Sudden cardiac death

Definition refers to the natural death due to cardiac causes with abrupt loss of consciousness and occurring within 1 hour of the onset of symptoms.

Additional criteria for the definition of SCD include the absence of trauma, and the unexpected timing and mode of death.

SCD may occur in patients with previously documented coronary artery disease or may be an initial event.

Sudden cardiac arrest highest risk is for patients with depressed left ventricular ejection fraction.

Despite cardiopulmonary resuscitation training, placement of automated external defibrillators survival rate remains low.

SCD often presents as the initial manifestation of cardiovascular disease in previously healthy people, and a concerning proportion of events occur individuals not identified as high risk by traditional measures.

Accounts for nearly half of all deaths from cardiovascular disease in the US.

SCD is a  leading cause of death worldwide.

Sudden cardiac death is the cause of about half of deaths due to cardiovascular disease and about 15% of all deaths globally.

More than 20,000 individuals are estimated to experience an unexplained cardiac arrest each year in the US alone.

More than half of the deaths from coronary heart disease occurs as cardiac arrest outside of hospitals or emergency departments within one hour of the onset of symptoms.

While most victims have coronary heart disease, the majority go undiagnosed prior to death.

A plurality of sudden cardiac death occurs in a population with no apparent cardiac risk factors, but the risk is greatest in patients with left ventricular ejection fraction of less than 30%, those with clinical heart failure, those with prior aborted cardiac arrest, or coronary artery disease.

The frequency of cardiac arrest due to coronary heart disease has increased a middle-aged men doing marathons and triathlons in the US.

Primary diagnostic tool to estimate the risk of sudden cardiac death (SCD) is left ejection fraction among patients with known heart disease.

Approximately 450,000 deaths annually in the US related to SCD.

Among patients who reach in intensive care unit for mechanical ventilation and cardiocirculatory support, hypoxic-ischemic brain injury is the most common cause of death.

hypoxic-ischemic encephalopathy is the leading cause of death and disability among adults with coma who have been resuscitated after out of hospital, cardiac arrest.

Brain hypoperfusion may contribute to cerebral hypoxia, exacerbate brain damage, and lead to poor neurologic outcomes.

Three times more common in men than in women, reflecting a similar pattern for coronary artery disease.

Low serum calcium levels are associated with increased risk of sudden cardiac death in the community (Yarmohammadi Y).

Both hyperkalemia and hypokalemia are associated with cardiac arrhythmias and sudden cardiac death.

Hypokalemia and other electrolyte disturbances account for most sudden deaths in patients with eating disorders.

Both high and low serum magnesium levels are associated with increased mortality and sudden death.

Hyponatremia and hypernatremia are not associated with arrhythmias or sudden death.

More prevalent in Black patients, in patients with diabetes mellitus, and those with chronic kidney disease.

White men have the highest death rates, five followed by men of other races, women of nonwhite races and lastly, white women.

May be a result of acute ischemia without infarction, acute myocardial infarction, electrical instability induced by coronary artery disease, or some other problem which would be coincidental to coronary artery disease.

Sudden cardiac death is described as a natural death due to cardiac causes, associated with abrupt onset of loss of consciousness and occurring within one hour of the onset of symptoms.

Risk inversely related to cardiorespiratory fitness.

It may occur in patients with previously documented coronary artery disease or it may be an initial event.

Extreme emotional states/stress can result in the markedly heightened autonomic nervous system activity that can lead to malignant ventricular arrhythmias followed by ventricular fibrillation and death.

Incidence ranges from 0.36-1.28 per 1000 persons per year which leads to approximately 400,000 deaths in the US. annually.

70-90% of total incidence occurs in men.

The age-adjusted national incidence of SCD is 60 per 100,000 persons.

Incidence decreasing about 15-19% due to timely myocardial reperfusion, use of drugs, and defibrillator implantation.

Most common cause is coronary artery disease.

