ARDS(Acute Respiratory Distress Syndrome)/Noncardiogenic Pulmonary Edema Epidemiology 70% mortality rates in people who develop ARDS.

Pathophysiology Disruption of the alveolar-capillary membrane is caused and an increase in pulmonary capillary permeability, destruction of the capillary lining and increases in osmotic forces act to draw fluid into the interstitial space and contribute to interstitial edema. This increases the thickness of the respiratory membrane and limits diffusion of oxygen. Assessment Findings Determine PMHX and/or if the pt has been exposed to any hazards. Dyspnea, confusion and agitation are often found. Fatigue and reduced exercise ability may also be present. Abnormal findings can be orthopnea, paroxyxmal nocturnal dyspnea(trouble breathing while asleep) or sputum production. The prominent findings are generally those associated with the primary underlying lung insult, but will most likely include tachypnea, tachycardia, crackles(rales) in both lungs, wheezing may be present if there is an element of bronchospasm. Severe tachypnea, central cyanosis and signs of imminent respiratory failure are seen in severe cases. Management Removal of pt from activities or hazards that they were involved in or exposed to are the priority treatment. O2, IV, cardiac monitoring, pulse ox, suctioning if needed to keep patent airway, provide fluids if hypovolemia exists. If pt is demonstrating signs of respiratory failure, provide ppv with bvm while preparing CPAP.

Asthma Epidemiology Asthma afflicts 4-5% of the US population. Deaths from asthma have significantly increased in the last decade. Most occur in patients 45y/o or older and the death rate for black patients is twice as high then in white patients. 50% of patients that die from asthma do so before reaching the hospital. Pathophysiology Within minutes of exposure to triggers, or asthma inducing factors, a two-phase reaction occurs. The first phase is characterized by the release of chemical mediators such as histamine. These mediators cause contraction of the bronchial smooth muscle and leakage of fluid from peribronchial capillaries which results in both bronchoconstriction and bronchial edema. These two factors significantly decrease expiratory air flow, causing the typical asthma attack. The second phase starts usually 6-8 hours after the exposure. This late phase is characterized by inflammation of the bronchioles as cells of the immune system(eosinophils, neutrophis and lymphocytes) invade the mucosa of the respiratory tract. This leads to additional swelling of the bronchioles and edema and a further decrease of in expiratory air flow. Assessment Findings Most common presenting symptoms are dyspnea, tachypnea, wheezing and cough. As severity increases the pt may exhibit hyperinflation of the chest due to air trapping in the alveoli and start to use accessory muscles. Also, one to two word dyspnea, pulsus paradoxus(dropping of bp 10mmhg or more with inspiration), tachycardia and decreased O2 saturation on pulse ox. If hypoxia occurs pt may become agitated and anxious. Management Correct hypoxia, reverse bronchospasm, reduce inflammation. O2 @100% high flow, IV, cardiac monitor The most commonly used drugs to reversing brochospasms are albuterol or levalbuterol(xopenex), in conjunction with ipratropium bromide(atrovent). These can be easily administered with a small volume, oxygen powered nebulizer. Monitor the pts response by noting improvement in PEFR, capnography and pulse ox readings.

Chronic Bronchitis Epidemiology COPD found in 25% of all adults. Chronic bronchitis alone affects 1 in 5 adult males. Patients with COPD have a 50% mortality within 10 years of the diagnosis. Pathophysiology Gas exchange is decreased because of the lowered alveolar ventilation, which ultimately results in hypoxia and hypercarbia. Hypoxia may increase red blood cell production, which in turn leads to polycythemia. Physiologically, an increased PaCO2 causes pulmonary vasoconstriction, resulting pulmonary hypertension and, eventually, cor pulmonale. Assessment Findings Try to get PMHX as the pt is usually a heavy cigarette smoker, but this disease may occur in nonsmokers as well. There may be a history of frequent respiratory infections. Pt usually produces a considerable amount of sputum daily. Clinically, the patient is described as having a productive cough for at least 3 months per year for 2 or more consecutive years. Patients with the disease tend to be overweight and can be cyanotic or blue bloaters. Auscultation of the thorax often will reveal rhonchi due to occlusion of the larger airways with mucus plugs. Pt may also show s/s of right heart failure such as jvd, ankle edema and hepatic congestion. Management Relieve hypoxia and reverse bronchoconstriction. First establish an airway, place the pt in a seated or semiseated position to assist the accessory respiratory muscles. Apply pulse ox and administer supplemental O2 to keep saturation levels above 90%. If hypoxia or respiratory failure is evident, then increase the concentration of O2 being administered. Be prepared to assist breathing efforts with bvm. CPAP may prove beneficial and can, in some instances, prevent the need for endotracheal intubation. It is best to keep PEEP pressures less than 10cm/H2O. Regardless, intubation may be required if CPAP fails and respiratory failure is imminent. Establish an IV w/ns or lactated ringers at a TKO rate. More aggressive fluid administration is suggested if signs of dehydration are present. This may also aid in loosening thick mucus secretions. Then, if ordered by medical control, administer a bronchodilator medication, such as albuterol though a small volume nebulizer. Consider the addition of iprtropium bromide(atrovent) during the initial nebulizer treatment. Corticosteroids are also commonly used in the early management of patients.

