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Infection Control A. Spread of an infection occurs when a pathogen is able to overcome the barriers of the host. Three elements must be present for an infection to spread; 1) Source The primary source of an infection in hospitals are people or contaminated objects. People may also serve as their own source of infection via endogenous flora called autogenous infection. Microorganisms differ in their relative virulence. Highly virulent organisms need be present in small numbers to cause infection. Others need high numbers or an immunocompromised host. Most noscomial pneumonia is bacterial in nature. 2) Host The presence of microorganisms in a host is called colonization. Whether a host actually becomes infected depends on both the organisms virulence and hosts resistance. 3) Transmission Route There are 5 routes for transmission of pathogens; i) Contact Most important and most common. Can occur directly or indirectly. (Staphylococcus, P. aeruginosa) ii) Droplet Occurs when individuals discharge large contaminated liquid droplets into the air by coughing, sneezing, or talking. The max range of these droplets is about 3 feet. (Haemophilus influenzae) iii) Airborne Occurs when the spread of contaminated droplet nuclei or dust particles become residue in evaporated water droplets. Because of their small size, they can remain suspended in air for a long time. (TB, measles) iv) Common Vehicle Occurs via host exposure to pathogens in contaminated food or water. (Food Salmenollosis and hep A, Water Shigellosis, cholera) v) Vectorborne Occurs when transmission occurs when an infectious agent transfers from one host to another usually via animals, bugs. 4) Spread of Infection to Lungs i) Infectious agents can reach the lungs via 3 mechanisms. First aspirate contaminated oropharyngeal or gastric secretions. Second, by inhaling droplets or contaminated particles, and third by spread from a distant infection site via blood.

B) Infection Control aims at breaking the chain of events that cause the spread of an infection. 1) Decrease Host Susceptibility Most difficult and least feasible. (Immunizations) 2) Eliminate Source of Pathogens It is impossible to eliminate all pathogens.

3) Interrupting the routes of Transmission Using specialized equipment handling procedures, barrier/isolation precautions, and use of single pt disposable equipment. C) Equipment Processing 1) Cleaning Removing dirt and organic material from equipment 2) Disinfection Destroys the vegetative forms of pathogenic organisms but cannot kill bacterial spores i) Pasteurization Application of moist heat at temperatures below the boiling point of water. ii) Chemical Disinfection application of chemical solutions to contaminated surfaces or equipment. Put into solution, let soak, rinse in sterile water. 3) Sterilization Complete destruction of all forms of microbial life. i) Incineration ii) Boiling iii) Autoclaving steam under pressure iv) Ionizing radiation: x-rays and gamma rays.

II) Physical Principles of Respiratory Care A) States of matter Solid, liquid, gas B) Internal Energy of matter a. Potential energy energy of position b. Kinetic energy energy of motion C) Internal Energy and Temperature a. Absolute Zero No kinetic energy b. Temperature Scales i. K = C + 273 ii. C= 5/9 (F-32) iii. F= (9/5 x C) + 32 c. Heat and the First Law of Thermodynamics i. Energy cannot be created nor destroyed, only transformed in nature. d. Heat transfer i. Conduction ii. Convection iii. Radiation iv. Evaporation/Condensation D) Properties of Liquid a. Pressure in liquids i. Pascals Principle Pressure is the same at any depth regardless of depth because its pressure acts in all directions. b. Buoyancy (Archimedes Principle) i. An object in water appears to weigh less than in air. This is due to liquid pressure creating an upward or supporting force. c. Viscosity i. The force opposing a fluids flow. Most important in laminar flow when the fluid moves in discrete cylindrical layers called streamlines. d. Cohesion and Adhesion i. Cohesion the attractive force between like molecules ii. Adhesion the attractive force between unlike molecules e. Surface Tension a force exerted by like molecules at a liquids surface. i. Laplaces Law Pressure varies directly with the surface tension of a liquid and inversely with its radius. f. Capillary Action i. The phenomenon in which a liquid in a small tube move upward against gravity. It uses adhesion and cohesion. Adhesion by liquid on the walls of the tube and creates a concave meniscus. Because surface tension acts to maintain the smallest possible liquid gas interface, instead of just the edges being pulled, the whole surface is pulled up.

g. Partial Pressures (Daltons Law) i. Relationship among the partial pressure and the total pressure in a gas mixture. The total pressure of a mixture of gases must equal the sum of the partial pressures of all the components of gas. h. Solubility of Gases in Liquids (Henrys Law) i. Predicts how much gas will dissolve in a liquid. At a given temperature, the volume of gas that dissolves in a liquid is equal to its solubility coefficient times its partial pressure. E) Fluid Dynamics a. Pressure in Flowing Fluids i. For any given tube length, flow resistance equals the difference in pressures between the two points along the tube divided by the actual flow. b. Patterns of Flow i. Laminar Flow 1. Discrete cylindrical layers or streamlines ii. Turbulent Flow 1. Fluid molecules form irregular eddy currents in a chaotic pattern. iii. Transitional Flow 1. A mixture or laminar and turbulent flow to an overall driving pressure. F) Flow, Velocity and Cross-Sectional Area a. Flow- bulk movement of a volume of fluid per unit of time. b. Law of Continuity Velocity of fluid moving through a tube at a constant flow varies inversely with the available cross-section area. c. The Bernoulli Effect When a fluid flows through a tube of uniform diameter, pressure decrease progressively over the tube length. However, when it passes through a constriction the pressure drop is much greater. d. Fluid Entrainment If an open tube is placed distal to a constriction, this negative pressure can actually pull another fluid into the primary flow stream. e. Coanda Effect Is the tendency of a fluid jet to stay attached to an adjacent curved surface that is very well shaped. (ie if one holds the back of a spoon in the edge of a stream of water running freely from a tap, the stream of water will deflect from the vertical to run over the back of the spoon)

III) The Respiratory System

Neonatal A. Development of the Respiratory system XXX B. Transition from Uterine to Extrauterine Life XXX a. Placental Circulation b. Fetal Circulation c. Cardiopulmonary Events at Birth C. Postnatal Lung Development XXX D. Compliance, Airway Resistance, and Pressure-Volume Relationships a. Compliance How easily if deforms and returns to original shape

b. Airway Resistance the pressure gradient required to produce flow through an airway. The rate at which the lungs and airways empty is termed time constant. Adult A. Thorax the rib cage, thoracic vertebrae, and sternum a. Three compartments mediastinum, and left and right plural cavities. B. Mediastinum divides the thorax vertically and separates the left and right cavities C. Lungs a. Top apices b. Hilum medial surface opening to the lungs contains bronchi, blood vessels, lymphatics, and nerves. c. Each lung is divided into lobes and separated by fissures. Right upper, middle, lower. Left Upper, Lower. d. Pleura Thin layer or tissue lining the inside of the chest walls (Parietal) and surface of lungs. (Visral) e. Costophrenic Angle The costal pleura lines the inner surface of the rib caf and the mediastinal pleura cover the mediastinum and the diaphragmatic pleura covers the diaphragm. The acute angle where the costal pleura join the diaphragmatic pleura is the costophrenic angle. f. Sternum dagger-shaped bony structure in the median line at the front of the chest. It serves as a point of attachment for the costal cartilages and numerous muscles. It consists of the upper triangular manubrium, the long, narrow body, and the pointed lower xiphoid process. D. Muscles a. Diaphragm Large muscle that arises from the lumbar vertebrae, the costal margin, and the xiphoid process. b. Intercostal muscles i. External arise from the lower edge of each rib ii. Internal lie beneath the external c. Scalene Muscle d. Sternomastoid e. Pectoralis Major f. Abdominal Innervations of the Lung the autonomic NS provide motor and sensory pathways to the lung A. Somatic Innervation a. Innervation of the diaphragm and the intercostals b. Phrenic nerve innervate the diaphragm B. Autonomic Innervation

a. Via the branches or the paired vagus nerves and the upper 4 or 5 thoracic sympathetic ganglia b. Efferent pathways i. Each vagus nerve, on entry to the chest, sends a branch that curves back up to the larynx. These branches are the recurrent laryngeal nerves. Each nerve also gives off a branch called the superior laryngeal nerve. The external branch supplies the cricothyroid muscle. The internal brach provides sensory fibers to the larynx c. Afferent Pathways i. Most from lungs are CNS to Vagal in origin. 1. Strech receptors located on smooth muscle of the bronchi and the bronchioles. 2. Inflation Receptors though to adjust the depth of inspiration 3. Irritant receptors Subepithelial tissue of large airways. 4. J receptors respond to an increase in pulmonary capillary pressures. When high as in CHF, result in rapid, shallow breathing. Vascular Supply composed of pulmonary and bronchial circulations. A. Pulmonary Circulation a. Originates in the right side of the heart. Oxygen depleted mixed venous blood returns to the heart via the inferior and superior vena cavae. Blood is pumped to the lungs by the R ventricle through the pulmonary artery. B. Bronchial Circulation a. Mixed venous blood in the pulmonary arteries lack sufficient oxygen for the metabolic needs of the lung. A separate arterial supply called the bronchial circulation also accompanies the bronchi. Anatomy of the Respiratory Tract A. The nose most adults are nose breathers. Nasal polyps or mucosal edema sometimes prohibit nasal breathing. The flared openings called alae with a space on each side called vestibule, which have hairs whi ch act as a filter. The nasal passages are separated by septum. They also have turbinates that divide the cavities into superior, middle and inferior. The nose warms inspired air close to body temperature (37C). B. Paranasal Sinuses Chronic sinus infections are a source of contaminated materials that may be aspirated into the lower respiratory tract. C. Oral Cavity - Palate separated the nasal from the oral. Soft and hard.

D. Pharynx naso- , oro- and hypo. The entire surface is lined with stratified squamous epithelium. Eustachian tubes run to middle ear. Oro uvula to the epiglottis and base of tongue. Hypo epiglottis and the larynx E. Larynx Complex structure located immediately below the pharynx. It hangs from the hyoid bone at the base of the tongue. It can be felt at the adams apple. It consists of 9 cartilages and numerous muscles and ligaments. They combine to protect the lower airway during breathing and swallowing. The major function is sound production. The epiglottis is flat cartilage that extends from the base of the tongue backwards and upwards, it simply diverts food into the esophagus. F. Vallecula a small space between the tounge and the epiglottis. G. Glottis true vocal cords. Made of muscle, ligament, and submucosal soft tissue H. Cricoid cartilage lower boarder of the larynx. It is the only rigid structure that completely encircles the airway Lower Respiratory Tract A. Trachea Beginning of the conducting system and braches to 2 mainstem bronchi. There is a sharp cartilage at the point of the tracheal bifurcation called the carina and divides flow right and left. B. Transitional and Respiratory Zone a. Terminal bronchioles begin at 17 generation b. Two principal alveolus i. Type I squamous pneumocytes 1. Opening between type I cells are pores of Kohn ii. Type II granular pneumocytes iii. Alveolar Macrophage phagocytic cells that clear bacteria and other material invading the alveoli. Do not originate in the lung c. Intercommunicating Channels i. Pores of Kohn ii. Canals of Lambert Other Functions of the Lungs In addition to gas exchange, perform other functions related to homeostasis. The pulmonary circulation also acts as a filter for the systemic circulation. It traps particles before they enter the systemic circulation, where blockages could be life-threatening. The lung releases substances in response to physiological or immunological challenges. Angiotensin is converted to its active form by the lung. Adenosine triphosphate and norepinephrine are partially removed from the blood and inactivated by the lungs.

IV) Cardiovascular System

V) Ventilation A. Mechanics of Ventilation a. Two cycles 1. Inspiration 2. Expiration b. The volume moved is the tidal volume i. Removes CO2 and supplies O2 c. Vital Capacity B. Pressure Differences During Breathing a. Ventilation occurs because of pressure gradients created by expansion and contraction of the thorax. b. Pressure at airway opening (0 or atmospheric pressure) c. Pressure at body surface (also 0) d. Alveolar pressure (interpulmonary pressure) varies during breathing e. Plural pressure usually negative f. Pressure gradients involved in ventilation i. Transrespiratory ii. Transpulmonary iii. Transthoracic C. Forces opposing inflation of the lung a. Elastic forces i. Tissue of the lungs and thorax, along with surface tension in the alveoli b. Frictional Forces i. Resistance to gas flow and tissue movement during breathing VI) Gas Exchange and Transport A. Diffusion gas movement between the lungs and tissues occur by simple diffusion B. Alveolar Carbon Dioxide the PACO2 varies directly with the bodys production of carbon dioxide and inversely with alveolar ventilation C. Alveolar Oxygen Tension The most important factor is the inspired partial pressure of oxygen PA02 = FiO2 x (Pb-47) PaCO2/0.8 If the pt is breathing with Fi02 of 60 or greater PA02 = FiO2 (Pb-47) PaCO2 D. Changes in Alveolar Gas Partial Tensions Nitrogen plays no role in gas exchange but it does occupy space and exert pressure E. Oxygen Transport a. Dissolved in plasma b. Erthrocyte intracellular fluid

F. Normal loading and unloading oxygen Oxyhemoglobin dissociation curve

G. Abnormal Hemoglobins a. Methemoglobin (metHb) abnormal form in which the heme-complex normal ferrous ion loses an electron and is oxidized to its ferric state. IN this state it cannot combine with oxygen resulting in a special form of anemia called methemoglobinemia. Most common cause is nitrite poisoning. In this state the blood turns a brown color. Treated with methylene blue or ascorbic acid. b. Carboxyhemoglobin is a chemical combination of hemoglobin with carbon monoxide. Hemoglobi ns affinity for CO2 is more than 200 times greater then for oxygen. H. Impaired Oxygen Delivery When oxygen delivery falls short of cellular needs hypoxia occurs. Hypoxia occurs if (1) the arterial blood oxygen content is decreased (hypoxemia),(2) cardiac output or perfusion is decreased (shock or ischemia), or (3) abnormal cellular function prevents proper uptake of oxygen (dysoxia). a. Hypoxemia occurs when the PA02 is decreased to lower then the predicted normal based on the age of the pt. b. Decreased PaO2 may be caused by low ambient PaO2 (mountain sickness, high altitudes), hypoventilation, impaired diffusion, V/Q imbalances, and right to left anatomical or physiological shunt I. Impaired Carbon Dioxide removal a. Inadequate Minute Ventilation

i. Decreased tidal volume, atelectasis, neuromuscular disorders, impeded thoracic expansion b. Increased Dead space ventilation i. Rapid shallowbreathing ii. Increased physiological dead space c. V/Q imbalances

