R6 Hypertension

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Author:
jknell
ID:
204422
Filename:
R6 Hypertension
Updated:
2013-03-09 12:38:06
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Renal II
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Hypertension
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  1. Hypertension
    prevalence
    • -1 in 3 Americans
    • -Increases with age: 7.3% in adults 18-39 years, 32.6% in 40 to 59 years, 66.6% in pts >60 years
    • -African Americans tend to develop HTN earlier than whites
    • -Second most prevalent cause of ESRD in the US - increasing BP correlates to increase risk

    • *We have increased awareness and the % treated, but less than 48% of patients with HTN have controlled blood pressures
    • *Only 15% of pts with diabetes and HTN have controlled BP
  2. Hypertension
    complications
    • -TIA, stroke
    • -Retinopathy
    • -Peripheral vascular disease
    • -Renal failure
    • -LVH, CHD, HF

    *antihypertensive treatment reduces the risk of all of these complications
  3. Hypertension
    SBP vs DBP, risk factors for organ damage
    • Increase Systolic BP (even isolated increased SBP) is the more powerful cardiovascular risk factor
    • (systolic>>diastolic BP elevations)
    • Concomitant risk factors: serum cholesterol, ♂, family history of CVD, smoking, race (black)
  4. Hypertension
    Monitoring and staging
    • Measure with sphygmomanometer: BP cuff
    • -If the cuff is too small --> artifactual increase in BP
    • -Home monitoring: better detection and treatment (white coat HTN, masked HTN, Labile HTN)
    • -Nocturnal Dip: BP dips when sleeping

    • -Normal: <120/80
    • -Prehypertesion: 120-139/80-89
    • -Stage 1 HTN: 140-159/90-99
    • Stage 2 HTN: ≥160/100
  5. Hypertension
    Nocturnal dipping
    Normally, BP dips at night (sleep)

    Pts with kidney disease often lack the nocturnal dip, some are even "reverse dippers"

    • African American Study of Kidney disease... pts with decreased GFR
    • -20% dipped at night (nl)
    • -40% didn't dip (or dipped less than normal)
    • -40% rose at night
  6. Blood pressure
    MAP = (CO)*(SVR)

    -↑BP must result from either ↑ CO, or ↑SVR (or both)
  7. Blood pressure regulation and kidney function
    • Hypertension follows the kidney
    • Pressure natriuresis - salt sensitivity
    • Relationship between progression of renal disease and HTN
    • Generations of vasoactive hormones
    • Role of Renal nerves in BP regulation
  8. RAAS
    role in BP regulation
    • Angiotensin II has effects on:
    • -Brain, pituitary gland
    • -Heart
    • -Kidney and Adrenal gland
    • -Vasculature

  9. Hypertension
    Primary vs Secondary
    Primary or Essential (unknown cause)

    • Secondary
    • -Renal parenchymal disaese
    • -Renovascular HTN
    • -Pheochromocytoma
    • -Isolated Systolic HTN
  10. Renal Parenchymal Disease
    • Proposed mechanism:
    • -Decreased sodium/water excretion
    • -Increased RAAS activity
    • -Increased renal nerve activity
    • -Decreased Nitric oxide activity

    • Clinical findings:
    • -Increased BUN/Creat
    • -Proteinuria
    • -Evidence of renal and/or systemic disease
    • -Presence of edema
    • -HTN difficult to control
  11. Renal artery stenosis
    • -Limits transmission of blood pressure to the kidneys
    • -One kidney model: RAAS system activated to try and restore volume to normal
  12. Renovascular hypertension
    • Proposed mechanism:
    • -Decreased renal perfusion pressure secondary to stenosis
    • -Increased RAAS activity
    • -Decreased salt and water

    • Clinical findings:
    • -HTN difficult to control
    • -Hypokalemia
    • -Response to RAAS blockers
    • -Atherosclerotic lesions: elderly patient, previous history of HTN
    • -Fibromuscular dysplasia: young female, no fhx
    • -Renal artery stenosis on imaging
    • -Asymmetric kidney size (long-standing disease can cause damage to the contralateral kidney)

    -Stenosis ≠ disease; must have significant stenosis
  13. Primary aldosteronism
    Prevalence varies by region (~20% of patients with resistant and/or severe hypertension)

    • Proposed mechanisms:
    • -Increased Na reabsorption in the distal tubule
    • -Activation of the sympathetic nervous system
    • -Aldosterone producing adenoma
    • -Bilateral adrenal hyperplasia

    • Clinical findings:
    • -Hypokalemia
    • -Muscle weakness
    • -Poliuria
    • -Nocturia
    • -Response to mineralocorticoid receptor blocker
    • -Increased cardiovascular risk
    • **No edema
    • **High aldo, suppressed renin
  14. Suspected primary aldosteronism
  15. Secondary aldosteronism
    • high aldosterone AND high renin
    • Edema
  16. Pheochromocytoma
    • Proposed mechanism:
    • -Catecholamine secreting tumor

