CC
A 57-year-old male with a history of hypertension, coronary artery disease (CAD), and hypercholesterolemia is referred to your office for evaluation of a biopsy-proved mandibular dentigerous cyst. The perioperative cardiovascular risk assessment includes recognition of risk factors such as a history of ischemic heart disease, heart failure, cerebrovascular disease, insulin-dependent diabetes mellitus, or renal insufficiency (preoperative serum creatinine ≥2.0 mg/dL). Risk stratification allows for evaluation of the risk of cardiac complication and for optimization before surgery.
HPI
The patient is diagnosed with a small dentigerous cyst of the posterior mandible.
The preoperative assessment includes inquiry into the patient’s cardiovascular system review. This includes any symptoms such as angina (the two major types of angina are stable angina, which occurs with exertion, and unstable angina, which occurs at rest), dyspnea, syncope, and palpitations; history of heart disease, including ischemic, valvular, or cardiomyopathic disease; and a history of hypertension, diabetes, chronic kidney disease, and cerebrovascular or peripheral artery disease. Positive symptoms or recent significant health events are indicators for additional preoperative questioning and testing. In addition, the patient’s metabolic equivalent of task levels (METs) in performing daily activities is necessary to ascertain functional status or capacity. One MET is defined as 3.5 mL of O 2 uptake/kg per minutes, which is the resting oxygen uptake in a sitting position. Typically, METs of 4 or higher (climbing a flight of stairs or walking up a hill), in the absence of cardiac complaints, preclude the need for further cardiac testing (gold standard is the cardiac stress test) for non–high-risk surgeries.
Risk assessment is not exclusively for patients with known cardiac disease because a significant number of patients have undiagnosed heart disease. The guidelines published by the American College of Cardiology (ACC)/American Heart Association (AHA) outline the algorithm for cardiovascular risk assessment in individuals undergoing noncardiac surgery.
The current patient denies any cardiovascular complaints, including chest pain, shortness of breath, and dyspnea on exertion. He reports that he is able to climb a flight of stairs without difficulty (MET > 4).
PMHX/PDHX/medications/allergies/SH/FH
The patient has a history of hypertension, CAD, and hypercholesterolemia, for which he has been taking medications for the past 15 years. He denies any history of previous myocardial infarction (MI), cerebrovascular accident, or recent hospitalization. (With a history of CAD, formal recommendations should be sought from the patient’s cardiologist regarding the holding of any antiplatelet therapy during the perioperative period.) The patient’s last physical examination was several months ago, when a number of minor adjustments were made to his medications. His past surgical history includes an appendectomy and cholecystectomy under general anesthesia without any perioperative complications. (A positive history of adverse events with anesthesia is significant in assessing the future risk of surgery under general anesthesia.) His medications include atenolol (a beta-blocker), lisinopril (an angiotensin-converting enzyme [ACE] inhibitor), atorvastatin (an HMG-CoA reductase inhibitor, a cholesterol-lowering medication), and aspirin. He has smoked one pack of cigarettes per day for the past 20 years and admits to a sedentary lifestyle. He has no symptoms of depression. (Depression is a common comorbid condition in patients with CAD and a well-documented risk factor for recurrent cardiac events and death.) His family history is significant for the death of his father at age 50 years from a massive acute myocardial infarction (AMI).
Examination
General. The patient is a moderately obese male in no distress.
Vital signs. Normal except for a baseline blood pressure of 155/88 mm Hg (stage 1 hypertension).
Maxillofacial: Minimal expansion of the buccal cortex of the left posterior mandible is noted.
Cardiovascular. The cardiovascular examination shows the following:
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Inspection : The chest wall appears normal. The point of maximum impulse is located at the normal position along the midclavicular line at the fifth intercostal space.
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Auscultation: No audible bruits are heard using the bell of the stethoscope. This portion of the examination includes auscultation for bruits at the neck (carotid), midabdomen (aorta), and lateral flanks (renal). (Audible bruits would be indicative of significant atherosclerotic plaques, suggestive of systemic atherosclerosis.) Auscultation of the heart reveals a regular rate and rhythm, no murmurs, normal S1 and S2 with no S3 (usually abnormal in patients >40 years old; common early finding of heart failure caused by left ventricular volume overloading or dilation) or S4 noted (caused by poor compliance and stiffness of the left ventricles).
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Jugular venous pressure: Within normal limits at 3 cm above the sternal angle. (Jugular venous distension is a sign of venous hypertension, most commonly secondary to right-sided heart failure.)
