Your SlideShare is downloading. ×
Hypertension
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×

Saving this for later?

Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime - even offline.

Text the download link to your phone

Standard text messaging rates apply

Hypertension

2,343
views

Published on

Hypertension overview for medical students

Hypertension overview for medical students

Published in: Health & Medicine

1 Comment
3 Likes
Statistics
Notes
  • Very elucidative. Excellent didactic rationale. Is it possible to have this presentation in pwp? anacampa@usp.br
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Views
Total Views
2,343
On Slideshare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
269
Comments
1
Likes
3
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. 1
  • 2. Hypertension
  • 3. Definition of Blood PressureThe pressure exerted by blood against the artery through which it flows Blood pressure = cardiac output X systemic vascular resistance CO X SVR = BP 3
  • 4. Hypertension is defined: As the level of blood pressure linked with a doubled increased long-term risk for adverse events ORHypertension is ... “the level ofblood pressure at which thebenefits of action (i.e. therapeuticintervention) exceed those ofinaction.” 4 Evans and Rose Brit Med Bull
  • 5. 5
  • 6. 6
  • 7. Definition of Hypertension JNC - VII BHSNormal <120/<80 Optimal <120/<80Prehypertension 120-139/80-89 Normal <130/<85Stage 1 140-159/90-99 High Normal 130-139/85-89Stage 2 >160/>100 Hypertension Chobnian JAMA 2003;289:2560 Grade 1 140-159/90-99 Grade 2 160-179/100-109 Grade 3 >180/>110 Isolated syst. hypertension Grade 1 140-159/<90 Grade 2 >160/<90 Williams BMJ 2004;328;634 7
  • 8. What guidelines are used to categorize HTN?The Joint Committee on Prevention,Evaluation, and Treatment of HighBlood Pressure (JNC 7) guidelinesprovide the most current guidelineshttp://www.nhlbi.nih.gov/hbp/detect/categ.htm 8
  • 9. 9
  • 10. JNC 6 Report 10
  • 11. 11
  • 12. Prevalence65 million Americans have hypertension(HTN)Of those diagnosed with HTN < 50%have their blood pressure under controlLack of treatment leads to seriouscomplications 12
  • 13. High Prevalence of Hypertension Worldwide 60 55 Prevalence of hypertension (%) 49 49 47 42 38 38 40 28 20 0 USA Italy Sweden England Spain Finland Japan* Germany Adults aged 35–64 y (data are age- and sex-adjusted), except* (adults aged ≥ 30 y) Hypertension defined as BP ≥ 140/90 mmHg or on treatment Wolf-Maier et al. JAMA. 2003;289:2363−2369;13 Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912.
  • 14. Prevalence of Hypertension 14
  • 15. Awareness, Treatment and Control of Hypertension is Rather Low Worldwide Proportion of patients in the population (%)Country Aware Treated Controlled*Japan 16.0 – 4.1England 35.8 24.8 10.0Germany 36.5 26.1 7.8Spain 38.9 26.8 5.0Sweden 48.0 26.2 5.5Italy 51.8 32.0 9.0USA 69.3 52.5 28.6 * BP < 140/90 mmHg Wolf-Maier et al. Hypertension. 2004;43:10–17; 1515 Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912.
  • 16. BP Control Rates Trends in awareness, treatment, and control of high blood pressure in adults ages 18–74 National Health and Nutrition Examination Survey, Percent II II II (Phase 1) (Phase 2) 1976–80 1988–91 1991–94 1999–2000Awareness 51 73 68 70Treatment 31 55 54 59Control 10 29 27 34 16
  • 17. 17
  • 18. 18
  • 19. Benefits of Lowering BP Average Percent ReductionStroke incidence 35–40%Myocardial infarction 20–25%Heart failure 50% 19
  • 20. Risk of CV Mortality Doubles With Each 20/10 mmHg BP Increase• Meta-analysis of 61 prospective, observational studies• 1 million adults aged 40–69 y with BP > 115/75 mmHg• 12.7 million person-years 10 8-fold 8relative CV riskFold increase in 6 4-fold 4 2-fold 2 1-fold 0 115/75 135/85 155/95 175/105 SBP/DBP (mmHg) 20
  • 21. Each 2 mmHg Decrease in SBP Reduces CV Risk by 7–10% • Meta-analysis of 61 prospective, observational studies • 1 million adults aged 40–69 y with BP > 115/75 mmHg • 12.7 million person-years 7% reduction in risk of IHD and other 2 mmHg vascular disease decrease in mortality mean SBP 10% reduction in risk of stroke mortality 2121 Lewington et al. Lancet. 2002;360:1903–1913.
