Hipertensi : Suatu Petunjuk Praktis Meningkatkan Kepatuhan Pengobatan Antihipertensi

Bagi para farmasis klinik, kepatuhan pengobatan pasien, terutama pada pasien dengan penyakit kronik mrupakan faktor yang sangat krusial agar tujuan terapi dapat tercapai. Di sini tentu sangat diperlukan peran serta aktif dari farmasis. Tidak hanya diperlukan kapasitas & kompetensi multidisiplin ilmu yang baik seperti farmakoterapi dan pharcovigilance namun juga diperlukan kemampuan komunikasi terhadap pasien yang baik.

Berikut ini merupa materi yang saya comot dari suatu web yang menyediakan continuing education bagi para farmasis yg saya rasa sangat bermanfaat bagi para farmasis khsusunya farmasis klinik dan komunitas. Maaf saya belum sempat men-translate-nya karena keterbatasan waktu. Selamat belajar!

Introduction

Hypertension, also known as high blood pressure, is a chronic medical condition affecting more than 65 million Americans.1 Generally asymptomatic in presentation, hypertension often remains undetected in patients who fail to engage in regular physician visits and/or health screening. Despite efforts in recent years to raise awareness of the long-term implications of high blood pressure, the prevalence of hypertension continues to rise.1 Controlling hypertension is essential to decreasing the prevalence of cardiovascular morbidity and mortality among Americans, especially ethnic minorities living in this country. It is well-established that undetected, untreated, and even undertreated hypertension increases the risk of acute myocardial infarction (AMI), cerebral vascular disease (CVD), chronic renal failure (CRF), and heart failure.1-3 As health care professionals in the position to greatly enhance hypertensive management, pharmacists must understand the etiology and pathophysiology, as well as the treatment, of hypertension. Furthermore, pharmacists must aid in providing patients with a full understanding of the risks of untreated hypertension, as well as the benefits of remaining adherent to medication therapy despite a lack of symptoms.

Definition

The pressure exerted on the arterial wall is considered the arterial blood pressure. Arterial blood pressure is commonly reported in 2 measurements, the systolic and the diastolic blood pressures. The systolic blood pressure is recorded during the contraction of the heart, and the diastolic blood pressure is recorded during the filling of the heart chambers. Systolic blood pressure, therefore, represents the higher value; while diastolic blood pressure represents the lower value. Blood pressure is recorded in millimeters of mercury (mm Hg) and is generally documented as systolic blood pressure over diastolic blood pressure. Blood pressure can be defined as the product of cardiac output and total peripheral resistance. Therefore, alteration of either cardiac output or total peripheral resistance will result in an overall change in blood pressure. Blood pressure is not a static value and will vary depending on the time of day, as well as the level of physical activity.2 Additional factors with the potential to affect blood pressure include fluid retention, psychological conditions, medications, and the even body position.

The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) provides the most commonly used guidelines for the staging and management of hypertension and is most currently in its seventh report.3 The JNC 8 is not expected to be available for public review and comment until Summer 2011 and the final version may not be available until Spring 2012. According to the JNC 7, normal blood pressure is defined as a systolic blood pressure (SBP) less than 120 mm Hg and a diastolic blood pressure (DBP) less than 80 mm Hg. Further staging of hypertension is as follows:

− Pre-Hypertension: SBP 120 to 139 mm Hg or DBP 80 to 89 mm Hg
− Stage 1 Hypertension: SBP 140 to 159 mm Hg or DBP 90 to 99 mm Hg
− Stage 2 Hypertension: SBP ≥ 160 mm Hg or DBP ≥ 100 mm Hg3

The established blood pressure goal for the general population is less than 140/90 mm Hg; however, this blood pressure goal has been lowered to less than 130/80 mm Hg for those with diabetes or chronic kidney disease.3

Diagnosis

Blood pressure readings should be taken at every office visit for patients aged 18 years and older. Patients should be advised to withhold from the use of nicotine or caffeine for at least 30 minutes prior to blood pressure testing. Blood pressure cuffs must be appropriately sized, ensuring that at least 80% of the arm circumference is covered. Patients should be allowed approximately 5 minutes to relax themselves prior to testing, and should be instructed not to talk during the procedure. Clothing should be removed, if possible, from the arm being tested. Patients should be seated with arm at heart level, legs uncrossed, and flat on the floor.

