Navdeep Singh Marivic Zerrudo

Navdeep Singh Marivic Zerrudo
HYPERTENSION Navdeep Singh Marivic Zerrudo

introduction The heart is a hollow muscular organ that is somewhat pyramid and lies within the pericardium in the mediastinum. Reference: Snell

Surfaces of the heart Sternocostal surface Diaphragmatic surface
Base of the heart Apex of the heart

Borders Apex – left ventricle, 5th left intercostal space 3.5 in from the midline Superior – formed by the roots of the great blood vessels, extends from a point on the 2nd left costal cartilage 0.5 in from the edge of the sternum to a point on the 3rd right costal cartilage from the edge of the sternum Right border – right atrium, extends from a point on the 3rd right costal cartilage 0.5 in from the edge of the sternum downward to a point on the 6th right costal cartilage 0.5 in from the edge of the sternum

Borders Left border – left ventricle, extends from a point on the 2nd left costal cartilage 0.5 in from the edge of the sternum to the apex beat of the heart Inferior border – right ventricle and the apical part of the left ventricle, extends from a point on the 6th right costal cartilage 0.5 in from the edge of the sternum to the apex beat

Anatomy of the Heart

Heart anatomy Chambers Right atrium Right ventricle Left atrium
Left ventricle

Atrioventricular valves Mitral valve Tricuspid valve
Specialized excitatory and conducting myocytes Valves Semilunar valves Aortic valve Pulmonary valve Atrioventricular valves Mitral valve Tricuspid valve Sinoatrial (SA) node pacemaker of the heart Atrioventricular (AV) node Bundle of His Right and left bundle branches

Blood supply: (3) Major Epicardial Coronary arteries:
a. Left Anterior Descending Artery - Anterior wall - Anterior two thirds of septum - Entire apex of heart, circumferentially b. Left Circumflex Coronary Artery - Posterior, lateral left aspect of heart. c. Right Coronary Artery - Posterior one third of septum, inferior aspect, and posterior wall of heart

Blood Vessels: types Arteries and arterioles – carry blood away from the heart Arterioles – control conduits - Has a strong muscular wall that can close the arteriole completely or can, by relaxing, dilate it several fold, thus, can regulate blood flow and pressure Capillaries – where nutrient and gas exchange occur Veins and venules – carry blood toward the heart. - much less smooth muscle

Hypertension Definitions:
A progressive cardiovascular syndrome arising from complex and interrelated etiologies Early markers of the syndrome often are present before elevated blood pressure is observed. Therefore, hypertension cannot be classified solely by discrete blood pressure thresholds. Progression is strongly associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidney, brain vasculature, and other organs and lead to premature morbidity and death. Pharmacy Times (Hypertension: Beyond JNC 7) page 32, March 2006

Epidemiology prevalence of hypertension
blood pressure levels rate of age-related blood pressure increase Hypertension is present in all populations It accounts for 6 % of deaths worldwide. Reference: Harrison vary among countries and among subpopulations within a country.

Epidemiology Top ten provinces with the highest hypertension prevalence Guimaras (80.1%) Camiguin (60.4%) Quirino (54.1%) Sultan Kudarat (51.4%) Pasay City (50.7%) Muntinlupa City (50.6%) Las Pinas (49.1%) Davao Oriental (44.8%) Catanduanes (40.9%) Kalinga (39.3%). Reference:

Epidemiology Bottom ten province/area with the lowest hypertension prevalence San Juan (0%) Marinduque (2.6%) Tawi Tawi (3.0%) Navotas (4.6%) Northern Samar (5.2%) Misamis Occidental (8.3%) Masbate (8.5%) Bataan (10.4%) Siquijor (10.43%) Sorsogon(11.4%) Reference:

Mortality Statistics > Hypertensive heart disease (2004) by country
RANK COUNTRIES DEATHS # 1 United States: 23,761 deaths # 2 Germany: 13,253 deaths # 3 Brazil: 11,561 deaths # 4 Romania: 9,347 deaths # 5 Mexico: 3,795 deaths # 6 Colombia: 3,672 deaths # 7 Japan: 3,375 deaths # 8 South Africa: 3,216 deaths # 9 Poland: 2,741 deaths # 10 Hungary: 2,713 deaths Reference:

Epidemiology Prevalence of Hypertension in the U.S. (HARRISON’S INTERNAL MEDICINE) 33.5 % among Hispanic Blacks 28.9 % among Hispanic Whites 20.7 % among Mexican Americans Out of the world, incidence of high blood pressure is highest in African Americans 36.7% of African American men have high blood pressure One in three blacks have hypertension 30% of African American male deaths are connected to hypertension/high blood pressure 27.9% of Latin American male deaths are connected to hypertension/high blood pressure Reference:

Epidemiology In the United States, average systolic blood pressure is higher for men than for women during early adulthood. At age 60 and older, systolic blood pressures of women are higher than men. Diastolic blood pressure increases progressively with age until about 55 years old, after which, it tends to decrease.

Epidemiology Philippines 9.6M are hypertensive
15.4M are predisposed to be hypertensive among adults, 20 years and over for over 5 years, hypertension ranks as the fifth leading cause of morbidity Reference:

epidemiology Hypertension increases with age.
Among aged ≥ 60, prevalence is 65.4 %. In African Americans, it appears earlier. Obesity and weight gain are strong and independent risk factors. Sixty percent of hypertensive patients are > 20 % overweight.

TYPES OF HYPERTENSION PRIMARY HYPERTENSION
90 % of all cases, high BP with na apparent cause Factors – genetics, race, gender, age, diet, weight, lifestyle SECONDARY HYPERTENSION 10 % of all cases, high BP by pre-existing physical condition such as kidney or thyroid condition

Mechanisms of Hypertension
intravascular volume autonomic nervous system renin-angiotensin-aldosterone system vascular mechanisms.

Intravascular volume Primary determinant of arterial pressure over the long term Cardiac output Directly related to stroke volume and heart rate Directly related to arterial pressure There is an increase with arterial pressure with increased cardiac output. This occurs with increased blood volume. CO = SV x HR Arterial pressure = CO x TPR

Autonomic Nervous System
Maintains cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. Adrenergic reflexes modulate blood pressure over the short term. Adrenergic function with hormonal and volume related factors contributes to the long term regulation of blood pressure.

Renin- Angiotensin-Aldosterone System
It contributes to blood pressure regulation via the vasoconstrictor properties of angiotensin II the sodium retaining properties of aldosterone. Renin is an aspartyl protease found in the kidney. Active renin once relased into the circulation cleaves angiotensinogen to form an inactive decopeptide, angiotensin I. A converting enzyme, located primarily but not exclusively in the pulmonary circulation, converts angiotensin I to the active octapeptide, angiotensin II. Angiotensin II further stimulates release of aldosterone.

Primary Stimuli for Renin Secretion Decreased NaCl transport in the thick ascending loop of Henle Decreased pressure or stretch within the renal afferent arteriole Sympathetic nervous system stimulation of renin-secreting cells via ß1 adrenoreceptors

Vascular mechanisms The decrease in lumen size of blood vessels significantly increases resistance. This contributes to increased peripheral resistance. This may occur in cases of arteriosclerosis where there is plaque formation in the vessel wall reducing the diameter of a lumen. The stiffness of a blood vessel also contributes to resistance. It is found in most hypertensive patients and in the elderly.

Identifiable causes of hypertension
Chronic kidney disease Renal parenchymal disease Altered excretory function – defects in renal excretion of salt and water Altered RAAS – ischemic changes resulting from intrarenal scarring may activate the RAAS abd contribute to hypertension in patient with early or advanced renal failure Coarctation of the aorta

Cushing’s syndrome glucocorticoid excess resulting from exogenous glucocorticoid therapy Hypertension may occur because cortisol has mineralocorticoid-like effects and therefore leads to the retention of sodium and water Other glucocorticoid excess states – remediable hyperaldosteronism Chronic steroid therapy

