The patient is unconscious and breathing rapidly. As you kneel to feel a radial pulse, you discover the pulse is weak and rapid. The femoral and carotid pulses are stronger. After opening the airway and applying high-flow oxygen, vital signs are assessed revealing a pulse of 130 bpm and blood pressure 90/38. Your partner comments, “The patient is in shock.” So what is this shock thing?

Shock occurs when the circulatory system doesn’t have enough pressure to allow oxygen to reach all of the organs. Supplying organs and body tissues with oxygenated blood is known as perfusion. Components responsible for maintaining perfusion include the heart, blood vessels and blood. Shock should be considered a sign, not a diagnosis. Treatment is based on the underlying cause. There are five types of shock: cardiogenic, distributive, obstructive, dissociative and hemorrhagic.

Cardiogenic shock occurs when the heart fails to pump adequately. Decreased cardiac output can be caused by extremes in heart rate — either too slow or too fast, a decrease in force of pumping caused by a myocardial infarction (MI) or damaged heart valves.

Distributive shock is a distribution problem. The blood vessels make up the network responsible for distributing blood to the body. When these vessels leak or become too large or dilated, blood pressure will go down resulting in shock. Common causes of distributive shock are anaphylaxis, sepsis and trauma to the spinal cord.

Obstructive shock occurs when a physical obstruction alters the body’s ability to maintain perfusion. Causes include pulmonary embolism, tension pneumothorax and pericardial tamponade.

Dissociative shock presents with normal heart function, intact and responsive blood vessels, and plenty of blood. Perfusion problems occur because the blood has a decreased ability to carry oxygen to the tissues. Causes of dissociative shock are CO poisoning, cyanide poisoning and anemia.

Excessive blood loss results in hemorrhagic shock. Internal bleeding from ulcers or ruptured aneurisms as well as external bleeding caused by traumatic events can result in hemorrhagic shock.

The body will try to compensate as it progresses into shock. Initial drop in blood pressure is recognized by sensors in the carotid arteries and aorta, triggering a release of epinephrine. Epinephrine increases heart rate, makes the heart beat harder and constricts the blood vessels. This allows the body to maintain blood pressure and vital organ perfusion.

This early stage of shock is called compensated shock. Patients in compensated shock will have an increase in heart rate and pale skin caused by vasoconstriction. Their blood pressure may be normal. Epinephrine also causes anxiety and sweating (diaphoresis). Diaphoresis is first seen on the forehead and upper lip. These patients will reap the most benefit from treatment.

The goal of the EMT is to recognize what may be subtle signs, such as diaphoresis, and try to determine the cause of the shock. Additional signs and symptoms can help with recognition. Anaphylaxis can present with hives (urticaria), and mottling can be seen with sepsis. Cardiogenic shock may have chest pain and palpitations. Venous distention and shortness of breath are common findings in obstructive shock.

If the cause of shock isn’t stopped, the continued release of epinephrine will eventually cause enough vasoconstriction to shut off blood supply to distal tissues. These tissues will soon become damaged because they lack oxygen and release acids as they begin to die, causing the blood vessels to dilate. As vessels dilate blood pressure begins to drop. This takes oxygenated blood away from vital organs. System-wide damage begins. This stage of shock is known as progressive or decompensated shock. These patients are in imminent danger of dying. Recognition, aggressive treatment and appropriate transport are crucial for patient survival.

Patients who remain in shock will eventually reach irreversible shock. In this stage, known as Multiple Organ Dysfunction Syndrome (MODS), enough damage has been done to the organs to cause the failure of body systems. Patients who reach this irreversible stage of shock will die. Death may be immediate or several days later due to organ failure.

Shock treatment is straight forward. Supply oxygenated blood to the tissues and you stop the cause. Unfortunately, some situations make this difficult. Care begins by assuring the appropriate depth and rate of ventilation and administration of high-flow oxygen. Perfusion can be assisted by placing the patient supine. Keep the patient warm. Treatment then focuses on the cause. If the EMT suspects an MI, the administration of aspirin and nitro may be indicated. In the case of anaphylaxis, EpiPens may be lifesavers. Patients hemorrhaging must have the bleeding stopped. Other causes of shock, such as sepsis, pulmonary embolism and tension pneumothorax, may require more advanced care. Shock should still be recognized and patients treated symptomatically.

In cities with specialized hospitals, destinations should be selected appropriately. Trauma patients go to trauma centers and cardiac patients go to cardiac centers. If specialty centers aren’t available, the EMT should notify the receiving facility as soon as possible to allow them time to prepare.

Based on physical assessment and history, you determine your patient’s in anaphylactic shock. After conferring with the MD over the radio, you administer the patient’s EpiPen. You assure the airway remains patent and continue administration of high-flow oxygen. The patient is transported supine and kept warm with a blanket. Early notification of the receiving facility allows for preparation of advanced airways, antihistamines and steroids. The patient shows signs of improvement, and the MD compliments you for your quick thinking and intervention.