VII) Acid-Base Balance Bicarbonate and nonbicarbonate buffer systems are the immediate defense against the accumulation of hydrogen ions A. Lungs The lungs can lower H2CO3 by eliminating CO2. B. Kidneys Physically remove H+ from the body i. Excretion eliminate through urine ii. Secretion renal tubule cells actively transport substances into the tubule lumens fluid or filtrate iii. Reabsorption active or passive transport of the filtrate substances back into the tuble cell and then into the blood of nearby capillaries C. Normal Acid base balance Normally the kidneys maintain a bicarb of 24 mEq/L and lungs maintains a PCO2 or 40 mm Hg i. An increase in pH leads to academia ii. A decreased in pH leads to alkalemia a. Primary Respiratory Disturbances i. Respiratory Acidosis 1. Caused by depressed ventilation, CNS depression ii. Respiratory Alkalosis 1. Caused by hyperventilation, b. Primary Metabolic Disturbances i. Metabolic Acidosis 1. Caused by (1)fixed acid accumulation in the blood (2) an excessive loss of HCO3 from the body ii. Metabolic Alkalosis 1. Caused by (1) loss of fixed acids (2) gain of blood buffer base c. Compensation restoring pH to normal D. Clinical Acid-Base States a. pH i. 7.35 7.45 b. PaCO2 i. 35 45 mm Hg c. HCO3 i. 22 26 mEq/L

VIII) Regulation of breathing A. Medullary Respiratory Center The dorsal respiratory groups (DRG) contain mainly inspiratory neurons where the ventral respiratory groups (VRG) contain both inspiratory and expiratory neurons a. DRG Mainly inspiratory neurons that are located bilaterally in the medulla. These neurons send impulses to the motor nerves or the diaphragm and external intercostals muscles, providing the main inspiratory stimulus b. VRG i. Located bilaterally in the 2 different nuclei and contain both inspiratory and expiratory neurons. Ins send motor impulse through the vagus nerve to the laryngeal and pharyngeal muscles abducting the vocal cords and increasing the diameter of the glottis c. Inspiratory Ramp Signal i. The muscles do not receive a instantaneous burst of signals but a gradually increase at the end of expiration creating a ramp signal B. Pontine Respiratory Center a. Apneustic Center i. Ill defined because its existence and function can only be demonstrated if its connections to the higher pneumotaxic center and vagus nerve are severed b. Pneumotaxic Center i. Bilateral group of neurons located in the upper pons. It controls the switch off point of the inspiratory ramp signal, thus controlling time. Strong signals increase the respiratory rate and weak prolong inspiration thus increasing tidal volume. C. Reflex Control of Breathing a. Hering-Breuer Inflation Reflex i. Generated by stretch receptors in the smooth muscles of both large and small airways. When inflation stretches these receptors, they send inhibitory impulses through the vagus nerve to the DRG neurons, stopping further inspiration. b. Deflation Reflex i. Sudden collapse of the lung stimulates strong inspiration efforts c. J receptors i. Alveolar inflammation processes (pneumonia), pulmonary vascular congestion (CHF), and pulmonary edema stimulate theses receptors, causing rapid shallow breathing and a sensation of dyspnea d. Peripheral Proprioceptors

i. Located in muscles, tendons, and joints as well as pain receptors in muscles can skin. Stimulation increases inspiratory activity and causes hyperena D. Chemical Control of Breathing a. Central Chemoreceptors i. Hydrogen ions stimulate highly responsive chemosensitive nerve cells located in the medulla. Which are extremely sensitive to CO2 in an indirect fashion, since they are not in direct contact with arterial blood. Instead they are bathed in CSF, separated from the blood by the semipermeable membrane called the blood brain barrier. It is impermeable to hydrogen and bicarb but is freely permeable to carbon dioxide. When, PaCO2 rises, CO2 diffuses rapidly through the bloodbrain barrier into the CSF. In the CSF the CO2 reacts with H+ and HCO3-. The H+ ions generated in this reaction stimulate the central chemoreceptors, which in turn stimulate the medullary inspiratory neurons. Therefore arterial PCO2 is indirectly the primary min-to-min control of ventilation. b. Peripheral Chemoreceptors i. Carotid Bodies 1. Located bilaterally in the bifurcations of the common carotid arteries 2. Aortic bodies located in the arch of the aorta 3. They are stimulated by decreased PaO2, Increased PaCO2, and Decreased pH

Bedside Assesment A. Interviewing and Medical History a. Est rapport between clinician and pt b. Obtain essential dx info c. Help monitor changes in pts symptoms and response to therapy B. Common Cardiopulmonary Symptoms a. Dyspnea shortness of breath perceived by the pt b. Orthopnea SOB when the pt is reclining postion c. Platypnea SOB in upright position d. Cough Forceful expiratory maneuver that expels mucus and foreign material from the airways i. Effectiveness depends on the pts ability to take deep breaths, lung recoil, strength of expiratory muscles, and level of airway resistance e. Sputum Production i. Phlegm mucus that comes from the tracheobronchial tree that are not contaminated by oral secretions ii. Sputum from the lungs that passes through the mouth iii. Purulent contains pus cells iv. Fetid foul smelling v. Mucoid clear and thick f. Hemoptysis coughing up blood or blood streaked sputum. Where hematemesis is vomiting blood. g. Chest Pain i. Pleuritic located laterally in position, worsens on deep, sharp stabbing pain ii. Nonpleuritic located center of the anterior chest and may radiate to the shoulder and back h. Fever may occur with something as simple as viral infection of the upper airway or as serious as bacterial pneumonia or TB. Pts with fever will have an increased metabolic rate, and thus an increased oxygen consumption and carbon dioxide production. This may lead to acute respiratory failure. i. Pedal Edema swelling of the lower extremities. Most often occurs with heart failure which causes an increase in the hydrostatic pressure of the blood vessels in the lower extremities. Pts with chronic hypoxemic lung disease are esp prone to right-side heart failure (cor pulmonale) C. Physical Exam a. 4 steps (1) inspection, (2) palpitation, (3) Percussion, (4) auscultation b. General Appearance i. Diaphoresis (sweating) ii. Facial expression

c. Level of Consciousness i. Sensorium d. Vital Signs i. Body Temperature 1. 98.6 F (37 C) 2. Febrile (fever) a. Indicates metabolic rate 3. Hypothemia a. Exposure to cold, shivering, head injury, stroke e. Pulse i. 60 100 beats a min ii. >100 tachycardia iii. <60 bradycardia iv. Pulsus paradoxus increasing heart rate on inhalation v. Pulsus alternans alternation of strong and weak pulse f. Respiratory rate i. 12-18 breaths a min 1. >18 tachypnea 2. <12 bradypnea g. Blood Pressure i. Systolic peak force exerted in the major arteries during contraction of the left ventricle 90-140 mm HG ii. Diastolic is force remaining in the major arteries during relaxation or the ventricles 1. Hypotension > 2. Hypertension < 3. Korotkoff sound D. Examination of the head and neck a. Head i. Nasal Flaring ii. Cyanosis iii. Pursed-lip breathing b. Neck i. Position of the trachea 1. Trachea shifts away from midline in certain thoracic disorders. 2. In general the trachea shifts toward an area of the collapsed lung ii. Jugular venous distension 1. Right side heart failure 2. Hypervolemia

3. When venous return to the right atrium is obstructed by mediastinal tumors c. Examination of lungs and thorax i. Inspection 1. Thoracic configuration a. Anteroposterior diameter i. Abnormal increase is barrel chest ass. With emphysema b. Pectus carinatum abnormal protrusion of the sternum c. Pectus excavatum depression of part or all of the sternum d. Kyphosis spinal deformity in which the spine has an abnormal AP curvature e. Scoliosis spinal deformity in which the spine has a lateral curve f. Kyphoscoliosis combination of kyphosis and scoliosis 2. Breathing pattern and effort a. Increased work of breathing may result in retractions, intermittent sinking inward of the skin overlying the chest wall b. Abdominal paradox inward movement of the anterior abdominal wall during inspiration c. Apnea no breathing d. Biots respiration irregular breathing with long periods of apnea e. Cheyne-stokes irregular type of breathing; breaths increase and decrease in depth and rat with periods of apnea f. Kussmauls respiration deep and fast respirations g. Apneustic breathing prolonged inspiration h. Asthmatic breathing prolonged exhalation i. Palpation i. Vocal femitus vibrations created by the vocal cords during speech ii. Tactile fremitus vibrations of speech felt on the chest wall j. Thoracic expansion i. Normal thumb distance is 3-5 cm ii. Reduced in COPD and neuromuscular disorders k. Subcutaneous Emphysema i. Crepitus

3. Percussion of the chest a. Percussion over lung fields i. Normal resonance moderately low-pitched sound ii. Increased louder and lower than normal iii. Decreased - opposite of resonance 4. Ausculation of the lungs a. Stethoscope (1) bell (2) diaphragm (3) tubing (4) earpiece b. Normal breath sounds i. Vesicular Low pitch, peripheral lung areas ii. Bronchovesicular moderate pitch, moderate intensity, around the sternum and between scapulae iii. Tracheal high pitch, loud intensity, over the trachea Abnormal Breath sounds i. ii. iii. iv. Electrocardiogram and lab test assment A. EKG inexpensive, noninvasive and easy to use a. Basic principles i. Depolarization - stimulation of the polarized cells causes an influx of sodium into the interior portion of the cell ii. Repolarization rapid return of the cell to the polarized state iii. Automaticity ability of the cells to depolarize without direct stimulation b. Conduction System i. Sinoatrial Node (SA) ii. Interatrial conduction tract (Bachmann;s bundle) iii. Internodal atrail conduction tracts iv. Atrioventricular node (AV) v. Left and Right Bundle branch vi. Purkinje fibers vii. Ectopic beats any heartbeat originating outside the SA node Crackles, Wheezes Rhonchi Stridor

c. Basic ECG Waves i. P-Wave depolarization of the atria ii. QRS Complex depolarization of the ventricle (0.12 sec) iii. S wave negative deflection after R wave iv. T wave wave of repolarization in the ventricles immediately after depolarization v. PR Interval represents the time in which impulses begins in the SA node and travels across the atria (0.20 sec)

d. Interpreting the ECG i. Identifying rate 1. Number of P waves in 6 sec x 10 a. 0.04 sec = 1 small block b. 0.20 sec = 5 small blocks ii. Recognizing Arrthymias 1. Normal Sinus Rhythm 2. Sinus Tachycardia a. Rate exceeding 100 beats per min b. Causes: anxiety, pain, fever, hypoxemia 3. Sinus Bradycardia a. Rate less than 60 beats per min 4. Sinus Arrhythmia a. I r r e g u l a r s p a c

ing between the QRS complex b. Most cases dont need treatment 5. First degree heart block a. PR interval >0.20 sec i. Common following an MI that damages the AV node, or complications of medications like digoxin or Beta-blockers 6. Second Degree Heart Block

a. Type I (Wenckebach or Mobitz type I) i. Progressive prolongation of the PR interval until one does not pass at all b. Type II (Mobitz Type II) i. Series of nonconducted P waves followed by a P wave that is conducted to the ventriles

7. Third Degree Heart Block a. The atria and ventricle are paced at independent rates

8. Atrial Flutter a. Saw-tooth pattern

9. Premature Ventricular Contraction (PVC) a. Ectopic beats b. Bigeminy if every other beat i. Causes: Caffine, nicotine, or ischemia of the myocardium 10. Ventricular Tachycardia a. A run of 3 or more PVCs 11. Ventricular Fibrillation a. Erratic quivering of the Ventricular muscle

Laboratory Tests A. Complete Blood Count (CBC) a. Detailed descriptions of circulating white blood cells (WBC), called leukocytes, and red blood cells (RBC) called erythrocytes. The WBC is made up of 5 different types of cells. RBC are evauluated for size and hemoglobin content. i. White Blood Cells 1. Elevation of WBC count is known as leukocytosis. It can be cause by a number of problems known including stress, infection and trauma. The degree of leukocytosis is a function of the severity of the problem and the condition of the pts immune system. 2. WBC below normal is leucopenia. Occurs when the pts immune system is overwhelmed by an infection of suppressed by disease or therapy. Diseases of the bone marrow, such as lymphoma; chemotherapy; and radiation therapy for cancer are common causes of leucopenia. Common in elderly pt with sever pneumonia that is overwhelming the immune system. 3. Differential of the White Blood Cell Count a. Used to determine the differential of the WBC count to determine that exact number of each type of WBC present in the circulating blood. Cell Type Relative Value Absolute Causes for Abnormalities Value Neutrophils 40-75% 1800-7500 Increased with bacterial infections and trauma; reduced with bone marrow disease Eosinophils 0-6% 0-600 Increased with allergic reactions and parasitic infections Basophils 0-1% 0-100 Increased with allergic reations Monocytes 2-10% 90-1000 Increased wihth invasion of foreign material (TB) Lymphocytes 20-45% 900-4500 Increased with viral and other infections; reduced with immunodeficiency problems ii. Red Blood Cell Count 1. Low is anemia and suggests production by the bone marrow is inadequate or excessive blood loss occurred. 2. Elevated is polycythemia and occurs when the bone marrow is stimulated to produce extra RBCs in response to low blood oxygen levels (termed secondary polycythemia) a. Polycythemia helps prevent the negative side effects of reduced PO2 in the blood by increasing the oxygencarrying capacity. Pts who live in high altitude and those

