You may have heard about the H's and T's of cardiac arrest. Maybe yes maybe no. In this article, we have made it simple and clear for you regarding the topic.

Many different traumatic and medical conditions can lead to cardiac arrest in both adults and children. This includes electrical abnormalities, inherited disorders and structural changes in the heart.

It is of great importance to determine and treat the cause of cardiac arrest. Fortunately, many causes of cardiac arrest are reversible. These conditions are often referred to by the mnemonic “H’s and T’s of cardiac arrest”.

The H’s and T’s of cardiac arrest is a mnemonic used to help recall the major contributing factors to pulseless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia.

H's and T's of Cardiac Arrest

Without taking much time lets start with the H"s

The H's


Hypovolemia basically refers to a lack of circulating body fluids, principally blood volume. This is usually caused by some form of bleeding, anaphylaxis, or pregnancy with a gravid uterus.

Severe burns can also lead to hypovolemia. Hypovolemia from blood loss is a leading cause of death in traumatic cardiac arrest. External blood loss is usually obvious (e.g., trauma, hematemesis, hemoptysis), but may be more challenging to diagnose when occult (e.g., gastrointestinal bleeding or rupture of an aortic aneurysm)

Peri-arrest treatment includes giving IV fluids preferably warmed crystalloids and blood transfusions, and controlling the source of any bleeding either by direct pressure for external bleeding, or emergency surgical techniques such as esophageal banding, gastroesophageal balloon tamponade, thoracotomy in cases of penetrating trauma or significant shear forces applied to the chest, or exploratory laparotomy in cases of penetrating trauma, spontaneous rupture of major blood vessels, or rupture of a hollow viscus in the abdomen.


Hypoxemia is low levels of circulating oxygen in the blood, which can lead to hypoxia at the tissues. A lack of oxygen delivery to the heart, brain, and other vital organs.

In most cases, hypoxemia is a consequence of asphyxia, which accounts for most of the non-cardiac causes of cardiac arrest. The conditions that can cause hypoxia are:

Rapid assessment of airway patency and respiratory effort must be performed. If the patient is mechanically ventilated, the presence of breath sounds and the proper placement of the endotracheal tube should be verified.

Treatment may include providing oxygen, proper ventilation, and good CPR technique. In cases of carbon monoxide poisoning or cyanide poisoning, hyperbaric oxygen may be employed after the patient is stabilized.

Hydrogen ions (acidosis)

When you hear of hydrogen ions you think of something to do with acids right? In this case, acidosis can be either metabolic or respiratory.

An abnormal pH in the body as a result of lactic acidosis which occurs in prolonged hypoxia and in severe infection, diabetic ketoacidosis, renal failure causing uremia, or ingestion of toxic agents or overdose of pharmacological agents, such as aspirin and other salicylates, ethanol, ethylene glycol, and other alcohols, tricyclic antidepressants, isoniazid, or iron sulfate.

Acidosis of any kind is most likely detrimental to the circulation as it causes peripheral vasodilatation, negative inotropy and impaired oxygen uptake in the lungs.

An arterial blood gas is a quick and accurate method to determine if a patient is acidotic.

This can be treated with proper ventilation, good CPR technique, buffers like sodium bicarbonate, and in select cases may require emergent hemodialysis.

Hyperkalemia or hypokalemia

Both excess and inadequate potassium can be life-threatening.

Electrolyte abnormalities can cause cardiac arrhythmias or cardiac arrest, and life-threatening arrhythmias are associated most commonly with potassium disorders, particularly hyperkalemia. Potassium is an electrolyte that plays a role in maintaining the normal contraction of the myocardium. If levels become too high or too low, cardiac arrest may ensue.

Evaluation of serum potassium must take into consideration the effects of changes in serum pH. When serum pH decreases (acidemia), serum potassium increases because potassium shifts from the cellular to the vascular space; the process that is reversed when serum pH increases (alkalemia).

Causes of hypokalemia include excessive vomiting/diarrhea or the use of diuretics. Chronic kidney disease can also lead to potassium loss.

Treatment may include a controlled but rapid infusion of potassium. Hyperkalemia may be caused by kidney disease, diabetes and as a side effect of certain drugs.

Hyperkalemia can be treated by administering sodium bicarbonate or calcium chloride or by performing dialysis.


Hyperkalemia is the most common electrolyte disorder associated with cardiac arrest. It is usually caused by impaired excretion by the kidneys, drugs or increased potassium release from cells and metabolic acidosis with hyperkalemia occurring in up to 10% of hospitalized patients.

There is no steadfast numeric limit universally used to define hyperkalemia, but 5.5 mmol-1 is commonly recognized. As the potassium concentration increases above this value the risk of adverse events increases and the need for urgent treatment increases.

