Paramedic Care: Principles & Practice

Paramedic Care: Principles & Practice
Volume 3, 5e Chapter 1 Pulmonology

Multimedia Directory Slide 22 Gas Exchange Animation Slide 82 Inspiratory Wheezing Animation Slide 122 ARDS Animation Slide 125 COPD Video

Standard Medicine (Respiratory)

Competency Integrates assessment findings with principles of epidemiology and pathophysiology to formulate a field impression and implement a comprehensive treatment/disposition plan for a patient with a medical complaint.

Introduction Respiratory system: responsible for providing oxygen to tissues; removing metabolic waste product, carbon dioxide. Oxygen required for conversion of essential nutrients into energy; must be constantly available to all tissues.

Introduction Intrinsic risk factors: influenced by or are from within patient; genetic predisposition. Certain respiratory conditions increased in patients who have underlying cardiac or circulatory problems. Patient's level of stress may increase severity of respiratory complaint.

Introduction Extrinsic risk factors: external to patient; increase likelihood of developing respiratory disease. Most important risk factor: cigarette smoking. Environmental pollutants another factor. Teaching Tips Respiratory emergencies are some of the most common responses for the EMS provider. It is important for the students to understand the importance of managing respiratory emergencies.

Review of Respiratory Anatomy and Physiology
Upper airway responsible for warming and humidifying incoming air. Air enters upper airway through nose. Passes through external nares (nostrils); enters nasal cavity. Nasal cavity divided into two chambers by nasal septum. Anterior portion has many hair follicles that help trap large dust particles. Teaching Tips This is a review of previously discussed material. Revisit the previous topics concerning anatomy of the respiratory system.

Figure 1-1 Overview of the upper and lower airways.

Upper Airway Between each set of turbinates is passageway (meatus); leads to paranasal sinuses. Turbinates cause turbulence in incoming airflow. Mucus constantly produced. Cilia: thin, fingerlike projections; ability to contract in single direction.

Figure 1-2 Anatomy of the upper airway.

Upper Airway In nose, cilia produce steady posterior flow of mucus, removing any entrapped particles. Once mucus and entrapped particles reach nasopharynx, they are swallowed and removed via digestive tract. Class Activities Because this is review material, have students split into groups and present a portion of the respiratory system to the rest of the class. Then you can gauge which content students need to practice more with.

Upper Airway Kiesselbach's plexus, in lower nasal septum, warms inspired air. Paranasal sinuses: air cavities in frontal, ethmoid, sphenoid, maxillary portions of skull. Superior portion of nose contains nerve fibers important to sense of smell (olfactory sense).

Figure 1-3 Paranasal sinuses.

Upper Airway Pharynx: funnel-shaped structure that connects nose and mouth to larynx. Three divisions: Nasopharynx Oropharynx Laryngopharynx

Upper Airway In addition to speech, larynx is filtering device for digestive/respiratory tracts. During inspiration, three paired cartilages remain separated; epiglottis sits upright so air can enter trachea. With swallowing, epiglottis tips backward; cartilage pairs close, diverting food to esophagus.

Lower Airway During inspiration, air exits upper airway; passes through larynx into trachea. Trachea :11 cm in length; composed of series of C- shaped cartilaginous rings. Stimulation by food or other ingested products triggers coughing response.

Lower Airway At carina, trachea divides into right and left mainstem bronchi. Mainstem bronchi divide into secondary (lobar) bronchi; ultimately divide into bronchioles, or small airways. Both upper airway and lower airway must be patent so air may pass through bronchial system into alveoli.

Lower Airway Bronchioles become terminal bronchioles. Terminal bronchioles divide into respiratory bronchioles. Airway shifts from being conduit for air to organ of gas exchange.

Figure 1-4 Anatomy of the lower airway.

Lower Airway Respiratory bronchioles divide into alveolar ducts. These terminate in alveolar sacs (alveoli). Estimated 300 million alveoli in lungs. Most gas exchange (oxygen and carbon dioxide) takes place in alveoli.

Gas Exchange Animation
Questions: 1. What is the function of the alveolus? 2. What type of cell makes up the pulmonary capillaries? 3. What two gases are exchanged in the alveolus? 4. What is this process of gas exchange called? Click here to view an animation on the topic of alveolar gas exchange. Back to Directory

Figure 1-5 The alveoli and the pulmonary capillaries.

Lower Airway Pulmonary capillaries: carry carbon-dioxide-rich blood from heart into lungs and oxygen-rich blood away from lungs for return to heart. Alveolar lining, supportive tissue, and capillaries make up respiratory membrane.

Lower Airway Alveoli moistened and kept open because of chemical called surfactant. Alveolar macrophages part of immune system; function to digest particles, bacteria, and other foreign material.

Lower Airway Lungs main organs of respiration. Right lung has three main divisions or lobes; left lung has only two. Covered by connective tissue (pleura). Pleural fluid: serves as lubricant for lung movement during respiration.

Lower Airway Blood supplied to lungs: pulmonary vessels and bronchial vessels. Pulmonary arteries transport deoxygenated, carbon– dioxide–rich blood from heart and lungs for oxygenation. Pulmonary veins transport oxygenated blood from lungs back to heart.

Physiologic Processes Major function of respiratory system is to exchange gases with environment. Gas exchange: oxygen taken in; carbon dioxide eliminated. Oxygen diffuses into bloodstream through lungs. In lungs, carbon dioxide exchanged for oxygen and excreted from lungs.

Physiologic Processes Ventilation: mechanical process of moving air in and out of lungs. Body structures must be intact: chest wall, nerve pathways, diaphragm, pleural cavity, brainstem. Chest wall protects heart, lungs, other organs of thorax; diaphragm separates thorax and abdomen.

Physiologic Processes Ventilation has two phases: inspiration and expiration. During inspiration, air drawn into lungs. During expiration, air leaves lungs. Phases depend on changes in volume of thoracic cavity.

Physiologic Processes Inspiration always active process, requiring energy. Inspiration dependent on intact chest wall and intact pleural cavity. During expiration, chest wall and diaphragm recoil to normal resting state. Expiration passive process; does not require energy. Class Activities Map a molecule of oxygen moving through the body, beginning with inhalation and ending with a target organ. Briefly discuss different areas where respiratory emergencies may affect its travel through the body.