with chronic lung diseases are most likely to experience chronic hypoxia b. Hemoglobin is a protein substance with the unique ability to bind with oxygen. Normal levels are 12-16 g/gL c. Hematocrit level is the ratios of RBC volume to that of whole blood. A low reading occurs with anemia, a high with polycythemia. The hematocrit level (40-50% of blood volume) is a reflection of the hydration status of the pt. Dehydration causes it to increase where over hydration causes it to decrease. iii. Platelet Count 1. Smallest formed element in the blood and important for coagulation. 2. Reduction in bone marrow disease, or disseminated intravascular coagulation. This also causes the pt to bruise easily and at a greater risk for hemorrhage B. Blood Chemistry Tests a. Electrolyte Concentrations not measured to make a dx, but to identify the general health status of the pt and the side effects of certain medications. i. Sodium (135-145 mmol/l) 1. Low Hyponatermia and may occur with diuretic, diarrhea, or certain kidney problem. May cause confusion, decreased mental alertness, muscle twitching and possibly seizures. 2. High Hyper natremia and occurs with renal disease, and excessive water loss ii. Potassium (3.5-5.3 mmol/l) 1. Low hypokalemia and occurs when potassium-containing fluids are lost in excessive amounts, such as with diuretics, vomiting and diarrhea. Leads to weakening of the cardiac muscles which reduces cardiac output. 2. High Hyperkalemia and occurs with renal disease and tissue trauma, which cuases a release of intracellular potassium into the plasma. Leads to feelings of tiredness, weak and nausea. Could cause difficulty in ventilator weaning. iii. Chloride (4-60 mmol/l) 1. Low Hypochloremia and occurs with prolonged vomiting, resulting in the loss of HCl, chronic respiratory acidosis, and certain renal diseases 2. High hyperchloremia and occurs with prolonged diarrhea, certain kidney disease and some cases of hyperthyroidism

iv. Total CO2 represents the level of HCO3- in venous blood. Because the CO2 concentration is higher in venous blood than it is in arterial blood, the normal venous HCO3- level is slightly higher than that seen in the ABG analysis. Any abnormality that causes KCO3- level to increase will lead to elevation of the total CO2 on the venous chemistry panel. Disorders that causes the blood HCO3- to decrease will lead to abnormally low total CO2. b. Sweat Chloride i. Pt with cystic fibrosis have increased levels of chloride in their sweat because of their inability to reabsorb it. Thus these pts will have abnormally elevated chloride levels in their sweat. Important in diagnosing CF. ii. Anion Gap 1. Balance normally exists between cations and anions in the serum. Evaluation of this balance is done by determining the anoin gap, which if the difference between the concentration level of the primary cation (Na+) and the primary anions (HCO3- and Cl-). The anion gap is calculated by adding the HCO3- and the Clvalues and subtracting this from the serum sodium. Normal is 8-16 mEq/L. Elevation suggests metabolic acidosis, and further evaluation is needed. iii. Renal Function 1. Blood Urea Nitrogen (BUN) Urea is a waste product of metabolism that is excreted by healthy adults. 2. Creatinine waste product of muscle metabolism and filtered out of the body by the kidneys. Normal levels are 0.7-1.3 mg/dL. Diseases of the kidney that result in a significant proportion of the renal nephrons becoming dysfunctional cause the level to increase iv. Serum Enzymes 1. Enzymes are present in most body cells. Damage to these tissues causes the release of certain enzymes into the circulating blood. Measurements of the serum enzymes can be helpful in confirming a suspected diagnosis in confirming a suspected diagnosis. a. Aspartate Aminotransferase (AST) highest concentrations are found in pts with liver disease, ie hepatitis, and the second day after a MI. b. Alanine Aminotransferase (ALT) increased with liver diseases like hepatitis.

c. Akaline Phosphatase (ALP) present in bones, kidney, spleen and intestine. Damage to these tissues causes an elevation in serum levels. d. L-Lactate Dehydrogenase (LDH) high concentrations in the heart, liver, skeletal muscle, brain, kidney and RBCs. Elevated levels in conditions like hepatitis, renal disease, shock, MI, trauma, widespread carcinoma, and megaloblactic anemia. e. Creatine Kinase (CK) occurs in brain, skeletal muscle and heart. CK from the brain does no cross the blood-brain barrier and does not appear in the serum, so elevated levels are indicative of heart or skeletal muscle disorders. Elevation of the type only found in the heart (CK-MB) is suggestive of an MI v. Serum Glucose 1. Breakdown of carbohydrates results in the production of serum glucose, which is metabolized by the cells for energy. Insulin in necessary for cells to utilize the glucose circulating in the blood. Pts with DM have reduced insulin production and therefore do not use glucose normally. a. Hyperglycemia elevation of BG. May be seen in pt with metabolic acidosis and consistent with diabetic ketoacidosis and represents a potentially life-threatening condition if not treated immediately. b. Hypoglycemia Low BG. May be drug induced, associated with digestive problems or related to inadequate dietary intake of carbohydrates. Pts often will complain of weakness, shaking, headache, lethargy, and excessive sweating. May lead to difficulty in ventilator weaning. Normal is 70-105 mg/dL. C. Microbiology Tests a. Sputum Gram Stain i. Used to recognize organism causing the infection and making it easier to treat. 1. 1st smears sputum on glass slide and stains the sample and examines with microscope 2. The sample with numerous pus cells and few or no epithelial cells is most likely a true sample from the lung and is reflective of the infection source.

Analysis and Monitoring of Gas Exchange A. Analysis versus Monitoring a. Although the term analysis is defined broadly as study or interpretation, analysis in a clinical laboratory has a special meaning, as does the term monitoring. In clinical practice, laboratory analysis refers to discrete measurements of fluids or tissue that must be removed from the body. Such measurements are made by a laboratory analyzer. Conversely, monitoring is a device that provides the appropriate data to the clinician in real time, usually without removal of samples from the body. B. Invasive Versus Noninvasive a. Invasive requires insertion of a sensor or collection device into the body b. Noninvasive is a means of gathering data externally. C. Measuring FIO2 a. 2 Types of electrochemical oxygen analyzers i. Polarographic (Clark) electrode 1. Similar to those used in blood gas analyzers. This system consists of a platinum cathode and a silver-silver chloride anode. Oxygen molecules diffuse through the sensor membrane into the electrolyte, where a polarizing voltage causes electron flow between an anode and cathode. While silver is oxidized at the anode, the flow of electrons reduces oxygen to hydroxyl ions at the cathode. The more O2 molecules that are reduced, the greater the electron flow is across the poles. The resulting change in current is proportional to the PO2, with its value displayed on a galvanometer. Displays in 10-30 sec. ii. Galvanic fuel cell 1. Use a gold anode and a lead cathode. Current flow across these poles is generated by the chemical reaction itself. Thus, unless accessories such as alarms are included, a galvanic cell needs no external power. Slower to display results, almost 60 sec. b. Procedure i. First must be calibrated. Usually 2 point test, usually 100% O2, and room air 21%. c. Problem solving i. Because o2 analyzers include replaceable components that deteriorate over time, the best way to avoid is through preventive maintenance, which should include both scheduled parts replacement and routine operational testing by biomed. Detailed records must be kept. ii. The most common causes of analyzer malfunction are low batteries (Clark), sensor depletion, and electronical failure.

iii. Inaccurate readings also can occur with electro-chemical analyzers, resulting from either condensed water vapor or pressure fluctuations. Galvanic cells are particularly sensitive to condensation. To avoid this problem during continuous use are humidified circuits, the clinician should be place the analyzer sensor proximal to any humidification device. D. Sampling for Arterial Blood Gas a. Indication i. The need to evaluate ventilation (PaO2), acid-base (pH and PaCO2), Oxygenation (Pa02 and SaO2) status, and the oxygen-carrying capacity of blood. ii. The need to assess the pts response to therapy and/or diagnostic tests (O2 therapy) iii. The need to monitor the severity and progression of a documented disease process b. Contraindications i. Negative results of modified Allen test are indicative of inadequate blood supply to the hand and suggest the need to select another extremity for the puncture site. ii. Arterial puncture should not be performed through a lesion or distal to surgical shunt. For example, arterial puncture should not be performed on a pt undergoing dialysis. If there is evidence of infection or peripheral vascular disease involving the selected limb, an alternate site should be selected iii. Because of the need for monitoring the femoral puncture site for an extended period, femoral punctures should not be preformed outside the hospital. iv. A coagulopathy or medium to high dose anticoagulation therapy, such as heparin or warfarin (Coumadin), streptokinase, of tissue plasminogen activator may be relative contraindication. c. Precautions and/or Complication viii. Arterial occlusion i. Arteriospasm ix. Vasovagal response ii. Air or clotted blood x. Pain emboli iii. Anaphylaxis from local anesthetic iv. Pt or sample contamination v. Hematoma vi. Hemorrhage vii. Trauma to the vessel

d. Assessment of Need i. The following findings may make it easier for the clinician to decide whether arterial blood sampling is needed: 1. History and physical indicators, such as positive smoking history, recent onset of difficulty breathing independent of activity level or trauma 2. Presence of other abnormal diagnostic tests or indexes, such as abnormal pulse oximetry reading or chest x-ray examination 3. Initiation, change, or discontinuation of therapy 4. Projected surgical interventions for pts at risk 5. Projected enrollment in a pulmonary rehab program e. Frequency i. The frequency with which sampling is repeated should depend on the clinical status of the pt and the indication for performing the procedure. Because repeated punctures at a single site can cause injury, clinicians should consider either finding alternate sites or using indwelling catheter. f. Monitoring i. The following should be monitored as part of the arterial blood sampling: 1. FIO2 or prescribed flow 2. Proper application of oxygen mask 3. Mode of ventilator support and settings 4. Pulsatile blood return 5. Presence of air bubbles or clots in the syringe or sample 6. Appearance of the puncture site after application of pressure and before dressing 7. Pts respiratory rate, temp, position and level of activity, clinical appearance 8. Ease of obtaining sample E. Oximetry a. The measurement of blood hemoglobin saturations using spectrophotometery. The principle is every substance has a unique pattern of light absorption. A substances pattern of light absorption varies predictably with the amount present, this is known as the Lambert-Beer Law. b. 2 types of oximetry used in clinical practice i. Hemoximetry (co-oximetry) 1. Measurement of oxygen saturation of hemoglobin in arterial blood. Used to monitor tissue and organ oxygenation in surgical patients. ii. Pulse Oximetry

1. Inexpensive and portable noninvasive monitoring device that provides estimates of arterial blood oxyhemoglobin saturation levels. 2. Instrumentation a. spectrophotometry b. photoplethysmography F. Capnometry and Capnography a. Capnometry the measurement of CO2 in respiratory gases. A capnometer is the device that measures the CO2. Capnography is the graphic display of CO2 levels as they change during breathing.

Pulmonary Function Testing A. PFTs a. Lung Volumes and capacities b. Flow rates of gases through the airways c. Ability of the lungs to diffuse gases B. Purpose a. Identification and quantification of changes in pulmonary function b. Epidemiological surveillance for pulmonary disease c. Assessment of postoperative pulmonary risk d. Aid in the determination of pulmonary disability e. Evaluation and quantification of therapeutic effectiveness C. Equipment a. Devices that measure gas volume i. Water-sealed spirometers ii. Bellow spirometers iii. Dry rolling seal spirometers b. Devices that measure gas flow i. Pneumotachometers ii. Thermistors iii. Turbinometers iv. Sonic devices v. Peak flow meters D. Lung volumes and capacities

a. Lung Volumes i. Tidal Volume ii. Inspiratory reserve volume (IRV) iii. Expiratory reserve volume (ERV) iv. Residual volume (RV)

b. Capacities i. Total Lung Capacity (TLC) ii. Inspiratory capacity (IC) iii. Functional residual capacity (FRC) iv. Vital capacity (VC) E. Pulmonary Mechanics: Spirometry a. Forced expiratory volume b. Forced Inspiratory flow rate

c. Forced expiratory flow d. MVV

An example of a correctly performed FVC maneuver. Upon producing the peak expiratory flow, flow diminishes in a nearly linear fashion. Repeated maneuvers lead to reproducible flows, albeit that the FVC maneuver appears to be terminated prematurely at least once.

The second figure shows 5 reproducible maximum expiratory flow-volume curves. In some cases the middle portion of the curve is convex towards the volume axis, in other cases it displays a shoulder instead. These variations often relate to variations in body position during the maneuver. If trunk, neck and head are kept straight while looking forward the shape of the curve may be different from the one obtained when the subject bends over during the maneuver. This is because the former position may straighten the trachea, thereby stretching it and increasing its stiffness (consult reference below). It is therefore recommended to standardize body posture; it is best if the subject sits or stands straight up, with the chin tilted slightly upwards throughout the maneuver. This also prevents saliva from dripping into the equipment or tubing.

Reversible airway obstruction The curve delimited by the interrupted line represents the predicted flow-volume curve. The convexity of the curve towards the volume axis before bronchodilatation points to peripheral airway obstruction. There is significant bronchodilator responsiveness, with normalization of the FVC, signifying very significant reversibility of expiratory airway obstruction. The illustration also shows the inspiratory and expiratory flow-volume curve during normal tidal breathing.

Severe airway obstruction Immediately after the peak expiratory flow, the flow drops to low values until the end of the forced expiration. This pattern is compatible with severe airflow limitation. Expiratory flow during the normal tidal breathing is at the same level as during a forced expiration; this signifies the presence of a flow limiting segment during normal respiration, so that each normal expiration

is in fact a forced expiration at the expense of considerable work of breathing. The ventilator reserves in this pt are therefore minimal. During physical exercise Inspiratory flow can be relatively easily increased, unlike expiratory flow; therefore end-expiratory volume will increase sharply, exacerbating the hyperinflation of this pt. This pattern is encountered in the case of loss of elastic lung recoil associated with dynamic compression of the intrathoracic airways, such as occurs in pulmonary emphysema.

