Evaluation and Management of the Cardiac Patient for Office Oral Surgery

In the (lental profession we are often asked to provide care for a variety of medically comnpromised patients. One of the more frequent anid challeniginig is the patient afflicted with organic hear-t disease, atherosclerotic coronary artery disease (ASCAD), or congenital heart disease. Throughlouit the course of dental surgical in.lalagement, a great deal of physiological and psychological stiess caIn be directed toward these patieints. Physiologicallv, this stress is trainslated into a Ielease of circulating catecholamines mlanifestiing in miany bodxy functional changes, all designed to prepaie the patient for the imminent traumatic experieince flight or fright synvdromie. One of the organ systems which responds mar-kedlv to this stimulation is the cardiovascular svstem (elevations in heart rate, cardiac output, etc.). CoIsequenitly, a thorough evaluation and uniderstainding of the patient's cardiac status is vitally iimportant in insuring the patient's well-being duiriing the dcental visit. Cardiac disease can be generally classified into three basic categories for our purposes: 1. Congenital heart defects 2. Congestive heart failure (CHF) 3. Coronary artery disease (CAD)

In the (lental profession we are often asked to provide care for a variety of medically comnpromised patients. One of the more frequent anid challeniginig is the patient afflicted with organic hear-t disease, atherosclerotic coronary artery disease (ASCAD), or congenital heart disease.
Throughlouit the course of dental surgical in.lalagement, a great deal of physiological and psychological stiess caIn be directed toward these patieints. Physiologicallv, this stress is trainslated into a Ielease of circulating catecholamines mlanifestiing in miany bodxy functional changes, all designed to prepaie the patient for the imminent traumatic experieinceflight or fright synvdromie.
One of the organ systems which responds mar-kedlv to this stimulation is the cardiovascular svstem (elevations in heart rate, cardiac output, etc.). CoIsequenitly, a thorough evaluation and uniderstainding of the patient's cardiac status is vitally iimportant in insuring the patient's well-being duiriing the dcental visit.
Cardiac disease can be generally classified into three basic categories for our purposes: 1. Congenital heart defects 2. Congestive heart failure (CHF) 3. Coronary artery disease (CAD) Congenital Heart Defects The incideence of congenital heart defects is approximately 0.8% of all live births wlhiclh represeints 8 cases per 1,000 babies.' About .50% of' all defects present without cvaInosis, 25% with cyanosis, aInd 25% withl cliinical signs of obstructioin to 1)1ood flow that max or may inot result in lhvpoxia anId cyanosis. Shuintiing of blood througlh the septal defect caIn lead to hvpoxemia if the 10lood is directed froimi the riglht side of the heart to the left. This results in 1)lood0 bypassing the lungs without becomiing oxygenated. Small defects imax go unnoticed for many years and are usually physically well tolerated until the right heart develops hNipertrophy and congestive failie. The septalldefect mayx also slhuint blood fi-romi the left ventricle to the riglht ventricle iresultinig in left hear-t hvpertrophy, pulmoniar-y hypertensioin, anid subsequentlv left oI right heart failure.
Valvular defects, primarily aortic ancd mitial stenosis, can lead to elevated pressures in the left ventricle and left atriulm, respectively. Oftein the only symptom is gradually decreasing exercise toleiaince over several years. As the valvular disease pIrogresses, harsh murmurs develop indicating albormal blood currenits (i.e., Eddy waves). If sutddein death due to a rupture of a valve leaflet or papillary mulscle does not occur, the progression of valvular defects usuallv leads to congestive heart failuire.

Congestive Heart Failure
This entitv is defined as a functioinal state in which the heart is unable to meet the needs of the other organ systems, even as compensatory mechanisimis are at work. The causes of heart failure can be grouped into: 1) those resulting in the need for increased stroke volume, cardiac output, or impedaince to ejection, such as pulmonarv or systemic hvpertension; 2) those causiing abnormalities in coontractile functioni of the mivocardium, such as in cardiomvopathv; and 3) those causiIng restriction in fillinig suichi as valvular obstruction, or ventricular/peiricairdial stiffniess following mvocardial infarction.-A patieint with congestive heart failure often has a varietv of symptoms rangiing from dvspnea at rest, wheeziing or congested lungs in severe cases, to dvspnea only on mild exertion and a "chronic cigarette coughi." The term cardiac insufficiency is the most actcurate description of the milder form of failure.
Most patients with a history of cardiac disease requiring prior hospitalization will be oIn iiitltiple drugs. These usually include a diuretic (e.g., lasix), a cardiac glvcoside (e.g., digoxin), andI additional med-ications to control hypertension or arrlvlthmias. Clinically, these patients mav prese!-it. with anv combination of the following phvsicai findings: shortness of breath, orthopnea in the dental chair (inability to breathe in the supine position), various cardiac arrhythmias, pedal edema, cool and pale skin, and moist bronchial rales. Radiographicallv, on chest x-rav, there may be an enlargement of the cardiac silhouette (Kerlev-B-lines, and cephalization of vasculature). 3 A review of the patient's present medications is verv helpful, and mav lend important information as to the progress of the disease. Every drug that a patient is presentlv taking should be recor(led bv name and dosage and updated on a regular basis at subsequent visits. Cardiac glvcoside administration usuallv indicates moderate to serious myocardial disease. Diuretics including lasix and spironolactone drugs are given for mild to moderate hypertension, but mav be used with digoxin for congestive heart failure. Dental patients should continue these medications the day of treatment. The pulse rate and rhvthm ar-e important to monitor preoperativelv and during the surgical procedure.