    • Clinical findings:
    • -HTN sustained or paroxysmal plus/minus tachycardia
    • -orthostatic hypotension
    • -Evidence of cardiovascular complication (MI, LVH, cardiomyopathy, arrhythmias, CVA)

  17. Essential hypertension
    primary, idiopathic, genetic, familial
    • Strong genetic component; twin studies
    • Multifactorial disease
  18. Evaluation of hypertension
    • Lifestyle assessment:
    • -BMI
    • -Sodium intake
    • -Potassium intake
    • -Alcohol intake
    • -Smoking habits
    • -Exercise habits

    • Exclude secondary causes:
    • -Age of onset
    • -Spontaneous hypokalemia
    • -Labile hypertension
    • -Resistant hypertension
    • -Vascular bruits (RVH)
    • -Familial

    • Target organ injury:
    • -24 hour urine protein
    • -Serum Creatinine
    • -EKG or ECHO (LVH)
    • -Peripheral pulsations
    • -History of stroke
    • -History of myocardial infarction
    • -Heart failure
    • -Retinopathy
  19. Hypertension evaluation
    • 1. History and PE
    •  - Consequences of HTN: target organ damage
    •  - Cause of HTN (2° hypertension)

    • 2. Laboratory evaluation
    •  - Hemogram
    •  - Chemistry panel (BUN, creatinine, electrolytes)
    •  - EKG
    •  - Chest Xray
    •  - Urinalysis
  20. Antihypertensive treatment
    Lifestyle modifications
    • Lifestyle modification:
    • -Avoid excessive Na intake (<100mEq/d) (good luck!)
    • -Weight loss (BMI 18-25)
    • -Reduce sodium intake 
    • -Physical activity
    • -Adopt DASH eating plan
    • -Limit alcohol consumption
    • -Dietary potassium supplementation

  21. Substances that interfere with BP control
    • NSAIDs (nonselective and COX-2 selective) - increase BP through retention of sodium and water
    • Sympathomimetic agents (wt loss pills, cocaine)
    • Amphetamines
    • Exogenous glucocorticoids and mineralocorticoids
    • Antidepressants
    • Alcohol
    • Oral contraceptive pills
    • Immunosuppressants
    • Erythropoietin
    • Natural licorice
    • Herbal agents ephedra or ma huang
  22. Resistant hypertension
    • Elevated blood pressure on 3 anti-hypertensive meds
    • OR
    • Normal blood pressure on 4anti-hypertensive meds
  23. Antihypertensive medications
    • Central sympatholytics (clonidine, methyldopa)
    • β-blockers (many)
    • α-blockers (prazosin, doxazosin)
    • Angiotensin-receptor blockers (many)
    • Converting-enzyme inhibitors (many)
    • Thiazide diuretics (many)
    • Calcium channel blockers (many)
    • Direct vasodilators (hydralazine, minoxidil)
    • Renin inhibitors (aliskiren)
  24. RAAS
    • -Renin converts Angiotensinogen to Ang I
    • -ACE converts Ang I to Ang II
    • -Ang II acts on AT1 and AT2 (receptors)

    • Effects of AT1:
    • -Vasoconstriction
    • -Inotropism
    • -Glomerular filtration
    • -Renal blood flow
    • -Vascular hypertrophy
    • -LVH
    • -Fibrosis
    • -Oxidative stress
    • -Inflammation

    • Effects of AT2:
    • -Vasorelaxation
    • -Cellular growth inhibition

    • *Ang II causes increase Aldosterone
    • +inflammation
    • +Sodium reuptake
    • +K and Mg excretion
    • +CNS enhancement
    • +Myocardial fibrosis
  25. Angiotensin II receptors
    effects of blockade
    • Vascular AT1 receptor
    • -Constantly expressed
    • -Mediate vasoconstriction
    • -Mediate angiotensin II arterial wall growth effects

    • Vascular AT2 receptors
    • -Expressed only after injury (sustained hypertension might provoke expression)
    • -Mediate vasodilation
    • -Mediate antiproliferative actions
    • -Activate other factors (nitric oxide, tissue kinins)

    • Potential double action of selective AT1 blockers
    • -Directly block vasoconstrictor and growth actions of Ang II at AT1 receptors
    • -Increase circulating AngII
    • -Unblocked AT2 receptors (if expressed), stimulated by increased Ang II activity, mediate vasodilation and growth inhibition
    • -Net effect: AT1 blockade plus AT2 stimulation
  26. Ang II
    end organ damage
    • Damage:
    • -Atherosclerosis
    • -Vasoconstriction
    • -Vascular inflammation
    • -Endothelial dysfunction
    • -LVH
    • -Fibrosis (cardiac)
    • -Remodeling (cardiac)
    • -Apoptosis
    • -↑ Glomerular capillary pressure