  • 22. CVD Risk HTN prevalence ~ 50 million people in the United States. The BP relationship to risk of CVD is continuous, consistent, and independent of other risk factors. Each increment of 20/10 mmHg doubles the risk of CVD across the entire BP range starting from 115/75 mmHg. Prehypertension signals the need for increased education to reduce BP in order to prevent hypertension. 22
  • 23. 23
  • 24. 24
  • 25. Factors contribute to the development of primary HTN1. Sympathetic nervous system hyperactivity2. Renin-angiotensin-aldosterone system hyperactivity3. Endothelial dysfunction 25
  • 26. 26
  • 27. Types of HTN?Primary Secondary• ?? ‘essential’idiopathic • Caused by some other• Most common type medical problem or found in 90-95% of condition: those with HTN • High-dose estrogen• Cause not well • Renal artery stenosis understood • Pregnancy (PET) • Salt sensitive • Cushing’s syndrome • RAAS dependent • pheochromocytoma • Others? 27
  • 28. 28
  • 29. ABPM ?Renin level ?? 29
  • 30. What are the Symptoms?Symptoms may or may not be present• Dizziness (unsteadiness)• Early morning headacheactivity tolerance• Malaise, fatigue• Blurring of vision• Spontaneous nosebleed• Palpitations, angina, dyspnea• Early signs/symptoms are often missed 30
  • 31. 31
  • 32. 32
  • 33. 33
  • 34. BP measurementPhysical assessment • Proper size cuff• Height & weight applied 1 inch above• Blood pressure brachial arteryMeasuring BP • Inflate cuff to 30accurately: mmHg above initial• No smoking or caffeine radial pulse check If 30 minutes before BP elevated, wait 2• Rest for 5 minutes prior minutes, recheck to BP • Check BP in other arm• Apply cuff to bare arm 34
  • 35. BP Measurement TechniquesMethod Brief DescriptionIn-office Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm. 140/90Ambulatory BP Indicated for evaluation of “white-monitoring coat” HTN. Absence of 10–20% BP decrease during sleep may indicate increased CVD risk. 130/80Self-measurement Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN. 135/85 35
  • 36. 36
  • 37. White Coat and Ambulatory BP monitoring ABPM 37
  • 38. 38
  • 39. 39
  • 40. Key Messages For persons over age 50, SBP is a more important than DBP as CVD risk factor. Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range. Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN. Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive who require health-promoting lifestyle modifications to prevent CVD. 40
  • 41. Key Messages (Continued) Thiazide-type diuretics should be initial drug therapy for most, either alone or combined with other drug classes. Certain high-risk conditions are compelling indications for other drug classes. Most patients will require two or more antihypertensive drugs to achieve goal BP. If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic. 41
  • 42. Key Messages (Continued) The most effective therapy prescribed by the careful clinician will control HTN only if patients are motivated. Motivation improves when patients have positive experiences with, and trust in, the clinician. Empathy builds trust and is a potent motivator. The responsible physician’s judgment remains paramount. 42
  • 43. Complications of HTNThe higher the BP and the longer anindividual has hypertension, the higherthe risk of complications which include:• Hypertensive heart disease• Cerebrovascular disease• Peripheral vascular disease• Kidney disease• Retinal damage 43
  • 44. 44
  • 45. 45
  • 46. Complications of Hypertension Heart  resistance   workload  left ventricular hypertrophy • CAD, angina, MI • Heart failure 46
  • 47. Complications of Hypertension Brain • Atherosclerosis, stroke 47
  • 48. Complications of Hypertension Peripheral vascular Kidney disease disease • vessels less elastic • Aortic aneurysm or  decreased dissection perfusion renal Retinal damage failure • damage to blood vessels of the eye 48
  • 49. Acute ComplicationsHypertensive Sx: papilledema,Crisis: progressive renalSevere and abrupt failure,elevation of BP encephalopathyDiastolic over Most common120mm hg cause is untreated hypertensionHigh Mortality Goal: slowly decrease BP 49
  • 50. Classifications Hypertensive Crisis Hypertensive crisis is Hypertensive urgency: categorized by the BP is elevated but there degree of organ damage is no evidence of target Hypertensive organ damage emergency: BP is severely elevated and there is evidence of target organ damage • Especially brain 50