A single blood pressure reading is not adequate to diagnose hypertension. At least 2 readings, taken 1 to 2 minutes apart, should be recorded per office visit. These blood pressure readings should then be averaged. If blood pressure readings vary by greater than 5 mm Hg, 1 to 2 further readings should be obtained and an overall average of the readings should be calculated. Diagnosis of hypertension should be made only after an average of the total blood pressure readings is elevated, according to at least 2 different office visits.4,5

Etiology

The majority of hypertensive cases are considered essential hypertension, that is, of unknown or idiopathic etiology. In fact, more than 90% of hypertensive cases do not have a clear causative factor.6 Theories postulated to explain the etiology of hypertension are complex. Generally speaking, essential hypertension is thought to arise from a combination of lifestyle or environmental factors and genetic factors as discussed below.3,6,7

Lifestyle factors likely play a significant role in the genesis of hypertension within the American population. Diet can substantially contribute to an increase in blood pressure, primarily through the ingestion of high amounts of sodium, low amounts of potassium, or an overabundance of alcohol, as does tobacco dependence. American culture often promotes these detrimental choices through the increased availability and decreased cost of fast foods and processed foods.

Physical inactivity and weight gain seriously contribute to the development of hypertension, as well. Approximately 65% of adults in the United States have a body mass index (BMI) greater than 25 kg/m2 and more than 30% have a BMI greater than 30 kg/m.2,7 It is estimated that at least 122 million Americans are currently overweight or obese and less than 20% of Americans are involved in regular physical activity.3 Additionally, psychosocial factors like increased physiological and/or psychological stress, may also increase blood pressure.4,7

The prevalence of hypertension increases with age, rising to approximately 75% in those 70 years of age and older. Lifetime risk of the development of hypertension is approximately 90% in those who are not hypertensive between 50 and 60 years of age; this is also true for those 80 years of age and older.3 An increase in the older population of the United States and improvements in medicine will likely contribute to an increased overall prevalence of hypertension.

Genetic factors also contribute to the development of hypertension. Mutations in 10 genes have been implicated in the development of Mendelian forms of hypertension.2,6 The majority of genetic mutations resulting in hypertension do so through an alteration in the kidneys’ ability to maintain appropriate sodium balance.2,6 Single-gene mutations are rare, suggesting that the etiology of hypertension is most often the result of a combination of factors.6

Although more rare in nature, some cases of hypertension have a clear, discernible cause and are considered secondary hypertension. Secondary causes of hypertension may be suspected if patients present with a sudden onset of hypertension, show signs and symptoms of possible hypertension-related disease states, or do not respond to blood pressure lowering medication.3 The most notable causes of secondary hypertension are chronic renal disease (2% to 5%), Cushing’s syndrome (0.1% to 0.6%), pheochromocytoma (0.04% to 0.1%), renovascular disease (0.2% to 0.7%), and primary hyperaldosteronism (0.01% to 0.3%).4 Other disease-related causes of hypertension include obstructive sleep apnea and thyroid disease. If secondary hypertension is suspected, patients should undergo an appropriate work-up for diagnosis of the suspected causative disease state.3

Medications have also been commonly implicated in cases of secondary hypertension. Notably, sympathomimetic agents, such as pseudoephedrine and phenylephrine, are known to increase blood pressure. Since decongestants are over-the-counter (OTC) medications, pharmacists can suggest using an intranasal decongestant, rather than systemic, for the short-term treatment of nasal congestion in patients with hypertension or cardiovascular disease. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also known to increase blood pressure through renal sodium and water retention. NSAIDs are commonly used for the treatment of pain and this information should be an educational point when counseling both hypertensive and older patients.8-10 A number of other agents documented to increase blood pressure include oral contraceptives, tacrolimus, cyclosporine, COX-2 inhibitors, amphetamines, cocaine, ginseng, and some OTC dietary supplements.4,8 A thorough patient interview inquiring about OTC medication and dietary supplement use should be performed when hypertension remains uncontrolled despite adequate treatment. Ginseng and caffeine-containing energy drinks continue to be widely used and most individuals are not aware of the potential for adverse side effects; pharmacists should inquire with patients regarding the ingestion of these products.

