Sudden Cardiac Arrest and the H’s and T’s
Sudden cardiac arrest and sudden cardiac death can happen in every health care setting. Sudden cardiac arrest is a major health care problem in the United States that accounts for up to 350,000 deaths per year27. 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 interventions25.
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 “H’s and T’s”:
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 arrest25. 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 States6. Accidental hypothermia is defined as an involuntary drop of the core body temperature <35 degrees Celcius25. Hypothermia can be estimated and further subdivided by using the Swiss staging system18:
- 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 consciousness25. As core temperature decreases, sinus bradycardia tends to give way to atrial fibrillation followed by VF and finally asystole16. Arrhythmias other than VF tend to revert spontaneously as core temperature increases, and usually do not require immediate treatment25. Unless the patient goes into VF, rewarm using active external methods (e.g., forced warm air) and minimally invasively 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 hyperkalemia25. Potassium is an electrolyte which 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 values25. 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 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: 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 patients8. 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 increases25. The main causes of hyperkalemia are1:
- 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 sole cause in patients with advanced chronic kidney disease)
The treatment for hyperkalemia involves five key strategies26:
- Cardiac protection
- Shifting potassium into cells
- Removing potassium from the body
- Monitoring serum potassium and blood glucose
- Prevention of recurrence
Hypokalemia: Hypokalemia is the most common electrolyte disturbance in clinical practice9. It is seen in up to 20% of hospitalized patients17. Hypokalemia increases the incidence of arrhythmias and sudden cardiac death13. 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 include25:
- 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 hypokalemia7.
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 lungs22. Although severe acidemia frequently occurs in patients during and after cardiac arrest, the prognostic value of severe acidemia for neurologic outcomes is unknown23. 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 therapy21. 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 CPR3. 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 disease, 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 arrest25. 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 aspiration25. 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 hypotension25. 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.
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 suitable20. 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 reflexes25.
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)25. Give sodium bicarbonate (1–2 mmol kg-1) for the treatment of tricyclic-induced ventricular arrhythmias4.
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 injections15. Severe agitation, loss of consciousness, seizures, bradycardia, asystole or ventricular tachyarrhythmias can all occur25. When LAST is suspected, benzodiazepines are the drug of choice because they are an anticonvulsant without causing significant cardiac depression15. Although there are many case reports and case series of patients who were resuscitated after 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 ACLS2.
Beta-blockers: Beta-blocker toxicity causes bradyarrhythmias and negative inotropic effects that are difficult to treat and can lead to cardiac arrest25. 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 salts10.
Calcium channel blockers: Calcium channel blocker overdose is emerging as a common cause of prescription drug poisoning deaths5. 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 collapse25. 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 needed11.
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 treatment14. 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 arrest12. Specific treatments for cardiac arrest resulting from pulmonary embolism include administration of fibrinolytics, surgical embolectomy and percutaneous mechanical thrombectomy25.
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 vessel25. 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 CPR25.
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, J.R., Moses, V., & Bjornson, L. (2013). Errors in potassium measurement: a lab-oratory perspective for the clinician. North American Journal of Medical Sciences, 5, 255–259.
- Association of Anaesthetists of Great Britain and Ireland. (2010). Management of Severe Local Anaesthetic Toxicity.
- Barton, E.D. (1999). Tension pneumothorax. Current Opinion in Pulmonary Medicine, 5, 269–274.
- Bradberry, S.M., Thanacoody, H.K., Watt, B.E., Thomas, S.H., & Vale, J.A. (2005). Management of the cardiovascular complications of tricyclic antidepressant poisoning: role of sodium bicarbonate. Toxicology Review, 24,195–204.
- Bronstein, A.C., Spyker, D.A., Cantilena, Jr. L.R., Green, J.L., Rumack, B.H., & Giffin, S.L. (2009). 2008 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 26th annual report. Clinical Toxicology, 47, 911–1084.
- Brown, D.J., Brugger, H., Boyd, J., & Paal, P. (2012). Accidental hypothermia. New England Journal of Medicine, 367, 1930-1938.
- Cohn, J.N., Kowey,. P.R., Whelton, P.K., & Prisant, L.M. (2000). New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Archives of Internal Medicine, 160, 2429–2436.
- Einhorn, L.M., Zhan, M., & Hsu, V.D., et al. (2009). The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med, 169, 1156–1162.
