9781284139396_CH16_PPT_Comprehensive.pptx

Chapter 16 Respiratory Emergencies National EMS Education Standard Competencies Medicine 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....

Chapter 16 Respiratory Emergencies National EMS Education Standard Competencies Medicine 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. National EMS Education Standard Competencies Respiratory Anatomy, signs, symptoms, and management of respiratory emergencies including those that affect the – Upper airway – Lower airway National EMS Education Standard Competencies Anatomy, physiology, pathophysiology, assessment, and management of – – – – – – Epiglottitis Spontaneous pneumothorax Pulmonary edema Asthma Chronic obstructive pulmonary disease Environmental/industrial exposure National EMS Education Standard Competencies Anatomy, physiology, pathophysiology, assessment, and management of – – – – – – – Toxic gas Pertussis Cystic fibrosis Pulmonary embolism Pneumonia Viral respiratory infections Obstructive/restrictive disease National EMS Education Standard Competencies Anatomy, physiology, epidemiology, pathophysiology, psychosocial impact, presentations, prognosis, and management of – – – – – – – Acute upper airway infections Spontaneous pneumothorax Obstructive/restrictive lung diseases Pulmonary infections Neoplasm Pertussis Cystic fibrosis National EMS Education Standard Competencies Shock and Resuscitation Integrates comprehensive knowledge of causes and pathophysiology into the management of cardiac arrest and prearrest states. National EMS Education Standard Competencies Shock and Resuscitation Integrates a comprehensive knowledge of the causes and pathophysiology into the management of shock, respiratory failure, or arrest, with an emphasis on early intervention to prevent arrest. Introduction Respiratory disease is one of the most common pathologic conditions. – One of the most common EMS dispatches Epidemiology Asthma and COPD are among the top 10 chronic conditions causing restricted activity. Pneumonia is one of the most common fatal illnesses in developing countries. Epidemiology Some respiratory diseases are genetic while others are caused by external factors. – Many respiratory diseases are caused by a combination of factors. Anatomy and Physiology Respiratory system structures look like an inverted tree. © Jones & Bartlett Learning. Anatomy and Physiology Tracheobronchial tree – Carries air to the lungs – Extends from the larynx to the mainstem bronchi © Jones & Bartlett Learning. Anatomy and Physiology Bronchi – Mainstem bronchi branch into the lobes of the lungs, then into: Tertiary (segmental) bronchi Subsegmental bronchi Bronchioles Anatomy and Physiology Bronchioles © Jones & Bartlett Learning. – Gas exchange Anatomy and Physiology Bronchioles (cont’d) – Lack cilia – Have no protective mucus – Not shielded by smooth muscle or a more rigid structure Smooth muscle around the airway – Bronchoconstriction: smooth muscle narrows the airway Anatomy and Physiology Alveoli – Terminal airways and alveoli include branches 16 to 24 of the tracheobronchial tree. – Entire surface of alveoli and terminal bronchioles is covered in capillaries. – Participate in gas exchange Anatomy and Physiology Mediastinum: space in middle of the chest – Consists of: Heart Large blood vessels The large conducting airways Other organs Pulmonary Blood Flow Blood flows from the heart to the lungs via the pulmonary artery. – The pulmonary artery branches into smaller and smaller vessels. – More gas exchange takes place between lung bases and circulatory system. – Pulmonary capillaries are narrow. Polycythemia Cor pulmonale Perfusion Circulatory component of respiratory system – Blood must keep flowing through pulmonary vessels. – A large embolus can block blood flow to the lung. Mechanisms of Respiratory Control Cardiovascular regulation – Lungs are closely linked to cardiac function. – Heart changes have pulmonary consequences. – Left-sided heart failure progresses faster than right-sided heart failure. Mechanisms of Respiratory Control Cardiovascular regulation (cont’d) – Mild hypoxia causes an increase in heart rate. – Severe hypoxia causes bradycardia. – Uncorrected hypoxic insults may trigger lethal cardiac arrhythmia. Mechanisms of Respiratory Control Cardiovascular regulation (cont’d) – Various forms of heart failure caused by: Fluid-balance changes Right-sided heart pumping pressure Left-sided heart pumping pressure Mechanisms of Respiratory Control Muscular control – Body takes in air by negative pressure – Air pulled through mouth and nose, over turbinates, around epiglottis and glottis © Jones & Bartlett Learning. Mechanisms of Respiratory Control Muscular control (cont’d) – The thorax is an airtight box with the