Pathophysiology

Like the etiology of hypertension, the pathophysiology of hypertension is complex and multifactorial in nature. The most commonly recognized mechanisms include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). Increased activation of the sympathetic nervous system causes stimulation of the heart and kidneys. Cardiac output and vascular resistance are increased as a result.6 Arterial and aortic baroreceptors become reset to a higher pressure in the patient with hypertension. Angiotensin II may also contribute to exaggerated sympathetic stimulation. In addition, chemoreflex pathways may become altered in those experiencing apnea, leading to an overall increase in sympathetic stimulation. Ultimately, chronic sympathetic stimulation contributes to left ventricular hypertrophy and vascular remodeling.6

There are a number of ways RAAS is involved in the pathophysiology of hypertension. Increased blood pressure is primarily mediated through the effects of angiotensin II. Circulating angiotensin II causes constriction of the resistance vessels, as well as increased sympathetic stimulation. It also stimulates the synthesis of aldosterone, which causes sodium and water retention, leading to increased blood pressure. Furthermore, angiotensin II plays a role in cardiac and vascular cellular hypertrophy.2,6

Risks of Hypertension

Long-term implications of untreated or undiagnosed hypertension include heart attack, stroke, coronary heart disease, heart failure, and renal failure.1,7 Hypertension is the most common risk factor for cardiovascular morbidity and mortality and contributes to an estimated 7.1 million deaths per year.3,9 Cardiovascular risk doubles with every 20/10 mm Hg rise in blood pressure over 115/75.3 Controlling blood pressure can be highly beneficial in diminishing the risk of these cardiovascular events. Every 3 mm Hg drop in systolic blood pressure is estimated to provide a 5% decrease in coronary heart disease mortality and an 8% decrease in stroke mortality.7 Starting at 115/75 mm Hg, cardiovascular risk doubles with each increment of 20/10 mm Hg throughout the blood pressure range and persons who are normotensive at age 55 have a 90% lifetime risk for developing hypertension.3

Many significant risk factors involved in the development of hypertension continue to greatly afflict the population of the United States (U.S.), including obesity, diabetes, smoking, kidney disease, and hyperlipidemia.4,6,10 Sleep deprivation, sleep apnea, and stress exposure are also highly prevalent in American culture.11 Adequate control and appropriate therapeutic management of these risk factors is imperative to decreasing the overall prevalence and morality of hypertension.

Nonpharmacologic Treatment

According to the JNC 7, patients with a systolic pressure between 120 to 139 mm Hg or a diastolic pressure between 80 and 89 mm Hg should be considered prehypertensive; these patients may require health-promoting lifestyle modifications to prevent CVD.3 Lifestyle modifications are typically chosen as the first-line treatment for hypertension. When used in combination, diet and exercise have shown notable improvements in blood pressure, often achieving adequate control or providing the opportunity for lower doses of medication. Nonpharmacologic treatments are particularly beneficial in the African-American population, which often presents with higher blood pressure than non–African-Americans.7

Weight loss has been repeatedly documented as an important mechanism for preventing and treating hypertension. Studies have shown that even moderate weight loss can contribute to lowering blood pressure, whether or not the patient actually achieves a desirable body weight. Weight loss of approximately 5 kg has been shown to decrease blood pressure by 4.4/3.6 mm Hg on average.7 Furthermore, a weight loss of 10 kg sustained over 2 years has been shown to decrease blood pressure by 6/4.6 mm Hg.9 Initiating an exercise regimen involving high physical activity will aid in sustaining weight loss over time: regular aerobic exercise is recommended for 30 minutes a day, most days of the week.3 Attaining a BMI less than 25 kg/m2 is currently considered ideal for preventing and treating hypertension. Patients who are not currently overweight should be encouraged to maintain a BMI less than 25 kg/m.2,3,7

Diet is also a relatively effective approach to decreasing blood pressure. Initiation of a low-sodium, high-potassium diet is recommended for hypertension treatment and prevention. Overall blood pressure response to limiting sodium is variable and is often more beneficial in the African-American and older adult populations. It is hypothesized that these patient groups have a less responsive RAAS. Complete sodium restriction is not recommended. An Institute of Medicine committee determined that 1.5 grams of sodium daily is adequate; however, this is highly difficult to achieve in today’s culture.7 It is, therefore, recommended that 2.3 grams of sodium daily be used as an upper limit for the management of hypertension. Generally, sodium restriction should be achieved through the selection of foods low in sodium, especially by limiting the intake of processed foods. Pharmacists should discourage consumption of foods high in sodium, such as many canned soups or frozen dinners, fast foods, processed meats, and pickles. Patients recently diagnosed with hypertension may benefit from a visit with a clinical dietician to learn more about healthy food choices and to understand how to read food labels. Care also should be taken to limit adding excess salt to foods when dining or cooking.3,7

