You’re called to the scene where a 50-year-old male was working in his yard when his wife witnessed him collapse. He’s found pulseless and apneic with no signs of trauma. His wife is performing CPR when you arrive.
What are the five common causes of sudden death that could have led to his demise, and what are some symptoms the patient may have been experiencing in the hours or days leading to his arrest?
EMS providers are often faced with patients in cardiac arrest. Many of these patients have complicated medical histories and have been ill for a long period of time. This article will discuss the five major causes of acute sudden death that may occur without warning in previously healthy patients, with a focus on the etiology, recognition and treatment of these conditions. The article is written to better allow prehospital providers to consider these causes and initiate appropriate time-sensitive care whenever possible.
The five causes of sudden death discussed in this article are: fatal arrhythmias, acute myocardial infarction, intracranial hemorrhage/massive stroke (cerebrovascular accident), massive pulmonary embolism and acute aortic catastrophe.
There are many causes of fatal arrhythmias including cardiomyopathies,1,2 inherited defects in the conduction system (such as prolonged-QT syndrome or Brugada syndrome),3 and the most commonly associated factor: ischemic injury from acute myocardial infarction (AMI) or previous infarct.4 Electrolyte imbalance can lead to arrhythmias and sudden death, such as hyperkalemia seen in patients with end stage renal disease on hemodialysis and hypokalemia in patients taking diuretics. Both of these are usually asymptomatic, but can prolong the QT interval leading to torsades de pointes.5,6 Other potential causes of malignant arrhythmias include illicit drug ingestion, medications that prolong the QT interval, acute changes in pH, worsening heart failure, Wolff-Parkinson-White syndrome and commotio cordis following chest trauma.
A significant number of patients who suffer sudden cardiac death will have no preceding symptoms. Other patients may have a history of chest pain, shortness of breath, palpitations, dizziness or syncope. Thus, even healthy, relatively young patients with “minor complaints,” such as palpations, need to be taken seriously and should be carefully monitored en route to the hospital.
These complaints should always prompt EMS providers to consider arrhythmia as a potential cause of the patient’s symptoms. To that end, patients with these complaints always need what we refer to as the “opening gambit”: oxygen, oxygen saturation monitoring, IV access, continuous cardiac monitoring and a 12-lead ECG.
Sudden death from a cardiac cause accounts for the majority of events, with estimates as high as 80%.4 Less than 8% of patients who have arrested will survive to be discharged from the hospital, and those who do live are likely to present with shockable rhythms.7 (See Figure 1 download below.) Unfortunately, it appears that only about one quarter of out-of-hospital cardiac arrests will have unstable v tach or v fib, and the remaining 75% who present in pulseless electrical activity (PEA) or asystole will have a bleak prognosis.7
Early defibrillation is the reason patients in v fib have a four-fold increase in odds of survival compared to those found in PEA, and nearly 20-fold increase in odds of survival compared to patients found in asystole.8
In the case of v fib patients, it’s estimated that every one minute in delay of defibrillation will decrease the chance of survival by up to 10%.7 For this reason, encouraging automated external defibrillator (AED) placement wherever there are large crowds or sporting events is essential.
Key concepts: Fatal arrhythmias are a common cause of sudden death. Early recognition of patients at the risk for these arrhythmias and appropriate treatment of reversible causes saves lives.
Patients found in v fib or v tach stand a much greater chance of survival when early defibrillation and high-quality chest compressions are delivered.
2. Acute Myocardial Infarction (AMI)
Another cause of sudden death is AMI. Plaques that develop within arteries progress over time and eventually rupture and occlude blood flow. Much like a sprinter will feel a burn in his muscles as he fatigues at the end of a race, the lack of adequate oxygen delivered to the heart (ischemia) results in fatigue that causes the anginal symptoms experienced by most patients during acute coronary syndrome (ACS).9 If ischemia affecting a large enough area of the heart is prolonged, extensive cell death follows and results in an AMI. Damage to the conduction pathways within the heart can degenerate into bradycardia, heart block, unstable v tach, v fib or PEA with the common endpoint of asystole. In the hundreds of thousands of cardiac arrests in out-of-hospital settings each year, approximately 80% are thought to be related directly to ischemic heart disease.4
When a patient presents with symptoms suggestive of AMI, it’s critically important to obtain a 12-lead ECG, which can help confirm the diagnosis of ST elevation myocardial infarction (STEMI). However, only 20–60% of patients having an AMI will initially have an ECG showing a true STEMI on presentation.10 (See Figure 2 download below.)