Physiologic Processes Amount of airflow into lungs (ventilation) dependent not only on difference between pressure in atmosphere and that inside chest cavity; also on airway resistance and lung compliance.

Physiologic Processes The more airway resistance (or drag to flow of air), the less air flowing into chest cavity. Lung compliance: ease with which chest expands. Change in volume of chest cavity; results from specific change in pressure within chest cavity.

Physiologic Processes Volume of air entering lungs varies based on metabolic needs of patient. Factors such as age, sex, physical conditioning, medical illness will alter these volumes. Tidal volume: during quiet respiration, 500 mL of air move in and out of lungs of 70-kg adult.

Physiologic Processes Inspiratory reserve volume: lungs draw in additional volume of air beyond volume inspired during quiet respiration. Expiratory reserve volume: amount of air that can be forcibly expired out of lungs after normal breath. Residual volume: air remains in lungs at all times; maintains patency of alveoli.

Physiologic Processes Inspiratory capacity: sum of tidal volume and inspiratory reserve volume. Functional residual capacity: sum of expiratory reserve and residual volume. Vital capacity: amount of air measured from full inspiration to full expiration. Total lung capacity: total volume of air in lungs.

Physiologic Processes Minute respiratory volume: amount of air moved in and out of lungs during 1 minute. Minute alveolar volume: volume of air moving through alveoli in 1 minute. Forced expiratory volume (FEV): volume of air exhaled over measured period of time.

Physiologic Processes Peak flow: measures maximum rate of airflow during forced expiration. Anatomical dead space: air rests in trachea, mainstem bronchi, bronchioles; unavailable for gas exchange. Alveolar dead space: some alveoli unavailable for gas exchange.

Physiologic Processes Lower portions of brainstem (medulla) control ventilation; both inspiratory and expiratory center. Medullary signal transmitted through phrenic and intercostal nerves to muscles of ventilation; diaphragm and intercostal muscles.

Physiologic Processes Stretch receptors provide input to medulla's respiratory center. Prevents overinflation of lungs (Hering-Breuer reflex). Most important determinant of ventilatory rate is arterial PCO2. Increase in arterial PCO2 results in decrease in pH of blood.

Physiologic Processes Chemical receptors in medulla detect decrease in pH, which produces increase in ventilatory rate. Helps body eliminate excess CO2 and return pH to normal level. In patients with chronic obstructive pulmonary disease (COPD), body less responsive to changes in arterial PCO2.

Physiologic Processes Diffusion: gases move between alveoli and pulmonary capillaries. Oxygen moves from oxygen-rich alveoli into oxygen- poor capillaries. Carbon dioxide passes out of blood in response to gradient between concentration of carbon dioxide in blood in pulmonary capillaries and in alveoli.

Physiologic Processes Respiratory membrane must remain intact for gas exchange to occur. Endothelial lining of capillaries must be intact for exchange of oxygen and carbon dioxide to occur.

Physiologic Processes Problems with lung diffusion: Provide patient with high concentrations of oxygen. Medications such as diuretic agents or anti-inflammatory drugs given to reduce fluid and inflammation.

Physiologic Processes Lung perfusion: circulation of blood through lungs or pulmonary capillaries. Dependent on three conditions: Adequate blood volume Intact pulmonary capillaries Efficient pumping of blood by heart

Physiologic Processes Perfusion: adequate volume of blood in bloodstream. Oxygen transported in bloodstream: bound to hemoglobin or dissolved in plasma. Oxyhemoglobin: hemoglobin with oxygen bound. Deoxyhemoglobin: hemoglobin without oxygen.

Physiologic Processes Hemoglobin: four iron-containing heme molecules; protein-containing globin. Oxygen molecules bind to heme portion. Oxygen dissociation curve: fully oxygen-bound hemoglobin releases oxygen. Changes in body temperature, blood pH, and PCO2 can alter oxygen dissociation curve.

Physiologic Processes Carbon dioxide transported from cells to lungs: As bicarbonate ion (70%) Bound to globin portion of hemoglobin molecule (23%) Dissolved in plasma (measured as PCO2) (7%)

Physiologic Processes Majority of carbon dioxide transported in form of bicarbonate ion; released from red blood cells (RBCs) and transported in plasma. In lungs, reverse process takes place, producing water and carbon dioxide. Carbon dioxide diffuses into alveoli; eliminated during exhalation.

Physiologic Processes Carbaminohemoglobin: hemoglobin with carbon dioxide bound. Haldane effect: heme portion of hemoglobin molecule becomes saturated with oxygen; becomes acidic and more carbon dioxide released. Only fraction of carbon dioxide transported as gas.

Physiologic Processes For perfusion to take place: Adequate blood volume. Pulmonary capillaries able to transport blood through lung tissue; vessels must be open and not occluded, or blocked. Heart must pump efficiently to push blood through pulmonary capillaries to perfuse lung tissues.

Physiologic Processes To maintain perfusion, ensure patient has adequate circulating blood volume; improve pumping action of heart. Pulmonary respiration: occurs in lungs. Cellular respiration: occurs in peripheral capillaries.

Pathophysiology Any disease process that impairs pulmonary system will result in derangement in ventilation, diffusion, perfusion, or combination of these processes. Knowledge Application Respiratory physiology is very important in the management of respiratory emergencies. It is important to be able to tie the concepts of respiratory emergencies to the functions and structures within the body they affect. For example, correlate the pulmonary circulation with the disorders that affect it.

Pathophysiology Disruption in Ventilation
Disease states that affect upper respiratory tract result in obstruction of airflow to lower structures. Chest wall and diaphragm mechanical components essential for ventilation. Traumatic injuries to these areas will disrupt mechanics, causing loss of negative pressure within pleural space.

Pathophysiology Disruption in Ventilation
Any disease that impairs regulation of breathing alters ventilation. Abnormal respiratory patterns: Cheyne-Stokes respirations Kussmaul's respirations Central neurogenic hyperventilation Ataxic (Biot's) respirations Apneustic respiration

Pathophysiology Disruption in Diffusion
Any change in concentration of oxygen in alveoli can limit diffusion of oxygen and produce hypoxia. Any disease that alters structure or patency of alveoli will limit diffusion. Diseases alter thickness of respiratory membrane; fluid and inflammatory cells in interstitial space.

