Office Evaluation of Hypertension December 2, 2008.
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Transcript of Office Evaluation of Hypertension December 2, 2008.
Why do we (physicians) Why do we (physicians) get so excited about get so excited about
controlling hypertension?controlling hypertension? Coronary artery diseaseCoronary artery disease StrokeStroke End-stage renal diseaseEnd-stage renal disease Congestive heart failureCongestive heart failure
Isolated systolic and Isolated systolic and systolic / diastolic systolic / diastolic
hypertension in the elderlyhypertension in the elderly
Hypertension is the most common Hypertension is the most common disease specific reason for disease specific reason for Americans to visit a physicianAmericans to visit a physician
Present in over 50% of all Present in over 50% of all Americans over the age of 60Americans over the age of 60
Short-term benefit of treatment is Short-term benefit of treatment is greater than in young people greater than in young people because of overall greater because of overall greater cardiovascular riskcardiovascular risk
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md: NationalInstitutes of Health, National Heart, Lung, and Blood Institute. 2003; NIH Publication 03-5231.
Classification of blood Classification of blood pressurepressure
Normal BP: systolic < 120 and Normal BP: systolic < 120 and diastolic <80diastolic <80
Pre-hypertension: systolic 120-139 Pre-hypertension: systolic 120-139 or diastolic 80-89or diastolic 80-89
Classification of blood Classification of blood pressurepressure
Stage 1: systolic 140-159 or Stage 1: systolic 140-159 or diastolic 90-99diastolic 90-99
Stage 2: systolic > 160 or diastolic Stage 2: systolic > 160 or diastolic > 100> 100
Lower Blood Pressure is Lower Blood Pressure is BetterBetter
Not symptomatically hypotensiveNot symptomatically hypotensive Treated Blood Pressure must take Treated Blood Pressure must take
into account the risk of medicationsinto account the risk of medications Low diastolic pressures are probably Low diastolic pressures are probably
a marker for decreased arterial a marker for decreased arterial compliance in patients over age 65 compliance in patients over age 65 years (Hardening of the arteries)years (Hardening of the arteries)
Initial evaluationInitial evaluation
BP should be elevated on 2 BP should be elevated on 2 separate occasions: office, home, separate occasions: office, home, ambulatory monitorambulatory monitor
Rule out secondary causes Rule out secondary causes (correctable) of hypertension(correctable) of hypertension
Evaluate for end-organ damageEvaluate for end-organ damage Evaluate the patient’s overall Evaluate the patient’s overall
cardiovascular risk statuscardiovascular risk status
Secondary HypertensionSecondary Hypertension
Renovascular hypertension Renovascular hypertension (secondary hyperaldosteronism)(secondary hyperaldosteronism)
Primary hyperaldosteronismPrimary hyperaldosteronism Primary hyperparathyroidismPrimary hyperparathyroidism Cushing’s diseaseCushing’s disease PheochromocytomaPheochromocytoma
Secondary HypertensionSecondary Hypertension
Primary renal diseasePrimary renal disease HypothyroidismHypothyroidism Oral contraceptivesOral contraceptives Sleep apneaSleep apnea Coarctation of the aortaCoarctation of the aorta
Secondary HypertensionSecondary Hypertension
Renovascular hypertension Renovascular hypertension (secondary hyperaldosteronism)(secondary hyperaldosteronism)
Renovascular Renovascular hypertensionhypertension
Most common cause of secondary Most common cause of secondary hypertensionhypertension
Incidence 10-45% in severe or Incidence 10-45% in severe or refractory hypertensionrefractory hypertension
Clinical symptoms include ischemic Clinical symptoms include ischemic loss of renal function and loss of renal function and otherwise unexplained sudden otherwise unexplained sudden onset pulmonary edemaonset pulmonary edema
Secondary HypertensionSecondary Hypertension
Renovascular hypertension Renovascular hypertension (secondary hyperaldosteronism)(secondary hyperaldosteronism)
Primary hyperaldosteronismPrimary hyperaldosteronism Primary hyperparathyroidismPrimary hyperparathyroidism Cushing’s diseaseCushing’s disease PheochromocytomaPheochromocytoma
HyperaldosteronismHyperaldosteronism
Primary Hyperaldo-most common, Primary Hyperaldo-most common, prevalence around 1-2%prevalence around 1-2%
