The Reversible Causes of Cardiac Arrest

James Hobson   Published 18th February 2023

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The information on this page was accurate at the time of publication. Always consult current national and local guidelines. Content is for training purposes only.

Cardiac Arrest

Cardiac arrest is a sudden irregularity/loss of heart function, resulting in a loss of cardiac output. This requires resuscitation by following the Advanced Life Support Algorithm. You can learn more about resuscitation, including chest compressions, airway management, rhythm recognition and defibrillation in our Cardiac Arrest article.

While resuscitation is ongoing, the team should be considering the reversible causes of cardiac arrest. Reversible causes are those conditions that may be able to be corrected during the arrest to help achieve return of spontaneous circulation.

The Hs and Ts

The reversible causes of cardiac arrest can be broadly thought of as the Hs and Ts.

The Hs

Hypoxia

Hypovolaemia

Hypo/hyperkalaemia

Hypothermia

The Ts

Tension pneumothorax

Thrombus

Toxins

Tamponade

We'll go through each of these in this article.

Hypoxia

There is an inadequate supply of oxygen to the body tissues. This could be due to a problem picking up oxygen in the lungs (e.g. severe pneumonia), a problem transporting oxygen bound to haemoglobin (e.g. carbon monoxide poisoning) or an issue with offloading oxygen to the tissues (e.g. poor tissue perfusion).

Recognition

Signs of hypoxia:

  • Low oxygen saturation
  • Cyanosis of the skin or mucous membranes
  • Tachypnoea (prior to arrest)
  • Altered mental status (prior to arrest)
  • The patient may also have a history of respiratory disease or exposure to carbon monoxide

Treatment

  • Provide supplemental oxygen - 15L/min via non-rebreathe mask if breathing, or via bag-valve mask/ventilator
  • Identifying and treat the underlying cause
    • Intubation and mechanical ventilation if required
    • Pneumonia - sepsis screen and IV antibiotics
    • CO poisoning - secure airway and give 100% high-flow oxygen

Hypovolaemia

There is a loss of blood volume, which leads to a decrease in cardiac output and blood pressure. Hypovolaemia can result from problems like bleeding (e.g. from ruptured AAA or GI bleed), severe dehydration, burns and diarrhea or vomiting. Pay particular attention to those on blood thinning medications or with bleeding disorders.

Recognition

Signs of hypovolaemia:

  • Low blood pressure
  • Tachycardia (prior to arrest)
  • Decreased urine ouput (prior to arrest)
  • Signs of dehydration like dry mucous membranes or decreased skin turgor
  • Active bleeding
  • The patient may also have a history of recent blood loss, vomiting, or diarrhoea

Treatment

Treatment depends on the underlying cause.

  • For all causes - fluid resuscitation with IV crystalloid to restore circulating volume
  • For refractory hypovolaemia after 2000ml of fluids have been given, begin giving blood products
  • For haemorrhage - give blood products (packed red cells) from the start, instead of fluids
  • Other blood products (e.g. platelets, cryoprecipitate and fresh frozen plasma) may be needed to help stop bleeding and replace other blood components
  • Antifibrinolytic agents (e.g. tranexamic acid) can be given to help stabilise blood clotting
  • Vasopressors and inotropes can be given to help increase the blood pressure (by inducing vasoconstriction and increasing the force of contraction of the heart)

Hypo/Hyperkalaemia

Potassium is an important electrolyte responsible for maintaining the resting membrane potential of excitable cells, including cardiac muscle. Abnormal levels of potassium can cause reduced or increased cardiac muscle excitability, by changing the resting membrane potential baseline. This results in cardiac arrhythmias and, in severe cases, cardiac arrest. Untreated potassium derangement commonly results in ventricular fibrillation, a shockable rhythm.

