Emergency Medical Services. Группа авторов

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delayed onset of peak effect, protracted duration of action, and side effect profile, diuretics are rarely indicated in the prehospital setting [61]. The other treatment options (e.g., nitroglycerin and NIPPV) likely provide more benefit to the patient.

      Morphine, once a staple of therapy for ADHF and SCAPE, has also been largely supplanted by the other therapies. A review of the large ADHERE database found a significant association between receiving morphine and death, as well as several other adverse outcomes [62]. One explanation may be that as morphine causes hypotension, it takes away the therapeutic room available for the use of other medications that could be used to reduce preload and afterload, such as nitroglycerin. In addition, as a respiratory depressant, morphine may decrease the respiratory drive of an already struggling patient and worsen hypoxemic respiratory failure [63].

      Pneumonia and infectious respiratory disease

      In general, there are few specific field interventions for patients who are determined to have pulmonary infectious causes of their shortness of breath. Pneumonia treatment guidelines are universally focused on prompt diagnosis and early treatment with antibiotics.

      Pulmonary embolus

      Pulmonary embolus is another clinical condition that can present to EMS clinicians with respiratory distress. Classic risk factors for venous thromboembolism (VTE) include the Virchow triad of venous stasis, trauma, and hypercoagulability. There are many risk factors for VTE, but the ones that have been clinically validated by Wells criteria and the PERC rule for risk stratification include recent surgery or immobilization of an extremity, malignancy, exogenous estrogen use, and prior DVT [64]. Other notable risk factors include genetic deficiency of anticlotting factors, pregnancy, obesity, and extended travel.

      Pulmonary embolus is a challenging clinical diagnosis because the manifestations can be subtle. The most common symptom is dyspnea, and the most common clinical signs are tachycardia and tachypnea. The pulmonary exam is usually unremarkable, although examination of the extremities, particularly the legs, may reveal swelling, erythema, and possibly pain in a limb with a DVT. With the increased use of peripherally inserted central venous catheters, pulmonary emboli are also reported more frequently because of upper extremity DVTs [65]. Small emboli often present with respiratory distress. Larger emboli that cause lung infarction can present with findings such as pleuritic chest pain and hemoptysis, and those with massive saddle embolism cause findings suggestive of obstructive shock (Box 5.2). The latter can be detected by findings such as right axis deviation, right ventricle strain, and right bundle branch block on a 12‐lead ECG. Additional useful ECG features for pulmonary embolus include the presence of T‐wave inversions in both V1 and lead III, an S wave in lead I, and a Q wave and inverted T wave in lead III (S1Q3T3) [66]. Acute right ventricular dysfunction can also be visualized using portable ultrasonography.

      EMS treatment priorities include high‐flow oxygen, vascular access, and cardiac monitoring. A fluid bolus is reasonable in the patient who presents with a suspected massive pulmonary embolus and perfusion failure. In some patients, the presentation can take the form of a witnessed nontraumatic cardiac arrest with narrow complex pulseless electrical activity as the initial rhythm. The presence of respiratory distress, altered mental status, and a shock index (heart rate/systolic blood pressure) >0.8 have also been shown to be predictive of cardiac arrest in suspected pulmonary embolus patients [67]. A rapidly declining EtCO2 can also be a harbinger of impending arrest. Although the use of prehospital thrombolysis in these instances has been reported to be effective in selected cases, a randomized controlled clinical trial failed to show improved outcomes during cardiac arrest when t‐PA was administered compared to placebo for patients with refractory pulseless electrical activity [68, 69].

      Pneumothorax

      Spontaneous pneumothorax is an uncommon condition that can present with acute respiratory distress. Risk factors for the development of a spontaneous pneumothorax include smoking history, underlying lung disease (e.g., COPD, tumor, infection, or a connective tissue disorder), positive‐pressure ventilation, and being male, with a tall, slender build [70]. A spontaneous pneumothorax is typically caused by rupture of the alveolar air sacs (i.e., subpleural bleb), leading to air accumulation between the parietal and visceral pleura, followed by variable collapse of the lung. Tension pneumothorax is a life‐threatening condition that occurs when the intrathoracic pressure increases due to air trapping from a valve‐like defect in the visceral pleura. This results in hemodynamic compromise from impaired venous return and decreased cardiac output.

      Symptoms of spontaneous pneumothorax include dyspnea and pleuritic chest pain. The examination may reveal tachycardia, unilateral decreased breath sounds on the affected side, asymmetrical chest rise, and chest wall crepitus. Patients with a suspected simple pneumothorax should be monitored closely for evidence of tension physiology such as worsening respiratory distress, hypoxia, and hypotension. Jugular venous distension and tracheal deviation are late findings of tension pneumothorax and should not be relied on to confirm this diagnosis. If available, ultrasound can be a valuable tool to assess for a potential pneumothorax, with both high sensitivity and specificity [10, 11]. Imaging will reveal an absence of lung sliding on the affected side. Intubated patients receiving positive‐pressure ventilation are at greater risk for developing a tension pneumothorax and should be monitored closely.

      Patients should be treated with supportive care, including oxygen, as indicated. If tension pneumothorax is suspected, immediate chest wall decompression is indicated. This can be achieved through needle or finger thoracostomy, depending on clinician scope of practice and training [71, 72]. (See Chapter 40.)

      Tracheotomy

      The patient with a tracheotomy presents a special circumstance when experiencing respiratory distress. An initial consideration is whether the distress is directly related to the tracheotomy itself. If not, then assessment and treatment should proceed as it would otherwise, with the added benefit of an effectively secured airway already in place.

      Respiratory distress related to tracheotomies generally relates to complications that manifest as airway obstructions. Commonly, secretions are the culprit, causing mucus plugging or drying inside the cannula and resulting in various degrees of obstruction. Initially, EMS clinicians should attempt to suction the airway through the inner cannula of the tracheotomy tube. Except in children, whose tracheotomy tubes have no inner cannula, the clinician can remove it if suctioning is inadequate. If there is no relief, the clinician should suction through the tracheotomy tube. Small aliquots of saline instilled into the tube may help loosen secretions to improve suctioning results. In the event that an appropriately sized suction catheter cannot be passed into a tracheotomy tube, it may also be removed with important considerations.

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