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Peripheral pulses and extremities: No edema of the extremities (a sign of heart failure) or clubbing of the nail beds (seen with chronic pulmonary disease). (The peripheral pulses are inspected for symmetry and strength. [Pulsus alternans denotes an alternating strong and weak pulse and may signify left ventricular heart failure.].)
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Fundoscopic examination: Bilateral retinal plaques (secondary to atherosclerosis) and arteriovenous nicking (secondary to hypertension). (Examination of the retinas is an important part of a complete cardiovascular examination because it allows direct visualization of the microvasculature. Cotton-wool spots or dot or blot retinal hemorrhages are signs of diabetic retinopathy.)
Pulmonary. The chest is bilaterally clear on auscultation. (With left-sided heart failure, blood backs up into the pulmonary circulation, causing “congestion” and the leakage of fluid from the pulmonary capillaries into the interstitium; this leads to pulmonary edema [“wet lung”], which is detected as rales or crackles on auscultation of the lungs.)
Imaging
Other than a panoramic radiograph, no other routine radiographic imaging studies are indicated for excision of a cyst under intravenous (IV) sedation. A preoperative chest radiograph may be obtained in select patients based on the history and physical examination findings. Routine preoperative chest radiographs in asymptomatic, healthy adults is not indicated.
In the current patient, the panoramic radiograph demonstrated a 2-cm × 2-cm unilocular radiolucency of the posterior mandible, consistent with a dentigerous cyst.
Labs and other tests
The preoperative laboratory tests for the evaluation of a patient with significant cardiovascular disease (CVD) should be done in conjunction with the treating primary care doctor, cardiologist, or both.
A variety of stress tests, in conjunction with electrocardiographic (ECG) monitoring, may be performed to further risk stratify higher risk patients undergoing intermediate- to high-risk surgery. The cardiovascular system is tested, or “stressed,” either with physical activity (walking on a treadmill) or pharmacologically using vasodilators (e.g., adenosine or dipyridamole) or inotropes or chronotropes (e.g., dobutamine), to test for any significant myocardial ischemia. Determination of cardiac function and risk stratification are based on the duration of exercise, any symptoms that develop, and the presence of ECG findings such as flipped T waves or ST-segment depression or elevation. In addition to the ECG portion, stress testing may include imaging with echocardiography or myocardial perfusion with labeled radioisotopes.
Echocardiography is a diagnostic test performed to assess cardiac structure and function. Several parameters can be estimated from echocardiography, such as the degree of valvular insufficiency or stenosis, wall motion abnormalities, and the ejection fraction. The ejection fraction is the percentage of the stroke volume that is expelled from the left ventricle with systole; the normal range is 55% to 70%. Left ventricular systolic dysfunction is defined by an ejection fraction of 40% or less. An echocardiogram is not routinely ordered unless the patient is having active or new cardiac complaints.
Cardiac catheterization is the gold standard for evaluating the coronary anatomy and assessing for the presence of significant atherosclerosis. However, it is not routinely recommended for preoperative assessment, given the invasive nature of the procedure, unless the patient has a significant abnormality on cardiac stress testing and it is recommended by the consulting cardiologist.
Evaluation of blood cholesterol levels is also important for assessment of future risks of cardiovascular events. The ACC recommends targeting the low-density lipoprotein (LDL) level at below 100 mg/dL in individuals with CAD or diabetes mellitus. However, the target LDL level may be below 70 mg/dL, depending on the patient’s comorbidities. The target high-density lipoprotein (HDL) levels are above 40 mg/dL for males and above 50 mg/dL for females.
The current patient’s most recent testing was done at his last physical examination several months ago. His total cholesterol was 190 mg/dL, LDL was 125 mg/dL, and HDL was 37 mg/dL. The basic metabolic profile was within normal limits. (Levels of potassium must be monitored in the patients with hypertension who are taking diuretics.) A treadmill cardiac stress test done within the past year did not reveal any signs of myocardial ischemia.
A 12-lead ECG revealed no abnormalities. (ECG is an invaluable tool for obtaining information on cardiac conduction, chamber enlargement, electrolyte disturbances, drug toxicities, myocardial ischemia, and infarction. Elevation of the ST segment is strongly suspicious of myocardial injury, whereas ST depression is suggestive of myocardial ischemia.)
Assessment
A 57-year-old male with a history of CAD, hypertension, and hypercholesterolemia, requiring outpatient removal of a dentigerous cyst under IV sedation anesthesia.
