management of hypertension problems in gp

52
Management of Hypertension problems in GP Dr. Mostafa Rashed PGY2 Family Medicine Department HMC Dr. AbdulMutaleb al Qawasmeh

Upload: amir-mahmoud

Post on 15-Aug-2015

38 views

Category:

Health & Medicine


7 download

TRANSCRIPT

Management of Hypertension problems in

GPDr. Mostafa Rashed PGY2

Family Medicine DepartmentHMC

Dr. AbdulMutaleb al Qawasmeh

Mr Zaki is a 47 years old man, coming to your clinic to refill his medications. He has past medical history of DMll for 12 years, smoker. He works is an accountant for 20 years, doesn’t play any sports. His current medications are: sitagliptin 50/1000mg BID, diamicron 120 mg OD, Crestor 10 mg.

CASE 1

Vitals: BP: 147/96 bilaterally pulse:86 temperature:37.1 RBS:180 mg/dl BMI: 36

Physical examination:General : looks wellChest: clearCVS: loud S2 over 2nd midclavicular line on Rt side.Abdomen: soft, lax no organomegalyPeripheral pulses: week bilateral dorsalis pedis pulsations

Labs: CBC: NORMAL Kft: Scr:104, Na:141, K: 4.2 Albumin in urine 600 mg/day ECG:

What is the goal BP ? What are the important advices you would

tell the patient ? What is your management ?

Mrs Aziza is a 56 years old female coming to your clinic today for FU, she is a k/c of HTN ,osteoarthritis, bronchial asthma, GERD.

Her BA is controlled, her heart burn is not controlled all over the week, pt takes NSAIDs frequently for her osteoarthritis, pt is not following healthy diet where she eats most of her food with extra salt. She is unemployed doesn’t go out frequently. She has family history of HTN, DM, CAD, Breast cancer. Her home medications are lisinopril 20 mg, amlodipine 10 mg, hyrochlorothiazide 25 mg, pantoprazole 20 mg, diclophenac 100 mg.

CASE 2

Her home BP readings range between: systolic 150-180 mmhg, diastolic 90-110 mmhg

Vitals at your office:BP 172/105, PULSE 78, TEMP 36.8BMI 40EXAMINATION: No significant findings

What is your approach to this patient ?

 Based upon the average of two or more properly measured readings at each of two or more office visits after an initial screen

●Normal blood pressure: systolic <120 mmHg and diastolic <80 mmHg

●Prehypertension: systolic 120 to 139 mmHg or diastolic 80 to 89 mmHg (see "Prehypertension")

●Hypertension:•Stage 1: systolic 140 to 159 mmHg or diastolic 90

to 99 mmHg•Stage 2: systolic ≥160 mmHg or diastolic ≥100

mmHg

DEFINITION

Isolated systolic hypertension is considered to be present when the blood pressure is ≥140/<90 mmHg, and isolated diastolic hypertension is considered to be present when the blood pressure is <140/≥90 mmHg. Patients with blood pressure ≥140/≥90are considered to have mixed systolic/diastolic hypertension.

DEFINITION

Based upon ambulatory and home readings  Increasingly, the diagnosis of hypertension is made using ambulatory blood pressure monitoring (ABPM) or home blood pressure monitoring. While there is some debate about the most appropriate definition, the following diagnostic criteria were suggested by the 2013 ESH/ESC guidelines; meeting one or more of these criteria qualifies as hypertension:

●A 24-hour average of 130/80 mmHg or above ●Daytime (awake) average of 135/85 mmHg or above ●Nighttime (asleep) average of 120/70 mmHg or

above

DEFINITION

The 2007 United States Preventive Services Task Force (USPSTF) guidelines on screening for high blood pressure among adults recommend screening every two years for persons with systolic and diastolic pressures below 120 mmHg and 80 mmHg, respectively (normal blood pressure), and yearly for persons with a systolic pressure of 120 to 139 mmHg or a diastolic pressure of 80 to 89 mmHg (prehypertension)

Screening

The following tests should be performed in all patients with newly diagnosed hypertension