diaphragm at the bottom and the trachea at the top. – The diaphragm flattens during quiet breathing. Air is sucked in to fill the increasing space. Mechanisms of Respiratory Control Muscular control (cont’d) – Minute ventilation can be increased by: Deep breathing Rapid breathing Mechanisms of Respiratory Control Muscular control (cont’d) – Traumatic openings in thorax provide route for air to be sucked in Sucking chest wound © Jones & Bartlett Learning. Mechanisms of Respiratory Control Renal status – Kidneys play a part in controlling: Fluid balance Acid-base balance Blood pressure – Factor into pulmonary mechanics and oxygen delivery to body tissues Hypoventilation Carbon dioxide accumulates in the blood when the lungs fail to work properly. – Combines with water to form bicarbonate ions and hydrogen ions (carbonic acid) – Results in acidosis Hypoventilation Impaired ventilation is caused by a variety of factors. Hypoventilation Carbon dioxide level is directly related to pH. – As carbon dioxide rises, pH drops. – Hypoventilating patients usually have respiratory acidosis. Hypoventilation Causes of hypoventilation include: – Conditions that impair lung function Atelectasis Pneumonia Pulmonary edema Asthma COPD Hypoventilation Causes of hypoventilation include (cont’d): – Conditions that impair mechanics of breathing Flail chest Severe retractions Air- or blood-filled abdomen Obesity hypoventilation syndrome Hypoventilation Causes of hypoventilation include (cont’d): – Conditions that impair neuromuscular apparatus Head trauma, intracranial infections, brain tumors Serious spinal cord injury Guillain-Barré syndrome Amyotrophic lateral sclerosis (Lou Gehrig disease) Botulism Hypoventilation Causes of hypoventilation include (cont’d): – Conditions that reduce respiratory drive Intoxication Head injury Hypoxic drive Asphyxia Hypoventilation The ultimate manifestation is respiratory arrest followed by cardiac arrest. Initiate aggressive treatment to assist the patient’s respiratory efforts. Hyperventilation Occurs when people breathe in excess by increasing rate and/or depth of respiration – Releases more carbon dioxide than normal – Results in alkalosis – Called hysterical hyperventilation or hyperventilation syndrome if triggered by emotional distress or panic Hyperventilation Respiratory alkalosis causes numbness in hands, feet, and mouth. Respiratory alkalosis ultimately leads to carpopedal spasm. – Symptoms often cause more hyperventilation. Hyperventilation Having a patient rebreathe carbon dioxide can be dangerous. – Patients quickly exhaust the oxygen in the gas they are breathing. – Hyperventilation in a patient with acidosis may be the body’s attempt to raise the pH level. Hyperventilation Treatment may include: – Sedation (extreme measure) – Psychological support: Breathing with the patient Having the patient count to two between breaths Distraction techniques Having the patient sing a song Patient Assessment Respiratory assessment includes much more than listening to the patient’s lungs. – Many respiratory ailments are life threatening. – Respiratory assessment should be done early. Scene Size-Up Take standard precautions. Use proper PPE. Evaluate scene safety for: – – – – Diminished oxygen concentrations Carbon monoxide Irritant gases Highly contagious respiratory illness Scene Size-Up Respiratory diseases can impair: – – – – Ventilation Diffusion Perfusion Combination of all three Rapid-onset dyspnea may be caused by: – – – – Acute bronchospasm Anaphylaxis Pulmonary embolism Pneumothorax Scene Size-Up Paroxysmal nocturnal dyspnea – May signal left-sided heart failure Ability to move air may be hindered by factors that: – Limit diaphragm movement – Restrict chest wall movement – Disrupt the integrity of the thoracic cage Primary Survey Establish and maintain an open airway. Form a general impression. – Body type may be associated with condition Emphysema: barrel chest, muscle wasting, pursed-lip breathing, tachypnea Chronic bronchitis: sedentary, obese, sleeps upright, spits up secretions Primary Survey Assess oxygen demand and work of breathing. – Observe condition during typical exertion. – Tachycardia, diaphoresis, and pallor can be triggered by: Increased work of breathing Anxiety Hypoxia Primary Survey Position and degree of distress – The patient prefers sitting positions, such as the tripod position. – Lying flat may be a sign of sudden deterioration. – Head bobbing is an ominous sign. © Jones & Bartlett Learning. Primary Survey Breathing alterations – Can involve: Conducting airways (trachea, bronchi and bronchioles) Alveoli Muscles and nerves involved in breathing Rigid structure of the thorax Increased work of breathing – Patients using accessory muscles to breathe are in danger of