and if appropriately credentialed clinicians and resources are available.
A patient with a penetrating wound to the chest should have an occlusive dressing applied with watchful monitoring for the development of tension physiology. If tension develops, the dressing should be immediately vented. Some types of occlusive dressings provide one‐way air flow (pleural space to environment) to prevent the accumulation of gas in the pleural space that leads to a tension pneumothorax. Alternatively, an occlusive dressing may be left unsealed on one side or corner, which allows it to act like a one‐way flap valve.
A frequent concern with the management of patients with pneumothorax is air transport. Boyle’s law (P1 × V1 = P2 × V2) describes that the air in the pleural space will expand with decreasing atmospheric pressure associated with increasing altitude. The EMS clinician should be aware that helicopter transport is not typically associated with sufficient altitude to have a significant clinical effect. For example, most medical helicopters fly at 1,000–3,000 feet above the ground. But at 6,000 feet, an altitude sometimes associated with instrument flight conditions (e.g., inclement weather), the increase in size would be about 25% (e.g., V2 = P1 × V1/P2 = 760 mmHg × 100 cc/609 mmHg = 125 cc). The clinical effects of such an increase in pneumothorax size are very much patient specific, depending on such things as initial volume, lung compliance, and comorbid conditions. Patients generally should not be flown in fixed‐wing aircraft (especially without cabin pressurization) without tube thoracostomy decompression.
Summary
Oxygenation and ventilation are distinctly different but interrelated physiological processes. In general, adequate oxygenation requires sufficient ventilation to deliver gas to alveolar spaces, where oxygen can then enter pulmonary capillaries for transport to peripheral tissues. Pulse oximetry is a useful tool, except in cases of carbon monoxide poisoning, to help determine the extent of tissue oxygenation. Patients with respiratory distress or SpO2 less than 94% should receive supplemental oxygen. However, use of oxygen should not be indiscriminate.
Ventilation is about gas moving in and out of the lungs. Clearly, it can occur without oxygen, and, in that sense, is a distinct process. The adequacy of ventilation is generally assessed in terms of minute ventilation. Waveform capnography is a useful tool to both monitor ventilation and evaluate its effectiveness. NIPPV may provide needed support to an awake patient with inadequate ventilation but intact respiratory drive. Mechanical ventilation is the maximum ventilatory support tool. Especially in a dynamic prehospital environment, vigilant monitoring is imperative to promptly identify and address deficiencies in ventilation and oxygenation and complications arising from their treatment.
References
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4 4 McSwain SD, Hamel DS, Smith PD, et al. End‐tidal and arterial carbon dioxide measurements correlate across all levels of physiologic dead space. Respir Care. 2010; 55:288–93.
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8 8 Austin MA, Wills KE, Blizzard L, et al. Effect of high flow oxygen on mortality in chronic obstructive disease patients in the prehospital setting: randomized controlled trial. BMJ. 2013; 341: c5462.
9 9 Williams B, Boyle M, Robertson N, Giddings C. When pressure is positive: a literature review of the prehospital use of continuous positive airway pressure. Prehosp Disaster Med. 2013; 28:52–60.
10 10 Siegler J, Kroll M, Wojcik S, Moy HP. Can EMS providers provide appropriate tidal volumes in a simulated adult‐sized patient with a pediatric‐sized bag‐valve‐mask? Prehosp Emerg Care. 2017; 21:74–8.
11 11 Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000; 342:1301–8.
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13 13 Sanchez LD, Straszewski S, Saghir A, et al. Anterior versus lateral needle decompression of tension pneumothorax: comparison by computed tomography chest wall measurement. Acad Emerg Med. 2011; 18:1022–6.
14 14 Inaba K, Karamanos E, Skiada D, et al. Cadaveric comparison of the optimal site for needle decompression of tension pneumothorax by prehospital care providers. J Trauma. 2015; 79:1044–8.
15 15 American College of Surgeons, Committee on Trauma. Advanced Trauma Life Support: Student Course Manual. Chicago, IL: American College of Surgeons, 2018.
16 16 Jodie P, Hogg K. BET 2: Pre‐hospital finger thoracostomy in patients with chest trauma. Emerg Med J. 2017; 34:419.
17 17 Jodie P, Kerstin H. BET 1: Pre‐hospital finger thoracostomy in patients with traumatic cardiac arrest. Emerg Med J. 2017; 34:417–18.
CHAPTER 7 Hypotension and Shock
Francis X. Guyette, Raymond L. Fowler, and Ronald N. Roth
Introduction
Shock is a life‐threatening physiological state characterized by decreased tissue perfusion and end‐organ tissue dysfunction, and is a significant predictor for complications including death [1]. The presence of shock must be recognized and therapeutic interventions must be started early to prevent progression. Unfortunately, identification and treatment of shock in the out‐of‐hospital setting are fraught with many difficulties and potential pitfalls. Patient assessment is often limited by the challenging environment. The tools available for the diagnosis and treatment of shock in the field are limited. Even when shock is properly identified, the most appropriate management is often unknown or the subject of debate.
In the field, identification of shock relies primarily on recognition of signs and symptoms, including tachycardia, poor skin perfusion, and altered mental status. Note that hypotension, arbitrarily defined at a systolic blood pressure (sBP) of less than 90 mmHg, is not an adequate definition of shock and may not adequately reflect the onset of tissue hypoperfusion [2]. Unfortunately, the early stages of compensated shock, with only subtle alterations in physical findings, are easily overlooked or misinterpreted by clinicians. Physiological changes associated with age, pregnancy, or treatment for medical conditions such as beta‐blockers for hypertension, may also mask or alter the body’s compensatory responses. As a result, the patient with severe shock may present with near‐normal vital signs.
Pathophysiology
Shock is a complex physiological process defined as the widespread reduction in tissue perfusion leading to cellular and organ dysfunction and death. In the early stages of shock, a series of complex compensatory mechanisms act to preserve critical organ perfusion [3]. In general, the following relationships drive