Hypertension 2012


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Hypertension lecture prepared for B Soma Raju lecture incorporating major current concepts of Hypertension

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Hypertension 2012

  1. 1. Hypertension Dr Uday Prashant CARE Hospitals
  2. 2. Hypertension • • • • • Introduction & Definition. How to measure? Etiology Treatment Complications
  3. 3. Global Mortality 2000: Impact of hypertension and other health risk factors Developing region Developed region 0 1 2 3 4 5 6 7 8 Attributable mortality (in millions (total: 55,861,000) Adapted from Ezzati et al. Lancet 2002;360:1347–60
  4. 4. Hypertension Definition: the force exerted by the blood against the walls of the bleed vessels Adequate to maintain tissue perfusion during activity and rest Arterial blood pressure: primary function of cardiac output and systemic vascular resistance
  5. 5. Hypertesnion • Hypertension currently is defined as a usual BP of 140/90 mm Hg or higher, for which the benefits of drug treatment have been definitively established in randomized placebo-controlled trials. • For certain high-risk patients, especially those with CAD, the recommended medical treatment threshold recently has been lowered to 130/80 mm . 27/10/2013 6
  6. 6. Hypertension • The major factors which help maintain blood pressure (BP) include the sympathetic nervous system and the kidneys. • Optimal healthy blood pressure is a systolic blood pressure of <120 mmHg and a diastolic blood pressure of <80 and cardiovascular risk increases from BP >115/75 mm Hg
  7. 7. Hypertension Category Systolic Blood Pressure Diastolic Blood Pressure Normal < 120 <80 Pre-hypertension 120-139 80-89 Hypertension – Stage 1 140-159 90-99 Hypertension – Stage 2 >160 >100
  8. 8. Blood Pressure • Exhibits a normal or Guassian distribution within the population • Increasing blood pressure is associated with a progressive increase in the risk of stroke and cardiovascular disease • Risk however rises exponentially and not linearly with pressure 27/10/2013 9
  9. 9. 27/10/2013 10
  10. 10. Measurement
  11. 11. The force of the blood in its vessels is continually varying according to...the various distances of time after taking food...also from exercise, rest, different states of vigour or vivacity of the animal and many other circumstances.” Stephen Hales The first observer of mammalian blood pressure, summarizing his remarkable observations in dogs 277 years ago.
  12. 12. d How BP was measured first
  13. 13. Complex methods of BP measurement before sphygmomanometer discovered
  14. 14. Modern methods
  15. 15. BP measurement • BP should be measured at least twice after 5 minutes of rest, with the patient seated in a chair, the back supported, and the arm bare and at heart level. • A large adult-sized cuff should be used to measure BP in overweight adults because the standard-sized cuff can spuriously elevate readings. • Tobacco and caffeine should be avoided for at least 30 minutes. • BP should be measured in both arms and both patient & doctor should not be talking during BP measurement • after 3 minutes of standing, the latter to exclude a significant postural fall in BP, particularly in older persons and in those with diabetes or other conditions (e.g., Parkinson's disease) that predispose to autonomic insufficiency.
