Most dentists have witnessed a patient complaining of cardiac palpitations after administration of a local anesthetic with epinephrine or during forceful procedures. Frequently this is the result of benign dysrhythmias, such as extrasystoles (premature contractions), but they pass unnoticed because continuous ECG monitoring is usually not in place. Published guidelines for patient monitoring during sedation are consistent in requiring continuous assessment of oxygenation by pulse oximetry. This also provides continuous monitoring of pulse rate but not the specific rhythm, and guidelines for the use of ECG monitoring are less consistent. While stating that moderate and even deep sedation have minimal impact on cardiovascular function, the American Society of Anesthesiologists guidelines nevertheless require ECG monitoring for even moderate levels of sedation.16
This has no evidence-based scientific basis, but from the society's perspective, it is understandable. All monitoring systems used by anesthesiologists include electrocardiography, and any case scheduled initially for sedation may require instant conversion to a full general anesthetic. However, this requirement may be excessive for the dentist providing only moderate sedation, and guidelines published by the American Dental Association are more practical for the average moderate sedation–trained dentist.17
These guidelines do, however, require continuous ECG monitoring for deep sedation and general anesthesia, but its use for moderate sedation is suggested only for patients having significant cardiovascular disease. This would include patients who have known rhythm disturbances, including those managed with implanted pacemakers.
Legal controversies aside, there is an intangible reassurance provided by an ECG monitor that adds to that provided by periodic measurement of blood pressure and continuous pulse oximetry. This of course presumes the operator understands and can interpret electrocardiograms and is comfortable witnessing occasional benign dysrhythmias and the subtle mechanical nuances all monitors present during routine use. The precise interpretation of a particular dysrhythmia is not as important as recognizing that a disturbance is occurring and deciding whether it is compromising the patient's hemodynamic status. This will be our approach when addressing selected dysrhythmias and their management. A review of basic electrocardiogram interpretation has been published in a previous continuing education article in this journal.18
Bradycardia is defined as a heart rate of <60 beats/min, but symptoms normally do not arise unless the rate falls to <50 beats/min. Supraventricular bradydysrhythmias may be sinus or junctional in origin, or they may be caused by various degrees of atrioventricular block. In most cases, these events are vagally induced, but central nervous system depressants are potential culprits and may potentiate vagal activity when present. Hypoxemia can also be a common cause, and efforts should be made to investigate and correct this possibility.19
The precise diagnosis of the arrhythmia is not so important as evidence of hemodynamic compromise (hypotension) or ventricular ectopy (premature ventricular contraction [PVC]) due to ventricular escape. When either of these events is present, the bradycardia should be treated with atropine, as previously explained in the discussion of hypotension in this article.
If a bradyarrhythmia does not respond after 2 doses of atropine, a second or third degree atrioventricular block should be investigated. Second-degree type II and third-degree blocks are located below the atrioventricular node, where there is no parasympathetic innervation. Atropine is seldom effective for infranodal block, and these cases require EMS transport for eventual pacemaker insertion. If hypotension remains significant while awaiting EMS transport, the recommended treatment is epinephrine by continuous infusion titrated from 2–10 µg/min.19
This can be accomplished by adding 1 mL of 1
1000 epinephrine to a 500-mL bag of normal saline or 5% dextrose, which provides a concentration of 2 µg/mL. Titration with an infusion pump should commence at 1 mL/min with incremental increases guided by blood pressure and heart rate. An epinephrine infusion should be used only by those with advanced training and when continuous ECG monitoring and minute-by-minute blood pressure recording are in place.