Restrictive lung disease This is a characteristic pattern of a low FVC and comparatively high expiratory flow, giving the flow-volume curve a pointed cap appearance. Both FEV1 and FVC are well below predicted levels, but the FEV1/FVC ratio is normal or even high. Measurement of the total lung capacity may be considered to ascertain a restrictive ventilatory defect if its presence is not already evident from extrathoracic causes. If pathological changes of lung parenchyma are suspected it may be useful to assess the transfer factor for carbon monoxide, as the TL,CO is often diminished in interstitial lung disease. In general practice the prevalence of restrictive ventilatory defects is very low indeed. In only a moderate proportion of subjects referred to hospital with suspected restriction on the basis of the above criteria is a restrictive ventilatory defect confirmed by measurement of lung volumes (Aaron). Therefore entertain this 'diagnosis' only if spirometric findings and clinical symptoms are compatible with a restrictive syndrome. A general rule of thumb is that measurement of lung volumes should only be performed if FEV1%FVC > 55% and FVC%pred < 85%. This rule has a 96% sensitivity for predicting a low TLC and an 98% negative predictive power for excluding restriction (Glady). Quantifying severity of airway obstruction The European Respiratory Society, British Thoracic Society and American Thoracic Society (see international recommendations) have recommended to use the FEV1%(F)VC to decide whether

there is or is not airway obstruction, and to quantify its severity on the basis of the FEV1. Therefore these recommendations have been adopted in the SpirXpert software. However, do keep in mind that using the FEV1 to grade severity of airways obstruction is fraught with difficulties:

The recommendations relate to COPD and do not take account of coexisting restrictive ventilatory defects. Restrictive lung disease associated with an FEV1%(F)VC below a borderline leads to overestimating the severity of airway obstruction. Each assessment is very sensitive to how well the reference values adopted fit the population. In a large Dutch population, for example, adjustments of predicted values were required for FEV1 and FVC, but not for FEV1%FVC. The latter index has a strong point in its favor: even though predicted FEV1 and (F)VC differ widely in various parts of the world, differences in the level of these indices level out in the ratio, leading to remarkable international uniformity in the level of this index. In spite of ethnic differences in FEV1 and (F)VC, in western societies the FEV1%(F)VC differs little, if at all, between Caucasians and other ethnic groups, from childhood to old age. Publications from non-western countries seem to suggest that particularly in black women the FEV1/FVC ratio tends to be higher than in Caucasian women (see ethnic differences). With the potential exception of some non-western countries, therefore, FEV1%FVC offers a robust solution to diagnosing airway obstruction independent of ethnic differences in ventilatory function, but this is not the case for assessing its severity from the level of FEV11, in particular because of the paucity of predicted values for nonCaucasians. General practitioners tend to underestimate FEV1 by up to 280 mL, depending on equipment used and previous training (see FEV1 underestimated). In general this is to be expected if spirometric measurements are not performed by professionally trained personnel and do not conform to international recommendations. If FEV1%(F)VC is below normal limits, airway obstruction tends to be systematically overestimated when based on the level of FEV1.

In keeping with international recommendations the severity of airway obstruction is based on the level of FEV1%predicted. The SpirXpert scaling complies with the BTS classification: Obstruction FEV1%FVC FEV1%predicted None Mild > LLN < LLN > 60%

Moderate Severe


40-59 % < 40% FEV1%(F)VC (corrected for age and gender)

Expiratory airway obstruction No obstruction

above 5th percentile, and no bronchodilator response below 5th percentile and FEV1%pred >60% , or above 5th percentile and bronchodilator response below 5th percentile and FEV1%pred 40-59% below 5th percentile and FEV1%pred <40%

Mild obstruction

Moderate obstruction Severe obstruction

Bronchodilator response No response Mild response Marked response Possibly response

Criteria for grading of response Increase in FEV1 < 200 mL and < 9% initial FEV1 Increase in FEV1 > 200 mL and/or > 9% initial FEV1 Increase in FEV1 > 12% initial FEV1 and > 200 mL According to FEV1 no bronchodilator responsiveness, but increase in (F)VC > 340 mL and/or > 12% initial value and fall in FEV1%(F)VC < 2%: the increase in (F)VC might reflect better subject cooperation

Reversibility of airway obstruction No reversibility Partial reversibility Completely reversible Airway obstruction but no response to bronchilator drug In spite of the response to a bronchodilator drug the FEV1%(F)VC is still below the 5th percentile FEV1%(F)VC after the bronchodilator drug is above the 5th


VC too low Moderate Severe

Criterion below 5th percentile but SDS* > -3 SDS* < -3.0

FEV1 Too low

Criterion below 5th percentile

Humidity and Bland aerosol Therapy A. Humidity Therapy a. Physiological control of heat and moisture exchange i. Heat and moisture exchange is the primary function of the upper respiratory tract, mainly the nose. During inspiration through the nose, the tortuous path of gas through the turbinates increases contact between the inspired air and the mucosa. As the inspired air enters the nose, it warms (convection) and picks up water vapor from the moist mucosal lining (evaporation), cooling the mucosal surface. During exhalation, the expired gas transfers heat back to the cooler tracheal and nasal mucosal by convection. As the saturated gas cools, it holds less water vapor. Condensation occurs on the mucosal surfaces during exhalation, and water is reabsorbed by the mucus. In cold environments, the formation of condensate may exceed the ability of the mucus to reabsorb water (running nosw). ii. As inspired gas moves into the lungs, it achieves BTPS conditions (body temperature, 37C; barometric pressure; saturated with water vapor). This point, normally approximately 5 cm below the carina, is called the isothermic saturation boundary (ISB) b. Indications i. The primary goal is to maintain normal physiological conditions in the lower airways. Proper levels of heat and humidity help ensure normal function of the mucociliary transport system. ii. Administration of dry medical gases at flows greater than 4 L/min to the upper airway causes immediate heat and water loss, and if prolonged, causes structural damage. As the airway is exposed to relatively cold, dry air, ciliary motion is reduced, airways become more irritable, mucous production increases, and pulmonary secretions become thick and inspissated. iii. Prolonged breathing of improperly conditioned gases through a tracheal airway can result in hypothermia, inspissations of airway secretions, mucociliary dysfunction, destruction of airway epithelium, and atelectasis. iv. The amount of heat and humidity that a patient needs depends on the site of delivery. v. Warmed, humidified gases are used to prevent or treat a variety of abnormal conditions. For treatment of the hypothermic pt, heating and humidifying the inspired gas is one of several techniques used to raise core temperatures back to normal. Heated humidification is also used to prevent intraoperative hypothermia. c. Equipment

i. A humidifier is a device that adds molecular water to gas. This occurs by evaporation from a water surface, whether the surface of water is in a reservoir or is a sphere of water in suspension (nebulization). d. Physical principles governing humidifier function i. Temperature 1. The greater the temperature of gas, the more water vapor it can hold. Although the humidifier fully saturates the gas, the low operating temperature limits total water vapor capacity to approximately 9.4 mg/L water vapor, equivalent to approximately 21% of body humidity. ii. Surface area 1. The greater the area of contact between water and gas, the more opportunity for evaporation to occur. Passover humidifiers pass gas over a large surface area of water. More space-efficient ways to increase the water/gas surface-area ratio include bubble diffusion, aerosol, and wick technologies. 2. The bubble-diffusion technique directs a stream of gas underwater, where it is broken up into small bubbles. As the gas bubbles rise to the surface, evaporation increases the water vapor content within the bubble. For a given gas volume, the smaller the bubbles, the greater the water/air surface-area ration 3. Wick technologies use porous water-absorbent materials to increase surface area. A wick draws water, into its fine honeycombed structure by means of capillary action. The surfaces of the wick increase the area of contact between the water and gas, which aids in evaporation iii. Time of contact 1. The longer a gas remains in contact with water, the greater the opportunity for evaporation to occur. B. Types of humidifiers a. Bubble Humidifiers i. Breaks (diffuses) an underwater gas stream into small bubbles. ii. To warn of flow-path obstruction and to prevent bursting of the humidifier bottle, bubble humidifiers incorporate a simple pressure-relief valve, or pop-off. Releases above 2 psi. b. Passover Humidifiers i. Wick type 1. The wick (a cylinder of absorbent material) is placed upright in a water reservoir and surrounded by a heating element. Capillary action continually draws up from the reservoir and keeps the wick

saturated. As dry gas enters the chamber it flows around the wick, quickly picking up moisture and leaving the chamber fully saturated with water vapor. No bubbling occurs. ii. Membrane type 1. Separates the water from the gas stream by means of hydrophobic membrane. Water vapor molecules can easily pass through the membrane, but liquid water cannot. No bubbling occurs. iii. Advantages 1. The can maintain saturation at high flows 2. They add little or no flow resistance to spontaneous breathing circuits 3. Do not generate any aerosols, and thus pose a minimal risk for spreading infection c. Heat and Moistures Exchangers (HME) i. A passover humidifier that has been described as an artificial nose. ii. 3 types of HME 1. Simple Condenser a. Contain a condenser element with high thermal conductivity, usually consisting of metallic gauze, corrugated metal, or parallel metal tubes. On inspiration, inspired air cools the condenser element. On exhalation, expired water vapor condenses directly on its surface and rewarms it. On the next inspiration, cool, dry air is warmed and humidified as is passes over the condenser element. Can only recapture approximately 50% of pts exhaled moisture. 2. Hygroscopic condenser humidifiers a. Using a condensing element of low thermal conductivity (paper, wool, foam) b. Impregnating this material with a hygroscopic salt (calcium or lithium chloride). 3. Hydrophobic condenser humidifiers a. Use a water repellent element with a large surface area and low thermal conductivity. During exhalation, the condenser temperature rises to approximately 25C because of the conduction and latent heat of condensation. On inspiration, cool gas and evaporation cools the condenser down to 10C. This large temperature change results in the conservation of more water to be used in the humidifying the next breath.

C. Heating Systems a. Hot plate at the base of the humidifier b. Wraparound type that surrounds the humidifier chamber c. A yolk or collar, element sits between the water reservoir and the gas outlet d. An immersion type heater, with the element actually placed in the water reservoir e. Heated wire in the Inspiratory limb warming a saturated wick or hollow fiber D. Bland aerosol therapy a. Equipment for therapy i. Aerosol Generators 1. Large-volume jet nebulizers a. Pneumatically powered, attaching directly to a flow meter and compressed gas source. Liquid particle aerosols are generated by passing gas at a high velocity through a small jet orifice. The resulting low pressure at the jet draws fluid from the reservoir up to the top of a siphon tube, where it is sheared off and shattered into liquid particles. The large, unstable particles fall out of suspension or impact on the internal surfaces of the device, including the fluid surface (baffling). The remaining small particles leave the nebulizer through the outlet port, carried into the gas stream. A variable air entrainment port allows air mixing to increase flow rates and to alter FIO2 levels. 2. Ultrasonic Nebulizers a. USN electrically powered device that uses a piezoelectric crystal to generate aerosol. This crystal transducer converts radio waves into high-frequency mechanical vibrations (sound). These vibrations are transmitted to a liquid surface, where the intense mechanical energy creates a geyser of aerosol droplets. E. Problem Solving and Troubleshooting a. Cross contaminations and infection i. Water systems should be changed regularly b. Environmental safety i. Mainly when aerosol therapy is prescribed for immunosuppressed pts of for those with TB c. Inadequate mist production d. Over hydration e. Bronchospasm f. Noise

Aerosol Drug Therapy A. Characteristics of Therapeutic Aerosols a. Output i. Aerosol output is defined as the weight of mass of aerosol particles produced by a nebulizer. For drug delivery systems, emitted dose is often used to describe the mass of aerosol leaving the nebulizer. Aerosol density is the weight or mass of aerosol per unit volume of gas leaving the nebulizer. b. Particle Size i. Particle size depends on the substance being nebulized, the nebulizer chosen, the method used to generate the aerosol, and the environmental conditions surrounding the particle. c. Deposition i. Aerosol particles are deposited when they leave suspension in gas. Only a portion of the aerosol generated from a nebulizer (emitted dose) may be inhaled. A smaller fraction of fine particles may be deposited in the lung (respirable dose). Inhaled mass is the amount of drug inhaled. The proportion of the drug mass of proper size to reach the lower respiratory tract is the respirable mass. Not all aerosol delivered to the lung in retained. A significant percentage of the inhaled drug may be exhaled. Whether aerosol particles that are inhaled enter and are deposited in the respiratory tract depends on the size, shape, and motion of the particles and on the physical characteristics of the airway and breathing pattern. Key mechanisms of aerosol deposition include: 1. Inertial Impaction a. Occurs when suspended particles in motion collide with and are deposited on a surface. The greater the mass and velocity of a moving object, the greater is its inertia and the greater is the tendency of that object to continue moving alone that path. When a particle of sufficient mass is moving in a gas stream and that stream changes direction, the particle tends to remain on its initial path and collide with the airway surface. Because inertia involves both mass and velocity, the higher the flow of a gas stream, the greater is the tendency for particles to impact and be deposited in the airways. Turbulent flow patterns, obstructed or tortuous pathways and Inspiratory flow greater than 30 L/min are associated with increased inertial impaction.