It’s important to realize there are many mimics of AMI that require different management.11 Furthermore, there are many atypical presentations of AMI that won’t be immediately recognized if a provider isn’t aware of them. For example, it’s been estimated that as many as one in four patients with AMI won’t have chest pain.9 Missed cardiac ischemia is more common in patients with atypical symptoms, younger patients, the elderly, women and minorities.12
The five most common atypical symptoms of an AMI are:
3. Central nervous system (CNS) symptoms including syncope, presyncope, dizziness, and stroke-like symptoms;
4. Gastrointestinal symptoms including nausea and non-localizing mild abdominal discomfort; and
The classic presentation of AMI is chest pain. The pain is sometimes difficult to delineate from indigestion, but several factors are known to increase the likelihood that a patient’s chest pain is related to ischemia. Pain that’s similar to a previous heart attack, pain that radiates to either or both arms, and pain that’s precipitated by exertion increase the likelihood that a patient’s chest pain is associated with an AMI or ischemia preceding an AMI.10
Factors associated with chest pain that decrease the likelihood of an AMI or an ischemic etiology are pain that is sharp, stabbing, worse with respiration, positional or worse with pressure applied to the affected area.10 Pain relieved by nitroglycerin isn’t predictive of ischemic chest pain.10 It’s best to have a high index of suspicion for possible signs and symptoms of ACS and to remember: Atypical is typical! Doing more 12-lead ECGs rather than less should be the practice pattern for all providers working in EMS and EDs.
In the presence of an AMI, expedient transport to the nearest medical center that can offer specialized cardiovascular intervention is paramount. Minimizing the time to percutaneous intervention will improve the patient’s outcome and chance of survival.7 While en route to a specialized medical facility, remember that administration of aspirin has been shown to significantly improve mortality.7
Key concepts: Time is muscle, and early recognition of patients suffering an AMI, even in the absence of chest pain or ECG changes, will ensure the opportunity to intervene appropriately isn’t missed. EMS providers must maintain a high index of suspicion for AMI as patients will often not present with a “classic history.”
3. Intracranial Emergencies
Intracranial catastrophe is an often overlooked cause of sudden death. Unlike other tissues in the body, the brain has a uniquely limited capacity to tolerate low oxygen delivery. This is the same reason ensuring appropriate blood flow through maintaining adequate blood pressure and oxygenation in head trauma patients is emphasized in Prehospital Trauma Life Support (PHTLS) training. In the case of a cerebralvascular accident (CVA), the blood flow to a part of the brain has stopped due to either obstruction from an embolism or from the rupture of a vessel carrying blood to the affected area of the brain. (See Figure 3 download below.)
In nonhemorrhagic strokes, where thrombolytic therapy is thought to benefit certain subpopulations of patients when delivered within the first several hours, timely transport is imperative. These patients can present with syncope, vertigo, facial droop, dysarthria, unilateral weakness, unilateral loss of sensation or hemiparesis. Initial assessment should include a blood glucose measurement as hypoglycemia can mimic stroke-like symptoms. Cardiac monitoring is also important as strokes have been associated with ensuing fatal arrhythmias leading to sudden unexpected death.13
In the case of a massive hemorrhagic CVA, which is associated with markedly elevated blood pressures and obtundation, patients frequently die before the initiation of medical therapy.14 Declining mental status in particular is one of the early signs of increased intracranial pressure, a harbinger of impending fatal herniation of the brain. However, there are many patients who can potentially benefit from emergent therapy and thus transport shouldn’t be delayed so that timely diagnosis and management can be initiated at a medical center capable of providing advanced care. Either type of a CVA (hemorrhagic or nonhemorrhagic) can be devastating and can lead to lifelong disability or death even when treated early and aggressively.
The adage “time is brain,” copied from “time is muscle,” is meant to emphasize that in the cases where intervention is possible, the sooner it’s initiated, the more hopeful the patient’s prognosis will be.
Subarachnoid hemorrhage (SAH) is another CNS cause of stroke and sudden death. Most commonly a result of a ruptured intracranial aneurysm, SAH often presents with the rapid onset of a severe headache often referred to as a “thunderclap headache.” Other signs and symptoms may include nausea, vomiting, neck stiffness or focal neurologic deficits. Beware of patients who experience syncope during exertion, sexual intercourse, or after developing “the worst headache of their life,” as these are classic presentations of a subarachnoid hemorrhage due to a rupture of an arteriovenous malformation or cerebral aneurysm.
Key concepts: As with other causes of sudden death, patients with intracranial emergencies may have no preceding symptoms. However, signs and symptoms such as new or worsening headaches, focal neurologic complaints and declining mental status can be seen. A glucose value should always be obtained to avoid missing hypoglycemia and profound hyperglycemia. When transporting patients with suspected intracranial hemorrhage/CVA, it’s critical to avoid hypotension or hypoxia as both will significantly increase morbidity and mortality. To that end, paramedics should rarely use antihypertensives in patients suspected of a CVA and should carefully monitor oxygenation.