●Electrolytes and serum creatinine (to calculate the estimated glomerular filtration rate)

●Fasting glucose●Urinalysis●Lipid profile (total and HDL-

cholesterol,triglycerides)●Electrocardiogram (ECG)Additional tests — Additional tests may be

indicated in certain settings:

●The evidence supporting benefit from the treatment of hypertension

●The choice of antihypertensive drugs●The goal blood pressure

Hypertension in DM

BENEFIT OF TREATMENT : Early treatment of hypertension is particularly important in diabetic patients both to prevent cardiovascular disease and to minimize progression of renal disease and diabetic retinopathy 

Interventions to prevent hypertension include nonpharmacologic methods, such as weight reduction, increased consumption of fresh fruits, vegetables, and low-fat dairy products, exercise, salt restriction, and avoidance of smoking and excess alcohol ingestion. This is consistent with the American Diabetes Association 2015 guidelines, which state that, among patients with a systolic blood pressure of 120 to 139 mmHg, or a diastolic pressure of 80 to 89 mmHg, such nonpharmacologic methods should be used to reduce blood pressure. Pharmacological agents should be initiated in patients who develop hypertension (blood pressure ≥140/≥90 mmHg)

Management

 Major guidelines suggest that the goal blood pressure in patients with diabetes mellitus is less than 140/90 mmHg, although prior guidelines had suggested more intensive lowering to less than 130/80 mmHg . Two small trials (Normotensive ABCD and SANDS) and the large ACCORD BP trial addressed the value of lower goal blood pressures in patients with diabetes, with mean attained systolic pressures below 120 mmHg in the aggressive therapy groups in SANDS and ACCORD BP. A meta-analysis of the ACCORD BP, ABCD, and HOT trial (suggested that intensive blood pressure lowering in patients with diabetes significantly lowers the incidence of stroke (2 versus 3.1 percent) but does not significantly lower the risk of mortality (5.5 versus 6.3 percent) or myocardial infarction (7.9 versus 8.5 percent).

This is consistent with major guidelines published by members of the eighth Joint National Committee (JNC 8) and the European Societies of Hypertension and Cardiology (ESH/ESC)

GOAL BLOOD PRESSURE

A goal blood pressure of less than 130/80 mmHg in patients with diabetic nephropathy and proteinuria (500mg/day or more). Patients with moderately increased albuminuria are treated similarly to diabetic patients without proteinuria. 

CHOICE OF ANTIHYPERTENSIVE DRUGSOverall approach to selecting a therapy — The

choice of antihypertensive agents in diabetic patients is based upon their ability to do the following:

●Prevent mortality●Prevent adverse cardiovascular events, such

as myocardial infarction, stroke, and heart failure

●Prevent the progression of renal disease, if present

●In patients with severely increased albuminuria (formerly called "macroalbuminuria"), we treat with an ACE inhibitor or an ARB. We also use these drugs in patients with moderately increased albuminuria (formerly called "microalbuminuria

●In patients without increased albuminuria, initial monotherapy can consist of an ACE inhibitor, ARB, thiazide diuretic, or calcium channel blocker. However, because angiotensin inhibitors can prevent albuminuria, and because thiazide diuretics have the disadvantage of an adverse effect on glucose metabolism, many experts will choose an ACE inhibitor or ARB even in patients without albuminuria.

●In patients who require more than one drug to control their blood pressure, we treat with a combination of an ACE inhibitor (or ARB if unable to take an ACE inhibitor) and a dihydropyridine calcium channel blocker (eg, amlodipine).

Overall approach in diabetic patients who require antihypertensive therapy is as follows:

Why ACE INHIBITORS

?????

●They lower the blood pressure, although no drug is likely to be sufficient as monotherapy.

●They have no specific toxicity, except for cough and raising the plasma potassium concentration in patients with underlying hyperkalemia or renal insufficiency.

