Reversible Causes of Cardiac Arrest

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Introduction

Cardiac arrest can be defined as the “cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation”.¹

There are 1 to 1.5 cardiac arrests per 1000 hospital admissions per year. The annual incidence of out-of-hospital cardiac arrest (OHCA) is approximately 55 per 100,000 inhabitants with 72% of cardiac arrests occurring in the home or workplace (15%).²

Cardiac arrest can often occur as a result of underlying cardiac diseases such as ischaemic heart disease, heart failure and arrhythmias.³

Cardiac arrest can also occur due to non-cardiac causes such as toxins, pneumothorax or severe infection. 

This article will cover the reversible causes of cardiac arrest, including relevant investigations and management.

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Hypoxia

Hypoxia is the state of insufficient oxygen to maintain homeostasis at a cellular level.⁴ Sustained hypoxia is the most common non-cardiac cause of arrest.⁵

Aetiology

Causes of hypoxia include:

• Airway obstruction (e.g. choking, soft tissue obstruction resulting from a reduced level of consciousness)
• Asthma
• Drowning
• Hanging
• Asphyxia

Research into the sequence of events leading to cardiac arrest following hypoxia is limited, but current research assumes that hypoxia results in desaturation, a fall in blood pressure which then causes bradycardia finally progressing to cardiac standstill.⁵

Investigations

Relevant investigations in the context of hypoxia include:

• Bedside investigations: including capnography, oxygen saturations and respiratory rate
• Arterial blood gas

Management

Management priorities for correcting hypoxia during resuscitation include:^6,7

• Assess the airway for causes of obstruction such as angioedema, vomit or foreign body
• Initiate basic airway management to clear any obstructions and optimise oxygenation
• Auscultate to check for breath sounds and air entry when ventilating, and listen for stridor which may indicate airway obstruction
• Aim for a normal ventilation rate with the highest feasible oxygen concentration

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Hypovolemia

Hypovolaemia can be defined as a reduction in intravascular volume. Blood volume, reduced by fluid loss causes a reduction in pressure and cardiac output until cardiac arrest occurs.⁸

Aetiology

Causes of hypovolaemia include:⁶

• External blood loss (e.g. traumatic injuries, haematemesis)
• Internal blood loss (e.g. ruptured aortic aneurysm, gastrointestinal bleeding)
• Other causes of fluid loss (e.g. diarrhoea & vomiting, dehydration, renal disease)

Investigations

Relevant investigations in the context of hypovolemia include:

• Haemoglobin/haematocrit: may be low
• Arterial blood gas
• Focused Assessment with Sonography in Trauma (FAST): bedside ultrasound can be used to identify any internal bleeding

Management

Management priorities for correcting hypovolemia during resuscitation include:

• A full secondary survey will identify any external bleeding and some internal causes (e.g. distended abdomen)
• Catastrophic haemorrhage control (e.g. tourniquets, pelvic binders)
• Blood transfusion
• Fluid resuscitation
• Oxygen therapy

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Hypothermia

Hypothermia is defined as a core temperature below 35°C. Mild hypothermia is categorised as 32-35°C, moderate hypothermia as 30-32°C and a core temperature of below 30°C is defined as severe hypothermia.¹⁰

Aetiology

As the body temperature drops from its normal homeostatic state, the metabolic rate reduces and neural transmission is inhibited. As a result of a number of mechanisms such as lower myocardial contractility, reduced availability of oxygen at the tissue level, vasoconstriction, VQ mismatch and increased blood viscosity.¹¹

Initially sympathetic drive results in an increased heart rate and respiratory rate as well as shivering to produce heat. However, at (or below) 30°C the sympathetic drive stops, and this results in a fall in heart rate, blood pressure and cardiac output as well as ventilation. Fluid moves into extravascular spaces, and intravascular volume falls.¹²

Cardiac activity usually slows to sinus bradycardia before atrial arrhythmias begin, then ventricular arrhythmias occur which develop into asystole. 

