LOS ANGELES VALLEY COLLEGE Summer Semester, 2019

RESPIRATORY THERAPY 3 - Lab Instructors: Gregory Morrison, Cheryl Pearson Clinical Instructors – Patrick Kelly (PSJ & Northridge) & Edwin Khatchetourian (CHLA) Required Text. – RT III Syllabus (available Haiku site) Egan’s Fundamentals of Respiratory Care 11th edition RT III Lab task analysis – available on portal or Haiku site Equipment Theory for Respiratory Care by Gary White 5th Edition – Printed 2015 Cengage Publishing ISBN-13: 978-1439059593

Monday Lab 8:00 a.m. – 11:30 AHS 331 – Lecture – Professor Morrison Lab 12:30 p.m. - 5:00 p.m. AHS 331__Morrison & Pearson Clinic 3 days Tuesday – Thursday (except UCLA W-Fri) - 2 12 hr + 1 8 Hr Office Hours: Monday 4:30 - 6 AHS 309 Wens – Friday by appointment Week # Date Topic

I 07/8 Lecture – Monday through Friday 8-11:30 and Lab 12:30 -5:00

Tues – Friday LAB 8-11:30 & 12:30 -5:00 (1st week only) Monday Introduction: 8 a.m. Review R.T. 15 and RT 6 Final Exams; RT 15 course & clinic evaluations, RT 6 & 15 summary evaluations Module 1 Bedside assessment review (Chap. 16) Tuesday Lab - Module 2 Airway Clearance Therapy– Egan Chapter 43 Lab X ray review – Professor Santana Wens Lab Airway clearance continued Lab – Clinical Assessment + Aerosol Delivery Thursday Lecture Module 3 Pharmacology Egan Chapter 35 &39 Lab – Airway Clearance Friday Lecture Module 4 Airway Management Egan Chap. 33 Lab Airway management - II 07/15 Mon Lecture 8 -11:30 Module 4 airway management continued

7/15 Mon Lab - 12:30 – 5:00 Airway Management & Intubation

7/16 Tuesday 1st day of clinic Tues – Thurs (GAMC & UCLA W – Fri)

III 07/22 Monday Mid Term 8 – 10 Lab Lung Expansion Egan Chapter 39

4 07/29 Mon Lecture Module 5 Lung Expansion Lab – IPPB / Lung Expansion therapy

5 08/5 Monday Lecture Module 5 Lung Expansion & Course review Lab – Lab Airway management – Intubation & CPR review 08/8Thursday – Last day of Clinic 08/9 Friday RT III Final Exam 9:00 – 1:00 AHS 331

1 Grading: RT 3 Midterm 44 points Final Examination= 66 points 8 patient Profile/care plans due= 20 points Grade Totals – Mid Term = 44 points + Final= 66 points+ Pt Care Plans 20 points= 130 points Passing = 75%

Course Requirements – all of the following must be completed to successfully complete RT3 Mid Term Exam – 44 points 8 Patient Profiles - 20 points Final Exam - – 66 points must have passing grade on final exam to successfully Complete RT 3 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 Student must complete all required Clinical forms including physician interaction and attendance records

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) 947-2681 or TTD (818) 947-2680 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) 947-2412. Go to the Financial Aid Office in the Student Services Center, first floor. For more info: http://www.lavc.edu/financialaid/index.htmlindex.html .

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 (http://www.lavc.edu/writingcenter/handouts/plagiarism.html) and refer to the STANDARDS OF STUDENT CONDUCT AND DISCIPLINARY ACTION in the current Schedule of Classes and Catalog

Digital Literacy – All RT courses are web enhanced. All students are required to acquire and maintain a student email address and have computer access to download and print any course information on the RT 3 Haiku Educational Portal. https://www.myhaikuclass.com/morrisgs/rt3clinicalexperienceii/signup and entering SPP7V.

2 Summer Clinical Schedules - 4 weeks 7/16- 8/08/18

All Hospitals except CHLA, GAMC & UCLA) Tuesday 12 hr, Wed 12 hrs, Thursday 8 hours

CHLA – Tues 8 hrs, Wed 12 hr, Thurs 12 hr

UCLA & GAMC – Wed 12 hrs, Thurs 12 hrs, Fri 8 hours

RT 3 Student learning Outcomes Respiratory Therapy, 3 , Applications of Respiratory Therapy & Clinical Experience I

Course Objectives • Administer bronchial hygiene, lung expansion, respiratory medication, and airway management therapies to a patient.

• List and explain the indications, limitations, hazards, and contraindications of bronchial hygiene, respiratory medications, lung expansion, and airway management devices and therapies.

• Demonstrate clinical thinking skills by performing a bedside patient assessment and make recommendations for the appropriate bronchial hygiene, lung expansion, oxygen administration, or airway maintenance therapy.

• Identify & document the patient’s response to therapy

• Perform endotracheal suctioning on a patient with or without an artificial airway.

• Demonstrate teamwork skills in the clinical setting by communicating and collaborating with Respiratory therapists, nurses, doctors and other health care professionals.

Course Level Student Learning Outcome

Students can apply clinical assessment, lung expansion, bronchial hygeine, and airway management skills in the clinical setting.

Assessment Measures • Student Clinical Evaluations & oral examination - at the end of each clinical rotation the students will be evaluated by clinical staff & LAVC instructors on how well they applied course objectives in actual patient care setting .The evaluation includes technical competency, critical thinking, teamwork, interpersonal, and communication skills.

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LOS ANGELES VALLEY COLLEGE Respiratory Therapist Program RT 3 Clinical Objectives & Clinical Evaluation

Clinical Objectives RT 3: Orientation to Hospital-- Module 1 Clinical Bedside assessment • Identify and examine a patient to create a respiratory care plan • Assess chest expansion, respiratory movement, diaphragmatic excursion, and usage of respiratory muscles by a patient receiving respiratory care. • Perform auscultation on a patient and assess the adequacy of air movement. • Contrast breath sounds auscultated with normal breath sounds and categorize them as indications of a respiratory disorder. • Identify & document the patient’s response to therapy & therapeutic objectives

Module 2 Airway Clearance Therapy Clinical Objectives • Administer postural drainage to a patient, with attention to indications, goals and hazards (limited to clinics where chest physiotherapy is a respiratory therapy assignment). • Chart the postural drainage procedure according to department policy. • Given a patient situation, perform correctly cough instruction, percussion and vibrations in a chest physiotherapy regimen. • Given a patient situation, recommend, or assist in planning a suitable chest physiotherapy regimen, including duration and evaluation.

Module 2 Pharmacology Clinical Objectives • Administer aerosolized medications via small volume nebulizer, monitor response to therapy & document • Assist or instruct a patient in the use of an MDI, Dry Powder, continuous nebulizer, inline nebulizer or other specified aerosol unit: monitor response to therapy and document. • Explain indication, typical dosages, route, risks, hazards, side effects & contraindications for Respiratory, Cardiac, diuretic, antibiotic, diabetic, antithrombolytic, & sedation medications. • Identify which aerosolized medications can safely be administered together

Module 3 Airway Management Clinical Objectives

• Observe or assist at an oral or nasal intubation or ET tube stabilization. • Observe or assist at a tracheostomy. • Perform endotracheal suctioning on a patient with or without an artificial airway. • Measure a patient's endotracheal tube cuff pressure and volume. • Observe or assist at an extubation. • Observe or assist at a trach tube change. • Observe or assist at a bronchoscopy.

Module 4 Lung Expansion Therapy Clinical Objectives

• Administer IPPB therapy to a patient, demonstrating correct techniques. • Initiate incentive spirometry; instruct/monitor a patient in its use. • Assist a patient with a home IPPB order in discharge planning. • Administer alternative lung expansion therapy i.e. PEP, EZPAP, Flutter etc. Explain indications, risks, hazards, & contraindications for each therapy

4 RT 3 Module one Clinical Assessment (Egan’s Chapter 16)

Objectives – explain • How to perform a patient interview • What lung abnormalities are associated with common pulmonary symptoms • Normal & abnormal lung sounds • How to identify abnormal & normal breathing patterns • How & why we examine the precordium, abdomen, & extremities Patient assessment – why? • JCAHO requirement • Initial assessment – oxygen therapy, treatments, & ventilators • Significant Changes – i.e. new therapy or frequencies • Routinely – 4 days (old Medicare requirement)

• Interdisciplinary Plan of Care – Assessment is the 1st element of an interdisciplinary plan of care • Problem list – prioritized & safety problems identified • Therapeutic Goals & objectives – what specific goals do we want i.e. SPO2 > 92% What does within normal limits mean?????? i.e. WNL - • Interventions – i.e. – MD orders identified & listed. Which objectives do they meet??? • Outcome – tx’s discontinued after objectives met

• Medical History – Typical elements of an MD’s history • Chief Complaint – CC • History of present illness – HPI • Past Medical History – PMH • Family & social/environmental history – • Review of systems “head to toe”

5 Patient Interview – (Egan Box 16-1 page 322)

Why? • Establish rapport with patient • Obtain diagnostic information • Monitor changes in patient’s response to therapy

How? • Where do you stand or position yourself???? What if the patient is a child?? • Show respect for patients beliefs, attitudes, & rights • How do you identify the patient? – National safety goal requires 2 identifiers • How do you introduce yourself? – Who are you & why are you here? • What questions can you ask that will help you assess the patient? (Open ended, closed ended, neutral) • How long have you been in the hospital? • Do you use o2, meds, and inhaler therapy @ home? • How does your breathing feel today compared to yesterday? • When did your problems start?

Pain assessment- • How severe is the pain scale of 1-10? • Where is the pain located? • When does it occur??? i.e. @ noc, with exertion vs. at rest (at rest symptoms indicate increased severity or progression of disease) – Chest pain – • Pleuritic – caused by inflammation of pleural lining • Lateral or posterior • Increases with deep breath • Stabbing / sharp. List 2 diseases that could cause this type of pain • Nonpleuritic – angina, gastric - • Anterior or center of chest – radiating to extremities (name 3 types of patients who can have atypical chest pain = ACLS guidelines) • Center of chest • Pressure – occurs with exertion or stress What therapies are indicated for a patient with this type of pain? M.O.N.A?

6 Sputum production? • Cough - ????? Dry vs. productive (phlegm) • How much???? (How many teaspoons?), Color, thickness/viscosity • When??? @ Night vs. am • Sinus allergies????? Most asthmatics have significant sinus allergies & infection hx. • Hemoptysis – blood streaked sputum > 300 ml = massive What diseases are indicated by Hemoptysis??? Dyspnea assessment = S.O.B perceived by patient = WOB excessive for level of activity • When does occur? – acute vs. chronic • Orthopnea – when reclined – common in CHF ( increased in venous return when reclined) • Platypea – dyspnea when upright – arteriovenous / liver or congenital disorders • Physiologic causes • Hypoxia • Bronchospasm • Decreased Lung compliance List 2 possible diseases or pathophysiologic causes for each of the above 3 causes of dyspnea

• Severity of Dyspnea – (Egan Figure 16-1 “Borg” 0 – 10 scale page 324) • Minimal • Mild • Moderate • Severe • How does it feel? describe it?– i.e. “tightness” vs. “can’t take a deep breath” PT’s Physiologic degree of abnormality may not correlate with degree of dyspnea • Visual evaluation – What do you see “appears” to have what degree of dyspnea

Should Mechanically ventilated patients be assessed for Dyspnea? Why? Physical assessment – • Fever – height of fever may indicate they type & virulence of the infection – fever & cough indicate possible respiratory tract infection • Effects: • Increased oxygen consumption • Increased Co2 production • Increased lactate production • Physiologic response = hyperventilation

7 • Pedal edema – lower edema swelling • Indicates possible heart failure, COPD / cor pulmonale

• Clubbing of fingers – indicates chronic hypoxic cardiopulmonary disease (Egan figure 16-10 page 342)

• Cyanosis – • Peripheral cyanosis = poor blood flow • Central cyanosis = hypoxia

• Capillary refill - > 3 seconds – indicates poor cardiac output or poor vascular supply

• Physical Exam elements – Egan Box 15-3, 15-4, & 15-5

• Inspection – visual “overall” inspection • Hygiene, anxiety level, facial expressions / pain • Well nourished vs. weak & emaciated • Diaphoresis

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• Level of consciousness – alert & oriented, responsive to verbal or pain, unresponsive… • Caused by abnormal cerebral blood flow or oxygenation

• Vital signs • Temperature –

• HR – pulse Box 15-6 – rate, rhythm, & strength –

What is a “significant” drop in pulse pressure during inspiration called? What does it indicate? What is an alternating strong & weak pulse called? What does it indicate? Pressure applied while checking a carotid pulse can cause what physiologic response?

• RR – rate & rythym – regular or irregular or regularly irregular? • • BP – systolic / diastolic (S-P = pulse pressure)

• What is syncope?

• What are Korotkoff sounds?

• What does “Shock” mean?

• What are “Pressors”

• In Critical Care how do we define “unstable”

• SPO2 – 5th vital sign

9 Examination of the head & Neck • Cyanosis, nasal flaring, purse lip breathing – indicate hypoxia or respiratory distress • Neck Vein distension – What is the most common cause?

Examination of the Thorax & Lungs

Abnormal Breathing patterns – (Egan Table 16-2 page 334) • Retractions = increased use of accessory muscles –What 2 physiologic effects does this cause? • Intercostal • Supraclavicular • subcostal

What are the problems that cause the following breathing patterns?

• Paradoxical • Kussmaul • Cheyne-Stokes

Abnormal Chests – What type of respiratory problem do these cause? • Pectus excavatum • Pectus Carniatum • Kyphosis – AP deformity • Scolios – lateral deformity • Kyphoscoliosis

10 Palpation • Vocal Fremitus – vibrations created by vocal cords • Tactile Fremitus – felt – say “99” • Increased vibrations = increased consolidation • Crepitus – caused by air leak into skin / subcutaneous emphysema

What is the typical cause of subcutaneous emphysema? = (Crepitus - air leaks from lungs into subcutaneous tissue.)

Percussion – Dampened vs. hyperresonate • Loss of resonance indicates – increased lung density i.e. tumors, pneumonia • Increased resonance = decreased lung density i.e. air trapping

Which would you expect to find with a COPD patient?

Thoracic expansion – What chronic pulmonary disease causes an increased AP diameter?

Auscultation (Egan figure 16-6 page 337) • Technique • Start at bases – compare side to side – work towards lung apex • Note • Pitch • Intensity • Inspiratory – does the sound occur throughout the entire cycle vs. just the end? • Expiratory – end expiratory vs. throughout exp. cycle • Diminished? • Normal sounds • Tracheal – • Bronchvesicular – upper half of sternum – similar to tracheal • Vesicular – normal sounds over lung fields 11 Adventitious sounds–Egan Table 16-3 established by American Thoracic society (ATS)

• Crackles – discontinuous sounds – secretions vs. airways popping open • Inspiratory noises – What do fine late inspiratory crackles indicate? • May clear with coughing

• Wheezes – high pitched continuous sounds – indicates airway obstruction

• Rhonchi – low pitched continuous sounds

• Bronchial Breath sounds – abnormal if heard over peripheral lung fields – indicates increased lung density

• Diminished breath sounds – indicates obstruction to airflow, air trapping , or shallow respirations

• Pleural friction rub – ‘creaking pleural surfaces” – localized indicates pleural inflammation

• Stridor – upper airway noise – indicates serious upper airway obstruction • Fine • Coarse • Loud • Indications – • Higher pitch = narrower airway

12 ATS Lung / Auscultation Description Anatomy of the Respiratory System and Thorax The respiratory system can be separated into two tracts (upper and lower) The upper respiratory tract is comprised of the nose, paranasal sinuses, pharynx, and the larynx. The purpose of this tract is to purify, warm, and humidify ambient air before it reaches the gas exchange units. The lower respiratory tract begins with the trachea, the right main bronchus which divides into three lobar or divisions of the lung (upper, middle, and lower), the left main bronchus which divides into two lobes (upper and lower), followed by the bronchioles, and terminating at the alveoli (air sacs). In this tract, there are approximately 23 generations of airways; the first 16 are conducting airways while the last seven are respiratory airways ending in approximately 300 million alveoli, which form the gas exchange surface

13 Listening to the Lungs The lungs are auscultated with the diaphragm on the chest piece of a stethoscope with the patient breathing slowly and deeply through their mouth. The anatomical sites for lung auscultation are illustrated in below. Figures 3 and 4. Sites for Auscultation of the Lungs

There are some common errors to avoid: 1. Listening to breath sounds through a patients gown or clothes. 2. Allowing tubing to rub against bed rails or patient’s clothes. 3. Interpreting chest hair sounds as adventitious* sounds. 4. Auscultating on the convenient places only *Adventitious sounds: added sounds, or those superimposed on a patient's underlying breath sounds that usually indicate disease. Normal breath sounds consist of those heard over the entire lung field and consist of an inspiratory and expiratory phase. They are classified as:

Tracheal: These breath sounds are high-pitched and loud, with a harsh and hollow (or "tubular) quality. The inspiratory and expiratory phases are of equal duration, and there is a definite pause between phases. Tracheal breath sounds usually have very little clinical usefulness.