Coronary Artery Disease
This is a general term describing the inability of the coronary circulation to meet the required oxygen demands of the myocardium. The clinical manifestations of the disease are in the form of a varietv of complaints including exertional or non-exertional chest pain (angina pectoris) and/or tightness of varying intensity, duration, location, radiation, and quality, as well as associated symptoms such as nausea, vomiting and diaphoresis.
There are four types of angina pectoris associated with myocardial ischemiastable, unstable, preinfarction, and Prinzmetal angina. Approximatelv one-third of the patients with Prinzmetal angina (pain at rest) have no atherosclerotic arterial changes seen on angiography. This entity is supposedly caused by a coronary artery spasm and can occur at any time under any conditions, including non-stressful situations. Prinzmetal angina usually develops in the second and third decades of life and can be associated with sudden cardiac arrest. The greatest problem in the pre-surgical evaluation of what appears to be angina pectoris (AP) is its differentiation from other medical problems (Table 1).
The major difference between classical AP and GI disorders is that the former is usuallv brought on bv a fixed amount of exertion and subsides with rest, a pattern which seldom fits the latter. Musculoskeletal pain is usually slow in onset, of a longer duration, and duller in character.4 Pressure or bodily movement over the area intensifies this type of pain, but it must be kept in mind that AP has a wide variety of clinical presentations and is especially difficult to evaluate in the poor historian. Stable angina can be described as chronic, occurring predictably with exertion and alleviated quickly with rest and/or no more than three .4 mg nitroglycerine tablets sublingually on any one occasion. There is usually some event, such as exertion, overeating, or emotional upheaval that triggers the onset.
Unstable angina occurs while at rest, is not predictable in terms of precipitating factors, is triggered with minimal effort and lasts progressively longer than the stable type. If either the stable, unstable, or Prinzmetal types of angina seem to last longer, are more intense accompanied by hypotension and cardiac arrhythmias, a pre-infarction angina should be suspected. The treatment of the cardiac patient with dental pathology begins well before the actual surgery is contemplated, with the establishment of good rapport, reassurance, and good planning. Following the acquisition of the medical history, the patient should be classified according to the severity of the organic heart disease. Four classifications extending from the most benign to borderline complete heart failure have been proposed by the New York Heart Association.4 Class I patients that do not require special medicationssome clinical evidence of coronary artery or valvular disease disclosed bv tests as sophisticated as angiography to organic murmurs heard by chest auscultation are usually managed without any special precautions (except for antibiotic prophylaxis for patients with valvular heart disease).
Class IV patients with severe impairment of normal functional activities such as walking, household duties and require frequent rest periods should be treated in a hospital setting for even minor elective procedures. Class II and III patients vary from those taking multiple medications to patients who have cardiorespiratory impairment during recreational activities. These patients generally require more specialized care such as cardiac monitoring, and good pain control and sedation (as indicated) to reduce myocardial oxygen requirements while not compromising the blood pressure and respiration. Care must be exercised to adjust the dental chair in a semireclining rather than flat or full supine position that may impair breathing or increase the blood volume and cardiac work of the heart. Patients should continue their medication without interruption on the day of treatment and sublingual nitrates used prophylactically only if the patient is experiencing angina from anxiety of dental treatment. Exogenous vasoconstrictors are tolerated in low dosages with local anesthetics but even 3-4 ml of 1:100,000 dilution of epinephrine can increase serum catecholamine levels. For this reason, blood pressure and pulse rates and rhythm are recommended every 5 minutes for 20 minutes after injection. This may be done by the "floating" dental assistant or nurse who is free to take the vital signs.

Evaluation of Vital Signs
Blood pressurea baseline pressure immediately when a patient arrives at the office is more important than after resting comfortably in the chair or waiting room. This evaluates the cardiovascular response to stressful activities leading up to the patient's arrival which may even include the frustration of automobile traffic or just finding the office or a parking space. If an initial recording of greater than 140/90 decreases to below these values after resting, labile or unstable hypertension should be suspected. When compared to a patient who is consistently above 140/90 before and after stressful situations (stable hypertension), the labile patient will likely have extreme fluctuations in blood pressure with sympathetic stimulation from anxiety or catecholamine release.
Hvpotension during a procedure should not exceed 20-30% of the baseline systolic or diastolic pressures. If a drop in blood pressure occurs, treatment should be conservative including changing the chair to a Trendelenburg position (head down), intravenous fluids and oxygen by mask. Care should be exercised to prevent the administration of excessive fluids (i.e., dextrose in water or lactated Ringer's solution). A maximum of 5 ml of fluid per kilogram of body weight on a patient with heart disease can be given to help correct hypotension. More aggressive therapy should include ephedrine 12-25 mgm intravenously or intramuscularly. On the other hand, hypertension is best managed initially with cessation of the procedure. Administration of mask oxygen (not nasal cannula), and small amounts of intravenous analgesics titrated to control pain. Nitrous oxide, 35-50%, is very useful in the treatment of pain-induced hypertension. Several cases of hypertension (i.e., 220-260/110-140) have been managed initially, to relax the patient, by nitrous oxide analgesia with good success.

