I. time is always one in the ratio E. Time / I. time = 1/E Ratio i.e. 3 / 1 = 1/3 Ratio Calculating I. time & E time from I/E ratio & rate E ratio & 1 ( I. time) = parts per breath Total Breath time / parts per breath = time for each part I. time = 1 time part E. time = E ratio x time per part i.e. RR 15 ratio 1:2 1:2 = = 3 parts per breath 60 / 14 = 4 seconds per breath 4 / 3 = 1.3 per time part Time = 1.3 seconds E. time = 2.6 seconds Flow rate & time: Flow is in liters per second Convert to liters per second = L/min / 60 = L/second i.e. 30 l/min / 60 =.5 L/ second Time calculation using VT & Flow rate Convert L/ min to L/ second Flow L/sec / VT liters = I. time seconds i.e. 500 cc s with Flow 45 L/min 45 L/min / 60 seconds =.75 L/second VT / Flow =.5 L /.75 L/sec =.63 seconds Calculating I. time, E time & 1:E ratio Calculate total breath time 60 / rate Calculate I. time Flow L/sec / VT liters Calculate E. time = Total breath time I. time Calculate I : E ratio = E time / I time expressed as a ratio i.e. 500 cc s RR 20 & flow 30 L/min 60 / 20 = 3 seconds / breath VT / Flow =.5 L/.5 l /second = 1.0 sec I. time 3 seconds 1.0 = 2.0 seconds E time 2 / 1 = 1:2 I/E ratio 65

66 What is Pressure Control Ventilation? RT 4 Pressure Control Ventilation Pressure Control is the type of breath delivered, not the mode of ventilation. Many different modes are pressure controlled. PCV refers to the type of mechanical / controlled breath delivered in A/C, CMV, or SIMV modes. SIMV / PCV use PCV mechanical breaths & PSV spontaneous breaths. In pressure control, a pressure limited breath is delivered at a set rate. In this controlled mode of ventilation, the ventilator delivers a flow to maintain the preset pressure at a preset respiratory rate and during a preset inspiratory time. The pressure is constant during the inspiratory time and the flow is decelerating. If for any reason pressure decreases during inspiration, the flow from the ventilator will immediately increase to maintain the set inspiratory pressure The volume can vary from breath to breath if the patient s compliance and resistance changes. It is very important to set the alarm limits for expired VT & minute volume to adequate levels. The tidal volume is determined by the preset pressure limit. The inspiratory time is also set by the operator. (This is what makes PCV different from PSV). The I. time may be set directly or indirectly by setting an I/ E ratio (such as PCV on the 7200 ventilator). Set I.time is more common esp. in treating restrictive/ lung recruitment diseases such as ARDS. Set I/E ratios are helpful in using PCV on obstructive disease patients to prevent air trapping. The flow waveform is always decelerating in pressure control: this relates to the mechanics of targeting airway pressure: Flow slows as it reaches the pressure limit. Gas flows into the chest along the pressure gradient. o As the airway pressure rises with increasing alveolar volume the rate of flow drops off (as the pressure gradient narrows) until a point is reached when the delivered pressure equals the airway pressure: flow stops. Typical flow rates = ( Servo 300 Flow rates) The maximum available flow is 3.3 l/sec to 200 l/min for Adult and 0.56 l/sec to 33 l/min for Infant. The pressure is maintained for the duration of inspiration. Longer inspiratory times lead to higher mean airway pressures 66

67 Inspiratory rise time in PC is the time to peak inspiratory pressure and flow of each breath. It is set as % of the respiratory cycle time - from an extremely fast response to a low initial inspiratory flow. This is typically used to soften or ramp up to the onset of PIP by using lower flows. This is useful in patients with reduced inspiratory demands or high inspiratory airway resistance ( such as small or pediatric patients with small ETT s) The combination of decelerating flow and maintenance of airway pressure over time means that stiff, noncompliant lung units which are difficult to aerate are more likely to be inflated. Pressure Assist Control Ventilation, 1 second inspiratory time: note that the breaths are identical in duration, whether controlled or assisted. It is known that decelerating flow patterns improve the distribution of ventilation in a lung with heterogeneous mechanical properties (as in acute lung injury). Pressure control is also useful in patients whose airway cannot be fully sealed ( i.e. uncuffed ETT s. The reason for this is that, although volume is lost through the leak, the ventilator will continue to attempt to pressurize the airway for the duration of the Ti: a constant flow pattern will be measured if the leak is large enough. The trigger mechanism is the same as in volume control. The key advantage of pressure targeted ventilation is unlimited flow in inspiration to satisfy the patient s demands. The harder the patient draws in, the greater the pressure gradient, and the higher the flow. This also makes this a preferred breath type for sever obstructed & flow starved patients ( such as COPD or asthma) that require specific I. times & flow requirements. 67