Drug induced or drug related Oral contraceptives – hypertension occurs as a result of estrogen-induced increases in angiotensin synthesis in the liver Obstructive uropathy Primary aldosteronism and other mineralocorticoid excess states By inducing sodium and water retention leading to expansion of the ECF volume Often accompanied by hypokalemia because mineralocorticoids promote renal potassium excretion in the collecting duct of the nephron Pheochromocytoma Tumors of the adrenal medulla increases the secretion of the catecholamines leading to hypertension

Renovascular hypertension Result from complex interplay between activation of the renin-angiotensin-angiotensin-aldosterone system and the sympathetic nervous sytem Sleep apnea Thyroid or parathyroid disease

Genetics of Hypertension
Genetic abnormalities associated with several rare forms of hypertension, includes the following: mineralocorticoid-remediable aldosteronism 11beta-hydroxylase and 17alpha-hydroxylase deficiencies Liddle’s syndrome, the syndrome of apparent mineralocorticoid excess pseudohypoaldosteronism type Candidate genes angiotensinogen alpha-adducin, beta- and DA-adrenergic receptors beta-3 subunit of G proteins

Risk Factors: Modifiable Unhealthy lifestyle which include
Cigarette smoking unmanaged stress salty food consumption physical inactivity being overweight Reference: Non modifiable factors genetic predisposition to hypertension disease condition like diabetes heart disease kidney disease high cholesterol level stroke increasing age

Patient Evaluation: Objectives:
to assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment to reveal identifiable causes of high BP to assess the presence or absence of target organ damage and CVD

Patient Evaluation: Patient evaluation methods medical history
physical examination routine laboratory tests Urinalysis, CBC, electrolytes, renal function test, FBS, total cholesterol, HDL, 12-L ECG Optional laboratory tests Creatinine clearance, microalbuminuria, 24-hr urinary protein, blood calcium, uric acid, fasting triglycerides/LDL, HgbA1C, TSH, Echocardiography

Patient Evaluation: The physical examination includes the following:
an appropriate measurement of BP with verification in the contralateral arm; an examination of the optic fundi a calculation of body mass index (BMI) (measurement of waist circumference is also very useful) an auscultation for carotid, abdominal, and femoral bruits; a palpation of the thyroid gland a thorough examination of the heart and lungs an examination of the abdomen for enlarged kidneys, masses, distended urinary bladder, and abnormal aortic pulsation a palpation of the lower extremities for edema and pulses Neurological assessment.

Diagnosis: Because most individuals with hypertension do not exhibit any symptoms or feelings of malaise, they may assume that their blood pressure is normal. Occasionally, if blood pressure reaches extreme levels, individuals may experience some symptoms, such as the following: Dizziness Diplopia Headache Shortness of breath Chest pain Abdominal pain

JNC-7 Blood Pressure Classification
Systolic Pressure Diastolic Pressure < 120 < 80 Pre-hypertension 80-89 Hypertension Stage 1 90-99 Stage 2 >159 >100

Accurate Blood Pressure Measurement in the Office
Persons should be seated quietly for atleast 5 minutes in a chair, with feet on the floor, and arm supported at heart level. Caffeine, exercise, and smoking should be avoided for at least 30 minutes prior to measurement. Measurement of BP in the standing position is indicated periodically, especially in those at risk for postural hypotension, prior to necessary drug dose or adding a drug, and in those who report symptoms consistent with reduced BP upon standing. An appropriately sized cuff (cuff bladder encircling at least 80 percent of the arm) should be used to ensure accuracy.

Accurate Blood Pressure Measurement in the Office
At least two measurements should be made and the average recorded. For manual determinations, palpated radial pulse obliteration pressure should be used to estimate SBP— the cuff should then be inflated 20–30 mmHg above this level for the auscultatory determinations; the cuff deflation rate for auscultatory readings should be 2 mmHg per second. SBP is the point at which the first of two or more Korotkoff sounds is heard (onset of phase 1), and the disappearance of Korotkoff sound (onset of phase 5) is used to define DBP. Clinicians should provide to patients, verbally and in writing, their specific BP numbers and the BP goal of their treatment.

Treatment Although there is no known cure to hypertension, it is treatable using various pharmacologic and nonpharmacologic measures.

