systemic hypertension craig a chasen md facc
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Overview of HypertensionOverview of Hypertension
JNC VI on Prevention, Detection, Evaluation, and Rx of High Blood Pressure (1997)– 50 million hypertensive patients in the U.S.
National Health and Nutrition Examination Survey III (NHANES III) (1995)– only 21% are controlled to <140/90 mm Hg– 35% are unaware of their condition
High-normal BP is associated with an increased risk of cardiovascular disease– N Eng J Med 2001; 345: 1291-7
Joint National Committee VIJoint National Committee VI
Category Systolic BP Diastolic BP Optimal < 120 < 80 High normal 130 – 139 85 - 89 Mild HTN 140 – 159 90 - 99 Mod HTN 160 – 179 100 - 109 Severe HTN >180 > 110
MacMahon et al 1990MacMahon et al 1990
Diastolic BP increased by 5 mm Hg– 34% increase in stroke risk– 21% increase in coronary risk
Hypertension Adverse Effects:Hypertension Adverse Effects:Framingham StudyFramingham Study
Triples risk of stroke Triples risk of CHF Doubles risk of SCD Doubles risk of MI
Types of Variation in BPTypes of Variation in BP
Short-term: HR and RR, autonomic NS Daytime: degree of activity Diurnal: BP fall during sleep Seasonal: cold weather increases BP
Obtaining BP MeasurementsObtaining BP Measurements
Sitting > 5 minutes Appropriate cuff size Cuff level with heart Legs uncrossed Self vs. RN vs. MD*
* Mancia et al., Hypertension 1987;9:209
False BP ElevationsFalse BP Elevations
Examinee: pain, alcohol, caffeine Equipment: leaky bulb valve, noise Examiner: expectation bias, hearing Examination: cuff uncentered, narrow or
low; elbow too low
Australian Therapeutic TrialAustralian Therapeutic Trial
Overall, 80% of the patients with mild-mod. HBP placed on placebo maintained a diastolic BP < 100 mm Hg and, during the average 3-yr follow-up, had no excess CV events.
Only 12.2% of the placebo treated patients noted a rise in diastolic BP > 110 mm Hg.
Management Committee.Lancet 1980;1:1261
Cardiovascular Consequences Cardiovascular Consequences of Hypertensionof Hypertension
Increased cardiac afterload leads to LVH Increased LV mass is associated with
elevated CV morbidity and mortality independent of other risk factors
Pts with BP > 160/95 have CAD, PVD & CVA > 3x than in normotensives
BP, Stroke & CHDBP, Stroke & CHD
In nine prospective observational studies and 420,000 patients with DBP ranging from 70 – 110 mm Hg who were followed for 6 – 25 years, the associations (with the above CV events) were “positive, continuous and apparently independent”.
MacMahon et al. Lancet 1990;335:765Kaplan’s Clinical Hypertension 2002
Hypertension Treatment and Hypertension Treatment and CV Outcomes over 5 Yrs.CV Outcomes over 5 Yrs.
Reduce BP by 15/6 mm Hg Reduce stroke by 34% Reduce CHD by 19%
Patient EvaluationPatient Evaluation
Determine type of hypertension Identify target organ damage Assess risk for early CV event
Patient History: IPatient History: I
Duration and prior Rx Pharmaceutical profile Family history Symptoms of secondary causes Target organ damage Presence of other risk factors
Patient History: IIPatient History: II
Concomitant Diseases Dietary History Sexual Function Features of Sleep Apnea Ability to modify life-style
HBP and Cardiac Risk FactorsHBP and Cardiac Risk Factors
50+Sedentary lifestyle
15Diabetes
40Obesity
25HDL-C < 40 mg/dl
40LDL-C > 140 mg/dl
35Smoking
PercentCardiac Risk Factor
Kaplan NM. Dis Mon 1992; 38:769-838
Physical Examination: IPhysical Examination: I
Accurate measure of BP, BMI Fundoscopy Carotid and thyroid abnormalities Heart sounds, rhythm, size Rales, rhonchi on lung exam
Physical Examination: IIPhysical Examination: II
Renal masses, waist circumference Aorta bruits, femoral pulses Peripheral pulses and edema Neurologic assessment, i.e. congnitive
JNC VI: BP & RxJNC VI: BP & Rx
Blood Pressure Stage (mm Hg)
Risk Group A NO RISK FACTORS
Risk Group B ONE RISK FACTOR
Risk Group C DIABETES or ORGAN DAMAGE
High-Normal BP 130-139/85-89
Lifestyle Modification
Lifestyle Modification
Medication Lifestyle Modification
Stage 1 HTN 140-159/90-99
Lifestyle Modification (up to 12 mo)
Lifestyle Modification (up to 6 mo)
Medication Lifestyle Modification
Stage 2,3 HTN ≥160/≥100
Medication Lifestyle Modification
Medication Lifestyle Modification
Medication Lifestyle Modification
Lifestyle Changes for HTNLifestyle Changes for HTN::
Reduce excess body weight Reduce dietary sodium to < 2.4 gms/day Adequate dietary intake of K, Ca and Mg Limit daily alcohol consumption Moderate aerobic exercise each day Cessation of cigarette smoking Garlic, fish oils, co-enzyme Q ???