●They have no adverse effects on lipid metabolism.●They may lower the plasma glucose concentration by increasing

responsiveness to insulin. In one study, for example, 130 patients with type 2 diabetes were stabilized for three months; the subsequent administration of captopril for four months led to a reduction in hemoglobin A1C values from 8.6 to 6.5 percent with no change in insulin dose, dietary intake, or body weight . A possible effect of ACE inhibitors in reducing the incidence of new onset type 2 diabetes is discussed elsewhere.

●They protect against the progression of moderately increased albuminuria and severely increased albuminuria due to types 1 and 2 diabetes and have been evaluated for primary prevention of diabetic nephropathy.

●They may slow the progression of retinopathy.

Angiotensin-converting enzyme (ACE) inhibitors offer a number of advantages:

 If a beta blocker is given, carvedilol may be the drug of choice because of potential benefits on glycemic control and lower rate of development of moderately increased albuminuria compared with metoprolol. A loop diuretic is likely to be necessary in patients with renal disease or heart failure.

The presence of severe and symptomatic paroxysmal hypertension should always generate suspicion of a catecholamine-secreting pheochromocytoma. However, the reality is that this tumor is rarely found among such patients. In one report, the diagnosis was established in only 1 of 300 patients evaluated for pheochromocytoma. Up to 40 percent of patients in this series fulfilled the criteria for panic disorder.

Paroxysmal hypertension (pseudopheochromocytoma)

Pseudopheochromocytoma most likely involves activation of the sympathetic system; this has been shown from the following observations :

Paroxysmal nature Association with tachycardia in some patients Increase in plasma catecholamines

documented during attacks Increase in baseline plasma epinephrine and

metanephrines Response to alpha/beta blockade

In patients in whom the diagnosis of a pheochromocytoma has been excluded, who are considered to have pseudopheochromocytoma, hypertensive episodes are generally characterized by the following three features:

An abrupt elevation of blood pressure (which can be greater than 200/110 mmHg in some patients) that is documented by a clinician or home blood pressure monitor

Equally abrupt onset of distressful physical symptoms, such as headache, chest pain, dizziness, nausea, palpitations, flushing, and diaphoresis

Attacks are not triggered by fear or panic, although fear does occur as a consequence of the frightening physical symptoms

The duration of episodes can range from 10 minutes to many hours, with frequency ranging from several per day to once every few months. Between episodes, the blood pressure is normal or may be mildly elevated

CLINICAL MANIFESTATIONS

Anxiety. Hyperthyroidism Cluster or migraine headaches Hypertensive encephalopathy Coronary insufficiency. Renovascular hypertension Central nervous system lesions, such as stroke, tumor,

hemorrhage, compression of lateral medulla, and trauma Seizure disorder. Carcinoid Drugs – cocaine, lysergic acid diethylamide, amphetamine,

and clozapine. Tyrosine ingestion combined with monoamine oxidase

inhibitors.

Differential diagnosis

 Successful treatment of pseudopheochromocytoma is usually possible, it involves the use of the following three modalities, either alone or in combination:

●Antihypertensive agents●Psychopharmacologic agents●Psychological interventionAntihypertensive agents :Severe or very

symptomatic paroxysms often require acute intervention, either with an oral or IV agent, as well as chronic preventative therapy.

MANAGEMENT

Acute management of paroxysms :  Intravenous labetalol (beginning with a bolus of 20

mg initially, followed by 40 to 80 mg every 10 minutes to a maximum dose of 200 to 300 mg) is usually very effective. If the blood pressure elevation is not extreme, oral agents, such as clonidine, can be employed acutely. Response to oral labetalol is less predictable due to considerable inter-individual differences in bioavailability. An anxiolytic agent such as alprazolam, used alone or in combination with an antihypertensive agent, can also effect rapid improvement in both symptoms and blood pressure

Chronic preventive management: Since pseudopheochromocytoma involves activation of the sympathetic system, treatment with adrenergic blockade is more likely to be effective than management with agents such as angiotensin-converting enzyme (ACE) inhibitors and diuretics, which are directed at mechanisms other than the sympathetic nervous system. The combination of any beta blocker (eg, atenolol at a dose of 12.5 to 50 mg per day or bisoprolol 2.5 to 10 mg daily) and an alpha blocker (eg, doxazosin at a dose of 0.5 to 2 mg per day) is frequently effective as preventive therapy in reducing the magnitude of blood pressure elevation. Labetalol and carvedilol can also be effective but provide a less reliable degree of alpha and beta blockade. In addition, central alpha agonists (eg, clonidine) may be effective, but fatigue and somnolence usually hamper chronic administration. In patients who are normotensive between paroxysms, the risk of hypotension is often a limiting factor in prescribing an antihypertensive regimen.