Increased potassium intake has also been shown to improve blood pressure control, especially in the African-American population.7 An adequate potassium intake of 4.7 grams daily is recommended and should be achieved through increased intake of potassium-rich fruits and vegetables. Patients at risk for hyperkalemia because of decreased potassium excretion should not be advised to increase potassium intake. This includes patients with chronic kidney disease, adrenal insufficiency, diabetes, or heart failure. Caution is also advised in patients taking medications which inhibit potassium excretion including NSAIDs, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and potassium-sparing diuretics.7

The most widely studied and recommended diet for lowering blood pressure is the DASH diet. DASH stands for Dietary Approaches to Stop Hypertension. When studied, the DASH diet provided an average decrease in blood pressure of 5.5/3 mm Hg. The DASH diet consists of fruits, vegetables, poultry, fish, low-fat dairy, whole grains, and nuts. At the same time, it encourages decreased fats, sweets, and red meat. DASH, as with the other dietary measures discussed, is more beneficial in the African-American population. DASH is not recommended for those with chronic kidney disease because of the high protein and potassium content.3,7

Patients with hypertension who smoke should be strongly encouraged to stop, since cigarette smoking is a known independent risk factor for cardiovascular disease. There is evidence that pharmacist-directed smoking cessation programs are successful for smoking cessation.12-14 Lastly, excessive alcohol intake (≥ 2 drinks per day) has been shown to contribute to the development of hypertension. Moderation of alcohol consumption provides an approximate decrease in systolic blood pressure of 2 to 4 mm Hg.3 It is recommended that men drink no more than 2 drinks per day and women drink no more than 1 drink per day. One drink should be considered 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof liquor.3,7

Pharmacologic Treatment Selection

Pharmacologic treatment is necessary for many patients with hypertension. Over 75% of patients require 2 or more medications to achieve blood pressure goal.3,10 A number of pharmacologic classes have been utilized for blood pressure control including thiazides, loop diuretics, aldosterone antagonists, ACE inhibitors, ARBs, beta-blockers, calcium channel blockers, alpha-1 adrenoreceptor antagonists, central alpha-2 adrenoreceptor agonists, and direct vasodilators.3 Please refer to Table 1 for a list of examples of specific medications and their respective pharmacotherapeutic class and dosing range.