    • -↑ Proteinuria
    • -↑ Aldosterone release
    • -Glomerular sclerosis

    • *Stroke
    • *Hypertension
    • *Heart failure
    • *Myocardial infarction
    • *Renal failure
  27. ACE and ARB combination treatment
    • "Prils" and "sartans"
    • Both excellent first line therapies for HTN
    • Poor side effect profile in combination and little to no benefit
  28. Calcium antagonists
    • Available compounds:
    • -Phenylalkylamines: Verapamil ("V" for ventricles)
    • -Benzothiazepines: Diltiazem
    • -Dihydropyridines: nifedipine, amlodipine, felodipine, isradipine

    • Mode of action:
    • -Decrease cellular calcium entry through L-type channel
    • -Negative inotropic effect
    • -Reduction in total peripheral resistance
    • -Natriuresis
    • -Interference with Ang II, α1- and α2-mediated vasoconstriction

    • Indications:
    • -HTN
    • -Salt-sensitive HTN
    • -Diastolic dysfunction
    • -Variant angina
    • -Cerebral vascular disease
    • -Cyclosporine hypertension

    • Contraindications:
    • -Heart block and HF
    • -MI

    • Side effects:
    • -Tachycardia
    • -Edema
    • -Flushing
    • -Headache
  29. β-blockerss
    • Antihypertensive effects:
    • 1. Reduction in heart rate and CO
    • 2. CNS effect
    • 3. Inhibition of renin release
    • 4. Reduction in venous return and plasma volume
    • 5. Reduction in SVR
    • 6. Reduction in vasomotor tone
    • 7. Improvement in vascular compliance
    • 8. Resetting of baroreceptor levels
    • 9. Effects on prejunctional β-receptors: reduction in NE release
    • 10. Attenuation of pressor response to catecholamines with exercise and stress

    *Not often used in younger patients (bradycardia)
  30. α-2 agonists


    • -Methyldopa (Aldomet)
    •  -- Aldoclor = methyldopa + chlorothiazide
    •  -- Aldoril (Methyldopa + HCTZ)

    • -Clonidine (Catapres)
    •  -- Clorpres = Clonidine + chlorthalidone
  31. Direct vasodilators
    *Never used as first line defense; third choice...

    • Hydralazine
    • -mainly used in pregnancy
    • -part of triple therapy with diuretic and adrenergic inhibitors


    • Minoxidil
    • -only for severe refractory hypertension
    • -also used in Rogaine
  32. Efficacy of therapy
    • Monotherapy: completely satisfactory in ~60%
    • Combination: needed in ~40% of patients
    • Must choose/add a second drug with different action
  33. TZ diuretics - side effect
    Combination with beta blockers or ACE-In
    • TZ → decrease serum potassium
    • Beta blockers
    • -Combination therapy improved BP better than individual therapy alone
    • -Combination didn't drop serum potassium as much as Diuretics alone (less risk for hypokalemia)

    • ACE-In
    • -Combination blocks the adverse metabolic effects of TZ
  34. Combination antihypertensive treatment
    ACE-Inhibitors and CCB
    Different mechanism of action → Additive effect

    SBP and DBP drop significantly with combination (captopril + Nifedipine)
  35. Co-morbid conditions influencing antihypertensive drug choices
  36. Other antihypertensive agents
    • Sodium nitroprusside: IV, can titrate minute to minute
    • Glyceril trinitrate
    • Nicardipine
    • Verapamil
    • Fenoldopam
    • Hydralazine
    • Enalaprilat
    • labetalol
    • esmolol
    • phentolamine
  37. HTN classifications
    • Severe hypertension:
    • >180/110mmHg
    • Sx: often asymptomatic, HA, anxiety

    • Hypertensive urgency:
    • >180/110mmHg
    • Sx: severe HA, SOB, Edema
    • Management: lower BP, observe for 3-6hrs

    • Hypertensive Emergency = Malignant HTN:
    • >220/140mmHg
    • Sx: prolonged chest pain, motor impairment/neurologic deficit, altered mental status, uncontrolled bleeding, pulmonary edema, MI, CVA, Encephalopathy...
  38. Hypertension in the elderly
  39. Isolated systolic hypertension
    • Common in elderly
    • ↓ arterial "compliance" (↓ SV/PP) → ↑PP → ↑ SBP
  40. African americans and ESRD
    African Americans in HTN
    • -African Americans are over-represented in the ESRD population
    • -HTN is especially common (prevalence ~50%)
    • -Blacks are more hypersensitive to salt than whites

    -TZ are as effective in blacks and whites

    -Beta blocker efficacy white > black

    -Combination (TZ+BB) works additively in all patients

    -CCB have equal effects as initial (mono) therapy of htn for blacks and whites

    -Incidence of ESRD is lower with ACE-In
  41. Renal denervation
    New(er) treatment for treatment-resistant hypertension

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