Bronchial: Normally heard over the upper manubrium, these breath sounds directly reflect turbulent airflow in the main-stem bronchi. They are loud and high-pitched but not quite as harsh and hollow as tracheal breath sounds, the expiratory phase is generally longer than the inspiratory phase, and there is usually a pause between the phases.

Bronchovesicular: These breath sounds are normally heard in the anterior first and second intercostal spaces and posteriorly between the scapula, where the main-stem bronchi lie. The inspiratory and expiratory phases are about equal in duration, with no pause between phases. Bronchovesicular sounds are soft and less harsh than bronchial breath sounds and have a higher pitch than vesicular sounds.

14 Vesicular: Audible over peripheral lung fields, these breath sounds are soft and low-pitched, without the harsh, tubular quality of bronchial and tracheal breath sounds. The inspiratory phase is about three times longer than the expiratory, with no pause between phases

Breath sounds are considered abnormal if they are heard outside their usual location in the chest or if they are qualitatively different from normal breath sounds (e.g. decreased or absent). They are divided into two categories: (1) Continuous (2) Non-continuous lung sounds.

The pulmonary nomenclature developed and adopted by the American Thoracic Society and the American College of Chest Physicians, as published in the Essentials of Cardiopulmonary Physical Therapy describe all continuous adventitious sounds are referred to as wheezes and described as either high-pitched or low pitched. Wheezes represent airway obstruction, can be caused by broncho- constriction of smooth muscle or the presence of mucus. When a wheezes occur, it is significant. They are most common with expiration. However, they can occur during inspiration and this indicates that a severe airway obstruction is present. Low-pitched wheezes are often still referred to as ronchi.

Discontinuous adventitious sounds are classified as either: 1. Crackles sound like brief bursts of popping bubbles. They are most commonly associated with the sudden opening of closed airways.

2. Pleural Rubs are an indication of pleural inflammation and sounds like two pieces of sandpaper rubbing together throughout each inspiration and expiration.

15 COPD assessment & Treatment 101

16 Basic Respiratory Assessment = 4 basic Problems Problem Clinical Signs & Symptoms Stable / chronic Unstable/ Respiratory Failure

Oxygenation SPo2, PaO2 compared to FiO2 SPo2 88 – 92% with SpO2 < 84% required < 4l/min 02 Nasal Required FiO2 > A-a grad, a/A ratio, PO2/ Fio2 Cannula 60% (> than 6L o2 ratio nasal cannula) Ventilation ABG – Pco2 & pH RR 12 – 20 RR > 25 at rest RR Visible chest rise Poor chest rise VT - = chest rises & Breath sounds Diminished BS Auscultation auscultated Work of 3 How’s RR 12 – 20 RR > 25 Breathing How Deep = VT Visible chest rise Minimal chest rise How Fast = RR Minimal to mild Diminished or absent How Hard = accessory retractions at rest BS muscle use (retractions Mod to severe between, under, or above ribs retractions at rest Airway LOC Alert, oriented & ALOC – obtunded, Protection Cough Effort follows commands will not stay awake, Secretions – amount, color & Effective productive barely can follow Viscosity cough commands Moderate secretions Ineffective or weak productive several nonproductive cough times per day Copious secretions – large amounts every 1-2 hours Thick yellow, green or brown mucous NON Respiratory Hypotension < 100 Problems Acidosis pH < 7.25 CHF / Pulmonary edema Wet lungs / hypoxia Fever  101 Decreased HR < 60 Increased HR  120 at rest Anemia < 10 Hb Pain

17 Auscultation and Cough assessment basics

Breath Sound Description and typical cause

Clear Good airflow through main bronchial airways (Bronchovesicular)

Wheeze High pitched Usually expiratory (I & E = more severe) Caused by bronchoconstriction / bronchospasm of small to medium airways Ronchi (older term) Coarse rumbling or gurgling sound in large airways Caused by thick secretions in the bronchi Fine – Coarse Inspiratory and expiratory Improves with productive cough Crackles Wet Sound – like a wet sponge expanding after squeezing Fine – Coarse Usually inspiratory Caused by edema in Lung tissue / alveoli Diminished No sound Lack of airflow caused by 1. Obstructed Airway 2. Collapsed Lung – atelectasis or Pneumo Thorax 3. Exhausted or weak patient unable to breathe deeply

Cough assessment Typical Cause / Indication

Productive vs. Non Productive = cough effective enough to remove sputum Productive form the lungs Non Productive = 1. Cough is effective but no sputum present in the lungs 2. Effort is too weak /ineffective to remove sputum Tight /dry Cough Caused by bronchospasm – usually dry with minimal production 1st clinical sign of bronchospasm before wheezing Can be caused by small amount of mucous (sinus infection) Slightly wet/ loose Edema in Lung = CHF cough (Prof Greg term) Loose Cough Rumbling coarse caused by thick secretions in the large airways

18 Reasons for COPD admission to Acute Care and increased hypoxia “Why is my patient WOB increasing & SPO2 decreasing” Acute Condition Clinical Signs and Symptoms Treatment

Pneumonia / Loose cough Assess Cough effort and infection Coarse ronchi coarseness “Most common Yellow / green sputum Airway Suction reason” Diminished BS with weak cough effort Nebulizer TX’s with Can cause moderate to severe Bronchodilator & mucolytic hypoxia (Mucomyst) Fever Ambulate *** Fever with hypotension Hydrate = Septic Shock*** CPT PAP or Flutter devices (Accapella) Humidification of 02 Antibiotics

** NIPPV may give brief relief but will dry out lungs, prevent the patient from being able to cough and make this worse – avoid long periods of NIPPV. Give breaks Q2-4 hours**

Exacerbation / Wheezing Bronchodilators exhaustion Increased Accessory muscle use Steroids Agitated or fatigued –ALOC Long acting Inhalers Caused by acute Usually only mild or minimal increase Review treatment regimen bronchoconstriction, in Hypoxia and patient compliance increased work, Cough is dry or tight fatigue, or non- Secretions are clear or white – may be **NIPPV – this gives the best compliant with long thin or thick results & may avoid acting medications readmission or intubation**

Pulmonary Edema / Wet crackles in lung fields esp. middle Diuretics CHF exacerbation lobes Monitor I & O Tight /wet cough Clear foamy sputum ** NIPPV or CPAP give good Tachycardia results and patient should Palpitations improve within 30 minutes - Distended Neck Veins 1st hour** Edema swelling in extremities

19 Rapid Bedside Assessment You’re called to the bedside because the COPD patient is desaturating and appears in distress

I. LOC & Breathing (5- 10 seconds) Sit Him up and talk to him!!! A. LOC – Alert, oriented, & follows commands or  Obtunded – barely arousable vs. Agitated  Previous sedations – anti-anxiety, pain, or sleep aids  Blood Glucose levels  Blood Pressure – Hypotension???

B. Breathing – Is he moving any Air? Apnea vs. tachypnea?  RR  Chest Rise  Accessory Muscle use – how hard is he working?

II. SPo2 & Vital Signs – Stable vs. Unstable (ALOC, decreased BP & O2 > 6 l/min)

III. Auscultation – Breath sounds present vs. Diminished or absent

IV. Cough Assessment – weak vs. strong – loose vs. tight – productive vs. non productive

V. I & O

VI. Medication & Treatment orders

20 COPD Treatment Basics Oxygen Therapy – Typical Goal is SPO2 88 – 92% for moderate to severe COPD Avoid SPO2 > 96% (hyperoxia) – This can make the patient drowsy and suppress his respiratory drive

*** Progressive COPD typically does not require high Fio2 – O2 < 4l/min*** In the case of severe hypoxia the cause is usually I. Obstructed airway due to secretions Hypoventilation – not breathing deep enough

21 Arterial Blood Gases – What 2 things do you need to look at to interpret any diagnostic tests? Parameter Description Ranges

Oxygenation Parameters

PaO2 Partial pressure 80 – 100 mmHg = normal of oxygen in 60 – 80 = mild hypoxemia arterial plasma 50 – 60 = mod hypoxemia < 50 = severe hypoxemia 40 – 45 = venous oxygenation. SaO2 % Oxygen 95 – 100 % = normal Saturation of 92 – 95 % = mild hypoxemia. arterial blood 90 – 92 % = mod hypoxemia. < 90 % = severe hypoxemia 85 % = venous oxygenation

A – a gradient Difference 20 mmHg = normal on between the 21% oxygen level in >FIO2 = oxygenation Alveoli and problem. artery. >350 = Hypoxic respiratory Indicates level Failure of oxygenation + diffusion problems. a/ A ratio Ratio of Pa & .90 = normal (90%) PAo2’s esp. < .3 = severe hypoxemia useful with vent pt’s on high Fio2’s > 60% PaO2/ FiO2 Used with < 300 = early ARDS ratio ARDS 100- 200 = ARDS assessment & <100 associated with high NIH ARDS mortality Network – ARDSNET guidelines

22 Acid Base Parameters (Respiratory vs. Metabolic) Acid Base Parameters (Respiratory vs. Metabolic) Respiratory Component PCO2 Partial pressure 35 – 45 mmHg = normal of CO2 in < 40 = hyperventilation arterial plasma & respiratory alkalosis pCO2 = > 40 = hypoventilation ventilation. + Respiratory acidosis Metabolic Component HCO3 Bicarbonate 22-26 Buffer level in 24 meq = normal arterial blood **(if pCO2 = 40)** > 24 = metabolic alkalosis <24 = metabolic acidosis BE (Base Measurement + Or – 2 = normal Excess) of buffer level > 2 = metabolic alkalosis in blood, < -2 = metabolic acidosis measures = Base deficit metabolic Can be used to calculate increases or amount of HCO3 to treat an decreases in acidosis HCO3 production.

Rules of Respiratory /Metabolic Compensation H2O + CO2 < - > H2 CO3 < - > HCO3 + H - (which equation is this?) (Water + CO2 = Carbonic Acid = Bicarbonate)

Link to most important equations is healthcare http://www.globalrph.com/martin_4_most.htm

Respiratory Compensation: • Increasing CO2 = increasing acid = respiratory acidosis • Decreasing CO2 = decreasing acid = respiratory alkalosis • Respiratory compensation is immediate and used for short term or acute problems, i.e.… lactic acidosis, diabetic keto acidosis, etc.… • Respiratory compensation is never complete…only partially compensates • Cannot increase PaCo2 > 45 to compensate – cannot override the drive to breathe

23 Rules of Respiratory /Metabolic Compensation H2O + CO2 < - > H2 CO3 < - > HCO3 + H (Water + CO2 = Carbonic Acid = Bicarbonate)

Metabolic Compensation: • Increasing HCO3 and Base Excess levels = metabolic alkalosis. • Decreasing HCO3 and Base Excess levels = metabolic acidosis. • Metabolic compensation takes time and used for chronic problems, i.e.. COPD chronic CO2 retention…Uncompensated (Acute) • Metabolic compensation can be complete (Chronic)

Causative Agent vs. Compensating Factor (Who’s to blame?) • Causative agent will usually match the ph.

• Compensating factor will usually opposite of the pH

• COPD patients can have Acute Respiratory Failure (Uncompensated Resp. Acid) on Chronic Respiratory Failure (Compensated Respiratory Acidosis)

• COPD patients on the ventilator can have Acute Hyperventilation (Respiratory Alkalosis) on Chronic Respiratory Failure (resp. acidosis)

Acid Base Balance: • pH - < 7.40 = acidemia vs. > 7.40 = alkalemia. • Evaluate respiratory component. PCO2 < 40 = resp. alkalosis vs. > 40 = resp. acidosis. • Evaluate metabolic component BE > + 2 = met alkalosis vs. BE < -2 = met acidosis. • Determine causative agent (which component matches the pH) • Determine compensating factor (which component opposes the pH) • Determine degree of compensation, i.e.…complete vs. partial vs. uncompensated. • Failure to compensate indicates a CRITICAL situation = combined

Ventilation: • pCO2 = ventilation… • PCO2 < 40 = hyper ventilation vs. • > 40 = hypoventilation.

• “How well are they moving air compared to the patient’s effort /work of breathing (WOB), RR, Tidal volume + minute ventilation

24 Questions to Ask (Critical Thinking) Does the Patient: Assess for Normal, Abnormal or Critical Values = stable vs. unstable • Need more oxygen? Hypoxic, adequate, or hyperoxic? • Compare FiO2 to PaO2 = severity of lung disease.-

o PaO2 / FiO2, A-a gradient, & a/A ratios quantify the severity of the lung disease • Need to breathe more? Compare Ve to PaCO2 = efficiency of ventilation = % dead space). • Have normal pH or an acid base problem? (Sickness causes acidosis) • Have any Anemia problems – reduced Hb, Increased CoHb or Met Hb • Have signs, symptoms, diagnosis, or medical history that apply to the ABG results? • Have to WORK to maintain these ABG results…is he OK or tiring out? • Have a chronic disease like COPD? (How do know what the normal PaO2 & PCo2 are normal for this patient?)

25 Basic Concepts of Acid-Base Balance

1. Bicarbonate (HCO3¯) is the base in acid-base balance. It is the metabolic component.

2. Carbonic Acid (H2CO3) is the acid in acid-base balance.

3. Carbon Dioxide (CO2) is proportional to the amount of carbonic acid and is the respiratory component. (PCO2 x .03 = H2CO3 in meg/1).

4. Respiratory Acidosis means an elevated PCO2 (usually greater than 45 mmHg).

5. Respiratory Alkalosis means a decreased PCO2 (usually less than 35 mmHg).

6. Metabolic Alkalosis means a positive base excess and usually an elevated bicarbonate.

7. Metabolic Acidosis means a negative base excess (base deficit) and usually a low bicarbonate.

8. The pH is a measurement of H+. Alkalemia means an increased pH. Acidemia means a decreased pH.

9. The pH is a balance of bicarbonate and carbonic acid (expressed as PCO2).

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10. The primary component is either the metabolic or the respiratory component which causes a change in the pH. (maybe both)

11. The pH usually reflects the primary component(s).

12. The secondary component is the compensation mechanism. The secondary component is always the opposite of the primary component and usually pH.

13. Each component is compensated by its opposite. The respiratory component

(PCO2) is compensated by the metabolic component (HCO3¯).

14. There are only 14 possible ABG combinations, 4 are rarely every seen.

15. Acute means uncompensated. In an acute ABG, the pH reflects the primary component. The secondary component is within normal limits. Only the pH and the primary component are not normal.

16. Partially compensated means the secondary component is working to bring the pH back towards normal. The pH reflects the primary component and the secondary component is in the opposite direction.

17. Chronic or compensated means the secondary component has balanced the primary component in order to normalize the pH.