The main causes of hyperkalemia are:

  • Renal failure (i.e., acute kidney injury or chronic kidney disease)
  • Drugs (e.g., angiotensin-converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists (ARB), potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, beta-blockers, trimethoprim)
  • Tissue breakdown (e.g., rhabdomyolysis, tumor lysis, hemolysis)
  • Metabolic acidosis (e.g., renal failure, diabetic ketoacidosis)
  • Endocrine disorders (e.g., Addison’s disease)
  • Diet (may be the sole cause in patients with advanced chronic kidney disease)

The treatment for hyperkalemia involves five key strategies:

  1. Cardiac protection
  2. Shifting potassium into cells
  3. Removing potassium from the body
  4. Monitoring serum potassium and blood glucose
  5. Prevention of recurrence


Hypokalemia is defined as a serum potassium level <3.5 mmol-1 and severe hypokalemia is serum potassium <2.5 mmol-1. Hypokalemia is the most common electrolyte disturbance seen in up to 20% of hospitalized patients. It increases the incidence of arrhythmias and sudden cardiac death.

The main causes of hypokalemia include:

  • Gastrointestinal loss (e.g., diarrhea)
  • Drugs (e.g., diuretics, laxatives, steroids)
  • Renal losses (e.g., renal tubular disorders, diabetes insipidus, dialysis)
  • Endocrine disorders (e.g., Cushing’s syndrome, hyperaldosteronism)
  • Metabolic alkalosis
  • Magnesium depletion
  • Poor dietary intake

Treatment of hypokalemia depends on the severity and the presence of symptoms and ECG abnormalities.

The best course of action is the gradual replacement of potassium to normal serum levels. In an emergency, intravenous potassium is warranted, with the knowledge that many patients who are hypokalemic are also hypomagnesemia.

Repletion of magnesium stores will facilitate more rapid correction of hypokalemia and is recommended in severe cases of hypokalemia

A common presentation of hyperkalemia is in the patient with end-stage renal disease who has missed a dialysis appointment and presents with weakness, nausea, and broad QRS complexes on the electrocardiogram.


A low core body temperature defined clinically as a temperature of fewer than 35 degrees Celsius (95 degrees Fahrenheit).

The patient is re-warmed either by using a cardiac bypass or by irrigation of the body cavities (such as thorax, peritoneum, bladder) with warm fluids; or warmed IV fluids. CPR only is given until the core body temperature reached 30 degrees Celsius, as defibrillation is ineffective at lower temperatures.

Patients have been known to be successfully resuscitated after periods of hours in hypothermia and cardiac arrest.


There is an unclear association between hypoglycemia and sudden cardiac death. In the NICE-SUGAR trial, moderate and severe hypoglycemia were both associated with increased mortality. However, the administration of dextrose is also associated with worse outcomes.

Hypoglycemia was removed from the H's and T's of cardiac arrest by the American Heart Association in their 2010 ACLS update.

In the H's and T's of Cardiac Arrest, T follows H! Let's move on to the T's

Tablets or toxins

Early tracheal intubation of unconscious patients by trained personnel may decrease the risk of aspiration. Drug-induced hypotension usually responds to IV fluids, but occasionally vasopressor support (e.g., noradrenaline infusion) is required.

Some of the most common drugs involved in an overdose are benzodiazepines, opioids, tricyclic antidepressants, local anesthetics, beta-blockers, and calcium channel blockers.

Benzodiazepines: Overdose of benzodiazepines can cause loss of consciousness, respiratory depression, and hypotension. The drug of choice for the treatment of benzodiazepine overdose is Flumazenil which is a competitive antagonist of benzodiazepines and can be used when the patient does not have a history of risk of seizures.

Opioids: Excess opioid consumption via any route can lead to respiratory depression, respiratory insufficiency, and/or respiratory arrest. The opiate antagonist naloxone can reverse the respiratory effects of an opioid overdose. The preferred route for giving naloxone depends on the skills of the rescuer: intravenous (IV), intramuscular (IM), subcutaneous (SC), intraosseous (IO) and intranasal (IN) routes are all suitable. The initial doses of naloxone are 0.4–2 mg IV, IO, IM or SC, and may be repeated every 2–3 minutes.

Additional doses may be needed every 20–60 minutes. Intranasal dosing is 2 mg IN (1 mg in each nostril), which may be repeated every 5 minutes. Titrate the dose until the victim is breathing adequately and has protective airway reflexes.

Tricyclic antidepressants: Self-poisoning with tricyclic antidepressants is common and can cause hypotension, seizures, coma and life-threatening arrhythmias. Cardiac toxicity mediated by anticholinergic and Na+channel-blocking effects can produce a wide complex tachycardia (VT).

Give sodium bicarbonate (1–2 mmol kg-1) for the treatment of tricyclic-induced ventricular arrhythmias.

Local anesthetics: Local anesthetic systemic toxicity (LAST) is a serious but rare consequence of regional anesthesia and most commonly results from an inadvertent vascular injection or absorption of large amounts of drug from certain nerve blocks requiring large volume injections.

Severe agitation, loss of consciousness, seizures, bradycardia, asystole or ventricular tachyarrhythmias can all occur. When LAST is suspected, benzodiazepines are the drug of choice because they are an anticonvulsant without causing significant cardiac depression.