Goals of Therapy The ultimate public health goal of antihypertensive therapy is to reduce cardiovascular and renal morbidity and mortality. Since most persons with hypertension, especially those >50 years of age, will reach the DBP goal once the SBP goal is achieved, the primary focus should be on attaining the SBP goal. Treating SBP and DBP to targets that are <140/90 mmHg is associated with a decrease in CVD complications. In patients with hypertension and diabetes or renal disease, the BP goal is <130/80 mmHg.

treatment Non-pharmacologic Pharmacologic Lifestyle modification Thiaz
BB ACEI ARB ALDO ANT CCB

Achieving Blood Pressure Control in Individual Patients:
Therapy begins with lifestyle modification The maximum protection against combined cardiovascular endpoints is achieved with pressures <135–140 mmHg for systolic blood pressure and <80– 85 mmHg for diastolic blood pressure More aggressive blood pressure targets for blood pressure control (e.g., blood pressure < 130/80 mmHg) may be appropriate for patients with diabetes, CHD, chronic kidney disease, or with additional cardiovascular disease risk factors. In diabetic patients, effective blood pressure control reduces the risk of cardiovascular events and death as well as the risk for microvascular disease (nephropathy, retinopathy).

Risk reduction is greater in diabetic than in nondiabetic individuals. If BP goal is not achieved via lifestyle modification, thiazide-type diuretics should be used as initial therapy for most patients, either alone or in combination with one of the other classes (ACEIs, ARBs, BBs, CCBs) that have also been shown to reduce one or more hypertensive complications in randomized controlled outcome trials. If the initial drug selected is not tolerated or is contraindicated, then a drug from one of the other classes proven to reduce cardiovascular events should be substituted. Since most hypertensive patients will require two or more antihypertensive medications to achieve their BP goals, addition of a second drug from a different class should be initiated when use of a single agent in adequate doses fails to achieve the goal.

When BP is >20 mmHg above systolic goal or 10 mmHg above diastolic goal, consideration should be given to initiate therapy with two drugs, either as separate prescriptions or in fixed-dose combinations. The initiation of therapy with more than one drug increases the likelihood of achieving BP goal in a more timely fashion. The use of multidrug combinations often produce greater BP reduction at lower doses of the component agents, resulting in fewer side effects. The use of fixed-dose combinations may be more convenient and simplify the treatment regimen, and may cost less than the individual components prescribed separately.

Use of generic drugs should be considered to reduce prescription costs, and the cost of separate prescription of multiple drugs available generically may be less than nongeneric, fixed-dose combinations. The starting dose of most fixed-dose combinations is usually below the doses used in clinical outcome trials, and the doses of these agents should be titrated upward to achieve the BP goal before adding other drugs. Caution is advised in initiating therapy with multiple agents, particularly in some older persons and in those at risk for orthostatic hypotension, such as diabetics with autonomic dysfunction.

Lifestyle Modifications
Adoption of healthy lifestyles by all persons is critical for the prevention of high BP and is an indispensable part of the management of those with hypertension. Weight loss of as little as 10 lbs (4.5 kg) reduces BP and/or prevents hypertension in a large proportion of overweight persons, although the ideal is to maintain normal body weight. BP is also benefited by adoption of the Dietary Approaches to Stop Hypertension (DASH) eating plan which is a diet rich in fruits, vegetables, and lowfat dairy products with a reduced content of dietary cholesterol as well as saturated and total fat (modification of whole diet).

Lifestyle Modifications
Reduce dietary sodium intake to no 2–8 mmHg more than 100 mmol per day (2.4 g sodium or 6 g sodium chloride). Engage in regular aerobic physical 4–9 mmHg activity such as brisk walking (at least 30 min per day, most days of the week). Moderation of alcohol - limit consumption to no more than 2–4 mmHg consumption

Pharmacologic Treatment
A large number of drugs are currently available for reducing BP. More than two-thirds of hypertensive individuals cannot be controlled on one drug and will require two or more antihypertensive agents selected from different drug classes. In hypertensive patients with lower BP goals or with substantially elevated BP, three or more antihypertensive drugs may be required.