  • Hypokalaemia - K+ less than 3.5 mEq/L (symptoms usually arise below 3.0 or if the change is rapid)
  • Hyperkalaemia - K+ greater than 5 mEq/L (symptoms usually arise above 7.0 or if the change is rapid)

Recognition

Signs of potassium derangement:

  • ECG changes (see below)
  • Muscle weakness or paralysis
  • Decreased deep tendon reflexes
  • Nausea and vomiting
  • The patient may also have a history of kidney disease, certain medications, or nutritional deficiencies

Hyperkalaemia raises the resting membrane potential closer to the action potential threshold, and therefore initially increases tissue excitability. However the persistent depolarisation inactivates voltage-gated sodium channels, which leads to a reduction in total membrane excitability. Hence both hyper- and hypo- kalaemia exhibit signs of reduced excitability.

Treatment

Treat the underlying cause - e.g. vomiting, diarrhoea, review medications (such as diuretics, beta-2 agonists, laxatives etc)

Hypokalaemia

  • Potassium repletion with IV fluids containing pre-added KCl
  • Do not exceed 10–20 mEq/hour via peripheral vein, as potassium is highly irritant
  • Higher doses (up to 40 mEq/hour) can be administered through a central venous catheter
  • The patient should be placed on continuous cardiac monitoring during potassium replacement therapy


Hyperkalaemia

  • Stabilise the cardiac membrane with IV calcium gluconate (30ml of 10% solution)
    • Ensure the patient is on continuous cardiac monitoring, the ECG should begin to improve by 5 minutes
  • Short-acting insulin with dextrose (IV 10 units of Actrapid in 50mls of 50% dextrose over 15 mins)
    • Insulin shifts potassium intracellularly to lower serum K+. It is given with glucose/dextrose to prevent hypoglycaemia
  • Consider inhaled SABAs as an adjunct to insulin therapy to help drive K+ into cells (unlicensed use)
  • Consider haemodialysis as a definitive treatment in refractory hyperkalaemia

ECG changes in hypo/hyperkalaemia

Take a look at these ECGs and try describing them, which one is hyperkalaemia and which is hypokalaemia?

Click the dropdowns below to reveal the answers

Example ECG

12-lead ECG

  • Heart rate: ∼ 50/min (bradycardia)
  • Regular
  • Sinus rhythm
  • Normal cardiac axis
  • Normal PR interval (~ 0.16s)
  • Narrow QRS complexes (normal 80-100ms)
  • Tall, peaked T waves (normal height is less than 5mm in limb leads and less than 10mm in precordial leads)
  • No conduction blocks

Bradycardia and tall symmetrically peaked T waves are suggestive of hyperkalemia.

ECGs in hyperkalaemia can also show:

  • Broad/flattened P waves - lengthened PR interval (normal 0.12 to 0.20 secs)
  • Widened QRS complexes with unusual morphology
  • Conduction blocks (e.g. bundle branch blocks)
  • Development of sine wave appearance (see below)
    • Widened QRS complexes and peaked T waves fuse to create a sine wave pattern
    • The sine wave appearance is a "pre-terminal" rhythm, suggestive of impending VF or asystole

Hyperkalaemia ECG showing a sine wave morphology
Sine wave morphology in severe hyperkalaemia

Example ECG

12-lead ECG

  • Heart rate: ∼ 68/min
  • Regular
  • Sinus rhythm
  • Normal cardiac axis
  • PR interval ~ 0.20s (upper boundary of normal)
  • Narrow QRS complexes (~ 60ms)
  • ST depression in leads II, aVF and V3-V6
  • T wave inversion in leads II, III, aVF and V2-V6, all other leads have flattened T waves
  • Prominent U waves in leads II, III, aVF and V2-V6
  • No conduction blocks

Lengthened PR interval, narrow QRS, ST depression, T wave flattening/inversion and U waves are all suggestive of hypokalemia.

Hypothermia

Hypothermia is classified as when body temperature falls below 35°C, which can lead to arrhythmias (such as AF and VF) and heart blocks. Primary hypothermia occurs in individuals exposed to cold environments, especially in the elderly, infants and the homeless.

Secondary hypothermia occurs as a result of a condition affecting temperature regulation - examples include burns, surgery, sepsis, hypothyroidism, strokes, substance misuse.

