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© Springer Nature Switzerland AG 2021

R. Reti, D. Findlay (eds.)Oral Board Review for Oral and Maxillofacial Surgerydoi.org/10.1007/978-3-030-48880-2_13

13. Cardiovascular Disease

Damian Findlay1  , Gregory S. Tentindo1 and Robert Reti2

Oral Facial Surgery Institute, St. Louis, MO, USA

Southwest Oral Surgery, St. Louis, MO, USA

HypertensionIschemic heart diseaseAcute coronary syndromeCongestive heart failureValvular heart diseaseOrthotopic heart transplantMetabolic equivalents (METS)Angina


  • Persistently elevated arterial blood pressure of 130/80 or mm or higher Hg in adults.

  • Diagnosed by 2 elevated readings of at least 130/80 mmHg on 2 or more visits.

  • American Heart Association (AHA) and American College of Cardiology (ACC) update to the JNC 7 Classification [1]:

    • Normotension <120/80 mmHg

    • Elevated 120–129/<80 mmHg

    • Stage I 130–139/80–89 mmHg

    • Stage II >140/90 mmHg

Essential Hypertension (HTN)

  • Hypertension with no identifiable cause.

  • 90% of patients diagnosed with HTN have essential HTN [2].

  • Associated with the following defects:

    • Decreased vascular response to vasodilators such as prostaglandins and nitric oxide.

    • Renal defect which leads to retention of sodium chloride.

    • Increase in sympathetic tone.

    • Neural reflex defects.

    • Increased angiotensin II and renin secretion.

  • Risk factors associated with hypertension include the following:

    • Obesity and sedentary lifestyles

    • Diabetes

    • Alcohol

    • Aging

    • Smoking

    • OSA

    • Family history

    • Ethnicity (African American)

    • Sex (Males have higher rates of HTN)

Secondary Hypertension

  • Hypertension with an identifiable cause. Examples include the following:

    • Pheochromocytoma

    • Renal artery stenosis

    • Polycythemia vera

    • Cushing syndrome

    • Coarctation of the aorta

    • Hyperaldosteronism

    • Pregnancy

    • Renal parenchymal disease

  • Sequelae of untreated/poorly controlled hypertension (result of end organ damage):

    • Left ventricular hypertrophy

    • Ischemic heart disease

    • CHF

    • Renal insufficiency

    • Retinopathy and vision loss

    • Cerebrovascular accident

    • Peripheral vascular disease

Treatment of Hypertension

  • Secondary hypertension – treat underlying cause.

  • Lifestyle modification – weight loss, smoking cessation, decreased in sodium intake, exercise, and reducing alcohol consumption.

  • Pharmacologic therapy:

    • Calcium channel blockers – decrease the influx of calcium ions resulting in vasodilation and a reduction in blood pressure (e.g., amlodipine, felodipine, diltiazem, verapamil).

    • Ace inhibitors – block the conversion of angiotensin I to angiotensin II (AII). AII is responsible for vasoconstriction and liberating aldosterone. Inhibiting vasoconstriction and decreasing the effects of aldosterone results in a reduction in blood pressure (e.g., lisinopril, fosinopril, enalapril, captopril, ramipril).

    • Angiotensin II (AII) receptor blockers (ARBs) – block the effects of AII through antagonism of AII receptors leading to decreasing vasoconstriction and aldosterone secretion. (e.g., losartan, valsartan, olmesartan, telmisartan).

    • β-blockers  – block β-adrenergic receptors resulting in a decrease in myocardial contractility, decrease in renin production, and relaxation of smooth muscles (e.g.,metoprolol, atenolol, esmolol, carvedilol, labetalol).

    • Thiazide diuretics – block the reabsorption of NaCl in the distal convoluted tubule of the nephron leading to a contracted intravascular volume (e.g., hydrochlorothiazide, chlorthalidone).

    • Vasodilators – work by decreasing vascular smooth muscle tone (e.g., hydralazine, sodium nitroprusside).