Diuretics Low-dose thiazide diuretics are often used as first-line agents, alone or in combination with other antihypertensive drugs. Thiazides inhibit the Na+/Cl– pump in the distal convoluted tubule and, hence, increase sodium excretion. Long term, they may also act as vasodilators. Thiazides are safe, efficacious, and inexpensive and reduce clinical events. They provide additive blood pressure–lowering effects when combined with beta blockers, ACE inhibitors, or angiotensin receptor blockers.

Diuretics In contrast, addition of a diuretic to a calcium channel blocker is less effective. Usual doses of hydrochlorothiazide range from 6.25–50 mg/d. Owing to an increased incidence of metabolic side effects (hypokalemia, insulin resistance, increased cholesterol), higher doses are generally not recommended. The main pharmacologic target for loop diuretics is the Na+-K+-2Cl– cotransporter in the thick ascending limb of the loop of Henle. Loop diuretics are generally reserved for hypertensive patients with reduced glomerular filtration rates [reflected in serum creatinine > 220 mol/L (>2.5 mg/dL)], CHF, or sodium retention and edema for some other reason such as treatment with a potent vasodilator, e.g., minoxidil.

Diuretics Indapamide – non-thiazide sulfonamide diuretic with both diuretic and vasodilator activity Amiloride – inhibits smooth muscle responses to contractile stimuli, probably through effects on transmembrane and intracellular calcium movement that are independent of its action on sodium excretion Thiazide diuretics – appropriate for most patients with mild to moderate HTN and normal renal and cardiac fxn Loop diuretics – powerful for severe HTN Potassium-sparing diuretics – Useful both to avoid excessive potassium depletion, particularly in patients taking digitalis and to enhance the natriuretic effects of other diuretics

Diuretics Loop diuretics Drug Total daily oral dose Bumetanide
1As single dose or in two divided doses Drug Total daily oral dose Bumetanide 0.5 – 2 mg Ethacrynic acid 50 – 200 mg Furosemide 20 – 80 mg Torsemide 5 – 20 mg

Potassium-sparing diuretics & COMBINATION PREPARATIONS
TRADE NAME AGENT HYDROCHLOROTHIAZIDE Adactazide Spironolactone 25 mg 50 mg Aldactone Spironolactone 25, 50, 100 mg Dyazide Triamterene mg 25 mg Dyrenium Triamterene 50 or 100 mg Inspra 1 Eplerenone 25, 50 or 100 mg Maxzide Triamterene 75 mg Maxzide-25 mg Triamterene 37.5 mg Midamor Amiloride 5 mg Moduretic 1Eplerenone is currently approved for use only in HTN

THIAZIDES AND RELATED DIURETICS
DRUG TOTAL DAILY ORAL DOSE FREQUENCY OF ADMINISTRATION Bendroflumethiazide mg Single dose Chlorothiazide 0.5-2 g Two divided doses Chlorthalidone1 25-50 mg Hydrochlorothiazide mg Hydroflumethiazide mg Indapamide1 Methyclothiazide Metolazone1 Polythiazide 1-4 mg Quinethazone1 Trichlormethiazide 1Not a thiazide but a sulfonamide qualitatively similar to the thiazides

Blockers of the Renin-Angiotensin System
ACE inhibitors decrease the production of angiotensin II, increase bradykinin levels, and reduce sympathetic nervous system activity. Angiotensin II receptor blockers provide selective blockade of AT1 receptors, and the effect of angiotensin II on unblocked AT2 receptors may augment the hypotensive effect. Both classes of agents are effective antihypertensive agents that may be used as monotherapy or in combination with diuretics, calcium antagonists, and alpha-blocking agents. Side effects of ACE inhibitors and angiotensin receptor blockers include functional renal insufficiency due to efferent renal arteriolar dilatation in a kidney with a stenotic lesion of the renal artery.

Blockers of the Renin-Angiotensin System
Additional predisposing conditions to renal insufficiency induced by these agents include dehydration, CHF, and use of nonsteroidal anti- inflammatory drugs. Dry cough occurs in 15% of patients, and angioedema occurs in <1% of patients taking ACE inhibitors. Angioedema occurs most commonly in individuals of Asian origin and more commonly in African Americans than in Caucasians. Hyperkalemia due to hypoaldosteronism is an occasional side effect of both ACE inhibitors and angiotensin receptor blockers.