tiring out. Courtesy of Health Resources and Services Administration, Maternal and Child Health Bureau, Emergency Medical Services for Children Program. Primary Survey Primary Survey Increased work of breathing (cont’d) – Infants and small children are in danger of collapse of flexible sternum cartilage. – Profound intrathoracic pressure changes can cause peripheral pulses to weaken or disappear. Pulsus paradoxus Primary Survey Altered rate and depth of respiration – Patient with adequate rate but low volume will have inadequate minute volume. Respiratory rate × tidal volume = minute volume – Monitor trends in respiratory rates. – Note inspiratory-to-expiratory (I/E) ratio. Primary Survey Abnormal breath sounds – Auscultate lungs systematically. – Some conditions are gravity dependent and others diffuse throughout the lungs. © Jones & Bartlett Learning. Primary Survey Abnormal breath sounds (cont’d) – Breath sounds are created by airflow in the large airways. Tracheal Bronchial Bronchovesicular Vesicular Primary Survey © Jones & Bartlett Learning. Primary Survey Abnormal breath sounds (cont’d) – Some conditions cause normal breath sounds to be heard in abnormal places. – Sounds move better through fluid than through air. The “wetter” the patient’s lungs are, the louder the sounds. – The quality of sounds is dependent on the amount of tissue between the stethoscope and structures. Primary Survey Adventitious breath sounds – Extra sounds on top of other breath sounds – Continuous: can be heard across each breath Wheezes (diffuse or localized, monophonic or polyphonic) – Discontinuous: instantaneous pops, snaps, and clicks (crackles) Rales (high-pitched crackles) Rhonchi (low-pitched crackles) Primary Survey Abnormal breath sounds (cont’d) – Audible sounds include: Stridor—upper airway obstruction Grunting—lower airway obstruction Death rattle—patients can’t clear secretions – The most ominous sounds are no sounds. Primary Survey Abnormal breath sounds (cont’d) – Noisy breathing Snoring: Partial obstruction of the upper airway by the tongue Gurgling: Fluid in the upper airway Stridor: Narrowing from swelling – Quiet breathing Hyperventilation Shock Primary Survey Sputum – Has color or amount changed from normal? – Blood-tinged, pink froth is a warning sign. – Note purulent mucus. Primary Survey Abnormal breathing patterns – May indicate neurologic insults Brain trauma or any disturbance may depress respiratory control centers in the medulla. Brain injuries may damage or deprive blood flow. Primary Survey Most respiratory centers are in and around the brainstem. © Jones & Bartlett Learning. Primary Survey Injury to the spinal cord and certain illnesses may disable the respiratory muscles from functioning normally. – Tidal volume is shallow, and minute volume decreases. – Patients often need assisted ventilation. Primary Survey Circulation – Assess skin color. Note generalized cyanosis. Assess mucous membranes. © John Thys/Reporters/Science Source. Primary Survey Circulation (cont’d) – Cyanosis Healthy hemoglobin levels are 12 to 14 g/dL. Cyanosis begins at about 5 g/dL desaturation. – Chocolate brown skin May occur from high levels of methemoglobin – Pale skin Caused by a blood flow reduction to small vessels Primary Survey Circulation (cont’d) – Check for dehydration: Dry, cracked lips Dry, furrowed tongue Dry, sunken eyes Primary Survey Transport decisions – Usually transported to closest hospital If the patient is experiencing renal failure, consider a facility that can provide emergency dialysis. If multiple emergency departments are available, consider taking the patient to his or her preferred facility. History Taking Investigate chief complaint – Have patients explain what they are feeling in their own words. – Common complaints Increased cough Change in amount or color of sputum Fever Wheezing Dyspnea Chest pain History Taking The patient may know the exact problem. – – – – – – Asthma with fever Nondelivery of medication Travel-related conditions Dyspnea triggers Seasonal conditions Noncompliance with therapy History Taking SAMPLE history – Signs and symptoms – Allergies – Medications Antihistamines, antitussives, bronchodilators, diuretics, expectorants – Pertinent past medical history – Last oral intake – Events preceding the onset of the complaint Secondary Assessment Neurologic assessment – Note level of consciousness. Decline in partial pressure of oxygen: restlessness, confusion, and combative behavior Increase in partial pressure of carbon dioxide: sedative effects – If lungs are not functioning correctly, oxygen may not be delivered and carbon dioxide may not be removed. Secondary Assessment Neck exam – Jugular venous distention Common with asthma or COPD Rough measure of pressure in right