68 Indications for PCV Lung Recruitment PEEP, Pplat & decelerating Flow = alveolar opening Lung recruitment has gained widespread interest as a tool for the opening of closed lung units. The widespread use of low tidal volumes may increase the risk of reabsorption atelectasis in the basal parts of the lung, which eventually may lead to consolidation of the affected areas. This effect is further enhanced by high inhaled oxygen concentrations. In certain patients, the use of a recruitment maneuver may provide a long-term improvement in oxygenation. If a proper PEEP level can be determined and set, the effect will stabilize and further protect the lung by avoiding cyclical opening and closing of lung units Lung Protective Ventilation Pplat < 35cm H20 VT < 5-7 or 8-10 cc Kg Traditional ventilation patterns with high tidal volumes and low PEEP have recently been postulated to be important mechanisms for inducing and maintaining inflammatory reactions in the lung. The fact that this initial local reaction eventually may migrate to other parts of the body and induce secondary failure in remote organ systems is increasingly recognized. Flow starved & Obstructive Disease patients. Decelerating flow that adjust to patient demand Set I. time or I:E ratio to prevent air trapping Inverse Ratio for severe ARDS / shunt patients Prolonged I. time to increased MAP & improve oxygen diffusion Short E. time to allow minimal CO2 removal Disadvantages Air trapping increased Barotraumas & hemodynamic compromise Uncomfortable requires sedation to prevent WOB & asynchronous ventilation Hypercapnia Co2 s increased requires permissive hypercapnia strategy PCO2 < 60 with ph >

69 Disadvantages / hazards & Precautions of PCV versus Volume control Pressure control does not guarantee minute ventilation, and therefore requires more monitoring by the operator. The minute ventilation is a complex mix of the peak pressure, the Ti, the lung and chest wall compliance resistance in the airway and from other thoracic structures. If there is a rapid change in the compliance, then the patient may hypoventilate and become hypoxic This is a volume-pressure relationship in the same patient, on volume control ventilation (darker line) and pressure control ventilation (lighter line). Note that both modes achieve the same tidal volume, but the peak pressure is considerably lower in pressure control. This was achieved by using different flow patterns constant flow for volume breaths, decelerating for pressure breaths. In addition, the pressure breath used a slightly longer inspiratory time. To initiate pressure control is slightly more difficult than volume control. The PEEP and FiO2 are determined by lung mechanics and oxygenation targets. The inspiratory pressure is determined by looking for a tidal volume of 5-6ml/kg. The respiratory rate is determined by the minute volume requirement. The inspiratory time is usually set at 1sec, but can be increased if target tidal volume is not achieved 69

70 The patient remains hypoxic in spite of a plateau pressure >30cmH2O. In this way the mean airway pressure is used to increase overall lung volumes, and improve V/Q matching. Unfortunately, there is a limit to this process, auto-peep. Longer inspiratory times and faster respiratory rates predispose to alveolar gas trapping. Oxygenation parameters FiO2 Time increases MAP to increase oxygenation PEEP increase MAP Ventilation parameters Rate PIP / PCV increased PIP to increase VT time minimal Ventilation effect unless I. time is too short to allow alveolar opening WOB / Synchrony parameters MODE A/C or SIMV ( SIMV allows spont. Respirations can improve vent/ pt synchrony) I. time I. time must long enough meet pt demand & short enough allow adequate E. Time. Basic Ventilator Parameters Volume Control Pressure Control Controls Controls Rate Rate PEEP PEEP FiO2 FiO2 Flow rate ( I. time or I% for Servo) Tidal Volume Flow pattern ramp vs. Square Relative Advantages/Disadvantages Inspiratory Time ( Fixed I or I:E ratio) Peak Inspiratory Pressure Insp. Rise time Relative Advantages/Disadvantages Known TV No guarantee of TV Risk for barotrauma pressure limited decreases risk of barotrauma Uses Uses Most ventilated patients neonates 70

71 Patients in OR (including neonates) patients where pressure is a concern ARDS, asthmatics sometimes 71

72 Guidelines for Changing from Volume control to PCV Before Changing to PCV assess: P Plat reflects alveolar pressure required for current VT MAP indicates amount of MAP currently required for oxygenation I:E ratio I. time PEEP Fio2 VT Determine Goals VT range with max & Min PCV settings I:E ratio range I. time range Oxygenation goals Ventilation goals ( permissive hypercapnia?) Restrictive & Obstructive disease goals = respiratory pattern Hemodynamic goals Initial settings PCV = previous P plat I. time = ( compare to previous I. time on volume control) Rate same as volume ventilation PEEP same as volume control FiO2 same as previous setting Initial monitoring Delivered VT MAP SPO2 & clinical signs WOB / dysynchrony I:E ratio Hemodyanmics Why? Adjust PCV settings based on observed VT, I:E ratio, MAP, SPO2 & WOB Increase I. Time Deliver VT ( if no increase in VT is seen with increased I. time then Increase PIP Maintain desired I:E ratio Increase MAP Maintain synchrony Decrease I. Time Avoid over distention Reduce Hemodynamic ( decreased venous return) compromise Increase PIP increase to deliver VT Reduce PIP decrease VT prevent over distention, barotrauma & volutrauma 72