Ace inhibitors Captopril – oral: 25 mg, 50 mg tablets
Enalapril – oral: 5, 10, 20 mg tablets Parenteral: 1.25 mg enalaprilat/ml Benazepril Fosinopril Lisinopril Moexipril Perindopril Quinapril Ramipril Trandolapril

Aldosterone Antagonists
Spironolactone is a nonselective aldosterone antagonist that may be used alone or in combination with a thiazide diuretic. It may be a particularly effective agent in patients with low-renin essential hypertension, resistant hypertension, and primary aldosteronism. In patients with CHF, low-dose spironolactone reduces mortality and hospitalizations for heart failure when given in addition to conventional therapy with ACE inhibitors, digoxin, and loop diuretics.

Aldosterone Antagonists
Because spironolactone binds to progesterone and androgen receptors, side effects may include gynecomastia, impotence, and menstrual abnormalities. These side effects are circumvented by a newer agent, eplerenone, which is a selective aldosterone antagonist.

Beta Blockers Adrenergic receptor blockers lower blood pressure by decreasing cardiac output, due to a reduction of heart rate and contractility. Other proposed mechanisms by which beta blockers lower blood pressure include a central nervous system effect, and inhibition of renin release. Beta blockers are particularly effective in hypertensive patients with tachycardia, and their hypotensive potency is enhanced by coadministration with a diuretic. In lower doses, some beta blockers selectively inhibit cardiac receptors and have less influence on receptors on bronchial and vascular smooth muscle cells; however, there seems to be no difference in the antihypertensive potencies of cardio-selective and nonselective beta blockers.

Beta Blockers Certain beta blockers have intrinsic sympathomimetic activity, and it is uncertain whether this constitutes an overall advantage or disadvantage in cardiac therapy. Beta blockers without intrinsic sympathomimetic activity decrease the rate of sudden death, overall mortality, and recurrent myocardial infarction. In patients with CHF, beta blockers have been shown to reduce the risks of hospitalization and mortality. Carvedilol and labetalol block both receptors and peripheral -adrenergic receptors. The potential advantages of combined adrenergic blockade in treating hypertension remain to be determined.

Beta Blockers Propanolol – oral: 10, 20, 40, 60, 80 90 mg tab
4-8 mg/mL oral solution; Intensol 80 mg/mL sol Oral sustained-release: 60, 80, 120, 160 mg cap Parenteral: 1mg/mL for injection Metoprolol – oral: 50, 100 mg tab Oral sustained-release: 25, 50, 100, 200 mg tab Nadolol, Carteolol, Atenolol, Betalol, Bioprolol Pindolol, Acebutolol, Penbutolol Labetalol, Carvedilol

Adrenergic Blockers Postsynaptic, selective adrenoreceptor antagonists lower blood pressure by decreasing peripheral vascular resistance. They are effective antihypertensive agents, used either as monotherapy or in combination with other agents. However, in clinical trials of hypertensive patients, alpha blockade has not been shown to reduce cardiovascular morbidity and mortality or to provide as much protection against CHF as other classes of antihypertensive agents.

Adrenergic Blockers These agents are also effective in treating lower urinary tract symptoms in men with prostatic hypertrophy. Nonselective -adrenoreceptor antagonists bind to postsynaptic and presynaptic receptors and are primarily used for the management of patients with pheochromocytoma.

Sympatholytic Agents Centrally acting sympathetic agonists decrease peripheral resistance by inhibiting sympathetic outflow. They may be particularly useful in patients with autonomic neuropathy who have wide variations in blood pressure due to baroreceptor denervation. Drawbacks include somnolence, dry mouth, and rebound hypertension on withdrawal.

Sympatholytic Agents Peripheral sympatholytics decrease peripheral resistance and venous constriction by depleting nerve terminal norepinephrine. Although potentially effective antihypertensive agents, their usefulness is limited by orthostatic hypotension, sexual dysfunction, and numerous drug-drug interactions.

