Sudden Cardiac Death and Cardiac Arrest



Sudden Cardiac Death and Cardiac Arrest


Donna Gerity



Sudden cardiac death (SCD) is a major clinical and public health problem in the United States. The incidence of SCD is difficult to measure due to inconsistent methodology in classifying deaths. Various estimates of annual SCD events in the United States range from 200,000 to 450,000. The most widely used estimate is in the range of 300,000 to 350,000 deaths annually. Even with significant advances in management of coronary artery disease (CAD), and the treatment of heart failure, the overall incidence has remained unchanged as our population ages.1 CAD is present in as many as 80% of those individuals who experience SCD. Autopsy studies show that 50% of these sudden death patients have acute changes in coronary status, such as plaque, rupture, or thrombus.2 Survival rates for out-of-hospital sudden cardiac arrest (SCA) victims are low, with only 2% to 25% surviving to discharge in the United States. Those survivors of SCA have a high risk for future events. Therefore, the aim at decreasing SCD is to better identify and treat potential victims of SCD. Future events will be minimized if the incidence of CAD is reduced and primary and secondary prevention is provided.3,4


DEFINITION OF SUDDEN DEATH

SCD is defined as an unexpected death caused by cardiac causes that occurs within 1 hour of symptom onset. The person may or may not have known pre-existing heart disease. Cardiac arrest, usually caused by cardiac arrhythmias, is the term used to describe the sudden collapse, loss of consciousness and loss of effective circulation that precedes biologic death.5,6 A subclassification of sudden death uses the term instantaneous death, a death with immediate collapse without preceding symptoms. Other causes of death may also be instantaneous, such as stroke, massive pulmonary embolism, or rupture of an aortic aneurysm. It is also important to note that not all arrhythmic deaths are sudden. A patient may be successfully resuscitated from a cardiac arrest but may die days later from complications.7


PATHOPHYSIOLOGY AND CAUSE OF SCA

The epidemiology of SCD tends to follow that of coronary heart disease (CHD). The incidence of SCD increases with the aging population in both men and women, whites and nonwhites, just as ischemic heart disease increases. SCD occurs 75% more often in men. Hypertension, left ventricular hypertrophy (LVH), intraventricular conduction defect, hypercholesterolemia, vital capacity, smoking, relative weight, and heart rate were all noted as risk factors per the 26-year follow-up of the Framingham Study.8 SCD does appear to be increasing in women. From 1989 to 1999, SCD increased by 21% among women aged 35 to 44 years in the United States. During this same time frame there was a 2.8% decline among men of the same age group.1,9 Risk profiling for CAD is useful for identifying populations and individuals at risk, but does not identify an individual patient at risk for SCD. The inability to identify individuals is a major reason why SCD remains an important public health problem.10

There are several different arrhythmia mechanisms responsible for SCD. The most common arrhythmia leading to SCD appears to be ventricular tachycardia (VT) accelerating into ventricular fibrillation (VF), often followed by asystole or pulseless electrical activity (PEA). Acquired structural and functional changes that occur in a diseased heart, and genetic factors may contribute to sudden death. However, the mechanism that produces the potentially fatal arrhythmia among patients with CAD is difficult to define.11,12

The episode could be caused from pure ischemic injury because of occlusion of a major artery in a patient with a normal ventricle in whom VF develops in the first minutes of an acute infarction. The other type of mechanism is one in which a patient with a previous myocardial infarction (MI) has postinfarction scarring that provides the anatomic substrate for VT that leads to hemodynamic collapse and SCD. Patients could also have complex substrates consisting of dense scar tissue with aneurysms or other areas where disorganized arrhythmias predominate. This complex interaction and multiplicity of influences that occur in a cardiac arrest episode differ for all patients.2,7


