Emergencies

Automated External Defibrillators, Part 1 Introduction and Rationale

Dentistry Today June 1, 200311 Mins read1.6k Views

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Since August 2001, when Dentistry Today presented a series of articles on emergency cardiovascular care and the use of automated external defibrillators (AEDs), AEDs have become widely available for emergency use in the public sector. This 2-part series provides the most current information on the rationale and use of AEDs. Part 1 discusses types of cardiac emergencies, factors necessary for successful resuscitation from cardiac arrest, and the rationale behind the concept of early defibrillation. Part 2 will discuss available AEDs, how they are used, and their potential importance in dental practice.

Cardiovascular disease is the leading cause of death in the United States.^1-2 Of these deaths, approximately 1,000 occur daily as a result of out-of-hospital cardiac arrest.³ Most of these deaths are a result of ventricular fibrillation (VF).⁴ Though highly reversible with the prompt application of defibrillation, VF is otherwise fatal within minutes, even with the immediate provision of cardiopulmonary resuscitation.⁵ The overall survival rate of out-of-hospital cardiac arrest in the United States is estimated to be less than 5%.^2,6


Figure 1. Normal sinus rhythm (NSR).	Figure 2. Premature ventricular contractions (PVCs).

Figure 3. Ventricular tachycardia (V-tach or VT).	Figure 4. Coarse ventricular fibrillation (VF).

Figure 5. Fine ventricular fibrillation.	Figure 6. Myocardial contraction ceases (asystole, “silent heart”).

SUDDEN CARDIAC ARREST
Fifty percent of people in Western society with serious coronary artery disease (CAD) experience their first signs of the disease in a dramatic way—sudden cardiac arrest.⁷ The first sign of a progressive narrowing of the coronary arteries from a decades-long development of an atheroma (intra-arterial plaque) can be a rapid sequence of plaque rupture or erosion and formation of an occluding thrombus. This arterial obstruction leads to ischemia, an irritable myocardium, a sudden generation of ventricular fibrillation, collapse, and death. Whether the victim lives or dies at this point depends on whether the collapse has been witnessed; whether the people who respond are trained in basic life support, resuscitation, and defibrillation; and whether they access an emergency response system that can bring about early arrival of BLS (basic life support) and ACLS (advanced cardiovascular life support) resources.⁸

The heart is an organ composed of specialized muscle fibers (myocardium) that work synchronously to pump blood throughout the body. The right side of the heart pumps deoxygenated blood into the lungs; the left side pumps oxygen-rich blood into the systemic circulation. During systole, myocardial cells depolarize synchronously to produce ventricular muscle contraction, which increases intraventricular blood pressure until the pulmonic and aortic valves open and blood is ejected into the lungs or aorta. As blood is ejected from the heart, the intra-aortic pressure increases until it exceeds the pressure in the left ventricle and the aortic valve closes, ending systole. Diastole now starts, the ventricles refilling with blood. This process normally repeats itself 60 to 100 times a minute throughout the lifespan of the individual. The QRS complex is an indication of ventricular contraction (systole), while the interval between these complexes constitutes diastole (Figure 1).

Whenever normal function of the heart is compromised, signs and symptoms associated with decreased cardiac output are noted (eg, dusky skin color, cyanosis of mucous membranes, diaphoresis, and respiratory distress). If adequate blood supply to the cerebral circulation is maintained, the victim remains conscious, albeit exhibiting signs and symptoms of altered consciousness (eg, lightheadness and dizziness.) If cardiac output decreases significantly or ceases, consciousness is lost.

ACUTE CORONARY SYNDROMES (INCLUDING ACUTE MYOCARDIAL INFARCTION)
Though the mortality rate from coronary heart disease has steadily declined in the United States for the past 30 years, it remains the number one cause of death.⁷ Acute myocardial infarction (AMI, aka “heart attack”) occurs in approximately 1,100,000 Americans annually.¹ As described above, an AMI usually develops when a plaque ruptures and a blood clot forms in a coronary artery, compromising blood flow to a portion of myocardium—most commonly located in the left ventricle. Deprived of blood, these now ischemic myocardial cells can no longer function normally (contracting synchronously with other myocardial cells) to pump blood out of the heart into the systemic circulation. The heart has been weakened. The victim of an AMI usually retains consciousness, but exhibits symptoms associated with decreased cardiac output as well as complaining of retrosternal pain, described variably as crushing, burning, and constricting “like there is a heavy weight on my chest” and exhibiting the classical radiation patterns associated with AMI (eg, upper epigastric region, left arm, left neck, left mandible).