Sinus and Supraventricular Tachydysrhythmias
Tachycardia is defined as a heart rate >100 beats/min, but usually it is not until rates exceed 150 that patients become symptomatic. Transient episodes of tachycardia are triggered most often by pain, stress, and vasopressors included in local anesthetic solutions. It may be an indication that the sedation being administered is not sufficient to manage the patient's fear. It is important to establish whether the tachycardia is secondary to pain, stress, or vasopressors or whether the tachycardia is truly cardiogenic, which may lead to hypotension or myocardial ischemia. This tachycardia is almost always controlled by the sinoatrial node and is called sinus tachycardia; a P wave precedes each QRS complex. Sinus tachycardia can also be an initial reflex response to hypoxia or hypotension, and these should be considered before further treatment. Once these possibilities have been attended, persistent tachycardia may cause the patient to complain of palpitations. In this case, intravenous fluids should be administered to support blood pressure in the event the rapid heart rate is attempting to sustain the blood pressure in a hypovolemic patient. If the episode continues, a selective beta-1 receptor antagonist, such as esmolol (Brevibloc), can be administered. Due to its relatively brief duration of action (T1/2 ~9 minutes), esmolol is generally administered as a bolus of 0.5 mg/kg over 2 minutes followed by a continuous intravenous infusion. For office use, we suggest it be titrated intravenously in 20-mg increments every 2–3 minutes until the heart rate declines to an appropriate level. There is no maximum dose published for esmolol, but 80–100 mg is a reasonable limit before determining it is ineffective. If the tachycardia does not respond to this dosage or recurs after the effects of esmolol have waned, EMS transport should be considered. Compared with nonselective beta blockers, such as labetalol, esmolol is less likely to produce bronchospasm, but it must nevertheless be used with caution in patients with chronic obstructive pulmonary disease or asthma. Esmolol should be used only by those with advanced training and only when continuous ECG monitoring and minute-by-minute blood pressure recording are in place.
Sinus and supraventricular tachydysrhythmias are distinguished from ventricular dysrhythmias by narrow QRS complexes. If P waves are not evident preceding the QRS, the rhythm is not sinus in origin and is described as supraventricular. These dysrhythmias include atrial flutter, atrial fibrillation, and supraventricular tachycardia. It must be emphasized that atrial flutter and fibrillation are fairly common chronic conditions that are usually well tolerated due to medications that control ventricular rate. They introduce concern only when ventricular rate accelerates or they present as a new onset.
In contrast to atrial flutter and fibrillation, supraventricular tachycardia is not a chronic condition, although a patient may have a history of paroxysmal episodes. An onset of supraventricular tachycardia is always a concern. It is generally more rapid, producing heart rates >150 beats/min, and can be distinguished from the others by its regular ventricular rhythm (ie, regular R to R intervals). A precise diagnosis can be challenging, but the important feature determining a need for treatment is hemodynamic instability, that is, hypotension. Although adenosine is regarded as the drug of choice for confirmed supraventricular tachycardia, a beta blocker, such as esmolol, is also an option.19
Furthermore, esmolol is also an option in treating symptomatic atrial flutter and fibrillation. For this reason, esmolol is an acceptable choice for managing any of the atrial tachyarrhythmias. Compared with sinus tachycardias, any of the supraventricular dysrhythmias that become symptomatic are a far greater concern, and EMS transport should be arranged as treatment is rendered.
Extrasystoles (Premature Contractions)
Extrasystoles are ectopic impulses that occur in addition to the underlying rhythm and occur in most individuals. By convention, the term contraction is applied to these extra impulses, although a true mechanical contraction may not always occur. The source of these ectopic impulses can be anywhere throughout the atria and ventricles: premature atrial contractions, premature junctional contractions, or PVCs. In general, they are all relatively benign rhythms, and any new onset may reflect some sort of stress response that should be addressed.
PVCs are distinguished from other extrasystoles by their bizarre and widened QRS complex. They are generally benign, but when they occur with considerable frequency, they do have a greater potential for complications than other extrasystoles. They may produce hemodynamic instability or lead to lethal dysrhythmias, such as ventricular tachycardia and fibrillation. The Lown criteria are used to classify PVCs according to their frequencies and patterns ().20
After myocardial infarction, Lown classes 3–5 have been found to be associated with a greater risk for conversion to lethal dysrhythmias, but this correlation has not been established for other patients.20
Nevertheless, a reasonable caveat is that treatment is unlikely necessary for PVCs having a uniform appearance, regardless of frequency, unless the patient becomes hypotensive. For classes 3–5, treatment and EMS transport are reasonable decisions.