atrium © ejwhite/Shutterstock. Secondary Assessment Neck exam (cont’d) – Note trachea for deviation. Courtesy of Stuart Mirvis, MD. © Jones & Bartlett Learning Sign of tension pneumothorax Secondary Assessment Chest and abdominal exam – Pressing on the liver when the patient is in respiratory distress and semi-Fowler’s position will cause the jugular veins to bulge. Hepatojugular reflex – Feel for vibrations in the chest as the patient breathes. – Chest or abdominal trauma can cause respiratory distress. Secondary Assessment Examination of the extremities – – – – – – Edema Cyanosis Pulse Pulsus paradoxus Skin temperature Distal clubbing © Jones & Bartlett Learning. Photographed by Kimberly Potvin. © Mediscan/Visuals Unlimited. Secondary Assessment Vital signs – Patients under stress can be expected to have tachycardia and hypertension. – Ominous signs: Bradycardia Hypotension Falling respiratory rates Secondary Assessment Stethoscope – Diaphragm is for high-pitched sounds. – Bell is for low-pitched sounds. – The longer the tubing, the more extraneous noise that is heard. Secondary Assessment Pulse oximeter © Jones & Bartlett Learning. © Jones & Bartlett Learning. – This is a noninvasive way to measure the percentage of hemoglobin with oxygen attached. – Oxygen saturation over 94% is normal. Secondary Assessment Pulse oximeter (cont’d) – Oxygen saturation should match the patient’s palpated heart rate. – If hemoglobin level is low, the pulse oximetry result will be high. – The pulse oximeter does not differentiate between oxygen or carbon monoxide molecules. Secondary Assessment Pulse oximeter (cont’d) – Oxyhemoglobin dissociation curve Relationship between oxygen saturation and amount of oxygen dissolved in the plasma © Jones & Bartlett Learning. Secondary Assessment Peak expiratory flow – Maximum rate at which a patient can expel air – Normal values: 350 to 700 L/min Variable by age, sex, and height – Inadequate level: 150 L/min Reassessment Report changes in patient’s LOC or increased difficulty breathing. Contact medical control before assisting with prescribed medications, per protocol. Document changes and orders from medical control. Emergency Medical Care Provide supportive care. – Administer supplemental oxygen and provide monitoring and transport. Perform standard interventions. – – – – Oxygen (keep saturations above 94%) IV line Psychological support Position of comfort Decrease the Work of Breathing Muscles work harder during respiratory distress. – Use substantial energy to compensate for respiratory distress. Require more oxygen and ventilation May fatigue to point of decompensation Decrease the Work of Breathing To decrease the work of breathing: – – – – – Help the patient sit up. Remove restrictive clothing. Do not make the patient walk. Relieve gastric distention. Do not bind the chest or have the patient lie on the unaffected lung. Provide Supplemental Oxygen Administer in effective concentrations. – Reassess, then adjust as needed. – Pulse oximetry is a good guide to oxygenation. Concentrations higher than 50% should be used only with hypoxia that does not respond to lower concentrations. – Most patients with good oxygen saturation (at least 94%) do not benefit from supplemental oxygen. Administer a Bronchodilator Many can benefit from bronchodilation. – Those without bronchospasms will benefit only slightly. – Bronchodilators are ineffective in cases of: Pneumonia Pulmonary edema Heart disease Administer a Bronchodilator Fast-acting bronchodilators – Most stimulate beta-2 receptors in the lung. Provide almost instant relief – Ipratropium is now available as an aerosol or inhaler. – Sometimes prescribed with ipratropium in a premixed “cocktail.” Administer a Bronchodilator Aerosol therapy – Nebulizers deliver a fine mist of liquid medication. © Jones & Bartlett Learning. Need gas flow of at least 6 L/min to keep particles optimal size Administer a Bronchodilator Aerosol therapy (cont’d) – A nebulizer can be attached to: A mouthpiece A face mask A tracheostomy collar – A nebulizer can also be held in front of the patient’s face (blow-by technique) Administer a Bronchodilator Aerosol therapy (cont’d) – Can disperse other drugs through aerosols: Corticosteroids Anesthetic agents Antitussives Mucolytic agents Administer a Bronchodilator Metered-dose inhalers – These inhalers deliver the same amount of medication as aerosol treatment. – Ambulance metered-dose inhalers should have spacers. © Jones & Bartlett Learning. Administer a Bronchodilator Metered-dose inhalers (cont’d) – To avoid common errors, the patient should: Inhale deeply at discharge. Suck medication out of the bottom. Flow should be smooth and low pressure. Inhale deeply; hold breath for a few seconds. Make sure the inhaler