Immediate entry into the EMS (Emergency Medical Services) system (9-1-1) increases the likelihood of survival from this potentially life-threatening situation.⁹ Management of AMI in the dental environment follows the P-A-B-C-D protocol described for all emergency situations.¹⁰ P is position; A, airway; B, breathing; C, circulation; and D, definitive care. All are assessed and instituted as necessary. In the still-conscious patient, position is based on patient comfort (most persons with chest pain prefer to be upright), and A, B, and C are assessed as adequate. Definitive care (D) requires activation of EMS, monitoring of vital signs (every 5 minutes), and MONA: the administration of (M) morphine or, if available, nitrous oxide (50%) and (O) oxygen (50%), (N) administration of a dose (2 sprays on the tongue) of nitroglycerin unless contraindicated (eg, hypotension), and (A) one adult aspirin tablet (325 mg) to the patient. (Chewable aspirin is acceptable, as is pulverizing an aspirin tablet and placing it in water for the patient to drink.)¹¹

Figure 7. The adult chain of survival.

Figure 8. Defibrilation converts VF to a NSR.

AMI MAY PROGRESS TO CARDIAC ARREST
From 4% to 18% of AMI’s progress to cardiac arrest.¹² Ischemia makes the myocardium irritable and more likely to depolarize prematurely, provoking irregularities in the rhythm of the heart. Frequently noted at this time are premature ventricular contractions (PVCs) (Figure 2). In a PVC, the ischemic myocardium depolarizes prematurely, before the ventricles have refilled with blood following the previous contraction. No blood is ejected from the heart into the systemic circulation with a PVC, therefore no peripheral pulse is palpable. Cardiac output decreases and the symptoms described above increase in intensity. Since the majority of heartbeats are still normal, consciousness is retained, although at a diminished level (eg, “dizzy,” “lightheaded,” “faint”).

With prolonged ischemia the increasingly damaged area of myocardium may begin to initiate every heartbeat, a rhythm in which every beat is a PVC. This is ventricular tachycardia (also called V-tach or VT) (Figure 3). Although the heart is beating, blood is not being circulated (pulseless V-tach). Consciousness is lost, breathing ceases (respiratory arrest), and a palpable pulse is absent. Pulseless ventricular tachycardia is one form of cardiac arrest.

Immediate management includes positioning adult victims supine with their feet elevated slightly, managing the airway (head tilt—chin lift), assessing breathing (look, listen, feel) and delivery of 2 complete full ventilations, assessing circulation for not more than 10 seconds, and—in the absence of a palpable pulse—commencing chest compressions at a rate of 100 per minute in a ratio of 15 compressions to 2 ventilations.¹³ This will result in oxygenated blood being circulated to the myocardium and to the brain.

Since the myocardium receives its blood supply from the coronary arteries (which are branches of the aorta), the entire myocardium progressively becomes increasingly ischemic and increasingly irritable. Organized heartbeats cease as individual myocardial fibers depolarize in an increasingly chaotic fashion, producing a quivering of the heart (called coarse ventricular fibrillation, or VF) (Figure 4). With no cardiac output, but with the heart contracting chaotically up to 400 times per minute, the myocardium becomes progressively weaker, and the patient is closer to death (fine ventricular fibrillation) (Figure 5). Finally, myocardial contraction ceases (asystole, “silent heart”) (Figure 6).

It has been demonstrated that properly performed BLS can prolong the period of time the heart remains in VF and preserves functioning of both the heart and the brain.¹^4,15

SUDDEN CARDIAC DEATH
Fifty-two percent of deaths associated with acute coronary syndromes, including AMI, occur within the first hour following the onset of symptoms, prior to the victim reaching the hospital.⁷ In 17% of patients, ischemic pain is the first, last, and only symptom.16 Seventy to 80% of cardiac arrests occur in the home.¹⁷

With loss of consciousness, cessation of both breathing (respiratory arrest, apnea), and effective circulation (cardiac arrest), the victim appears lifeless (ie, “clinically dead”). However, cells in the body are still capable of metabolic activity. They continue to function, albeit with increasingly diminished effectiveness, until all remaining oxygen in the blood has been consumed, at which point biological (cellular) death occurs. Neurons in the cerebral cortex are the cells most sensitive to anoxia. Permanent neurological damage may develop following approximately 3 minutes of anoxia.¹⁸ Many adults in VF can survive neurologically intact even if defibrillation is performed as late as 6 to 10 minutes after sudden cardiac arrest, particularly if BLS is provided.¹⁵The term cardiopulmonary-cerebral resuscitation [CPCR] has been introduced to emphasize this important need.¹⁸ The period of time between clinical death and biological death offers a window of opportunity during which resuscitation (CPR) may be successful.