Lown Classification of Premature Ventricular Contractions*
There are many antidysrhythmic drugs advocated for treating patients with PVCs, but lidocaine is the safest and least sophisticated to administer. It can be administered as a single 0.5- to 1-mg/kg dose and repeated every 5 minutes up to 3 mg/kg. Its influence will generally last 15–20 minutes, after which a continuous infusion of 1–2 mg/min is required if the condition persists. However, when a patient remains symptomatic after 1 or 2 incremental doses or the condition recurs after its effects have waned, EMS transport should be arranged.
Before electing to use lidocaine for PVCs, it is important to confirm that the underlying rhythm is not a bradycardia, in which the PVCs represent efforts at ventricular escape. In this case, atropine should be administered to increase the underlying heart rate. The ventricular escape beats will then hopefully subside.
Unlike ventricular fibrillation, ventricular tachycardia may not be accompanied by cardiac arrest. It can be distinguished from atrial tachydysrhythmias by wide QRS complexes and the absence of atrial waveforms. It is not uncommon for patients to remain relatively stable while experiencing this dysrhythmia, but it can deteriorate rapidly to cardiac arrest. EMS transport should be summoned immediately. Current advanced cardiovascular life support guidelines suggest procainamide, amiodarone, and sotalol as preferred agents, but lidocaine is still regarded as an acceptable alternative and can be administered in the identical regimen addressed for management of PVCs. If the patient develops chest pain or becomes hypotensive, synchronized cardioversion is recommended if available. The office team should prepare for cardiac arrest, should it occur. provides an algorithm approach for managing atrial and ventricular tachydysrhythmias.
Figure 4. Sudden-onset tachycardia algorithm. Current advanced cardiovascular life support guidelines provide several suggestions for managing tachycardias. Although lidocaine is not listed as the preferred agent for ventricular tachycardia, it is nevertheless (more ...)
Chest Pain: Angina/Myocardial Infarction
When any of the previously discussed complications become extremely severe, they can either strain the heart or compromise coronary perfusion to the point that the patient may experience an episode of angina pectoris. However, this form of chest pain is most likely to occur if the patient has preexisting coronary artery disease. The event may represent an episode of stable angina or a more serious event labeled acute coronary syndrome. To understand this difference, a basic understanding of the pathogenesis of coronary artery disease must be appreciated.
The fundamental defect in coronary artery disease is stenosis, or narrowing of the lumen of coronary arteries due to atherosclerosis. The condition is not acutely life threatening so long as the lesion remains stable and does not rupture. The patient may experience chest pain if cardiac stress suddenly increases because coronary “supply” is outweighed by myocardial oxygen demand. 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 cardiac stress is reduced by calming the patient and perhaps administering a dose of nitroglycerin.
A more serious consequence occurs when atherosclerotic lesions become unstable and rupture, producing the so-called “acute coronary syndrome.” In this case, coronary perfusion becomes even further compromised. Added to the preexisting stenosis, debris from fractured atherosclerotic plaques obstructs coronary flow more severely and 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 undergo necrosis, defined as myocardial infarction. Therefore, the acute coronary syndrome is produced by unstable atherosclerotic lesions and manifests as either unstable angina or myocardial infarction, described collectively as acute coronary syndrome.
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, a complete primary assessment that includes not only blood pressure and heart rate but also hemoglobin saturation via pulse oximetry should be performed. This will assure that adequate oxygenation is present. Regardless of these results, supplemental oxygen should be provided via nasal cannula (4 L/min) or nasal hood (6 L/min). 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, nitroglycerin (either a 0.3- or 0.4-mg tablet or a 0.4-mg spray) should be administered sublingually, provided that the systolic blood pressure is >90 mm Hg. Nitroglycerin dilates systemic veins and reduces venous return, that is, 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 (eg, hypotension, 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.
Nitroglycerin is contraindicated if the patient has taken an erectile dysfunction agent, such as sildenafil (Viagra) and vardenafil (Levitra), within 24 hours or within 48 hours if tadalafil (Cialis) is used.21
Furthermore, we must reemphasize the importance of assessing blood pressure before administering nitroglycerin to any patient. In some cases of myocardial infarction, nitroglycerin can produce a more significant drop in blood pressure. This is particularly true if the infarction involves the inferior wall and right ventricle.22,23
Although this diagnosis requires 12-lead ECG analysis, successful management of these particular infarctions is dependent on improving preload, which is reduced by nitroglycerin. Systolic blood pressure >90 mm Hg should be confirmed before administering each dose.