contains medication. Keep the spacer and canister holder clean. Rinse the mouth after using a corticosteroid inhaler. Administer a Bronchodilator Failure of a metered-dose inhaler – The inhaler must be properly used. – Use is contraindicated if the patient cannot move enough air into the lungs. – The patient may not realize the inhaler is empty. – The patient may inhale at the wrong time. Administer a Bronchodilator Dry powder inhalers – The medication may be dispensed by means of a plastic disk. The patient inhales deeply to suck out the powder. – Other devices require the patient to insert a capsule of powdered medication. – These are rarely used during emergency care. Administer a Bronchodilator Leukotriene modifiers – Block bronchoconstricting chemicals (leukotrienes) Electrolytes – Magnesium may have a role in bronchodilation in severe asthma attacks. Administer a Bronchodilator Corticosteroids – Reduce bronchial edema – Adverse effects Cushing syndrome Rapid change in blood glucose levels Blunt the immune system – Must be discontinued slowly Administer a Bronchodilator Inhaled corticosteroids – Do not seem to have the same adverse effects as oral versions IV corticosteroids – Single bolus no apparent negative long-term effects – Methylprednisolone and hydrocortisone IV boluses Used for acute asthma attacks or acute COPD exacerbations Administer a Vasodilator Sequester more fluid in venous circulation and decrease preload – Nitrates can be used if the patient: Has adequate blood pressure Does not take a phosphodiesterase inhibitor – Morphine sulfate is not likely to increase venous capacity. Restore Fluid Balance Common to give fluid bolus to dehydrated, younger patients. – Elderly patients or patients with cardiac dysfunction could develop pulmonary edema. Assess breath sounds before and after. – Hydrating patients with pneumonia may cause the pneumonia to spread. Administer a Diuretic Helps reduce blood pressure and maintain fluid balance in patients with heart failure Helps remove excess fluid from circulation, keeping it out of the lungs of patients with pulmonary edema Administer a Diuretic Many diuretics cause potassium loss. – May lead to cardiac dysrhythmias and chronic muscle cramping Do not give diuretics to patients with pneumonia or dehydration. Support or Assist Ventilation Breathing may need more aggressive support if the patient becomes fatigued. – CPAP and BPAP may preclude intubation. – Patients may simply require bag-mask ventilation. Support or Assist Ventilation Continuous positive airway pressure – Used to treat: Obstructive sleep apnea Respiratory failure – Patients with obstructive sleep apnea wear a CPAP unit to maintain airway while they sleep. Support or Assist Ventilation CPAP (cont’d) – CPAP therapy may be delivered through a mask. Air is forced into the upper airway. Positive pressure is created in the chest. © Jones & Bartlett Learning. Support or Assist Ventilation Bag-mask ventilation – Pressure that is too high may: Cause tension pneumothorax Cause subcutaneous air Block venous returns – New guidelines emphasize: Lower ventilation rates Smaller volumes Lower pressures Support or Assist Ventilation Bag-mask ventilation (cont’d) – Ensure a seal. – If a patient is unwilling to use it, do not fight it. – Success is related to the patient’s respiratory rate after application. © Juanmonino/Getty. Support or Assist Ventilation Bilevel positive airway pressure (BPAP) – One pressure on inspiration and a different pressure during exhalation More like normal breathing More complex and expensive Support or Assist Ventilation Automated transport ventilators – Flow-restricted oxygen-powered ventilation Deliver a particular oxygen volume at a set rate Good for patients in cardiac or respiratory arrest Not intended to be used without direct observation Courtesy of Airon Corporation (www.AironUSA.com). Intubate the Patient Intubation is the last option for patients with severe asthma. Ventilate patients before cardiac arrest. Patients who are severely intoxicated or have had a stroke may have no gag reflex. Intubate the Patient With diabetes or overdose, an ampule of 50% dextrose or naloxone may change the need for intubation. – Use bag-mask ventilation for a few minutes to monitor effects. Inject a Beta-Adrenergic Receptor Agonist Subcutaneously Use if inhalation techniques are ineffective. – These agents may cause more tachycardia and hypertension. – Be careful using in elderly patients. Instill Medication Directly Through an Endotracheal Tube AHA guidelines discourage this practice. – IV or intraosseous medication administration is preferred. Anatomic Obstruction Pathophysiology – The tongue is the most common cause of airway obstruction if a patient is unresponsive. Anatomic