- El-Sherif, N., & Turitto, G. (2011). Electrolyte disorders and arrhythmogenesis. Cardiology Journal, 18, 233-245.
- Engebretsen, K.M., Kaczmarek, K.M., Morgan, J., & Holger, J.S. (2011) High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clinical Toxicology, 49, 277–283.
- Gunja, N., & Graudins, A. (2011). Management of cardiac arrest following poisoning. Emergency Medicine of Australia, 23, 16–22.
- Heit, J.A., Silverstein, M.D., Mohr, D.N., Petterson, T.M., O’Fallon, W.M., & Melton, III L.J. (2000). Risk factors for deep vein thrombosis and pulmonary embolism: a population-based case–control study. Archives of Internal Medicine, 160, 809–815.
- Kjeldsen, K. (2010). Hypokalemia and sudden cardiac death. Experimental and Clinical Cardiology, 15, e96–99.
- Konstantinides, S.V., Torbicki, A., Agnelli, G., et al. (2014) ESC guidelines on the diagnosis and management of acute pulmonary embolism. European Heart Journal, 35, 3033–69.
- Nagelhout, J.J. (2018). Local Anesthetics. 6th Edition. Nurse Anesthesia (pp. 119-125). St. Louis: Elsevier.
- Paal, P., Strapazzon, G., & Braun, P., et al. (2013). Factors affecting survival from avalanche burial – a randomised prospective porcine pilot study. Resuscitation, 84, 239–243.
- Paice, B.J., Paterson, K.R., Onyanga-Omara, F., Donnelly, T., Gray, J.M., & Lawson, D.H. (1986) Record linkage study of hypokalemia in hospitalized patients. Postgraduate Medical Journal, 162, 187–191.
- Pasquier, M., Zurron, N., & Weith, B., (2014). Deep accidental hypothermia with core temperature below 24 degrees C presenting with vital signs. High Altitude Medical Biology 15,58–63.
- Roberts, D.J., Leigh-Smith, S., Faris, P.D., et al. (2015). Clinical presentation of patients with tension pneumothorax: a systematic review. Annals of Surgery. Jan 5. [Epub ahead of print].
- Robertson, T.M., Hendey, G.W., Stroh, G., & Shalit, M. (2009). Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehospital Emergency Care, 13, 512–515.
- Rubens de Nadai, T., Nunes de Nadai, M., Albuquerque, A., Menezes de Carvalho, M., Celotto, A.C., & Evora, P.R. (2013). Metabolic Acidosis Treatment as Part of a Strategy to Curb Inflammation. International Journal of Inflammation, 1-4.
- Spindelboeck, W., Gemes, G., Strasser, C., Toescher, K., Kores, B., Metnitz, P., Haas, J., & Prause, G. (2016). Arterial blood gases during and their dynamic changes after cardiopulmonary resuscitation: A prospective clinical study. Resuscitation, 106, 24-29.
- Tetsuhara, K., Kato, H., Kanemura, T., Okada, I., & Kiriu, N. (2015). Severe acidemia on arrival not predictive of neurologic outcomes in post–cardiac arrest patients. American Journal of Emergency Medicine, 34, 425-428.
- Thompson, T.M., Theobald, J., Lu, J., & Erickson, T.B. (2014). The general approach to the poisoned patient. Disease a Month, 60, 509–524.
- Truhlar, A., Deakin, C.D., Soar, J., Khalifa, G.E., Alfonzo, A., Bierens, J.J., Brattebo, G., Brugger, H., Dunning, J., Hunyadi-Anticevic, S., Koster, R.W., Lockey, D.J., Lott, C., Paal, P., Perkins, G.D., Sandroni, C., Thies, K.C., Zideman, D.A., & Nolan, J.P. (2015). European Resuscitation Council guidelines for resuscitation 2015. Resuscitation, 95, 148-201.
- UK Renal Association. (2014). Treatment of acute hyperkalemia in adults. Clinical practice guidelines. London: UK Renal Association.
- Al-Khatib, S., Fonarow, G.C., Hayes, D.L., Curtis, A.B., Sears, S.F. Jr., Sanders, G.D., Hernandez, A.F., Mirro, M.J., Thomas, K.L., Eapen, Z.J., Russo, A.M., Yancy, C.W. (2013). Performance measures to promote quality improvement in sudden cardiac arrest prevention and treatment. American Heart Journal, 165(6), 862-868.