Emphysema Epidemiology The major factor contributing to emphysema is cigarette smoking. Significant exposure to environmental toxins is another contributing factor. It is more common in men than women. Pathophysiology Gradual destruction of the walls of the alveoli decreases the membrane surface area that lessens the area available for gas exchange that results in diffusion defects. Additionally the number of pulmonary capillaries in the lung is decreased and in turn increases the resistance to pulmonary blood flow which ultimately causes pulmonary hypertension which in turn may lead to right heart failure, cor pulmonale and death. Emphysema also causes weakening of the small bronchiole walls. This cause the lungs to lose their capacity to recoil and air becomes trapped in the lungs increasing the residual volume while the vital capacity remains relatively normal. The destroyed lung tissue(blebs) result in alveolar collapse. To counteract this, patients breathe with pursed lips to create positive pressure similar to PEEP to prevent alveolar collapse. Assessment Findings Find out PMHX of smoking habit. Physical exam will reveal a barrel chestYou may also not a prolonged expiratory phase and a rapid resting respiratory rate. They tend to be thin pink puffers due to excessive caloric intake use for respiration and due to polycythemia(excess RBC). Patients also tend to have hypertrophy of accessory respiratory muscles. S/S same as Asthma and Chronic Bronchitis. Management Relieve hypoxia and reverse bronchoconstriction. First establish an airway, place the pt in a seated or semiseated position to assist the accessory respiratory muscles. Apply pulse ox and administer supplemental O2 to keep saturation levels above 90%. If hypoxia or respiratory failure is evident, then increase the concentration of O2 being administered. Be prepared to assist breathing efforts with bvm. CPAP may prove beneficial and can, in some instances, prevent the need for endotracheal intubation. It is best to keep PEEP pressures less than 10cm/H2O. Regardless, intubation may be required if CPAP fails and respiratory failure is imminent. Establish an IV w/ns or lactated ringers at a TKO rate. More aggressive fluid administration is suggested if signs of dehydration are present. This may also aid in loosening thick mucus secretions. Then, if ordered by medical control, administer a bronchodilator medication, such as albuterol though a small volume nebulizer. Consider the addition of iprtropium bromide(atrovent) during the initial nebulizer treatment. Corticosteroids are also commonly used in the early management of patients.

Pneumonia Epidemiology It is the 5th leading cause of death in the US. A common medical problem in the very young, very old and those infected with HIV. Pathophysiology It is caused by a variety of infectious agents that invade the lungs. Bacterial and viral are the most common. The infection begins in one part of the lung and often spreads to nearby alveoli. The infection may ultimately involve the whole lung. Fluid and inflammatory cells collect in the alveoli and alveolar collapse may occur. Pneumonia is primarily a ventilation disorder. Assessment Findings The patient will generally appear ill, may report a recent hx of fever and chills, generalized weakness and malaise. Patient will c/o a deep, productive cough and may expel yellow to brown sputum, often streaked with blood. Many have associated plueritic(sharp or tearing) chest pain. Pneumonia involving the lower lobes of the lung, the patient may c/o nothing more that upper abd pain. Common findings are fever, tachypnea, tachycardia and a cough. Auscultation usually reveals crackles(rales) in the involved lung segment. There is usually decreased air movement in the areas filled with infection. Percussion of the chest may be dull and egophony may be noted. Management Purely supportive. Place the patient in a position of comfort, administer high flow high concentration O2, place on pulse ox, establish an IV with fluids given based on patients level of dehydration.

Pulmonary Embolism Epidemiology It accounts for 50,000 deaths per year in the US. 1 in 5 cases of sudden death are due to PE. 1 in 10 documented cases of PE result in death. PMHX of recent surgery, immobilized long bone fractures, bedridden condition, long distance travel immobilization, cancer, infection, thrombophllebitis, atrial fibrillation and sickle cell anemia all increase a patients risk of PE. Pathophysiology Sources of PE include air embolism(occurs during central line placement), fat embolism(occurs following a fracture), amniotic fluid embolism and blood clots. Foreign body emboli are also possible due to a venous catheter becoming dislodged. The majority of them are caused by blood clots formed in the deep venous system of the lower extremities. When a PE occurs, the blockage of blood flow through the affected artery causes the right heart to pump against increased resistance. This results in an increase in pulmonary capillary pressure. The area of the lung supplied by the occluded pulmonary vessel can no longer effectively function in gas exchange since it receives no effective blood supply. Assessment Findings Get PMHX to see if they have been immobilized from fracture, surgery or debilitating illness. Pt may show signs of labored breathing, tachypnea and tachycardia. In massive PE there may be signs of right heart failure such as jvd and falling bp. 50% of the cases will present with signs of DVT such as a warm, swollen extremity with a thick cord palpated along the medial thigh and pain on palpation or when extending the calf. Management Perform CPR if needed as in the case of cardiac arrest. Establish and maintain an airway, assist with ventilations if needed, administer high concentration O2. Establish an IV at TKO with ns or lactated ringers. Monitor vitals closely and place on cardiac monitor. Transport emergently.