The treating cardiologist was contacted for perioperative risk assessment for an elective low-risk surgery. (Procedures of the head and neck are classified as being either low or intermediate risk.) He stratified the patient as intermediate risk for surgery with a recommendation to continue the existing atenolol regimen without interruption. He noted that the aspirin could be held preoperatively, if necessary, to minimize potential bleeding complications and then resumed after surgery. (A preoperative medical evaluation serves to assess the patient’s risk of morbidity and mortality in the perioperative period. There is insufficient evidence to support the use of beta-blockers in patients undergoing low-risk procedures; however, they are continued during the perioperative period in patients already on a beta-blocker regimen.)
Treatment
After discussion of the risks, benefits, and alternatives, the patient elected to proceed with the procedure. He was instructed to withhold all his morning medications with the exception of his blood pressure pills, which were to be taken with a small sip of water. The patient was also counseled on the benefits of tobacco cessation and improved dietary and exercise habits.
Surgery was carried out with the patient monitored using the American Society of Anesthesiologists (ASA) I standards for outpatient procedures. (ASA I monitoring includes ECG, blood pressure, heart rate, and pulse oximeter monitoring.) IV anesthesia was planned using a combination of midazolam (Versed) and fentanyl. Five minutes into the procedure, the ECG showed multiple unifocal premature ventricular contractions (the most frequent mechanism is localized reentry) at the rate of about 10 per minute. The patient’s oxygen saturation declined from 98% on room air to 92% with 4 L/min oxygen flow via a nasal cannula. His oxygen flow was increased to 8 L/min, resulting in improvement of the oxygen saturation to 97%. The patient then suddenly became noticeably agitated, tachypneic with shallow breaths, and tachycardic, with a heart rate of 135 bpm. (Agitation can be a sign of hypoxia.) The procedure was aborted, and all IV anesthetics were halted. His blood pressure now measured 90/45 mm Hg (hypotensive). His condition continued to deteriorate, with ST-segment elevation and multifocal premature ventricular contractions showing on the ECG. He remained tachycardic with persistent hypotension. The patient emerged from anesthesia and complained of chest tightness while putting his fist over his chest (a positive Levine sign; the patient places their hand over the sternal region because of the dull, aching, squeezing discomfort of ischemic chest pain). A diagnosis of AMI was suspected, and emergency medical services (EMS) was immediately activated. EMS personnel arrived within minutes and transported the patient to a local hospital.
A suspected AMI should be managed with use of the AHA’s adult Advanced Cardiac Life Support (ACLS) algorithm for ischemic chest pain. The primary goal is to reduce the risk of death and the extent of permanent cardiac injury associated with AMI. Immediate treatment should include administration of supplemental oxygen to an oxygen saturation greater than 90% (to increase oxygen delivery), along with 325 mg (NN) of chewable aspirin or aspirin per rectum (to inhibit platelet function and clot propagation). Sublingual nitroglycerin (vasodilator) is administered to increase coronary blood flow, which reduces cardiac ischemia and therefore pain. If there are no signs or risks of heart failure, 25 mg (NN) of metoprolol tartrate has been shown to have beneficial effects. A clopidogrel loading dose of 300 mg (NN) if the patient is age 75 years or younger (if older than 75 years of age, give a loading dose of 75 mg (NN)), in addition to aspirin, aids in reperfusion. If chest pain is not resolved after giving nitrates and other medical therapy, morphine should be administered intravenously. The routine administration of morphine to all patients with ST-segment elevation myocardial infarction (STEMI) has been shown to have no clear clinical benefit and may cause harm. The mnemonic MONA (morphine, oxygen, nitroglycerin, and aspirin) outlines this treatment. Vital signs and oxygen saturation should be monitored during these interventions. IV access should be initiated immediately for drug delivery. A 12-lead ECG, serum cardiac markers, serum electrolytes and coagulation studies, and a portable chest radiograph should be obtained as soon as possible. The decision whether to treat the patient with pharmacologic agents, including IV heparin, glycoprotein IIb/IIIa receptor inhibitors, direct thrombin inhibitors, and nitroglycerin, is based on the ECG findings and continuous clinical assessment. In the setting of STEMI, rapid assessment and transport to a cardiac catheterization laboratory are essential; the goal is a door-to-balloon time under 90 minutes for revascularization of the affected vessel or vessels. Therapy becomes less effective with each minute its delivery is delayed.
Complications
The most feared complication of an AMI is sudden death (most commonly caused by ventricular fibrillation or myocardial rupture). The immediate- and long-term sequelae of an AMI are related to the extent and location of the necrotic myocardial tissue. Subsequent inflammatory and electrical conduction abnormalities that lead to mechanical dysfunction of the heart can be variable in both chronology and severity.
