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Medicine II: Lecture on Hypertension Lerrie Gutierrez, MD


The Seventh Report on the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-7) v Purpose Publication of many new studies Need for a new, clear, and concise guideline useful for clinicians Need to simplify classification of blood pressure Blood Pressure Measurement and Clinical Evaluation v Classification of Blood Pressure v Cardiovascular Disease Risk Hypertension prevalence: 50M people in the US The blood pressure relationship to risk of cardiovascular disease is continuous, consistent and independent of other risks Each increment of 20/10 mmHg doubles the risk of cardiovascular disease across the entire blood pressure range starting from 115/75 mmHg Prehypertension signals the need for increased education to reduce BP in order to prevent HPN v Benefits of lowering blood pressure Average percent reduction Stroke incidence: 35-40% Myocardial infarction: 20-25% Heart failure: 50% In stage I HPN and additional cardiovascular disease risk factors, achieving a sustained BP over 10 years will prevent 1 death for every 11 patients treated v Blood pressure control rates v Blood pressure measurement techniques In-office: Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm Ambulatory BP monitoring: indicated for evaluation of white coat HPN. Absence of 10-20% blood pressure decreased during sleep may indicated increased cardiovascular disease risk (Every 30 minutes, BP is recorded in a digital mode, then downloaded into the computer to be analyzed) Deepers: Decreased BP during sleep Non-deeper: increased risk Normally higher in the right arm Self-measurement Provides information on response to therapy. May help improve adherence to therapy and evaluate white coat HPN Cant monitor BP during sleep May not give accurate measurement v Patient evaluation: Laboratory tests and other diagnostic procedures Guidelines in measuring BP v Crossing legs will increase BP v Posture For patients who are older than 65 years, diabetic or receiving anti-hypertensive therapy, check for postural changes by taking readings immediately and 2 minutes after the patient stands Sitting pressure are usually adequate for routine followup. Patient should sit quietly with back supported for 5 minutes and arm supported at level of the heart v Circumstances No caffeine for preceding hour No smoking for preceding 15 minutes No exogenous adrenergic stimulants e.g. phenylephrine in nasal decongestants or eyedrops for pupillary dilation Quiet warm setting

Home reading taken under varying circumstances and 24 hour ambulatory recordings my be preferable and more accurate in predicting subsequent cardiovascular disease v Equipment Cuff size: The bladder should encircle and cover 2/3 of the length of the arm; if not, place the bladder over the brachial artery; if bladder is too small, spuriously high readings may result Manometer: Aneroid gauges should be calibrated every 6 months against a mercury manometer For infants, use ultrasound equipment, e.g. the Doppler method Factors that affect BP measurement v Instrumentation BP apparatus: Mercury, aneroid, digital Blood pressure cuffs (sizes), area of arm covered v Technique of BP measurement v Patient factor v Environment Timing of BP measurement v Diagnosis of HPN: Multiple readings taken at various times throughout the waking hours v Monitoring of HPN therapy: BP should be measured prior to intake of anti-hypertensive medications to determine the trough or nadir effect v False positive results: food intake, excess caffeine, smoking, cool environment, patient talking Patient position v BP usually taken in sitting position. Supine position increases SBP and decreases DBP by 2-3 mmHg v Sitting and standing BP needed to detect postural hypotension (elderly, DM) v Patient should sit quietly for 5 minutes before BP is taken Apprehension causes elevation of BP 20-30% of patients with office HPN are normotensive at home (White Coat HPN) Technique of Measurement v Step 1: With the arm supported at the level of the heart, inflate the cuff to a pressure approximately 30mmHg greater than the SBP (Estimated from disappearance of brachial arterial pulse on palpation) v Step 2: Place stethoscope lightly over the brachial artery and deflate slowly at a rate of 2-3 mmHg per heart beat v SBP: Pressure at which the brachial pulse can first be palpated or first heard by auscultation (Korotkoff phase I) v DBP Disappearance of pulse on auscultation (Korotkoff phase V) on most patients Abrupt muffling of pulse (Korotkoff phase IV) in those with more than 10mmHg between phase IV and V (Anemia, aortic regurgitation, thyrotoxicosis, high output states) v Measure BP initially on both arms and use arm with higher BP on subsequent measurements v Take BP at least twice on each visit allowing 1 to 2 minutes interval between measurements v Additional or continued measurements should be made if there is a more than 5 mmHg difference between 2 consecutive measurements v Recorded BP should be the average of the last 2 measurements