2. Gravimetric sedimentation a. Occurs when aerosol particles settle out of suspension and are deposited owing to gravity. The greater the mass of the particle, the faster it settles. Sedimentation occurs mostly in the central airways and increases with time, affecting the particles. 3. Brownian diffusion a. Primary mechanism for deposition of small particles, mainly in the respiratory region where bulk gas flow ceases and most aerosol particles reach the alveoli by diffusion. d. Aging i. Particles constantly grow, shrink, coalesce and fall out of suspension. The process by which an aerosol suspension changes over time is aging. How an aerosol ages depends on the composition of the aerosol, the initial size of its particles, the time in suspension, and the ambient conditions to which it is exposed. B. Hazards of aerosol therapy a. Adverse reaction to the medication being delivered i. Primary hazard b. Infection i. Can contribute to nosocomial infections by spreading bacteria by airborne route ii. The most common sources of bacteria are contaminated solutions, caregivers hands, and the pts own secretions c. Airway reactivity i. Cold and high-density aerosols can cause reactive bronchospasm and increased airway resistance, especially in pts with preexisting respiratory disease. Medicaitons, and distilled water have been associated with increased airway resistance and wheezing during aerosol therapy d. Pulmonary and systemic effects i. Are associated with the site of delivery and the drug being administered. Excess water can cause over hydration, and excess saline solution can cause hypernatremia e. Drug reconcentration i. During the evaporation, heating, baffling, and recycling of drug solution undergoing jet or ultrasonic nebulization, solute concentration may increase. This process can expose the pt to increasingly higher concentrations of the drug over the course of therapy. The result is

that a relatively large amount of drug remains in the nebulizer at the end of therapy. This increase in concentration usually is time dependent, the greatest effect occurring when medications are nebulized over extended periods, as in continuous aerosol drug delivery C. Aerosol Drug Delivery System Effective aerosol therapy requires a device that quickly delivers sufficient drug to the desired site of action with minimal waste and at a low cost. a. Metered Dose Inhalers i. The pressurized MDI (pMDI) is the most commonly prescribed method of aerosol delivery in the US. MDIs are portable, compact, and relatively easy to use. ii. Properly used, MDIs are at least as effective as other nebulizers for drug delivery. iii. Technique 1. As many as 2/3 of both pt and health professionals who teach MDI use do not perform the procedure properly. 2. Thorough preliminary pt instruction can last 10 to 30 minutes and should include demonstration, practice, and confirmation of pt performance.
Technique for use of a metered dose inhaler (MDI) -Shake canister vigorously for 5 seconds. -Uncap mouthpiece and check for loose objects in the device. -Insert MDI into spacer. Hold the MDI upright with the index finger on the top of the medication canister and the thumb supporting the bottom of the inhaler. You may need to use the other hand to hold the spacer. -Breathe out normally. -Close lips around spacer. For spacers that have a mask, hold the mask snugly to the face. If no spacer is available, close lips around mouthpiece or position it about 4 cm from the mouth. -Keep tongue away from the spacer opening or mouthpiece. -Press down the top of the medication canister with the index finger to release the medication. -At the same time as the canister is pressed, inhale deeply and slowly through the mouth until the lungs are completely filled; this should take four to six seconds. -Hold the medication in the lungs as long as possible (4 to 10) seconds before exhaling. If using a spacer, you may inhale a second time and hold the breath if needed. -If a second puff is needed, wait approximately 15 to 30 seconds between puffs, or long enough to perform the next inhalation properly. Shake canister again before use. Recap mouthpiece.

iv. MDI Accessory Devices 1. Flow-triggered MDI a. Autohaler designed to eliminate the need for handbreath coordination by automatically triggering in response to the pts Inspiratory effort. To use, the pt cocks a lever on the top of the unit, which sets in

motion a downward spring force. Using the closedmouth technique, the pt draws through the mouthpiece. When the pts flow rate exceeds 30L/min, a vane release the spring, which forces the canister down and triggers the MDI. 2. Spacers and Holding Chambers a. Are accessory devices designed to reduce both oropharyngeal and the need for hand breath coordination b. Dry Powder Inhalers i. The pt creates the aerosol by drawing air through a dose of finely milled drug powder. DPIs are relatively inexpensive, do not need propellants, and do not require the hand-breath coordination needed for MDI. However, dispersion of the powder into respirable particles depends on the creation of turbulent flow of the inhaler. Turbulent flow is a function of the ability of the pt to inhale the powder with a sufficiently high Inspiratory flow rate. ii. Technique 1. The most critical factor in using a DPI is the need for high Inspiratory glow. Pts must generate an Inspiratory flow rate of at least 40-60L/min to produce a respirable powder of aerosol. Because infants, small children(<5) and those not able to follow instructions cannot develop flow this high, these pt groups cannot use DPI. c. Pneumatic (Jet) Nebulizers i. Small-volume nebulizers 1. Gas-powered jet nebulizers have been in clinical use for more than 100 years. Most modern jet nebulizers are powered by high-pressure air or oxygen provided by a portable compressor, compressed gas cylinder, or 50 psi wall outlet. Because nebulizers used at home and hospital have small (<10 mL) medication reservoirs, they are called small volume nebulizers (SVN). 2. Nebulizer design, gas pressure and density and medication characteristics affect SVN performance. ii. Large volume Nebulizers 1. Used to provide continuous nebulization with a specialized large-volume nebulizer. 2. Special purpose large volume nebulizer is a Small Particle aerosol generator (SPAG)





a. Specifically designed for administration of ribavirin (Virazole) b. Caregiver is exposed to the drug aerosol c. If used through mechanical ventilator circuit, drug precipitation can jam breathing valves or occlude the ventilator circuit i. Fix by placing 1 way valve between SPAG and the circuit ii. Filtering out the excess aerosol particles before they reach the exhalation valve Ultrasonic Nebulizer i. Use piezoelectric crystal is used to produce an aerosol. The crystal transducer converts an electrical signal into high-frequency acoustic vibrations. These vibrations are focused in the liquid above the transducer, where they disrupt the surface and create oscillation waves. If the frequency of the signal is high enough and its amplitude strong enough, the oscillation waves form a geyser of droplets that break free as fine aerosol particles. They are capable of high aerosol outputs (0.2-0.5 mL/min) and higher aerosol densities than are conventional jet nebulizers. Hand-Bulb atomizer i. Hand-bulb atomizer, or nasal spray pump, is used to administer sympathomimetic, antimuscarinix, anti-inflammatory, and anesthetic aerosols to the upper airway. These agents are used to manage upper airway inflammation and rhinitis, to provide local anesthesia, and to achieve systemic effects. Selecting an aerosol drug delivery system i. The available drug formulation ii. Desired site of deposition iii. Pts characteristics (age, acuity or problem, alertness and ability to follow instructions) iv. Pts preference Controlling environmental contamination i. Nebulized drugs that escape from the nebulizer into the atmosphere or are exhaled by the pt can be inhaled by anyone in the vicinity of the treatment ii. The greatest occupational risk for RTs is believed to be associated with administration of ribavirin and pentamidine. Conjunctivitis, headachs, bronchospasm, shortness of breat, and rashes have been reported among those administering these drugs. Pts given

aerosolized ribavirin or pentamidine, must be treated in a private room, booth, or tent or at a special station designed to minimize environmental contamination. iii. Negative-pressure rooms 1. When ribavirin or pentamidine is given, the treatment is provided in a private room. The room should be equipped for negative pressure ventilation with adequate air exchanges (at least 6 per hour) to clear the room of residual aerosols before the next treatment. High-efficiency particulate air (HEPA) filters should be used to filter room or tent exhaust, or the aerosol should be scavenged to the outside.

Storage and Delivery of Medical Gases A. Gas Cylinders a. Are marked with metal stamping on the shoulders that supplies specific information. B. Cylinder Sizes a. E through AA C. Estimating the Duration of Cylinder Gas Flow a. Duration of flow = Contents/Flow b. Duration of Flow (min) = Pressure x Cylinder Factor / Flow (L/min) D E G H and K 0.16 0.28 2.41 3.14 D. Bulk Oxygen a. Holds at least 20,000 cubic feet of gas. May be stored in either gaseous or liquid form, but liquid storage is the most common. b. Gas Supply Systems i. Alternating supply system or cylinder manifold system ii. A cylinder supply system with reserve supply iii. Bulk gas system with a reserve E. Flow Restrictors a. Thorpe Tube i. Pressure compensated ii. Pressure uncompensated b. Bourdon Gauge i. Always used in combination with an adjustable device that is always used in combination with adjustable pressure-reducing valve.

Medical Gas Therapy A. Oxygen Therapy a. General Goals and Clinical Objectives i. Correct documented or suspected acute hypoxemia 1. Raising alveolar and blood levels of oxygen ii. Decrease the symptoms associated with chronic hypoxemia 1. COPD and some forms of interstitial lung disease report less dyspnea receiving supplemental oxygen iii. Decrease the workload hypoxemia imposes on the cardiopulmonary system 1. The cardiopulmonary system compensates for hypoxemia by increasing ventilation and cardiac output. B. Assessing the Need for Oxygen Therapy a. Use of laboratory measures to document hypoxemia i. Hemoglobin saturation and PaO2 b. Based on specific clinical problem or condition i. Postoperative, carbon monoxide poisoning, cyanide poisoning, shock, trauma, or acute myocardial infraction c. Clinical manifestation such as tachypnea, cyanosis, and distressed overall appearance C. Precautions and Hazards of Supplemental Oxygen a. Oxygen Toxicity i. Affects the lungs and CNS. Two primary factors determine the harmful effects of oxygen: PO2 and exposure time. The higher the PO2 and the longer the exposure the greater the likelihood of damage. Effects on CNS, including tremors, twitching, and convulsions, tend to occur when a pt is breathing oxygen at pressures greater the 1 atm ii. The toxicity of oxygen is caused by overproduction of oxygen free radicals. b. Depression of Ventilation i. When breathing moderate to high oxygen concentration, COPD pts with chronic hypercapnia tend to ventilate less. The primary reason some COPD pts hypoventilate when given oxygen is most likely suppression of the hypoxic drive. In these pts, the normal response to high PCO2 is blunted, the primary stimulus to breathe being lack of oxygen, as sensed by the peripheral chemoreceptors. The increase in the blood oxygen level in these pts suppresses peripheral chemoreceptors, depresses ventilator drive, and elevates PCO2. c. Retinopathy of prematurity

i. An abnormal eye condition that occurs in some premature or low-birthweight infants who receive supplemental oxygen. An excessive blood oxygen level causes retinal vasoconstriction, which leads to necrosis of the blood vessels. In response, new vessels form and increase in number. Hemorrhage of these new vessels causes scarring behind the retina. Scarring leads to retinal detachment and blindness. d. Absorption Atelectasis i. Breathing high levels of oxygen quickly depletes body nitrogen levels. As blood nitrogen decrease, the total pressure of venous gases rapidly decreases. Under these conditions, gases that exist at atmospheric pressure conditions, gases that exist at atmospheric pressure within any body cavity rapidly diffuse into the venous blood. This principle is used for removing trapped air from body cavities. For example, giving pts high levels oxygen can help clear trapped air from the abdomen or thorax. Unfortunately, this same phenomenon can cause lung collapse, especially if the alveolar region becomes obstructed. D. Oxygen Delivery Systems a. High Flow i. An air-entrainment or blending system is used. As long as the deliverd flow exceeds the patients flow, both systems can ensure a fixed FIO2. ii. Gas Mixing 20 30 20 Air value Desired FIO2 100 Oxygen value 100 70 50

30/50 = 0.6:1 b. Low Flow 1. Nasal Cannula a. A humidifier is used only when the input flow exceeds 4 L/min 2. Nasal Catheter 3. Trantracheal Catheter c. Reservoir i. Reservoir Cannula ii. Reservoir Mask

iii. Nonrebreathing reservoir circuit d. FIO2 Ranges i. Low (<35%) ii. Moderate (35-60%) iii. High (>60%) iv. Determining fixed or variable FIO2 1. Depends how much or the pts inspired gas it supplies. If the system provides the entire pts inspired gas, it remains stable. If it provides only some of the inspired gas, the pt must draw the remainder from the surrounding air e. Enclosures i. Oxygen tents 1. Croup tents ii. Hoods iii. Incubators E. Hyperbaric Oxygen Therapy a. Therapeutic use of oxygen at pressures greater than 1 atm b. Physiological Effects i. Air embolism and decompression sickness, high pressure exerts a physical effect on air or nitrogen bubbles trapped in blood or tissues c. Methods of Administration i. Multiplace ii. Monoplace chamber d. Indications i. Air embolism 1. Complications that can occur with certain cardiovascular procedures, lung biopsy, hemodialysis, and central line placement. It decreases the volume of air bubbles and helps oxygenate local tissue. ii. Carbon Monoxide Poisoning F. Other Medical Gas Therapies a. Nitric Oxide Therapy i. Mode of Action 1. Endogenous nitric oxide is normally produced from L-arginine in a reaction catalyzed by the enzyme nitric oxide synthase. Nitric oxide activates guanylate cyclase, which catalyzes the production of cGMP. Increased cGMP levels cause smooth-muscle relaxtion. Because it relaxes capillary smooth muscle, inhalation of nitric oxide improves blood flow to ventilated alveoli. The result is a reduction in intrapulmonary shunting, improvement in arterial

oxygenation, and a decrease in pulmonary vascular resistance and pulmonary arterial pressure. ii. Indications 1. In conjunction with ventilator support and other appropriate agents, is indicated for treatment of term and near-term (>34 weeks) neonates with hypoxic (type I) respiratory failure associated with pulmonary hypertension. iii. Dosing 1. 20 ppm 2. Treatment should be continued up to 14 days or until underlying oxygenation desaturation has resolved. Dosage can be reduced to 5 ppm at the end of 4 hours after initial treatment. iv. Withdrawing therapy 1. Nitric oxide level should be reduced to the lowest effective dose (ideally <5 ppm) 2. The pts condition should be hemodynamically stable and able to maintain adequate oxygenation while breathing a moderate FIO2 (< 0.4) on low levels of positive end expiratory pressure. 3. The pt should be hyperoxygenated just before discontinuation of inhaled nitric oxide 4. Preparations should be made to provide hemodynamic support should the pt need it. b. Helium Therapy i. Indications 1. Based solely on its low density. 2. Helium-oxygen therapy also has been found effective in the management of acute upper airway obstruction of varying origin, postextubation stridor in pediatric trauma pts, and refractory viral croup ii. Guidelines for use 1. Because helium is highly diffusible, mixtures of this gas generally should be administered with a closed system or with a smallvolume reservoir device. iii. Troubleshooting 1. The low density of helium mixtures makes them poor vehicles for aerosol transport. High-density bland water aerosols are difficult to deliver with helium mixtures, as are aerosolized drugs. 2. The low density of helium mixtures also makes coughing less effective

3. Hypoxemia associated with breathing helium mixtures. Although this problem may have been caused by using too low an oxygen concentration. Some commercial cylinders of helium-oxygen have been found to contain these gases in an unmixed, or separated, state. The only way to avoid this potential hazard is to analyze the oxygen concentration coming from the cylinder before administering the gas mixture to a pt