    • Alpha-2 adrenergic agonist – works on central adrenergic receptors leading to decreased norepinephrine release (e.g., clonidine).

    • Direct renin inhibitor – prevents renal release of renin with a subsequent decrease in AII production (e.g., aliskiren).

Patient Management

  • Obtain recent labs/studies to assess end organ damage (BUN/Creatinine, EKG, CBC).

  • Defer elective surgery if preoperative blood pressure is not controlled. Refer immediately to physician for hypertensive urgency (BP >180/120 with no signs/symptoms of end organ dysfunction). Patients are treated with oral antihypertensives with gradual reduction of BP over the course of a few days.

  • Metabolism of amide anesthetics can be reduced in patients taking beta-blockers [3].

  • Monitor blood pressure closely and be prepared to treat intraoperative hypertension and hypotension:

    • Ephedrine and phenylephrine are commonly used to treat hypotension. Be cautious of the reflex bradycardia with phenylephrine usage.

    • Patients taking antihypertensives should continue their medications. Know side-effect profiles of the antihypertensives that the patient is taking.

    • A basic metabolic panel should be taken on patients taking ARBs and ACE inhibitors to rule out hypokalemia.

    • Patients taking ARBs and ACE inhibitors are more prone to anesthesia-induced hypotension.

    • Monitor EKG intraoperatively to rule out myocardial ischemia.

    • Use local anesthesia with a vasoconstrictor judiciously based on recommendation of 0.4 mg of epinephrine according to the AHA recommendations.

    • Anxiolysis to reduce stress-induced hyper-tension.

    • Monitor for signs/symptoms of orthostatic hypotension due to antihypertensive medications.

    • Avoid medications that increase sympathetic tone (e.g., ketamine).

    • Contact EMS for evidence of a hypertensive crisis (BP 180/120 with signs/symptoms of myocardial ischemia, bradycardia, hypertensive encephalopathy, dyspnea, chest pain, confusion, nausea/vomiting, headache, seizures, and pulmonary edema). Hypertensive crisis- BP is gradually reduced to not lead hypotension and subsequent myocardial ischemia and cerebrovascular ischemia.

Atherosclerosis and Ischemic Heart Disease


Hardening of the arteries due to lipid accumulation within the arterial wall.

Risk Factors

  • Genetics – familial hyperlipidemia due to a mutated low density lipoprotein (LDL) receptor.

  • Dyslipidemia – Having a total cholesterol of 240 mg/dl increases the risk of a coronary event [2]. Elevated LDL levels correlate with an increased incidence of atherosclerosis and coronary artery disease (CAD). Elevated high density lipoprotein (HDL) levels correlated with being protective against atherosclerosis and CAD.

  • Tobacco – enhances oxidation of LDL, causes endothelial dysfunction, and causes increased platelet adhesiveness.

  • HTN – damages the endothelium which leads to increased permeability to lipoproteins.

  • DM – nonenzymatic glycosylation of LDLs increases the antigenicity of LDLs.

  • Metabolic syndrome – cluster of HTN, hyperlipidemia, insulin resistance, and abdominal obesity.

  • Lack of physical activity.

  • Estrogen status – Physiologic estrogen levels raise HDL and lower LDL. Menopausal women are at an increased risk for ischemic heart disease (IHD).

Pathophysiology of Atherosclerosis

  • Damage to the endothelium occurs.

  • Lipoproteins then traverse the intima and leukocytes are recruited via chemotaxis. Macrophages imbibe LDL to form foam cells.

  • Smooth muscle cells of the media layer secrete an extracellular matrix that traps the lipoprotein and gives bulk to the lesion.

  • This matrix gives rise to the fibrous cap. As the lesion increases in size, the fibrous cap thins. Rupturing of the fibrous cap, leading to exposure of the thrombotic lipid core, which is now exposed to the blood. This may lead to an acute coronary syndrome (ACS).