Pathophysiology Disruption in Diffusion
Similar effects produced by changes in permeability (leakiness) of pulmonary capillaries (noncardiogenic causes). Disease states alter pulmonary capillary endothelial lining.

Pathophysiology Disruption in Perfusion
Any disease state that reduces normal circulating blood volume will limit normal perfusion of lungs. Any reduction in normal circulating hemoglobin will affect perfusion. Pulmonary shunting: area of lung tissue ventilated, no perfusion occurs; oxygen not moved to circulatory system.

Assessment of the Respiratory System
Scene Size-Up Is scene safe to approach patient? Are there visual clues that might provide information regarding patient's medical complaint? Certain gases and toxic products causing respiratory complaints from patient may present significant risk to you; dust particles also a risk. Discussion Topics How does the assessment of a respiratory patient differ from assessment of other patients? What is important to consider when assessing respiratory patients?

Scene Size-Up Environments in which concentration of oxygen significantly reduced: grain silos, enclosed storage containers, any enclosed space with active fire. Specific protective items: hazardous materials suits, self-contained breathing apparatus (SCBA), supplemental oxygen.

Scene Size-Up HAZMAT teams required; contact dispatch. Using your eyes, ears, nose can lead to important, useful clues as you assess patient.

Primary Assessment General Impression Consider patient's position. Severe cases, patient will assume "tripod" position. Patients with severe respiratory distress display pallor and diaphoresis. Cyanosis late finding; may be absent even with significant hypoxia.

Figure 1-14 Tripod position.

Primary Assessment General Impression Assess mental status. Hypoxic patient: restless and agitated. Confusion with hypoxia and hypercarbia. Respiratory failure imminent: patient will appear severely lethargic and somnolent.

Primary Assessment General Impression Assess patient's ability to speak in full, coherent sentences. Rambling, incoherent speech indicates fear, anxiety, hypoxia. Respiratory effort: use of accessory muscles in neck and contractions of intercostal muscles indicate significant breathing effort.

Primary Assessment General Impression Nasal flaring Use of accessory respiratory muscles Cyanosis Pursed lips Tracheal tugging Identify life-threatening conditions resulting from compromise of ABCs.

Primary Assessment Airway Any significant abnormality in respiratory tract potentially life threatening. Noisy breathing nearly always means partial airway obstruction. Obstructed breathing not always noisy. Brain can survive only few minutes in asphyxia.

Primary Assessment Airway Artificial respiration useless if airway blocked. Patent airway useless if patient apneic. If airway obstruction, do not waste time looking for help or equipment. Act immediately.

Primary Assessment Airway If airway compromised, quickly institute basic airway management techniques. Once you have secured patent airway, ensure patient has adequate ventilation. Assessment should be brief and directed.

Primary Assessment Airway/Breathing Alterations in mental status Severe central cyanosis Absent breath sounds Audible stridor One- to two-word dyspnea Tachycardia ≥ 130 beats per minute

Primary Assessment Airway/Breathing Pallor and diaphoresis Presence of intercostal and sternocleidomastoid retractions Use of accessory muscles If any of these signs present, immediately resuscitate and transport.

Secondary Assessment History and physical exam determined by chief complaint or primary problem. Obtain SAMPLE history. Ask OPQRST questions. Obtain past history. Question patient or family about prior hospitalizations for respiratory disease.

Secondary Assessment Consider patients who have been previously intubated potentially seriously ill. Ask patient if he has known respiratory disease. Determine if disease affecting ventilation, diffusion, perfusion. History of medication use essential.

Secondary Assessment Pay particular attention to medications that suggest pulmonary disease. Ask if patient has home nebulizer unit. Ask about drugs for cardiac conditions. Inquire about medication allergies.

Secondary Assessment Pursed lips indicate significant respiratory distress. Examine nose, mouth, throat for signs of swelling or infection. Increase in amount of sputum suggests infection of lungs or bronchial passages. Look at jugular veins for evidence of distention.

Secondary Assessment Follow standard steps of patient assessment: inspection, palpation, percussion, auscultation. Inspection: examine anterior-posterior dimensions and shape of chest. Palpation: palpate chest, front and back, for abnormalities; tenderness, crepitus, subcutaneous emphysema.

Secondary Assessment Percussion: limit percussion to suspected cases of pneumothorax and pulmonary edema. Auscultation: auscultate chest; listen without stethoscope and from distance; note loud stridor, wheezing, or cough.

Figure 1-16 Inspection of the chest.

Secondary Assessment Normal Breath Sounds Bronchial (or tubular) Loud, high-pitched breath sounds heard over trachea Expiratory phase lasts longer than inspiratory phase

Secondary Assessment Normal Breath Sounds Bronchovesicular Softer, medium-pitched breath sounds heard over mainstem bronchi Expiratory and inspiratory phase equal Vesicular Soft, low-pitched breath sounds heard in lung periphery

Secondary Assessment Abnormal Breath Sounds Snoring Stridor Wheezing Rhonchi Crackles (rales) Pleural friction rub

Inspiratory Wheezing Animation
Questions: 1. Listen to the breath sound—inspiratory wheezing. Why does a wheeze sound this way? 2. What does wheezing indicate? 3. List three conditions in which you can hear wheezing. 4. How is wheezing treated? Click here to view an animation on the topic of inspiratory wheezing. Back to Directory

Secondary Assessment Examine extremities. Look for peripheral cyanosis (hypoxia). Swelling, redness, hard and firm cord (pulmonary embolism). Clubbing of fingers (hypoxemia). Carpopedal spasm (hyperventilation).

Figure 1-20b Characteristics of finger clubbing include large fingertips and a loss of the normal angle at the nail bed.

Figure 1-20c Characteristics of finger clubbing include large fingertips and a loss of the normal angle at the nail bed.

Secondary Assessment Vital Signs Tachycardia may indicate hypoxia. Pulsus paradoxus associated with COPD and cardiac tamponade. Elevated respiratory rate in patient with dyspnea caused by hypoxia. Persistently slow rate indicates impending respiratory arrest.