Autopsy studies reveal approximately 2/3 of unexpected deaths are cardiac in origin.

5-10% of SCD occur with no evidence of CAD or CHF, and SCD is the first manifestation of disease.

In patients with structural normal hearts and SCD mechanisms may relate to comorbid conditions such as obesity, epilepsy, fusion complexes on EKG or family histories of SCD.

Sudden death incidence has remained fairly constant and survival associated with cardiopulmonary resuscitation has not changed substantially in decades.

SCD is the most devastating manifestation of cardiac ventricular electrical arrhythmias.

Causes of SCD are divided into electrical and nonelectrical classifications.

Ventricular tachyarrhythmias account for most electrical causes of cardiac arrest.

Holter monitor studies reveal let 64.4% of patients with sudden cardiac death were preceded by ventricular fibrillation, 16.5% by btadyarrhythmias, 12.7% bt Torsades de pointes and 8.3% by ventricle tachycardia (Bayes de Luna A et al).

In the above study ischemic ST-Sigman changes before the arrhythmia were uncommon.

Stable risk factors that contribute to SCD include: anatomical defects, myocardial,scarring, CAD, and alterations in cardiac nerves.

SCD inducing transient factors include changes in local oxygen tension, pH and electrolyte imbalance such as hypokalemia, hypomagnesemia, hemodynamic changes, toxins, drugs, alcohol, and ischemia.

One or more transient factors may precipitate electrical instability

SCD criteria include the absence of trauma.

More than 95% of patients will experience an SCD within 10 minutes of ventricular tachycardia, ventricular fibrillation, pulseless electrical activity or asystole (Chugh SS et al).

Sudden cardiac arrests are the most common cause of deaths in the U.S. accounting for approximately 400,000 deaths annually.

Accounts for more than 50% of overall mortality from cardiovascular diseases.

Left ventricular ejection fraction is the most important predictor of sudden cardiac death after MI.

Between 370,000-750,000 hospitalized patients experience cardiac arrest and undergo cardiopulmonary resuscitation each year in the U.S.

More than 300,000 out of hospital cardiac arrests each year in the US with a survival rate of 7.9%, and the majority of survivors have ventricular fibrillation or pulseless ventricular tachycardia.

Patients presenting with ventricular fibrillation or pulseless ventricular tachycardia have a higher survival rate than patients with other rhythms.

Almost half of patients with atrial fibrillation remain remain refractory despite multiple defibrillation attempts.

The use of double sequential external defibrillation technique or VC change defibrillation can improve survival to hospital discharge in this setting.

Out of hospital events has an estimated incidence of 55 per 100,000 person-years or about 155,000 episodes annually in the U.S.

Acute coronary syndrome accounts for up to 60% of out of hospital cardiac arrests in which a cardiac clause has been identified.

The finding of ST segment elevation on a post resuscitation EKG has good positive predictive value for acute coronary lesions triggering the cardiac arrest.

There is a larger sub group of patients without ST segment deviation.

Incidence of out of hospital cardiac arrest in industrialized countries estimated to be 92 per hundred and 89 cases per hundred thousand population (Straus SM et al, Rea TD et al, Nichol G et al).

Out-of-hospital sudden cardiac death a leading health problem worldwide, accounting for 15-20% of all natural adult deaths and up to 50% of cardiovascular deaths.

Approximately 100,000 resuscitation attempts are made annually each year in the US and 40,000 patients survive to hospital admission (Schulman SP et al).

Ventricular tacchyarrhythmias initiating event in 80% of patients who develop out of hospital primary cardiac arrest during ambulatory electrocardiogram monitoring (Bayes De Luna).

In comatose survivors of out of hospital cardiac arrest, a target temperature of 31°C did not significantly reduce the rate of death or poor neurologic outcome at 180 days compared with the target temperature of 34°C.