18. Combined means BOTH the respiratory and metabolic components reflect the pH. In this case both components are primary and there is no compensation.

27 Normal COPD ABG’s • pH, 7.32 – 7.38 (compensated resp. acidosis). • PCO2, 45 – 65 (chronic CO2 retention). • PO2, 50 – 70 (chronic hypoxemia). • HCO3, 30 – 40 (metabolic compensation). • BE + 5 – 10 (metabolic compensation). • SaO2, 90 – 94 % (chronic hypoxemia + reduced hypoxic drive). • THb, 12 – 17 (chronic hypoxemia = polycythemia “more trucks.”

ACIDOSIS NORMAL ALKALOSIS

PCO2 >45 35-45 <35

pH <7.35 7.35-7.45 >7.45

BE <-2 +2 - -2 > +2

Oxford medical Sample ABG exam http://www.oxfordmedicaleducation.com/abgs/abg-examples/

Rule of Thump Blood Gas equations

(Ve 1) x (PaCO2 1) = (Ve 2) x (PaCO2 2) used to calculate how to change Ve to obtain a desired PCO2. ( Egan’s Chap 14 mini clinic page 289)

PaCo2 decrease by 1= pH increase by .01 or PaCo2 decrease by 10 = pH Increase by .1

PaCo2 increase by 1 = pH decrease by .006 or PaCO2 increase by 10 = pH Decrease by .06 (Egan’s Chapter 14 table 14-6 page 299)

Acute Increase of PaCO2 above 40 by 10 = imm HG increase in HCO3 This is buffering not compensation. (Egan Chapter 14 page 295)

28 pH PCO2 HCO3 BASE PO2 FIO2 Interpreted EXCESS

1. 7.26 56 24 -4 40 Air ______

2. 7.52 28 22 +4 51 40% ______

3. 7.60 55 51 +26 80 Air ______

4. 7.44 24 16 -6 56 Air ______

5. 7.38 76 42 +14 80 35% ______

6. 7.20 25 9 -17 115 Air ______

7. 7.56 44 38 +4 92 Air ______

8. 7.32 25 13 -12 106 Air ______

9. 7.60 25 24 +4 60 Air ______

10. 7.32 95 49 +15 45 50% ______

11. 7.56 32 28 +6 56 Air ______

12. 7.55 58 49 +20 99 Air ______

13. 7.20 78 30 0 37 Air ______

14. 7.46 26 18 -4 73 28% ______

15. 7.36 83 48 +15 41 45% ______

16. 7.54 29 24 +3 59 Air ______

17. 7.24 60 26 -2 47 Air ______

18. 7.20 38 15 -13 88 Air ______

29 Los Angeles Valley College Respiratory Therapist Program PATIENT PROFILE Student Name______Date Pt. Assessed______Diagnosis :( chief complaint) Primary: ______Admission Date ______: Age: ______yrs M / F

Secondary ( chronic diseases)______:______

History (smoking, previous surgeries, procedures) ______

______

Home O2 or RT treatments ______

Current oxygen Therapy – Device ______FiO2 ______Flow ______

Current RT Therapy Orders ______Therapeutic Objectives ______

Vital Signs: RR: ______, HR: ______, BP: ______/______, Temp:_____0C/F, SPO2 ______%

Physical: Skin Color: ______Edema ______vs. Dehydrated______Auscultation ______Chest Rise ______LOC ______Accessory muscle / wob______

Chest X-Ray: Date ____ /______

Hemodynamics: s, PA___/___, CVP Pres ____Troponin____, AST (SGOT)_____, Protime ___ EKG results ______LAB: Hb_____gms, Hmt ______%WBC____ BUN____ Creat____ K+____ Albumin____ Glucose ____ C&S ______Blood Culture______Lactate _____ Sputum Culture ______Other Abnormal Labs ______Most Recent ABG: Date ______Time______Device______Flow____ Vent Settings______FIO2 _____%, PO2 _____mmHg, PCO2 _____mmHg, pH _____, BE _____, HCO3______meq/l, A-a ______a/A Ratio ______PaO2 / FiO2 Ratio _____ O2 HB ____ THB ____ CoHb ____ Met HB ____

ABG Interp: ______

Oxygen or Ventilation Titration orders or Protocols ______Medications/IVs Med Dose Route Freq. Classification Considerations/side effects Pulmonary Medications

Cardiac Meds

Other 30 Patient Respiratory Care Plan - Initial Problems Goal / objective Interventions – RT Orders Current Date Problems progress / status Started ______Oxygenation SPo2 > ______O2 therapy Spo2 ______Spo2______PaO2>______Device ______ABG’s______Fio2______Other ______Flow/ Fio2 ______PaO2______Date S/U ______Resolved Date Other ______

Ventilation Pa Co2 >______< Ventilation Settings VE ______RR ______PaCO2 ______VT/ Chest RR > ______< ______Resolved Date rise______VT > ______<______NIPPV Setting ______Ve ______Ve > ______< ______PaCo2 ______Other ______Work Of Breathing RR > ______< ______RT Tx’s – date started ______RR > ____ < _____ RR______VT /chest rise device______VT /chest rise VT / Chest ______medications______rise______Acc. Muscle Minimal or no Accessory Freq ______Accessory muscle ______muscle use use______Breath sounds ______Other ______Date resolved ______Breath sounds ______Other ______

Airway protection LOC ______Directed cough ______LOC______ALOC Airway Suction ______Cough effort ______Cough effort _____ Cough effort Airway clearance ______Secretions Airway management ______Secretions Secretions ______Visc______Breath Sounds ______Amt______Other Date resolved Color ______Non RT Problems Cardiac Other ______/Hemodynamic Date resolved ______Acidosis ______Other______

Care Plan Recommendations: (titrate SO2 = 92%, treatments, diagnostic tests) ______

______

31 Module 2 Airway Clearance (formerly Bronchial Hygiene Therapy) Egan’s Chapter 43

Diseases associated with Abnormal Airway Clearance

• Cystic Fibrosis – most common cause • Increased mucous viscosity – abnormal sodium concentration • Bronchiectasis – increased mucous production & decreased airway patency • Bronchial hygiene is primary therapy – bronchodilator is secondary therapy • COPD????

• Foreign body obstruction

• Tumors

• Kyphoscoliosis

• Asthma / bronchitis

• Acute infections –

• Neuromuscular diseases & injuries

Causes of impaired Mucociliary Clearance in intubated patients (Egan’s Chap 43 Box 43-1 page 953)

• Endotracheal Tube • Tracheal suctioning • High FiO2’s • Anesthesia • Opiated / Narcotics

32

General Therapeutic goal – decrease WOB & improve gas exchange by mobilizing & removing retained secretions

Clinical Indications for airway Clearance Therapy (Egan’s box 43-2 page 954)

Acute conditions • Copious secretions

• Ineffective cough

• Acute respiratory failure with retained secretions

• Acute lobar atelectasis

• Low V/Q caused by lung infiltrates or consolidations –

What clinical signs & symptoms would indicate these conditions exists?

Questionable acute indications: • COPD exacerbation???????

• Pneumonia without clinically significant secretions???

• Asthma????

Prevention Airway Clearance therapy??? – Not proven effective except for 2 conditions • CF patients

• Ventilator or immobile Critical Care patients – i.e. rotating & vibration beds

Chronic Conditions • CF • Bronchiectasis • COPD with retained secretions • Ciliary Dyskinetic syndromes

33 Initial assessment of need for Airway Clearance Therapy – (Egan Box 43- 3 page 955)

• Patient history of chronic lung disease • Patient mobility • Artificial Airway • Compared to signs and symptoms

Signs and symptoms of retained secretions

• Mucous production vs. Effective Cough effort determine need for airway clearance therapy

• Increased hypoxia or O2 requirements ( PaO2 or SPo2 compared to FiO2)

• Ineffective Loose sounding Cough Effort = nonproductive or scant production of mucous

• Color or viscosity changes in mucous

• Diminished BS

• Coarse Ronchi that does not improve with coughing

• Poor chest rise

• Increased WOB

• Increased fever ( not specific of retained secretions)

What tests would you recommend if you assessed these clinical signs?

What results would you expect?

34 CPT / Postural Drainage Therapy

CPT • Chest physical therapy is a form of removing secretions by cupping your hand and clapping on a designated position of a lung field. There are 6 different positions, 4 of which are drained by positioning the body with the head down. Percussion is done for 3-5 minutes per position. A cough is encouraged after every position. Percussion can be done manually or automatic and usually requires assistance.

• Chest physical therapy (CPT) is the traditional airway clearance technique. The removal of obstructive, thick sticky secretions is important in preventing infections and helps ease breathing.

CPT consists of two parts: 1) postural drainage and 2) percussion and vibration: • Postural drainage pertains to placing the body in a position, which allows the mucus to drain from the smaller airways into the main airway with gravity. Two positions are in an upright sitting position and four positions are with the head tilted below the lungs. To obtain the head- down positions, the use of a pillow, a beanbag chair, or couch cushions work well.

• Percussion and vibration help loosen and mobilize secretions. Percussion is a repetitive tapping on the designated position and can be done with palm cups (of varying sizes), by hand, or with a manual percussor. If you choose to use your hands, the palm of your hand should be cupped to provide a pocket of air that cushions the percussion. Manual percussors have padding and Velcro to allow self-use. Vibration is done at the end of the position. After a big breath in, vibrate when the air is slowly blown out, for three big breaths.

35

• Techniques to improve percussion effectiveness include: • Avoid percussion over bony area’s i.e. Sternum, scapula & clavicle • Percuss over area’s where ribs are palpated • Use a thin sheet or cloth to protect patient skin but avoid dampening vibrations • Use good ergonomics – back supported & straight – raise bed • Alternate hands in sequence • Loose wrists with slow steady rhythm

36 Positions – ( Egan figure 43-2 page 958) – determine effected lobes to determine position

37

38 Complications, Risks & hazards (Egan table 43-3 page 958)

• Increased ICP > 20mm Hg

• Aspiration – uncontrolled airway

• Increased WOB

• Unstable spinal cord or other orthopedic injuries

• Hypoxia – increased V/Q mismatch Hypotension

• Pain

• Bronchospasm

• Acute Hypotension

• Vomiting

• Bronchopleural fistula

• Pulmonary hemorrhage

• Pulmonary Embolism

• Rib fracture

• Active hemoptysis

• Empyema or large pleural effusion

• Arrhythmias– What precautions or actions could you take to minimize these risks?

Assessing outcome (Egan’s box 43-5 page 959) What would tell you the patient is clearing his secretions and improving?

Could the patient’s auscultation or clinical signs look worse after CPT? Why?

39 What Lobes & segments are being treated?

40 Turning – Kinetic therapy or continuous lateral rotation – rotating on long axis • Rotating Beds – ( special beds with additional features = “overlays”) - • Manual turning/ repositioning of the patient • Therapeutic objectives • Promote lung expansion • Improve oxygenation • Prevent retained secretions • Indications • Immobile patients with high risk for pneumonia – • Acute Lung injury – “prone “ position – shown to improve oxygenation & lung expansion • Blood shifted away from “shunt” lung regions improving V/Q mismatch • Contraindications for Turning • Unstable spinal cord injury • Traction arm injuries • Increased intracranial Pressures ( ICP)– i.e. brain injury/ stroke patients

Coughing & expulsion breathing techniques • Directed Cough (Egan’s box 43-6 page 960)

• Indications / objectives

• Clears secretions from central airways

• Used to help patients with physical or clinical limitations for an effective cough

• Helps provide control over cough reflex

• Technique

• Position – whatever is most comfortable “ high fowlers”

• Breath control – slow deep inspiration through nose

• Strength exercises -

41 Modifications

• Post op “splinting”

• Abdominal

• “huff coughing” – same as FET

• Forced Expiration Technique (FET) • FET may be used in addition to some other form of ACT. It consists of one or two forced expirations (huffs) followed by relaxation and comfortable breathing. FET is repeated until secretions are mobilized to central airways where they can easily be coughed out. The huff can be started at different lung volume levels, to clear the mucus from the different sizes of airways.

42

• Active Cycle Breathing (ACB) (Egan’s box 43-7 page 962) – prevents bronchospasm • ACB technique consists of thoracic expansion exercises, breathing control, and the forced expiration technique (huff). Breathing control is passive normal breathing, using the diaphragm. It is used between the active parts of the cycle, to allow relaxation and to avoid airflow obstruction. Thoracic expansion exercises are deep breathing exercises with an emphasis on inspiration. Expiration is quiet and relaxed. These exercises help to loosen bronchial secretions. Forced expiration technique consists of two huffs or forced expirations, combined with periods of breathing control. At mid lung volume to low lung volume a huff will help to move secretions from the peripheral airways. At high lung volume a huff will mobilize secretions from the upper airways. These three stages are repeated until the huff becomes dry sounding and non-productive or it is time for a rest. Position placement is determined by where the secretions are heard or felt in the lungs.

• Autogenic Drainage (AD)(Egan’s figure 43-6 page 963) • This breathing technique takes cooperation and understanding of the different lung capacities. With good training the individual can identify which lung field the secretions are in. There are 3 phases:

• Phase I is the "un stick" phase, where very low lung volume, normal breathing helps move the secretions up the bronchial tree.

• Phase II is the "collect" phase, where small volume breathing is increased to a higher level, allowing for secretion collection in the central airways.

• Phase III is the "evacuate" phase, where breathing is normal to high volume breathing and secretions can be removed from the upper airways. A huff maneuver is used to remove secretions.

Contra indications for PAP or MIE ACT’s (Egan’s box 43 – 8 page 964

• Untreated Pneumothorax • Chest trauma • Head trauma or high ICP’s • Hemoptysis • High W.O.B. • Hypotension – low cardiace output • Nausea • Facial trauma or bleeding

43

Mechanical Insufflation – Exsufflation: MIE “cof-flator” – “In-Exsufflator”

• Designed in 1950’s for polio patients • The machine operates with a blower and a valve that applies a positive pressure first to give a deep breath in, and then shifts rapidly to negative pressure to create a high expiratory flow, like one has with a normal cough. It can be used on a person with a trach or someone without a trach through a face mask or mouthpiece. The circuit is a bacterial filter, a pressure tap, and a hose to the face mask or adapter to the trach tube. There are two models: one with automatic timing and one manual.

• Pressures should start low, about 10 20 cm as tolerated, and then build up to 40-45 cm to get deep insufflation. The timing for the positive-negative is one to two seconds. The positive and negative pressures are set about the same, though some people like the inspiratory pressure to be slightly less.

• The Cough Assist can be used with a facemask, mouthpiece or, with an adapter, to a patient's endotracheal or tracheostomy tube. This device can be used on adult and pediatric patients at home or in a hospital/institutional environment.

44

Positive Airway Pressure: PAP (Egan’s box 43-8 page 964) • PEP

• Positive expiratory pressure is self-administrating. The process is to take a deep breath in and blow out with moderate force, against a resistance. This resistance keeps the airways open allowing air to move secretions so they can be coughed out. 20 deep breaths against the resistance followed by a huff cough maneuver is the usual sequence.

• PEP valve may be used inline with nebulizer tx’s.

• Uses a variable expiratory resistance – “blow slow not hard”

• Secretions are mobilized by creating pressure “behind “ the secretions – i.e. “collateral ventilation / pores of Kohn”

• Best results involve CF patients

• Eliminates risks of postural drainage

• Self-administered

• PAP of 10-20 cm H20 during entire expiratory cycle

45 High-Frequency compression / Oscillation: • Flutter

• This is a hand held device that functions like PEP working from the inside out. Exhalation through the flutter results in a vibrating of the airway walls loosening secretions. The airways are open during expiration to mobilize secretions. The positioning or angle of the flutter will determine the vibration level. A huff cough maneuver is used to remove secretions.