Secondary Assessment Vital Signs Continually reassess respiratory rate and pattern. Tachypnea: respiratory pattern with rate that exceeds 20 breaths per minute. Bradypnea: respiratory pattern with rate slower than 12 breaths per minute.

Diagnostic Testing Pulse oximetry offers rapid and accurate means for assessing oxygen saturation. Applied to finger or earlobe. Pulse rate and oxygen saturation continuously recorded. Concentration of oxyhemoglobin displayed as percentage (hemoglobin oxygen saturation).

Figure 1-21 Sensing unit for pulse oximetry
Figure Sensing unit for pulse oximetry. This device transmits light through a vascular bed, such as in the finger, and can determine the oxygen saturation of red blood cells. To use the pulse oximeter, it is only necessary to turn the device on and attach the sensor to a finger. The desired graphic mode on the oximeter should be selected. The oxygen saturation and pulse rate can be continuously monitored.

Diagnostic Testing SpO2 reflects oxygen saturation of available hemoglobin. Pulse oximeters cannot discern between normal/abnormal levels of hemoglobin. Some newer pulse oximeters have capability of noninvasively measuring total hemoglobin (SpHb) in addition to SpO2 and other parameters.

Diagnostic Testing Handheld devices available for determining patient's peak expiratory flow rate (PEFR). Normal expected peak flow rate based on patient's sex, age, height. PEFR obtained using Wright spirometer. Peak rate of exhaled gas recorded in liters per minute.

Diagnostic Testing Capnography: noninvasive method of measuring levels of carbon dioxide (CO2) in exhaled breath. Capnometry: measurement of expired CO2. Capnography: graphic recording or display of capnometry reading over time. Class Activities If possible, demonstrate the use of a pulse oximeter, capnogram, or other tools used to assess respiratory illnesses. Take some time for students to become comfortable using them on one another.

Diagnostic Testing Capnograph: device that measures expired CO2 levels. Capnogram: visual representation of expired CO2 waveform. End-tidal CO2 (ETCO2): measurement of CO2 concentration at end of expiration (maximum CO2).

Diagnostic Testing PETCO2: partial pressure of end-tidal CO2 in mixed gas solution. PaCO2: partial pressure of CO2 in arterial blood. CO2 end product of metabolism; transported by venous system to right side of heart.

Diagnostic Testing CO2 pumped from right ventricle to pulmonary artery; enters pulmonary capillaries. Diffuses into alveoli; removed from body through exhalation. Decreased CO2 levels: shock, cardiac arrest, pulmonary embolism, bronchospasm, airway obstruction.

Diagnostic Testing Increased CO2 levels: hypoventilation, respiratory depression, hyperthermia. Capnometry provides noninvasive measure of CO2 levels. Colorimetric device: disposable CO2 detector; pH- sensitive, chemically impregnated paper encased within plastic chamber.

Figure The ability to noninvasively determine the amount of hemoglobin present (SpHb) is available on certain monitoring technologies. (© Dr. Bryan E. Bledsoe)

Diagnostic Testing Colorimetric devices cannot detect hypercarbia or hypocarbia. Electronic capnography detectors: infrared technique detects CO2 in exhaled breath; CO2 molecules absorb infrared light; can then be measured. Electronic ETCO2 detectors: qualitative or quantitative.

Figure Capnography devices provide a digital waveform (capnogram) that reflects the entire respiratory cycle.

Diagnostic Testing Capnogram: CO2 concentrations over time. Phase I: respiratory baseline. Phase II: respiratory upstroke. Phase III: respiratory plateau. Phase IV: inspiratory phase.

Diagnostic Testing Continuous waveform capnography: Continuous monitoring of airway placement and ventilation for intubated patients. Utility in monitoring nonintubated patients. CO2 detection useful in cardiopulmonary resuscitation (CPR).

Management of Respiratory Disorders
Management Principles Airway always has first priority. Any patient with hypoxia should receive oxygen. Any patient whose illness or injury suggests possibility of hypoxia should receive oxygen until pulse oximetry available. Teaching Tips Airway and breathing are the first components of the ABCs. Don't forget to focus on the importance of good basic skills of airway and breathing management, including ventilation.

Management Principles If question whether oxygen should be given, administer enough oxygen to maintain adequate SpO2 level (≥ 96%). Strive for normoxia; avoid both hypoxia and hyperoxia, if possible.

Management Principles Administering too much oxygen can worsen patient outcomes. Excess oxygen can result in formation of toxic chemicals (free radicals). These chemicals can damage body cells and tissues (oxidative stress). Provide just enough oxygen to treat hypoxia without causing hyperoxia. Points to Emphasize Oxygen should be treated like any other drug. You must be careful to provide just enough to treat hypoxia without causing hyperoxia.

Figure Excess amounts of oxygen (hyperoxia) have been associated with worsened outcomes in critically ill patients. Always provide enough oxygen to treat hypoxia but avoid hyperoxia.

Specific Respiratory Diseases
Upper Airway Obstruction Common causes: relaxed tongue, food, dentures, other foreign bodies. Can be result of facial or neck trauma, upper airway burns, allergic reactions, swelling. Severe signs: silent cough, cyanosis, and inability to speak or breathe.

Upper Airway Obstruction Unresponsive patient: snoring respirations, possibly tongue or denture obstruction. Speech indicates obstruction incomplete. If unresponsive and has been eating, suspect food bolus lodged in trachea.

Upper Airway Obstruction If burn present or suspected, assume laryngeal edema until proven otherwise. Watch for urticaria (hives). Intercostal muscle retraction and use of strap muscles of neck for breathing suggest attempts to ventilate against partially closed airway.

Upper Airway Obstruction Management based on nature of obstruction Blockage by tongue corrected by opening airway, using head-tilt, chin-lift; jaw-thrust; or jaw-thrust without head extension maneuver. Employ nasopharyngeal or oropharyngeal airway.

Upper Airway Obstruction Conscious Adult Determine if complete obstruction or poor air exchange. If severe obstruction or poor air exchange, provide rapid abdominal thrusts in rapid sequence until obstruction relieved.