The actual criteria for need and timing for activation of EMS transport are not well established. The package inserts for nitroglycerin formulations instruct patients with angina pectoris to access EMS transport when 3 doses of nitroglycerin over 15–20 minutes fail to relieve symptoms. Pollack and Braunwald24
have suggested that EMS transport is indicated after administration of 3 doses of nitroglycerin over a 15- to 20–minute period for stable angina but only 1 dose if angina is deemed unstable. Current American Heart Association guidelines25
address only suspected acute coronary syndrome (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 preexisting 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 the dental treatment is completed. In contrast, patients having no prior history of angina or who require more than their usual 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 when possible.
With activation of EMS transport, the decision has been made that the condition is possibly an acute coronary syndrome, and aspirin (300 mg) should be administered. This is accomplished ideally by chewing and swallowing either 3 or 4 chewable, flavored baby aspirins (81 mg each) or a regular 325-mg tablet. 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 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, that is, a nitroglycerin-like effect. Although morphine is ideal and thus 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 and often. 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 .
Figure 5. Chest pain algorithm. It may be difficult to determine whether sudden onset of chest pain is an episode of stable angina or acute coronary syndrome. If the episode was provoked in a patient with a known history of ischemic heart disease and spontaneously (more ...)
Cardiac arrest is the absence of a pulse. In the office setting, the ECG status will most likely commence with ventricular tachycardia, which deteriorates to ventricular fibrillation. This can subsequently deteriorate further to asystole or pulseless electrical activity. Cardiac arrest is most often attributed to myocardial infarction but may also be triggered by other factors, such as sustained hypoxemia due to severe respiratory depression or airway obstruction.
Once primary assessment confirms cardiac arrest, EMS transport must be obtained immediately and the office team should commence cardiopulmonary resuscitation following the 2010 American Heart Association guidelines as instructed in all health care provider courses in basic life support.26
An exemplary office protocol is presented in . Ventilations should be performed using a bag-valve-mask device (eg, Ambu-Bag) attached to a 100% oxygen source. Chest compressions must be rapid (100/min) with pauses after 30 compressions to allow for 2 adequate ventilations. There is little excuse for the entire office staff not being certified in basic life support at the health care provider level on a regular basis (ideally on an annual basis). Definitive treatment requires electrical defibrillation as soon as it is available. The beneficial role of cardiopulmonary resuscitation likely rests in its modest influence on coronary perfusion and minimizing hypoxemia, which may sustain electrical activity until defibrillation is available. Supporting this concept are data illustrating greatest success when cardiopulmonary resuscitation is initiated immediately and is followed by defibrillation within 5–8 minutes of cardiac arrest. For offices equipped with automated external defibrillators, the device should be turned on and its instructions followed. If an automated external defibrillator is not available, the office team should concentrate on proper delivery of cardiopulmonary resuscitation until EMS transport arrives.
Figure 6. Office protocol for basic life support.26 This algorithm summarizes the actions that should be followed when a patient unexpectedly loses consciousness and primary assessment reveals no evidence of breathing. Unlike the American Heart Association guidelines (more ...)
Although many sedation and all general anesthesia providers train in advanced cardiac life support, it is essential to appreciate that the bulk of this curriculum benefits patient management during the prearrest and postarrest period. The actual success of resuscitation from cardiac arrest is predicated on an effective basic life support protocol, including early defibrillation. However, once basic life support measures are in place, providers may proceed according to the American Heart Association cardiac arrest algorithm.19
An abridged version of this protocol is provided in . Once an advanced airway is in place, chest compressions should no longer be interrupted. A single ventilation can be provided every 6–8 seconds while compressions continue.
Figure 7. Abridged version of the advanced cardiovascular life support cardiac arrest algorithm. When cardiac arrest is determined, the emergency medical service (911) should be alerted and cardiopulmonary resuscitation commenced immediately as presented in (more ...)