73 RT 4 Inspiratory Time & Pressure Control Inspiratory Time has 3 purposes in PCV Improve Ventilatory / patient synchrony meet patient demand i.e. I/E ratio Ventilation - Assure Complete opening of alveoli to deliver tidal volume Oxygenation increase MAP to increase diffusion of O2 Synchrony Maintain I/ E ratio < ½ = enough time to exhale Normal I time = adults Obstructive patients require I / E ratio s < ½ to avoid air trapping Ventilation Minimum I. time to assure VT can be delivered with PPV time too short = reduced VT caused by PCV breath terminating before inspiratory flow has ceased Pres. I. flow I. flow cut off Note Insp flow terminated early = decreased VT = decreased ventilation I. time too long = I. time & PCV breath ending after inspiratory flow has stopped = Inspiratory pause / hold = excessive PPV & increased MAP with no improvement in VT Press Insp. Flow Inspiratory hold Note I.Flow terminates before end of PCV breath = inspiratory hold = increased MAP = decreased ventilation 73

74 Oxygenation Increasing I. time = Increased MAP = increased diffusion of oxygen Severe Shunt or refractory hypoxia Inverse Ratio Ventilation = long I. time > 1.5 seconds with short E time Increased oxygenation Decreased Ventilation caused by low RR & prolonged Inspiratory holds Uncomfortable & high risk Mode Requires sedation possible paralysis o Avoid barotruma o Avoid excessive PPV caused by dysynchrony o Minimize WOB Requires BP IV support because of high MAP s & sedation Requires Permissive hypercapnia strategy Excessive MAP may decrease Perfusion to non dependent lung area s Setting I. time Goals - Synchrony set I. time seconds to maintain I / Ratio > 1:2 Ventilation Increase I. time to maintain minimum VT Observe flow curve Observe VT as I. time is increased Increasing I. time with out Increased Vt = insp Hold Oxygenation Consider longer I. times to increase oxygenation by increasing MAP Consider Inverse ratio s to treat severe refractory hypoxemia i.e. ARDS 74

75 RT 4 Flow terminology Mechanical Ventilators are Flow Generators Expiratory support is almost always PEEP/CPAP, which elevates the baseline airway pressure. The description of the mode of ventilation refers to the method of inspiratory support, that is, how the patient is helped up the volume pressure curve. CPAP is elevated baseline airway pressure The classification of ventilators refers to the following elements (which vary from textbook to textbook): this is the clearest method: 1) Control: How the ventilator knows how much flow to deliver Volume Controlled (volume limited, volume targeted) and Pressure Variable Pressure Controlled (pressure limited, pressure targeted) and Volume Variable Dual Controlled (volume targeted (guaranteed) pressure limited) 2) Cycling: how the ventilator switches from inspiration to expiration: the flow has been delivered to the volume or pressure target - how long does it stay there? Time cycled - such in pressure controlled ventilation Flow cycled - such as in pressure support Volume cycled - the ventilator cycles to expiration once a set tidal volume has been delivered: this occurs in volume controlled ventilation. If an inspiratory pause is added, then the breath is both volume and time cycled 75

76 3) Triggering: what causes the ventilator to cycle to inspiration. Ventilators may be time triggered, pressure triggered or flow triggered. Time: the ventilator cycles at a set frequency as determined by the controlled rate. Pressure: the ventilator senses the patient's inspiratory effort by way of a decrease in the baseline pressure. 4) Flow: modern ventilators deliver a constant flow around the circuit throughout the respiratory cycle (flow-by). A deflection in this flow by patient inspiration, is monitored by the ventilator and it delivers a breath. This mechanism requires less work by the patient than pressure triggering. Breaths are either: what causes the ventilator to cycle from inspiration Mandatory (controlled) - which is determined by the respiratory rate. Assisted (as in assist control, synchronized intermittent mandatory ventilation, pressure support) Spontaneous (no additional assistance in inspiration, as in CPAP) 5) Flow pattern: constant, accelerating, decelerating or sinusoidal Sinusoidal = this is the flow pattern seen in spontaneous breathing and CPAP Decelerating = the flow pattern seen in pressure targeted ventilation: inspiration slows down as alveolar pressure increases (there is a high initial flow). Most intensivists and respiratory therapists use this pattern in volume targeted ventilation also, as it results in a lower peak airway pressure than constant and accelerating flow, and better distribution characteristics Constant = flow continues at a constant rate until the set tidal volume is delivered 76