46 IPV

• Intrapulmonary percussive ventilation is administered by a percussionator. Aerosolized air, in the form of mini-bursts, is delivered into the lungs. A constant pressure is maintained to keep the airways open. The bursts of air provide an air hammer affect opening the airways that have retained secretions. The huff cough is used for secretion removal.

Meta Neb - The MetaNeb® System is indicated for the mobilization of secretions, lung expansion therapy, the treatment and prevention of pulmonary atelectasis, and also has the ability to provide supplemental oxygen when used with compressed oxygen.

The MetaNeb® System is a therapeutic device that utilizes a systematic approach to enhance normal mucus clearance and resolve or prevent patchy atelectasis. CHFO (Continuous High Frequency Oscillation) mode is a pneumatic form of chest physiotherapy that delivers medicated aerosol while oscillating the airways with continuous pulses of positive pressure. In CPEP (Continuous Positive Expiratory Pressure) mode The MetaNeb® System provides medicated aerosol combined with continuous positive pressure to assist in holding open and expanding the airways.

47

CHFO is a pneumatic form of chest physiotherapy (Airway Clearance) that utilizes a systematic approach to enhance normal mucus clearance and resolve patchy atelectasis by:

1. Providing aerosolized medication and humidification to relax bronchial smooth muscle so that airway resistance is decreased, and at the same time hydrating thickened retained secretions; 2. Using specifically calibrated frequency and I:E ratio to create a mean airway pressure in order to maintain airway caliber, prevent premature closure, and expand collapsed lung regions. 3. Maintaining continuous high frequency oscillation during both inspiration and expiration to form a pressure gradient to the small airways where secretions are trapped. This pressure gradient creates an accelerated expiratory airflow that can be manipulated to assist in moving the secretions to the upper airways. 4. Delivering hyperinflation therapy through positive expiratory pressure that will aid patients in deep breathing and coughing.

The purpose of this therapy is to:

1. Prevent or reverse atelectasis; 2. Aid in the mobilization of retained secretions; 3. Reduce the incidence of air trapping.

48 The MetaNeb® System can be safely incorporated into a ventilator circuit in order to provide therapy with The MetaNeb® System on most ventilators. By simply utilizing the following components, CHFO therapy can be administered via The MetaNeb® System to a ventilated patient without breaking the circuit;

• spring-valve tee (normally used for in-line nebulizer treatments) • 15mm x 22mm adaptor (included in The MetaNeb® System circuit), and • black occlusion ring (also included with the circuit) to replace the green selector ring

49

• Vest – Therapy Vest “Theravest”

• The bronchial drainage system vest (e.g., the Vest Airway Clearance System®, formerly known as the therapy Vest® or the ABI Vest ®) is a portable device that provides external thoracic percussion. It consists of a non-stretching inflatable vest linked to an air pulse generator by two flexible hoses. The generator rapidly inflates and deflates the vest, gently compressing and releasing the chest wall to create airflow within the lungs. This process moves mucous toward the larger airways where it can be cleared by coughing. This airway clearance therapy is commonly referred to as high frequency chest wall oscillation.

• High frequency chest compression technique is self-administrating. An inflatable vest is placed over the chest with air pulsating through it. The pulsation helps force secretions toward the large airways so they can be coughed up. The pulsation frequency is increased throughout the treatment. The huff cough (forced expiration maneuver) is used to remove secretions.

What the advantages of these systems over traditional CPT?

Selection Criteria (Egan’s Table 43 page 956 -2 & Box 43-10 page 967) • Patient issues – motivation, goals, support systems

• Costs

• Fatigue to patient

• Physician goals

• Disease type & severity

• Patient’s learning & physical ability

• Skill of therapists

• Ease of learning & teaching

50 Bronchopulmonary Hygiene Algorithm (Egan’s’ 43-11 page 969)

• Productive Cough - Weak effort vs. chronic or copious secretions • Non Productive Cough – Weak cough vs. amount of secretions

When do you know it’s time to suctions?

51

RT 3 Module 3 – Pharmacology Typical Aerosolized Medications Principles of Pharmacology

Drug administration: delivery to respiratory tract via aerosol. • Advantages: topical delivery vs. systemic . Lower dosages . Rapid onset . Targeted delivery . Less systemic effect

Pharmacokinetic Phase: time, course, and disposition of a drug. • Based on: • Absorption • Distribution – Ionized ( Atrovent) vs.Non Ionized ( atropine) • Metabolism • Elimination

L/T Ratio - (Egan Figure 35-1) – efficiency of aerosol delivery to lungs

• Lungs – topical delivery = therapeutic effect • GI Tract – systemic absorption from oral pharynx = side effects

Pharmacodynamic phase – Drug actions /effects on the body (Egan table 35-1, 35-2 page 718 & 719)

• Adrenergic – stimulate sympathetic system ( epinephrine, norepinephrine) • Antiadrenergic – blocks sympathetic system – blocks receptor site for epinephrine • Chloinergic – stimulates parasympathetic system ( acetylcholine) • Anticholinergic – blocks parasympathetic system (Para sympatholytic) – blocks receptor site for acetylcholine • Muscarinic – Drug that stimulates acetylcholine receptors specifically at parasympathetic nerve ending sites

What effect does each of the 4 classifications have on the Cardioplumonary system? Give one medication example of each of the 4 classifications.

52

• How can inhaled medications be administered? (Egan Chapter 39) • Types of Inhalers • Metered Dose Inhalers - (MDI’s) gas & liquid medicine

• Dry Powder Inhalers – turbo inhalers & Discs

• Spacers – mixing or holding… can use a mask for small children

• Nebulizers – higher doses & require less patient effort than MDI

• Require a compressed gas source.i.e. pulmo-aide or Pari Neb

• psio-electric neb’s i.e.. Aeroneb (vibrating mesh) or ultra-sonic. Portable – battery packs

53 Spacers + Chambers (holding vs. Mixing)? - # of Puffs = the dose

1. Shake medication & Prime if new or used for a few months

2. Blow out slowly

3. Breathe in through spacer & Pump - Slowly

A. Holding Chamber Pump then breath in B. Mixing Chamber or No Chamber ( Pump after starting to breath in)

4. Hold breath for 6-10 seconds

5. “don’t count a bad puff”

6. How much medicine do I have left?

Dry Powder Inhalers – click “once” & breathe In Fast & hold breath 6- 10 seconds

– take a second breath but only click once

See YouTube links Airway Clearance files in RT 3 Haiku site

54 Asthma Plan basics:

• Prevent attack – know my triggers

• Know my signals – “signs & symptoms” – Red, yellow or green

• Take my rescue medicine

• Relax, relax, relax – blow out slow – “pursed lip breathing”

• How am I now? – Is my plan working?

• If it’s not working try it again or get more help

• Knowing what to do means “No Fear” = Control

55 How do I know how sick I am? • Peak Flow meters • Breath in Deep

• Blast the air out “blow out the fire”

• Green Zone – your best day

• Yellow Zone - ¾ of your best day Relax Use your rescue inhaler Check yourself again in 20 minutes Yellow Zone signs – 1. coughing 2. wheezing 3. sneezing 4. short of breath when I try to exercise

• Red Zone – ½ of your best day Relax Use your inhaler Now!!!!!! Check yourself again If you are not a lot better get help RED ZONE SIGNS 1. Short of breath while not moving 2. Sucking in at neck or under sternum 3. Blue color on fingers, hands, lips, gums 4. Feeling worse after using inhaler • When do I stay home? – Yellow Zone after using my inhaler

• When do I go to the doctor or ER Red Zone – esp. if you’ve used your inhaler and you’re still in the “RED” When the Plan’s not working!!!!!!!

• Types of doctors that treat asthma • Primary care doctors • ER doctors • Pediatricians • Allergists • Pulmonologists

56 Types of Medications – bronchodilators vs. anti-inflammatory

Most of the work done in developing new Rescue Medication is finding drugs that have very specific actions, with the fewest side effects. The Beta2 receptor is the target for all of these drugs. Beta1 is the other receptor that is most often stimulate along with the Beta2 receptor. Beta1 receptors are primarily cardiac in action, increasing heart rate and contractility (strength of the heartbeat). The less Beta1 action, the less cardiac side effects like tachycardia (fast heart rate). Medications like Albuterol, Bitolterol, Terbutaline, and Metaproterenol have very specific Beta2 TM action with minimal Beta1. The former "over-the-counter" medications, like Primatine Mist , had strong Beta1 & Beta2, plus Alpha effects. Alpha-receptor stimulation causes major vasoconstriction (increases blood pressure), mild bronchoconstriction, and a small amount of increased cardiac contractility.

SABA’s – Short Acting Beta Agonists • Fast acting / Rescue medications - “stays in your pocket” • Sympathomimetics – mimic rescue systems – BETA 1 & BETA 2 • Increases nerve signals to open airway – “broncho-dilator” = BETA 2 • Side effects – HR, tremors, nausea, headaches, “allergic” / rebound bronchospasm, • Underdosing or too little too late - • Overdosing – sign of loss of control of disease – • Loss of effectiveness / tolerance • Daily use > Q 4 hours indicates need for long acting medication

• Albuterol (Proventil, Ventolin) – Racemic Albuterol ( R and S isomer) • Nebulized dosage = 2.5mg in 3 ml NS ( most common Beta 2 agonist with less HR effects compared to earlier meds ( such as Bronkosol, Isuprel, & Alupent) • MDI Dose – 2- 4 puffs (.09mg each) Q4-6 hours PRN • onset – 5- 10 minutes • Peak 20 minutes • Duration 3- 4 hours • Most commonly used “Rescue medication” • Continuous Nebulizer dosage 7.5 – 20 mg per hour ( ER tx) • Can lower serum “K” potassium levels •

57 Alupent ( Metaproterenol) • Nebulizer dosage.2 cc’s - .3 cc’s (10-15 mg)in 3 ml NS • MDI dosage 2-4 puffs (.65 mg each) 4-6 PRN • ( stronger HR & tremor side effects but is commonly used for patients that have allergic or poor tolerance to Albuterol ) • NEVER USE MORE THAN ONE SYMPATHOMIMETIC

• • • • • • • • Xopenex – Levalbuterol – refined form of Albuterol – (Single R isomer of Racemic Albuterol) • Dosage 1.25 mg adults - .63 mg infants & peds • Longer acting 6-8 hours • Less cardiac side effects – • Possible beneficial anti-inflammatory effects • Can improve benefits in combination therapy with Atrovent & Pulmicort • More expensive • Available in MDI form now.

58

• Brethine (terbutaline sulfate). .( comes in injectable vials) • 25 - .50 mg - .25 - .5 Ml in 3ml NS • weaker beta 1 & Beta 2 typically used in patients sensitive to other Beta 2 – i.e. Albuterol • duration 4- 6 hours ( also available in tablet form)

• Maxair(Maxair™ Autohaler™ pirbuterol acetate inhalation aerosol) is: • 1-2 puffs ( .20 mg each) 4-6 hours • A rescue inhaler for asthma • A breath-actuated inhaler- no coordination necessary • Not available in nebulized form

59 Racemic Epinephrine – (nebulized epinephrine) original Emergency treatment for Asthma.

• Racemic - of, relating to, or constituting a compound or mixture that is composed of equal amounts of dextrorotatory and levorotatory forms of the same compound – who cares;)

• Strong sympathomimetic – not specific • Beta 1 – increase HR – Used in ACLS to treat profound bradycardia & asystole • Beta 2 – fast acting Bronchodilator – • Onset 3-5 minutes • Peak 5-20 minutes • Duration – 0.5 – 2hours ( Beta 1 & alpha systemic effects can last longer)

• Alpha effects – vasoconstriction = Increase BP & decreased topical edema

• Dosage – 2.25% - .25 - .50 ml’s in 3 cc’s NS q1 – q4hr prn

• Brand names – Vaponephrin, asthmanefrine, micronefrin & Primatene mist ( over the counter inhaler)

• Indications: • Upper airway / laryngeal edema – What are 2 common causes of acute upper airway edema that typically indicate the use of racemic epinephrine SVN tx’s.

• What is the most common adverse reaction? • Why is this no longer the preferred short acting aerosolized medication for the treatment of asthma?

60

Anticholinergics – Short Acting Muscarinic Agent SAMA • ( Primary medication for chronic bronchitis) • parasympatholitic – “block parasympathetic signals such as bronchoconstriction & bradycardia” • can be used with Sympathomimetics – “synergist effect” • may also be used if patient is using Beta Blocker ( i.e. Inderal or “Lol’s”)

• Atrovent – Ipratropium Bromide ( fast acting & drying) • 0.5 mg in 3 ml unit dose for nebulizer • MDI dose 2-4 puffs (.07 mg each)QID • Blocks signals that are closing the airway • Atrovent & Albuterol Mix = “Combivent”- MDI or “Duo Neb” – nebulizer • Can dry airways – • Peanut allergy alert & Glaucoma alert

• • •

• Atropine Sulfate – SAMA • Dosage .5 - 1 ml ( .4 mg per 1 ML injectable vial) • No MDI form

61 Long acting / Control medications –“stays at home” – Long Acting Muscarinic Agents (Egan Table 35-3 page 723)

Spriva – Tiotropium Bromide– Long Acting Muscarinic Agent LAMA • Once a day dose ( 18 micro grams) • Dry capsule ( Handi-haler ) only

• Tudorza “ Pressair” (Aclidinium bromide) o BID – 1 puff

62 Inhaled Corticoid Steroids – MDI liquid or DPI - Dry powder (Egan Table 35-5 page 728)

Older Steroids FDA approved before 2000 • Azmacort (Triamcinolone acetonide), 2- puffs BID • Aerobid (flunisolide), 2 puffs BID • Flovent(fluticasone Propionate 44, 110, & 220, mcg dosages) 1-2 x day • QVAR/ Vanceril (Beclomethasone dipropionate ) 2 puffs 1-2 times per day

Newer Steroids – FDA approved after 2000

• Pulmicort Turbuhaler - The medication in PULMICORT TURBUHALER is called budesonide, a synthetic corticosteroid. Corticosteroids are natural substances found in the body that help fight inflammation. Corticosteroids are used to treat asthma because they reduce swelling and irritation in the walls of the small air passages and ease breathing problems. When inhaled regularly, Corticosteroids also help prevent asthma attacks.

• Pulmicort Respules – nebulized form of Pulmicort. • .25 to 1.0 mg in 2ml unit dose 1-2 times per day • do not mix with other inhaled medications • may be mixed with Xopenex • used for chronic Asthma to reduce use of prednisone

• Cicloneside “ Alvesco” • 1-2 puffs BID – 80 or 160 mcg • No Shaking needed

63

• Asmanex – Mometasone furoate – “Twisthaler” – Ped 110 and adult 220 mcg doses – Q Day

WHAT IS THE MOST COMMON SIDE EFFECT OF USING INHALED CORTICOID STERIODS?

HOW CAN THIS BE PREVENTED?

WHERE IS THE BEST PLACE TO STORE THESE?

64 LABA’s • Long Acting Broncho-dilator adrenergic / sympathomimetic– Egan Table 32-2 • Serevent ( Salmeterol Xinfoate) 50 mcg - • also available in discus or in combo with Flovent ( Advair) BID • typically used for exercise induced or nocturnal asthma • Onset 5 min , Peak – 3- 5 hours, Duration – 12hours • Associated with asthma deaths – when used as a rescue medication

• Foradil ( Formoterol) • BID- onset 15 minutes , Peak 30 – 60 minutes, duration 12 hour • Dry powder MDI only

• Brovana( Arfomoterol)

• 15 mcg Bid Peak 15 minutes, Peak 30 – 60 minutes, Duration 12 hours

What is a “Black box” or “ Boxed” FDA warning?

Why do all LABA’s have this warning?

