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    Inside Dentistry

    March 2011, Volume 7, Issue 3
    Published by AEGIS Communications


    Chest Pain

    By Daniel Becker, DDS

    The acute onset of chest discomfort is frightening to both the patient and the dentist. The patient’s discomfort may be the result of gastrointestinal reflux, bronchospasm, or other noncardiac conditions, but for safety’s sake it should be presumed related to coronary artery disease. In this case the condition is labeled angina pectoris. The event may represent an episode of stable angina or a more serious event labeled acute coronary syndrome (ACS). To understand this difference, a basic understanding of the pathogenesis of coronary artery disease must be appreciated.

    Ischemic heart disease is a condition in which coronary perfusion is inadequate for myocardial oxygen requirements. The fundamental defect is stenosis of the coronary arteries due to atherosclerosis and for this reason the condition is also referred to as coronary artery disease (CAD).

    Atherosclerosis produces a narrowing or stenosis of the coronary arteries. The condition is not acutely life-threatening as long as the lesion remains stable and does not rupture. The patient may experience chest pain if cardiac stress suddenly increases because the coronary “supply” is outweighed by myocardial oxygen demand (MVO2). These episodes of chest pain are regarded as stable angina and can be precipitated by the stress of dental treatment. The angina will dissipate when the cardiac stress is reduced.

    A more serious consequence occurs when atherosclerotic lesions become unstable and rupture producing the so-called ACS. In this case, coronary perfusion becomes even further compromised. Added to the pre-existing stenosis, debris from fractured atherosclerotic plaques obstructs coronary flow more severely, and the subsequent chest pain is described as unstable angina. This form of angina can occur at rest or with stress and may evolve to thrombosis with total occlusion of a coronary vessel. If this occurs, myocardial cells will begin the process of necrosis, defined as myocardial infarction. Therefore, ACS is produced by unstable atherosclerotic lesions and manifests as either unstable angina or myocardial infarction. Table 1 illustrates the distinctions among various coronary syndromes.

    Stable angina reflects a stable atherosclerotic lesion producing a constant degree of stenosis. Pain occurs when myocardial oxygen demand becomes excessive due to exertion or stress. In contrast, ACS occurs when the atherosclerotic lesion becomes unstable and ruptures. After disruption of a vulnerable plaque, patients experience ischemic discomfort (unstable angina) resulting from a more severe reduction of flow through the affected coronary artery. The flow reduction may evolve to a complete thrombosis causing myocardial infarction and may or may not be evident on an ECG tracing as an elevated ST segment; STEMI vs NSTEMI. In either case, serum markers are positive for myocardial cell necrosis. Patients who present with chest pain at rest or a new onset are presumed to be experiencing an ACS.

    The dentist can do little to improve coronary blood flow. Patient management must be devoted to reducing cardiac stress and subsequent myocardial oxygen requirement, which hopefully will render the compromised coronary perfusion adequate. When a patient experiences chest pain, perform a complete primary assessment that includes not only blood pressure and heart rate, but also hemoglobin saturation via pulse oximetry if available. This will ensure that adequate oxygenation is present. Regardless of these results, supplemental oxygen should be provided via nasal cannula (4 L/minute) or nasal hood (6 L/minute). Any benefit of supplemental oxygenation has not been established for patients who sustain normal hemoglobin saturation on room air, but short-term administration has no adverse effects. Comforting the patient may reduce stress-induced increases in heart rate and blood pressure. If pain persists, a single tablet of nitroglycerin (0.4 mg tablet) should be administered sublingually. Nitroglycerin dilates systemic veins and reduces venous return, ie, preload. This reduction in diastolic wall tension or stress may also allow improved coronary perfusion, especially in the subendocardial regions. Nitroglycerin can be repeated every 5 minutes until symptoms improve or side effects such as hypotension or reflex tachycardia occur. Hypotension is particularly troublesome because it could compromise coronary perfusion further, and reflex tachycardia increases myocardial oxygen demand. Although reclined patients are not likely to experience these problems, blood pressure and pulse should be assessed before administering each subsequent dose of nitroglycerin.