  16. 16. Assessment of hypertension How often should BP be measured • 5 yearly - adults up to 80 years • Annually - high normal (130-139 or 85-89) & anyone with high readings at any time Confirmation of hypertension • If BP high – repeat monthly over 4-6 months. (Unless BP very high, then measure more frequently) • Do not treat on basis of one isolated reading BHS guidelines NICE BP confirmation If Initial BP > 140/90 repeat monthly for 2 months
  17. 17. Indications for ABPM 24 hour BP monitoring • Possible ‘white coat’ hypertension • Informing equivocal treatment decisions • Evaluation of nocturnal hypertension • Determining efficacy of drug treatment over 24 hours • Evaluation of symptomatic hypotension • Unusual BP variability • Diagnosis & treatment of hypertension in pregnancy • Evaluation of drug resistant hypertension
  18. 18. Aetiology of Hypertension • Primary – 90-95% of cases – also termed “essential” of “idiopathic” • Secondary – about 5% -10% of cases – Renal or renovascular disease – Endocrine disease • • • • Phaeochomocytoma Cusings syndrome Conn’s syndrome Acromegaly and hypothyroidism – Coarctation of the aorta – Iatrogenic • Hormonal / oral contraceptive • NSAIDs Kieran McGlade Nov 2001 Department of General Practice QUB
  19. 19. Causes of Secondary HTN • Common – Intrinsic renal disease – Renovascular disease – Mineralocorticoid excess – Sleep Breathing disorder • Uncommon – – – – Pheochromocytoma Glucocorticoid excess Coarctation of Aorta Hyper/hypothyroidism
  20. 20. 27/10/2013 22
  21. 21. RISK FACTORS FOR HYPERTENSION • • • • • • • • • Age Weight Race, Genetics Diet (High Sodium) Smoking Excess Alcohol Sleep apnea Stress – Mental and emotional Hormonal disorders – Hypothyroidism, POCD, Syndrome X, Cushings • Drugs – Cyclosporine, Steroids , NSAIDS etc
  22. 22. Contributory factors • Overweight • Excess alcohol Men 3 units/day; Women 2 units/days • Excess salt intake • Lack of exercise • Environmental stress
  23. 23. Examination • Appropriate measurement of BP in both arms • Optic fundi • Calculation of BMI ( waist circumference also may be useful) • Auscultation for carotid, abdominal, and femoral bruits • Palpation of the thyroid gland.
  24. 24. Examination-contd. • Thorough examination of the heart and lungs • Abdomen for enlarged kidneys, masses, and abnormal aortic pulsation • Lower extremities for edema and pulses • Neurological assessment
  25. 25. Investigation of the New Hypertensive • • • • • • • • History and examination Exclude secondary Hypertension Urea and electrolytes FBP and ESR ECG Lipid profile Urine CUE Chest x-ray Kieran McGlade Nov 2001 Department of General Practice QUB
  26. 26. Clinical clues to renal vascular disease • History Onset of hypertension before 30 years or after 50 years of age Abrupt onset of hypertension Severe or resistant hypertension Symptoms of atherosclerotic disease elsewhere Negative family history of hypertension Smoker Worsening renal function after renin-angiotensin inhibition Recurrent “flash” pulmonary edema Examination Abdominal bruits Other bruits Advanced fundal changes Laboratory Findings Secondary aldosteronism Higher plasma renin level Low serum potassium level Low serum sodium level Proteinuria, usually moderate Elevated serum creatinine level Unilateral small (atrophic) kidney size by ultrasound examination . Kieran McGlade Nov 2001 Department of General Practice QUB
  27. 27. Etiology of Primary HT • Age <40 yrs; IDH (Isolated Diastolic HT) increased CO. High RAAS & sympathetic activation • Age 40-60 yrs SDH (Systolic & Diastolic HT); increased PVR • Age >60 yrs ISH (Isolated Systolic HT); 1)Increased arterial stiffness - widened pulse pressure. 2)Reduced GFR, Na & water retention
  28. 28. Distribution of Hypertension Subtype in the untreated Hypertensive Population in NHANES III by Age ISH (SBP 140 mm Hg and DBP <90 mm Hg) SDH (SBP 140 mm Hg and DBP 90 mm Hg) IDH (SBP <140 mm Hg and DBP 90 mm Hg) 100 17% 16% <40 40-49 16% 20% 20% 11% 70-79 80+ 80 Frequency of hypertension 60 subtypes in all untreated 40 hypertensives (%) 20 0 50-59 60-69 Age (y) Numbers at top of bars represent the overall percentage distribution of untreated hypertension by age. Franklin et al. Hypertension 2001;37: 869-874.
  29. 29. Classification Important because • Younger Hypertensive patients drugs which act on RAAS & Beta Blockers are important. • Older patients CCB`s first choice and evidence of volume overload present diuretics
  30. 30. Pulse Pressure PP = SBP – DBP • Increase in pulse pressure (PP) indicates greater stiffness in large conduit arteries, primarily the thoracic aorta. • PP, therefore, is a surrogate measure of dynamic, cyclic stress during systole. • PP may be a better marker of increased CV risk than either systolic BP or diastolic BP alone in older persons.