65

Combination Medications LABA & Inhaled Corticosteroids (ICS)

• Advair = Flovent & Serevent

o BID dosages (100,250, 500/50 mcg Flovent/ Serevent)

• Symbicort – ( Pulmicort & Floradil) o BID doses (80 & 160 Pulmicort)

• Breo “Ellipta” (Flovent and Vilanterol) o BID doses (100 /25 mcg)

• Dulera –( Asmanex & Floradil) o BID doses (100/5 & 200/5)

66 LABA LAMA Combination – COPD Therapy Link to Astra Zeneca site LAMA LABA site https://www.bevespiaerosphere.com/lama-laba-dual- bronchodilation.html?source=BEV_N_H_620&umedium=CPC&uadpub=Bing&ucampaign =Unbranded_-_Treatment-Medication&ucreative=LAMA- LABA_Combination&uplace=laba&cmpid=1&gclid=CLDfmfed99sCFcaTxQIdUgYNZA&gcl src=ds

Anoro Elliptica

o Anoro Ellipta (Vilanterol/umeclidinium) is a dry powder inhaler licensed for once- daily maintenance treatment of chronic obstructive pulmonary disease (COPD).

Triple combination DPI – LABA, LAMA, ICS = Trelegy – Vilanterol + Umeclidinium Bromide + Fluticasone https://www.trelegy.com/meet- trelegy/index.html?bing=e_&rotation=71700000033372484&banner=58700003893001830&kw=3121 0984392&cc=BF842B9C99C4&pid=43700031210984392&gclid=CLCZzqeZ5-ICFR- kxQIdzLwOcA&gclsrc=ds

67 Nasal Steroids – Nasonex, Vancenase, Flonase – now over the counter

Nonsteroidal Antiasthma Medications - (Egan Table 35-6 page 730)

Mucous Controlling Agents -

• Mucous blockers – Mast Cell stabilizers - blocks production of mucous i.e. chronic asthma

• Chromolyn Sodium(Intal, Nasalcrom) • Dosage 20 mg. 2 ml unit dose 2-4 times per day • Used for persistent asthma with secretions • MDI – QID dose

• Tilade – Nedocromil Sodium – QID MDI

• Hypertonic Saline – for CF as therapy forces fluid to come out of cells to dilute the muous

• Side effects airway irritation & hemoptysis

• Mucolytics – break down proteins to thin secretions

• Acetylcysteine – Mucomyst , Mucocil – • Dose 3 ml 10% solution • May be instilled ( most effective to remove plugs) as well as nebulized • Liquefy thick secretions • Irritation to airways – not recommended for long term use • Aerosolized drug – leaves sticky film on tubing, filters, and internal ventilator sensors

Dornase Alfa – Pulmozyme (used in Cystic Fibrosis patients) (Egan Figure 35-5) • 2.5 mg unit dose 1-2 times per day • use separate nebulizer do not mix with other aerosol meds • Clone of Pancreatic Dornase – missing in CF patients • Reduces viscosity in infected secretions. • Natural enzyme with few side effects • More expensive then other mucolytics

68

Aerosolized Anti-infectious Agents: (Egan Table 35-8 page 732)

• Pentamadine Isethoionate: Nebupent- antiprotozoan agent to treat Pneumocystis carinii (PCP) pneumonia in immune compromised patients i.e. AIDS. • Indication : • Second line therapy to prevent PCP in high risk patients ( HIV +) • Previous PCP episodes • CD4 ( T4 cell helper) lymphocyte < 200/ mm • Has been shown to be effective if given in IV form ( eliminates exposure issue with aerosol) • Dosage: • 300 mg powder in 6 ml sterile h20 once every 4 weeks • Hazards / side effects : ( similar to symptoms of PCP) • Respiratory – • Bronchial irritation & bronchospasm (what could be done to minimize this?) • Dizziness, nausea, rashes, metallic taste • PCP symptoms – night sweats, chills • Renal Failure • Staff exposure issues / nebulizer requirements • MMAD 1- 2 um • “respirgard” filter on exhalation – prevent aerosol exposure • negative pressure room or isolation chamber ( Aerostar) • HEPA fit tested mask

• Ribaviran (Virasol): antiviral – tx. For Respiratory Syncytial Virus ( RSV)

• Indications:

• Treat seasonal RSV ( self limiting respiratory disease in infants & children • questionable effectiveness vs. cost

• hazards / precautions • rashes, conjunctivitis, eyelid erythema • Can effect or occlude ventilator expiratory valves or filters (what precaution should be taken if this is nebulized inline on a vent pt?) • Small Particle Aerosol Generator ( SPAG) large volume small particle nebulizer required to deliver to small aerosol to small airways • Expiratory “ respirgard” filter to minimize staff exposure • RSV patients – respiratory / aerosol isolation – mask

• Dosage – 6 g in 300 gm sterile h20(20mg / ml) via SPAG q 12 -18 for 3-7days

69

• Tobramycin (TOBI) : antibiotic – pseudomonas aeruginosa pneumonia

• Indication: - • Chronic Pseudomonas – common infection in chronic respiratory disease patients such as CF

• Hazards / Precautions ( Egan Box 29-5) • Cannot be mixed or nebulized with other aerosolized medications • Less side effects with aerosolized TOBI • Possible ototoxicity ( hearing damage) • Staff exposure issues – filter, thumb valve / PARI neb,& isolation mask • Fetal harm – avoid exposure to pregnant women • Bronchospasm & airway irritation

• Dosage: 300 mg / 5m l ampule ( adults & children > 6 ) ( 20 30 mg in NICU) BID – 28 days on & 28 days off

• Zanamivir ( Relenza): antiinfluenza agent – antiviral – neuraminidase inhibitor

• Indication : treatment for high risk ( cardio – pulmonary disease) patients for influenza A+B • Binds Virus agents together to prevent spread of disease • Hazards / precautions: • Bronchospasm • Allergic reactions • Under treat of underlying bacterial infection hidden by viral infection • Dosage : • Dry powder dose – 5 mg per inhalation BID x 5 days

• Amphotericin B: antifungal agents – No FDA approved aerosolized antifungal agents

• Indication: Treat patients at risk(i.e. CF, Lung transplant , & chronic steroid use.) from fungal infections & minimize toxic effects of systemic antifungal agents –

• Dosage – no standard dose response yet.

• Colistimethate Sodium – Colistin – Treatment for sensitive strains of Pseudomonas Aeruginosa ( CF) and for Acinetobacter baumanni • Side effects- • bronchospasm – • eliminated through urinary system • Neurotoxic – and neuromuscular blockade – possible respiratory failure

70 New Directions for Aerosolized Medications Inhaled Pulmonary Vasodilators – indicated for Pulmonary Hypertension

Treatment for Pulmonary Arterial Hypertension PAH for in adults with ARDS or PPHN in NICU INOmax – Inhaled Nitric Oxide – inhaled gas @ 10 - 40 parts per million • Selective Pulmonary Vasodilator • Active agent for smooth muscle relaxation = vasodilation • Combines with oxygen quickly – eliminated as Meth hemoglobin

Nebulized Prostaglandins- a prostaglandin (a hormone-like substance that occurs naturally in the body). Prostaglandins help to control functions in the body such as blood pressure and muscle contractions.

Veletri - Epoprotenal Epoprostenols -

Ventavis – Iloprost – • Administered with I-neb or Prodose nebulizer • Synthetic prostacyclin PGi = pulmonary vasodilation • Side effects – syncope , cough, and headaches

Flolan - epoprostenol sodium

What is Sildenafil? What is its role in PAH treatment?

Antidiabetic Agents

Exubera – inhaled human insulin • Not indicted for COPD, lung disease, or smoking patients

71 RT 3 Module 3 Oral Airway Medications (Egan’s table 25-3 page 530 & 531 summary table of treatment of Asthma or COPD)

Systemic Corticosteroids: Prednisone • Respiratory Indications: (suppress inflammation) • Initial assessment of COPD • Acute exacerbation of COPD • Severe chronic asthma – failure to respond to inhaled steroids or other meds. • Idiopathic Pulmonary fibrosis – bronchiolitis common

• Hazards / Precautions: • Edema / fluid retention– “moon face” • Petechia – small hemorrhage or blood vessel rupture near skin • Osteoporosis • Immune suppression – increase infection risk – esp. respiratory of opportunistic organisms

• Dosage: (0.5 – 1.0 mg / Kg / day) • Typical dosage 5 – 50 mg per day for 10 – 14 days • Dosage is typically reduced slowly = wean patient off • Tablets – 1,5,20, & 50 mg How would you assess that the effectiveness of the Prednisone therapy?

Methylxanthines: aminophylline / theophylline – Thodur, Slo Bid

• Indications: ( questionable results) • COPD – debilitating COPD despite other treatments • Acute severe Asthma – controversial older method – not common front line therapy • Nocturnal Asthma • Apnea of prematurity – used in NICU on premature neonates to prevent apnea

• Hazards / Precautions: • Must be in therapeutic range to be effective – 8 – 10 mg / ml ( blood level) • Above therapeutic range = toxic > 15 mg / ml • Toxic levels can cause cardiac arrhythmias • High levels can be increased by : • Hepatic metabolism disorders • Acute viral infections • Cardiac failure • Drug interaction i.e. erythromycin, cimetidine • Low levels can be caused by • Cigarette smoking • Phenobarbital ( increase liver clearance ) • Nausea, vomiting , tremors, palpitations, headaches, seizures

• Dosage – based on maintaining blood level in therapeutic range 8-10 mg / ml • 300 – 1200 mg mg / day divided by Q6 to until therapeutic range is reached

72 Anti-leukotrienes – (Egan Table 35-6) now over the counter allergy treatments.

Non-Steroidal Antiasthma Agents - stops cascade of inflammation Singulair (Helps to relieve a broad range of seasonal allergy symptoms for a full 24 hours • Is a seasonal allergy medicine that specifically blocks leukotrienes, an underlying cause of allergy symptoms • Is a once-a-day tablet • Is available in oral granules and cherry chewable tablets for children as young as 2 years • Is approved to help control asthma • Is not a steroid

Zyflo, (Zieluton)

Accolate (Zafirlukast) (age 5-11) or 20 mg (12 – adult) twice a day

Xolair (Omalizumab) - allergy tx for ages 12 & above was approved in 2003 as a new class of therapy, known as anti-IgE, for patients with moderate to severe persistent allergic asthma. IgE is an antibody that we all have and it is responsible for causing allergic problems in some people. It may reduce allergic reactions by causing free IgE to disappear from the body so that the IgE cannot attach to pollen (and other substances that are present). Used for controlling persistent asthma – not for rescue

73 RT 3 Module 4 Airway management Clinical Objectives: • Perform & assist intubation & extubation safely • Obtain sputum specimen • Assess need for artificial airway • List & explain hazards of airway suction • Assess proper placement of artificial airways • Assist with bronchoscopy • List & explain complications of insertion of artificial airways

Basic skills in airway management

• Airway Clearance • Suction • Oral Pharyngeal • Nasal tracheal • Endotracheal

• Artificial Airway Insertion • Oral pharyngeal • Nasal Pharyngeal • Endotracheal

• Assist in performing special airway procedures • Bronchoscopy

Suctioning: use of negative pressure to remove secretions from Upper airway – main stem bronchi

Bronchoscopy – use of suction to remove secretions or specimens from beyond main stem bronchi

Airway suctioning (Egan AARC guidelines box 36-1 page 741)

• Oral airway suction – use rigid suction ( Yankauer) tube – suction above vocal cords

74

• Indications: • Large amount of secretions or soft foreign body obstruction • Minimize oral secretions from pooling around cuff of ETT • Minimize oral secretions draining into lungs esp. with uncuffed ETT’s ( i.e. neonate) • Minimize risk of aspiration for oral / gastric secretions into lungs • Prior to deflating cuff for ETT reposition or extubation • Good oral care minimizes need for invasive endotracheal suction • Decrease risk of VAE ( formerly VAP) Hazards/ precautions – What are three possible risks for oral suction?

• Endotracheal Suction – flexible suction to remove secretions from trachea - main stem Bronchi • Indications : • Inability to generate an effective cough • Evidence ( x-ray ) of retained secretions • Increased PIP on VC or decreased VT on PCV • Visible or easily heard secretions in airway • Obtain Sputum specimen • Suspected aspiration of oral or gastric secretions

• Hazards: • Hypoxia: Why? = Loss of FRC / Increased Atelectasis • Vagal nerve response: What are the 2 most common vagal responses? • Airway spasm • Bleeding • Increased ICP • Pain • Interruption of mechanical Ventilation • Infection – invasive

•

75 Equipment : (Egan Box 36-1 page 742) • Suction – wall suction vs. electric ( Gompco) • Suction regulator: What pressures are safe for Adults, pediatrics, & neonates? o Adults 100 – 120 mm Hg o Children 80 – 100 mm Hg o Infants 60 – 80 mm Hg • Secretion trap • Sterile gloves • Standard precautions – goggles????? • Oxygen • Sterile saline for lavage • Sterile h20 to clear tubing • Suction catheter – size?? Adults 12 – 14 fr, Pediatric 10 – 12 fr , neonatal 6-8 fr o Adults & peds – inner diameter x 2 then use next size down o Neonates ETT size chart Weight Tube Size Oral Tube Length at Lip Nasal Tube Length at Nose Suction Tube Size (kg) (mm) (cm) (cm) (Fr) <1.0 2.5 5.5 7.0 6 1.0 2.5-3.0 6.0 7.5 6 2.0 3.0 7.0 9.0 6 3.0 3.0 8.5 10.5 6 3.5 3.0-3.5 9.0 11.0 8 4.0 3.5 9.0 11.0 8

• Single use Suction Catheter kits • Components of a catheter ( Egan Figure 36 -2) • What is a “Murphy hole” • What does the position of the holes effect?

76 Closed Suction Catheter Kits (indications – Egan Box 36-2)

•

• • • • • • • • • • Advantages: • Decreased infection control issues – patient & staff • Reusable system – cost effective • Ventilator circuit is not opened = minimal O2 , PEEP, FRC ,heliox, or Nitric oxide loss • Easily Performed by one person • Easy to instill saline lavage • Can measure depth of catheter for insertion – color coded

• Disadvantages: • Initial Cost > than 1or 2 suction kits • Additional weight on ETT. What is the risk to the patient? • Catheter can be left in ETT= airway obstruction. What clinical signs would indicate this? • Potential leak in Ventilator circuit = vol. loss. How could you tell if the catheter leaks? • Less control / stiffer catheter = potential inability to reach deep into airway • Airway damage from catheter hitting same location

• Procedure: • Assess for indications & potential risk • Assemble equipment • Pre-oxygenate or hyper ventilate. What are the risks? What techniques can you use? • Insert catheter – How do you determine correct depth? Sterile technique? • Apply suction – 10 15 seconds. Rotate during withdrawal. • Patient recover & reoxygenate • Reinsert catheter – sterile technique? Rinse catheter? • Monitor patient

77

• Minimizing Risks: • Atelectasis • Minimize suction time • Minimize suction pressure • Hypoxemia – What clinical symptoms / problems can hypoxia cause? • Hyper oxygenate • Maintain PEEP – avoid hand bagging, Closed suction • Airway trauma • Use Correct suction depth – don’t bang on the carina • Soft catheter – i.e. red robin • Murphy hole arrangement • Correct suction setting • Airway obstruction • Check catheter is completely withdrawn • Infection – Sterile technique, closed suction, good oral suction

• Nasotracheal Suction – (Egan’s Box 36-2 page 745 AARC Guideline) Most important trick is to keep patient’s head in sniffing (Peds) or hyperextended adults = opens the airway (just like CPR)

What position does the RN put the patient’s head in when inserting an NG tube? • Indication: retained secretions without an artificial airway

• Hazards / precautions • Same as endotracheal • Upper airway bleeding & trauma – List 3 techniques that can use you minimize this? • Contamination of lungs ( sterile) with upper airway secretions ( non sterile)

• Oral Tracheal Suction – use of an oral airway

78

• Sputum Collection: ( via suction) • Indication: ineffective cough to produce secretions because of weakness or artificial airway

• Equipment: • Sputum trap ( Luken’s trap or De Lee) ( Egan figure 33-5) • Saline for lavage – Why can’t you use sterile h20 to lavage or rinse the specimen?