Psychopharmacologic agents : Adding an antidepressant is usually dramatically effective in eliminating paroxysms and restoring a normal quality of life in patients in whom severe or very symptomatic paroxysms recur despite alpha and beta blockade, particularly when the disorder is substantially affecting quality of life. Even when the patient rejects the possibility of an emotional basis, an antidepressant drug, such as a selective serotonin reuptake inhibitor (eg, paroxetine or citalopram at a starting dose of 10 to 20 mg per day), or a tricyclic antidepressant, such as desipramine (starting dose 10 to 25 mg per day), perhaps initially combined with an anxiolytic agent, such as clonazepam (0.5 to 1 mg twice daily), can eliminate attacks. There are inadequate data to indicate whether one antidepressant agent or class is more effective than any other.

A cure is sometimes possible in patients who are willing to consider the possibility that the disorder is linked to emotional factors. However, many patients, particularly those whose psychological well-being depends upon continued repression of deep-seated, potentially overwhelming, emotions, cannot and will not consider such a possibility. Their refusal to pursue psychotherapy should be honored. It is never appropriate to coerce a patient into psychotherapy, which would be fruitless and potentially harmful

Isolated systolic hypertension (ISH) has generally been defined as a systolic blood pressure above 160 mmHg, with a diastolic blood pressure below 90 mmHg.

However, as used in the eighth Joint National Committee report and supported by other experts, a systolic blood pressure of 140 mmHg is the upper limit of normal at all ages

Treatment of hypertension in the elderly patient, particularly isolated systolic hypertension

although adverse outcomes that can be ascribed only to excessive blood pressure lowering with antihypertensive drugs are probably not common in patients with isolated systolic hypertension, cardiovascular events can occur if the diastolic pressure is reduced below the level needed to maintain perfusion to vital organs, particularly the heart. Recommended a minimum posttreatment diastolic pressure of 60 mmHg overall or 65 mmHg in patients with known coronary artery disease unless symptoms that could be attributable to hypoperfusion occur at higher pressures

 A number of issues need to be considered before initiating antihypertensive drug therapy in the elderly :

●Lower initial doses (approximately one-half that in younger patients) should be used to minimize the risk of side effects.

●Elderly patients may have sluggish baroreceptor and sympathetic neural responses, as well as impaired cerebral autoregulation. Thus, in the absence of a hypertensive emergency or urgency, blood pressure should be lowered gradually over a period of weeks to months rather than hours to days in order to minimize the risk of ischemic symptoms, particularly in patients with orthostatic hypotension. This approach is consistent with recommendations made by the ESH/ESC. Even more caution is advised in the very old, although the benefits from careful therapy probably outweigh the risks in these patients.

●The trials showing benefit from the treatment of hypertension in the elderly were performed in relatively fit patients. Greater caution should be applied to frail patients, and treatment may be withheld if orthostatic hypotension is limiting.

Problem of orthostatic hypotension:  A potential limiting factor to the use of

antihypertensive drugs is that orthostatic (postural)and/or postprandial hypotension are found in as many as 20 percent of elderly patients with isolated systolic hypertension. Hypertensive older adults with orthostatic hypotension are significantly more likely to fall than those without orthostatic hypotension. In addition, antihypertensive treatment in elderly patients is associated with an increased risk of hip fracture during the first one to two months following initiation of therapy

In older adults with isolated systolic hypertension, we recommend lowering the systolic pressure to less than 150 mmHg compared with higher values. This evidence-based recommendation is consistent with guidelines produced by the  (ESH/ESC),  (JNC-8), (AHA), the American Society of Hypertension/InternationalSociety of Hypertension (ASH/ISH), and the Canadian Hypertension Education Program (CHEP) .There is general agreement supporting a blood pressure goal of less than 150/90 mmHg among adults 80 years and older. In patients aged 60 to 79 years, we also suggest lowering the systolic pressure to less than 140 mmHg if it can be achieved without producing significant side effects. This opinion-based suggestion is broadly consistent with the ESH/ESC, AHA, ASH/ISH, and CHEP guidelines.

