Sudden Cardiac Arrest and the Hs and Ts
Sudden cardiac arrest and sudden cardiac death can happen in every healthcare setting. Sudden cardiac arrest is a major healthcare problem in the United States that accounts for up to 350,000 deaths per year.27 Irrespective of the cause of cardiac arrest, early recognition and calling for help, including appropriate management of the deteriorating patient, early defibrillation, high-quality cardiopulmonary resuscitation (CPR) with minimal interruption of chest compressions and treatment of reversible causes, are the most important interventions.25
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. Determining and treating the cause of cardiac arrest is critical to improving patient outcomes. Fortunately, many causes of cardiac arrest are reversible, including the conditions listed below. These conditions are often referred to by the mnemonic “Hs and Ts”:
Cardiac arrest caused by pure hypoxemia is uncommon. Hypoxemia is low levels of circulating oxygen in the blood, which can lead to hypoxia at the tissues. Hypoxemia is normally a consequence of asphyxia, which accounts for most of the non-cardiac causes of cardiac arrest.25 The following is a list of some of the causes of hypoxemia according to Truhlar:
- Airway obstruction: soft tissues (coma), laryngospasm, aspiration
- Avalanche burial
- Central hypoventilation – brain or spinal cord injury
- Chronic obstructive pulmonary disease
- High altitude
- Impaired alveolar ventilation from neuromuscular disease
- Tension pneumothorax
- Traumatic asphyxia or compression asphyxia (e.g. crowd crush)
Treating the cause of hypoxia/hypoxemia must be done quickly because this is one of the potentially reversible causes of cardiac arrest. Proper oxygenation and ventilation are key to restoring adequate amounts of oxygen into the system and negating the lethal cardiac rhythm.
One common cause of cardiac arrest is hypovolemia, which can develop due to a reduced intravascular volume (i.e. hemorrhage). It can occur as a result of extreme sweating, severe diarrhea and/or vomiting, and even severe vasodilation. 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).25 Treatment of hypovolemia includes rapid infusion of preferably warmed crystalloids and/or blood products while treating the original cause of the hypovolemia.
Every year approximately 1,500 people die of primary accidental hypothermia in the United States.6 Accidental hypothermia is defined as an involuntary drop of the core body temperature <35 degrees Celsius.25 Hypothermia can be estimated and further subdivided by using the Swiss staging system.18
- Hypothermia I – mild hypothermia (conscious, shivering, core temperature 32–35◦C)
- Hypothermia II – moderate hypothermia (impaired consciousness without shivering, core temperature 28–32◦C)
- Hypothermia III – severe hypothermia (unconscious, vital signs present, core temperature 24–28◦C)
- Hypothermia IV – cardiac arrest or low flow state (no or minimal vital signs, core temperature <24◦C)
- Hypothermia V – death due to irreversible hypothermia (core temperature <13.7◦C)
The risk of hypothermia is increased by alcohol or drug ingestion, exhaustion, illness, injury or neglect especially when there is a decrease in the level of consciousness.25 As core temperature decreases, sinus bradycardia tends to give way to atrial fibrillation followed by VF and finally asystole.16 Arrhythmias other than VF tend to revert spontaneously as core temperature increases, and usually do not require immediate treatment.25 Unless the patient goes into VF, rewarm using active external methods (e.g., forced warm air) and minimally invasive methods (e.g., warm IV infusions).25
Electrolyte abnormalities can cause cardiac arrhythmias or cardiac arrest, and life-threatening arrhythmias are associated most commonly with potassium disorders, particularly hyperkalemia.25 Potassium is an electrolyte that plays a role in maintaining normal contraction of the myocardium. If levels become too high or too low, cardiac arrest may ensue. The precise values that trigger treatment decisions will depend on the patient’s clinical condition and rate of change of electrolyte values.25 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.8 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.25 The main causes of hyperkalemia are:1
- 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:26
- Cardiac protection
- Shifting potassium into cells
- Removing potassium from the body
- Monitoring serum potassium and blood glucose
- Prevention of recurrence
Hypokalemia is the most common electrolyte disturbance in clinical practice.9 It is seen in up to 20% of hospitalized patients.17 Hypokalemia increases the incidence of arrhythmias and sudden cardiac death.13 Hypokalemia is defined as a serum potassium level <3.5 mmol-1 and severe hypokalemia is a serum potassium <2.5 mmol-1 25. The main causes of hypokalemia include:25
- 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 hypomagnesimic. Repletion of magnesium stores will facilitate more rapid correction of hypokalemia and is recommended in severe cases of hypokalemia.7
Hydrogen Ion (Acidosis):
Acidosis can be either metabolic or respiratory. Either cause can lead to cardiac arrest. 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.22 Although severe acidemia frequently occurs in patients during and after cardiac arrest, the prognostic value of severe acidemia for neurologic outcomes is unknown.23 An arterial blood gas is a quick and accurate method to determine if a patient is acidotic. If a patient has respiratory acidosis, they can be treated by providing adequate ventilation. Metabolic acidosis is one of the most common abnormalities in patients suffering from serious diseases, and there have been numerous etiologies and treatments of the underlying disease as the basis of therapy.21 A common intervention to treat metabolic acidosis may be by the administration of sodium bicarbonate.