Recognition

Signs of hypothermia:

  • Low core temperature (below 35°C)
  • Bradycardia (initially tachycardic)
  • Bradypnoea (initially bradycardic)
  • Altered mental status
  • Shivering (typically stops as hypothermia gets worse)
  • Rigidity (pseudo-rigor mortis)
  • History of cold exposure

Treatment

The treatment for hypothermia is core rewarming.

  • Remove wet clothing and ensure the room is warm
  • Apply continuous core temperature monitoring - oesophageal (best option), rectal or bladder
  • External rewarming - warm blankets or Bair Hugger™
  • Internal rewarming - warmed IV fluids, warm thoracic/peritoneal cavity lavage, warm air ventilation
  • Extra-corporeal rewarming - warm the blood with haemodialysis or Extra-Corporeal Membrane Oxygenation (ECMO)

Tension pneumothorax

A tension pneumothorax is a life-threatening progressive accumulation of air in the pleural space. Pressure builds up in the thorax and can compress the heart and great vessels.

A one-way valve mechanism develops in the visceral (as shown below) or parietal pleura. Air can enter the pleural space on inspiration, but not exit. The pressure in the chest gets progressively higher. This causes collapse of the ipsilateral lung, and compression of the contralateral lung, trachea, heart and superior vena cava. The inferior vena cava becomes angulated.

Respiratory function decreases and venous return to the heart is reduced. Cardiac output falls.


Pathogenesis of tension pneumothorax
Pathogenesis of tension pneumothorax


Recognition

Signs of tension pneumothorax:

  • Low blood pressure
  • Tachycardia
  • Low oxygen saturation
  • Dyspnoea
  • Pleuritic chest pain
  • Asymmetrical chest expansion
  • Hyper-resonance to percussion
  • Reduced/absent breath sounds
  • Tracheal deviation away from affected side

Treatment

  • Give high-flow oxygen
  • Needle decompression - insert a wide-bore cannula into the pleural space through the second intercostal space (mid-clavicular line) or the fourth/fifth intercostal space (mid-axillary line)
  • After decompression - insert definitive chest drain

Thrombus

The formation of a clot, obstructing blood flow to/from the heart. There are two types we're concerned about:

  • Pulmonary embolism – pulmonary artery obstruction
    • Venous thromboembolism from DVT (surgery, immobilisation, long haul travel)
    • Fat embolism (long bone fractures)
    • Air embolism (IV lines, penetrating trauma)
    • Amniotic fluid embolism (amniotic fluid and fetal debris enter maternal circulation – e.g. placental abruption)
  • Acute coronary syndrome – coronary artery obstruction
    • Atherosclerosis (plaque rupture)
    • Coronary ulceration/fissure/dissection (results in thrombus)
    • Infectious embolism (Infective Endocarditis)

Recognition

Pulmonary

  • Dyspnoea
  • Tachycardia, hypotension, tachypnoea
  • Pleuritic chest pain
  • Haemoptysis
  • Low O2 saturations
  • Drop in end-tidal CO2

Coronary

  • Typically central crushing chest pain radiating to left arm/jaw (but may be atypical - e.g. epigastric pain, back pain, sharp pain, no pain)
  • Tachycardia
  • Syncope
  • ECG and troponin findings
  • Consider if in VF/VT - coronary occlusion is the most common cause

Treatment

The treatment for thrombosis involves restoring blood flow to the affected area.

Pulmonary

  • IV fluids (if hypotensive) and high-flow oxygen
  • Thrombolysis with alteplase (tPA)
  • Embolectomy – if thrombolysis is contraindicated (intracranial haemorrhage, stroke, recent surgery) or unsuccessful
  • Consider ECMO

Coronary

  • IV fluids (if hypotensive) and high-flow oxygen
  • Dual anti-platelet therapy (aspirin + antiplatelet agent - e.g. prasugrel or clopidogrel)
  • Emergency PCI (can be done with CPR ongoing) or thrombolysis if PCI unavailable (alteplase)
  • Consider ECMO

Toxins

There are a variety of toxic substances that can induce cardiac arrest, so there are no specific tests or clinical features. Consider depending on:

  • Items found with the patient – blister packs, needles etc
  • The patient's medical history (e.g. drug abuse history, current medications)
  • Medication that could taken from family and friends
  • Were any interacting drugs prescribed? (Look at the drug chart)
  • Herbal supplements or OTC medications
  • Send blood and urine samples to toxicology

Recognition

You may see signs such as:

  • Bradycardia
  • Reduced GCS
  • Dilated or constricted pupils
  • Seizures
  • Flaccid paralysis
  • Vomiting
  • ECG changes

Treatment

Early tracheal intubation of unconscious patients decreases the risk of aspiration.