Structural Abnormalities


Coronary Heart Disease

CHD is the major structural abnormality found in most SCA victims. In 80% of patients who have had an SCA, CAD is present. SCA is often the first manifestation of CHD.10,13 Pathology studies of SCD patients have shown that coronary atherosclerosis is the major predisposing cause. Plaque rupture and plaque erosion are the underlying pathologies in the majority of cases of SCD. Evidence shows a difference in the mechanism of MI and death between men and woman. Men tend to have coronary plaque rupture, while women tend to have plaque erosion.14 Data from the Nurses’ Health Study of 121,701 women have shown that 94% of women who had SCD had one risk factor for heart disease.9 The evolution and clinical manifestation of CHD leading to SCA has been identified as four separate stages (Fig. 27-1). The first stage is atherogenesis, which is the beginning of plaque formation and occurs over a long period of time. This stage should be thought of as the stage that determines risks for CHD. The
second stage is the transitional stage where changes in plaque anatomy and pathophysiology are taking place. During this stage, the disease has moved from quiet to active. The third level of the process is the acute coronary syndrome phase when the acute ischemic event may be triggered by plaque disruption and the onset of the thrombotic process. The time to a fatal arrhythmia is close, leaving less time for preventative actions. The final phase is the arrhythmogenesis, when an interaction is occurring between the active ischemic process and the onset of cardiac arrhythmias.15






Figure 27-1 Evolution and clinical manifestations of risk for sudden cardiac death due to coronary artery disease. The cascade identifies four levels of progression beginning with plaque formation and development, progressing to an active state, then to acute coronary syndromes (ACS), and ending with life-threatening arrhythmias of SCD. (Used with permission from Myerburg, R. J. [2002]. Scientific gaps in the prediction and prevention of sudden cardiac death. Journal of Cardiovascular Electrophysiology, 13, 709-723.)

Changes in coronary artery blood flow from other causes such as coronary vasospasms or nonatherosclerotic coronary artery abnormalities can also provoke ischemia and create myocardial electrical disturbances and the development of VF. Structural coronary artery abnormalities without atherosclerosis are rare and include congenital lesions, coronary artery emboli from aortic valve endocarditis, or from thrombotic material released from prosthetic aortic or mitral valve.16


Cardiomyopathy

The second largest group of patients who experience SCD includes patients with cardiomyopathy. Severely depressed left ventricular function is an independent predictor of SCD in patients with ischemic and nonischemic cardiomyopathy. An ejection fraction equal to or less than 0.35 is considered the most powerful predictor of SCD. Improved treatment options for patients with heart failure provide them with better long-term survival. However, there is an increasing proportion of patients with heart failure who die suddenly.16 Three primary prevention studies have shown reduction in total mortality for ischemic and nonischemic cardiomyopathy patients. The Multicenter Automatic Defibrillator Implantation Trial (MADIT II) has shown that the implantable cardioverter defibrillator (ICD) will reduce total mortality in patients with ischemic cardiomyopathy with ejection fractions less that 0.30. The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) enrolled patients with either ischemic or nonischemic cardiomyopathy with ejection fractions less than 0.35, and NYHA classes II and III heart failure. The results confirmed reduced mortality in the ischemic patients, but also in the nonischemic cardiomyopathy patients. The Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial also showed reduction in death from arrhythmias with ICD therapy.17, 18, 19

LVH has been established as an independent risk factor for SCD. ECG changes consistent with LVH and echocardiography evidence have both been associated with sudden and unexpected cardiac death.8,20 The underlying causes for myocardial hypertrophy include hypertensive or valvular heart disease, obstructive and nonobstructive hypertrophic cardiomyopathy (HCM), and right ventricular hypertrophy secondary to pulmonary hypertension or congenital heart disease. All of these conditions are associated with increased risk of SCD, but it has been suggested that people with severely hypertrophic ventricles are especially susceptible to SCD.16