Table 1. Review of Oral Anti-Hypertensive Medications2,3,16

  US BRAND NAMES SIDE EFFECTS PREGNANCY RISK
Hydrochlorothiazide Microzide® Orthostatic hypotension
Photosensitivity
Hypokalemia
B
Chlorthalidone Thalitone® Photosensitivity
Hypokalemia
Epigastric distress
B
Metolazone Zaroxolyn® Photosensitivity
Hypokalemia
Orthostatic hypotension
Hyperuricemia
B
Furosemide Lasix® Electrolyte depletion
Photosensitivity
Ototoxicity
Nephrotoxicity
C
Bumetanide Bumex® Electrolyte depletion
Hyperuricemia
Ototoxicity
Nephrotoxicity
C
Torsemide Demadex® Electrolyte depletion
Ototoxicity
Nephrotoxicity
GI effects
B
Spironolactone Aldactone® Hyperkalemia
Gynecomastia
Fatigue
Menstrual changes
C
Eplerenone Inspra™ Hyperkalemia
Hypertriglyceridemia
Dizziness
B
Lisinopril Prinivil®; Zestril® Angioedema
Cough
Hyperkalemia
Dizziness
C (1st trimester);
D (2nd/3rd trimester)
Enalapril Vasotec® Angioedema
Cough
Hyperkalemia
Dizziness
C (1st trimester);
D (2nd/3rd trimester)
Ramipril Altace® Angioedema
Cough
Hyperkalemia
Hypotension
C (1st trimester);
D (2nd/3rd trimester)
Benazepril Lotensin® Angioedema
Cough
Hyperkalemia
Headache
D
Losartan Cozaar® Fatigue
Hypotension
Hyperkalemia
Angioedema (rare)
C (1st trimester);
D (2nd/3rd trimester)
Valsartan Diovan® Hyperkalemia
Dizziness
Hypotension
Increased BUN
D
Irbesartan Avapro® Hyperkalemia
Orthostatic hypotension
Dizziness
Upper Respiratory Infection
C (1st trimester);
D (2nd/3rd trimester)
Candesartan Atacand® Hyperkalemia
Hypotension
Increased serum creatinine
Dizziness
C (1st trimester);
D (2nd/3rd trimester)
Metoprolol Tartrate Lopressor® Bradycardia
Dizziness
Fatigue
AV Block
C
Metoprolol Succinate Toprol-XL® Bradycardia
Dizziness
Fatigue
AV Block
C
Atenolol Tenormin® Bradycardia
Dizziness
Fatigue
AV Block
D
Bisoprolol Zebeta® Fatigue
GI effects
Chest pain
Dyspnea
C
Carvedilol Coreg® Hypotension
Dizziness
Fatigue
Bradycardia
Edema
AV Block
C
Labetalol Trandate® Orthostatic hypotension
Dizziness
Fatigue
Nausea
C
Amlodipine Norvasc® Peripheral edema
Flushing
Fatigue
Dizziness
C
Felodipine Plendil®; Renedil® Headache
Peripheral edema
Flushing
Tachycardia
C
Nifedipine Adalat® CC; Nifediac CC®; Nifedical XL®; Procardia XL® Flushing
Peripheral edema
Dizziness
Headache
Heartburn
C
Diltiazem Cardizem® CD; Cardizem® LA; Cartia XT®; Dilacor XR®; Tiazac® Edema
Headache
AV Block
Bradycardia
Hypotension
C
Verapamil Calan®;
Calan® SR;
Covera-HS®; Isoptin® SR; Verelan®;
Verelan® PM
Headache
Gingival hyperplasia
Constipation
Hypotension
Edema
AV Block
C
Doxazosin Cardura®; Cardura® XL Dizziness
Headache
Fatigue
Edema
Orthostatic hypotension
C
Terazosin Hytrin® Dizziness
Muscle weakness
Edema
Orthostatic hypotension
C
Prazosin Minipress® Dizziness
Palpitation
Headache
Drowsiness
Orthostatic hypotension
C
Clonidine Catapres-TTS®-1; Catapres-TTS®-2; Catapres-TTS®-3; Catapres®; Duraclon® Xerostomia
Drowsiness
Dizziness
Constipation
Headache
C
Methyldopa Aldomet® Peripheral edema
Dry mouth
Drowsiness
B
Hydralazine Apresoline® Orthostatic hypotension
Peripheral edema
Tachycardia
Dizziness
Fluid/Sodium retention
C
Minoxidil Loniten® ECG changes
Hypertrichosis
Peripheral edema
Fluid/Sodium retention
C
Aliskiren Tekturna® Orthostatic hypotension
Rash
Increased creatinine
Hyperkalemia
Diarrhea
C (1st trimester);
D (2nd/3rd trimester)
BUN = blood urea nitrogen; AV = atrioventricular; ECG = electrocardiogram

 

All patients should begin therapy with lifestyle modifications; however, if unable to adequately control blood pressure alone, pharmacotherapy is initiated in combination with lifestyle changes. The choice of initial therapy for the majority of patients has been the topic of considerable study and debate. Recent consensus guidelines and clinical reviews have concluded that the degree of blood pressure reduction correlates positively to the reduction in cardiovascular risk, rather than the initial antihypertensive drug prescribed.15-17 This assumes that the patient does not have a compelling indication for a particular drug, such as a beta-blocker or verapamil for rate control in those with atrial fibrillation. Thus, a consensus is emerging that, at the same level of blood pressure reduction, most antihypertensive agents will provide a similar degree of cardiovascular protection.18

While thiazide diuretics have long been considered first-line agents of choice, they may not be optimally effective as monotherapy in some patients. In actual practice there is wide interpatient variability. Some patients will respond well to one drug or drug class, and not another. However, making this determination a priori is not always possible. Perhaps the JNC 8 guidelines will inform clinicians better on initial drug selection. For now it seems prudent to base the initial choice on the level of blood pressure control needed, the presence of compelling indications or concurrent diseases, the potential for drug interactions, the adverse effect profile, warnings, precautions, contraindications, history of response, and affordability.