Cardiac arrhythmias are commonly seen during an AMI. Infarction of specialized myocardial tissue, such as the sinoatrial node, atrioventricular node, or bundle branches, can lead to a variety of arrhythmias and conduction blocks. Ventricular fibrillation is a nonperfusing rhythm that needs to be rapidly identified and treated via the ACLS protocol.
Impaired myocardial function can cause failure of the heart to adequately pump blood into the systemic circulation, with subsequent congestion of blood into the pulmonary circulation, resulting in congestive heart failure. AMI may also lead to cardiogenic shock, which is defined as tissue hypoperfusion secondary to heart failure, resulting in decreased cardiac output and hypotension.
Ischemia or necrosis of specific anatomic locations may result in mechanical dysfunctions such as rupture of the papillary muscles, ventricular septal perforation, or rupture of the ventricular free wall and subsequent cardiac tamponade (usually resulting in death). Other long-term complications include pericarditis (inflammation of the pericardium) and thromboembolic events originating within the cardiac chamber secondary to endothelial injury, stasis of blood, and turbulent flow.
Discussion
The prevalence of CVD in the United States was updated in 2019 by the AHA reporting that 48% of people 20 years of age or older have CVD, which includes coronary heart disease, heart failure, stroke, and hypertension. It is estimated that cardiac deaths and MI occur in 0.2% (50,000 deaths) of all cases of surgery under general anesthesia annually. As the baby boomer population ages and the number of patients undergoing elective surgery increases, perioperative cardiovascular evaluation should be performed meticulously in patients at risk.
The causes of MI span a broad range of pathologic processes, including atherosclerosis with thromboembolic events, vascular syndromes, coronary aneurysms, primary and drug-induced coronary spasms (cocaine), severe conditions of oxygen demand with hypotension (aortic stenosis, sepsis), and hyperviscosity states (polycythemia vera). Signs and symptoms of AMI are not always evident. Approximately 20% of patients who sustain an AMI are asymptomatic and have retrospective positive ECG findings. This is particularly significant in patients with diabetes, who may not experience painful symptoms because of underlying peripheral neuropathy.
Studies have provided evidence that the use of beta-blockers reduces morbidity and mortality in patients with AMI and those in heart failure caused by left ventricular systolic dysfunction. By reducing the sympathetic drive to the myocardium (and hence workload), beta-blockers have been shown to reduce the rate of reinfarction and recurrent ischemia. In addition, ACE inhibitors, sodium-glucose cotransporter-2 inhibitors, hydralazine plus nitrate, and mineralocorticoid receptor antagonists have been proven to increase survival rates in patients with AMI.
With progressive ischemia and subsequent MI, the ECG findings include T-wave inversions (ischemia), ST-segment elevation (suggestive of acute myocardial infarct), ST-segment depression (nontransmural infarct or ischemia), and the development of Q waves (indicative of MI). The leads in which an ST-segment elevation occur correspond to the area of cardiac injury. On a 12-lead ECG, leads V1 through V6 are designated as the precordial chest leads, and leads I, II, III, aVL, aVR, and aVF are the limb leads. Whereas an inferior infarct commonly presents with abnormalities in leads II, II, and aVF, findings on leads V1 through V6 represent injury to the anterior wall.
Cardiac enzymes are plasma diagnostic markers released during myocardial necrosis. Based on the onset of injury, concentration, and metabolic half-life of the enzymes released, myocardial cell necrosis can be confirmed. In addition, the approximate time of infarction can be predicted. Several enzymes are used, including creatine kinase, creatine kinase–myocardial band (CK-MB), and troponin I or T. Creatine kinase and myoglobin are not specific to myocardial tissue and can be elevated from other causes. The CK-MB enzymes can also be found in skeletal muscles and are not as cardiac specific for myocardial tissue. Troponins T and I are currently the markers of choice for determining acute cardiac injury because they have higher cardiac specificity and are much more sensitive than the CK-MB enzyme. Troponin levels can be detected as soon as 4 to 8 hours after injury and may remain elevated until 5 to 9 days later. Myocardial muscle creatinine kinase isoenzymes are helpful in detecting reinfarction as levels typically peak at 24 hours, with a return to the normal range in 48 to 72 hours.
In summary, a thorough patient history and physical examination are essential in determining the general health and preoperative risk of the patient. This should be done in cooperation with the patient’s primary care physician and cardiologist when indicated. In the event of an AMI in the office setting, early detection of symptoms is critical ( Fig. 110.1 ). Management should follow ACLS guidelines, including defibrillation for indicated arrhythmias; early initiation of the appropriate pharmacologic agents; and timely transfer to the hospital setting, where continued medical therapy and cardiac catheterization can significantly increase the likelihood of patient survival.