77 Accelerating = flow increases progressively as the breath is delivered. This should not be used in clinical practice. 6) Mode or Breath Pattern: there are only a few different modes of ventilation: CMV = Conventional controlled ventilation, without allowances for spontaneous breathing. Many anesthesia ventilators operate in this way. Assist-Control = Where assisted breaths are facsimiles of controlled breaths. Intermittent Mandatory Ventilation = Which mixes controlled breaths and spontaneous breaths. Breaths may also be synchronized to prevent "stacking". Pressure Support = Where the patient has control over all aspects of his/her breath except the pressure limit. High Frequency Ventilation = where mean airway pressure is maintain constant and hundreds of tiny breaths are delivered per minute. 77

78 RT 4 Ventilator Waveforms & Graphics Ventilator Waveforms Waveforms usually plot one of three parameters (pressure, flow, or volume) against time. Time is plotted on the horizontal (x) axis and the other parameter is plotted on the vertical (y) axis. The ventilator has default settings for the scales used to depict the graphics; sometimes these scales need to be changed in order for the user to see certain details of a breath or to see several breaths on the screen for comparison. Figure 1 shows a pressure-time graphic of three breaths. The first breath (A) shows a negative deflection, representing the patient s triggering of the breath. The ventilator sensitivity is set so that an inspiratory effort by the patient will trigger the delivery of a breath. The second breath (B) is not triggered by the patient, but is, instead, initiated by the machine (time triggered). The third breath (C) shows an improperly set sensitivity; the patient is having to generate a large negative inspiratory pressure before the trigger point is reached and a breath is given. This increases the work of breathing and is very uncomfortable for the patient. Making the machine more sensitive will correct this problem. The patient s inspiratory effort should result in an immediate flow of gas. The usual sensitivity setting for a pressure-triggered breath is 1 to 2 cm H2O. It should be noted that if the inspiratory flow is inadequate, the patient may generate a large negative inspiratory effort and continue pulling as the breath is being delivered. This will make the pressure waveform look irregular and nonlinear as the breath is given. Increasing the flow should correct this. If the pressure-time waveform shows a breath-triggering problem not related to sensitivity, the RCP should consider checking the gas source, the driving pressure, and the machine calibration. Time, pressure, and flow are the most common triggering mechanisms. 78

79 Figure 3 shows a side-by-side comparison of the pressure-time, volume-time, and flow-time waveforms for volume-control versus pressure-control ventilation over four breaths. Both examples show that the ventilator settings include 10 cm H2O of PEEP, shown by the baseline tracing at +10 on the pressure-time waveforms. On both tracings, the first and last breaths are mandatory, the first breath is time triggered, and the last three breaths are patient triggered (as seen in the triggering deflection on the pressure-time waveform). Pressure support of 20 cm H2O is being delivered during the two spontaneous (second and third) breaths). 79

80 Finding Auto PEEP Auto PEEP (also called intrinsic PEEP) and air trapping are other problems that can be uncovered by examining the waveforms. AutoPEEP often happens in patients with high respiratory rates or high minute volumes, or when PEEP settings are at 10 cm H2O or higher. The basic problem occurs when inspiration starts before the end of the previous breath (before a completion of exhalation). When auto PEEP is present, there will be an increase in the work of breathing when the patient initiates a breath. This occurs because the patient must create a larger negative pressure (or negative flow) to reach the set trigger point. Work of breathing is also increased as auto PEEP causes the diaphragm to be flattened, reducing the effectiveness of the muscle s contraction. The volume-time and flow-time waveforms show this problem during the expiratory phase of the breath, as shown in Figure 4. At the end of exhalation, the volume-time waveform approaches the baseline then starts upward immediately with the next breath. Conversely, at the end of exhalation on the flow-time curve, there is an abrupt movement up to the baseline and an immediate starting of inspiratory flow for the next breath. When the problem of auto PEEP is seen on the ventilator s waveforms, the RCP needs to consider several possible causes and remedies. The patient may need suction in order to clear obstructing secretions out of the airways, or it may be time for a bronchodilator treatment, which can increase airway diameter. More air is exhaled as a result of these actions, reducing the trapped air. Increasing the flow rate, decreasing the inspiratory time, or decreasing the tidal volume can prolong expiratory time and allow for more exhalation. Other possibilities include decreasing the breath rate while increasing the tidal volume, moving to a larger endotracheal tube, or changing to a different mode of ventilation. 80