Patients presenting with Stage 1 hypertension without contraindications should be initiated on monotherapy with a thiazide diuretic such as hydrochlorothiazide (HCTZ) or chlorthalidone. Other pharmacologic classes may be considered for Stage 1 hypertension in cases where the thiazides are contraindicated or are not tolerated, or if the patient has a compelling indication for a different drug. Patients unable to achieve adequate blood pressure control may be started on combination therapy. For example, the use of a thiazide diuretic in combination with a drug that acts on the RAAS yields synergistic antihypertensive effects. Furthermore, many of these agents are commercially available in a fixed-dose combination as a single tablet or capsule (Table 2). The use of these formulations should result in improved adherence and possibly lower unit costs, especially for those that are generically available (e.g., losartan plus HCTZ). Pharmacists should recall that chronic administration of diuretics can be associated with metabolic complications, such as hypokalemia, hypomagnesemia, and hyperuricemia in a dose-related fashion. Polyuria is a common adverse effect of diuretics and can lead to noncompliance.

Table 2. Selected Diuretic Combination Medications2,3,16

FIXED COMBINATION ANTIHYPERTENSIVES
Combination Brand Name Available Dose (mg)
ACEI + HCTZ
Benazepril/HCTZ
Captopril/HCTZ
Enalapril/HCTZ
Lisinopril/HCTZ
Moexipril/HCTZ
Quinapril/HCTZ
Lotensin®
Capozide®
Vaseretic®
Prinzide®, Zestoretic®
Uniretic®
Accuretic®
5/6.25, 10/12.5, 20/12.5, 20/25
25/15, 25/25, 50/15, 50/25
5/12.5, 10/25
10/12.5, 20/12.5, 20/25
7.5/12.5, 15/25
10/12.5, 20/12.5, 20/25
ARB + HCTZ
Candesartan/HCTZ
Eprosartan/HCTZ
Irbesartan/HCTZ
Losartan/HCTZ
Olmesartan/HCTZ
Telmisartan/HCTZ
Valsartan/HCTZ
Atacand HCT®
Teveten HCT®
Avalide®
Hyzaar®
Benicar HCT®
Micardis HCT®
Diovan HCT®
600/12.5, 600/25
16/12.5, 32/12.5
75/12.5, 150/12.5, 300/12.5
50/12.5, 100/25
20/12.5, 40/12.5, 40/25
40/12.5, 80/12.5
80/12.5, 160/12.5
Renin Inhibitor + HCTZ
Aliskiren/HCTZ
Tekturna HCT® 150/12.5, 150/25, 300/12.5, 300/25
HCTZ = hydrochlorothiazide

 

The question of therapeutic equivalency of HCTZ, as compared with chlorthalidone is another area of debate.19-22 Investigators have correctly observed that chlothalidone is more potent and has a longer half-life and duration of action than HCTZ (chlorthalidone 12.5 mg is approximately equivalent to HCTZ 25 mg).19 However, in actual practice, HCTZ is more often prescribed. A recent, large-scale retrospective cohort analysis demonstrated that chlorthalidone reduces cardiovascular events more than HCTZ.20 These investigators concluded that chlorthalidone may be preferred over HCTZ for treating hypertension in patients at high risk for cardiovascular events.

Most patients presenting with Stage 2 hypertension should be started on 2-drug combination therapy. It is recommended that 1 of the 2 agents be a thiazide diuretic, unless contraindicated. Options for the second pharmacologic agent include an ACE inhibitor, ARB, beta-blocker, or calcium channel blocker. Use of 2 pharmacologic classes generally aids in achieving the blood pressure goal more readily. After initiation of pharmacologic therapy, patients should follow-up on a monthly basis until the goal blood pressure is achieved. Medication dosages should be optimized and additional medications may be added as needed and as tolerated. When choosing whether to increase medication dosage or initiate an additional agent, multiple factors should be considered. Patients should be questioned about antihypertensive drug adherence. In situations where patients claim good compliance, yet arterial pressures remain high, the clinician may need to corroborate the patient’s claim with a phone call to the dispensing pharmacy or use pill counts. Patients should also be questioned about the use of nonprescription agents, such as NSAIDs, pseudoephedrine, ginseng, caffeine consumption, and use of energy drinks before adding additional medications.