Obstruction Assessment: – Risks include: Decreased level of consciousness – Audible signs include: Sonorous respirations Gurgling Squeaking and bubbling Stridor Anatomic Obstruction Management – Obstructive sleep apnea may be caused by excess soft tissue in the airway. Can be manually displaced Recovery position Inflammation Caused by Infection Pathophysiology – Infections can cause upper airway swelling. Can lead to laryngotracheobronchitis Common cause of croup – Stridor – Hoarseness – Barking cough Inflammation Caused by Infection Pathophysiology (cont’d) – Poiseuille law: as the diameter of a tube decreases, resistance to flow increases. © Jones & Bartlett Learning. Inflammation Caused by Infection Assessment – Croup and tonsillitis are common, but other conditions are rare. – They are critical emergencies when they occur. – Avoid manipulating the airway. Inflammation Caused by Infection Management – Airway may be entirely obscured. Laryngoscopy may worsen swelling. – Have partner press on the chest while you check for a bubble stream. If this effort fails, cricothyrotomy may be necessary. Aspiration Inhalation of anything other than breathable gases – Water, blood, vomitus, food, or foreign bodies Patients at risk: – Tube-fed patients placed supine after a large meal – Geriatric patients with impaired swallowing – Unresponsive patients Aspiration Pathophysiology – Aspiration has high mortality Common but profoundly dangerous complication in cardiac arrest and unresponsive patients Assessment – Determine scenario of sudden onset dyspnea Immediately after eating? Gastric feeding tube? Aspiration Management – Avoid gastric distention when ventilating. Use nasogastric tube to decompress the stomach. – Monitor the patient’s ability to protect the airway; use an advanced airway when needed. – Treat with suction and airway control. Obstructive Lower Airway Diseases Cause airflow obstruction to the lungs – Emphysema and chronic bronchitis (COPD) – Asthma © Jones & Bartlett Learning. Obstructive Lower Airway Diseases Physical findings: – – – – Pursed lip breathing Increased I/E ratio Abdominal muscle use Jugular venous distention Asthma Pathophysiology – Increased tracheal and bronchial reactivity Causes widespread, reversible airway narrowing (bronchospasm) Jones & Bartlett Learning; © Scott Rothstein/Shutterstock. Asthma Pathophysiology (cont’d) – Patients with potentially fatal asthma often have severely compromised ventilation all the time. Serious risk if acute bronchospasm is triggered or infection Asthma Reactive airway disease – Bronchospasms are caused by triggers. – The patient may be asymptomatic between attacks. Status asthmaticus – Severe, prolonged asthmatic attack that does not stop with conventional treatment – Dire medical emergency Asthma Assessment – Patient in status asthmaticus Struggling to move air through obstructed airways Prominent use of accessory muscles Hyperinflated chest Inaudible breath sounds Exhausted, severely acidotic, and dehydrated Asthma Assessment (cont’d) – Bronchospasm Constricting muscle surrounding bronchi May occur from stimulation by an allergen or irritants Wheezing: air forced through constricted airways Asthma Assessment (cont’d) – Bronchial edema Swelling of the bronchi and bronchioles causes turbulent airflow, wheezing, and air trapping. Bronchodilator medications do not work. – Increased mucus production Thick secretions contribute to air trapping. Dehydration makes secretions thicker. Asthma © Jones & Bartlett Learning. Asthma Management – Bronchospasm Treatment: nebulized bronchodilator medication – Bronchial edema Treatment: corticosteroids – Excessive mucus secretion Treatment: improve hydration, mucolytic agents Asthma Management (cont’d) – Transport considerations Infection or continuous exposure to a trigger: consider removing patient No improvement in peak flow: consider corticosteroids Undernourished or dehydrated: consider IV fluids Advanced life support more than a few minutes away: consider transport to nearest ED Chronic Obstructive Pulmonary Disease Pathophysiology – Emphysema damages or destroys terminal bronchiole structures. Alveoli have less surface area for gas exchange. – Restrictive lung diseases caused by trauma and diseases of the bones/muscles impair the ability to move air. Chronic Obstructive Pulmonary Disease Pathophysiology (cont’d) – Chronic bronchitis Sputum production most days of the month for 3 or more months of the year for more than 2 years Excessive mucus production in the bronchial tree, accompanied by chronic or recurrent productive cough Chronic Obstructive Pulmonary Disease Assessment – Emphysema Barrel chest from chronic lung hyperinflation Tachypnea Use muscle mass for energy to breathe Chronic Obstructive Pulmonary