81 Airway collapse may also be the cause of auto PEEP. In this situation, adding PEEP can help prop or splint the airways open and stop the air trapping. Patients with chronic obstructive pulmonary disease are more prone to have this problem as the normal supporting structures in the lung are weakened or destroyed by the effects of the disease. The amount of PEEP to add should be determined by having an expiratory pause or hold at the end of exhalation and observing the airway-pressure measurement; as it stabilizes, it will show the amount of auto PEEP or intrinsic PEEP. The RCP should set the PEEP level at no more than 85% of the measured auto PEEP level and should be sure to adjust the low-peep alarm to the appropriate level. 4 It should be kept in mind that adding PEEP can present other problems related to barotrauma, decreased venous return, decreased cardiac output, and increased hyperinflation. Using Loops Loops allow the practitioner to analyze the inspiratory and expiratory phases of each breath using either flow-volume or pressure-volume tracings. On the flow-volume loop, volume is plotted on the x axis and flow on the y axis. Positive flow from a positive-pressure breath often appears above the horizontal axis, with expiratory flow below the axis, but this pattern may be reversed, depending on the ventilator being used. In the examples given here, positive flow from the ventilator (during inspiration) will be above the horizontal axis and negative flow (during exhalation) will be below the axis. On most pressure-volume loops, the pressure is plotted on the x axis; volume, on the y axis. Patient-triggered breaths will look different from time-triggered or machine-triggered breaths on the pressure-volume loops as the patient generates a negative pressure at the beginning of inspiration. Figure 5 shows a patient-triggered breath and the resulting pressure-volume loop that traces the inspiration and exhalation. Figure 6 shows a decelerating-ramp flow pattern on a flow-volume loop. It shows the rapid increase in flow of early inspiration reaching peak flow, then decreasing to the end of inspiration and reaching zero flow. There is no time factor in these tracings, and exhalation follows immediately after the inspiratory phase on each of these loops. Figure 5. Patient-triggered breath. Figure 6. Decelerating-ramp flow pattern on a flow-volume loop. A point can sometimes be determined, early in the inspiratory phase, at which there is a change in the slope of the line that shows a more rapid increase in volume per unit of pressure. This is the lower inflection point. In the pattern of a typical pressure-volume loop on inspiration (with no PEEP 81

82 added), the lower inflection point is thought to show the point at which alveoli begin to fill rapidly and alveolar recruitment begins. Some have recommended setting the PEEP level just above the lower inflection point, but this point can change (depending on inspiratory flow, with higher flows being related to a lower inflection point that is also higher). At the other end of the inspiratory tracing on the pressure-volume loop, overdistension from too great an inspiratory volume will show up as a bird-like beak as the lung s maximum volume is reached in the face of continued inspiratory flow. The point at which this line begins to flatten and form the beak is the upper inflection point. 82

83 Figure 7 shows the lower inflection point (with tracings showing how this changes with increasing flow) and the upper inflection point for a delivered volume that is at the maximum setting (overdistension would begin to show up if delivered volume were increased). Figure 8 shows the beak representing overdistension as too much volume is delivered. In this situation, the volume needs to be reduced to avoid the problems related to overdistension (barotrauma, volutrauma, decreased venous return, and decreased cardiac output). Comparisons of flow-volume loops can help assess the effectiveness of a bronchodilator. In patients with obstructive disease, the prebronchodilator line shows a scooped-out pattern on the expiratory side representing decreased expiratory flows and airway obstruction. Following the bronchodilator, the scooped-out appearance will often change to a more linear shape from peak expiratory flows down to the end of exhalation, which reflects the positive effect of the bronchodilator in relieving the obstruction. 6 If the ventilator is delivering a decelerating flow, but the flow-volume loop shows a flattened inspiratory flow (similar to that of a flow-limited breath), there may be something that is artificially limiting flow. In this situation, the RCP should check for a bent or kinked endotracheal tube, tube occlusion (possibly because the patient is biting the tube), a saturated heat-moisture exchanger, or an occluded expiratory filter. Patient comfort and the effectiveness of ventilation are two important aspects of care that can be improved using the information provided by the graphics monitor. The RCP should go to the bedside and observe the patient-ventilator system in conjunction with the breathing pattern. Ventilator graphics constitute a valuable tool, and a thorough understanding of the associated patterns, problems, and corrections will help the RCP provide high-quality, effective care. Figure 7. Lower and upper inflection points for a delivered volume Figure 8. The beak represents overdistension as too much volume is delivered 83

84 Pressure/volume loops can also be used to determine the appropriate PEEP level. If an inflection point appears on the inspiratory limb, the PEEP should be set at that level of pressure. The inflection point represents an improvement in compliance from alveolar recruitment. The dashed lines represent the change in slope (compliance) on either side of the arrow (inflection point) Flow/volume loops help in evaluating whether airway obstruction lessens after bronchodilator therapy. Improvement would result in a higher peak expiratory flow (top half). Keep in mind that these breaths are not forced exhalations. If there are higher expiratory flows from a reduction in airway obstruction, there would be less of a scooped appearance during mid to end exhalation. 84