• Is a nasal tracheal specimen considered a sterile specimen? • Is a NT suction specimen the same as an “induced” specimen? • What is an induced specimen? • How is a sputum induction performed? What equipment medication / solution is used? Why? • What are 2 indications for an induced specimen? • What are the hazards or risks of a sputum induction?

• What precautions can you take to minimize the risks?

79 Bacterial growth in secretions and on suctioning equipment of orally intubated patients: a pilot study American Journal of Critical Care, March, 2002 by Mary Lou Sole, F. Elizabeth Poalillo, Jacqueline F. Byers, Jeffery E. Ludy * BACKGROUND Contamination of equipment, colonization of the oropharynx, and microaspiration of secretions are causative factors for ventilator-associated pneumonia. Suctioning and airway management practices may influence the development of ventilator-associated pneumonia. * OBJECTIVES To identify pathogens associated with ventilator-associated pneumonia in oral and endotracheal aspirates and to evaluate bacterial growth on oral and endotracheal suctioning equipment. * METHODS Specimens were collected from 20 subjects who were orally intubated for at least 24 hours and required mechanical ventilation. At baseline, oral and sputum specimens were obtained for culturing, and suctioning equipment was changed. Specimens from the mouth, sputum, and equipment for culturing were obtained at 24 hours (n = 18) and 48 hours (n = 10). * RESULTS After 24 hours, all subjects had potential pathogens in the mouth, and 67% had sputum cultures positive for pathogens. Suctioning devices were colonized with many of the same pathogens that were present in the mouth. Nearly all (94%) of tonsil suction devices were colonized within 24 hours. Most potential pathogens were gram-positive bacteria. Gram-negative bacteria and antibiotic-resistant organisms were also present in several samples. * CONCLUSIONS The presence of pathogens in oral and sputum specimens in most patients supports the notion that microaspiration of secretions occurs. Colonization is a risk factor for ventilator-associated pneumonia. The equipment used for oral and endotracheal suctioning becomes colonized with potential pathogens within 24 hours. It is not known if reusable oral suction equipment contributes to colonization; however, because many bacteria are exogenous to patients' normal flora, equipment may be a source of cross-contamination. ********** Pneumonia is the second leading cause of nosocomial infection in the United States. (1) According to the Centers for Disease Control and Prevention (CDC), (2) median rates of ventilator-associated pneumonia (VAP) are 4.2 to 16.3 cases per 1000 ventilator days in adult critical care units. Rates for VAP are highest in trauma, burn, and neurosurgical units. (2) The estimated occurrence of VAP in critical care units is 10% to 65%, with mortality rates of 20% to 70%. (3-8) when VAP occurs, the likelihood of death increases 3- to 4-fold. (7) In recent studies, (8,9) VAP increased hospital length of stay by 16 to 17 days and increased costs by almost $30 000 per case. Assessment of potential risk factors for VAP is important so that strategies to reduce risk can be implemented. The CDC (1) groups risk factors for nosocomial pneumonia into 5 categories: host factors, surgery, medications, invasive devices, and respiratory equipment. Harris et al (10) proposed that 3 factors contribute to VAP in trauma patients: host, treatment-related, and infection control-related factors. These factors lead to either inhalation or aspiration of pathogens into the respiratory tract. Research on the potential role of airway management in the pathogenesis of VAP is limited. Airway management includes maintenance of the artificial airway (use of an endotracheal tube or tracheostomy), suctioning of the artificial airway and the mouth, and related care such as oral hygiene. Because most instances of VAP are due to aspiration of bacteria from the oropharynx, (1) airway management practices may influence development of VAP. The purpose of our study was to identify potential pathogens in oral and endotracheal aspirates and on suctioning equipment that may contribute to VAP. The 3 research questions were as follows: 1. What potential pathogens for VAP are cultured from oropharyngeal and endotracheal aspirates of intubated patients? 2. What potential pathogens are cultured from oral suction devices (ie, Yankauer suctioning tube), the internal lumen of the common connection section of the suction tubing, and the distal connection of the in-line suction catheter? 3. How/where is the tonsil suction device stored? Background and Significance Aspiration of secretions into the lower part of the respiratory tract is a risk factor for pneumonia. (1,6,10-12) Many potential pathogens endogenous to the normal oral flora, such as Staphylococcus aureus and various species of Streptococcus, may be introduced into the lower part of the respiratory tract during intubation. (7,13) Once a patient is intubated, microaspiration of secretions from above the cuff of the endotracheal tube may occur. Oral secretions can be colonized with endogenous and/or exogenous pathogens. Exogenous pathogens, such as gram-negative bacteria and antibiotic-resistant organisms, can be introduced into a patient's mouth secondary to lack of handwashing and through

80 devices such as oral suctioning equipment. (1) Some organisms, such as Pseudomonas, can be transmitted either endogenously or exogenously. A review by Kollef (6) on the epidemiology and prevention of VAP emphasized the role of subglottic secretions in the development of VAP. As secretions pool above the cuff of the endotracheal tube, bacteria and secretions can gain access to the lower part of the respiratory tract by leaking around the cuff. Oral secretions may become the subglottic secretions that pool above the cuff and lead to microaspiration of secretions into the lower parts of the airway. Bonten et al (14) reported that oropharyngeal colonization and duration of mechanical ventilation were the most important risk factors for VAP caused by enteric gram-negative bacteria and Pseudomonas. Other factors that may contribute to microaspiration include sedation, decreased level of consciousness, and use of nasoenteric tubes. (10,15) Today, endotracheal suctioning is commonly performed with in-line (closed) suction catheters. (16) Although research on in-line suctioning is limited, cited advantages include prevention of suction-induced hypoxemia, convenience, decreased exposure of healthcare staff to patients' secretions, and cost-effectiveness when patients require frequent suctioning. (17- 21) Since the advent of in-line suctioning, the procedures for oral and endotracheal suctioning have changed. Historically, a single-use sterile catheter was used to suction secretions from the endotracheal tube. Once secretions were cleared from the endotracheal tube, the same catheter was used to suction secretions from the oropharynx, and then the catheter was discarded. The in-line catheter is designed only for suctioning secretions from an endotracheal tube or tracheostomy. Another device is needed to suction secretions from the oral cavity. Many caregivers use reusable equipment, such as a tonsil suction device (eg, Yankauer device), to suction the oral cavity. In addition, the suction connecting tubing and the suction canister are often used for both the in-line catheter and the tonsil suction device, requiring that the in-line suction catheter be disconnected from the suction tubing when oral suctioning is done. Rinsing of both in-line and oral suctioning devices is recommended after use (17,22); however, rinsing is not consistently done, and secretions often accumulate in the suction devices as well as in the connecting tubing. (18,23) No standard for storing the tonsil suction device exists. Studies on colonization of in-line suctioning equipment are limited. In-line suction catheters become colonized with bacteria as soon as the catheters are used on patients; however, the catheters have not been associated with an increased risk of pneumonia. (24) In one study, (9) use of in-line suctioning reduced the prevalence of VAP. Prolonged use of ventilator tubing and in-line suction devices has been recommended to reduce the prevalence of VAP (25); however, devices and equipment for management of oral secretions were not examined. Product literature (26) for in-line suctioning equipment states that the tubing used for suctioning should not be used for both bronchial and oral suctioning; however, no data are published to substantiate that claim. In-line suctioning practices may contribute to the pathogenesis of VAP. First, the mouth is not usually suctioned after each episode of endotracheal suctioning. Secretions then may pool in the oropharynx and contribute to microaspiration and VAP. Second, the reusable tonsil suction device may become colonized from bacteria exogenous to a patient's normal flora and contaminate the oropharynx. Third, using the same suction tubing for both oral and endotracheal suction devices may lead to contamination of the in-line suction catheter at the common connection between the 2 devices. Figure 1 shows the proposed role of airway management in the management of VAP.

81 RT 3 Module 4 Airway Management Artificial Airways

Pharyngeal airways: (Egan Box 36-3 page 745 AARC guidelines of airway emergencies) • Indications: to prevent obstruction of pharyngeal airway caused by: • Tongue falling back – pharyngeal airways pull the tongue forward away from posterior pharynx. • Loss of muscle tone in unconscious patient causes tongue to fall back • Can be used to secure ETT & prevent obstruction of ETT due to biting • Upper airway trauma • Assist in Bag mask Ventilation – Apnea & CPR • Assist in nasal tracheal or oral tracheal suctioning • Temporarily stabilize unusual upper airway anatomy i.e. coanal atresia – Pierre Robin syndrome • Massive secretions or hemoptysis in oral pharynx

• Oral Pharyngeal airways: (Egan chapter 33 figure 33-6 ) • Insertion techniques( Egan Chapter 34 – Basic Life support) • Inserted into mouth & over tongue • Initial insertion is with tube upside down then twisted into position as it is inserted past the tongue. (tongue may also be displaced using a tongue depressor) • Jaw Trust maneuver may also be used to assist insertion

• Size selection – corner of the mouth to the angle of the jaw

• Airway types – • Guedel – single airway down middle of tube • Berman – 2 channels down each side of the airway

• Hazards / precautions – List 3 physiologic responses can occur when inserting & placing an oral airway? • Contraindicated for conscious or semi conscious patients****

82 Nasal Pharyngeal airways • Indications – when oral airway cannot be used • Semiconscious or conscious patient • Unable to open jaws • Severe oral airway trauma • Assist with nasal tracheal suction

• Insertion Technique – what should be used to minimize nasal airway irritation & bleeding before the airway is inserted? What position should the patient’s head be in?

The insertion of a nasopharyngeal airway involves the following steps: 1. Determine and select the correct tube length by measuring from the tip of the nose to the earlobe. Use a tube with the largest outer diameter that will fit the patient’s nostril. 2. Lubricate the tube with water, water-soluble jelly, or lidocaine jelly, which will alleviate discomfort ******( what special risk is associated with topical Lidocain)?. 3. Reassure the patient and familiarize him or her with the procedure. 4. Insert the airway into the nostril up to the end of the nasal trumpet. 5. Have the patient exhale with the mouth closed. (If the tube is in the correct position, air can be felt exiting from the tube opening.) 6. Open the patient’s mouth, depress the tongue, and look for the tube’s tip just behind the uvula.

• Size selection (26-32 french) • Diameter- size of the nail bed on little finger • Length – earlobe to tip of nose

83 Laryngeal Mask airways – LMA’s

84 Laryngeal masks are used in anesthesia and in emergency medicine for airway management. They comprise a tube with an inflatable cuff that is inserted into the pharynx.

• They cause less pain and coughing than an endotracheal tube, and are much easier to insert. However, a standard laryngeal mask airway does not protect the lungs from aspiration, making them unsuitable for anybody at risk of this complication.

• The device is useful in situations where a patient is trapped in a sitting position, suspected of trauma to the cervical spine (where tilting the head to maintain an open airway is contraindicated), or when intubation is unsuccessful.

• The device sits tightly over the top of the larynx. It avoids tracheal intubation and can be used with spontaneous respiration or artificial ventilation.

• However, it may not protect the airway from the aspiration of regurgitated material.

• It has found favor in day case surgery. Patients who have been treated with a laryngeal mask airway claim it does not irritate the throat as intubation typically does.

• If use of a laryngeal mask airway is not suitable or appropriate, an endotracheal tube may be used to facilitate ventilation and prevent aspiration

85 Combi - Tube

86 King Airway

• You tube video http://www.youtube.com/watch?v=ca710sG4-ck

87 Tracheal airways – (Egan table 36-1 Advantages & disavantages of treacheal routs page 750 ) Tracheostomy (surgically inserted into trachea) & Endotracheal tubes (oral or nasal tubes inserted through pharynx into trachea). What physiologic systems are bypassed?

• Endotracheal Tubes

• Indications: Emergency or short term artificial airway. How long an ETT should be used? • Assist with mechanical ventilation • Improve effectiveness of bag ventilation • Provide stable airway in unconscious or semiconscious patient • Apnea • Foreign body obstructions • Upper airway edema – (emergency tx only) • Assist with endotracheal suction - copious secretions & pt. is unable to remove effectively

• Oral intubation advantages • Insertion is faster • Less trauma to nasal airway • Tolerates larger tube = decreased airway resistance ( Poiseuille’s law) • Less nasal inflammation=Decreased inflammation & nasal secretions i.e. sinusitis • Easier passage of bronchoscope

• Nasal intubation Tube advantages • More comfortable over long term use • Less gag & retching • Easier to keep tube secured • Insertion can be performed blind (with minimal sedation) • Easier & more effective oral care • Patient cannot bite ETT – no need for oral airway

• Specialized ETT tubes ( Egan figures 33 -7– 9) • Double lumen tubes • Used to ventilate only one lung. Why? • Used to assist jet high frequency ventilation

88 • ETT tube components – what are the functions of the following? • Pilot balloon • Cuff – high vol. low pressure • 15 mm adapter • tapered tip • I.D • O.D. • Centimeter marks • Murphy holes • Radiopaque indicator marks

EET tube sizes (Egan Table 36-2 Size & lip position guidelines page 753)

• Neonate 2.5 – 4.0 position 6-10 cm at the lip based on weight & gestational age • Pediatric 4- 6.0 • Small adult or ped > 16 yr. 6.5 – 7.0 • Women 7.5 – 8.0 position 19- 21 • Men 8.0 – 9 (although 7.5 is still very common) position 21 -23 • Height is the most important factor not weight

Tracheostomy tubes: - long term use – requires surgery - (Egan page 761 Comparison of Trach’s & Percutaneous vs. Open surgery) • Indications: • Long term artificial airway • Assist with mechanical ventilation • Chronic ineffective cough i.e. neuromuscular patients • Permanent upper airway obstruction • Radical neck surgery – i.e. cancer, trauma, burn • Emergency laryngeal edema i.e. epiglottitis

• Advantages: • More comfortable over long term use – eliminates oral hygiene & pain issues. • Patient can be fed • Patient “looks” better – face is not obstructed • Easier to keep secured • Easier to reinsert or exchange - RT procedure using obturator • Can use uncuffed tubes – What are the advantages of an uncuffed trach? • What is a Jackson trach? • Patient can talk – i.e. fenestrated tubes & passey Muir speaking valves 89 What is a percutaneous dilation mean? What does Trach care mean? What does changing a trach mean? Can an RT change a trach? What does plugging a trach mean? What is a trach button? What does trach decannulation mean? What is a Passey Muir valve? What is the most important safety rule before using a PMV?

• Hazards / precautions: • Infection control – i.e. colonization of pathogens ( Egan Box 36– 7 page 768) 90 • Tracheal injury ( Egan’s figure 36-33 page 769) • Hemorrhage – erode innominate artery • Permanent scar • Greater expense – why? • Persistent open stoma • Bypass upper airway humidification • Reduce airway diameter = fixed increased airway resistance

91 Cuff Pressures & volumes – Egan Figure 36-34 page 769)

• When should a cuff be inflated? • What is the appropriate Cuff Pressure? Why?

o Hint 30 cm H20 = 22 MMhg • What is minimum occluding volume technique? • What is minimal leak technique? • Alternative cuffs – used to minimize mucosal trauma • Foam cuffs • Lanz tube – self regulating external valve

Cuff Pressure  Minimal Occluding Volume

 Minimal Leak Method

 Direct Measurement

Cuff leaks (36-8 page 774 – Cuff Leak Algorithm) What are the causes cuff leaks? How can you tell which one is the cause and how do you fix it?

 Low volume in the cuff

 Hole in cuff

 Leaking pilot balloon

 Cuff is inflated in the upper airway

Trach Tube size (Egan’s table 36-5 page 762)

 Neonates 2.5 cuffless  Infants 3-3.5 cuffless  Pediatric 4-6.0 – age /4 + 4 = size  Adults 6-9.0 cuffed

92

• Routine Trach Care: ( Egan Box 36 – 8 page 771) How often is trach care performed?