  31. 31. Renal mechanisms • Many forms of experimental and human hypertension, the fundamental abnormality is an acquired or inherited defect in the kidneys' ability to excrete the excessive sodium load imposed by a modern diet high in salt.[22] • As humans evolved in a low-sodium/highpotassium environment, the human kidney is illequipped to handle the current exposure to high sodium and low potassium – Hence low salt diet is important
  32. 32. Neural mechanisms • Sympathetic overactivity has been demonstrated in early primary hypertension and in several other forms hypertension, associated with obesity, sleep apnea etc • deactivation of inhibitory neural inputs (e.g., baroreceptors) & activation of excitatory neural inputs (e.g., carotid body chemoreceptors, renal afferents), • an implantable carotid baroreceptor pacemaker and • catheter-based radiofrequency ablation of the renal sympathetic nerves
  33. 33. Hypertension Treatment • If the lifestyle modifications described are not adequate to bring the blood pressure to goal • <140/90 mm Hg for most individuals; • <130/80 mm Hg for those with diabetes or renal insufficiency), Start drug therapy
  34. 34. Lifestyle Recommendations for the Treatment of Hypertension 1. 2. 3. 4. 5. 6. 7. Healthy diet; High in fresh fruits, vegetables and low fat dairy products, low in saturated fat and salt in accordance with the DASH diet Regular physical activity: optimum 30-60 minutes of moderate cardiorespiratory activity 4-7/week Low risk alcohol consumption (≤2 standard drinks/day and less than 14/week for men and less than 9/week for women) Maintenance of ideal body weight (BMI 18.5-24.9 kg/m2) Weight loss (> 5 Kg) in those who are over weight (BMI>25) Waist Circumference < 102 cm for men < 88 cm for women Restriction of salt intake to less than 100 mmol/day in individuals considered salt-sensitive, such as: Canadians of African descent, age over 45, individuals with impaired renal function or with diabetes. Smoke free environment
  35. 35. Lifestyle Recommendations for Hypertension Dietary • Fresh Fruits • Vegetables • Low Fat dairy products • Low saturated fat diet in accordance with the DASH diet Dietary Sodium Restrict to target range of 65-100 mmol/day (Most of the salt in food is hidden and comes from processed food) Dietary Potassium If required, daily dietary intake >80 mmol Calcium supplementation No conclusive studies for hypertension Magnesium supplementation No conclusive studies for hypertension http://www.hc-sc.gc.ca/hpfb-dgpsa/onpp-bppn/food_guide_rainbow_e.html
  36. 36. Lifestyle Recommendations for Hypertension Physical Activity Should be prescribed to reduce blood pressure F Frequency - Four to seven days per week I Intensity - Moderate T Time - 30-60 minutes Type Dynamic exercise - Walking, jogging - Cycling - Non-competitive swimming T Exercise should be prescribed as adjunctive to pharmacological therapy
  37. 37. Lifestyle Recommendations for Hypertension Alcohol Low risk alcohol consumption • 0-2 standard drinks/day • Men: maximum of 14 standard drinks/week • Women: maximum of 9 standard drinks/week A standard drink is about 43 mL or 1.5 oz of spirits (40% alcohol), 341 mL or 12 oz of beer (5% alcohol) or 142 mL or 5 oz of wine (12% alcohol).
  38. 38. Lifestyle Recommendations for Hypertension Stress Management Stress management Hypertensive patients in whom stress appears to be an important issue Behaviour Modification Individualized cognitive behavioral interventions are more likely to be effective when relaxation techniques are employed.