  • 51. GOAL: Reduce ComplicationsJNC 7 guidelinesrecommend a targetBP of less than140/90Patients with renaldisease or diabetesneed BP less than130/80 51
  • 52. What Reduces Risk of Complications?REDUCING MODIFIABLE RISK FACTORS IS A KEY INTERVENTION Goal = Patient teaching to reduce risk factors Drug therapy is initiated if lifestyle changes are not effective to control BP 52
  • 53. Management of HypertensionDepends on risk groupLifestyle modificationsDrug therapy is initiated if lifestylemodifications do not achieve goalAdd or change drugs if goal not achieved 53
  • 54. TREATMENT: Lifestyle ModificationLose excess weightCut back on saltExercise regularlyCease alcohol intakeAdopt the DASH eating plan to decreasecholesterol intakeSTOP smoking 54
  • 55. DASH Diethttp://www.nhlbi.nih.gov/health/public/heart/hDietary Approaches to StopHypertension = DASH• A diet rich in fruits, vegetables and low-fat dairy products with reduced fat content• Limits sodium intake to 2.4 g/day 55
  • 56. Non-pharmacologic Managementof Hypertension Weight management • DASH Low sodium-low fat diet Smoking cessation Restrict alcohol and caffeine Regular aerobic exercise Stress management • bio-feedback, relaxation, yoga, Tai Chi 56
  • 57. 57
  • 58. Drug Therapy for HTNDiuretics Beta adrenergic• Flush excess water blockers and sodium from the Three classes: body • Cardioselective• Thiazide diuretics • Non-selective• Loop diuretics: • Combined alpha- furosemide (Lasix) beta-blockers• Potassium sparing: Aldactone 58
  • 59. The Majority of Hypertensive Patients Need Combination Therapy to Achieve BP Goals Trial (SBP achieved) ASCOT-BPLA (137 mmHg) ALLHAT (138 mmHg) IDNT (138 mmHg) RENAAL (141 mmHg) UKPDS (144 mmHg) ABCD (132 mmHg) MDRD (132 mmHg) HOT (138 mmHg) AASK (128 mmHg) 1 2 3 4 Bakris et al. Am J Med. 2004;116(5A):30S–38S; Average number of antihypertensive medications59 Dahlöf et al. Lancet. 2005;366:895–906.
  • 60. Pharmacologic Management of HypertensionAlpha-adrenergic blockers• Suppress nerve impulses to blood vessels, which allows blood to pass more easily so BP goes ↓ • prazosin (Minipress)Calcium channel blockers• decrease the influx of Ca++ into muscle cells • Act on vascular smooth muscles (primary arteries) to decrease spasm and promote vasodilation • Amlodipine (Norvasc); felodipine (Plendil) 60
  • 61. Pharmacologic Management of HypertensionAngiotensin Angiotensin IIconverting enzyme receptor blockers(ACE) inhibitors (ARB)• Decrease effect of • Prevent action of RAA system: angiotensin II and Capoten, Lisinopril produce vasodilation• Diabetes mellitus • losartan (Cozaar) w/proteinuria, heart failure 61
  • 62. Pharmacologic Management of Hypertension Vasodilators Alpha-receptor • Direct arterial agonists vasodilation • Clonidine • Sodium nitroprusside • Acts on central (Nipride) nervous system • Often used in • Lowers peripheral hypertensive crisis vascular resistance 62
  • 63. Why don’t some patients respond to therapy?Non-adherence to Drug related causestherapy Other conditions • Patients don’t take Secondary their HTN meds → complications!!! hypertension • Cost, inadequate Volume overload teaching, side effects, inconvenient dosing 63
  • 64. Causes of Resistant Hypertension Improper BP measurement Excess sodium intake Inadequate diuretic therapy Medication • Inadequate doses • Drug actions and interactions (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives) • Over-the-counter (OTC) drugs and herbal supplements Excess alcohol intake Identifiable causes of HTN 64
  • 65. Summary Key PointsTwo types of HTN: primary & secondaryInadequate BP control leads to seriouscomplications including STROKEKey point: risk factor modificationTreatment focuses on lifestylemanagement and drug therapyJNC 7 provides the most currenttreatment guidelines for hypertension 65
  • 66. Identifiable Causes of Hypertension Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease 66
  • 67. Pheochromocytoma0.01-0.1% of HTN population • Found in 0.5% of those screenedM=F3rd to 5th decades of lifeRare, investigate only if clinically suspicion: • Signs or Symptoms • Severe HTN, HTN crisis • Refractory HTN (> 3 drugs) • HTN present @ age < 20 or > 50 ? • Adrenal lesion found on imaging (ex. Incidentaloma) 67
  • 68. Pheo: Signs & SymptomsThe five P’s: • Pressure (HTN) 90% • Pain (Headache) 80% • Perspiration 71% • Palpitation 64% • Pallor 42% • Paroxysms (the sixth P!)The Classical Triad: • Pain (Headache), Perspiration, Palpitations • Lack of all 3 virtually excluded diagnosis of pheo in a series of > 21,0000 patients 68