Successful resuscitation from cardiac arrest is dependent upon a number of factors, collectively termed the “Chain of Survival.”¹⁹ The adult chain of survival consists of 4 links: (1) early access to EMS (9-1-1); (2) early BLS; (3) early defibrillation; and (4) early ACLS (advanced cardiovascular life support) (Figure 7). The most important component in the chain is the elapsed time between collapse and the implementation of defibrillation^.20-22The shorter this time span, the greater the chance of successful resuscitation. The likelihood of successful resuscitation from out-of-hospital cardiac arrest decreases by approximately 7% to 10% per minute, even with the administration of effective BLS.²³

On arrival at the scene of a cardiac arrest, the initial rhythm found by paramedics in approximately 80% of adult victims is VF^23,24, though recent studies demonstrate that this number appears to be decreasing²⁵. In the absence of BLS and defibrillation, VF tends to convert to asystole within a few minutes. Electrical defibrillation is the most successful treatment for VF. Decreasing the time from collapse of the victim to defibrillation increases the likelihood that the initial rhythm noted will be ventricular tachycardia or coarse VF, both of which have a greater likelihood of successful conversion to a functional (perfusing) normal sinus rhythm. Delays in the administration of defibrillation increase the likelihood that the initial observed rhythm will be fine VF or asystole, neither of which has a significant chance of successful conversion to a functional rhythm.²⁶ BLS does not convert VF into a functional rhythm; however, BLS does appear to prolong the period in which the heart remains in VF, contributing to the preservation of both heart and brain function.^14,15

In VF, the myocardium is beating in a chaotic, uncoordinated manner. Defibrillation delivers an electric shock across the victim’s chest, traveling through the myocardium, depolarizing all myocardial fibers simultaneously, essentially “turning off” the heart. As repolarization occurs (myocardial fibers possess the property of automaticity), it is hoped that a more synchronous, functional rhythm such as NSR will develop (Figure 8).

SURVIVAL FROM OUT-OF-HOSPITAL CARDIAC ARREST
In the United States, fewer than 5% of victims of out-of-hospital cardiac arrest are resuscitated and survive to be discharged from the hospital neurologically intact.¹⁵ Restoration of a perfusing cardiac rhythm requires prompt implementation of BLS followed by defibrillation within a few minutes of the initial arrest. As noted, from the time of collapse until defibrillation, survival rates decrease at about 7% to 10% per minute. When defibrillation is delayed, survival rates decrease to approximately 50% at 5 minutes, 30% at 7 minutes, approximately 10% at 9 to 11 minutes, and 2% to 5% beyond 12 minutes.^23,24

Early defibrillation (shock delivered within 5 minutes of receipt of an EMS call) is a high-priority goal of EMS care.²⁷ Unfortunately, this goal is achieved only on rare occasion. Cities such as New York City and Chicago have EMS response times of 11.4 minutes and 16 minutes, respectively.28,29 Not surprisingly, survival rates from out-of-hospital cardiac arrest are quite low; 1.4% and 2.0%, respectively.

Significantly higher survival rates from out-of-hospital cardiac arrest can be obtained if the collapse is witnessed, which is likely to occur in the dental office. BLS and defibrillation are likely to be performed within minutes (if a defibrillator is available). In the setting of supervised cardiac rehabilitation programs, 90 of 101 victims (89%) were resuscitated (the highest rate ever reported for out-of-hospital cardiac arrest).³⁰

The desirable time interval from EMS call (9-1-1) to delivery of shock (less than 5 minutes) cannot be reliably achieved with conventional EMS services. Public Access Defibrillation (PAD) is a public health initiative that aims to shorten this interval by placing AEDs in the hands of trained laypersons throughout the community. It has been stated that PAD has the potential to be the single greatest advancement in the treatment of VF cardiac arrest since the development of CPR.31 Studies of PAD have demonstrated survival rates as high as 56%, twice those previously reported for the most effective EMS systems^23,32-34.

References

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