For the primary cause of cardiac arrest to be hypothermia, very low temperatures are required which is unusual in the United Kingdom.¹²

Drowning is a potential cause of hypothermia.¹¹

Hypothermia protects vital organs such as the brain and therefore good neurological and functional recovery in patients who have experienced long periods of circulatory arrest is possible in the context of hypothermia.¹²

Risk factors

Hypothermia affects two main patient groups:

• Winter sports participants
• Urban poor (e.g those experiencing homelessness, drug and alcohol addiction and poor socioeconomic conditions)

Investigations

Relevant investigations in the context of hypothermia include:

• Core temperature: using a low reading thermometer, a tympanic in spontaneously breathing patients and oesophageal in patients with ET or supraglottic devices in situ.
• Arterial blood gas
• Full blood count: as fluid moves to intravascular spaces, haematocrit may rise. Estimate a rise of 2% for each 1 degree fall in core temperature. If haematocrit is lower than expected consider blood loss
• Urea & electrolytes: assess for hypoglycaemia and hyperkalemia. Serum potassium may increase with rewarming. Hyperkalaemia is indicative of cell necrosis and very high levels are associated with higher mortality. Rewarming is contraindicated if levels are >10mmol/L.
• Calcium
• Magnesium
• Coagulation profile: blood viscosity is reduced in hypothermia and coagulopathy similar to disseminated intravascular coagulopathy is common. Thrombocytopenia may occur as a result of marrow suppression or hepatosplenic sequestration.
• Amylase

When interpreting a blood gas from a hypothermic patient, take into account that blood gas machines rewarm samples to 37°C. These values can be corrected mathematically but are difficult to interpret. Therefore use uncorrected values to guide practice.

Management

Management priorities for correcting hypothermia during resuscitation include:¹¹

• Chest compression and ventilation rate should remain as per normothermic guidelines (120bpm and 12 ventilations per minute)
• Aim for a normal CO₂ on arterial blood gas (uncorrected)
• If ventricular fibrillation (VF) persists after 3 shocks, delay further shocks until the core temperature is >30°C
• Reduced metabolism means drugs should be withheld if the core temperature is <30°C. Timing intervals should be doubled if the core temperature is 30-34°C (e.g. 6-10 minutes for adrenaline).
• Rewarming should be performed with extracorporeal life support (ECLS) preferably with extracorporeal membrane oxygenation (ECMO) over cardiopulmonary bypass (CRB).
• Should return of spontaneous circulation (ROSC) be achieved, follow standard post-resuscitation care guidelines

When managing hypothermic cardiac arrest, prioritise steady rewarming and maintaining physiological supportive measures such as oxygenation, correction of electrolyte and metabolic disturbances, and supporting intravascular volume.¹²

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Hypo-/hyperkalaemia (electrolytes)

Hypokalemia and hyperkalemia are common electrolyte disorders caused by changes in potassium intake, altered excretion, or transcellular shifts.¹³

Hyperkalaemia is defined as plasma potassium in excess of ≥5.5 mmol/L whilst hypokalaemia is defined as a serum potassium level of <3.5 mmol/L.^14,16

It is important to consider hypo-/hyperkalaemia in all patients presenting with cardiac arrest.

Aetiology

Causes of hyperkalemia include:

• Renal impairment
• Medications (e.g. ACE-inhibitors)
• Diabetic ketoacidosis
• Trauma
• Burns

For more information, see the Geeky Medics guide to hyperkalaemia. 

Investigations

Use point of care testing to check electrolytes during the management of cardiac arrest. 

Management

Management priorities for correcting hypo/hyperkalaemia during resuscitation include:

• Confirm hyperkalemia using blood gas analyser
• 10ml calcium chloride 10% IV by rapid bolus injection
• Give 10 units soluble insulin and 25g glucose IV by rapid injection to shift potassium into cells.
• Monitor blood glucose: administer 10% glucose infusion guided by blood glucose to avoid hypoglycaemia.
• Shift potassium into cells: give 50 mmol sodium bicarbonate (50 mL 8.4% solution) IV by rapid injection.
• Consider dialysis for refractory hyperkalemia cardiac arrest to remove potassium from the body.
• If prolonged CPR is required, consider the use of a mechanical chest compression device.