HCM is a familial cardiac disease that occurs in 1 out of 500 people. Often the disease goes undiagnosed and is the most common cause of sudden death in people under 30 years of age.21,22 Sudden death often occurs with vigorous exercise is this group of patients. Various risk factors for SCD with HCM include family history of sudden death, documented nonsustained VT, recurrent and unexplained syncope, and extreme thickness of 30 mm or more of the left ventricle. Polymorphic VT and VF are thought to be the initial rhythm for patients with HCM who experience SCD.7,16 Genetic studies of HCM have confirmed autosomal dominate inheritance patterns. Typically HCM is caused by mutations in any one of 10 genes that encode proteins of the cardiac sarcomere. DNA testing can identify patients with HCM at an early onset, helping to modify medical therapy and recommendations for placement of an implantable defibrillator, or withdrawing from intense physical activities and competitive sports.22


Valvular Heart Disease

The risk of sudden death in patients with valve disease is low but present. After prosthetic or heterograft aortic valve replacements, patients are at risk for SCD caused by arrhythmias, prosthetic valve dysfunction, or existing CHD. The risk of SCD after surgery peaks at 3 weeks and plateaus after 8 weeks. Sudden death can also occur with exertion in young adults with congenital aortic stenosis. The mechanism is uncertain but thought to be from sudden changes in ventricular filling or aortic obstruction with secondary arrhythmias.7 Mitral valve prolapse is associated with a high incidence of symptomatic atrial and ventricular arrhythmias; however, whether it causes SCD is unresolved.16

Rare reports of sudden death have been reported from coronary embolism due to valvular vegetations, which trigger a fatal ischemic arrhythmia. Endocarditis of the aortic or mitral valve may cause deterioration of the valvular apparatus, and abscesses of the valvular rings or septum leading to sudden death.16



SCD without Structural Heart Disease

A reported 5% to 10% of those patients who experience SCD have no apparent structural heart disease.2,20 There are many potential causes (Display 27-1) of SCD in this small percentage of patients. The most common of these electrophysiological abnormalities are long QT syndrome (LQTS), short QT syndrome (SQTS), Brugada syndrome, and catecholaminergic polymorphic VT (CPVT). LQTS is either congenital or acquired by use of drugs, such as antiarrhythmic and psychotropic drugs, or with electrolyte imbalances. See Display 27-2 for a list of the most common drugs responsible for acquired LQTS. The list of drugs that are generally accepted to have an increase risk of torsades de pointes is ever expanding, and can be found at online sites such as www.qtdrugs.org. Torsades is a type of polymorphic VT, which leads to syncope or SCD. SQTS is relatively newly defined syndrome, with short refractory periods both in the atria and the ventricles. Brugada syndrome is a genetic disease characterized by a right ventricular conduction delay. CPVT is characterized by
ventricular arrhythmias that develop during physical activity in the presence of a normal resting ECG.20,23




Congenital Long QT Syndrome

Patients with the classic long QT intervals corrected for heart rate (QTc interval) are at increased risk for torsades.20,23,24 Congenital long QT is hereditary; mutations in eight genes have been identified. The most common mutations are LQT1 (42%), LQT2 (45%), and LQT3 (8%). Most mutations affect the cardiac potassium-channel genes KCNQ1 and KCNH2 and cause the most frequent forms of long QT. An impaired sodium channel gene, SCN5A, is the cause for LQT3. However, the mutation LQT4 has been identified as a mutation from a membrane adaptor protein, and not an ion channel.12,23 QT interval duration was identified as the strongest predictor of SCD, even before genetic mutation identification. A QTc greater than 500 ms in a patient identified with an affected gene carries the highest risk of syncope or SCD by the age of 40.20 Two patterns of long QT have been reported: the Romano Ward syndrome, which is an autosomal dominant syndrome, and the Jervell and Lange-Nielsen syndrome. The latter is autosomal recessive, more severe, and often associated with congenital deafness.20,25