Although there are many case reports and case series of patients who were resuscitated after the administration of IV lipid emulsion, evidence for its benefit in treating local anesthetic-induced cardiac arrest is limited.

Despite the paucity of data, patients with both cardiovascular collapse and cardiac arrest attributable to local anesthetic toxicity may benefit from treatment with intravenous 20% lipid emulsion in addition to standard ACLS.

Beta-blockers: Beta-blocker toxicity causes bradyarrhythmias and negative inotropic effects that are difficult to treat and can lead to cardiac arrest. Improvement has been reported with glucagon (50–150 mcg kg−1), high-dose insulin and glucose, lipid emulsions, phosphodiesterase inhibitors, extracorporeal and intra-aortic balloon pump support, and calcium salts.

Calcium channel blockers: Calcium channel blocker overdose is emerging as a common cause of prescription drug poisoning deaths. Overdose of short-acting drugs can rapidly progress to cardiac arrest and overdose by sustained-release formulations can result in delayed onset of arrhythmias, shock, and sudden cardiac collapse.

Treatment can include the administration of calcium chloride 10% in boluses of 20 ml (or equivalent dose of calcium gluconate) every 2-5 minutes in severe bradycardia or hypotension followed by an infusion.

Toxins may be evidenced by items found on or around the patient, the patient's medical history (i.e. drug abuse, medication) taken from family and friends, checking the medical records to make sure no interacting drugs were prescribed or sending blood and urine samples to the toxicology lab for the report.

Herbal supplements and over-the-counter medications should also be considered narcotics.

Cardiac tamponade

Blood or other fluids building up in the pericardium can put pressure on the heart so that it is not able to beat. This condition can be recognized by the presence of narrowing pulse pressure, muffled heart sounds, distended neck veins,(Becks triad), electrical alternans on the electrocardiogram, or by visualization on echocardiogram.

Beck triad is a collection of three clinical signs associated with pericardial tamponade which is due to an excessive accumulation of fluid within the pericardial sac. The three signs are:

low blood pressure (weak pulse or narrow pulse pressure); muffled heart sounds, raised jugular venous pressure

This is treated in an emergency by inserting a needle into the pericardium to drain the fluid (pericardiocentesis), or if the fluid is too thick then a subxiphoid window is performed to cut the pericardium and release the fluid.

Tension pneumothorax.

The build-up of air into one of the pleural cavities, which causes a mediastinal shift. When this happens, the great vessels (particularly the superior vena cava) become kinked, which limits blood return to the heart.

A tension pneumothorax develops when there is a buildup of air in the pleural space.

Diagnosis of tension pneumothorax in a patient with cardiac arrest or hemodynamic instability must be based on clinical examination.

The symptoms include hemodynamic compromise (hypotension or cardiac arrest) in conjunction with signs suggestive of a pneumothorax (preceding respiratory distress, hypoxia, absent unilateral breath sounds on auscultation, subcutaneous emphysema) and mediastinal shift (tracheal deviation and jugular venous distention)

The tracheal shift often requires a chest x-ray to appreciate

This is relieved by a needle thoracotomy (inserting a needle catheter) into the 2nd intercostal space at the mid-clavicular line, which relieves the pressure in the pleural cavity.

Thrombosis (myocardial infarction)

Coronary heart disease is the most frequent cause of out-of-hospital cardiac arrest. Although a proper diagnosis of the cause may be difficult in a patient already in cardiac arrest, if the initial rhythm is VF it is most likely that the cause is coronary artery disease with an occluded large coronary vessel.

Treatment options include immediate coronary angiography, primary percutaneous coronary intervention (PPCI) or other interventions such as (more rarely) pulmonary embolectomy.

Ongoing CPR and immediate access to the catheterization laboratory may be considered if a prehospital and in-hospital infrastructure is available with teams experienced in mechanical or hemodynamic support and rescue PPCI with ongoing CPR

If the patient can be successfully resuscitated, there is a chance that the myocardial infarction can be treated, either with thrombolytic therapy or percutaneous coronary intervention.

Thromboembolism (pulmonary embolism)

Cardiac arrest resulting from acute pulmonary embolism is the most serious clinical presentation of venous thromboembolism. In most cases originating from a deep venous thrombosis (DVT). Hemodynamically significant pulmonary emboli are generally massive and typically fatal.

Common symptoms preceding cardiac arrest are sudden onset of dyspnea, pleuritic or substernal chest pain, cough, hemoptysis, syncope, and signs of DVT (e.g., unilateral, low extremity swelling). However, pulmonary embolism may not be symptomatic until it presents as sudden cardiac arrest

Administration of thrombolytics can be attempted, and some specialized centers may perform thrombectomy, however, the prognosis is generally poor.


Cardiac arrest can also occur after a hard blow to the chest at a precise moment in the cardiac cycle, which is known as commotio cordis. Other traumatic events such as high speed car crashes can cause sufficient structural damage to induce arrest.

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