Hypotension may respond to IV fluids and vasopressor support (e.g., noradrenaline infusion) if required. Correct hypoxia, acidosis, electrolyte abnormalities and hypo/hyperthermia.

Definitive management depends on the toxin (often unknown toxin and dose), but most don’t have an antidote.

  • Activated charcoal can reduce GI absorption and increase elimination of many poisons. Effective up to 1 hour post ingestion
  • Opioid toxicity – naloxone
  • Sodium channel blocker – sodium bicarbonate infusion
  • Benzodiazepines – flumazenil
  • Amphetamines – benzodiazepines
  • Digoxin - digoxin-specific antibody

Continue with the standard ACLS protocol if toxin is unknown.

Tamponade

This is a condition where there is an accumulation of fluid or blood in the pericardial sac, leading to compression of the heart (especially the thinner-walled right ventricle), venous congestion and a decrease in cardiac output.

Causes include aortic dissection, cardiac wall rupture, pericarditis, cardiac surgery, malignancy and chest trauma.

Recognition

Signs of tamponade may include:

  • Tachycardia
  • Hypotension
  • Muffled heart sounds
  • Distended neck veins
  • The patient may also have difficulty breathing, chest pain and dysphagia

Beck's triad

Beck's triad for cardiac tamponade is:

  • Hypotension
  • Distant heart sounds
  • Distended neck veins

Treatment

Treatment for tamponade involves draining the fluid from the pericardial sac.

Small effusions can be medically managed with NSAIDs or colchicine. When a pericardial effusion causes tamponade, surgical intervention is required:

  • Surgical drainage – pericardiotomy
    • Preferred in haemopericardium, trauma, purulent effusion or neoplastic disease
    • Where there is potential for complications or immediate reaccumulation
    • For example, where tamponade is caused by ventricular rupture or aortic dissection the pericardial sac will fill faster than it can be drained by pericardiocentesis
  • Needle aspiration - pericardiocentesis
    • Preferred when there is no haemorrhage, trauma, neoplasm or purulence OR as emergency management in cardiac arrest/peri-arrest
    • Perform under guidance of ultrasound or fluoroscopy
    • If no imaging is immediately available, it is possible to go in blind using anatomical landmarks only

Be cautious with fluid resuscitation - excessive fluids will exacerbate tamponade.

Avoid anaesthesia or positive pressure ventilation - both decrease venous return and can lead to massive hypotension.

Additional causes

In addition to the reversible causes of cardiac arrest, there are many other potential causes. Some of these include:

  1. Arrhythmias - abnormal heart rhythms such as SVT, AF or heart blocks which can progress to a cardiac arrest rhythm
  2. Trauma - a blow to the chest can lead to cardiac arrest without causing hypovolaemia/tension pneumothorax/tamponade or any cardiac damage - known as commotio cordis
  3. Other electrolyte abnormalities - such as hypoglycaemia, hyper/hypomagnesaemia, hyper/hypocaalcaemia
  4. Neurological - neurological insults can lead to cardiac arrest, such as subarachnoid haemorrhage, intracranial haemorrhage, ischaemic stroke or seizures
  5. Electric shock - exposure to a high-voltage shock can disrupt the heart's electrical activity
  6. Hypertrophic cardiomyopathy - a genetic condition in which the heart muscle becomes abnormally thick, leading to increased risk of arrhythmias and sudden cardiac arrest
  7. Congenital heart defects - some individuals may be born with structural abnormalities in the heart that increase the risk of cardiac arrest