Lung Expansion Therapy A. Intro a. Pulmonary complications are the most common serious problems seen in patients who have undergone thoracic or abdominal surgery. Lung expansion therapy includes IPPB, IS, CPAP, and PEP. B. Causes and types of atelectasis a. Reabsorption atelectasis i. Occurs whenmucus plugs are present in the airways and block ventilation of the affected region b. Passive atelectasis i. Caused by persistent use of small tidal volumes by the pt. This is common when general anesthesia is given, with the use of sedation and bed rest, when deep breathing is painful as when broken ribs are present or surgery has been performed on the upper abdominal region. Weakening or impairment of the diaphragm also can contribute to passive atelectasis c. Lobar actelectasis i. Occurs in about 5% of pts who have undergone lung resection. This type of atelectasis significantly lengthens the pts stay in the ICU and hospital. This cause of lobar atelectasis often centers around a large mucus plug but is often the result of multiple factors. C. Indications a. Pts who have difficulty taking deep breaths without assistance include those with neuromuscular disorders, those who are heavily sedated, and those who have undergone upper abdominal or thoracic surgery. D. Clinical signs a. Recent abdominal or thoracic surgery b. History of chronic lung disease and/or cigarette smoking. c. The physical signs may be absent or very subtle if the pt has minimal atelectasis. When it involves a more significant portion of the lungs, the pts respiratory rate will increase proportionally. Fine, late-inspiratory crackles are heard over the affected area. Crackles are produced by the sudden opening of distal airways with deep breathing. E. Incentive Spirometry a. Designed to mimic natural sighing by encouraging pts to take slow, deep breaths. b. Physiological Basis i. The basic maneuver is a sustained, maximal inspiration. c. Indications

i. Treat existing atelectasis. It may also be used as a preventive measure when conditions exist that makes the development of atelectasis likely. d. Contraindications i. Unable to cooperate or follow instructions e. Hazards i. Dizziness and numbness around the mouth associated with respiratory alkalosis F. Intermittent Positive Pressure Breathing (IPPB) a. Definition and Physiological i. The application of inspiratory positive pressure to a spontaneously breathing pt as an intermittent or short term therapeutic modality. ii. It reverses the normal spontaneous pressure gradients. Positive pressure at the airway opening creates the needed pressure at the airway opening creates the needed pressure gradient to flow into the lungs b. Indications i. The need to improve lung expansion 1. The presence of clinically important pulmonary atelectasis when other forms of therapy have been unsuccessful or the pt cannot cooperate 2. Inability to clear secretions adequately because of pathology that severely limits the ability to ventilate or cough effectively and failure to respond to other modes of treatment ii. The need for short term noninvasive ventilator support for hypercapnic pt (as an alternative to intubation and MV) iii. The need to deliver aerosol medication 1. Although some authors oppose the use of IPPB in the treatment of sever bronchospasm, a closely supervised trail of IPPB treatment using other techniques has been unsuccessful 2. IPPB may be used to deliver aerosol medications to pts with ventilator muscle weakness or fatigue or chronic conditions in which intermittent noninvasive ventilator support is indicated. c. Contraindications i. Although no absolute contraindications to the use of IPPB therapy (except tension pneumothorax) have been reported, the pt with any of the following should be carefully evaluated before a decision is made to initiate IPPB therapy: 1. ICP >15 mmHg 2. Hemodynamic instability 3. Recent facial, oral, or skull surgery

4. Tracheoesophageal fistula 5. Recent esophageal surgery 6. Active hemoptysis 7. Nausea air swallowing 8. Active untreated TB 9. X-ray of bleb 10. Singulus (hiccups) d. Hazards and complications i. Increased airway resistance ii. Barotraumas, pneumothorax iii. Nosocomial infection iv. Hyperventilation/hypocapnia v. Hemoptysis vi. Hyperoxia when oxygen is the gas source vii. Gastric distention viii. Secretion impaction (inadequate humidity) ix. Psychological dependence x. Impedance of venous return xi. Exacerbation of hypoxemia xii. Hypoventilation xiii. Increased V/Q mismatch xiv. Air trapping, autoPEEP, over distended alveoli e. Assessment of Need i. Presence of atelectasis ii. Reduced time volumes or VC precluding an effective cough iii. Neuromuscular or skeletal disorders associated with decreased in lung volumes and capacities iv. Fatigue or muscle weakness with impending respiratory failure v. Presence of acute, severe bronchospasm or exacerbated COPD that fails to respond to other therapy vi. With demonstrated effectiveness, the pts preference for a positive pressure device should be honored f. Assessment of Outcome i. Tidal volume during IPPB greater than during spontaneous breathing ii. FEV1 or peak flow increase iii. Cough more effective with treatment iv. Secretion clearance enhanced as a consequence of deep breathing and coughing v. CXR improved vi. BS improved

vii. Favorable pt subjective response g. Monitoring i. Items from the following list should be chosen as appropriate for the specific pt: 1. Machine performance 2. Respiratory rate and volume 3. Perk flow or FEV1/FVC 4. Pulse rate and rhythm from ECG 5. Pt subjective response (pain, discomfort, dyspnea) 6. Sputum production (quantity, color, consistency and odor) 7. Mental function 8. Skin color 9. BS 10. Blood pressure 11. Arterial Hg saturation by Pulse Oximetry 12. ICP in pt for whom ICP is of critical importance 13. CXR h. Troubleshooting i. Sensitivity 1. Seen by large negative pressure swings early in inspiration 2. Alter sensitivity so only 1-2 cm H2o are needed to trigger ii. Pressure drop after inspiration begins or fails to rise until they very end of the machine breath; the problem is too low a flow. Increase flow until system pressure rises steadily and holds near the preset value. iii. Too high a flow will cause the device to cycle off prematurely. A lower flow setting flow setting will usually resolve this. iv. The device will cycle off prematurely when airflow is obstructed v. Leaks will cause the device to not reach its preset cycling pressure and thus not cycle off. To troubleshoot leaks check the differentiate between the machine and pt interface. Machine leaks most commonly occur at the connection points such as the nebulizer or exhalation valve. A torn or improperly seated exhalation valve diaphragm will cause a large leak. Leaks at the pt interface usually occur at the mouth or the nose.

Bronchial Hygiene Therapy A. Physiology of airway clearance a. Normal Clearance i. Requires a patent airway, a functional mucociliary escalator, and an effective cough. The mucus itself originates from the goblet cells and submucosal glands, although Clara cells and tissue fluid transudation also contribute to airway secretions. ii. Phases of cough 1. Irritation a. An abnormal stimulus provokes sensory fibers in the airways to send impulses to the brains medullary cough center. The stimulus is normally inflammatory, mechanical, chemical, or thermal. 2. Inspiration a. Once these afferent impulses are received, the cough center generates a reflex stimulation of the respiratory muscles to initiate a deep inspiration, about 1-2 L. 3. Compression a. Reflex nerve impulses cause glottis closure and a forceful contraction of the expiratory muscle. 4. Expulsion a. The glottis opens, initiating the expulsion phase. With the glottis open, a large pressure gradient is established between the alveoli and the airway opening. Together with the continued contraction of the expiratory muscles, this pressure gradient causes a violent, expulsive flow of air from the lungs b. Abnormal Clearance i. Any abnormality that alters airway patency, mucociliary function, or the effectiveness of the cough reflex can impair airway clearance and cause retention of secretions. Retention of secretions can result in full or partial airway obstruction. Full obstruction or mucus plugging, can result in atelectasis and impaired oxygenation due to shunting. By restricting airflow, partial obstruction can increase the work of breathing and lead to air trapping, over distention, and ventilation/perfusion imbalances. In the presence of pathogenic organisms, retention of secretions can lead to infections. Infectious processes, in turn, provoke an inflammatory response and the release of chemical mediators

ii. In critically ill pts with artificial airways, the tube presence in the trachea increases mucus secretion, while the tube cuff mechanically blocks the mucociliary escalator. In addition, the movement of the tube tip and cuff can cause erosion of the tracheal mucosa and further impair mucociliary clearance. Last, artificial tracheal airways impair the compression phase of the cough reflex by preventing closure of the glottis. Although suctioning is used to aid secretion clarance, it too can cause damage to the airway mucosa and thus impair mucociliary transport. Inadequate humidification can cause inspissations of secretions, mucus plugging, and airway obstruction. High FIO2 can impair mucociliary clearance, either directly or by causeing acute tracheobronchitis. Several common drugs including some general anesthetics and narcotic-analgesics, can depress the mucociliary transport. Last, several diseases commonly seen in critical care are associated with poor secretion clearance. c. General goals i. The primary goal of bronchial hygiene therapy is to help mobilize and remove retained secretions, with the ultimate aim to improve gas exchange and reduce the work of breathing. d. Indications i. Acutely ill pts with copious secretions ii. Pts in acute respiratory failure with clinical signs of retained secretions iii. Pts with acute lobar atelectasis iv. Pts with V/Q abnormalities due to lung infiltrates or consolidation e. Determining the need i. An ineffective cough, absent or increased sputum production, labored breathing pattern, decreased breath sounds, crackles or rhonchi, tachypnea, tachycardia, or fever indicates a potential problem with retained secretions B. Bronchial hygiene methods a. Postural drainage therapy i. Involves the use of gravity and mechanical energy to help mobilize secretions, improve V/Q balance, and normalize the FRC b. Coughing and related expulsion techniques c. PAP adjuncts d. High-frequency compression oscillation methods i. A variable air-pulse generator ii. A nonstretch inflatable vest e. Mobilization and exercise

Mechanical Ventilation How Ventilators Work A. Internal Function a. User Interface Certain controls on a control panel b. Control System interprets the operators settings and produces and regulates the desired output B. Power Source or Input power a. Electorally Powered Ventilators i. Wall Outlet (AC) ii. Battery (DC) b. Pneumatically Powered Ventilators i. Use a 50 psi gas source and have built in internal reducing valves so that the operating pressure is lower than the source pressure 1. Pneumatic Ventilators a. May use needle valves, Venturi entrainers, flexible diaphragms, and spring loaded valves to control flow, volume delivery, and inspiratory and expiratory function 2. Fluidic Ventilator a. Rely on special principles to control gas flow, specifically the principles of wall attachment and beam deflection c. Combined Power Ventilator i. The gas sources, mixtures of air and oxygen, allow for a variable FIO2 and may be also supply the power for ventilator function ii. The electrical power may be used to control capacitors, solenoid, and electrical switches that regulate phasing or inspiration and expiration and the monitoring of gas flow. These functions may be controlled by a microprocessor. d. Positive and Negative Pressure Ventilators i. Ventilator gas flow into the lungs is based on two different methods of changing the transrespiratory pressure at the airway opening minus pressure at the body surface. A ventilator can control pressure either at the mouth or around the body surface C. Control Systems and Circuits a. Open and Closed Loop Systems to Control Ventilator Function i. Open loop Not microprocessor controlled (unintelligent) ii. Closed Loop compare the set control variable to measured control variable (intelligent) b. Control Panel (User Interface)

i. Located on the surface of the ventilator and is monitored and set by the ventilator operator c. Pneumatic Circuit i. A series of tubes that allow gas to flow inside the ventilator and between the ventilator and the pt. The pressure gradient created by the ventilator with its power source generates the flow of this gas. D. Power Transmissions and Conversion Systems a. Compressors (Blowers) i. Reduce internal volumes, resulting in a change in pressure. b. Volume Displacement Designs i. Such as bellows, pistons, concertina bags, and bag in a chamber c. Flow Control Valves i. Control or direct gas flow by opening and closing either completely or in small increments

How a Breath is Delivered A. Factors Controlled and Measured by the Ventilator During Inspiration a. How the manufacturer designed the ventilator b. How it is set by the operator c. Pressure Controlled Breathing i. The pressure waveform in a specific pattern d. Volume Controlled Breathing i. Maintains the volume waveform in a specific pattern e. Flow Controlled Breathing i. The flow and volume waveforms remain unchanged, but the pressure waveform changes with alterations in lung characteristics f. Time Controlled Breathing i. Both the pressure and volume waveforms are affected by changes in lung characteristics B. Four Phases of a Breath and Phase Variables a. Change from exhalation to inspiration b. Inspiration c. Change from inspiration to exhalation d. Exhalation e. Beginning of Inspiration: Trigger Variable i. Time Trigger 1. The breath begins when the ventilator has measured an elapsed amount of time ii. Patient Triggering 1. Pts often attempt to breath spontaneously during mechanical ventilation; therefore machines have been developed that sense this effort a. Pressure Triggering i. Usually set at -1 cm H2O b. Flow Triggering i. Occurs when the ventilator detects a drop in flow through the pt circuit during exhalation. c. Volume Triggering i. Occurs when the ventilator detects a small drop in volume in the pt circuit during exhalation f. Inspiratory Factors: The Limit Variable i. Pressure Limiting 1. Allows pressure to rise to a certain value but not exceed it ii. Volume Limiting

Controlled by an electronically operated valve that measures the flow passing through during a specific interval. The colume may be set by the operator, or the ventilator may have a bag, bellows, or piston cylinder that contains a fixed volume. With either type of machine, a maximum volume that can be delivered is established. iii. Flow Limiting 1. Only a certain amount of flow can be provided g. Termination of the Inspiratory Phase: Cycle variable i. Volume-Cycled Ventilation 1. Breath is terminated when the set volume has been delivered a. Set Volume vs actual delivered volume i. Tubing Compressibility ii. System Leaks ii. Time Cycled 1. The inspiratory phase ends when a predetermined time has elapsed iii. Flow-Cycled 1. The ventilator cycles into the expiratory phase once the flow has decreased to a predetermined value during inspiration iv. Pressure-Cycled Ventilation 1. When a preset pressure threshold is reached at the mouth or upper airway, a ventilator set to pressure cycle ends inspiration v. Inflation Hold (Inspiratory Hold) 1. Designed to maintain air in the lungs at the end of inspiration, before the exhalation valve opens. The pressure reading peaks during inspiration and the levels to a plateau (Plateau pressure) h. Types of Breath i. Mandatory Breath 1. The ventilator determines the start time or tidal volume ii. Spontaneous Breath 1. Started by the pt, and the tidal volume delivered are based on pt demand rather than a value set by the operator i. Expiratory Phase: The Baseline Variable i. Definition of Expiration 1. The period between inspirations ii. Baseline Pressure 1. The pressure level from which a ventilator breath begins iii. Time-limited Exhalation


1. Some ventilators have a mode that allows the operator to control (inspiratory time) and (expiratory time). iv. Expiratory Hold 1. It allows the pt to exhale completely, then pauses before the next breath is delivered.