85 RT 4 Advanced Modes of Ventilation Basic Modes of Ventilation Assist Control - all mechanical Breaths SIMV Combination of Mechanical & Spontaneous Breaths CPAP all spontaneous breaths Basic Breath Types Mechanical Breath types Volume cycled typical volume mode Set volume Set Flow rate can use Square or Ramp flow waves PIP & PPlat varies Pressure Cycled ( i.e. IPPB, Bird, older neonatal, & transport ventilators)l Set PIP Set flow some have demand valves to increase flow Volume varies time varies ( some vents adjust I. Time ) Pressure Limited / Controlled Ventilation - PCV Pressure Plateau delivery Time cycled I. time Flow varies responds to patient demand Decelerating Flow to achieve stable PIP through out breath Volume varies - Spontaneous Breath Types Pressure Support Pressure assisted breath Pressure Plateau delivery Flow varies Decelerating flow to achieve PIP throughout breath Volume varies Flow cycled I. time varies Basic Characteristics of a PPV breath ask these questions for both mechanical & spontaneous breaths: How is it triggered? assist vs. control flow trigger vs. neg pressure trigger How is flow delivered set, ramp, decelerating How is Volume controlled How is PIP controlled How is PIP delivered i.e. P Plateau How is I. time cycled time vs. flow Terminal flow???? How is peak inspiratory flow controlled set, decelerating, Rise time???? 85

86 Advanced Modes Support modes Treat restrictive disease by improving gas distribution Pressure Plateau Deceleration Flow Flow set by patient demand Increased MAP using prolonged I. time Provide stable Vt s & VE Weaning Modes Provide Target Volumes & minute ventilation Adjust PPV support based on patient demand Support Modes (Improvements on Inverse Ration Ventilation allow spontaneous breaths) Active expiratory valve If a patient tries to exhale during the inspiration, pressure increases. When it increases 3 cm H2O above the set inspiratory pressure level, the expiratory valve opens and regulates the pressure down to the set inspiratory pressure level. Airway Pressure Release Ventilation APRV Prolonged I. Times = increased MAP = Increased Diffusion Short E. times to allow release of CO2 Requires permissive Hypercapnia strategy Active exhalation Valve - allows for Spontaneous Breaths during I. time Requires minimal sedation & avoids paralysis agents Bi Level Puritan Bennett 840 The Bi-level Mode is a pressure controlled breathing mode giving the patient the opportunity for unrestricted spontaneous breathing. In this mode the ventilator uses two shifting pressure levels and the patient can breathe spontaneously at both these levels. It is also possible to support the patient breaths with PSV 86

87 Weaning Modes Auto Weaning Modes Pressure Regulated Volume Control PRVC ( SERVO) Mechanical Breaths are PCV in type PIP adjusts to maintain a targeted Minute Ventilation VE All the advantages of PCV with a Volume guaranteed tricky because it targets VE not VT Volume Targeted ( 840) or Volume Control ( SERVO & Draeger) Similar to PRVC P. Plat & I. Time are controlled A low VT & High Vt are set PIP adjusts to maintain targeted VT The start-up sequence is 4 breaths. The first breath is given with a support of 10 cm H2O. From that breath the ventilator continually calculates and regulates the pressure needed to deliver the preset tidal volume. During the remaining 3 breaths, the maximum pressure increase is 20 cm H2O for each breath. PRVC is a controlled mode of ventilation that combines the advantages of Volume Controlled and Pressure Controlled Ventilation. The Servo-i delivers the preset tidal volume with the lowest possible pressure. The first breath delivered to the patient is a Volume Controlled breath. The measured plateau pressure is used as the pressure level for the next breath. The pressure is constant during the set inspiratory time and the flow is decelerating The set tidal volume is achieved by automatic, breath-by-breath pressure regulation. The ventilator will adjust the inspiratory pressure control level, according to the mechanical properties of the airways/lung/thorax, to the lowest possible level to guarantee the preset tidal volume. If the measured tidal volume increases above the preset, the pressure level decreases in steps of maximum 3 cm H2O between consecutive breaths until the preset tidal volume is delivered. Maximum available pressure level is 5 cm H2O below preset Upper Pressure Limit 87