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Patient Evaluation v Evaluation of patients with documented risk factors has 3 objectives Assess lifestyle and identify other cardiovascular risk factor or concomitant disorder that affects prognosis and guides treatment Reveal identifiable causes of high BP Assess the presence or absence of target organ damage and cardiovascular disease Cardiovascular Disease Risk Factors v HPN v Cigarette smoking v Obesity (BMI > 30kg/m2) v Physical inactivity v Dyslipidemia v DM v Microalbuminuria or estimated GFR <60 ml/min v Age (Older than 55 years for men, 65 for women) v Family history of premature cardiovascular disease Identifiable causes of HPN v Sleep apnea v Drug induced or related causes v Chronic Kidney Disease v Primary Aldosteronism v Renovascular disease v Chronic steroid therapy and Cushings syndrome v Pheochromocytoma v Coarctation of the aorta v Thyroid or parathyroid disease Target Organ Damage v Heart LVH Angina or prior MI Prior coronary revascularization Heart failure v Brain: Stroke or transient ischemic attack v Chronic kidney disease v Peripheral artery disease v Retinopathy Laboratory Tests v Routine test ECG Urinalysis Blood glucose and hematocrit Serum K, Cr, or the corresponding GFR and Calcium Lipid profile, after 9 to 12 hours fast, that include HDL and LDL cholesterol and triglycerides v Optional test: Measurement of urinary albumin excretion or albumin/creatinine ratio v More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved Treatment Overview v Goal of Therapy Reduce cardiovascular disease and renal morbidity and mortality Treat BP < 140/90 or BP <130/80 in patients with diabetes or chronic kidney disease Achieve SBP goal especially in persons older than 50 years of age v Lifestyle Modification Weight reduction: 5-20 mmHg/ 10 kg weight loss Adopt dietary approach high in fiber eating plan Dietary sodium reduction (100 mEq/mL, 2.5 or 6 g of Sodium) Physical activity: 30 minutes of aerobic exercise for 4x a week Moderation of alcohol consumption: 3 oz of alcohol