In individuals with long QT, ventricular arrhythmias often occur in the setting of stress and activity, but also can occur during rest and sleep. Exercise, particularly swimming, is often a trigger for arrhythmias in the LQT1 patients. LQT2 patients have arrhythmias that are triggered during both rest and emotion, often associated with acoustic stimuli. The LQT3 patients are more prone to having arrhythmias at rest and during sleep.20,26 Avoidance of competitive sports is recommended for LQT1 and LQT2 patients, but not for LQT3 patients.22


Brugada Syndrome

Brugada syndrome is an inherited disease that is associated with a high incidence of sudden death. A mutation of cardiac sodiumchannel gene SCN5A, has been identified in about 20% of persons with the syndrome, and occurs more often in men. The Brugada syndrome is confirmed with ST-segment elevation in the precordial leads, right bundle-branch block (RBBB) conduction pattern, and history of SCD. The ECG changes may be present all the time or elicited when antiarrhythmic drugs are given that block sodium channels (Chapter 15).20,27,28 Fever has been reported to unmask ECG changes of Brugada syndrome and elicit an electrical VT storm.29 Globally, the syndrome is more prevalent in areas of southeast Asia.23


Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White (WPW) is associated with an accessory pathway that allows for conduction between the atria and ventricles. Normally, WPW is associated with nonlethal arrhythmias. However, if atrial fibrillation develops and conduction is rapid over the accessory pathway, the ventricular rate can become so fast that the rhythm degenerates into VF. SCD in the setting of WPW is quite low, and has been reported at 0.39% per year.23,30


Catecholaminergic Polymorphic Ventricular Tachycardia

CVPT is a catecholamine-dependent arrhythmia that occurs in the absence of a long QT interval. The arrhythmia often occurs during physical activity or emotional distress; therefore, β-adrenoceptorblocking agents can be helpful in treating this condition. The first episode often occurs during childhood. The arrhythmia is characterized by bidirectional and polymorphic VT. The condition is rare, and is related to a genetic disorder. CPVT is caused by mutations involving the cardiac ryanodine receptor, and calsequestrin, a calcium-buffering protein.20,23,31


MANAGEMENT OF SCA

The outcome of cardiac arrest is determined by how promptly treatment is initiated with advanced cardiac life support (ACLS). To improve outcome from SCA, the following must occur as rapidly as possible: (1) early recognition of warning signs, (2) early activation of the emergency medical system, (3) early basic cardiopulmonary resuscitation (CPR), (4) early defibrillation, and (5) early ACLS. These events have been described as “links in a chain of survival,” because they are all connected and indispensable to the overall success of emergency cardiac care.32,33

Although this section summarizes ACLS recommendations for the adult patient, it is not a complete reference. For each cardiac nurse, participation in an ACLS provider course by the American Heart Association (AHA) is strongly recommended. In addition, the most current version of Emergency Cardiac Care, Basic Life Support for Healthcare Providers, and The Textbook of Advanced Cardiac Life Support should be used as definitive references.


Adult Advanced Cardiac Life Support

ACLS teaches the appropriate skills and knowledge, as determined by leaders in emergency cardiovascular care (ECC), to improve survival from SCA and acute life-threatening cardiopulmonary events. ACLS includes early recognition of prearrest, basic life support, the use of airway and circulation adjuncts, cardiac monitoring, and defibrillation and other arrhythmia control techniques. ACLS also includes establishment of intravenous access, drug therapy, and postresuscitation care. This section focuses on defibrillation and ACLS management of pulseless cardiac arrest. Postresuscitation management of SCA survivors is also included. For discussions of basic and complex arrhythmias, conduction disturbances, electrophysiology studies, hemodynamic monitoring, acute coronary syndrome, pacemakers, and implantable defibrillators, respectively, refer to Chapters 15, 16, 18, 21, 22, and 28, respectively.

In 2005, the AHA updated the guidelines for CPR and ECC.32 The guidelines are based on the 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. The classes of recommendation for ACLS management are based on evidence evaluation (Display 27-3).