88 Volume Assured Spontaneous Breaths Volume Assured Pressure Support VAPS ( Bird VIP) & Pressure Support Volume Guarantee PSVG Draegar Spontaneous breathing modes that target spontaneous breaths using a volume target PSV is adjusted to maintain VT or VE Very comfortable mode allows pt. to control spontaneous support Apnea causes mode to be turned off & PT returns to PCV Proportional assist Ventilation is a new mode in which the ventilator guarantees the percentage of work which it does, in the face of changes in respiratory system compliance/elastance and resistance. The pressure Proportional assist ventilation delivered varies from breath to breath, due to changes in elastance, resistance and flow demand. Usually this is set to overcome 80% of the work of breathing: for example, the pressure required to overcome this may be 14cmH2O. So this mode is interactive, as the ventilator varies its output to maintain its proportion of the workload. A version of this is available in some Draeger ventilators, and is called proportional pressure support. Auto mode allows ventilator to switch between support to weaning modes based on patient effort. Auto mode is an interactive mode of ventilation. The combined control and support function of the ventilator adapts to the patient s breathing capacity. Auto mode allows the patient to go into a Support Mode automatically if he triggers the ventilator, thereby better adapting ventilation to patient effort. If the patient is not making any breathing effort the ventilator will deliver controlled breaths. Auto mode gives both the patient and clinician an optimal means of commencing the weaning period at the time of initiating ventilator therapy. Essentially the ventilator works in two modes: Control or Support. When the patient, in Control Mode, makes an inspiratory effort, the ventilator reacts by supplying a supported breath.three different coupling modes combining control and support are available: Volume Control Volume Support PRVC Volume Support Pressure Control Pressure Support High Frequency Ventilation High MAP is constant = increased FRC Ventilation is a result of a constant flow of air caused by high frequency Hz pulses of air achieved by Flow interruption Infant Star 950 Flow oscillation Sensormedics Jet flow requires a double lumen ETT or ETT adapter We know that cyclical opening and closing of injured lung units damages them (particularly if tidal volumes are large). We would prefer if the patient could be ventilated at the top of the volume pressure curve, at high lung volumes, without phasic changes. This can be achieved using high frequency oscillation, but adult oscillators are not widely available. For the majority of patients, increasing mean airway pressure without increasing peak pressure means prolonging the inspiratory time in a pressure control mode. The longer the inspiratory time (Ti), the better the oxygenation benefit. 88

89 RT 4 Non invasive Ventilation Clinical Objectives: List & describe the goals & indications for NPPV Explain criteria for appropriate patient selection Differentiate between different types of interfaces, modes, & ventilators List & explain complications & hazards of NPPV List & explain factors that can predict success of NPV Initiate & manage NPPV in the acute care setting Definition Non Invasive Positive Pressure Ventilation NPPV or NIPPV - NIV Application of positive pressure via the upper respiratory tract to augment ventilation by use of a nasal or full face mask instead of an ETT or Tracheostomy tube. Goals of NIV Egan Table 45-1 Acute Care Setting Improve gas exchange Avoid Intubation Decrease Mortality Decrease Vent LOS Decrease Hospital LOS Decrease VAP Relieve Resp. Distress symptoms Improve Vent patient Dysynchrony Maximize Patient Comfort Long - Term Care Setting Relieve or improve symptoms Enhance Quality of Life Avoid Hospitalizations Increase survival Increase mobility Types of NPPV ventilators IAPV pneumobelt 1930 s rubber belt strapped to diaphragm Rocking Beds 1950 s rocks patient from trendelenberg to reverse trendelenberg Negative Pressure Ventilators 1920 s iron lung & chest cuirass IPPB 1947 use declined in 1980 s after studies showed little improvement in COPD pt s Nasal Mask CPAP 1989 big study BIPAP uses CPAP with the addition of PSV in both Spontaneous (S) or Spontaneous / Timed (ST) mode using a back up rate 89

90 Acute & Chronic Indications for NPPV (Egan box 45-2) Acute Cardiogenic Pulmonary Edema (most dramatic acute care results esp. avoiding intubations) COPD exacerbations / impending respiratory failure Asthma questionable results - Community acquired Pneumonia questionable & only indicated if underlying COPD is present w/ pneumonia Hypoxemic Respiratory failure questionable results unless COPD is underlying Do not intubate patients relieve WOB in end stage patients comfort care Post operative patients reduce intubation & ventilator LOS DNI Comfort measure patients Prevention of reintubation Prevention of post extubation respiratory failure ARDS/ ALI General Indication impending Respiratory Failure O2, Ventilation or WOB) Chronic Indications increases Nocturnal/ hypoventilation PaO2, decreases PaCo2 & decreases fatigue to respiratory muscles) Sleep Apnea nocturnal hypoventilation maintains airway reduces PaO2 increases REM COPD muscles recover & improved quality of sleep Restrictive Lung disease spinal Cord injury neuromuscular chest wall abnormalities Obesity Hypoventilation Syndrom ( OHS) 90