Goal blood pressure

In general, three classes of drugs are considered first-line therapy for the treatment of hypertension in elderly patients: low-dose thiazide diuretics (eg, 12.5 to 25 mg/day of chlorthalidone), long-acting calcium channel blockers (most often dihydropyridines), and ACE inhibitors or ARBs. A long-acting dihydropyridine or a thiazide diuretic is generally preferred in elderly patients because of increased efficacy in blood pressure lowering

DRUGS

Preferred initial therapy with a long-acting dihydropyridine calcium channel blocker. If additional therapy is required, a long-acting ACE inhibitor/ARB can be added to achieve the desired combination regimen. This suggestion differs slightly from the ESH/ESC and the (JNC-8) guidelines in the following way: ESH/ESC suggests that monotherapy should consist of either a long-acting calcium channel blocker or a thiazide diuretic and combination therapy can consist of any two drugs from the three previously mentioned drug classes, JNC-8 suggests that, of the three major drug classes, there is no preference for either monotherapy or combination therapy

DEFINITION Resistant hypertension — Resistant

hypertension is defined in the 2008 American Heart Association scientific statement and the 2013 guidelines from the European Societies of Hypertension and Cardiology (ESH/ESC) as blood pressure that remains above goal in spite of concurrent use of three antihypertensive agents of different classess. Thus, patients whose blood pressure is controlled with four or more medications should be considered to have resistant hypertension

Resistant hypertension

RISK FACTORS: Patient characteristics that predict difficult to control hypertension include higher baseline blood pressure (particularly systolic), presence of left ventricular hypertrophy, older age, obesity, African-American race, chronic kidney disease, and diabetes.

Suboptimal therapy — Suboptimal therapy is a common cause of resistant hypertension It is most often due to the lack of administration of more effective drugs and failure to prevent volume expansion with adequate diuretic therapy

Lifestyle and diet — Obesity, a high-salt diet, physical inactivity, and heavy alcohol intake all contribute to hypertension, although not all have been examined specifically among patients with resistant hypertension.

The contribution of dietary salt to resistant hypertension was examined in a randomized trial in which twelve patients with resistant hypertension were assigned to low (50 meq/day)- or high (250 meq/day)-sodium diet for one week [23]. After a two-week washout, the patients received the other diet. Switching from the high- to low-salt diet was associated with an average reduction in office blood pressure of 23/9 mmHg, and a reduction in the 24-hour ambulatory blood pressure of 20/10 mmHg.

Medications — A variety of medications can raise the BP and, in some cases, reduce the response to antihypertensive drugs. The most commonly implicated agents are over-the-counter and prescribed medications including nonsteroidal anti-inflammatory drugs (NSAIDs), including some but not all (eg, celecoxib) of the selective cyclooxygenase-2 (COX-2) inhibitors.

The NSAIDs that raise blood pressure can interfere with the antihypertensive effect of virtually any agent, except calcium channel blockers. A presumed mechanism by which the blood pressure rises is a reduction in sodium excretion, thereby increasing the intravascular volume.

Other agents that may contribute to hypertension include sympathomimetics (diet pills, decongestants, amphetamine-like stimulants), glucocorticoids, herbal preparations, estrogen-containing contraceptives, and antidepressants.

Extracellular volume expansion — Relative or absolute volume expansion is frequently at least partially responsible for an inability to control hypertension BP. Underlying renal insufficiency, sodium retention due to therapy with vasodilators,and/or ingestion of a high-salt diet (which can be assessed by measuring sodium excretion in a 24-hour urine collection) all may play a role.