• Changing a trach tube ( Egan page 772 ) • Indications: • Changing to smaller size – i.e. weaning patient off trach • Changing to same size – or changing to fenestrated tube • Changing tube to replace leaking cuff (Egan figure 33 -31 & 32 ) • Unable to repair leaking pilot balloon ( Egan figure 33 -31)

• Securing ETT’s & Tracheostomy tubes • Note ETT tube position before securing tube – cm mark compared to????

• Adhesives??? What are the risks of using adhesives?

• How is ETT placement confirmed?

• What is proper placement of an ETT?

• What are the indications an ETT is too low?

• What ventilator alarms should you observe?

• What are the indications an ETT is too high?

• What ventilator alarms would you observe

• How do you reposition a tube that is 2 low? How many people does it take?

• How do you reposition a tube that is too high? How many people does it take?

93 RT 3 Module Intubation

Alternative techniques to establish an airway (Egan’s table 36-1 Advantages of different tracheal routes page 750)

• Oral Airway • Nasal Airway • Mask Ventilation • Transtracheal Jet Ventilation • Retrograde Intubation • Laryngeal Mask Airway • Light Wand • Blind Nasal Intubation • Combitube • Emergency Cricothyrotomy Devices

INDICATIONS for ENDOTRACHEAL INTUBATION

• Endotracheal intubation is indicated in several clinical situations including • acute hypoxemic • hypercapnic respiratory failure • impending respiratory failure – If Non Invasive is ineffective or not indicated • This procedure is also used to protect the airway in conditions of upper airway obstruction, either mechanical or from airway pathology. • Patients at risk for aspiration, most commonly from central nervous system derangements may benefit from elective intubation. • Performed for many operative procedures; at times to facilitate certain diagnostic procedures (ex. computed tomographic scan /bronchoscopy); and to aid in respiratory hygiene. • Another potential indication for EI includes the need to hyperventilate by mechanical ventilation, attempting to reduce intracranial pressure

AIRWAY ANATOMY

Endotracheal intubation can be performed either orally or nasally, although oral intubation is the more commonly used technique. The nasopharynx and oropharynx lead to the laryngopharynx (hypopharynx). At the base of the tongue, the epiglottis separates the larynx from the laryngopharynx. The epiglottis serves as a protective mechanism for preventing aspiration by covering the opening of the larynx (i.e. the glottis) during swallowing.

The larynx, establishes the boundary of the upper and lower airway. The glottis divides the larynx into a superior compartment (from the laryngeal outlet to the vocal cords) and an inferior compartment (from the vocal cords to the lower border of the cricoid cartilage), which leads to the trachea. In the adult, the airway is narrowest at the vocal cords and in small children at the cricoid cartilage ring.

The trachea begins at the level of the cricoid cartilage and extends to the carina. The carina (at the level of the angle of Louis, about T5) is the point of airway bifurcation, leading to the left and right main stem bronchi. The right main stem bronchus is less angulated from the trachea than is the left 94 main stem bronchus (25 versus 45 degrees) and therefore is more prone to intubation if an endotracheal tube (ETT) is inserted too far.

EQUIPMENT (Egan Box 36– 3 page 753)

Laryngoscope

The laryngoscope is comprised of 2 separate parts; a handle which contains a light source and a blade. Blades are either curved (Macintosh) or straight (Miller):

Macintosh blades come in sizes 1-4, with an average adult requiring a size 3.It is inserted anteriorly to the epiglottis into the vallecula. The advantage of this blade is that it minimizes trauma to teeth, does not come in contact with the epiglottis and allows more room in the oropharynx.8However, with this blade the epiglottis may be in the way of visualizing the vocal cords. Miller blades come in sizes 0-4 with sizes 2 and 3 fitting an average adult. 8Straight blades are inserted posterior to the epiglottis, thus providing better visualization of the larynx. 8

Endotracheal tubes

Endotracheal tubes (ETT) are sized by either the internal diameter (2.5 to 10 mm) or the external diameter with sizes 2-9 French (Fr).Usually, adults use size 7 to 9 Fr ETTs. Smaller size ETTs are easier to insert, but larger size tubes have less airway resistance and allow for better suctioning and less work of breathing. A stylet can be inserted inside the ETT to help the tube conform to the airway and may facilitate insertion into the larynx and trachea. However, stylets have been associated with pharyngeal or laryngeal trauma.

Medications

Proper sedation should be used in all conscious and hemodynamically stable patients. In addition, neuromuscular blockers are often used to facilitate intubation.

What side effects does sedation typically cause?

95 Emergency Equipment

Resuscitation equipment, medications, oxygen, and alternative airway equipment should always be readily available during all intubation procedures.

PATIENT ASSESSMENT

Once it is determined that a patient requires EI, an assessment of the airway is necessary. Difficult intubation is a potentially serious complication of EI and patients should be examined for signs of a difficult airway. Table 2 lists signs of potential airway difficulties. If a patient is suspected of having a difficult airway, an immediate consultation with an expert in airway management should be made. However, in an emergency situation or when a difficult airway is not anticipated, a clinician may be required to manage a patient’s airway until appropriate help is available.

Signs of potentially difficult airways.

• Difficulties with positioning of the neck: arthritis, trauma, or previous surgery

• Anatomical variations: small mouth, large tongue, bull neck, receding lower jaw, high arched palate, marked obesity

• Limitation of mouth opening

• Stridor or other signs of upper airway inflammation from epiglottitis, laryngeal infection or burn

• Trauma to the larynx or trachea

• Congenital malformation of face, head and neck

PREPARATION

Prior to performing EI, all equipment, medication, emergency supplies, and support staff should be in place. In addition, patients should be monitored before, during and after intubation for blood pressure, heart rate, and pulse oximetry. Continuous pulse oximetry has been shown to reduce the risk of hypoxemia associated with emergency intubation. 11 An ECG monitor should also be used, when available. 5

All equipment should be checked including assembling the laryngoscope to verify a proper light source. If a stylet is used it should be inserted into the ETT with a water soluble lubricant. The end should then be bent to facilitate intubation, ensuring that the style does not protrude the end of the ETT. The balloon should be checked by inflating 10 cc of air with a syringe. An additional ETT (one size smaller), stylet, and laryngoscope should be readily available prior to attempting intubation.

96 TECHNIQUE Basic steps

• Assemble & check equipment • Position the patient • Preoxygenate the patient • Insert laryngoscope • Visualize glottis • Displace epiglottis • Insert tube • Assess position • Stabilize ETT/ confirm placement

The oral route for intubation is preferred since it can usually be performed more rapidly and provides for better visualization. In addition, the mouth can accommodate a larger tube than the nose. Nasal intubation in certain emergency situations can be used with blind insertion to secure the airway. With known or suspected neck trauma or cervical spine instability, nasal bleeding, upper facial fractures, and certain skull fractures, the nasal route is contraindicated. Instead, spine stabilization and use of a bronchoscope with cricoid pressure is preferred.

The patient should be prepared by removing any dental appliances (ex. dentures). Then proper sedation (and neuromuscular blockers, if used) administered. The patient must be positioned so that easy access is obtained. The head is placed in the “sniffing position” with the lower portion of the cervical spine flexed. Preoxygenation is then performed with 100% oxygen for 2 to 3 minutes via bag-mask ventilation.

The laryngoscope must be held with the left hand. The patient’s mouth opened with the right hand and the blade placed into the right side of the patient’s mouth, sweeping the tongue to the left. The tip of the straight blade is inserted posterior to the epiglottis, while the tip of the curved blade placed anterior to the epiglottis into the vallecula. The handle is then raised up and away from the patient without leverage until the vocal cords are visualized. The clinician’s wrist should not be bent as this may cause damage to the teeth. Once the vocal cords are seen, the ETT is passed through cords with the right hand and advanced to 20-26 cm, as measured at the teeth or with the cuff just below the vocal cords. The laryngoscope is then withdrawn and the cuff is inflated.

If intubation is delayed, no more than 30 seconds should pass without ventilation.3Therefore, if intubation is not performed within this time period, the procedure should be stopped and the patient ventilated with bag-mask ventilation prior to reattempting the procedure.

The Sellick maneuver can be used to facilitate intubation and reduce the risk of aspiration. The technique requires an assistant to apply pressure to the cricoid member posteriorly. The cricoid

97 cartilage is held firmly between the finger and thumb. It is then pressed posteriorly so that the esophagus can be compressed between the horizontal portion of the cartilage and cervical spine.

To assess proper placement of the ETT, the chest and abdomen are inspected for movement. If the tube is properly placed, symmetric movement of the thorax with minimal movement of the abdomen should be seen with each ventilation. Breath sounds should first be assessed over the epigastric area and then over left and right lung fields. Equal breath sounds are typically heard bilaterally with proper endotracheal intubation. If breath sounds are heard over the epigastric area only, it is likely that an esophageal intubation has occurred.

If breath sounds are heard over one hemi thorax, but are diminished or absent over the other hemi thorax, the tube should be left in place. The ETT should be withdrawn 2-3 cm and chest auscultated to check breath sounds again. A common complication of EI is right main stem intubation.9Since the right main stem bronchus has a straighter alignment with the trachea than the left main stem bronchus, an ETT advanced too far will typically enter the right main stem bronchus. In this situation, breath sounds may be heard more prominently or exclusive over the right lung field. Although a deep ETT placement is the most common case of unequal breath sounds, it is important to remember that other clinical conditions can cause unequal breath sounds including consolidation, obstruction, pneumothorax, hemothorax, and pleural effusion.

ETT placement can also be confirmed by use of an end-tidal CO2monitoring. A chest radiograph should always be done in emergency intubations to confirm ETT placement since equal breath sounds can be heard in up to 60% of right main stem intubations. Fiberoptic bronchoscopy has been suggested as a more reliable means of confirming ETT position over clinical assessment. 16

98 COMPLICATIONS

Complications of endotracheal intubation

• Esophageal Intubation

• Mainstem Intubation

• Perforation or laceration of upper esophagus, vocal cords, larynx

• Laryngospasm or bronchospasm

o How could you tell before you extubate that your patient may be at risk for laryngospasm?

o How could you tell after Extubation?

o What would the treatments be for post Extubation stridor?

• Dental and soft-tissue trauma

• Dysrhythmias

• Hypertension/Hypotension

• Aspiration of oral or gastric contents

99 Extubation Technique (Egan AARC clinical practice guidelines Box 36-3) • Indications • Weaning patient from need of mechanical ventilation. • Removal of obstructed or suspected obstructed ETT. What are the signs of an obstructed ETT? • Removal of ETT to be replaced with tracheostomy tube • Procedure • Assemble equipment – i.e. oxygen, bag & mask, suction, medication???

o How do you choose the correct oxygen device? o What are your options fo oxygen deivice • Preoxygenate patient • Suction ETT • Suction above cuff • Deflate cuff. Is it safe to cut the pilot balloon instead of deflating cuff? • Remove tube – 2 techniques • During deep inspiration • During cough – What are the risks & advantages? • Administer oxygen • Administer humidity or cool aerosol. Why?? • Assess patient ( Egan mini clinic page 690) • What are the 3 major risks / hazards of extubation? • How can these risks be minimized?

100 101

102 103 Fiberoptic endotracheal intubation is a useful technique in a number of situations. It can be used when the patient's neck cannot be manipulated, as when the cervical spine is not stable. It can also be used when it is not possible to visualize the vocal cords because a straight line view cannot be established from the mouth to the larynx. Fiberoptic intubation can be performed either awake or under general anesthesia and it can be performed either as the initial management of a patient known to have a difficult airway, or as a backup technique after direct laryngoscopy has been unsuccessful. As with all other procedures, the keys to the success of this technique involve adequate planning and patient preparation.

Position While the sniffing position is required for most direct laryngoscopies, it is not essential for fiberoptic guided intubation. The chin lift and jaw thrust maneuvers, and protrusion of the tongue, move the soft tissues and improve the view through the fiberscope. These maneuvers also help to prevent airway obstruction in the sedated patient. Most anesthesiologists prefer to stand at the head of the patient, as they do for direct laryngoscopy. The advantage of this position is that anatomical structures are visualized as most anesthesiologists are accustomed to seeing them. Alternatively, the operator can stand in front of the patient, as do most otolaryngologists.

Fiberoptic Endotracheal Intubation Procedure

Indications Anticipated difficult intubation (upper airway abnormality) Endotracheal intubation when neck extension is not desirable (cervical spine injury, rheumatoid arthritis)

Contraindications Inability to oxygenate Major bleeding

Technique

1. Oral route preferable 2. Topical anesthesia with 2% lidocaine on a base of the tongue, hypopharynx and vocal cords (aerosolized 10% lidocaine may also be used) 3. Sedation with midazolam (adult dose 1 to 2.5 mg IV) and fentanyl (adult dose 25-100 mcg IV) 4. "Jaw thrust" maneuver improve visualization 5. Apply oral airway or "bite block" to protect the equipment. Apply 100% oxygen via face mask (oxygen may also be delivered via bronchoscope channel) 6. After the bronchoscope is lubricated and loaded with an endotracheal tube it is introduced strictly in the midline following the base of the tongue, pass the uvula, behind the epiglottis and between the vocal cords. (see video on the left below). 7. Additional topical lidocaine is applied as necessary. 8. Once the main carina is visualized endotracheal tube is introduced by rotating movement over the bronchoscope. Proper position (3-5 cm above the carina) is evaluated and the tube secured. (see video on right below)

104 Advantages Excellent airway visualization Minimal hemodynamic stress

Disadvantages Costs associated with the need for special equipment and skill

Complications Oxygen desaturation Bronchospasm (inadequate local anesthesia)

Glidescope

105 Module 3 Bronchoscopy

Bronchoscopy-(AARC Clinical Practice Guidelines Egan figure 36-5 page 784) Not typically done in NICU due to small airways I. Types – Therapeutic vs. Diagnostic – ( Equipment - Egan Box 36-9)

Rigid Bronchoscope – hollow tube functions as airway and allows ventilation – Preferred method for foreign body removal form large airways

Flexible Bronchoscope – (Egan Figure 36-47) Allows observation of peripheral locations in the lung & avoids mechanical distortion of the airways. Indicated in Diagnostic Bronch’s Diagnostic vs. Therapeutic Bronch’s 1. Suspected Foreign body Foreign body obstruction 2. Suspected pathology secretions/ hemoptysis 3. Congenital abnormality Mass or tumor 4. Persistent problems Atelectsis / edema/

II. Risks A. bleeding B. edema / spasm – broncho & larygospasm C. pneumothorax D. trauma E. hypoxia – what are the 3 most likely causes?

106 107 Broncho alveolar Lavage BAL

108 Module 3 Thoracentesis & Special Procedures 1. Fluid removed form pleural space – needle in 6th- 8th intercostal space 2. Sitting up position if possible 3. 22-23 gauge needle for local anesthesia 4. Needle inserted just above rib to avoid nerves & vessels that run below ribs 5. 16 gauge needle for evacuation 6. Therapeutic – remove fluid to reduce cardio-pulmonary stress 7. Diagnostic – A. Clear, serous, or transudate associated w/ CHF B. Opaque, milky, cloudy, bloody or exudate fluid associated w/ infections, trauma, tumors – indicates need for cytology & chemistry testing Chest Tubes – Tx for gas or fluid in pleural space. > 20 % I. X-ray determination – dark w/ lung markings = air , white = fluid II. Medistinal shift III. Unequal BS – hypoxia IV. Insertion of large needle – emergency w/ stop cocks – needle aspiration using transilluminator – showing “Halo” V. Air drainage – tube inserted on anterior chest 2nd intercostal space @ mid clavicular line VI. Fluid drainage – 4-5thintercostal space mid axillary VII. More the one chest tube may be inserted into same space – “new coiling “ types of tubes increase surface area for sx

109 Suction Chest Drainage systems Water seal system to secure low pressure sealed suction – 1, 2, 3 bottle or disposable setups I. Collection chamber – proximal to pt tubing collects pleural drainage II. Water seal chamber – 2cm of water – shows respiration effort (spont vs. mechanical) & air leaks if bubbling III. Suction Control chamber – level of water determines amount of suction pressure usually 15 – 20 cm – bubbling show max suction achieved – excess air bubbles through water IV. Chest is placed on water seal without suction for 24 hours prior to removal V. Instruct pt to exhale & valsava during removal VI. 10% pneumo’s w/ minimal symptoms are usually not treated or may be treated w/ 100% N2 washout VII. 20% pneumo w/ symptoms usually indicates chest tube chest x-rays indicated w/ increase resp and post removal

110 Heliox Instructions • Indication – acute upper airway obstruction i.e.. Foreign body , mass or tumor or severe asthma airway obstruction • Delivery method – • Non Rebreather with humidifier • Circulaire nebulizer • supplemental oxygen – a 6 l o2 nasal cannula of may be used along with Heliox • Heliox Delivery % • 60% He & 40% O2 • 70% He & 30 % O2

Set Flow to keep reservoir bag inflated during peak inspiration. Flow rate conversion 1:4 to 1 l/ min – Heliox is less dense so actual flow is higher than set flow.