Pulse
Preoperative pulse rate and rhythm should be recorded prior to local anesthesia. Slight intraoperative changes are expected, but particularly in patients taking beta-adrenergic blocking agents, excessive rises in heart rate can cause mvocardial ischemia. A simple but practical formula of svstolic blood pressure times heart rate (rate-pressure product) can be a useful guide to ischemia in cardiac disorders. If the product is greater than 12-14,000 (i.e., 140 rate and 100 systolic pressure), undesirable increases in myocardial oxygen consumption are likely to occur. Conversely, bradycardia in a cardiac patient usuallv indicates either drug toxicitv, heart block, or hypoxia. The level of consciousness will be helpfuil in deciding whether treatment with fluids and vasopressors is required.
Arrhvthmias which mav develop, re(quire rapid recognition with the aid of an electrocardiograph and treatment. Generally speaking, supraventricular arrhythmias are usually hemodynamically insignificant compared to the ventricular ones, unless the ventricular response to the supraventricular rhythm is such that left ventricular filling is decreased and oxvgen demands are not met. This can be seen with atrial flutter (rate 300) with 2:1 block giving a ventricular rate of 150 which is too fast to allow proper filling. This type of arrhythmia re(uires early management with initial administration of edrophonium chloride 5-15 mgm intravenously, a short-acting parasvmpathomimetic which increases vagal activitv and slows the heart rate. Some patients may need rapid digitalization. If the arrhythmia is refractory to these treatments, one may consider cardioversion at 40 watt-seconds, direct current shock with a cardiac defibrillator to correct the atrial arrhythmia. Ventricular arrhythmias are almost alwavs more life-threatening, and these include frequent premature ventricular contractions, ventricular tachycardia, and ventricular fibrillation. Occasional premature ventricular contractions (pvc's) are usually benign unless occurring at a rate greater than 6 pvc's per minute as documented on electrocardiogram. If ventricular tachycardia develops, it should be treated with lidocaine 1 mgm/kgm intravenously followed by a continuous drip of 1-4 mgm/minute and transportation of the patient to the nearest emergency room.
Cardiac monitoring with standard leads is the best way to continuously evaluate pulse rate and rhvthm. But, with a minor adjustment in the placement of leads,5 the rhythm strip can also depict any changes in ST segments and T waves, which can reflect myocardial perfusion abnormalities such as myocardial or endocardial ischemia, or myocardial infarction.
Electrocardiographic monitoring is often advisable even for minor surgical procedures in the cardiac patient. The anterior, inferior, and lateral myocardium can be evaluated simply by shifting the classical standard three leads across the chest. These modifications significantly increase the amount of information obtained from cardiac monitoring, and improve our ability to properly manage the cardiac patient. The normal placement of the chest leads is shown in the diagram (Fig. 1). Bv cwvitching the leads in any of the three positioIns (Figs. 2, 3 and 4), the anterior, inferior, and the lateral mvocardial areas can be monitored. The anterior mvocardium can be seen by lead placement (Figs. 2 and 3) and the inferior-lateral areas (Fig. 4) with the ECG monitor switched to lead 2 position. rents can be seen. The advantage of this lead arrangement is the chest leads do not need to be shifted around as in the previous monitoring pattern. Both mvocardial ischemia and cardiac arrhythmias can be seen with either setting. Since ischemia is more commonlv seen in the antero-lateral mvocardium than in the inferior myocardium the modified V5 lead is most helpful."The following case illustrates the electrocardiographic pattern using the lead positioning in Figure 4.   Niodlified chest lead po1sitioni to moniitor lateral invocardiollm (NICL 5) imlonlitor selector on1 lead 2.
If the patient needs to have simultaneous monitoring of the anterior and lateral myocardium, lead placement in Figure 4 is most useful. With the monitor on lead 2 and the chest leads in Figure 4, electrical current from the inferior myocardium can be seen. By changing the switch on the cardiac monitor to lead 1, the anterior and lateral myocardium cur- A 52-year-old female with a previous history of anterolateral myocardial infarction in October, 1981, presents for major oral surgerv. She has a continual, unstable angina and is taking nitroglycerine as necessarv. In the modified V) lead position the QRS height, p wave configuration, and the ST segments are slightlv different from the conventional lead 2 position. With the history of anterolateral myocardial infarction, this lead pattern should be monitored continuously. Lead 2 can also be readily obtained should an inferior myocardial ischemia or a cardiac arrhythmia occur. Summary The cardiac patient represents a significant proportion of the medically compromised patient population. Consultation with the patient's cardiologist is advisable. The general dentist involved in their care should also be well versed in their proper eval-uation and management in order to provide safe, effective treatment and avoid serious complications. An overview of our approach has been presented.