Calcium Channel Blockers
Calcium antagonists reduce vascular resistance through L-channel blockade, which reduces intracellular calcium and blunts vasoconstriction. This is a heterogeneous group of agents that includes drugs in the following three classes: phenylalkylamines (verapamil), benzothiazepines (diltiazem), and 1,4- dihydropyridines (nifedipine-like).

Calcium Channel Blockers
Used alone and in combination with other agents (ACE inhibitors, beta blockers, adrenergic blockers), calcium antagonists effectively lower blood pressure; however, it is unclear if adding a diuretic to a calcium blocker results in a further lowering of blood pressure. Side effects of flushing, headache, and edema with dihydropyridine use are related to their potencies as arteriolar dilators; edema is due to an increase in transcapillary pressure gradients, not to net salt and water retention.

Direct Vasodilators These agents decrease peripheral resistance and concomitantly activate mechanisms that defend arterial pressure, notably the sympathetic nervous system, the renin- angiotensin-aldosterone system, and sodium retention. Usually, they are not considered first-line agents but are most effective when added to a combination that includes a diuretic and a beta blocker.

Direct Vasodilators Hydralazine is a potent direct vasodilator that has antioxidant and nitric-oxide enhancing actions, and minoxidil is a particularly potent agent and is most frequently used in patients with renal insufficiency who are refractory to all other drugs. Hydralazine may induce a lupus-like syndrome, and side effects of minoxidil include hypertrichosis and pericardial effusion

Choice of Antihypertensive drug based on patient characteristics
Diabetic patients and those with chronic kidney disease: use ace inhibitors or angiotensin II to delay nephropathy. Young patients : use beta blockers Coronary artey disease patients : use beta blockers, Ca- antagonists. Avoid hydralazine. Heart failure patients : use ACE-inhibitors and/or diuretics. Generally avoid beta blockers and Ca-antagonists.

Athletes : Avoid beta blockers and diuretics. Broncho-pulmonary disease patients : Use verapamil and other Ca-antagonists. Avoid beta blockers. Peripheral Vascular disease patients : Use calcium-antagonists, vasodilators, or ACE- inhibitors. Avoid beta blockers. Dyslipidemic patient : Avoid beta blockers and diuretics.

End stage renal disease patients : use Ca- antagonist, diuretics and centrally acting agents. Caution on ACE- inhibitors. For stroke patient : Use ACE-inhibitors and/or diuretics. Elderly patients : Use diuretics. Generally use lower dosages.

Followup and Monitoring:
Once antihypertensive drug therapy is initiated, most patients should return for followup and adjustment of medications at monthly intervals or until the BP goal is reached. More frequent visits will be necessary for patients with stage 2 hypertension or with complicating comorbid conditions. Serum potassium and creatinine should be monitored at least one to two times per year. After BP is at goal and stable, followup visits can usually be at 3- to 6-month intervals.

Followup and Monitoring:
Comorbidities such as HF, associated diseases such as diabetes, and the need for laboratory tests influence the frequency of visits. Other cardiovascular risk factors should be monitored and treated to their respective goals, and tobacco avoidance must be promoted vigorously. Low dose aspirin therapy should be considered only when BP is controlled because of the increased risk of hemorrhagic stroke when the hypertension is not controlled.

Benefits of Lowering Blood Pressure
In clinical trials, antihypertensive therapy has been associated with reductions in (1) stroke incidence averaging 35–40 percent (2) myocardial infarction (MI), averaging 20–25 percent (3) HF, averaging >50 percent

Benefits of Lowering Blood Pressure
It is estimated that in patients with stage 1 hypertension (SBP 140–159 mmHg and/or DBP 90–99 mmHg) and additional cardiovascular risk factors, achieving a sustained 12 mmHg reduction in SBP over 10 years will prevent 1 death for every 11 patients treated. In the added presence of CVD or target organ damage, only nine patients would require such BP reduction to prevent one death.

Resistant hypertension
Refers to patients with blood pressures persistently >140/90 mmHg despite taking three or more antihypertensive agents, including a diuretic, in reasonable combination and at full doses. Resistant or difficult-to-control hypertension is more common in patients >60 years than in younger patients.