Contraindications / Hazards – • SpO2 <92% on 6l n/c & 60% He / 40% O2 non Rebreather (discontinue Heliox and return to 100% Hi Flow O2)

• Do not use in line with any Puritan Bennett ventilator

• Never Use Heliox without humidity or Aerosol

• Mucous plugging

• To calculate the duration of a K or H cylinder of a Heliox mixture use the following formula: • Duration of H cylinder HeO2= • 2.508 x (gauge reading psig -500 psig safety factor) (Observed oxygen flow meter setting) x (Mixture Conversion Factor) • Example: • Given: Observed Tank Gauge Reading - 1800 psig • Observed oxygen flow meter setting - 10 L/min • 180 minutes = 2.50 x (1800-500 psig) • 10 L/min x 1.805 Change H cylinder when the gauge pressure is 500 psig.

111 RT 3 Module 5 Lung Expansion Therapy Clinical Objectives: • List & explain causes of atelectasis • Identify which patients lung expansion therapy is indicated for • Describe clinical findings seen in atelectasis • Describe how lung expansion therapy works • List & explain indications, risks, hazards, & complications of lung expansion therapy • Describe gas flow & mechanical operation of lung expansion devices • Use critical thinking skills to select the appropriate mode of lung expansion therapy

Lung expansion therapy: a variety of respiratory care modalities designed to prevent or correct atelectasis. These include: (The most common form of respiratory procedures utilized in care of high- risk patients) • IPPB • Incentive Spirometry • CPAP • PEP therapy

Atelectasis: abnormal collapse of distal lung parenchyma (reduced FRC – typically the basal or dependent lobes)

Complications / risks associated with atelectasis: • Pneumonia • Increased length of stay • Decrease respiratory reserve • Reduced surfactant production • V/Q mismatch = hypoxia (Which type of V/Q mismatch is caused by atelectasis?) • Decreased mucokinesis • Low grade fever • Increased pain / splinting

112 Types of Atelectasis • Gas absorption (Resorption) atelectasis: a blockage occurs in the airway- preventing ventilation downstream - resulting in eventual removal of remaining gas & alveolar collapse. If obstruction occurs in a large bronchus = lobar atelectasis What treatment would you recommend?

• Compressive atelectasis: Occurs when something outside the lung presses on lung tissue causing it to collapse. (Egan’s Figure 42-1 page 939) This occurs when there is a decreases in the Transpulmonary Pressure Gradient ( PL) PL = Alveolar Pressure (Pav ) – Pleural pressure (Ppl)

What are the 2 ways to accomplish this using lung expansion therapies?

• Passive atelectasis-: Occurs when patients do not take periodic deep breaths (sighs)

What Patients are “at-risk” for Atelectasis? • Post-op thoracic or abdominal surgery patients • Any heavily sedated patient • Patients who have neuromuscular diseases / spinal cord injuries • These diseases may weaken breathing muscles • Patients who are unable to ambulate / bedridden • Patients with chest trauma or chest wall injury • Poor nutrition / weak patients • Incisions close to diaphragm = increase risk

113 How do we know if someone has an Atelectasis? • “Gold Standard” - evidence of atelectasis on a chest x-ray (CXR) • increase opacity • reduced FRC / lung volume • shift of trachea, heart or mediastinum • elevated diaphragm • displacement of interlobular fissures • crowding of pulmonary vessels • narrowing of space between ribs • air bronchogams ( lung condensed around airways )

• Clinical signs: • Medical history – Identify potential risk What are they? • Increased RR • Auscultation • Fine late crackles • Diminished BS • Fever ( if pneumonia is present) • Tachycardia ( indicates pain or hypoxia)

Lung Expansion Therapy = increased transpulmonary pressure Gradient (P alv – P plueral)

Techniques to increase gas distribution Egan page 251 .

• Fick’s first law of diffusion : V gas =[ A x D ] (P1 – P2) T

• Gas takes time: Hold your breath • Apply pressure evenly i.e. plateau Variable Flow delivery i.e. Ramp flowrate vs. square – Breath slow • Increase pressure gradient – Breath Deep • How would you coach the patient to increase gas distribution?

114 Module 5 INCENTIVE SPIROMETRY (AARC Guidelines Egan Box 42-1) • Used primarily as a preventative or prophylactic treatment • Patient are encouraged to take slow - deep inspirations ten times every hour • Patients are taught to perform 5-10 second breath holds at maximal inhalation for each of the 10 hourly breaths

• Advantages of I.S. Therapy (Egan Boxes 42–1, 2, 3, 4 page 941) • Patients can self-administer as often as they like • Relatively easy to learn and perform • Very rare side effects • Inexpensive way of preventing pulmonary complications

• Reasons Why I.S. May Not Be Appropriate – • Patient is not alert or cannot follow instructions • Patient cannot hold mouthpiece in their mouth • Patient has a large atelectasis that must be treated with more aggressive measures • Patient cannot create a large enough breath for I.S. to be of any real value (VC< 10 cc’s per Kg IDBW)

• Prior to Teaching I.S. do the following: • Check the chart for; • Order; Admitting Dx; evidence of any recent surgery (when?; type?); evidence of any previous pulmonary problems (COPD; asthma?); Chest X-ray reports • At the bedside check for; • mental status; ability to comprehend; pain level; evidence of any pulmonary problems (tachypnea &/or S.O.B.?)

• What to Focus on During I.S. Instruction • What is I.S. • Why is the patient going to learn how to perform it • How often should the patient perform it • Does the patient have any questions

115

• Types of I.S. Devices ( Egan figure 43-3 & 4 ) • Volume Oriented devices • Actually measure & display the amount of air patient inhaled • Requires a large bulky bellows • Now uses a device that is based on flow through a restricted orifice sacrificing accuracy for convient size

• Flow Oriented devices (Tri flow) – Flow x time - volume • Uses flow through a restricted orifice to estimate the volume of air inhaled based on duration of inspiration

116 Module - IPPB Intermittent Positive Pressure Breathing – IPPB (EGAN – AARC guidelines, 42-2 & boxes 42-–6, 7, 8, 9, 10)

(IPPB) as Method of Enhancing Lung Expansion

• Definition - Lung expansion therapy utilizing positive airway pressure for periods of 15 - 25 minutes to enhance resting lung ventilation by increasing the patients tidal volume (VT)

How Positive Pressure Ventilation Differs from Normal • In normal breathing, inspiratory pressures are negative while expiratory pressure are positive • In IPPB, both inspiratory pressures & expiratory pressure are positive

Indications for IPPB • Patient has an atelectasis that is not responding to I.S. therapy • Patient cannot perform I.S. therapy • This may also be a problem with IPPB!! • Poor cough effort & secretion clearance due to inability to take a deep breath • Short term ventilator support when patient is hypercapnic • Enhancement of aerosol medication delivery in patient unable to take a deep breath

Contraindications to IPPB • Untreated pneumothorax • High intracranial pressure (>15 mm Hg) • Active hemoptysis • Radiographic evidence of a bleb • Nausea • Tracheoesophageal fistula • Recent esophageal surgery • Hypotension

117 Hazards & Complications of IPPB • Barotrauma (pneumothorax) • Hyperventilation (dizziness) • Gastric distension (secondary to air swallowing) • Decrease in venous return (possible drop in BP) • Increased airway resistance • May actually cause bronchospasm in some patients!

Monitoring the IPPB Treatment • What is the pulse & respiratory rate prior to treatment? • What are the patients breath sounds; their color; respiratory effort; mental state - prior to the Tx? • What is the patients SpO2 or peak flow before the treatment (if giving bronchodilators) • PIP, Tidal volume, RR, effort, tolerance, position

• mask vs mp vs trach

• sputum production

118 Equipment Needed for IPPB • IPPB Ventilator - • Bennett “PR series” ventilator OR Bird “Mark series” ventilator • IPPB tubing circuit • “Universal” disposable circuits now used • Additional equipment “possibly” needed; • Mouth seal & nose clips for patients who cannot use mouthpiece • Mask (if mouth seal is not available) • Connector for using circuit with trach patient Typical IPPB Ventilators • Bird mark Series • Identify the following : • HIGH PRESSURE INLET • PRESSURE CHAMBER • PRESSURE CONTROL LEVER • AMBIENT CHAMBER • ENTRAINED AIR INLET FILTER • MANUAL ON-OFF CONTROL ROD (red) • SENSITIVITY CONTROL LEVER • FLOWRATE CONTROL KNOB • PRESSURE MANOMETER • AIR-MIX CONTROL KNOB • MAIN BORE OUTLET • SMALL-BORE DRIVELINE CONNECTION • EXPIRATORY TIME FOR APNEA (RATE CONTROL KNOB)

119 Bird Ventilators Description • Bird Mark – 7 • Pneumatically powered assist/controller pressure ventilator for delivery of IPPB therapy.

• Requires gas source of 50 pounds per square inch. • Bird Mark - 8 • Same features as Mark-7 plus adjustable expiratory flow rate providing positive (PEEP)/negative (NEEP) end expiratory pressure.

• Bird Mark - 10 • Leak compensating IPPB ventilator with Mark-7 features.

• Bird Mark - 14 • Leak compensating IPPB ventilator with Mark-7 features plus extended range of flow and pressure.

Puritan Bennett Ventilators • Puritan Bennett AP-4 • Electrically powered IPPB with AP-5 features plus cover and handle modifications for storage and transport. Convenient for homecare or hospital use.

• Puritan Bennett AP-5 • Electrically powered IPPB therapy unit with internal motor/compressor. Ideal for homecare or hospital use. 120

121 IPPB Circuit features:

What does a universal circuit mean?

What does a single limb circuit mean?

Which devises use this type of circuit?

What does a double limb circuit mean?

• Main bore outlet connection • Nebulizer drive line and Exhalation valve drive line adapter • Patient connection & mouthpiece • Nebulizer cup • Exhalation valve outlet

Key Elements of IPPB Instruction • Explain what is IPPB • Why is the patient going to be receiving IPPB treatments • How long is each treatment & how often will they receive it • What should they do during the treatment • Any questions they have of you

What SHOULD the patient do during IPPB? • Patient starts their breath; the machine cycles on • Patient relaxes and lets the machine fill their lungs • Patient should NOT be actively breathing after the machine cycles (turns on) • Patient will exhale normally in a relaxed way through the mouth when machine ends inspiration (pre-set pressure is reached)

What should the therapist emphasize during the treatment? • Make sure patients keep lips sealed tight around the mouthpiece • Coach patient to not actively breath • “Relax and let the machine fill your lungs!” • Make sure patient does not breath too rapidly during treatment • This will cause dizziness secondary to hyperventilation

122 Key Aspects & Terms Associated with IPPB ventilators • Patient initiates the breath and machine is able to detect the patient’s effort and then starts delivering gas into the mouthpiece • The ability of machine to detect the patients need for a breath is called “sensitivity” • Sensitivity should be set so that machine will begin breath at a pressure that is 1 or 2 cmH2O pressure below zero (or -1 to -2 cmH2O pressure)

These machines are “pressure cycled” • This means that inspiration ends when a preset pressure is reached in the circuit • Preset pressure is set by the therapist • Typical pressure ranges (15 - 25 cmH2O) • Pressures higher than 25 associated with “air swallowing” particularly with mouth seal or mask treatments • Pressures less than 15 may be insufficient to increase the tidal volume (VT)

Characteristics of Pressure Cycling • Any leak in the “circuit” or in the patient will cause the machine to not end inspiration (cycle off) • Patient can easily end the breath by • Blowing back into the mouthpiece • Putting their tongue over the mouthpiece • Pressure cycled machine can NOT guaranteed to deliver any specific volume to the patient • Volume delivered is based upon; • The patients ability to relax and let the machine deliver the breath • The pressure level set by the therapist • The higher the pressure level set - the greater the volume delivered to the patient (ideally)

123 Module 5 CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP) • A simple approach which maintains some positive pressure in the airway at the end of exhalation • Net effect of CPAP is that FRC is increased • There is a high correlation between improvement of atelectasis and the patient having a higher than normal FRC

Beneficial Effects of CPAP • Recruitment of collapsed alveoli • The work of breathing is decreased as lung compliance (stretchability) improves • Improvement of gas distribution • Improvement in secretion removal

Indications for Use of CPAP • Treatment of post-operative atelectasis • Should be used continuously • Has been used in the treatment of cardiogenic pulmonary edema

Contraindications to CPAP • If blood pressure is very low • Diastolic of <50 mm Hg • If patient has one or more of the following; • Facial trauma (cannot use mask CPAP) • Nausea • Untreated pneumothorax • Elevated intracranial pressure (ICP)

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Hazards of the Use of CPAP • Barotrauma (pneumothorax) • Gastric distension • Air-trapping • Decrease in BP • Can be very uncomfortable to the face of patient using mask CPAP

What Does CPAP Accomplish? • Increases the FRC by increasing the amount of air in the chest at the end of exhalation • The net effect of increasing FRC is to; • Re-open any atelectasis areas • Improve any hypoxemia that may be resulting from the atelectasis • CPAP is also used to treat sleep apnea secondary to upper airway obstruction

125 Module 5 Airway Clearance / Lung expansion Procedures • PEP Therapy – Flow Restrictors

• IPV –

• Flutter Valve Therapy

• MetaNeb -

126 EZPAP Therapy – aggressive tx for atelectasis

• Delivered with high flow oxygen • Uses venturi entrainment system to generate • Inspiratory Positive pressure – 8 – 10 cm H20 • Variable high flow • Constant expiratory pressure – 10 – 20 cm H20 • Can be used inline with SVN TX. • Can be used on nonresponsive patients • Increases & sustains patient’s FRC = improved gas distribution to bases & dependent lung areas • Increases mucokinesis via PEP The system simplifies providing positive airway pressure. Connect to a flow meter (wall air or O2 for enhanced FiO2), adjust to 5–15 lpm, and instruct patient to breathe diaphragmatically through the mouthpiece or mask. There is no heavy or expensive equipment to roll around. While monitoring with a pressure gauge, slowly adjust the flow meter until the desired airway pressures are reached. The therapeutic pressure range is usually between 5 and 30 cm H2O. Slow inhalations and exhalations should maintain adequate airway pressure throughout the breathing cycle. The patient receives a positive pressure inspiratory assist when inhaling to hold open the airways, and the elevated positive pressure is maintained throughout the breathing cycle; the breath hold is positive pressure. When exhaling, the patient breathes against the resistance caused by airflow, creating the positive expiratory pressure. The expiratory resistance provides PEP therapy to further splint open the airways and reinflates the alveoli through collateral ventilation. EzPAP may be used in conjunction with aerosol medications (nebulizer) via a 22-mm connection between the EzPAP device and the patient

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