Tension pneumothorax is defined as hemodynamic compromise in a patient with an expanding intrapleural air mass. It is a treatable cause of cardiac arrest and should be excluded during CPR.3 A tension pneumothorax develops when there is a buildup of air in the pleural space. The buildup causes a shift in the mediastinum and venous return to the heart is obstructed, which can lead to cardiac arrest. Tension pneumothorax can occur in a variety of clinical situations including trauma, asthma, and other respiratory diseases, but can also be iatrogenic following invasive procedures (e.g., attempts at central venous catheter insertion).25 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).19 Treatment of a tension pneumothorax is either needle compression and/or thoracostomy with chest tube placement.
Cardiac tamponade occurs when the pericardial sac is filled with fluid under pressure, which leads to compromise of cardiac function and ultimately cardiac arrest.25 It may be caused by trauma to the chest such as a gunshot wound or by inflammation of the pericardium. Thoracotomy or pericardiocentesis is used to treat cardiac arrest associated with suspected traumatic or non-traumatic cardiac tamponade. The use of ultrasound guidance during pericardiocentesis is preferred, if available.
Airway obstruction and respiratory arrest secondary to a decreased conscious level is a common cause of death after self-poisoning (benzodiazepines, alcohol, opiates, tricyclics, barbiturates).24 Early tracheal intubation of unconscious patients by trained personnel may decrease the risk of aspiration.25 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.
Overdose of benzodiazepines can cause loss of consciousness, respiratory depression, and hypotension.25 The drug of choice for the treatment of benzodiazepine overdose is Flumazenil. Flumazenil is a competitive antagonist of benzodiazepines and can be used when the patient does not have a history of risk of seizures.
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.20 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.25
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).25 Give sodium bicarbonate (1–2 mmol kg-1) for the treatment of tricyclic-induced ventricular arrhythmias.4
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.15 Severe agitation, loss of consciousness, seizures, bradycardia, asystole or ventricular tachyarrhythmias can all occur.25 When LAST is suspected, benzodiazepines are the drug of choice because they are an anticonvulsant without causing significant cardiac depression.15 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.2
Beta-blocker toxicity causes bradyarrhythmias and negative inotropic effects that are difficult to treat and can lead to cardiac arrest.25 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.10
Calcium channel blockers:
Calcium channel blocker overdose is emerging as a common cause of prescription drug poisoning deaths.5 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.25 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 as needed.11
Cardiac arrest from acute pulmonary embolism is the most serious clinical presentation of venous thromboembolism, in most cases originating from a deep venous thrombosis (DVT).14 The 2014 European Society of Cardiology Guidelines on the diagnosis and management of acute pulmonary embolism define “confirmed pulmonary embolism” as a probability of pulmonary embolism high enough to indicate the need for specific treatment.14 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.12 Specific treatments for cardiac arrest resulting from pulmonary embolism include administration of fibrinolytics, surgical embolectomy and percutaneous mechanical thrombectomy.25
Coronary heart disease is the most frequent cause of out-of-hospital cardiac arrest. Although 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.25 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.25
Being able to think through the reversible causes of sudden cardiac arrest will give your patient the best chance of survival as the appropriate diagnosis is made and interventions initiated.
- Asirvatham JR, Moses V, Bjornson L. Errors in potassium measurement: a lab-oratory perspective for the clinician. North American Journal of Medical Sciences. 2013;5:255-259.
- Association of Anaesthetists of Great Britain and Ireland. Management of Severe Local Anaesthetic Toxicity. 2010.