Disease Assessment (cont’d) – Causes of diffuse wheezing: Left-sided heart failure (cardiac asthma) Smoke inhalation Chronic bronchitis Acute pulmonary embolism – Cause of localized wheezing: obstruction from foreign body or tumor Chronic Obstructive Pulmonary Disease COPD with pneumonia – Often have lung infection – Check for: Fever Change in sputum Other infection signs Breath sounds consistent with pneumonia Chronic Obstructive Pulmonary Disease COPD with right-sided heart failure – Look for: Peripheral edema Jugular venous distention with hepatojugular reflux End inspiratory crackles Progressive increase in dyspnea Greater-than-usual fluid intake Improper use of diuretics Chronic Obstructive Pulmonary Disease COPD with left-sided heart failure – Can be caused by any abrupt left ventricular dysfunction Chronic Obstructive Pulmonary Disease Acute exacerbation of COPD – Sudden decompensation with no co-pathologic conditions – Often from environmental change or inhalation of trigger substances Chronic Obstructive Pulmonary Disease End-stage chronic COPD – The lungs no longer support oxygenation and ventilation. – It is difficult to tell whether the situation can be resolved. – Secure documentation of patient’s wishes. – Follow local protocol or contact medical control. Chronic Obstructive Pulmonary Disease COPD and trauma – COPD lessens a patient’s ability to tolerate trauma. – Monitor closely. – “Normal” Oxygen saturation might be less than 90%. Achieving a saturation of 98% is unrealistic. Chronic Obstructive Pulmonary Disease Management – Immediate help can help improve immediate distress. – Determine what caused the situation to worsen enough for the patient to call for help. – Paramedics must understand: Hypoxic drive Positive end-expiratory pressure (auto-PEEP) Chronic Obstructive Pulmonary Disease Hypoxic drive – When breathing stimulus comes from decrease in PaO2 rather than increase in PaCO2 – Affects only a small percentage during end stage of disease process – Must decide whether to administer oxygen Chronic Obstructive Pulmonary Disease Hypoxic drive (cont’d) – It is impossible to tell which patients breathe because of hypoxic drive. – Verbal and physical stimulation to encourage breathing. – Skin appearance may remain perfused if the patient becomes apneic. Chronic Obstructive Pulmonary Disease Hypoxic drive (cont’d) – Provide artificial ventilation and consider intubation if a patient becomes apneic. – Intubation may mean the patient remains on the ventilator until the end of life. – Oxygen saturation values are less useful in patients with COPD. Chronic Obstructive Pulmonary Disease Auto-PEEP – Allow complete exhalation before the next breath during ventilation. Otherwise, pressure in the thorax will continue to rise (auto-PEEP). – If auto-PEEP is a possibility, patients should be ventilated at four to six breaths/min. Pulmonary Infections Pathophysiology – Infections are caused by: Bacteria Viruses Fungi Protozoa – Infectious diseases cause: Swelling of the respiratory tissues Increase in mucus production Production of pus Pulmonary Infections Pathophysiology (cont’d) – Resistance to airflow increases when the airway diameter is narrowed (Poiseuille law). – Alveoli can become nonfunctional if filled with pus. Pulmonary Infections Pathophysiology (cont’d) – At greater risk of pneumonia: Older people People with chronic illnesses People who smoke Anyone who is not ventilating efficiently Those with excessive secretions Those who are immunocompromised Pulmonary Infections Assessment – Patients usually report: Several hours to days of weakness Productive cough Fever Chest pains worsened by cough Pulmonary Infections Assessment (cont’d) – May start abruptly or gradually – During physical examination, patient may: Look grievously ill Or may not be coughing Present with crackles Have increased tactile fremitus and sputum production Have bronchial or bronchovesicular breath sounds over areas of consolidation Pulmonary Infections Assessment (cont’d) – Pneumonia often occurs in the lung bases. – Patients are often dehydrated. – Supportive care includes: Oxygenation Secretion management (suctioning) Transport to the closest facility Pulmonary Infections Management – Upper airway infections require aggressive airway management. – Lower airway infections need supportive care and transport. Atelectasis Pathophysiology – Disorders of alveoli Collapse from proximal airway obstruction or external pressure Fill with pus, blood, or fluid Smoke or toxin damage Atelectasis Pathophysiology (cont’d) – It is common for some alveoli to collapse. Sighing, coughing, sneezing, and changing positions help open closed alveoli. – When alveoli do not reopen, entire lung segments eventually collapse. – Atelectasis increases