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Tension pneumothorax

A pneumothorax is a collection of air in the pleural space (between the lung and chest wall).¹⁶

A tension pneumothorax is the continued collection of this air causing compression of the structures in the chest (including the heart), leading to haemodynamic compromise.¹⁸

Clinical features of a tension pneumothorax include tracheal deviation, absent breath sounds (unilateral) and cyanosis.

Aetiology

Causes of tension pneumothorax include:¹⁸

• Traumatic: penetrating injuries to the chest (e.g. gunshot or stab wound), rib fractures
• Medical: mechanical ventilation, asthma

Investigations

Relevant investigations in the context of tension pneumothorax include:

• Chest X-ray (do not delay treatment whilst arranging/awaiting a chest X-ray)

Management

Management priorities for correcting tension pneumothorax during resuscitation include:^18,19

• Needle decompression: insert a large-bore cannula (e.g. orange 14G or grey 16G) into the 2nd intercostal space (above the 3^rd rib), along the mid-clavicular line.
• Subsequent decompressions should be placed laterally to the initial one – but a chest drain should be prioritised if the equipment is readily available.
• In an out-of-hospital trauma cardiac arrest, bilateral needle decompression should be completed as part of the traumatic cardiac arrest algorithm.
• Thoracostomy should be completed as soon as equipment and qualified staff are available, followed by a chest drain insertion to either 4th or 5th intercostal space at the anterior axillary line (with subsequent x-ray to confirm correct placement and reinflation of the lung)

For more information, see the Geeky Medics guide to the emergency management of pneumothorax.

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Cardiac tamponade

Cardiac tamponade results from the presence of blood or fluid in the pericardial space (the sac around the heart). This limits the filling of the ventricles, reducing stroke volume and cardiac output, and causing cardiac arrest.¹⁹

Aetiology

Causes of cardiac tamponade include:²²

• Trauma to the chest/heart (e.g. penetrating injuries)
• Ventricular wall rupture following a myocardial infarction (MI)
• Metabolic causes (e.g. chronic kidney disease leading to an accumulation of toxins and fluid)
• Infection of the pericardium

Investigations

Relevant investigations in the context of cardiac tamponade include:²¹

• Echocardiogram
• ECG
• Chest X-ray
• CT imaging

Management

Management options for correcting cardiac tamponade during resuscitation include pericardiocentesis or resuscitative thoracotomy.

Pericardiocentesis²³

Using a large needle and catheter, the blood/fluid can be drained directly from the pericardial sac by entering through the chest wall. Fluoroscopy, CT or echocardiography can be used to guide the clinician, ensuring the correct siting of the needle. Apical, subcostal or parasternal approaches can be used as the entry site.

Resuscitative thoracotomy²⁴

A left-sided approach should be used to open the chest, using a scalpel from the sternum to the 5th intercostal space, and continuing to the posterior mid-axillar line. If right thorax injuries are also suspected, a clamshell approach should be utilised.

Rib spreaders should then be used to visualise the pericardium. A small incision into the pericardium, avoiding the myocardium, can then aid in removing fluid and clots.

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Toxins

Poisoning rarely causes cardiac arrest. It is important to consider the direct effects of drugs on the patient or potential anaphylaxis following medication administration.^5,9

Aetiology

Causes of cardiac arrest as a result of toxins include:²⁵

• Medication overdose: common medications that result in cardiac arrest include tricyclic antidepressants, beta blockers and opioids
• Illicit drug use (e.g. opiates or cocaine) can result in long QT and pulseless arrest

Investigations

Relevant investigations in the context of toxins include:⁹

• Urea and electrolytes: for potential electrolyte disturbance
• Core temperature: drug overdose can result in hypo/hyperthermia

Assess pupils as these may be affected by the toxin (e.g. pupillary constriction in opioid overdose). A collateral history may identify details of events leading up to the cardiac arrest (e.g. history of new medication).