91 Predictors for success in Acute care setting (Egan Box 45-3, 4, &5) Absence of severe pneumonia (pneumonia reduces success rate even in COPD pt s) Minimal air leak - PaCo2 > 45 but < 92mm Hg (impending respiratory failure but not apnea or complete arrest) ph < 7.35 but > 7.22 improvement in gas exchange within 30 minute to 2 hours improvement in respiratory rate, WOB & Heart rate Selection Criteria for Acute care patients Use of accessory muscles Paradoxical breathing RR > 25 / minute Moderate to severe dypsnea / WOB PaCo2 > 45 w/ ph <7.35 PaO2 / Fio2 ration < 200 Exclusion Criteria for Acute care patients Severe pneumonia w/ copious secretions Apnea / complete respiratory arrest Uncooperative patient behavior Unstable / critical hemodynamic or cardiac function High risk of aspiration - ALOC Anatomical abnormalities Significant air leak / pneumothorax Selection Criteria for Chronic Patients Identify symptoms of chronic hypoventilation & lack of quality sleep Weight gain Fatigue Increased PaCo2 > 45 mmhg Decreased SPo2 < 88% FVC < 50% predicted NIF < -60 cm H20 Sleep Study CPAP is indicated for most sleep apnea Severe Chronic COPD may need BIPAP COPD patient evaluation Evaluated after receiving optimal acute medical care & symptoms persist PaCo2 > 55 PaCo2 > 50 with recurrent hospitalization ( 2 per 12 months) or recurrent nocturnal hypoxia / desaturization Exclusion Criteria for Chronic Patients Same as acute care Unsupportive family Lack of financial resources 91

92 Expected Results of Changing NIV Settings Egan Table 45-1 What results would you expect if you increase or decrease these parameters Setting Adjustment Anticipated Results IPAP EPAP FiO2 Rate Rise Time What Criteria do you use to set the following Parameters? IPAP EPAP FiO2 Rate Rise Time 92

93 Aerosolized Medication Delivery inline vs. removal of NIV What are the advantages if you remove NIV to give SVN Tx? Which patients or conditions would you recommend this for? What are the advantages to giving SVN inline with BiPAP? What patients or conditions would you recommend this for? Where do you place the nebulizer inline? Between Mask and exhalation port What adjustments or issues will you observe? Can you give MDI s inline? What adjustments could you make? 93

94 Patient interfaces (disposable vs. long term ) Full Face mask acute care only increased risk of aspiration & claustrophobia Nasal Mask acute or Chronic care Head Gear / straps Size gauge Anti suffocation valve built into mask ( incase of NPPV failure or circuit disconnect) Circuit with exhalation valve ( built in port vs. whisper swivel) Chin strap ( for mouth breathers using nasal mask) Foam adapter to minimize leaks & patient discomfort i.e. foam bridge Sizing instructions Egan figure 42-1,2,3,4,and 5,6) size gauges available for both masks Nasal Mask above nose bridge, below nostrils, & above lip Nasal Pillows ( uses Adam s circuit) Face Mask above nose bridge ( at dorsum of nasal bridge), below lower lip, surrounding mouth Total Face mask ( one size covers from top of head to below chin ( figure 42-7) Mask too small or large = increased leaks ( esp. into eyes & at corner of mouth) NNPV Ventilators Noninvasive Ventilators CPAP & BIPAP blower driven ventilators Nasal CPAP Remstar ( home units have controls locked out) BIPAP PRO home version of BIPAP 94

95 BIPAP ST How is EPAP maintained? IPAP inspiratory PIP ( plateau press delivery) EPAP expiratory CPAP ( same as CPAP) IPAP EPAP = PSV IPAP = EPAP = CPAP mode S mode all spontaneous no back up RATE S/T mode spontaneous / timed mode back up rate up to 30 I. Time Flow is determined by patient effort & leak ( same delivery as PSV) FiO2 Fio2 is variable O2 is bled in separately from external source Fio2 is monitored by titrating SPo2 - difficult to deliver > 50% Separate Low pressure alarm system available required for acute care use BIPAP Vision more sophisticated micro processor & internal Fio2 Same settings as S/T Fio2 setting still variable dependent on flow but can also deliver 100% Leak can be monitored Volumes can be monitored Improved leak compensation & flow delivery Can be used on pediatric patients with flows as low as 30 l/min Critical Care Ventilators Esprit ( Respironics ) a critical care ventilator with NPPV mode PB 840 NPPV mode 7200 & traditional ventilators limited use because of air leaks CPAP with PSV SIMV with volume or pressure control delivery Humidification Required for chronic home care use usually passover humidifier ( low resistance) Common on newer NPPV ventilators Usually not used for short term ( <24 hours) acute or trial NPPV use. 95