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.

Hypertension with no identifiable cause.

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

Secondary hypertension – treat underlying cause.

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

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].

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).

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).

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.

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.

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).

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.

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.

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.

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).

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.

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%).