  39. 39. Impact of Lifestyle Therapies on Blood Pressure in Hypertensive Adults Intervention Amount SBP/DBP 1.8g or 78 mmol/d -5.0 / -2.7 per kg lost -1.1 / -0.9 - 3.6 drinks/day -3.9 / -2.4 Aerobic exercise 120-150 min/week -4.9 / -3.7 Dietary patterns DASH diet Hypertensive Normotensive -11.4 / -5.5 -3.6 / -1.8 Reduce foods with added sodium Weight loss Alcohol intake Applying the 2005 Canadian Hypertension Education Program recommendations: 3. Lifestyle modificationsto prevent and treat hypertension Padwal R. et al. CMAJ ・ SEPT. 27, 2005; 173 (7) 749-751
  40. 40. Lifestyle Therapies in Hypertensive Adults: Summary Target Intervention Reduce foods with added sodium < 100 mmol/day Weight loss BMI <25 kg/m2 Alcohol restriction Less or equal to 2 drinks/day Exercise at least 4 times/week Dietary patterns DASH diet Smoking cessation Smoke free environment Waist Circumference < 102 cm for men < 88 cm for women
  41. 41. DEVELOPMENT OF ANTIHYPERTENSIVE THERAPIES Effectiveness Tolerability 1940s 1950 1957 1960s Direct vasodilators Peripheral sympatholytics 1970s Alpha blockers 1980s 1990s ACE inhibitors ARBs 2007 DRIs Thiazide diuretics Ganglion blockers Central alpha2 agonists Veratrum alkaloids Non-DHP CCBs DHP CCBs Beta blockers DHP, dihydropyridine; CCB, calcium channel blocker; ARB, angiotensin II receptor blocker; DRI, direct renin inhibitors
  42. 42. Clinical Trials in Patients With Disorders Related to Hypertension Heart failure/ Post-MI Diabetes 1990-1995 Renal disease Atherosclerosis 1996-1999 CVA/ Dementia LVH Dyslipidemia 2000 2001 2002 2003 2004-2008 SOLVD ELITE-2 VAL-HeFT AASK IDNT HOPE CAPTOPRIL UKPDS RALES I-PRESERVE RENAAL SAVE IRMA2 PROGRESS ALLHAT LIFE SCOPE CHARM EPHESUS VALIANT INVEST ASCOT ACCORD DREAM EUROPA/ ON-TARGET/ PEACE TRANSCEND
  43. 43. Hypertension Antihypertensive Drug Therapy
  44. 44. Landmark Trials in treatment of Hypertension • HOT, STOP, SHEP – Blood pressure lowering benefits all including elderly pts. • ALLHAT – largest hypertensive trial by any drug achieving target BP is most important • ASCOT-BPLA – ACE inhibitors with CCB`s better than Beta Blockers with diuretics • ON TARGET, ROADMAP – ARB`s better • SIMPLICITY – Renal denervation in Resistant Hypertension
  45. 45. Combinations should be initiated early • BP is maintained by complex regulatory and counter regulatory mechanisms. • Blocking of one pathway causes excess activation of other system and offsets BP reduction achieved by single drug. • Therefore combination therapy should be initiated first line instead of waiting for maximally tolerated dose of single drug
  46. 46. Combination therapy • Most trials showed that use of standard doses of any class of anti HT caused 8 mm Hg reduction Syst BP and 4 mm in Diastolic and increasing to max tolerated dose 9-10 mm reduction 5-6 mm in diastolic • Whereas low dose combination drugs caused 14-20 mm Hg reduction in BP with less side effects • Some meta analysis showed 5 times BP reduction more when combination drugs used than doubling the dose of single BP drug.
  47. 47. What Hypertensive drugs are best? • Young start with ARB and add on Beta Blockers or Diuretics • Old start with CCB and combine with ARB or Diuretics • B blockers are no longer first line drugs for BP unless they had IHD. • After 2006 ON TARGET results ARB score over ACEI • IHD pts Beta Blockers should be preferred unless contra indicated. • Diabetics and also with LV dysfunction - ACEI/ARB`s evaluate renal function. • Stroke & PVD pts CCB`s better
  48. 48. Slow approach is better • Many physicians control a patient's hypertension rapidly and completely. • Regardless of which drugs are used, this approach often leads to undue fatigue, weakness, and postural dizziness, • which many patients find intolerable, particularly when they felt well before therapy was begun.