Upper Airway Obstruction Unconscious Adult Use head-tilt, chin-lift; jaw-thrust; or jaw-thrust without head extension maneuver in attempt to open airway. Begin CPR. If obstruction persists and ventilation cannot be provided, visualize airway with laryngoscope.

Upper Airway Obstruction Grasp obstruction with Magill forceps and remove. Airway obstruction caused by laryngeal edema, establish airway by head-tilt, chin-lift; jaw-thrust; or jaw- thrust without head extension maneuver. Administer supplemental oxygen. Attempt bag-valve-mask (BVM) ventilation.

Upper Airway Obstruction Start IV with crystalloid solution. Administer intramuscular epinephrine. Administer diphenhydramine (Benadryl).

Adult Respiratory Distress Syndrome (ARDS) Life-threatening condition; adversely affects gas exchange in lungs. Caused by fluid accumulation in interstitial space within lungs. Fluid accumulation result of increased vascular permeability and decreased fluid removal from lung tissue.

Adult Respiratory Distress Syndrome (ARDS) Mortality high (70%). Death as result of respiratory failure, failure of organ systems (liver and kidneys). Underlying conditions results in inability to maintain proper fluid balance in interstitial space.

Adult Respiratory Distress Syndrome (ARDS) Increases in pulmonary capillary permeability, destruction of capillary lining, and increases in osmotic forces act to draw fluid into interstitial space and contribute to interstitial edema. Increases thickness of respiratory membrane; limits diffusion of oxygen.

Adult Respiratory Distress Syndrome (ARDS) Specific clinical symptoms related to underlying cause of ARDS. Patients experience gradual decline in respiratory status. Dyspnea, confusion, agitation with noncardiogenic pulmonary edema. Tachypnea and tachycardia. Teaching Tips Specific respiratory diseases are treated based on the underlying cause. It is more important to stress the priorities of care for airway and breathing rather than attempting to diagnose the respiratory problem.

Adult Respiratory Distress Syndrome (ARDS) Crackles (rales) audible in both lungs. Pulse oximetry: low oxygen saturations with advanced disease. Management of patient's underlying medical condition hallmark of treatment for this disorder.

Adult Respiratory Distress Syndrome (ARDS) Treatment of gram-negative sepsis with appropriate antibiotics, removal of patient from inciting toxin, rapid descent to lower altitude with HAPE most important therapies. Often supplementation essential.

Adult Respiratory Distress Syndrome (ARDS) Establish intravenous access; provide fluids only if hypovolemia exists. Establish cardiac monitoring. Suctioning of lung secretions. Use positive pressure ventilation. Continuous positive airway pressure (CPAP) can avoid need for endotracheal intubation and mechanical ventilation.

Adult Respiratory Distress Syndrome (ARDS) Maintain cardiac monitoring and pulse oximetry. Transport facility capable of advanced hemodynamic monitoring (Swan-Ganz catheter) and mechanical ventilation support.

Click here to view an animation on the topic of ARDS.
ARDS Animation Questions: 1. List three causes of ARDS. 2. What substance in the alveoli is destroyed by ARDS? 3. List three pathologic features of ARDS. 4. What process of respiration is affected by ARDS? 5. How are levels of PO2 and PCO2 affected by ARDS? Click here to view an animation on the topic of ARDS. Back to Directory

Obstructive Lung Diseases Emphysema Chronic bronchitis Asthma Asthma genetic predisposition. COPD directly caused by cigarette smoking and environmental toxins.

Obstructive Lung Diseases Abnormal ventilation common feature. Obstruction primarily in bronchioles. Bronchospasm occurs. Increased mucus production by goblet cells that line respiratory tree. Inflammation of bronchial passages results in accumulation of fluid and inflammatory cells.

Click here to view an animation on the topic of COPD.
COPD Video Questions: 1) Explain the pathophysiology of COPD. 2) What disorders make up COPD? 3) What type of lung sounds would you expect to find during a COPD exacerbation? 4) How is a COPD exacerbation treated? Click here to view an animation on the topic of COPD. Back to Directory

Emphysema Destruction of alveolar walls distal to terminal bronchioles. More common in men than women. Contributing factors: cigarette smoking, exposure to environmental toxins. Decreases alveolar membrane surface area, lessening area available for gas exchange. Discussion Topics Several different pathophysiologies are covered in this chapter. Assign groups to cover different topics and find unique ways to discuss them with the class. Perhaps students can build case studies around a patient and have the other students try to determine the cause and treatment of each.

Emphysema Increased ratio of air to lung tissue; diffusion defects. Increases resistance to pulmonary blood flow. Ultimately causes pulmonary hypertension, leading to right-heart failure, cor pulmonale, and death.

Emphysema Weakening of walls of small bronchioles. When destroyed, lungs lose capacity to recoil; air becomes trapped in lungs. Patients breathe through pursed lips; creates continued positive pressure similar to positive end-expiratory pressure (PEEP); prevents alveolar collapse.

Figure Initiation of ARDS In septic ARDS, bacterial toxins cause inflammation that damages the alveolar and capillary walls. 2. Onset of Pulmonary Edema The damaged alveolar and capillary walls become more permeable, allowing plasma and other substances to enter the interstitial space, thus causing fluid entry into the alveoli.

Emphysema Irreversible airway obstruction. Patients susceptible to acute respiratory infections and cardiac arrhythmias. Dependent on bronchodilators, corticosteroids, supplemental oxygen.

Emphysema Weight loss, increased dyspnea on exertion, limitation of physical activity. Rarely associated with cough. Barrel chest evidenced by increase in anterior/posterior chest diameter. Tend to be pink in color; polycythemia. Hypertrophy of accessory respiratory muscles.

Emphysema Clubbing of fingers common. Breath sounds diminished. Signs of right-heart failure: jugular vein distention, peripheral edema, hepatic congestion.

Chronic Bronchitis Increase in number of goblet (mucus-secreting) cells in respiratory tree. Production of large quantity of sputum. Often occurs after prolonged exposure to cigarette smoke. Alveoli not severely affected and diffusion remains normal. Class Activities Each respiratory complaint has different components of history, physical exam, and treatment. Have students attempt to figure out the matching respiratory disease when given clues in pathophysiology, assessment, or management.