    The actual need and timing for activation of EMS transport are not well established. The package inserts for nitroglycerin formulations instruct patients to access EMS when three doses of nitroglycerin over a period of 15 to 20 minutes fail to relieve symptoms. Pollack and Braunwald1 have suggested that EMS transport is indicated after administration of three doses of nitroglycerin over a 15- to 20-minute period for stable angina, but only one dose if angina is deemed unstable. Current American Heart Association guidelines2 address only suspected ACS (unstable angina or myocardial infarction) and encourage immediate EMS transport. They do not address stable angina. However, it may be impossible for the dentist to ascertain if the condition represents a stable or unstable event, and personal judgment must be used regarding subsequent action. For a patient with pre-existing coronary disease, chest pain provoked by a particularly stressful intervention may well represent a typical episode of stable angina. In this case, the patient will respond nicely after a primary assessment or a single dose of nitroglycerin and could very well be sent home after their dental treatment is completed. In contrast, the patient having no prior history of angina—or one that requires more than a single dose to relieve symptoms—should be transported to an emergency department for further evaluation. In all cases, it is professionally courteous to inform the patient’s primary physician as soon as possible.

    With the activation of EMS transport, the decision has been made that the condition is possibly an ACS and 300 mg of aspirin should be administered. Ideally, this is accomplished by chewing and swallowing three to four baby aspirins. Platelet aggregation is a key factor during coronary thrombosis and the maximum antiplatelet influence of aspirin is achieved within 1 hour of administration. Nitroglycerin can be continued every 5 minutes provided that systolic pressure is at least 90 mm Hg and the heart rate is within normal limits. If pain is severe and persistent, an opioid (narcotic) can be administered. Opioids not only relieve pain and anxiety, but also reduce peripheral resistance (afterload) and venous capacitance (preload). This reduces myocardial oxygen demand, ie, a nitroglycerin-like effect. Although morphine is the conventional agent recommended, fentanyl and nalbuphine are acceptable alternatives. Opioids are more likely to produce hypotension if nitroglycerin has been administered and the clinician should monitor blood pressure carefully. An opioid should be considered only if an intravenous infusion is in place and the clinician is familiar with its use. A suggested algorithm for management of chest pain is provided in Table 2.

    The most feared sequel to an ACS is a lethal cardiac arrhythmia leading to cardiac arrest. If this occurs, the office team should administer cardiopulmonary resuscitation (CPR) as instructed in all healthcare provider BLS courses. Ventilation should be performed using a bag-valve-mask device (eg, Ambu-Bag) attached to a 100% oxygen source. Chest compressions must be rapid (100/minute) with pauses after 30 compressions to allow for two adequate ventilations. There is little excuse for the entire office staff not being certified in BLS at the healthcare provider level on an annual basis.

    Early cardiac arrest is due to ventricular tachycardia or fibrillation and definitive treatment requires electrical defibrillation as soon as it is available. The beneficial role of CPR likely rests in its modest influence on coronary perfusion, which may sustain electrical activity until defibrillation is available. Supporting this concept are data illustrating greatest success when CPR is initiated immediately and is followed by defibrillation within 5 to 8 minutes of cardiac arrest. For offices equipped with automated electronic defibrillators (AED), the device should be turned on and dictated instructions followed. While waiting for EMS to arrive, opioid increment may be considered if there is IV access.

    References

    1. Pollack CV Jr, Braunwald E. 2007 update to the ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: implications for emergency department practice. Ann Emerg Med. 2008;51(5):591-606.

    2. O’Connor RE, Brady W, Brooks SC, et al. Part 10: Acute Coronary Syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(Suppl 3):S787-S817.

    About the Author

    Daniel Becker, DDS
    Associate Director of Education BLS and ACLS Instructor
    General Practice Residency American Heart Association
    Miami Valley Hospital
    Dayton, Ohio


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