Aka Conn’s Syndrome (1955)Aka Conn’s Syndrome (1955) Hypertension, hypokalemiaHypertension, hypokalemia Adrenal adenoma, bilateral adrenal Adrenal adenoma, bilateral adrenal
hyperplasiahyperplasia
Cushing’s SyndromeCushing’s Syndrome
Excess glucocorticoid-either Excess glucocorticoid-either exogenous or endogenousexogenous or endogenous
Hypertension results from the Hypertension results from the mineralocorticoid effect of the mineralocorticoid effect of the excess glucocorticoidsexcess glucocorticoids
PheochromocytomaPheochromocytoma
Very rareVery rare Episodic headache, sweating and Episodic headache, sweating and
tachycardiatachycardia 50% have paroxysmal HTN, the 50% have paroxysmal HTN, the
rest apparently have “essential” rest apparently have “essential” HTNHTN
Features of Essential Features of Essential Hypertension without End Hypertension without End
organ damageorgan damage NoneNone
Initial evaluationInitial evaluation
BP should be elevated on 2 BP should be elevated on 2 separate occasions: office, home, separate occasions: office, home, ambulatory monitorambulatory monitor
Rule out secondary causes Rule out secondary causes (correctable) of hypertension(correctable) of hypertension
Evaluate for end-organ damageEvaluate for end-organ damage Evaluate the patient’s overall Evaluate the patient’s overall
cardiovascular risk statuscardiovascular risk status
Cardiovascular risk factorsCardiovascular risk factors
SmokingSmoking Diabetes mellitusDiabetes mellitus DyslipidemiaDyslipidemia Physical inactivityPhysical inactivity Chronic kidney diseaseChronic kidney disease
Symptoms of target organ Symptoms of target organ damagedamage
HeadacheHeadache Transient weakness or blindnessTransient weakness or blindness Loss of visual acuityLoss of visual acuity Chest painChest pain DyspneaDyspnea ClaudicationClaudication
Aggravating factorsAggravating factors
Drugs: estrogens, adrenal steroids, Drugs: estrogens, adrenal steroids, sympathomimetics, and NSAIDSsympathomimetics, and NSAIDS
Diet: salt, alcohol, caffeine, and Diet: salt, alcohol, caffeine, and weightweight
Family historyFamily history RaceRace Sleep apneaSleep apnea
Symptoms of secondary Symptoms of secondary causescauses
Muscle weaknessMuscle weakness Spells of tachycardia, sweating, Spells of tachycardia, sweating,
and tremorand tremor Thinning of the skinThinning of the skin Flank painFlank pain
Clues to the presence of Clues to the presence of Secondary HypertensionSecondary Hypertension
Young age of onsetYoung age of onset Sudden onset of HTNSudden onset of HTN Uncontrolled/Refractory HTNUncontrolled/Refractory HTN Malignant HTN (End organ Malignant HTN (End organ
damage)damage) Features of a recognized Features of a recognized
underlying causeunderlying cause
Is there evidence for end-Is there evidence for end-organ damage?organ damage?
RetinopathyRetinopathy Heart rhythm, extra soundsHeart rhythm, extra sounds Bruits (renal artery variety may Bruits (renal artery variety may
suggest a secondary cause)suggest a secondary cause) PulsesPulses EdemaEdema RalesRales
LaboratoryLaboratory
Electrolytes (Na+, K+, Cl-, CO2-)Electrolytes (Na+, K+, Cl-, CO2-)
CreatinineCreatinine
UrinalysisUrinalysis
Tests to pursue secondary Tests to pursue secondary causes of hypertensioncauses of hypertension
Serum renin and aldosteroneSerum renin and aldosterone 24 hour urine collection for 24 hour urine collection for
metanephrinesmetanephrines Dexamethasone suppression testDexamethasone suppression test Serum calciumSerum calcium Renal angiogram Renal angiogram
Lifestyle modificationLifestyle modification
Weight loss for the overweightWeight loss for the overweight Increased aerobic physical activityIncreased aerobic physical activity Moderate sodium restrictionModerate sodium restriction Moderate alcohol consumptionModerate alcohol consumption Minimize caffeine consumptionMinimize caffeine consumption
Pharmacologic treatmentPharmacologic treatment
Low renin*older*thin*black
- thiazide diuretics- calcium channel blockers- alpha blockers
Essential Hypertension High renin*younger*overweight
- beta blockers- angiotensin converting enzyme inhibitors- angiotensin II receptor antagonists
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md: NationalInstitutes of Health, National Heart, Lung, and Blood Institute. 2003; NIH Publication 03-5231.