Neoplasms of the Lung Epidemiology Lung cancer is the leading cause of cancer-related death in the US in both men and women. Most patients are between the ages of 55 and 65. Most patients die within 1 year of diagnosis. Pathophysiology The most common type of lung cancer, adenocarcinoma, arises from glandular-type(i.e. mucus producing) cells found in the lungs and bronchioles. Assessment Findings The first priority is to address signs of severe respiratory distress. Look for AMS, 1 to 2 word dyspnea, cyanosis, hemoptysis and hypoxia as noted by pulse ox. Severe uncontrolled hemoptysis can be a particularly life threatening presentation. Physical findings are nonspecific. Patients with advanced disease have profound weight loss, cachexia(general physical wasting and malnutrition), Crackles, rhonchi, wheezes and diminished breath sounds may be heard in the affected lung. Management Administer supplemental O2 as needed based on the clinical status and pulse ox measurement. Support ventilations and intubate if needed. Be aware of any advanced directives. Establish an IV and provide fluids if signs of dehydration are present. Transport the patient and monitor mental status, vital signs and oxygen status as appropriate.

Upper Respiratory Infection Epidemiology These are the most common infections for which patients seek medical attention. Pathophysiology The majority of URIs are caused by viruses, but a variety of bacteria may also produce infection of the upper respiratory tract. The most significant is group A streptococcus, which the causative organism in strep throat and accounts for 30% of URIs. Fortunately, most URIs are self-limiting illnesses that resolve after several days of symptoms. Assessment Findings Patients with URIs will often show these accompanying symptoms such as fever, chills, myalgias(muscle pain) and fatigue. Rhinitis(nose) s/s include runny nose, congestion, sneezing and rhinorrhea Pharyngitis(pharynx) s/s include sore throat, pain on swallowing, erythematous pharynx,tonsil enlargement, pus on tonsils, cervical lymph node enlargement Otitis Media(middle ear) s/s include ear pain, decreased hearing, red bulging eardrum, pus behind eardrum, lymph node enlargement in front of or behind ear Laryngitis(larynx) s/s include sore throat, hoarseness, pain on speaking, red pharynx, hoarse quality to voice, cervical lymph node enlargement Epiglottitis(epiglottis) s/s include sore throat, drooling, ill appearing, upright position Sinusitis(sinuses) s/s include h/a, congestion, tenderness over the sinuses, worsening of pain with leaning forward, yellow nasal discharge Management Focus attention on the patients airway and ventilation. Give supplemental O2 to any patient with underlying pulmonary disease and transport facility that is able to treat their condition. Continue monitoring with pulse ox and ecg during transport.

Spontaneous Pneumothorax Epidemiology There are 18 cases for every 100,000 people with recurrence in 50% of the patients within 2 years. There is a 5:1 ratio of male to female patients. Pathophysiology The negative pressure that normally exists in the pleural space is lost. This prevents proper expansion o f the lung in concert with the chest wall. A pneumothorax occupying 15-20% of the chest cavity is generally well tolerated by the patient unless there is significant underlying lung disease. Assessment Findings Patient presents with a sudden onset of sharp, pleuritic chest or shoulder pain. The symptoms are precipitated by coughing or lifting. Dyspnea is common along with tachypnea , diaphoresis and pallor. Management Most cases require only supplemental O2, monitoring and transport. Be careful when ventilating, too much pressure may result in a tension pneumothorax.

Hyperventilation Syndrome Epidemiology

Pathophysiology This frequently occurs in anxious patients. The pt often senses that he cannot catch his breath. The pt will then begin to breathe rapidly. Hyperventilation in a purely anxious patient results in the excess elimination of CO2 causing a respiratory alkalosis. This increases the amount of bound CA, producing a relative hypocalcemia. This results in cramping of the muscles of the feet and hands, which is called carpopedal spasm. Assessment Findings You may get a hx of fatigue, nervousness, dizziness, dyspnea, cp, numbness and tingling the mouth, hands and feet. An anxious pt will present with tachypnea and tachycardia, spasm of the fingers and feet may also be present. If the pt has a hx of seizures, the hyperventilation may precipitate a seizure. Management Reassure the pt, instruct the pt to control their respiratory rate and depth, place pt on pulse ox and provide supplemental O2 if indicated.