NIH Consensus Conference on Physical NIH Consensus Conference on Physical Activity and CV Health (1995)Activity and CV Health (1995)
Review of 47 studies of exercise and HTN 70% of exercise groups decreased SBP by
an avg. of 10.5 mm Hg from 154 78% of subjects decreased DBP by an avg.
of 8.6 mm Hg from 98 Beneficial responses are 80 times more
frequent than negative responses
Hagberg, J., et.al., NIH, 1995: 69-71
Medical Therapy and Medical Therapy and Implications for Exercise TrainingImplications for Exercise Training
Pharmacologic and nonpharmocologic treatment can reduce morbidity
Some antihypertensive agents have side-effects and some worsen other risk factors
Exercise and diet improve multiple risk factors with virtually no side-effects
Exercise may reduce or eliminate the need for antihypertensive medications
Oral Contraceptives and HBPOral Contraceptives and HBP
BP rises a little in most women on OCs RR=1.5 for current users vs. never users
– 41 cases per 10,000 person-years of OC use
RR=1.1 for current users vs. previous users ERT is associated with lower BPs
Drug Therapy of Hypertension:Drug Therapy of Hypertension:CV Events ReductionCV Events Reduction
Diuretics BBs ACEIs CCBs
Randomized controlled trials
Slow BreathingSlow Breathing
Guided slow breathing to < 10 /min 15 minutes, 3-4 times per week Sustained reductions in SBP & DBP FDA approved July 2002 J Hum Hypertension 2001;15:263 Am J Hypertension 2001;14:74
Malignant Hypertension:Malignant Hypertension:Treatment ITreatment I
Loop diuretic Nitroprusside* Fenoldopam Labetolol Enalaprilat
Malignant Hypertension:Malignant Hypertension:Treatment IITreatment II
Esmolol* Hydralazine Nitroglycerin CCBs Phentolamine
Hypertension and PregnancyHypertension and Pregnancy
5% enter pregnancy with chronic HTN BP > 140/90 @ < 20 wks IUP, > 6 wks PP Drug of choice: alpha-methyldopa 10% develop gestational HTN > 20 wks PE = HTN + proteinuria (300 mg/24 hrs) Eclampsia = PE + seizures
Rx of acute, severe HBP Rx of acute, severe HBP in Pre-eclampsiain Pre-eclampsia
Hydralazine Labetolol Nifedipine Nitroprusside
Renovascular Hypertension:Renovascular Hypertension:IncidenceIncidence
Unselected hypertensives 1% Resistant to 2 drug therapy 10% Severe, rapidly progressive HBP 15% Accelerated-malignant HBP 32%*
4%*
Renovascular Hypertension:Renovascular Hypertension:Clinical Clues & TestingClinical Clues & Testing
Low suspicion No testing No clinical clues
Moderate suspicion Non-invasive Severe HBP (DBP > 120) Abdominal or flank bruit
High suspicion Angiography Severe HBP + elevated Cr Malignant HBP
Mann/Pickering. Ann Int Med 1992;117:845
Renovascular Hypertension:Renovascular Hypertension:Diagnostic TestsDiagnostic Tests
Captopril-enhanced renal scan Doppler ultrasonography Gadolinium MRA Spiral CT Angiography
EB Pedersen’s GuidelinesEB Pedersen’s Guidelines
Moderate or high index of suspicion No to mod. renal failure [Cr < 2.3]
Doppler vs. (ACEI) Renography, if ++ then Spiral CT vs. MRA, if ++ then, angiography
Severe renal impairment No doppler, no renography MRA preferred, o/w spiral CT or angiography
Renovascular Hypertension:Renovascular Hypertension:Medical TreatmentMedical Treatment
Aggressive BP control Lipid reduction therapy Antiplatelet therapy
Renovascular Hypertension:Renovascular Hypertension:TreatmentTreatment
Renal Artery Revascularization– Intolerant of medical Rx– Unresponsive to medical Rx– Progressive renal impairment
Renovascular Hypertension:Renovascular Hypertension:TreatmentTreatment
In patients with a high likelihood of success and low risk of complications, such as the majority of patients with fibromuscular hyperplasia and uncomplicated atherosclerotic RVHT, it is usually reasonable to proceed directly to revascularization.