Establishing the Need for Mechanical Ventilation A. Acute Respiratory Failure a. Recognizing the pt in distress i. Evaluation of the pts level of consciousness ii. Assess color, and texture of the pts skin iii. Check vital signs (respiratory rate, heart rate, blood pressure, body temperature, and SpO2) b. Definition of Respiratory Failure i. Respiratory activity is absent or is insufficient to maintain adequate oxygen uptake and carbon dioxide clearance. ii. Lung failure accompanied by hypoxemia 1. Result of severe V/Q mismatch iii. Pump failure accompanied by hypercapnia 1. The ventilator pump consists of the respiratory muscle, thoracic cage, and nerve centers that control ventilation B. Patient History and Diagnosis a. Central Nervous System Disorders i. Disorders associated with the CNS, such as depression of the respiratory centers induced by drugs or trauma, can lead to significant reductions in minute ventilation and alveolar ventilation. b. Neuromuscular Disorders i. Motor nerve damage ii. Problems with transmission of nerve impulses at the neuromuscular junction iii. Muscle dysfunction iv. Nervous system disorders v. Drugs that affect the neuromuscular function c. Increased Work of Breathing C. Physiological Measurements in acute Respiratory failure a. Ventilator Mechanics i. Maximum Inspiratory Pressure ii. Vital Capacity 1. Ability to take in a large volume of air is considered important to the production of a cough strong enough to clear the airway iii. Peak Expiratory Flow Rate and FEV1 1. A good indicator of whether the pt is maintaining adequate airway patency iv. Respiratory Rate and Minute Ventilation 1. Normal rate is 12-20 2. Rates exceeding 35 are inadequate alveolar ventilation

v. Failure of Ventilation and Increased Dead Space 1. PaCO2 of more than 50 55 mm Hg with a decreased pH (<7.25) indicates acute hypoventilation or acute hypercapnic respiratory failure vi. Failure to Oxygenate 1. PaO2 is 80-100 mm Hg on room air D. Overview of Criteria for Mechanical Ventilation a. Support the pulmonary system so that it can maintain an adequate level of alveolar ventilation b. Reduce the work of breathing until the cause of respiratory failure can be identified and treated c. If possible, restore arterial and systemic acid-base balance to levels that are normal for the pt d. Increase oxygen delivery to and oxygenation of body and organs and tissues e. Prevent complications associated with mechanical ventilation

Selecting Ventilatory and Mode A. Full and Partial Ventilatory support a. Full ventilatory support (FVS) i. Provides all the energy necessary to maintain effective alveolar ventilation b. Partial ventilatory support (PVS) i. Is any degree of mechanical ventilation in which set machine rates are lower than 6 breaths/min and the pt participates in WOB to help maintain effective alveolar ventilation. B. Mode of ventilation and breath delivery a. Type of breath delivery i. Mandatory 1. Breaths for which the ventilator controls the timing or tidal volume or both. ii. Spontaneous 1. The pt controls the timing and tidal volume iii. Assisted 1. Have characteristics of both mandatory and spontaneous breaths. All or part of the breath is generated by the ventilator, which dose part of the WOB for the pt. b. Targeted control variable i. Volume 1. Volume is constant and independent of what happens to pressure when the pts lung characteristics (CL and RAW) change or when the pts effort change 2. Advantages it guarantees a specific volume delivery and VE, regardless of lung compliance and resistance or pt effort. 3. Disadvantage can cause the peak and alveolar pressure to rise, leading to alveolar over distention. However, this type of problem is reversible. When lung conditions improve, less pressure is required and ventilating pressures decline. ii. Pressure 1. Pressure remains constant whereas volume delivery changes as lung characteristics change. 2. Advantages a. Allows the RT to set a maximum pressure, which reduces the risk of over distention of the lungs by limiting the pressure put on the lungs. b. The ventilator delivers a descending flow pattern during PV.

3. Disadvantages a. Volume delivery varies b. Clinicians are less familiar with it c. VT and VE decrease when lung characteristics deteriorate c. Continuous Mandatory Ventilation i. All breaths are mandatory and can be volume or pressure targeted. Breaths also can be pt triggered or time triggered. ii. Controlled Ventilation 1. Is appropriate only when a pt can make no effort to breath or when ventilation must be completely controlled. Pts who are obtunded because of drugs, cerebral malfunction, spinal cord or phrenic nerve injury, or motor nerve paralysis may be unable to make voluntary efforts, therefore control ventilation is appropriate for them. iii. Assist/Control Ventilation 1. Time triggered or pt triggered. The operator sets a minimum rate, sensitivity level and type of breath (volume or pressure) iv. Volume-targeted Continuous Mandatory Ventilation 1. PC-CMV all breaths are time or pt triggered, pressure targeted (limited), and time cycled. v. Intermittent Mandatory Ventilation and Synchronized Intermittent Mandatory Ventilation 1. Periodic volume or pressure targeted breaths occur at set intervals. Between mandatory breaths, the pt breaths spontaneously at any desired baseline pressure without receiving a mandatory breath. SIMV originally designed to eliminate the problem of breath stacking. The mode is used when the goal is to have the pt breathe spontaneously without receiving a mandatory breath with even effort. d. Spontaneous Modes i. Spontaneous Breathing 1. Also called T-piece. Used to evaluate a pts readiness to have ventilation discontinued. ii. CPAP 1. May be useful for improving oxygenation in pts with refractory hypoxemia and a low FRC, as can occur with ALI iii. PSV 1. The ventilator provides a constant pressure during inspiration once it senses that the pt has made an inspiratory effort. PSV is

always an assist mode. The flow curve resembles a descending ramp, and the pt can vary the inspiratory flow on demand. a. To overcome WOB for spontaneously breathing pts, including those on CPAP, SIMV, through the ventilator circuit and the ETT b. To reduce WOB further in CPAP, SIMV by setting the pressure level higher than that required to overcome system resistance c. To provide full ventilatory support in the assist mode, in which each pt breath is a PS breath. The PT must have a dependable, intact respiratory center and a fairly stable lung condition for this use to because VT can vary. iv. Bilevel positive airway pressure 1. Also called bipap is another form of pressure ventilation used most often in NPPV. Bi-level Intermittent positive airway pressure (bilevel IPAP or APRV) is intended for pts with ARDS. C. Closed Loop Ventilation a. Dual control: Volume Delivered Every Breath i. Called pressure augmentation (PAug), guarantees volume delivery with every breath. The ventilator begins with a pt-triggered, pressuretargeted breath but targets the volume preset by the operator and delivers that volume every breath. b. Dual Control Pressure Ventilation with Breath-by-Breath Volume Target i. PRVC delivers pt or time-triggered, pressure-targeted, time-cycled breaths. During breath delivered and compares it to the tidal volume set on the controls. If the volume delivered is less than the set tidal volume, the ventilator increases pressure delivery progressively over several breaths until the set and the targeted are about equal. If the measured volume is too high, the pressure is reduced until the set and monitored volumes are about equal. The ventilator does not allow the pressure to rise higher than 5 cm H2O below the upper pressure limit setting. As the pt improves, less pressure is required to deliver the set volume. The ventilator progressively lowers the pressure but does not allow it to drop below the set baseline PEEP. D. Less Frequently Used Closed Loop Modes a. Mandatory Minute Ventilation (MVV) i. Primarily used to wean pts from the ventilator b. Airway Pressure Release Ventilation (APRV)

i. Designed to use 2 levels of CPAP and to allow spontaneous breathing at both levels when spontaneous effort is present. Both pressure levels are time triggered and time cycled. For initial setup, an optimum high SPAP level is determined much as the optimum PEEP or an ideal Paw is determined for improving oxygenation. The high CPAP is interrupted intermittently to allow pressure to drop very briefly (for about 1 second or less) to a lower CPAP level. Reducing the CPAP reduces the FRC and allows pt exhalation and ventilation. Expiratory flow generally is not permitted to return to baseline, therefore autoPEEP is intentionally present; this helps maintain an open lung and prevents repeated collapse and reexpansion of alveoli. c. Proportional Assist Ventilation (PAV) i. Is a different approach to mechanical ventilation because pressure, flow, and volume delivery are proportional to the pts spontaneous effort. The amount of pressure depends on: 1. The amount of inspiratory flow and volume demanded by the pts effort 2. The degree of amplification selected by the clinician ii. The ventilator measures airway flow and pressure and compares pt demand with the gain (amplification) set by the operator. The amount of flow provided to the pt is based on the result of this comparison. The more the pt effort increases, the greater the flow the ventilator provides

Initial Ventilator Settings A. Initial Settings during Volume Ventilation a. Setting Minute Ventilation i. Normal body metabolism results in total body oxygen consumption of about 150 mL/min and carbon dioxide production of about 200 mL/min. The primary goal of VV is to achieve a desired VE that matches the pts metabolic needs and accomplishes adequate gas exchange. b. Tidal Volume and Rate i. Normal spontaneous VT is about 5 7 mL/kg with a spontaneous rate of 12 18 breaths/min and a spontaneous VE of about 100mL/kg of IBW ii. For ventilated pts, a range of 6 12 mL/kg of IBW c. Tubing Compliance i. Reflects the amount (in mL) of gas compressed in the ventilator circuit for every centimeter of water pressure generated by the ventilator during inspiratory phase d. Mechanical Dead Space Considerations i. The volume of gas that is rebreathed during ventilation B. Inspiratory Flow and Flow Pattern a. The flow setting on a mechanical ventilator estimates the delivered flow of inspired gas. b. High flows shorten TI and may result in higher peak pressures and poor gas distribution. c. Slower flows may reduce peak pressures, improve gas distribution and increase Paw at the expense of increasing TI. This may cause cardiovascular side effects and shorten TE, leading to air trapping. d. Flow Patterns i. Constant Flow 1. Also called square waveform. A constant flow pattern provide the shortest TI of all the available flow patterns with an equivalent peak flow rate setting ii. Ascending Ramp 1. Provides an increase flow. No studies support the use iii. Sine Flow 1. The tapered flow at the end of inspiratory phase may contribute to a more even distribution of gas in the lungs than flow of the constant flow ventilator iv. Descending Ramp

1. Flow is greatest at the beginning of inspiration, when the pt flow demand is most often the highest. Occurs naturally in pressure ventilation C. Determining Initial Settings During Pressure Ventilation a. Setting Baseline pressure-physiological PEEP i. FRC decreases when a pt is intubated or placed in the supine position In most situations it is appropriate to use minimum levels of PEEP (35 cm H2O) b. Determining Tidal Volume in Pressure Ventilation i. In any pressure targeted breath the change in pressure between baseline and PIP is what is set to establish the VT delivery. Volume delivery will also be affected by the pts lung characteristics and any pt effort that is present c. Initial settings for PSV i. Usually started after the pt has been on full ventilatory support and is being moved to partial support to begin the process of discontinuing ventilation. PSV is used to support spontaneous breaths in a pt with an artificial airway when SIMV or CPAP modes are used. The pressure is set at a level sufficient to prevent a fatiguing workload on the respiratory muscles. ii. The goal of PSV 1. The help increase VT (5-12 mL/kg) 2. To decrease respiratory rate (<25-20 breaths/min) 3. To decrease work of breathing associated with breathing through an artificial airway D. Initial Settings for Pressure Control Ventilation (PCV) a. Rate, TI, and I:E are set the same as they are in VV. The pressure gradient is adjusted to establish a volume delivery based on pt lung characteristics and effort. If volume readings are not available, an initial pressure of 10-15 cm H2O with simultaneous volume measurement and adjustment is appropriate. PIP cannot exceed the set pressure (< 30 cm H2O). PCV has been shown to improve oxygenation, and gas exchange, increase Paw, facilitate lung healing, and reduce the following: PIP, required applied PEEP< VE, respiratory work, need for sedation, and ventilation time.

Final Considerations in Ventilator Setup A. Selection of Additional Parameters and Final Ventilator Setup a. Fractional Inspired O2 i. The goal is to achieve a PaO2 between 60-100 mm Hg Desired FIO2 = PaO2 (desired) x FIO2 (known) / PaO2 (known) ii. It is advisable to select a high initial FIO2 setting (0.5 1.0) to benefit pts with presumed severe hypoxemia iii. Any procedure that might be risky for the pt needs to be performed with 100% O2 iv. A SpO2 of >92% is a common acceptable goal. An ABG should be collected within 10-20 mins to assess the adequacy of ventilation v. An FIO2 > 0.65 increases the risk of oxygen toxicity and intrapulmonary shunting. b. Sensitivity Setting i. Is normally set so that pts can easily flow or pressure trigger a breath 1. Flow Trigger a. The exhalation valve does not have to close during flow triggering b. There is a flow of gas in the circuit during exhalation when flow triggering is selected. c. Humidification i. Normal spontaneous breathing provides 100% relative humidity at 37 C and contains 44 mg/L of water. Conditioning typically occurs down to the forth of fifth generation of subsegmental bronchi and is called isothermic saturation boundary. The heating system should provide at least 30 mg H2O/L of absolute humidity at a range of 31 35 C. ii. Heated Humidifiers 1. Avoid the need to open the ventilator circuit to refill the device. 2. Whenever the temperature in the pt circuit is less than the temperature of gas leaving the humidifier, condensate will accumulate in the circuit. iii. Heat Moisture Exchangers 1. Can provide from 10 14 mg/L of water at VT or 500 to 1000mL. More efficient hygroscopic heat and moisture exchangers (HHME) can provide from 22-34 mg/L at similar volumes. 2. HMEs should be taken out of line during delivery of an aerosolized medication d. Alarms

i. Low pressure 1. Usually set 5-10 cm H2O below PIP ii. High Pressure 1. Usually set about 10 cm H2O above PIP iii. Low PEEP/CPAP 1. Usually set at about 2-5 cm H2O below the PEEP level iv. Apnea Alarms 1. Period of no more than 20 seconds v. Low Gas Source 1. Can be critical for newer microprocessor ventilators that rely on high pressure gas to function. vi. Low Exhaled VT 1. 10 15 % below set VT vii. Low Exhaled Minute Volume 1. 10-15% below average VE e. Periodic Hyperinflation or Sighing i. Deep breaths and sighs have been used before and after suctioning a pt ii. A normal sigh in a spontaneously breathing, nonintubated pt occurs every 6 mins. f. Final Considerations i. Check ventilator and circuit function to ensure they are operating correctly and no significant leaks are present ii. Fill the humidifier with sterile water and set the humidifier temperature so that the final gas temperature at the airway will be approximately 31-35 C or place HME iii. Place a temperature monitoring device neat the pt connector when heated humidification is used iv. Check FIO2 v. Adjust Alarm vi. Be sure monitoring ECG is connected to pt vii. Have an emergency airway tray is available in case the pts airway is removed of damaged viii. Provide suctioning equipment ix. Select a volume-monitoring device and an oxygen analyzer if one is not available with the ventilator x. Keep a manual resuscitation bag with the ventilator B. Settings for Specific pt Situations a. COPD i. Have increased Raw and may have increased Cl

