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INTRODUCTION Public health policy supports best practice and appropriate use of prescription drugs. Emphasis should be placed on prevention of physician-­ associated iatrogenic errors during professional training by teaming physicians with pharmacists who ­ will help recognize prescription errors and help with drug interactions. Health care is not as safe as it should be. Data indicates that avoiding prescription errors can prevent at least 44,000 deaths and perhaps as many as 98,000 deaths annually in the United States (1). Trust is at the core of any clinical relationship between doctor and patient (2,3). Careful and individualized use of diagnostic and therapeutic resources in specific situations is not sufficiently emphasized in most residency programs and thus is not extended into medical practice (4). Avoidance of iatrogenic complications from medi­ cations demands attention at an early stage of treatment (5). Health care providers also need to be cognizant of the fact that many patients who do not want to take drugs ­ will use side effects they read or hear about as an excuse not to take a drug. In many cases, a so-­ called side effect may be true and unrelated to the drug, especially if not previously reported. Therefore, the provider needs to take a detailed history from the patient before concluding it is a drug allergy. Note that many antiarrhythmics affect CYP systems in the liver and alter drug metabolism of many drugs, not just cardiovascular ones. The same is true for lipid-­ lowering agents. Thus, a good knowledge of the pharmacology of the drugs being prescribed is critical in avoiding iatrogenicity. Hypertension, which affects 80 million ­ people in the United States (6), is the most readily treatable cause of premature death (7) and an in­ de­ pen­ dent predictor of sudden cardiac death (8). Increased blood pressure predisposes individuals to left ventricular hypertrophy, a predictor of arrhythmias including ventricular ectopy and arrhythmic death (9,10,11). Blood pressure control has become one of the greatest challenges in improving cardiovascular health. National and regional health initiatives have sought to increase public awareness of the benefits of lowering blood pressure (12,13). From 2011 to 2014, hypertension was controlled in about 52% of Americans adults, a higher level of control than in most other parts of the world (6). Tolerability of initial antihypertensive agents from the 1950s to 1970s was poor with resultant meager adherence. Since the 1980s, newer classes of longer-­ acting medi­ cations with generally better tolerability and fewer side effects ­ were instituted. However, CHAPTER 10 Antihypertensive Drug–­Induced Iatrogenic Cardiovascular Syndromes Rigas G. Kalaitzidis and George L. Bakris 102 / Antihypertensive Drug–Induced Iatrogenic Cardiovascular Syndromes adverse effects potentially related to antihypertensive therapy are still pres­ ent (see ­ Table 10-1). Older guidelines suggest antihypertensive agents should be titrated ­ until the maximum tolerability is achieved, a strategy that ­ favors side effects. ­ Today, in clinical practice, at least 60% of patients require more than one agent to achieve­TABLE 10-1 ​ Antihypertensive drugs and cardiovascular side effects Drugs Side Effects Cardiovascular Effects Thiazides and thiazidelike diuretics (e.g., hydroclorothiazide, chlorthalidone, indapamide) Hypovolemia Hypersensitivity Hypokalemia Hypomagnesemia Hypercalcemia Hyperuricemia Cardiac arrhythmias Increased ventricular ectopy Sudden death Loop diuretics (e.g., furosemide, torsemide) Hypovolemia Hypersensitivity Ototoxicity Hypokalemia Hypomagnesemia Cardiac ­arrhythmias Potassium-­sparing diuretics (e.g., spironolactone, eplerenone, amiloride, triamterene) Hyperkalemia Hypotension Dizziness Headache Nausea Cardiac arrhythmias Wide QRS accelerated rhythm Sudden ­death Beta-­blockers (metoprolol, atenolol, carvedilol, nebivolol) Cold hands and feet Tiredness Fatigue Reduced exercise ­ tolerance Reduced sexual function Increased risk of diabetes with all (except nebivolol and carvedilol) Bradycardia Hypotension Low-­ output cardiac failure Cardiogenic shock Prolonged QT interval Torsade de pointes Cardiac arrest RAAS inhibitors; ACE inhibitors (captopril, enalapril, ramipril, lisinopril); ARBs (losartan, telmisartan, olmesartan); renin inhibitors (aliskerin) Hyperkalemia Cardiac arrhythmias Bradycardia Calcium channel blockers (diltiazem, verapamil); dihydropyridines (amlodipine, nifedipine) Hypokalemia Hyperglycemia Oliguric renal failure Acute pancreatitis Respiratory distress syndrome Hypotension Sinus bradycardia Atrioventricular block Vasodilatory shock Pulmonary edema Sinus tachycardia Alpha-1 blockers (doxazosin, terazosin) Orthostatic symptoms Increased risk of cardiac heart failure Central alpha-2 agonists (moxonidine, clonidine, alpha methyldopa) Nausea Allergic skin reaction Dry mouth Increased mortality and morbidity Greater likelihood of hospitalization for heart failure and acute myo­ car­ dial infarction blood pressure control. Prospective studies and guidelines support the addition of a second agent over doubling the dose of the existing therapy (14). This approach is supported ­ because of better efficacy and fewer side effects. Diuretics and beta-­ blockers ­ were major breakthroughs in the early 1960s and remained the corner­ Diuretics / 103 hyponatremia...


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