Block/Pickering. Semin Nephrol 2000;20:474
PheochromocytomaPheochromocytoma
HBP, palpitation, sweating, HA Plasma / spot urine: metanephrines CT scan with adrenal cuts/ MRI If adrenal cuts nl : 131I–MIBG scan Phentolamine / Phenoxybenzamine
Primary AldosteronismPrimary Aldosteronism
HBP, weakness, alkalosis, hypokalemia Upright PAC/PRA ratio, if > 25, then Saline 500 cc/hr X 4 or NACl 10g/day X 3 Adrenal CT + P: 18-OH corticosterone Suppression scintiscan: NP-59 + dexameth Surgical therapy vs. spironolactone
Primary Aldosterone ExcessPrimary Aldosterone Excess
Aldosterone producing adenoma Bilateral adrenal hyperplasia Glucocorticoid-remediable
– chimeric11B-hydroxylase – aldosterone synthase gene– Glucocorticoids suppress ACTH
Adrenal carcinoma Extra-adrenal tumors
Corticosteroid induced HBPCorticosteroid induced HBP
Obesity, purple striae, osteopenia, DM Must r/o depression, alcoholism 1 mg dexamethasone (dexa) overnight
plasma suppression test Low dose dexa suppression test (urinary);
24-hr urinary free cortisol; plus sleeping midnight plasma cortisol test
Localization of Cortisol Localization of Cortisol ExcessExcess
Localization Pituitary Adrenal Ectopic CTH Corticotropin normal/high Low High CRH Response No response No response Dexa 8 mg Suppression No supp. No suppression Adrenal CT Nl/enlarged Tumor Nl/enlarged Pituitary CT Tumor Normal Normal Inferior petrosal Central/periph No central/peri
sinus sampling gradient gradient
Secondary HypertensionSecondary Hypertension
Hormonal: thyroid, hyperpara, acromegaly Neurologic: brain tumors, quadriplegia Acute physical stress: burns, resp distress Increased volume: EryP Rx, SIADH, PRV Chemical agents: cyclosporine, tacrolimus Sleep apnea
Reasons for Decline in CHD Reasons for Decline in CHD deaths from 1980-1990deaths from 1980-1990
43% from improved Rxs (i.e. CABG) 29% from secondary prevention (i.e. BP) 25% from primary prevention (i.e. BP)
Hunink et al JAMA1997;277:535
Exaggerated BP Response Exaggerated BP Response to Exerciseto Exercise
Among normotensive men who had an exercise test between 1971-1982, those who developed HTN in 1986 were 2.4 times more likely to have had an exaggerated BP response to exercise
Exaggerated BP Response Exaggerated BP Response to Exerciseto Exercise
Exaggerated BP was change from rest in SBP >60 mm Hg at 6 METs; SBP > 70 mm Hg at 8 METs; DBP > 10 mm Hg at any workload.
CARDIA study: subjects with exaggerated exercise BP were 1.7 times more likely to develop HTN 5 years later
J Clin Epidemiol 51 (1): 1998
Sleep, BP and CV EventsSleep, BP and CV Events
Inverted Dippers Non-dippers Excessive Dippers Dippers
Treatment of Orthostatic Treatment of Orthostatic HypotensionHypotension
Avoid overtreatment of BP Slow rising from chair/bed Supportive panty hose Avoid dehydration Volume expanders Sympathomimetics
NHANES III, phase 2NHANES III, phase 2HypertensionHypertension
Awareness 68.4% Treated 53.6% Controlled 27.4%