v Pharmacologic Treatment Without compelling indications (increased BP only) Stage 1 HPN Thiazide type of diuretics for most May consider ACEIs, Angiotensin receptor blockers, Beta blockers, CACB, or combination Stage 2 HPN 2 drug combination for most (usually thiazide and ACEI, or ARB, or BB, or CACB) With compelling indications: Drugs for the compelling indication, other anti-hypertensive drugs as needed v Classification and management of BP for adults v Follow-up and monitoring Patients should return for follow-up and adjustment of medications until BP goal is reached More frequent visits for stage II HPN or with complicating comorbid condition Serum K and Cr monitored 1-2 times per year After BP at goal and stable, follow-up visits at 3 to 6 months interval Co-morbidities, such as HF, associated disease such as DM and the need for laboratory tests influence frequency of visits LVH v Independent risk factor that increases the risk of cardiovascular events v Regression of LVH occurs with aggressive BP management, weight loss, sodium restriction, and treatment with all classes of drugs except the direct vasodilators, hydralazine and minoxidil Peripheral Arterial Disease (PAD) v PAD is equivalent in risk to ischemic heart disease v Any class of drugs can be used in most PAD v Beta blockers may increase morbidity because alpha adrenergic stimulation is unopposed v Other risk factors should be managed aggressively v Aspirin should be used HPN in Older Persons v More than 2/3 of people over age 65 have HPN v This population has the lowest rate of BP control v Treatment, including those who with isolated systolic HPN, should follow the same principles outlined or general care of HPN v Lower initial drug doses maybe indicated to avoid symptoms; standard doses and multiple drugs will be needed to reach BP targets Postural hypotension v Decrease in standing SBP >10 mmHg, when associated with dizziness/ fainting, more frequent in older patients with DM, taking diuretics, venodilators and some psychotropic drugs v BP in these individuals should be monitored in the upright position v Avoid volume depletion and excessively rapid dose titration of drugs Dementia v Dementia and cognitive impairment occur more commonly in patients with HPN v Reduced progression of cognitive impairment occurs with effective anti-hypertensive therapy HPN in Women v Oral contraceptives may increase BP and BP should be checked regularly. In contrast, hormonal replacement therapy does not raise BP
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v Development of HPN: Consider other forms of contraception v Pregnant women with HPN should be followed up carefully. Methyldopa, beta blockers, and vasodilators preferred for safety of the fetus. ACEIs and ARBs are contraindicated in pregnancy Children and Adolescents v HPN defined as BP of 95th percentile or greater, adjusted for age, height and gender v Use lifestyle interventions first, then drug therapy for higher levels of BP or if insufficient response to lifestyle modifications v Drug choices similar in children and adults, but effective doses are smaller v Uncomplicated HPN not a reason to restrict physical activity Hypertensive Emergencies and Urgencies (Under discretion of physician) v Patients with marked BP elevations and acute target organ damage (encephalopathy, MI, unstable angina, pulmonary edema, eclampsia, stroke, head trauma, life-threatening arterial bleeding or aortic dissection) require hospitalization and parenteral drug therapy v Patients with markedly elevated BP but without target organ damage usually do not require hospitalization, but should receive immediate combination oral anti-hypertensive therapy Additional considerations in Anti-Hypertensive Drug Choices v Potential favorable effects Thiazide type diuretics useful in slowing demineralization in osteoporosis Beta blockers useful in treatment of atrial tachyarrhythmias/ fibrillation, migraine, thyrotoxicosis (short-term), essential tremor, or perioperative HPN CACB useful in Reynauds syndrome and certain arrhythmias Alpha-blockers useful in prostatism v Potential unfavorable effects Thiazide diuretics should be used cautiously in gout or a history of significant hyponatremia Beta blockers should be generally avoided in patients with asthma, reactive airway disease, or second or third degree heart block ACEIs or ARBs are contraindicated in pregnant women or those likely to be pregnant (anyone who is still menstruating) ACEIs should not be used in individuals with a history of angioedema Aldosterone antagonists and potassium-sparing diuretics can cause hyperkalemia Strategies for improving adherence to Regimens v Clinician empathy increases patient trust, motivation, and adherence to therapy v Physician should consider the patients cultural beliefs and individual attitudes in formulating therapy Causes of Resistant HPN v Improper BP measurement v Excess sodium intake v Inadequate diuretic therapy v Medication Inadequate doses Drug actions and interactions (NSAID, illicit drugs, sympathomimetic drugs, oral contraceptives) Over-the-counter drugs and herbal supplements v Excess alcohol intake v Identifiable causes of HPN

ADDITIONAL NOTES: Definition of Hypertension v The level of blood pressure at which the benefits (minus the risks and costs) of action exceed the risk and costs (minus the benefits) of traction v Definition of hypertension is somewhat arbitrary and usually taken as that level of pressure associated with a doubling of long-term risk v Increased relative risk in patients with increased blood pressure (systolic and diastolic) v The issue of what blood pressure level should be taken to signify hypertension is further complicated by its typically marked variability. v White Coat Hypertension: Both transient and persistent elevations in pressure commonly seen when it is taken in the physicians office or hospital (with marked tendency to develop true hypertension) v Borderline Hypertension: For describing diastolic pressure that only occasionally exceed 90mmHg (Labile) Blood Pressure Classification (JNC-7) SBP DBP Normal < 120 And < 80 Pre-HPN (early) 120-139 Or 80-89 Stage 1 HPN 140-159 Or 90-99 Stage 2 HPN > 160 Or >100 Types of HPN v Primary (Essential): 90% v Secondary: 10% Blood Pressure v CO x TPR v MAP = CO x TPR

