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Cardiovascular

 Tachycardia, arrhythmias, hypotension

 Jugular venous distension in obstructive and cardiogenic shock states

 Tracheal deviation away from the affected side in tension pneumothorax

Central nervous system

 Agitation, confusion

 Alterations in level of consciousness

 Coma

Respiratory

 Tachypnea, dyspnea

Skin

 Pallor, diaphoresis

 Cyanosis (in obstructive and cardiogenic shock cases), mottling

In the noisy field environment, EMS clinicians often measure blood pressure by palpation rather than auscultation. Blood pressure by palpation provides only an estimate of sBP [7]. Without an auscultated diastolic pressure, the pulse pressure (the difference between systolic and diastolic pressure) cannot be calculated. A pulse pressure less than 30 mmHg or 25% of the sBP may provide an early clue to the presence of hypovolemic or obstructive shock [3]. Conversely, a wide pulse pressure may be indicative of distributive shock. Dividing the pulse rate by the sBP typically produces a ratio of approximately 0.5 to 0.8, which is called the “shock index.” When that ratio exceeds 0.9, then a shock state may be present [8].

Previously healthy patients with acute hypovolemic shock may maintain relatively normal vital signs with up to 25% blood volume loss [3]. Sympathetic nervous system stimulation with vasoconstriction and increased cardiac contractility may result in normal blood pressure in the face of decreasing intravascular volume, especially in the pediatric population. In some patients with intra‐abdominal bleeding (e.g., ruptured abdominal aneurysm, ectopic pregnancy), the pulse may be relatively bradycardic despite significant blood loss [9].

EMS personnel may equate “normal” vital signs with normal cardiovascular status [5]. The field team may be lulled into a false sense of security initially if the early signs of shock are overlooked, and then they are caught off guard when the patient’s condition dramatically worsens during transport. Following trends in the vital signs may also help identify shock before patients reach abnormal vital sign triggers. Early recognition and aggressive treatment of shock may prevent progression to the later stages of shock that can result in the death of potentially salvageable patients [10].

Prehospital hypotension may predict in‐hospital morbidity and mortality in both trauma and medical patients [11–13]. Medical patients may have a 30% higher mortality if there has been prehospital hypotension [11]. Trauma patients with prehospital hypotension have similar outcomes, even with subsequent normotension in the emergency department. This emphasizes the importance and value of accurate in‐field assessments, so that the next echelon of patient care can be informed and aware of the potential for critical illness or injury.

Despite their questionable value, orthostatic vital signs are often evaluated in the emergency department, and occasionally in the field. A positive orthostatic vital sign test for pulse rate would result in a pulse increase of 30 beats/min after 1 minute of standing [14]. Symptoms of lightheadedness or dizziness are considered a positive test. Occasionally, orthostatic vital signs are performed serendipitously by the patient who refuses treatment while lying down, then stands up to leave the scene, and suffers a syncopal or near‐syncopal episode. This demonstration of orthostatic hypotension is often helpful in convincing the patient to consent to treatment and transport. However, EMS clinicians should not routinely obtain orthostatic vital signs, and they should not equate absence of orthostatic response with euvolemia.

Capillary refill, an easy test to perform in the field setting, is not a useful test for mild‐to‐moderate hypovolemia [15]. Moreover, environmental considerations, such as cold temperatures and adverse lighting conditions, also affect the accuracy of this technique for shock assessment.

On‐scene estimates of blood loss by EMS clinicians may influence therapeutic interventions, including fluid administration. However, studies suggest that field clinicians are not accurate at estimating spilled blood volumes [16].

Hypoxia is a common manifestation of shock states. Patients in various stages of exsanguination may not have sufficient blood volume to perfuse adequately the body with oxygen. Unfortunately, pulse oximetry alone cannot detect the adequacy of oxygen delivery. Pulse oximetry may fail to detect a pulse (and give inaccurate oxygen saturation readings) when blood flow is reduced [15, 17]. Like pulse oximetry, capnography may also serve as an important tool in the evaluation and treatment of shock in the prehospital setting [18–21]. Exhaled end‐tidal carbon dioxide (EtCO₂) levels vary inversely with minute ventilation, providing feedback regarding the effect of changes in ventilatory parameters [22, 23]. Additionally, changes in EtCO₂ are virtually immediate when the airway is obstructed or the endotracheal tube becomes dislodged [24]. EtCO₂ concentration may be influenced by factors other than ventilation. For example, levels are reduced when pulmonary perfusion decreases in shock, cardiac arrest, and pulmonary embolism [25–27]. EtCO₂ is most useful as an indicator of perfusion when minute ventilation is held constant (e.g., when mechanical ventilation is applied) [19, 25]. Under these conditions, changes in EtCO₂ levels reliably indicate changes in pulmonary perfusion. In any patient suffering from a potential shock state, diminished EtCO₂ should be a warning of the critical nature of the patient’s problem.