Causes of resistant hypertension
Improper Blood Pressure Measurement Volume overload Excess sodium intake Volume retention from kidney disease Inadequate diuretic therapy

Causes of resistant hypertension
Drug-induced or other causes Nonadherence Inadequate doses Inappropriate combinations Nonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitors Cocaine, amphetamines, other illicit drugs Sympathomimetics (decongestants, anorectics) Oral contraceptive hormones Adrenal steroid hormones Cyclosporine and tacrolimus Erythropoietin Licorice (including some chewing tobacco) Selected over-the-counter dietary supplements and medicines (e.g., ephedra, ma huang, bitter orange) Associated conditions Obesity Excess alcohol intake

Orthostatic Hypotension
BP measurements are typically recorded in the sitting position. This practice, while convenient for the practitioner, limits the ability to diagnose OH. Normally, standing is accompanied by a small increase in DBP and a small decrease in SBP when compared to supine values. OH is present when there is a supine-to-standing BP decrease >20 mmHg systolic or >10 mmHg diastolic.

There is more OH in diabetic individuals. There is a strong correlation between the severity of OH and premature death as well as increased incidents of falls and fractures. The causes of OH include severe volume depletion, baroreflex dysfunction, autonomicinsufficiency, and certain venodilator antihypertensive drugs, especially alpha blockers and alpha-beta blockers. Diuretics and nitrates may further aggravate OH.

In treating older hypertensive patients, clinicians should be alert to potential OH symptoms such as postural unsteadiness, dizziness, or even fainting. Lying and standing BPs should be obtained periodically in all hypertensive individuals over age 50. OH is a common barrier to intensive BP control that should be clearly documented; if present, drug therapy should be adjusted accordingly and appropriate warnings given to patients.

Hypertensive Crises: Emergencies and Urgencies
Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction. They require immediate BP reduction (not necessarily to normal) to prevent or limit target organ damage. Examples include hypertensive encephalopathy, intracerebral hemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm, or eclampsia.

Hypertensive urgencies are those situations associated with severe elevations in BP without progressive target organ dysfunction. Examples include upper levels of stage II hypertension associated with severe headache, shortness of breath, epistaxis, or severe anxiety. Majority of these patients present as noncompliant or inadequately treated hypertensive individuals, often with little or no evidence of target organ damage. Early triage to establish the appropriate therapeutic strategies for these patients is critical to limiting morbidity and mortality.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of BP and parenteral administration of an appropriate agent. The initial goal of therapy in hypertensive emergencies is to reduce mean arterial BP by no more than 25 percent (within minutes to 1 hour), then if stable, to 160/100–110 mmHg within the next 2–6 hours. Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable in the initial treatment of hypertensive emergencies or urgencies.

If this level of BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented in the next 24–48 hours. Exceptions to the above recommendation Patients with an ischemic stroke in which there is no clear evidence from clinical trials to support the use of immediate antihypertensive treatment patients with aortic dissection who should have their SBP lowered to <100 mmHg if tolerated patients in whom BP is lowered to enable the use of thrombolytic agents.

Some patients with hypertensive urgencies may benefit from treatment with an oral, short-acting agent such as captopril, labetalol, or clonidine followed by several hours of observation. However, there is no evidence to suggest that failure to aggressively lower BP in the ER is associated with any increased short-term risk to the patient who presents with severe hypertension. Such a patient may also benefit from adjustment in their antihypertensive therapy, particularly the use of combination drugs, or reinstitution of medications if noncompliance is a problem.

Most importantly, patients should not leave the ER without a confirmed follow up visit within several days. Unfortunately, the term “urgency” has led to overly aggressive management of many patients with severe, uncomplicated hypertension. Oral loading doses of antihypertensive agents can lead to cumulative effects causing hypotension.

PREVENTION Primary - measures include activities that help avoid hypertension Example : avoid fatty foods or exercise daily like atleast minutes walking Secondary - identify and treat asymptomatic persons who have already developed risk factors or preclinical disease but in whom the condition is not clinically apparent Example : early case finding and screening tests Tertiary - activities involve the care of established disease, with attempts made to restore to highest function, minimize the negative effects of disease, and prevent disease-related complications

Navdeep Singh Marivic Zerrudo

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