Management

Management priorities for correcting toxins during resuscitation include:⁹

• Review poisons guidance (e.g. Toxbase) for advice regarding specific toxins
• Consider the use of reversal agents and antidotes as appropriate
• Supportive measures should continue until ROSC is achieved

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Thrombosis

A thrombus is a blood clot which can become dislodged and obstructs blood vessels. Thrombosis is a cause of cardiac arrest (typically pulmonary embolism (PE) and/or myocardial infarction (MI)) 

Management of cardiac arrest following suspected PE

A thrombus may become dislodged resulting in obstruction of the lung vasculature, resulting in right ventricular strain and overload. This causes cardiogenic shock and a reduction in preload and subsequent circulatory failure.²⁵

Relevant investigations in the context of PE include:⁹

• Low ETCO₂ readings <1.7kPA or 13mmhg may support a diagnosis of PE

Management priorities for correcting PE during resuscitation include:¹⁰

• If PE is the known cause of cardiac arrest, use thrombolytic drugs or surgical embolectomy or percutaneous mechanical thrombectomy.
• When thrombolytic drugs have been administered consider continuing CPR for 60-90 minutes before terminating resuscitation attempts.

Management of cardiac arrest following a suspected coronary thrombosis

A thrombus obstructing cardiac vessels will result in acute myocardial infarction. This results in necrosis of myocardial tissue and cardiac failure.

Relevant investigations in the context of coronary thrombosis:⁹

• Gather a collateral history if possible, presentations that may be suggestive of coronary thrombosis include chest pain prior to arrest, known coronary artery disease, initial rhythm VF or pulseless VT.
• Post resuscitation 12-lead ECG showing ST elevation

Management priorities for correcting coronary thrombosis during resuscitation include:^9,27.28

• Patients who have sustained ROSC and STEMI on post-ROSC ECG should receive primary percutaneous coronary intervention (PPCI) within 120 minutes of diagnosis.
• For NSTEMI consider patient characteristics and ECG findings
• Perform urgent angiography <120 mins if ongoing myocardial ischemia is suspected or if the patient remains haemodynamically unstable. 
• PCI is preferred over thrombolytic drugs as a reperfusion method

Beware of the risk of haemorrhage secondary to thrombolysis (haemorrhagic stroke occurs in 0.5-1% of patients).²⁸

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Key points

• Ensure effective basic life support is initiated prior to addressing reversible causes of cardiac arrest
• Consider the history of events in order to identify the likely cause of cardiac arrest
• To correct hypoxia, the focus should be on establishing/maintaining a patent airway and optimising oxygenation
• Complete a comprehensive secondary survey to identify sources of fluid loss in hypovolaemia
• In hypothermia, focus on steady rewarming and maintaining physiological supportive measures
• Consider electrolyte disturbance such as hypo/hyperkalaemia in all patients presenting with cardiac arrest
• If tension pneumothorax is suspected, complete a thoracostomy as soon as qualified staff are present and insert a chest drain at the earliest opportunity.
• Use bedside echocardiogram to identify cardiac tamponade
• Poisoning is rarely a cause of cardiac arrest related to toxins, consider the effects of prescribed or illicit drugs.
• If pulmonary embolism is suspected, consider continuing CPR for 60-90 minutes before terminating resuscitation attempts following the use of thrombolytic drugs.
• PPCI is the preferred reperfusion method when coronary thrombosis is suspected, prioritise PPCI within 120 minutes of ROSC if possible

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Reviewer

Craig Prentice

Lead ACP

Surrey and Sussex Healthcare NHS Trust

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Editor

Dr Chris Jefferies

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References

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