Incidence of ventricular fibrillation or pulseless ventricular tachycardia as the first recorded rhythm in out of hospital cardiac arrest has dropped in recent decades: the incidence today is 23% compared to 70% 30 years ago (Nichol G et al, Weisfeldt M et al).

Non-tachycardic SCD including pulseless electrical activity and asystole incidence has increased while tachyarrhythmia SCD incidences have decreased.

Although evidence of coronary artery disease is subsequently identified in 80% of patients with SCD, most deaths occur in apparently normal and asymptomatic adults with no previous history of CAD.

More than half of men and close to 70% of women who die of sudden cardiac arrest have no clinical history of heart disease before their cardiac arrest.

Only half of patients with sudden death outside hospitals are known to have coronary heart disease before their death.

High-risk patients with acute MI have SCD rates higher than 30% but account for a small minority of the total number of cases.

More than half occur before the age of 65.

63% of deaths from cardiovascular disease in 1998 were sudden and unexpected and mostly attributed to coronary artery disease.

End result of usually ventricular fibrillation or ventricular tachycardia.

Among the leading causes of cardiac arrest in hospitalized patients are ventricular fibrillation and pulseless ventricular tachycardia from primary electrical disturbances or cardiac ischemia.

Survival from ventricular fibrillation or pulseless ventricular tachycardia improved if defibrillation therapy is provided rapidly.

Patients with ventricular fibrillation or pulseless ventricular tachycardia should receive defibrillation within 2 minutes of event.

A retrospective observational study from the National Registry of Cardiopulmonary Resuscitation (NRCPR) revealed cardiac arrest in 253 US and Canadian hospitals, the rate of survival to hospital discharge following ventricular fibrillation or pulseless ventricular tachycardia was 36% and following asystole or pulseless electrical activity survival was 11% (Nadkarni VM et al).

Bradyasystole is the first rhythm in as many as 52% of cardiac arrests and many patients with initial ventricular fibrillation deteriorate to bradyasystole after defibrillation attempts.

Fewer than 3% of patients presenting with bradyasystole survive to discharge from hospital.

Only 20-40% of cardiac arrests occur in the context of an acute myocardial infarction with intracoronary thrombus.

Structural heart disease with atherosclerosis, cardiomyopathy, or valvular disease present in more than 90% of adults who have sudden cardiac death caused by ventricular arrhythmias.

Accounts for approximately 50% of all subsequent cardiac deaths among patients who have survived an acute myocardial infarction.

Women with SCD less likely to have a history of cardiovascular disease, structural heart disease, or left ventricular dysfunction than men with SCD.

In the Nurses’ Health Study 2/3 of SCD victims had no history of cardiac disease.

Women with torsades de pointes may be a greater risk of sudden death than men (Makkar RR).Are you

Women with coronary artery disease have a lower risk of ventricular arrhythmias and sudden cardiac death than men.

Clinically the only established predictor is severely decreased left ventricular systolic function (Chugh SS et al).

Ejection fraction data alone isn’t sufficient for sudden cardiac death risk prediction as it lacks sensitivity and specificity.

Less than one third of all SCD cases have severely decreased less LV ejection fraction that would qualify them for an implantable cardioverter defibrillator.

Sudden cardiac death comprises the majority of cardiac deaths among postmenopausal women with CAD, and left ventricular ejection fraction, heart failure, myocardial infarction, and GFR lower than 40 mls per minute, atrial fibrillation, physical inactivity, and diabetes were independently associated in a large multi-center sampling of women with coronary artery disease.

Incidence increases with age and overall is 3-4 times more common in men than women, reflecting the similar pattern for CAD.

In young athletes-risk between 1 per 100,000 and 1 per 300,000 per year.

Young individuals age 35 years or less with sudden cardiac death often have structurally normal hearts.

More than 3% of post acute myocardial infarction patients experience sudden cardiac death.

In young athletes-most common cause is hypertrophic cardiomyopathy a familial autosomal dominant disorder.

In young atheletes five times more common in males than females.