Electrical Therapy of Malignant Arrhythmias

Defibrillation and cardioversion are a delivery of electrical energy that totally depolarizes and stuns the myocardium, which allows the sinus node to resume its function as the pacemaker for the heart. Defibrillation is, by definition, the therapy for VF. Cardioversion, which is a synchronized shock, is the electrical therapy for all other tachyarrhythmias. Transcutaneous and transvenous pacing are additional types of electrical therapy used in ACLS
for patients with hemodynamically compromised bradycardias (Chapter 28).



Early Defibrillation

VT and VF are the most common arrhythmias during cardiac arrest, although the incidence of VF seems to be declining as reported by two studies from European cities, and from analysis of cardiac arrest events in Seattle, Washington from 1980 to 2000.33,34 Defibrillation is the definitive therapy for cardiac arrest caused by VF. Rapid, early defibrillation is a key step and the most important intervention likely to save lives. Survival rates are best when immediate bystander CPR is provided and defibrillation occurs within 3 to 5 minutes.35,36 A major obstacle to rapid, early defibrillation is that most cardiac arrests occur outside of the hospital, indicating a need for public health initiatives to improve early recognition of heart attack signs and symptoms.1 The widespread use of automated external defibrillators (AEDs) assists in making early defibrillation a reality by expanding the number of rescuers available to treat SCD. The AHA integrates the use of AEDs with basic life support skills because VF is the most common rhythm found in adults with witnessed, nontraumatic SCA.32,33


Defibrillators.

Defibrillators are the power source used to deliver the electrical therapy. Defibrillators typically include a capacitor charger, a capacitor to store energy, a charge switch, and discharge switch to complete the circuit from the capacitor to the electrodes. The capacitor charger converts power from a low-voltage source, such as direct current, to a voltage level sufficient for a shock. Portable defibrillators derive their power from a battery, which must be kept charged. Electrical output of defibrillators is quantified in terms of Joules (J), or watt-seconds, of energy.33

Defibrillators deliver energy to the electrode in either a biphasic or a monophasic waveform. Biphasic waveforms deliver current in a positive direction for a specific duration, and then reverse the current to a negative direction for the remaining discharge. A monophasic waveform delivers the current in one polarity or direction. Studies show that biphasic waveforms achieve shock success rates at lower energies, 150 J compared to 200 J, and produce less ST-segment change than shocks delivered with monophasic waveforms.37, 38, 39 Lower energy requirements reduce the size and weight of the defibrillator, which in turn increases public access to AEDs because they are easier to handle, less expensive, and more convenient.

Rapid defibrillation can be performed with manual, automatic, or semiautomatic external defibrillators. Well-trained personnel, often ACLS responders, who are able to interpret cardiac rhythms on a rhythm strip or monitor, must operate manual defibrillators. Automatic advisory or semiautomatic external defibrillators have been developed for use by first responders. AEDs are accurate and easy to use and, unlike standard defibrillators, have detection systems that analyze the rhythm and advise the operator to shock when VF/VT characteristics are determined. Thus, successful defibrillation can be achieved without requiring the operator to have rhythm recognition skills. AEDs are attached to the patient with the use of adhesive sternal and apex pads that are connected to a cable, allowing for “hands-free defibrillation.” AEDs were shown to help emergency personnel deliver the first shock on an average of 1 minute sooner than personnel using conventional defibrillators.40 Early defibrillation with an AED has been shown to significantly increase survival in both out-of-hospital and in-hospital cardiopulmonary arrests.32,41


Transthoracic Impedance.

The ability to defibrillate requires the passage of sufficient electric current through the heart. Current flow is determined by transthoracic impedance (TTI), or resistance to current flow, and the selected energy (Joules). If TTI is high, a low-energy shock may fail to produce sufficient current to defibrillate. The factors that determine TTI include energy setting, electrode size and composition, electrode-skin interface, number of and time between previous electrical discharges, electrode pressure, ventilation phase, and electrode placement.42,43

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Sudden Cardiac Death and Cardiac Arrest
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