4. Pulmonary Embolism (PE)
PE classically occurs more frequently in the elderly, cancer patients, patients who recently underwent surgery, patients on estrogen-containing medications, the bedbound and those who’ve previously had a deep venous thrombosis (DVT) or PE. Virchow’s Triad describes the three factors that are ultimately found to cause almost every PE:
1. Stasis of blood flow (e.g., immobilization);
2. A hypercoagulable state (e.g., estrogen therapy, smoking and inherited causes); and
3. Vascular injury (e.g., trauma—even relatively minor).
However, a PE can occur in patients with none of these risk factors known prior to presentation. Alarmingly, in one study it was estimated that sudden death was the first manifestation of PE in as many as 25% of patients. Of these, dyspnea and chest pain were the predominantly associated symptoms.15 Unexplained dyspnea should always raise the suspicion of a pulmonary embolism.
A PE occurs when a thrombus, commonly from a lower extremity DVT, becomes dislodged and embolizes via the inferior vena cava to the right side of the heart. Once ejected from the right ventricle, it enters the pulmonary circulation where it wedges into the branches of the pulmonary arteries, inhibiting blood flow through the lung. This also reduces oxygenation of venous blood prior to its return to the rest of the body. If the blood clot is large enough, cardiovascular collapse will occur as a result of obstructive shock. The left ventricle will be unable to deliver enough blood to the brain and body, resulting in the patient becoming hypotensive and obtunded.
Many patients who have a PE will often present with sinus tachycardia early on without any other findings. The combination of tachycardia, decreased oxygen saturation and pleuritic chest pain should prompt the provider to consider PE. Although associated with PE, hemoptysis is rarely, if ever, present. In the presence of a large PE, an initial ECG may show signs of right heart strain16 (see Table 1 and Figure 4 downloads below), although further testing will be required to confirm the diagnosis.
In patients suspected of having a PE, it’s important to secure the ABCs (airway, breathing, circulation) with oxygen, pulse oximetry, IV access, cardiac monitoring and obtaining a 12-lead ECG while expediting transport. In cases of cardiovascular collapse or submassive PE with imminent collapse, interventions such as thrombolytic therapy or endovascular clot removal can not only be lifesaving, but also prevent progression to right heart failure. Thus, early recognition and timely transport is essential to the patient’s outcome.
Key concepts: While acute pulmonary embolism often presents with pleuritic chest pain, signs and symptoms such as unexplained tachycardia, syncope, hypoxia, hypotension, anxiety and/or right heart strain should immediately prompt a provider to consider the diagnosis of PE. In such cases, supportive care and timely transport can be not only lifesaving, but also prevent long-term consequences from right heart failure and pulmonary hypertension.
5. Aortic Catastrophe
Lastly, acute aortic catastrophe, namely dissection or aneurysmal rupture, can cause sudden death. In patients with vascular disease (often the result of long-term comorbidities such as hypertension, high cholesterol or smoking), turbulent blood flow in the aorta can lead to outpouchings (aneurysms) of the arterial wall at points of stress due to weakening of the vessel from atherosclerosis.
While initially benign, as these aneurysms grow in diameter over the years, they become increasingly at risk for rupture.17
An aortic aneurysm, although generally painless, can cause pain that radiates to the back or flank when acutely expanding or upon rupturing. Aortic rupture results in extensive internal bleeding. After exsanguination from the rupture, but prior to death, PEA is likely to be encountered due to extensive volume loss.18 Whenever a patient over the age of 60 has a chief complaint of back, flank or abdominal pain, it’s essential aortic aneurysm always be high on the differential diagnosis.18 A large pulsatile mass palpated in the mid-abdomen makes the diagnosis much more likely, though is often not appreciated. These patients will require management in an intensive care unit and, very likely, surgery if the aneurysm is rapidly expanding or has already ruptured.
If the aorta’s wall is weakened by chronic changes from vascular disease, it becomes more susceptible to shearing stress that can tear the normal layers of the aorta apart. There are three layers of the healthy aorta that keep blood within the artery. Hypertension can cause blood to “dissect” through the innermost layer into the middle layer and then proceed to tear the wall of the aorta apart internally in a phenomenon called aortic dissection.17 This distinguishes a dissection from an aneurysm because in aneurysms the three layers of the aorta remain intact and instead bulge out together from their normal position. (See Figure 5 download below.)