Figure 1-35 Chronic mucus production and plugging of the airways occur in chronic bronchitis.

Chronic Bronchitis Gas exchange decreased because of lowered alveolar ventilation; results in hypoxia and hypercarbia. Patient often has history of heavy cigarette smoking; may occur in nonsmokers. History of frequent respiratory infections.

Chronic Bronchitis Produce considerable quantities of sputum daily. Productive cough for 3 months per year for 2 or more consecutive years. Overweight; can be cyanotic ("blue bloaters"). Rhonchi; occlusion of larger airways with mucus plugs.

Chronic Bronchitis May exhibit signs and symptoms of right-heart failure. Management goal: relieve hypoxia and reverse bronchoconstriction. Supplemental administration of oxygen. Establish airway. Apply pulse oximeter; determine blood oxygen saturation (SpO2).

Chronic Bronchitis Administer supplemental oxygen at low flow rate; maintain oxygen saturation greater than 90 to 95%. Support ventilation with BVM assistance. CPAP in COPD. Intubation may be required if CPAP fails and respiratory failure imminent.

Chronic Bronchitis Place saline lock. Fluid administration if dehydration. If ordered by medical direction, administer bronchodilator medication (albuterol, levalbuterol, metaproterenol) through small-volume nebulizer.

Asthma Chronic inflammatory disorder of airways. Airflow obstruction and hyperresponsiveness often reversible with treatment. Induced by "triggers" or "inducers." Environmental allergens major cause of inflammation.

Asthma Triggers: cold air, exercise, foods, irritants, stress, certain medications. First phase of reaction: release of chemical mediators such as histamine. Contraction of bronchial smooth muscle; leakage of fluid from peribronchial capillaries. Bronchoconstriction; bronchial edema.

Asthma Decreased expiratory airflow, causing "asthma attack." Often, asthma attacks resolve spontaneously in 1–2 hours. May be aborted by inhaled bronchodilator medications such as albuterol.

Figure 1-36 (a) Normal airway, (b) asthmatic airway, and (c) asthmatic airway during an attack.

Asthma 6–8 hours after exposure to trigger, second reaction occurs. Inflammation of bronchioles as cells of immune system invade mucosa of respiratory tract. Additional edema; swelling bronchioles; decrease in expiratory airflow.

Asthma Second-phase reaction will not typically respond to inhaled beta-agonist drugs. Anti-inflammatory agents such as corticosteroids required. Consider immediate threats to airway, breathing, circulation. Focused history; physical examination.

Asthma Symptoms: dyspnea, wheezing, cough. Hyperinflation of chest; tachypnea. As hypoxia develops, patient may become agitated and anxious. Patient's medications help confirm history of asthma. Determine when symptoms started; what attempts to abort attack.

Asthma Prior history of intubation and mechanical ventilation should heighten index of suspicion. Asthmatic on continuous corticosteroid therapy is high- risk patient. Emphasis on exam of chest and neck. Note abnormal breath sounds such as wheezing or rhonchi.

Asthma Increase in respiratory rate earliest symptom of respiratory problem. Pulse oximetry adjunct to respiratory assessment. More severe asthma attack, lower PEFR. Continuous waveform capnography can assist in identifying asthma; determine severity of airflow obstruction.

Asthma Acute asthma exacerbation will exhibit "shark fin" configuration on capnogram. Patients tend to hyperventilate to maintain adequate oxygenation. Treatment: correct hypoxia, reverse any bronchospasm, treat inflammatory changes associated with disease.

Asthma Administer supplemental oxygen to correct hypoxia. Establish intravenous access; place patient on electrogardiogram (ECG) monitor. Inhaled beta-agonist preparations such as albuterol or levalbuterol in conjunction with ipratropium bromide. Treat inflammation with a corticosteroid.

Asthma Drugs administered with small-volume, oxygen- powered nebulizer. The longer the time interval from onset of asthma attack until treatment, the less bronchodilator medications will work. Fatigued patient can quickly develop respiratory failure and require intubation and mechanical ventilation.

Asthma Status asthmaticus: severe, prolonged asthma attack; cannot be broken by repeated doses of bronchodilators. Serious medical emergency: requires prompt recognition, treatment, transport.

Asthma Status asthmaticus: greatly distended chest from continued air trapping. Breath sounds (wheezing) absent. Patient exhausted, severely acidotic, dehydrated. Recognize respiratory arrest imminent; prepare for endotracheal intubation. Transport immediately.

Asthma Common in children. Pathophysiology and treatment same as in adults, with altered medication dosages.

Upper Respiratory Infection (URI) Can make many existing pulmonary diseases worse or lead to direct pulmonary infection. Best defense against spread is common practices (good hand washing and covering mouth during coughing and sneezing).

Upper Respiratory Infection Viruses cause majority of URIs; variety of bacteria may also produce infection. Streptococcus accounts for 30%. URIs are self-limiting illnesses; resolve after several days of symptoms. Symptoms: fever, chills, myalgias, fatigue.

Upper Respiratory Infection Diagnosis and treatment based on history and physical findings. No intervention required except in children with epiglottitis and complicated infections in which pus may occlude airway. Give oxygen supplementation to treat hypoxia (avoid hyperoxia).

Upper Respiratory Infection Acetaminophen or ibuprofen for fever, headache, myalgias. Drink plenty of fluids. Saltwater gargles for throat discomfort. Decongestants and antihistamines to reduce mucus secretion. Encourage patients treated with antibiotics to continue these agents.

Pneumonia Infection of lungs; common medical problem, especially in aged and those infected with HIV. Leading causes of death in both groups; fifth overall cause of death in U.S. Risk factors: history of alcoholism, cigarette smoking, exposure to cold temperatures.

Pneumonia Collection of related respiratory diseases caused when variety of infectious agents invade lungs. Defect in mucus production, ciliary action, or both. Bacterial and viral pneumonias most frequent; fungal and other forms of pneumonia exist.

Figure Types of pneumonia: (a) Bronchopneumonia with localized pattern. (b) Lobar pneumonia with diffuse pattern within the lung lobe. (c) Interstitial pneumonia is typically diffuse and bilateral.