Complications of Atherosclerosis

  • Embolization of an atherosclerotic plaque to distant sites and can cause infarction of the affected organ (e.g., CVA).

  • Weakening of vessel walls that may lead to aneurysm formation.

  • Peripheral artery disease.

  • Renal artery stenosis.

  • Myocardial infarction.

Ischemic Heart Disease (IHD)

  • Disease process secondary to stenotic coronary arteries that leads to ischemic sequelae from a myocardial oxygen supply and demand imbalance.

  • Myocardial oxygen is dependent on oxygen supply and coronary blood flow. Myocardial oxygen demand is determined by wall stress, heart rate and contractility.

Consequences of IHD

Stable Angina

Transient chest discomfort due to a fixed atheromatous plaque secondary to a myocardial oxygen supply and demand imbalance.

  • Symptoms include dyspnea on exertion, retrosternal chest pain that may radiate to the arm or jaw. Patients will often describe the symptoms as a pressure or an elephant sitting on their chest. Patients may place a clenched fist over the sternum (Levine’s sign). Symptoms normally appear when a vessel is at least 70% stenotic. The symptoms normally cease after 5–10 minutes with rest.

  • Diagnostic workup – EKG may show ST depression or T wave inversion. Stress testing is done (bike, treadmill, or pharmacologic) to assess cardiac reserve. Pharmacologic testing may be carried out with dipyridamole thallium in persons unable to exercise. Echocardiogram is used to assess wall function, ejection fraction, and valvular function. Coronary angiography is used to assess stenotic coronary arteries (gold standard).

Acute Coronary Syndrome

Disease processes along a continuum secondary to a ruptured atherosclerotic plaque with subsequent formation of a thrombus within the coronary vessel.

  • Unstable angina occurs secondary to a coronary thrombus that is partially occlusive. Patients have chest pain that is not relieved by rest. Can see signs of ischemic changes on an EKG with negative cardiac enzymes.

  • Non-ST segment elevation MI – due to partially occlusive thrombus that results in a subendocardial infarction. Patients present with chest pain, nausea, dyspnea, and diaphoresis. EKG shows ST depression or T wave inversion. Will see elevated serum biomarkers such as troponins and CK-MB. (CK-MB is used to assess for early reinfarction due to its shorter half-life in comparison to troponins.)

  • ST segment elevation MI due to an occlusive thrombus that results in a transmural infarct. Will see ST segment elevations and serum biomarkers. Symptoms similar to NSTEMI.

Complications of MI (STEMI or NSTEMI) –may lead to fatal arrhythmias, conductions blocks, cardiogenic shock, ventricular wall rupture, and heart failure.

Treatment of IHD

  • Nitrates – cause venodilation, which decreases preload (determinant of wall stress) and dilates coronary arteries.

  • Beta-blockers and calcium channel blockers decrease oxygen demand by decreasing heart rate and contractility.

  • Ranolazine – inhibits sodium channels in myocardial cells, which leads to less intracellular calcium and decreased contractility.

  • Percutaneous coronary intervention balloon-tipped catheter is placed in a peripheral artery and maneuvered into the stenotic coronary vessel. A bare metal or drug eluting stent is then deployed to increase the patency of the coronary vessel. Patients are placed on antiplatelet drugs to decrease coronary thrombosis, as the stents are thrombogenic (drug-eluting stents are more thrombotic than bare metal stents). Drug-eluting stents decrease the rate of epithelialization.

  • Coronary artery bypass grafting (CABG) grafting done to bypass obstructive coronary vessels. Preferred for multivessel disease.

Treatment of MI

  • Morphine used for analgesia and anxiolysis.

  • Oxygen – increases oxygen supply to the myocardium.

  • Nitrates – improve coronary flow.

  • Aspirin decreases platelet aggregation.

  • Beta-blockers – decrease myocardial oxygen demand.

  • Transfer to hospital (remember time is myocardium) for PCI with stent deployment or fibrinolytic therapy if the hospital does not have interventional cardiology capabilities.