Compelling Indications

Patients may present with one or more comorbid disease states that may or may not be related to hypertension. These disease states are considered compelling indications and include heart failure, diabetes, chronic kidney disease, postmyocardial infarction, and necessity for recurrent stroke prevention. Evidence-based literature supports use of certain pharmacologic classes of medications in these conditions (Table 3). For example, patients with hypertension and chronic, stable renal impairment would benefit from an ACE inhibitor or an angiotensin II receptor antagonist to decrease the progression of hypertensive nephropathy. Similarly, patients with systolic heart failure would benefit from an ACE inhibitor, beta-blocker, and possibly an aldosterone antagonist. Thus, medication selection for hypertensive treatment in patients with concurrent diseases should be selected based on the most recent literature and the JNC recommendation.3

Table 3: Evidence-Based Medication Recommendations by Compelling Indication2,3,16

Compelling Indication Recommended Medications
Heart Failure Loop diuretic
Beta-blocker
ACE Inhibitor
ARB
Aldosterone Antagonist
Postmyocardial Infarction Beta-blocker
ACE Inhibitor
Aldosterone Antagonist
High Coronary Disease Risk Diuretic
Beta-blocker
ACE Inhibitor
Calcium Channel Blocker
Diabetes Beta-blocker
ACE Inhibitor
ARB
Calcium Channel Blocker
Chronic Kidney Disease ACE Inhibitor
ARB
Recurrent Stroke Prevention Diuretic
ACE Inhibitor
ACE = angiotensin-converting enzyme; ARB = angiotensin II receptor blocker

 

There are numerous possible patient scenarios in which one antihypertensive drug or combination may be preferred over another; however, illustrating each is beyond the scope of this lesson. Some examples include hypertensive women of child bearing age, or those who are already pregnant. In these situations, drugs such as ACE inhibitors, ARBs, and direct renin inhibitors should be avoided. Instead, a drug such as methyldopa or labetalol would be preferred. African-American patients generally respond better to thiazide or calcium channel blocker monotherapy, as opposed to ACE inhibitor or beta-blocker monotherapy.3 Whereas younger, white patients respond better to ACE inhibitors or ARBs and beta-blockers as compared with calcium-channel blockers and thiazides.3Scenarios where a beta-blocker may be preferred include hypertensive patients with benign essential tremor, migraine headache, and symptomatic hyperthyroidism, as well as for rate control in patients with atrial fibrillation or flutter.3 This illustrates the importance of obtaining a complete medical history for each patient, and individualizing the antihypertensive regimen as clinically appropriate.

The Pharmacy’s Role in Increasing Antihypertensive Adherence

With the increasing need for multiple medications to achieve adequate blood pressure control, pharmacist intervention will remain an important component of hypertensive patient care. As stated earlier, more than 75% of patients with hypertension require 2 or more drugs to achieve their blood pressure goal.3,10 Other patients remain undiagnosed, undertreated, uncontrolled, or resistant (unable to achieve goal with 3 or more medications).

A number of studies have documented the positive impact pharmacists can make by collaborating with physicians to improve blood pressure control in patients with hypertension in a variety of health-system settings.23-25 Pharmacists are well-suited to improve long-term medication adherence by providing multilevel feedback to prescribers and educating patients about various aspects of hypertension. This includes the consequences of uncontrolled or untreated disease, especially target organ damage; as well as providing proof regarding the benefits of optimal blood pressure control.

Patient adherence to pharmacologic therapy is of the utmost importance for adequate hypertensive control. It has been estimated that approximately 50% of patients with newly diagnosed hypertension are still continuing treatment at 12 months.26 A number of factors may contribute to nonadherence: patients may experience adverse effects, causing them to self-adjust or discontinue their medications; or the asymptomatic nature of hypertension may encourage patients to perceive that the side effects of these medications are unwarranted. Pharmacists must engage in conversation with their patients regarding both the risks associated with untreated hypertension and the expectations of possible side effects when a new medication is initiated. It is important for patients to take ownership and responsibility for risk factor reduction through lifestyle modification. Another way pharmacists can assist patients is by recommending the use of ambulatory blood pressure monitoring devices. This may allow patients to take a more active role in managing their blood pressure and should, theoretically, improve medication compliance.

Other contributing factors to nonadherence include patients’ inability to comply with complicated dosing schedules when taking multiple blood pressure lowering medications, along with other medications. Pharmacists should engage in monitoring the refill history of patients that may not be adequately filling their medications as prescribed. Possible options for improvement may be informing patients about the benefits of a pill box or attempting to contact the physician regarding combination therapies that may simplify the patient’s medication regimen. In an attempt to make the taking of a patient’s antihypertensive medication more routine, the pharmacist should assist patients with identifying regular, daily activities that may aid in remembering drug administration. For example patients should tie together the drug administration with brushing his/her teeth, drinking a morning cup of coffee, or other routine daily activity.