the chance of pneumonia. Atelectasis Assessment – Affected area can harbor pathogens that result in pneumonia. Check if a patient with fever has had recent chest or abdominal surgery. Atelectasis Management – Postsurgical patients encouraged to: Get out of bed. Cough. Breathe deeply. Use the incentive spirometer. © age fotostock/Alamy. Cancer Pathophysiology – Lung cancer is one of most common forms of cancer. Cigarette smoking Exposure to occupational lung hazards, secondhand smoke Cancer Assessment – Hemoptysis is often the first sign – Frequently accompanied by COPD and impaired lung function – Often metastasizes in the lung from other body sites Cancer Assessment (cont’d) – Other cancers may invade the lymph nodes in the neck. – Radiation and chemotherapy might cause pulmonary complications. – Tumors or treatments may cause pleural effusion. Cancer Management – Little prehospital treatment for pleural effusions or hemoptysis – Sometimes called for end-of-life issues Toxic Inhalations Pathophysiology – Damage depends on water solubility of toxic gas. Toxic Inhalations Assessment – Highly water-soluble gases react with moist mucous membranes. Causes upper airway swelling and irritation – Less water-soluble gases get deep in lower airway. More damage over time Toxic Inhalations Assessment (cont’d) – Moderately water soluble gases have signs and symptoms between irritation and pulmonary edema. Mixing drain cleaner and chlorine bleach may produce an irritant chlorine gas. Industrial settings often use irritant gas-forming chemicals. Toxic Inhalations Management – Immediately remove exposed patients from contact with gas. – Provide 100% oxygen or assisted ventilation. – If exposure is to slightly water-soluble gases, patients may have acute dyspnea hours later. Consider transport to closest ED for observation. Pulmonary Edema Pathophysiology – Fluid buildup in lungs when blood plasma fluid enters lung parenchyma – Classifications: High pressure (cardiogenic) High permeability (noncardiogenic) Pulmonary Edema Assessment – By time crackles can be heard, fluid has: Leaked out of capillaries Increased diffusion space between capillaries and alveoli Swollen alveolar walls Begun to seep into alveoli Pulmonary Edema Assessment (cont’d) – Listen to lower lobes through the back. – Crackles are heard higher in the lungs as the condition worsens. – In severe cases, watery sputum, often with a pink tinge, will be coughed up. Acute Respiratory Distress Syndrome Pathophysiology – Seldom seen in field – Caused by diffuse damage to alveoli from: Shock Aspiration of gastric contents Pulmonary edema Hypoxic event Acute Respiratory Distress Syndrome Assessment – Document oxygen saturation, breath sounds, and any sudden changes. – Monitor ventilation pressures. Pneumothorax Pathophysiology – Air collects between visceral and parietal pleura. – Weak spots (blebs) can predispose a person. Pneumothorax Assessment – Patients may have: Sharp pain after coughing Increasing dyspnea in subsequent minutes or hours Pneumothorax Management – Most patients will not require acute intervention. – They should receive oxygen and close monitoring of their respiratory status. Pleural Effusion Pathophysiology – Blister-like sac of fluid formed when fluid collects between visceral and parietal pleura © Jones & Bartlett Learning. Pleural Effusion Assessment – It can be hard to hear breath sounds. – The patient’s position will affect the ability to breathe. Management – Fowler’s position likely most comfortable – Supportive care during transport to hospital Pulmonary Embolism Pathophysiology – Pulmonary circulation compromised by: Blood clot Fat embolism from broken bone Amniotic fluid embolism during pregnancy Air embolism from neck laceration or faulty IV Pulmonary Embolism Pathophysiology (cont’d) – A large embolism usually lodges in a major branch of the pulmonary artery. Prevents blood flow – Venous blood cannot reach the alveoli. Pulmonary Embolism Assessment – Early presentation: normal breath sounds, good peripheral aeration – Classic presentation: sudden dyspnea and cyanosis, sharp pain in the chest Cyanosis does not end with oxygen therapy. Pulmonary Embolism Assessment (cont’d) – Often begins in large leg veins, then migrate into pulmonary circulation – Thrombophlebitis: high risk © Jones & Bartlett Learning. Pulmonary Embolism Management – Bedridden patients are often given: Anticoagulants Special stockings/other devices to reduce blood clot formation – Greenfield filter: opens to catch clots traveling from the legs in the main vein Pulmonary Embolism Management (cont’d) – Saddle embolus: exceptionally large embolus lodging at left/right pulmonary artery bifurcation May be immediately fatal Cape cyanosis despite CPR and ventilation