Pneumonia Infection begins in one part of lung; spreads to nearby alveoli. Infection may involve entire lung. As disease progresses, fluid and inflammatory cells collect in alveoli; alveolar collapse may occur. Primarily ventilation disorder.

Pneumonia Patients appear ill; recent history of fever and chills ("bed shaking"). Weakness; malaise; deep, productive cough; yellow to brown sputum, often streaked with blood. May be associated pleuritic chest pain.

Pneumonia Fever, tachypnea, tachycardia, cough. Respiratory distress may be present. Auscultation of chest crackles (rales). Diagnosed: physical examination, X-ray findings, laboratory cultures. Primary treatment: antibiotics. Administer supplemental oxygen to correct hypoxia.

Pneumonia Severe cases: ventilatory assistance; endotracheal intubation required. Establish intravenous access. Administering fluids for dehydration appropriate; overhydration can worsen respiratory condition. Antipyretic agents (acetaminophen or ibuprofen) to reduce high fever.

Pneumonia Patients over age 65: high mortality and complication rates. Transport to facility capable of handling significant complications associated with disease for this population.

Severe Acute Respiratory Syndrome (SARS) Viral respiratory illness; first appeared in southern China in November 2002. SARS-associated coronavirus (SARS-CoV). Spread by close person-to-person contact; incubation period 2–7 days.

Severe Acute Respiratory Syndrome (SARS) Considered contagious as long as symptoms. All personnel should use appropriate personal protective equipment (PPE) on every call or as directed by local health authorities. First address signs of severe respiratory distress.

Severe Acute Respiratory Syndrome (SARS) Patients with underlying respiratory disease and chronic illnesses at increased risk. Symptoms: sore throat, rhinorrhea, chills or rigors, myalgias, headache, diarrhea; progress to cough, sputum production, respiratory distress, eventual respiratory failure.

Severe Acute Respiratory Syndrome (SARS) Management: treat as with suspected pneumonia or respiratory illness. Supplemental oxygen to correct hypoxia. Establish intravenous access. Severe cases: ventilatory assistance and endotracheal intubation required.

Severe Acute Respiratory Syndrome (SARS) If SARS suspected, notify receiving hospital so that appropriate measures can be taken for isolation of patient and protection of health care workers.

Middle East Respiratory Syndrome (MERS) First reported in Jordan and Saudia Arabia in 2012. Characterized by fever, cough, and shortness of breath. Causes death in 3-4 patients of every 10 infected. Spread from person-to-person through close contact.

Middle East Respiratory Syndrome (MERS) Some will develop nausea, vomiting, and diarrhea. People with coexisting illnesses can develop pneumonia and renal failure. Standard respiratory illness protection measures are recommended (similar to those employed for SARS).

Lung Cancer Leading cause of cancer-related death in U.S. in both men and women. Between ages of 55 and 65 years. Four types based on predominant cell type. 20% cases involve only lung tissue. 35% spread to lymphatic system. 45% have distant metastases.

Lung Cancer Risk factors: cigarette smoking; environmental exposure to asbestos, hydrocarbons, radiation, fumes from metal production; home exposure to radon. Vast majority caused by carcinogens from cigarette smoking.

Lung Cancer Adenocarcinoma: most common type; glandular-type cells found in lungs and bronchioles. Small-cell carcinoma ("oat cell" carcinoma): bronchial tissues. Epidermoid carcinoma: bronchial tissues. Large-cell carcinoma: bronchial tissues.

Lung Cancer Bad prognosis; most patients die within year of diagnosis. Address signs of severe respiratory distress. Severe uncontrolled hemoptysis can be life-threatening presentation. Cough, dyspnea, hoarseness, vague chest pain, hemoptysis.

Lung Cancer Metastatic symptoms: headache, seizures, bone pain, abdominal pain, nausea, malaise. Profound weight loss, cachexia, crackles (rales), rhonchi, wheezes, diminished breath sounds.

Lung Cancer Administer supplemental oxygen. Be attentive for any do not resuscitate (DNR) order or advance directive (living will). Follow your local protocol regarding these legal instruments. Consult medical direction if questions arise.

Lung Cancer IV of 0.9% normal saline; provide fluids if dehydration. Follow your local protocol regarding access of permanent indwelling catheters in place.

Toxic Inhalation Causes pain, inflammation, destruction of pulmonary tissues. Consider in any dyspneic patient. Causes: superheated air, toxic products of combustion, chemical irritants, inhalation of steam.

Toxic Inhalation Severe inhalations; disruption of alveolar-capillary membranes may result in life-threatening pulmonary edema. Determine nature of inhalant or combusted material.

Toxic Inhalation Several products result in formation of corrosive acids or alkalis: Ammonia (ammonium hydroxide) Nitrogen oxide (nitric acid) Sulfur dioxide (sulphurous acid) Sulfur trioxide (sulfuric acid) Chlorine (hydrochloric acid)

Toxic Inhalation Determine duration of exposure, whether patient was in enclosed area, if experienced loss of consciousness. Pay attention to face, mouth, throat. Note burns or particulate matter. Wheezing: bronchospasm. Crackles: pulmonary edema.

Toxic Inhalation After ensuring safety of rescue personnel, remove patient from hazardous environment. Establish and maintain open airway. Administer humidified oxygen to correct hypoxia. Place saline lock for venous access. Transport promptly.

Carbon Monoxide Inhalation Carbon monoxide: odorless, tasteless, colorless gas produced from incomplete burning of fossil fuels and carbon-containing compounds. #1 cause of poisoning in industrialized countries. Potentially life threatening because it binds to hemoglobin molecule.

Carbon Monoxide Inhalation Receptor sites on hemoglobin can no longer transport oxygen to peripheral tissues. Hemoglobin with carbon monoxide bound is carboxyhemoglobin. Result is hypoxia at cellular level; ultimately, metabolic acidosis.

Carbon Monoxide Inhalation Determine source of exposure, length, location. Signs and symptoms: headache, nausea and vomiting, confusion, agitation, loss of coordination, chest pain, loss of consciousness, seizures. Skin cyanotic or bright cherry red.