In older atheletes the incidence ranges from 1 per 15,000 to 1 per 18,000.

In young people has an incidence between 1 and 5 per 100,000 patients.

In young people autopsy studies most commonly reveal hypertrophic cardiomyopathy, coronary artery anomalies and myocarditis.

In young people, 10-20% have no findings at autopsy and are unexplained.

Most patients who die suddenly without known symptoms of chest pain have underlying coronary artery disease.

Most patients who die in such a manner would not have qualified for receiving an ICD device for primary prophylaxis.

Early defibrillation is the most important intervention with survival decreasing 10% with each minute delay in its institution.

The incidence of cardiac arrest and sudden-death doing long-distance running races is 1 per 184,000 an 1 per 259,000 participants, respectively (The Race Associated Cardiac Arrest Event Registry (RACER) Study Group).

In the above study it was estimated that 0.2 cardiac arrests and 0.14 sudden deaths per 100,000 runner-hours at risk, using average running times of four and two hours for marathon and half marathon, respectively.

Event rates of cardiac arrest and sudden-death among marathon and half marathon runners are relatively low compared with other athletic populations: Collegiate athletes one death per 43,770 participants per year, triathlon participants one death per 52,630 participants, and previously healthy middle-aged joggers one death per 7620 participants (Harmon KG et al, Harris KM et al, Thompson PD et al).

The risk associated with long distance running events is equivalent or lower than the risk with other vigorous physical activities.

Men are more likely than women to have cardiac arrest and sudden-death with exertional cardiac arrest, and this is explained by a higher prevalence of both occult hypertrophic cardiomyopathy and early onset atherosclerosis in men.

The rates for cardiac arrest and death was a 3 to 5 times higher in marathoners as compared to half marathon runners.

Hypertrophic cardiomyopathy is the primary cause of death in young competitive athletes and is also the leading cause of death in marathon runners.

Epinephrine is the vasopressors of choice for cardiopulmonary resuscitation, the prognosis for patients who require this agent is extremely poor, regardless of the dose given.

Even if spontaneous circulation returns after in hospital cardiac arrest, approximately 60% of patients will not survive hospital discharge.

High mortality after CPR associated with postcardiac arrest syndrome involving global ischemic reperfusion injury, myocardial stunning, and anoxic brain injury (Negovsky VA).

The administration of supplemental oxygen to patients after cardiac arrest is controversial: there is a paradox when oxygen is delivered to an injured brain as too much oxygen may increase oxygen radical production and possibly trigger cellular damage and apoptosis (Becker LB).

Oxidative stress from reactive oxygen species formed after reperfusion may increase cellular death by diminishing mitochondrial oxidative metabolism, disrupt normal enzyme activity, and damage lipid membranes via peroxidation.

Post-ischemic hyperoxic reperfusion may worsen brain injury via cellular inflammation of the neurons or their microenvironment.

Debate exists about the level of oxygenation after resuscitation of whether conservative oxygen level targets (PaO2 68-75 mmHg) versus standard oxygen targets (PaO2 98-105 mmHg) are most beneficial.

Traditional risk factors include: older age, male sex, history of hypertension, diabetes, dyslipidemia, family history of premature coronary artery disease, current and past smoking history.

Among patients with out of hospital cardiac arrest, treatment with the intravenous or intraosseous calcium compared with saline did not significantly improve sustained return of spontaneous circulation.

In patients with refractory out of hospital, cardiac arrest, extracorporal CPR and conventional. CPR has similar effects on survival with a favorable neurologic outcome (Suverin MM).

Guidelines for post resuscitation care, recommend active fever prevention for 72 hours in comatose patients who have been resuscitated after an out of hospital cardiac arrest.
Active device-based fever prevention for 36 or 72 hours after cardiac arrest did not result in significantly different percentages of patients dying or having severe disability or coma (Hadsager C).

Leave a Reply

Your email address will not be published. Required fields are marked *