- Barton ED. Tension pneumothorax. Current Opinion in Pulmonary Medicine. 1999;5;269-274.
- Bradberry SM, Thanacoody HK, Watt BE, Thomas SH, Vale JA. Management of the cardiovascular complications of tricyclic antidepressant poisoning: role of sodium bicarbonate. Toxicology Review. 2005;24;195-204.
- Bronstein AC, Spyker DA, Cantilena LR Jr., Green JL, Rumack BH, Giffin SL. 2008 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th annual report. Clinical Toxicology. 2009;47:911-1084.
- Brown DJ, Brugger H, Boyd J, Paal P. Accidental hypothermia. New England Journal of Medicine. 2012;367:1930-1938.
- Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Archives of Internal Medicine. 2000;160:2429-2436.
- Einhorn LM, Zhan M, Hsu VD, et al. The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med. 2000;169:1156-1162.
- El-Sherif N, Turitto G. Electrolyte disorders and arrhythmogenesis. Cardiology Journal. 2011;18:233-245.
- Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clinical Toxicology. 2011;49:277–-83.
- Gunja N, Graudins A. Management of cardiac arrest following poisoning. Emergency Medicine of Australia. 2011;23:16-22.
- Heit JA, Silverstein MD, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ III. Risk factors for deep vein thrombosis and pulmonary embolism: a population-based case–control study. Archives of Internal Medicine. 2000;160:809-815.
- Kjeldsen K. Hypokalemia and sudden cardiac death. Experimental and Clinical Cardiology. 2010;15:e96-99.
- Konstantinides SV, Torbicki A, Agnelli G, et al. ESC guidelines on the diagnosis and management of acute pulmonary embolism. European Heart Journal. 2014;35:3033-69.
- Nagelhout JJ. Local Anesthetics. 6th Edition. Nurse Anesthesia. 2018:119-125. St. Louis: Elsevier.
- Paal P, Strapazzon G, Braun P, et al). Factors affecting survival from avalanche burial – a randomised prospective porcine pilot study. Resuscitation. 2013;84:239-243.
- Paice BJ, Paterson KR, Onyanga-Omara F, Donnelly T, Gray JM, Lawson DH. Record linkage study of hypokalemia in hospitalized patients. Postgraduate Medical Journal. 1986;162:187-191.
- Pasquier M, Zurron N, Weith B. Deep accidental hypothermia with core temperature below 24 degrees C presenting with vital signs. High Altitude Medical Biology. 2014;15:58-63.
- Roberts DJ, Leigh-Smith S, Faris PD, et al. Clinical presentation of patients with tension pneumothorax: a systematic review. Annals of Surgery. Jan 5, 2015. [Epub ahead of print].
- Robertson TM, Hendey GW, Stroh G, Shalit M. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehospital Emergency Care. 2009;13:512–515.
- Rubens de Nadai T, Nunes de Nadai M, Albuquerque A, Menezes de Carvalho M, Celotto AC, Evora PR. Metabolic acidosis treatment as part of a atrategy to curb inflammation. International Journal of Inflammation. 2013:1-4.
- Spindelboeck W, Gemes G, Strasser C, Toescher K, Kores B, Metnitz P, Haas J, Prause G. Arterial blood gases during and their dynamic changes after cardiopulmonary resuscitation: A prospective clinical study. Resuscitation. 2016;106:24-29.
- Tetsuhara K, Kato H, Kanemura T, Okada I, Kiriu N. Severe acidemia on arrival not predictive of neurologic outcomes in post–cardiac arrest patients. American Journal of Emergency Medicine. 2015;34:425-428.
- Thompson TM, Theobald J, Lu J, Erickson TB. The general approach to the poisoned patient. Disease a Month. 2014;60:509-524.
- Truhlar A, Deakin CD, Soar J, Khalifa GE, Alfonzo A, Bierens JJ, Brattebo G, Brugger H, Dunning J, Hunyadi-Anticevic S, Koster RW, Lockey DJ, Lott C, Paal P, Perkins GD, Sandroni C, Thies KC, Zideman DA, Nolan JP. European Resuscitation Council guidelines for resuscitation 2015. Resuscitation. 2015;95:148-201.
- UK Renal Association. Treatment of acute hyperkalemia in adults. Clinical practice guidelines. 2014; London: UK Renal Association.