Medication costs may also become problematic for patients, particularly those with multiple disease states requiring treatment, limited prescription drug coverage, or patients reaching the gap in Medicare coverage. Consulting the patient’s physician regarding the availability of generic medications rather than brand-only selections may provide the patient with a lower cost burden and an incentive to adhere to their blood pressure lowering therapy. Counseling patients about the benefits of adhering to lifestyle modifications to increase the possibility of achieving lower medication dosages or complete medication discontinuation may also aid in decreasing overall medication costs. Patients should be routinely asked about their level of physical activity and dietary factors, such as sodium intake.

Aside from patient adherence, the availability of OTC medications that increase blood pressure may also prompt a pharmacist’s intervention. Counseling patients filling prescriptions for blood pressure lowering medications about the effects of NSAIDs, pseudoephedrine, and some dietary supplements may reduce the possibility for the subsequent development of unrecognized drug-induced hypertension. Aiding patients with the selection of appropriate alternatives to these medications is a key role for pharmacists in hypertensive patient care.10

The pharmacist can also increase antihypertensive drug adherence by advising patients in advance about any potential adverse effects, such as a cough resulting from an ACE inhibitor, constipation with verapamil, erectile dysfunction, or orthostatic hypotension with vasodilator therapy (among the many other possible adverse effects from other classes). Furthermore, patients should be counseled about the potentially life-threatening adverse effects, such as angioedema with ACE inhibitors. Patients should be warned that a case of angioedema involving any part of the airway, such as the tongue, larynx or pharynx, should be considered a medical emergency.

Prescriber feedback does not necessarily translate into improved patient adherence, but if possible, prescribers should be made aware of patients who do not regularly refill their medication. Likewise, the pharmacist should engage the physician each time adverse effects are suspected or reported by the patient. Prescribers may need to be contacted for a possible dosage adjustment, potential drug interactions, or when therapeutically equivalent agents are available generically. Pharmacists with direct patient care responsibilities should pay careful attention to comorbid conditions, such as dyslipidemia and tobacco dependence, and collaborate with the physician, if possible, to address these issues with pharmacotherapy when appropriate. Patients should understand that hypertension is asymptomatic and, as a result, they may not feel any positive physical changes during treatment; however, effective antihypertensive therapy will help protect them from stroke, coronary events, heart failure, and the progression of renal disease, as well as the progression to more severe hypertension.

Conclusion

Hypertension is a highly prevalent condition affecting millions of Americans. When hypertension remains undiagnosed or untreated, patients are at increased risk for cardiovascular morbidity and mortality. Blood pressure control often requires the use of multiple medications from different pharmacological classes, along with lifestyle modifications, to achieve an appropriate blood pressure goal. Complicated by its often unknown etiology and asymptomatic presentation, patient understanding of hypertension is often incomplete. Pharmacists play a vital role in the management and the success of hypertensive patient care. Improving patient adherence, educating patients about the risks of hypertension, and aiding in the appropriate selection of OTC therapies are some of the ways pharmacists can contribute to improving the care of patients with hypertension.

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Taken from : http://www.powerpak.com/course/content/107594

Original Title : Understanding Hypertension: A Practical Guide for Increasing Antihypertensive Adherence

3 thoughts on “Hipertensi : Suatu Petunjuk Praktis Meningkatkan Kepatuhan Pengobatan Antihipertensi

  1. pak zulfan.. bagaimana menurut anda suatu pernyataan:
    “bagi pasien hipertensi harus minum obat seumur hidup.”

    trus.. jika pusing, sebaiknya minum obat pusing atau bisa langsung minum obat HTnya

    thank u..

    • Kalo menurut saya kuncinya tetap ada di diagnosisnya & modifikasi gaya hidup om. Liat dulu penyebabnya apa, lifestyle kah, obat kah, atau memang primary hypertension. perubahan gaya hidup sebelum HT sulit dikontrol menjadi sangat penting apapun penyebab HT-nya. Lihat perkembangan tensinya setiap kontrol ke dokter. Menurut salah satu penelitian ( ), pada pasien hipertensi esensial sedang, terapi anti HT mungkin saja dihentikan tentu saja dengan pengawasan rutin dan -sekali lagi- modifikasi gaya hidup.

      kalo bisa dipastikan pusingnya disebabkan HT & pusingnya masih bisa ditahan, maka ga perlu minum analgesik. Tapi kalo misalnya ga tertahankan bisa dikasih Paracetamol yg relatif aman & ga berinteraksi dgn obat2an Anti HT.

      Kalo ad ayg salah koreksi ya bro.hehe..

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