  49. 49. Circumstances Requiring Rapid Treatment of Hypertension Accelerated-malignant hypertension with papilledema Cerebrovascular Hypertensive encephalopathy Atherothrombotic brain infarction with severe hypertension Intracerebral hemorrhage Subarachnoid hemorrhage Cardiac Acute aortic dissection Acute left ventricular failure Acute or impending myocardial infarction After coronary bypass surgery Renal Acute glomerulonephritis Renal crises from collagen-vascular diseases Severe hypertension after kidney transplantation Excessive circulating catecholamines Pheochromocytoma crisis Food or drug interactions with monoamine oxidase inhibitors Sympathomimetic drug use (cocaine) Rebound hypertension after sudden cessation of antihypertensive drugs Eclampsia Surgical Severe hypertension in patients requiring immediate surgery Postoperative hypertension Postoperative bleeding from vascular suture lines Severe body burns Severe epistaxis
  50. 50. Diuretics • Until now, hydrochlorothiazide (HCTZ) in doses of 12.5 to 25 mg has been the overwhelming choice and is the diuretic combined with various beta blockers, ACEIs, ARBs, and DRIs • However, HCTZ in these doses has not been shown to reduce morbidity or mortality. • Conversely, chlorthalidone, 12.5 to 25 mg, has shown benefit in National Institutes of Health (NIH)–sponsored trials (HDFP, MRFIT, SHEP, ALLHAT). • After many years of not being prescribed, chlorthalidone is now being recommended as an appropriate diuretic.[44,45]
  51. 51. Resistant Hypertension • This is diagnosed when blood pressure can not be reduced to below 140/90 mmHg despite a triple drug regimen. • Patients with resistant hypertension are often referred to a hypertension specialist and the cause for the resistance is often found and overcome.
  52. 52. Hypertensive Crises • Accelerated Hypertension is used BP readings are greater than 180/120. • If there is end-organ damage, but no intracranial pressure increases, this is called hypertensive emergency. • Lastly, if there is end-organ damage and papilledema (due to raised intracranial pressure), the term Malignant hypertension is used.
  53. 53. Indications for specialist referral (Part 1) Urgent treatment needed • Accelerated hypertension (severe hypertension and grade III-IV retinopathy) • Particularly severe hypertension (>220/120mmHg) • Impending complications (e.g. TIA, LVF)
  54. 54. Indications for specialist referral Part 2 Possible underlying cause Any clue in history or examination of a secondary cause, eg. low potassium with increased or high normal plasma sodium (Conn’s syndrome) • Raised serum creatinine • Proteinuria or haematuria • Sudden onset or worsening of hypertension • Resistant to multi-drug regimen (> 3 drugs) • Young age (any hypertension <20 years; needing treatment <30 years)
  55. 55. Indications for specialist referral (Part 3) Therapeutic problems • Multiple drug intolerance • Multiple drug contraindications • Persistent non-adherence or non-compliance Special situations • Unusual blood pressure variability • Possible ‘white coat’ hypertension • Hypertension in pregnancy
  56. 56. Complications A) Acute B) Chronic
  57. 57. Acute complications
  58. 58. Hypertension chronic complications • Major risk factor for: – cerebrovascular disease – myocardial infarction – heart failure – peripheral vascular disease – renal failure 27/10/2013 66
  59. 59. Complications of chronic hypertension Heart • Pressure Overload Hypertrophy, arrythmias • Heart Failure ( Systolic & Diastolic) • Accelerated atherosclerotic disease - UA, MI • Arterial (Aortic) aneurysm, dissection, and rupture. Kidney • Glomerulosclerosis -Reduction GFR, Albuminuria, ESRD • Renal artery stenosis – shrunken kidney. Retina • Hemorrhages, retinopathy, vitreous hemorrhage, retinal detachment CVS • Stroke, intracerebral and subaracnoid hemorrhage. • Cerebral atrophy and dementia
  60. 60. Retina Normal and Hypertensive Retinopathy A B C Normal Retina Hypertensive Retinopathy A: Hemorrhages B: Exudates (Fatty Deposits) C: Cotton Wool Spots (Micro Strokes)
  61. 61. Benefits of Lowering BP Average Percent Reduction Stroke incidence 35–40% Myocardial infarction 20–25% Heart failure 50%
  62. 62. Future Perspectives • The measurement of BP will become more accurate for diagnosis and cardiovascular risk stratification with the greater use of out-of-office measurements (ABP) and assessments of vascular health by measures of vascular compliance (Pulse pressure), central aortic pressure, and inflammatory biomarkers. • Future research on underlying mechanisms of primary hypertension should aim to make treatment less empiric and more effective than current practice.
  63. 63. THANK YOU