For normal cell respiration, the body requires a constant supply of oxygen. When this is interrupted for more than 3 minutes (except when there is severe hypothermia), lactic acidosis and cell death occur. This can rapidly lead to cardiorespiratory arrest if left untreated. Patients may become severely hypoxic due to acute respiratory failure, airway obstruction or acute lung injury.

Hypoxia in cardiac arrest is treated by ensuring that the patient's lungs are adequately ventilated with as near to 100% oxygen as possible. The patient also receives good‐quality chest compressions, which deliver oxygenated blood to the major organs (RCUK [232]).

Hypovolaemia in adults results in PEA and is usually caused by severe blood loss. The most common causes of severe blood loss are:

Although blood loss may be overt, it may not become apparent until the patient collapses. The treatment for hypovolaemia is identifying and stopping the source of fluid or blood loss, and replacing the circulating volume with the appropriate fluid.

A large‐scale Cochrane review found no evidence that the use of colloids improves a patient's survival compared to the use of crystalloids (Lewis et al. [134]). Both colloids and crystalloids are solutions used to restore circulating volume. Colloids have larger molecules than crystolloids and can be synthetic (e.g. starches, dextrans or gelatins) or naturally occurring (e.g. albumin or fresh frozen plasma). Crystalloids are salt based (e.g. saline or Hartmann's solution) and contain smaller molecules than colloids. Furthermore, due to the considerable expense of colloids, fluid resuscitation is normally started with a crystalloid (e.g. 0.9% sodium chloride or compound sodium lactate solution). An acute loss of 30–40% of total blood volume (1500–2000 mL) will require blood product replacement. This will become a life‐saving therapy if more than 40% (>2000 mL) of the total blood volume is lost (Shander et al. [251]).

An imbalance of potassium affects both the nerve conduction and the muscular function of the heart. A severe rise or fall in potassium can cause arrhythmias, which will cause cardiac arrest. Hypokalaemia is defined as plasma potassium below 3.5 mmol/L. It may be classified as (RCUK [232]):

The causes of hypokalaemia are:

The immediate treatment for hypokalaemia that has resulted in cardiac arrest is to give concentrated infusions of potassium while carefully monitoring serial potassium measurements. During cardiac arrest or in an emergency, potassium levels can be checked promptly via a venous or arterial blood gas. Prolonged CPR attempts may be required in order to allow for potassium replacement.

Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L. It may be classified as (Wilkinson et al. [285]):

Patients who are most at risk of hyperkalaemia are those with renal failure, heart failure and/or diabetes (Adamson [4]). The immediate treatment for severe hyperkalaemia is to give intravenous calcium gluconate, which protects the myocardium (Wilkinson et al. [285]). Efforts should then move to the ‘shifting’ or removal of excess potassium. Methods for achieving this include administering a combination of insulin and glucose via rapid infusion in an attempt to move the potassium into the cells. Alternatively, removal via dialysis can be considered in specialist centres with the ability to do so.

Hypothermia is defined as a core temperature below 35°C and is classified as (Malhotra et al. [142]):

Temperature is normally tightly regulated but is less well controlled in the very young, the elderly, and those with chronic disease, injury or intoxication. As the body cools, the metabolic rate falls and neural transmission is inhibited. Multiple derangements occur, which ultimately lead to reduced tissue oxygenation, including (Malhotra et al. [142]):

Initially, in an attempt to retain heat and body temperature, the sympathetic drive increases the heart rate and respiratory rate, and heat is produced via shivering. At around 30°C, this process ceases and ventilation, heart rate, blood pressure and cardiac output fall. Intravascular volume falls due to a cold diuresis and fluid shifts into the extravascular space. Sinus bradycardia develops followed by atrial fibrillation. Below 28°C, ventricular arrhythmias (including VF) may occur before the patient finally goes into asystole (Schober et al. [244]).

Hypothermia should be suspected in any submersion or immersion injury. Resuscitation in the presence of hypothermia should continue until the patient is warmed to normothermia or as near to it as possible. Resuscitation attempts in a patient who is hypothermic may therefore be prolonged. Conversely, it is important to be mindful that a prolonged resuscitation attempt may lead to a patient who was normothermic at the onset of cardiac arrest becoming hypothermic (RCUK [232]).

The most common cause of thromboembolic or mechanical circulatory obstruction is a massive pulmonary embolus (Konstantinides et al. [128]). Options for definitive treatment include thrombolysis, cardiopulmonary bypass and operative removal of the clot (RCUK [232]).

Acute coronary syndromes (ACS) are a group of clinical conditions, all of which usually present with chest pain or discomfort resulting in myocardial ischaemia:

Commonly, an ACS is initiated by the rupture or erosion of an atherosclerotic plaque within a coronary artery. This causes:

The above process causes a rapid and critical reduction in blood flow to the myocardium. The degree and extent of this reduction in blood flow are largely determined by the clinical presentation and type of ACS (RCUK [232]).

Tamponade is where there is an acute effusion of fluid in the pericardial space, which is usually blood but can be malignant or infected fluid (Schiavone [243]). As the collection of fluid increases, the heart is splinted until it can no longer beat (tamponade).

The most common cause of a sudden tamponade is penetrating chest trauma, in which case resuscitative thoracotomy may be indicated. Otherwise, pericardiocentesis should be performed (Fitch et al. [84]). If resuscitation is successful, follow‐up surgery may also be required (Harper [100]).

Poisoning rarely leads to cardiac arrest but it is a leading cause of death in patients less than 40 years old; self‐poisoning with therapeutic or recreational drugs is the main reason for hospital admission in this group of patients (Truhlar et al. [274]). There are few specific therapeutic measures for poisons that are useful in the immediate situation. The emphasis must be on intensive supportive therapy, with correction of hypoxia, acid/base balance and electrolyte disorders. Specialist information and guidance can be obtained from pharmacists and the TOXBASE website (https://www.toxbase.org).

A tension pneumothorax can develop from either a spontaneous pneumothorax or a traumatic pneumothorax (RCUK [232]). The most common causes are:

A breach in the pleura allows air to flow into the pleural space during inhalation but it is retained in the pleural cavity during exhalation. Thus, the air cannot exit, and this leads to a gradual increase in the intrapleural cavity pressure, inducing an interthoracic shift. During tension pneumothorax, the affected lung completely collapses and the contralateral lung and heart are pressurized (Choi [45]). The result is severe dyspnoea and cyanosis due to hypoxia, in addition to hypotension caused by restriction of the venous return to the heart (Roberts et al. [235]). Ultimately, a tension pneumothorax is an acute emergency and can lead to death if it is not imminently treated. During cardiac arrest, a tension pneumothorax should be treated with immediate needle decompression (Choi [45]). The procedure involves insertion of a large‐bore cannula into the second intercostal space at the mid‐clavicular line on the affected side (RCUK [232]). The aim is to expel the pressure and create an outlet for trapped air. This should be followed up with the insertion of a chest drain.