Factors which determine Blood Pressure v CO Stroke Volume Preload Blood volume: Neurohormonal factors renal sodium and water handling Venous compliance: Neurohormonal factors Inotropy: Neurohormonal factors Heart Rate: Neurohormonal factors v TPR Vascular anatomy Vascular factors Tissue factors Neurohormonal factors Neural Control of the Heart v Parasympathetic Bradycardia Decreased CO Acetylcholine Muscarinic Receptors
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v Sympathetic Tachycardia Increased contractility Increased CO Norepinephrine 1-adrenergic receptors Hypertension v Increased CO Increased Preload Increased fluid volume Renal sodium and water retention m Stress decreased filtration surface m Reduced nephron number decreased filtration surface Excess sodium intake Volume redistribution Genetic Cell membrane alteration Stress Sympathetic nervous system reactivity Renin-angiotensin excess v Increased peripheral resistance Functional constriction Genetic Cell membrane alteration Stress Sympathetic nervous system reactivity Renin-angiotensin excess Structural hypertrophy Endothelium derived growth factors Obesity Hyperinsulinemia Genetic Cell membrane alteration Stress Sympathetic nervous system reactivity Renin-angiotensin excess Hypertension v Media/ lumen ratio increased v LVH v Decreased arterial elasticity v Decreased myocardial contraction and relaxation Baroreceptor Mechanism v (In young individuals) increased ECF, increased CO, decreased TPR increased BP v (In old individuals and in latter stages) Decreased blood volume, decreased CO, increased TPR Pathology in HPN: arterioles v Increased sympathetic outflow to resistance vessels? v Wall remodeling (Wall thickening, lumen narrowing, connective tissue changes) v Network remodeling? v Damaged endothelial dilation v Altered expression of receptors and contractile proteins in SMC Renal Sodium Retention in HPN v Pressure natriuresis: Increased arterial pressure increased peritubular hydrostatic pressure decreased sodium reabsorption v Resetting in the presence of HPN: increased renal vascular resistance increased filtration fraction increased peritubular oncotic pressure increased sodium reabsorption Sympathetic Nervous System in HPN v Sympathetic Nervous System is a critical initiating factor in HPN but play little in the maintenance of chronic elevation of BP v Sympathetic Nervous System is a facilitator of chronic HPN; there is an inappropriately high sympathetic nervous system activity in early and late HPN v Increased number of adrenergic neurons and increased activity of rostroventrolateral medulla in animal models

v Lesions in anteroventral hypothalamus or NTS raise BP; lesions in RVLM, AV3V, posterolateral hypothalamus and area postrema decrease blood pressure v Angiotensin, Neuropeptide Y, cGRP and ANP modulate sympathetic nervous function v Sympathetic overactivity v Psychosocial, physical, mental stress, and sympathetic nervous system Circulating Humoral Factors v Renin-angiotensin system v Vasopressin v Endogenous ouabain v Thyroid hormone v Parathyroid hormone v Mineralocorticoid v Glucocorticoids v Endogenous natriuretic peptides v Insulin, insulin-like factors v Sex steroids v Various growth factors v Serotonin v Neuropeptide Y v Adrenomedulin v cGRP v Metabolic factors (Glucose, uric acids, lipids) Nitric Oxide v Vasodilation v Inhibits vasoconstriction v Anti-thrombotic v Anti-inflammatory v Anti-proliferative v Scavenges superoxide anion Diseases Associated with Endothelial Dysfunction and Reduced NO Production v HPN v Obesity v Dyslipidemias v Diabetes v Heart Failure v Atherosclerosis, Cigarette smoking, Aging and Vascular Injury Increased TPR v Increased vascular smooth muscle reactivity v Renal homeostatic mechanism Renin-angiotensin system Renal sodium handling v Sympathetic overactivity v Endothelial dysfunction v Neurohumoral/ hormonal factors v Intracellular alterations v Genetics v Insulin resistance v Salt intake v Obesity v Stress

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