  • 69. Pheo: Paroxysms, ‘Spells’10-60 min durationFrequency: daily to monthlySpontaneousPrecipitated: • Diagnostic procedures, I.A. Contrast (I.V. is OK) • Drugs (opiods, unopposed β-blockade, anesthesia induction, histamine, ACTH, glucagon, metoclopramide) • Strenuous exercise, movement that increases intra-abdo pressure (lifting, straining) • Micturition (bladder paraganlgioma) 69
  • 70. Pheo: ‘Rule of 10’10% extra-adrenal (closer to 15%)10% occur in children10% familial (closer to 20%)10% bilateral or multiple (more iffamilial)10% recur (more if extra-adrenal)10% malignant10% discovered incidentally 70
  • 71. Plasma MetanephrinesNot postural dependent: can drawnormallySecreted continuously by pheoSEN 99% SPEC 89%False Positive: acetaminophenAssay not widely available yet 71
  • 72. Localization: ImagingCT abdomen • Adrenal pheo SEN 93-100% • Extra-adrenal pheo SEN 90%MRI • > SEN than CT for extra-adrenal pheoMIBG Scan • SEN 77-90% SPEC 95-100% 72
  • 73. 73
  • 74. Renovascular Hypertension 74
  • 75. 75
  • 76. Endocrine HypertensionCatecholamine producing tumoursMineralocorticoid hypertensionRenin-dependent hypertensionHyperthyroidism and hypothyroidismAcromegalyHyperparathyroidism 76
  • 77. Typical clinical scenariosDifficult hypertension with hypokalaemia,on polypharmacy- referred toendocrinologist for exclusion of 2aryhypertensionCoincidentaloma of adrenal withhypertension, on polypharmacyWhich drugs are permissible, and after howmuch delay should there be beforeinvestigation? 77
  • 78. Mineralocorticoid hypertension- in whom should it be suspected?Diagnosis should be suspected in patient withhypertension, spontaneous hypokalaemia(<3.5mmol/l), and alkalosis.Severe hypokalaemia (<3.0) on diureticsInvestigate patient hypertension refractory toconventional therapy, or adrenal coincidentalomaRecent onset of hypertensionNormokalaemia present in >35% patients on lowsalt diet 78
  • 79. Clinical features of hyperaldosteronismMild to severe hypertensionSodium retention + intravascular vol exp→mineralocorticoid escapeResetting of osmostat (thirst provoked at higher [Na+])K+ loss (kaliuresis) +/- low serum K+ (unprovoked: rule outdiuretics, laxatives, vomiting, herbal supplements)Suppression of renin generation (rule out drugs,excessivedietary sodium intake)Polyuria, nocturia,fatigue,cramps, Mg++↓Exclude liquorice abuse / carbenoxolone therapyNB minor mineralocorticoids DOC, compound B 79
  • 80. Imaging in 1ary hyperaldosteronismHigh resolution CT scanning with thin (2-3mm)slicesBilateral adrenal venous catheter (measure cortisol,adrenaline + aldosterone) remains gold standard –operator dependent: right adrenal notoriouslydifficult to cannulate. Give iv ACTH (2μg/min)during sampling to magnify difference betweentumour and non-tumorous sideNon-tumorous side PAC = peripheral valuebecause of suppressed PRA 80
  • 81. Glucocorticoid remediable hyperaldosteronism GRA (FH1)Due to aberrant expression of chimeric geneformed by unequal recombination of promoterand initial parts of CYP11B1 and section ofCYP11B2 with aldosterone synthase activityAldosterone under ACTH controlAutosomal dominant: FH of early onset BP↑ withCVA ,K+↓High levels of 18-hydroxy and 18-oxocortisolRx : chronic administration of low dose GC,spironolactone, or amiloride 81
  • 82. Liddle syndromeFamilial BP↑, unprovoked K+↓, PRA↓, andundetectable PACAutosomal dominant, caused by constitutiveactivation of distal renal epithelial sodiumchannel (β,γ C-terminal subunit mutationsprevent trafficking of channel)Treated by amiloride 82
  • 83. Liddles – low renin, low aldoLicorice and SAME -- low renin, low aldoRenal artery stenosis and renin-secretingtumors -- high renin, high aldoAdrenal hyperfunction -- low renin, highaldo 83
  • 84. Renin AldoLiddle low lowLicorice low lowRAS high highConn’s low high 84
  • 85. Renin-Angiotesnin- Aldosterone SystemA drop in BP or blood Stimulates adrenalvolume causes kidneys to glands to releasesecrete renin, a renin aldosteroneprecursor to This prompts theangiotensin I kidneys to retain sodiumAngiotensin-converting and waterenzyme turns The increased volumeangiotensin I into and vasoconstrictionangiotensin II, a potent raise BPvasoconstrictor 85
  • 86. 86
  • 87. 87