Treatment Used to Prevent Recurrent Episodes

  • Beta-blockers decrease myocardial oxygen demand and contractility via antagonism of beta-adrenergic receptor. Beta-blockers also increase the amount of time spent in diastole, which is the phase when coronary perfusion occurs (e.g., metoprolol, carvedilol, labetalol).

  • Calcium channel blockers decrease myocardial oxygen demand and contractility via antagonism of calcium channels. Calcium channel blockers increase the amount of time spent in diastole, which is the phase when coronary perfusion occurs (e.g., amlodipine, nifedipine, verapamil, diltiazem).

  • Nitrates – cause venodilation, which decreases preload (determinant of wall stress) and dilates coronary arteries (e.g., isosorbide mononitrate, isosorbide dinitrate).

  • ADP receptor inhibitors – decrease ADP activation of platelet aggregation to prevent coronary thrombosis. Examples are clopidogrel, prasugrel, and ticagrelor (reversible ADP inhibitor).

  • ACE inhibitors decreases the angiotensin II vasoconstriction, which decreases the afterload. ACE inhibitors also decrease aberrant cardiac remodeling (e.g., lisinopril, enalapril, quinapril, captopril).

  • Statins HMG Coa reductase inhibitors that decrease circulating LDL levels decreasing the rate atheroma formation (e.g., simvastatin, atorvastatin).

Patient Management

  • Assess functional capacity. Metabolic equivalents (METS) are physiologic measures of the amount of energy expended during activities compared to energy expenditure at rest. 1 MET is based on the basal oxygen consumption of a 40-year-old, 70-kg male. This helps with risk stratification of functional capacity.

    • >10 METS excellent functional capacity (jumping rope or strenuous sports).

    • 7–10 METS good functional capacity (jogging or calisthenics).

    • 4–6 METS moderate functional capacity (power walking, sexual activity, leisure biking).

    • <4 METS poor functional capacity ( watching television, writing). Patients with less than 4 metabolic equivalents should undergo noninvasive cardiac testing. Consider treating patients with less than 4 metabolic equivalents in the hospital setting.

  • Non-cardiac surgery can be carried out 6 weeks after an episode of ACS.

  • Anxiolysis to prevent increasing myocardial oxygen consumption.

  • Supplemental oxygen.

  • Ensure profound analgesia to prevent sympathetic stimulation.

  • Provide adequate fluid infusion to prevent hypotension. Must use judiciously in patients with concomitant CHF.

  • Avoid sympathomimetic agents as they increase heart rate and blood pressure (e.g., ketamine).

  • Be judicious with usage of drugs that can depress myocardial contractility and decrease blood pressure (e.g., propofol).

  • Consult the patient’s physician to help with risk stratification.

  • Use adjunctive hemostatic agents in patients on antiplatelet therapy.

  • Monitor EKG for occult signs of cardiac ischemia.

  • Maintain heart rate and BP within 20% of preoperative values.

  • Consider treating high-risk patients in a hospital setting.

Congestive Heart Failure (CHF)

  • Condition characterized by the inability of the heart to pump enough blood to meet the metabolic demands of the body.

  • Compensated heart failure is due to compensatory mechanisms such as an increase in sympathetic tone that decreases pulmonary congestion and fluid retention.

  • Decompensated heart failure is due to acute or gradual onset of signs and symptoms of pulmonary and systemic congestion.

  • Systolic failure due to impaired contractility of the heart or high afterload (chronic volume overload from mitral and aortic regurgitation, dilated cardiomyopathies, HTN, aortic stenosis). Ejection fraction <40%.

  • Diastolic failure due to impaired diastolic relaxation or ventricular failing of the heart (caused by left ventricular hypertrophy, restrictive cardiomyopathy, myocardial fibrosis, myocardial infarction). Can have preservation of the ejection fraction (>50%).

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Jul 23, 2021 | Posted by in Oral and Maxillofacial Surgery | Comments Off on Disease
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