Other agentsOther agents
Alpha 2 central blockersAlpha 2 central blockers
Direct vasodilatorsDirect vasodilators
Sympathetic blockersSympathetic blockers
Thiazide diureticsThiazide diuretics
Mechanism of action is unclear but probably is Mechanism of action is unclear but probably is a combination of mild plasma volume a combination of mild plasma volume decrease plus decreased intracellular calcium decrease plus decreased intracellular calcium concentration leading to vasodilationconcentration leading to vasodilation
CheapCheap
EffectiveEffective
Very low incidence of side effects at low dosesVery low incidence of side effects at low doses
Thiazide diuretics provide Thiazide diuretics provide cardioprotection in:cardioprotection in:
Left ventricular hypertrophyLeft ventricular hypertrophy Type 2 diabetes mellitusType 2 diabetes mellitus Previous myocardial infarctionPrevious myocardial infarction Previous strokePrevious stroke Current cigarette smokingCurrent cigarette smoking HyperlipidemiaHyperlipidemia Atherosclerotic cardiovascular Atherosclerotic cardiovascular
diseasedisease
Angiotensin converting enzyme Angiotensin converting enzyme inhibitors: agents of choice in inhibitors: agents of choice in
hypertension and ….hypertension and ….
Congestive heart failureCongestive heart failure ST elevation myocardial infarctionST elevation myocardial infarction Non-ST elevation anterior Non-ST elevation anterior
myocardial infarctionmyocardial infarction Diabetes mellitusDiabetes mellitus Proteinuric chronic renal failureProteinuric chronic renal failure
Angiotensin converting Angiotensin converting enzyme inhibitors and enzyme inhibitors and
angiotensin receptor blockers angiotensin receptor blockers used together are indicated used together are indicated
in:in:
Congestive heart failureCongestive heart failure
Proteinuric chronic renal failureProteinuric chronic renal failure
Angiotensin converting Angiotensin converting enzyme inhibitors act enzyme inhibitors act
by ...by ...
Decreasing angiotensin IIDecreasing angiotensin II Increasing kinin levels (block Increasing kinin levels (block
kininase activity)kininase activity) Decrease aldosteroneDecrease aldosterone Increase insulin sensitivityIncrease insulin sensitivity
Angiotensin II receptor Angiotensin II receptor antagonistsantagonists
Impair binding of angiotensin II to Impair binding of angiotensin II to AT1 receptorsAT1 receptors
No cough (no increased kinin No cough (no increased kinin levels)levels)
No reduction in AT2 receptor No reduction in AT2 receptor activity (arterial hypertrophy, activity (arterial hypertrophy, improved left ventricular activity improved left ventricular activity after ischemia)after ischemia)
Angiotensin receptor Angiotensin receptor antagonistsantagonists
Production of angiotensin II in the heart Production of angiotensin II in the heart may be through another enzyme may be through another enzyme (chymase), therefore AII receptor (chymase), therefore AII receptor antagonists may be more effective than antagonists may be more effective than ACE inhibitors locallyACE inhibitors locally
No change in insulin sensitivity (kinin No change in insulin sensitivity (kinin mediated)mediated)
Indications for and efficacy of ARB’s are Indications for and efficacy of ARB’s are not different from ACE inhibitorsnot different from ACE inhibitors
Direct Renin InhibitorsDirect Renin Inhibitors
Aliskiren approved by the FDA in Aliskiren approved by the FDA in August 2007August 2007
Inhibits renin production in the JG Inhibits renin production in the JG cellscells
Trade name TekturnaTrade name Tekturna Studies ongoing, not yet in Studies ongoing, not yet in
widespread clinical usewidespread clinical use
Beta blockers (without Beta blockers (without intrinsic sympathomimetic intrinsic sympathomimetic activity) are indicated in:activity) are indicated in:
Post myocardial infarctionPost myocardial infarction Stable patients with congestive Stable patients with congestive
heart failureheart failure Rate control in atrial fibrillationRate control in atrial fibrillation Control of angina pectorisControl of angina pectoris
Calcium channel blockersCalcium channel blockers
DihydropyridinesDihydropyridines
VerapamilVerapamil
DiltiazemDiltiazem
Calcium channel blockers: no Calcium channel blockers: no absolute indication in absolute indication in
treatment of hypertension treatment of hypertension but are helpful in:but are helpful in:
Rate control in atrial fibrillationRate control in atrial fibrillation
Control of angina pectorisControl of angina pectoris
May be preferred in obstructive May be preferred in obstructive airway diseaseairway disease
Dihydropyridines: side Dihydropyridines: side effectseffects
HeadacheHeadache DizzinessDizziness FlushingFlushing Edema (due to a redistribution of Edema (due to a redistribution of
fluid from vascular to interstitial fluid from vascular to interstitial space)space)
PregnancyPregnancy
Alpha Methyl DopaAlpha Methyl Dopa LabetalolLabetalol CCBCCB Diuretics +/-Diuretics +/- No ACE-I or ARBNo ACE-I or ARB