1. If possible use noninvasive ventilation to help avoid problems associated with artificial airway use. Bi-PAP is ideal for pts with COPD 2. If intubation is necessary, orotracheal intubation recommended 3. VC or PC-CMV may unload the work of the respiratory muscle more the SIMV. Using pt-triggered CMV in alert pt with COPD may increase the risk of hyperinflation and elevated lung pressures, and this mode should be monitored carefully 4. Adjuct the peak inspiratory flow to meet the pts demand in BV using the descending ramp waveform: flow >60 L/min and up to 100 L/min 5. In pt with COPD and asthma, where the airway obstruction and resistance are high, an initial VT of 8-10 mL/kg with a rate of 8-12 breaths/min and Ti 0.6 to 1.2 sec 6. PEEP < 5 cm/H2O or about 50% of auto-PEEP should be used initially 7. Monitor for and minimize dynamic hyperinflation by setting the lowest possible VE that produces acceptable gas exchange, targeting the pt baseline PaCO2 and pH 8. Provide the longest expiratory time possible. This might include decreasing TI, increasing TE, reducing f and/or VT, and accepting hypercapnia. (PaCO2 50-60 mm Hg, pH 7.30 to 7.40) 9. If the pt is initiating inspiration once ventilation has started and auto-PEEP is present, set PEEP near 80% of the auto-PEEP level, but do not exceed it. 3-5 cm H2O is often adequate. If PIP begins to rise because PEEP is increased, the safe PEEP level has probable been exceeded and will result in lung over inflation 10. P-Plateau should be monitored and maintained at <30 cm H2O to avoid alveolar over distention and lung injury. Accurate measurement of P-Pl may require sedation and paralysis. The decision to medicate pts is generally based on physician preference and institutional policy 11. Maintain PaO2 at 55-75 mm Hg or near the pts normal rate, with FIO2 <0.5, unless the pts condition worsens and he requires more oxygen. b. Neuromuscular Disorders

i. Myasthenia gravis, amyotropic lateral sclerosis, muscular dystrophy, poliomyelitis or post-polio syndrome, Guillian-Barre, tetanus, cervical spine injury, botulism and others ii. Ventilation is often needed because of progressive respiratory muscle weakness that eventually leads to respiratory failure iii. Guidelines 1. Full or partial support 2. Negative or PPV 3. Noninvasive or invasive 4. A/C 5. Volume Ventilation 6. High Vt (12-15 mL/kg) 7. RR - 8-12 8. Inspiratory flow >60 L/min to meet pt need 9. Flow waveform: constant or descending 10. PEEP of 5 11. FIO2 0.21 c. Asthma i. VC or PC are acceptable modes. With AV/PC being easier to keep pressures controlled ii. Keep peak and plateau minimized. PIP may be high due to the high Raw and use of high inspiratory gas flows. Plateau pressures must still be kept low (<30 cm H2O) despite high PIP iii. Maintain oxygenation by using an FIO2 as needed to keep PaO2 from 60 100 mmHg, usually > 0.50. Monitor hemodynamic status to be sure cardiac output is stable iv. Permissive hypercapnia (PaCO2 45-80 mmHg) is acceptable as long as pH range is acceptable (7.1-7.2) v. If the ventilator cannot be matched to accommodate the pt needs, the use of sedatives and paralytics may be necessary. The use of sedation and paralytics may permit resting of fatigued muscles, particularly during the first 24 hrs. vi. When the pts are spontaneously breathing and/or triggering breaths, setting the PEEP at about 80% of auto PEEP may make triggering easier. In some cases, applied PEEP may recruit lung units that are collapsed and may also assist with expired gas flows. In other cases it may worsen the pts conditions. If PIP increases with the application of PEEP, decrease the PEEP.

vii. Avoid reducing auto PEEP by providing long expiratory times: RR <8; VT 4-8 mL/kg; TI <1 sec; inspiratory gas flows = 80 to 100 L/min with descending wave flow viii. The occurrence of barotraumas in the form of pneumothorax, is not uncommon in these pts. d. Closed head injury i. Following head injury, protect the airway because the pt with altered levels of consciousness may be unable to do so. There is a high risk for vomiting and aspiration. Orotracheal intubation is often required. ii. AC/PC and PEEP can increase ICP. These pts often have normal lungs, so high alveolar pressure can be transmitted to the blood vessels, thus affecting venous return to the heart. Monitoring for elevated ICP can help evaluate this effect. iii. Monitor for increased ICP and hypoxemia so that a rapid increase in ventilation and oxygenation can be instituted if needed or if recommended by institutional policy. iv. When there is acute uncontrolled increased ICP, maintain PaCO2 from 25-30 mm Hg or titrate the ICP if its being monitored. v. If iatrogenic hyperventilation is used, this should only be temporary with PaCO2 gradually returning to normal levels in 24-48 hours, allowing acid-base balance to restore itself. Sudden increases in PaCO2 could trigger increases in cerebral blood flow and ICP. A normal response to acute increases in ICP is hypertension with bradycardia and is called cushing response. vi. Ventilator settings include 1. Provide full support to start 2. Either AC/VC or PV can be used 3. Maintain VT from 8-12 mL/kg while maintaining plateau <30 4. RR of 15-20 to provide normal acid base status, as long as auto PEEP is avoided 5. FiO2 of 100% initially and titrated as needed to keep PaO2 from 70-100 mm Hg 6. High inspiratory flows >60 L/min to keep TI short about 1 sec using a descending or constant flow wave form 7. PEEP 0-5 cm H2O as long as ICP is being measured and kept below 10 mm Hg vii. Suctioning and CPT can dramatically increase ICP, but maintaining a clear airway is also essential. Bronchial hygiene therapy must be done with extreme caution

viii. Monitor for complications of pulmonary infections and pulmonary emboli e. Acute Respiratory Distress Syndrome i. Choose a mode capable of supporting oxygenation and ventilation such as AC/VC or PC ii. Maintain Sao2 >88 to 90%. Start at 100% oxygen. To support oxygenation, use PEEP at a level that prevents alveolar collapse and overdistention to prevent lung damage. PEEP may allow reduction of FiO2 to safe levels. When oxygenation is inadequate, sedate, paralyze and change the pt position. CO and Hb levels should be optimized. High PEEP may allow reduction of FiO2 safer level iii. Keep Plateau <20 cm H2O by lowering VT 4-6 mL/kg. Allow PaCO@ to rise above normal is necessary, unless there is a risk of increased ICP or contraindications exist that demand a more normal PaCO2 or pH. Rapid rises in PaCO2 should be avoided f. Acute Carcinogenic Pulmonary Edema and CHF i. Select a mode that reduces WOB. This can be CPAP, which can improve oxygenation, reduce PaCO2, reduce the WOB, and reduce myocardial work. NPPV in pts with CHF may allow sufficient time for pharmacological treatment to become effective ii. When life threatening hypoxemia occurs with severe CHF, PEEP, and/or PPV may have beneficial effects on myocardial function and improve oxygenation iii. Careful evaluation of the effects of PPV on hemodynamics is essential. This may include the use of a pulmonary artery catheter in severe cases, particularly if PEEP >10-15. However, the use of pulmonary catheters carries a risk of increases mortality and morbidity and is controversial iv. The use of AV/CV or PC is recommended to avoid spontaneous breathing, which may divert increased blood flow and oxygen consumption to the respiratory muscle v. VT is from 8-20 mL/kg; RR >10, and peak flow of >60 L/min using descending or constant waveforms. TI range from 1-1.5 sec vi. Set a PEEP of 5-10 to support cardiac function vii. Start Fi02 at 100 and titrate quickly with SaO2 >90% viii. Monitor SaO2, ABGs, urine output, electrolytes, and systemic hemodynamics

Initial Assessment of the Mechanically Ventilated Pt A. Documentation of the Pt-Vent System a. Ventilator Flow Sheet i. Perform Vent Checks 1. Before an ABG 2. When there are new orders 3. Before hemodynamic data or bedside PFTs are done 4. When vent changes are made 5. When an acute change occurs in the pts condition 6. When the vents performance is questionable b. Compliance i. Static Compliance 1. 70-100 mL H2O (Cs = VT / Plateau EEP) a. Low can be caused by: air trapping, pulmonary edema, atelectasis, consolidation, pneumonia, pneumothorax, hemothorax, and pleural effusion ii. Dynamic Compliance 1. Cd = VT/PIP-EEP 2. Decreases whenever Cs decreases or Raw increases

Vent Graphics

Hemodynamic Monitoring A. Cardiac Cycle a. Systole i. The heart muscle contracts and ejects blood b. Diastole i. When the heart relaxes and fills with blood B. Ventricular Events a. Ventricular systole begins with a period of isovolumetric contraction, which coincides with the peak of the R wave on the ECG. As the ventricles contract, the mitral and tricuspid valves close, producing the first heart sound (S1). b. During this period of contraction, the left ventricular pressure increases from 0 to about 80 mm Hg and the right ventricular pressure increases from 0 to about 12 mm Hg. The volume of blood in the ventricle remains constant because the AV valves and the semi lunar valves are closed. c. As the ventricle contraction continues, the left ventricular pressure exceeds the aortic diastolic pressure and the right ventricular pressure exceeds the pulmonary artery and diastolic pressure; a period of ejection begins as blood flows rapidly out of the ventricle across the semi lunar valves. The pressure in the aorta and pulmonary artery continue to rise toward their peak systolic pressure during this ejection phase

Pathology A. Obstructive Airway disease a. Chronic obstructive pulmonary disease (COPD) is a term applied to a group of common chromic pulmonary disorders that are characterized by a variety of pathologic conditions that cause a reduction of airflow into and out of the lungs. b. Chronic Bronchitis i. Anatomic Alterations of lungs 1. Chronic inflammation and swelling of the peripheral airways 2. Excessive mucus production and accumulation 3. Partial or total mucus plugging 4. Hyperinflation of alveoli 5. Smooth muscle constriction of bronchial airways ii. Etiology 1. Smoking 2. Atmospheric pollutants 3. Infection 4. Gastroesophegeal Reflux Disease (GERD) iii. General Management 1. Pt Education a. Pulmonary rehabilitation 2. Behavioral management a. Avoidance of smoking and inhaled irritants b. Avoidance of infections c. Emphysema i. Anatomic Alterations of the Lungs 1. Permanent enlargement and destruction of the air spaces distal to the terminal bronchioles 2. Destruction of the pulmonary capillaries 3. Weakening of the distal airways, primarily the respiratory bronchioles 4. Bronchospasm 5. Air trapping ii. Etiology 1. Cigarette smoking 2. Genetic predisposition a. Alpha-1-antitrypsin deficiency 3. Occupational exposure to chemical irritants 4. Exposure to atmospheric pollutions iii. Additional treatments 1. Antibiotics

2. 3. 4. 5. iv. PFTs 1.

Inoculations against influenza and pneumonia Alpha-antitrypsin therapy Lung volume reduction therapy Lung transplant

Expiratory Maneuver Findings a. All reduced 2. Lung Volumes and Capacities a. VT, RV, FRC, TLC Up b. VC, IC, ERV Down

d. Asthma i. Anatomic Alterations of the Lungs 1. Bronchospasm 2. Excessive production of thick, whitish tenacious bronchial secretions 3. Air trapping 4. Mucus plugging and in, severe cases, atelectasis ii. Etiology 1. Extrinsic (allergic) a. Episodes associated with exposure to antigenic agent 2. Intrinsic (nonallergic) a. Not linked to a specific antigen 3. Exercise and Cold Air Exposure 4. Industrial Pollutants or Occupational Exposure 5. Drugs, food additives, and food preservatives 6. GERD 7. Nocturnal Asthma 8. Emotional Stress 9. Premenstrual Asthma (Catamnemail Asthma) 10. Risk Factors a. Residence in large, urban area, esp inner city b. Exposure to 2nd hand smoke c. Parent with asthma d. Respiratory infections in childhood e. Low birth weight f. Obesity iii. Medications 1. Xanthines 2. Corticosteroids 3. Other anti-inflammatory agents

a. Cromolyn sodium (intal) b. Nedocromil sodium (tilade) 4. Leukotriene inhibitors a. Montelukast (singular) b. Zafirlukast (Accolate) c. Zileuton (Zyflo) iv. PFTs 1. Expiratory Maneuver Findings a. All Decreased 2. Lung Volumes and Capacities a. Vt, RV, FRC, TLC increased b. VC, IC, ERV decreased e. Bronchiectasis i. Anatomic Alterations of the Lungs 1. Chronic dilation and distortion of one or more bronchi as a result of extensive inflammation and destruction of the bronchial wall cartilage, blood vessels, elastic tissue, and smooth muscle components 2. Varicose Bronchiectasis a. The bronchi are dilated and constricted in an irregular fashion similar to varicose veins, ultimately resulting in a distorted, bulbous shape b. Cylindrical Bronchiectasis i. Bronchi are dialated and have regular outlines similar to a tube. The dilated bronchi fail to taper for 6 to 10 generations and then appear to end abruptly because of mucus obstruction c. Saccular Bronchiectasis i. The bronchi progressively increase in diameter until the end in large cyst like sacs in the lung parenchyma d. Chronic dilation and distortion of bronchial airways e. Excessive production of often foul smelling sputum f. Smooth muscle constriction of bronchial airways g. Air trapping h. Atelectasis i. Hemorrhage 2nd to bronchial arterial erosion 3. Etiology a. Acquired i. Recurrent pulmonary infections

ii. Bronchial obstruction b. Congenital i. Kartageners syndrome ii. Hypogammagloblinemia iii. Cystic Fibrosis 4. General Management a. Medications i. Xanthines ii. Expectorants iii. Antibiotic