Carbon Monoxide (CO) Inhalation Signs of hypoxia (peripheral cyanosis or confusion). Carboxyhemoglobin levels measured noninvasively in prehospital setting through CO-oximetry. Can detect carboxyhemoglobin, methemoglobin, oxyhemoglobin, deoxyhemogobin.

Carbon Monoxide Inhalation Ensure safety of rescue personnel. Remove patient from site of exposure. Ensure and maintain airway. Administer supplemental oxygen at highest possible concentration. Apply tight-fitting nonrebreather mask. Use of CPAP for moderate to severe exposures.

Carbon Monoxide Inhalation Assist respirations. If shock present, treat. Prompt transport essential. Effectiveness of hyperbaric oxygen therapy in carbon monoxide poisoning remains unclear.

Pulmonary Embolism Blood clot (thrombus) or other particle that lodges in pulmonary artery, blocking blood flow through vessel. Condition potentially life threatening; can significantly decrease pulmonary blood flow, leading to hypoxemia.

Pulmonary Embolism 1 in 5 cases of sudden death caused by pulmonary emboli. Any condition that results in immobility of extremities can increase risk. Risk factors: venous pooling that occurs during pregnancy, cancer, infections, thrombophlebitis, atrial fibrillation, sickle cell anemia.

Pulmonary Embolism Sources: air embolism, fat embolism, amniotic fluid embolism, blood clots. Major derangement is perfusion disorder. Involved lung segment still ventilated, producing ventilation-perfusion mismatch.

Pulmonary Embolism Acute pulmonary embolism: sudden onset of severe unexplained dyspnea. May be recent history of immobilization (hip fracture, surgery, debilitating illness). Labored breathing, tachypnea, tachycardia, signs of right-heart failure.

Pulmonary Embolism Always examine extremities. In up to 50% of cases, deep venous thrombosis evident. Warm, swollen extremity with thick cord palpated along medial thigh; pain on palpation or when extending calf. Petechiae on arms and chest wall.

Pulmonary Embolism First priorities are ABCs. Large pulmonary embolism may lead to cardiac arrest; perform CPR if needed. Establish and maintain airway. Assist ventilations as required. Administer supplemental oxygen at highest possible concentration.

Pulmonary Embolism Endotracheal intubation may be required. Place saline lock. Requires high index of suspicion; high complication rate; significant mortality. Monitor patient's vital signs; cardiac rhythm. Quickly transport.

Spontaneous Pneumothorax Occurs in absence of blunt or penetrating trauma. 5:1 ratio of male-to-female patients. Risk factors: tall, thin stature; history of cigarette smoking. Develops between ages of 20 and 40 years. Higher incidence with COPD.

Spontaneous Pneumothorax Derangement in ventilation; negative pressure that normally exists in pleural space is lost. Prevents proper expansion of lung in concert with chest wall. Sudden onset of sharp, pleuritic chest or shoulder pain. Dyspnea commonly reported.

Spontaneous Pneumothorax Tachypnea, diaphoresis, pallor; cyanosis rarely found. Symptoms and pulse oximetry readings are guides to therapy. Supplemental oxygen required. Patients who require positive pressure ventilation by mask or endotracheal tube at risk for tension pneumothorax.

Hyperventilation Syndrome Rapid breathing, chest pains, numbness, other symptoms associated with anxiety or situational stress. Consider indication of serious medical problem until proven otherwise. Carpopedal spasm: cramping of muscles of feet and hands.

Hyperventilation Syndrome History of fatigue, nervousness, dizziness, dyspnea, chest pain, and numbness and tingling around mouth, hands, feet. If history of seizure disorder, hyperventilation episode may precipitate seizure.

Hyperventilation Syndrome Primary treatment is reassurance. Instruct patient to voluntarily reduce respiratory rate and depth of breathing. Check the oxygen saturation by applying a pulse oximeter. Pulmonary embolism or acute myocardial infarction can exhibit similar symptoms.

Central Nervous System (CNS) Dysfunction Relatively rare; consider possibility in any dyspneic patient. Causes: head trauma, stroke, brain tumors, various drugs. Be alert for nonrespiratory-system problems such as CNS trauma or drug ingestion.

Central Nervous System Dysfunction Establish and maintain open airway. If respiratory depression noted or if respirations absent, initiate mechanical ventilation. Administer supplemental oxygen. Establish saline lock for venous access.

Dysfunction of Spinal Cord, Nerves, or Respiratory Muscles Can lead to hypoventilation and progressive hypoxemia. Spinal cord trauma, polio, amyotrophic lateral sclerosis (ALS), myasthenia gravis, viral infections, tumors. At risk of developing pneumonia. Always question about injuries or falls.

Dysfunction of Spinal Cord, Nerves, or Respiratory Muscles If doubt about possible injury, immobilize cervical spine. Numbness, pain, sensory dysfunction. Problems with peripheral nervous system (PNS). Protect airway; support ventilation. Establish airway; ventilatory support.

Summary Respiratory emergencies commonly encountered in prehospital care. Important to recognize that all respiratory disorders may produce derangements in ventilation, perfusion, or diffusion.

Summary Recognition and treatment must be prompt.
Understanding underlying cause of respiratory disorder can guide therapy.

Summary Primary treatment is to correct hypoxia.
Necessary steps include establishing and maintaining airway, assisting ventilations as required, administering supplemental oxygen.

Summary Appropriate pharmacological agents may be ordered by local protocols. Primary responsibility never changes: Make sure your patient has open airway and is breathing well enough to maintain normoxia.

Summary Whenever airway and breathing are affected, astute paramedic will treat abnormalities as they are found. Oxygen is primary medication of choice, but remember to use it sparingly.

Summary Your goal is normoxia, not hyperoxia; hyperoxia and hypoxia both have dangerous effects on patient. Tools such as capnography, end-tidal CO2, pulse oximetry, carbon monoxide detectors available for determining respiratory patient's status.

Summary Do not become lulled by technology nor allow technology to replace good old-fashioned assessment and common sense. When combined with thorough physical assessment and proper judgment, these tools can be invaluable in guiding patient care and progress.

Paramedic Care: Principles & Practice

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Paramedic Care: Principles & Practice

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