.

Secondary causes of hypertension — Patients with resistant hypertension are much more likely to have an identifiable cause of hypertension (ie, secondary hypertension). The most common are primary aldosteronism and renal artery stenosis, chronic kidney disease, and obstructive sleep apnea (table 2). Less common causes include pheochromocytoma, Cushing's syndrome, and aortic coarctation

Primary aldosteronism — Primary aldosteronism has been reported in approximately 10 to 20 percent of patients with resistant hypertension. Otherwise unexplained hypokalemia is the major clue to the presence of primary hyperaldosteronism. However, more than 50 percent of patients with proven primary hyperaldosteronism are normokalemic at presentation. Thus, the absence of hypokalemia does not exclude this disorder.

Renal artery stenosis — Renal artery stenosis is a common cause of resistant hypertension and can be due to either atherosclerotic disease or, in younger patients, fibromuscular dysplasia.

Chronic kidney disease — As renal function declines in patients with chronic kidney disease, there is an increasing need for additional antihypertensive medications. Diuretics play a central role. Diuretics should be pushed until the blood pressure goal.

Obstructive sleep apnea — Obstructive sleep apnea is common among patients with resistant hypertension who are referred for sleep studies.

Most common causes of 2ry hypertension

Hypertensive emergency in adults (often defined as systolic blood pressure ≥180 mmHg and/or diastolic blood pressure ≥120 mmHg) can be associated with a variety of acute, life-threatening complications, These include hypertensive encephalopathy, retinal hemorrhages, papilledema, or acute and subacute kidney injury.

Management of severe asymptomatic hypertension 

Hypertensive urgency is the relatively asymptomatic patient with a blood pressure in the "severe" range (ie, ≥180/≥120 mmHg), often a mild headache, but no signs or symptoms of acute end-organ damage, as with hypertensive emergencies, occurs more frequently among patients who have been nonadherent with either their chronic antihypertensive drug regimen or their low-sodium diet. Severe hypertension can also develop in medication-adherent patients following ingestion of large quantities of salt and can be controlled by resuming a low-salt diet.

How quickly should the blood pressure

be reduced?

The blood pressure should be reduced over a period of hours to days, although slower reductions may be needed in older adult patients at high risk for cerebral or myocardial ischemia resulting from excessively rapid reduction of blood pressure.

What is the blood pressure target during this period of time? − The blood pressure should usually be lowered to <160/<100mmHg. However, the mean arterial pressure should not be lowered by more than 25 to 30 percent over this relatively short period of time. Thus, the short-term blood pressure target may need to be above 160/100 mmHg in patients who present with very high pressures. This approach has not been well studied and is based mostly upon experience. In the long-term, the blood pressure should usually be reduced further (eg, <140/<90 mmHg).

If the blood pressure needs to be lowered over a period of hours, we use oral furosemide, oral clonidine, or oral captopril.

Rapidity of blood pressure lowering — The rapidity with which blood pressure should be brought to safe levels is controversial and not based upon high-quality medical evidence. In the absence of symptoms, a gradual reduction in pressure is suggested over a period of several hours to several days

To achieve relatively rapid initial blood pressure reduction, we use one of the following agents:

●Oral furosemide (if the patient is volume overloaded) at a dose of 20 mg (or higher if the renal function is not normal)

●Oral clonidine (but not intended as long-term therapy) at a dose of 0.2 mg

●Oral captopril (if the patient is not volume depleted) at a dose of 6.25 or 12.5 mg

However, sublingual nifedipine is contraindicated in this setting and should not be used, cerebral or myocardial ischemia or infarction can be induced by aggressive antihypertensive therapy if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation. This has been most often described with sublingual nifedipine, which may produce an unpredictable and uncontrolled blood pressure reduction as well as severe ischemic complications. This was a major reason why the use of nifedipine capsules for hypertension is not approved by the United States Food and Drug Administration (US FDA), and why most hospitals' intensive care units and emergency departments restrict the use of this medication.

WARNING