Aortic dissection often presents with chest pain, described as “ripping” or “tearing” radiating to the back. Pain from aortic dissection is sudden and maximal in intensity at onset for the majority of patients.10
This is unlike angina, which builds in intensity and is rarely felt as ripping or tearing. In approximately one third of patients with aortic dissection, there will be a greater than 15 mmHg difference in systolic blood pressure between the upper extremities and approximately one quarter will have a diastolic murmur.19 However, neither of these findings are likely to be appreciated in the field. Patients are usually elderly (on average 65 years old), hypertensive (approximately 50% of patients), and sometimes have neurological deficits (less than 1 in 5 patients with dissection).20
It’s important to realize aortic dissection can often mimic ACS.11 As the treatment for ACS requires anticoagulation, appropriate recognition of a dissection saves lives as incorrectly diagnosing a dissection as ACS and treating with anticoagulation can lead to aortic rupture. Thus, any interventions beyond aspirin for chest pain should be pursued only after the diagnosis of dissection has been considered and thoughtfully ruled out.
Key concepts: Aortic rupture from aneurysm or dissection requires the thoughtful practitioner to first consider the diagnosis in any patient with chest pain, flank pain, abdominal pain or sudden collapse.
This is particularly true in elderly patients with hypertension who present with either ripping or tearing chest pain in the case of dissection, or in the case of ruptured aortic aneurysm patients presenting with severe back, flank or abdominal pain. Reducing hypertension and tachycardia while expediting transfer to a specialized medical center is critical.
Through improved awareness, the skilled provider will be able to more efficiently initiate appropriate therapy and avoid the pitfalls of misdiagnosis and resultant unintended harm to the patient. It’s held true for centuries that history and physical examination are an essential guide to the medical management of our patients, and these shouldn’t be undervalued. It’s also important to remember the basics: securing ABCs, opening the gambit and expediting transport to a qualified medical center.
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2. O’Mahony C, Elliott P, McKenna W. Sudden cardiac death in hypertrophic cardiomyopathy. Circ Arrhythm Electrophysiol. 2013;6(2):443–451.
3. Bastiaenen R, Behr ER. Sudden death and ion channel disease: Pathophysiology and implications for management. Heart. 2011;97(17):1365–1372.
4. Myerburg RJ, Junttila MJ. Sudden cardiac death caused by coronary heart disease. Circulation. 2012;125(8):1043–1052.
5. Krahn LE, Lee J, Richardson JW, et al. Hypokalemia leading to torsades de pointes. Munchausen’s disorder or bulimia nervosa? Gen Hosp Psychiatry. 1997;19(5):370–377.
6. Alpert MA. Sudden cardiac arrest and sudden cardiac death on dialysis: Epidemiology, evaluation, treatment, and prevention. Hemodial Int. 2011;15(Suppl 1):S22–S29.
7. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(4):e78–e140.
8. Teodorescu C, Reinier K, Uy-Evanado A, et al. Survival advantage from ventricular fibrillation and pulseless electrical activity in women compared to men: The Oregon Sudden Unexpected Death Study. J Interv Card Electrophysiol. 2012;34(3):219–225.
9. Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263.
10. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629.
11. Brywczynski J, Mckinney J, Brown A, et al. STEMI mimics: Five cases that look & sound like a STEMI, but may not be. JEMS. 2013;38(12):38–43.
12. Jones ID, Slovis CM. Pitfalls in evaluation the low-risk chest pain patient. Emerg Med Clin North Am. 2010;28(1):183–201.
13. Sörös P, Hachinski V. Cardiovascular and neurological causes of sudden death after ischaemic stroke. Lancet Neurol. 2012;11(2):179–188.
14. Huang J, van Gelder JM. The probability of sudden death from rupture of intracranial aneurysms: a meta-analysis. Neurosurgery. 2002;51(5):1101–1107.
15. Lucena J, Rico A, Vázquez R, et al. Pulmonary embolism and sudden-unexpected death: Prospective study on 2477 forensic autopsies performed at the Institute of Legal Medicine in Seville. J Forensic Leg Med. 2009;16(4):196–201.
16. Hunt JM, Bull TM. Clinical review of pulmonary embolism: Diagnosis, prognosis, and treatment. Med Clin North Am. 2011;95(6):1203–1222.
17. Ashley EA, Niebauer J. (2004.) Cardiology explained: Chapter 12: Aneurysm and dissection of the aorta. NCBI Bookshelf. Retrieved Feb. 2, 2014, from www.ncbi.nlm.nih.gov/books/NBK2210/.
18. Pierce LC, Courtney DM. Clinical characteristics of aortic aneurysm and dissection as a cause of sudden death in outpatients. Am J Emerg Med. 2008;26(9):1042–1046.
19. Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA. 2002;287(17):2262–2272.
20. Siegal EM. Acute aortic dissection. J Hosp Med. 2006;1(2):94–105.
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