Hypertension opd by 8Ti9QMoo


									JI Frances Cruz
   level of blood pressure at which the institution of
    therapy reduces blood pressure–related
    morbidity and mortality
   doubles the risk of cardiovascular diseases,
    including coronary heart disease (CHD),
    congestive heart failure (CHF), ischemic and
    hemorrhagic stroke, renal failure, and peripheral
    arterial disease
   often associated with additional cardiovascular
    disease risk factors, and the risk of
    cardiovascular disease increases with the total
    burden of risk factors
   present in all populations except for a small
    number of individuals living in primitive,
    culturally isolated societies
   Cardiovascular morbidity and mortality
    increase as both systolic and diastolic blood
    pressures rise, but in individuals over age 50
    years, the systolic pressure and pulse
    pressure are better predictors of
    complications than diastolic pressure.
 primary determinant of arterial pressure
 When NaCl intake exceeds the capacity of the kidney
  to excrete sodium, vascular volume initially expands
  and cardiac output increases
 The effect of sodium on blood pressure is related to
  the provision of sodium with chloride; non-chloride
  salts of sodium have little or no effect on blood
 May be a consequence of a decreased capacity of the
  kidney to excrete sodium, due to either intrinsic renal
  disease or to increased production of a salt-retaining
  hormone (mineralocorticoid) resulting in increased
  renal tubular reabsorption of sodium
 Maintains cardiovascular homeostasis via pressure,
  volume, and chemoreceptor signals
 Adrenergic reflexes modulate blood pressure over the
  short term, and adrenergic function, in concert with
  hormonal and volume-related factors, contributes to
  the long-term regulation of arterial pressure
 Chronic administration of agents that block
  adrenergic receptors may result in upregulation, and
  withdrawal of these agents may produce a condition
  of temporary hypersensitivity to sympathetic stimuli
 Arterial baroreflex is mediated by stretch-sensitive
  sensory nerve endings located in the carotid sinuses
  and the aortic arch
 Contributes to the regulation of arterial pressure
  primarily via the vasoconstrictor properties of
  angiotensin II and the sodium-retaining properties of
 Angiotensin II is the primary trophic factor regulating
  the synthesis and secretion of aldosterone by the
  zona glomerulosa of the adrenal cortex.
 Aldosterone is a potent mineralocorticoid that
  increases sodium reabsorption by amiloride-sensitive
  epithelial sodium channels (ENaC) on the apical
  surface of the principal cells of the renal cortical
  collecting duct
   Vascular radius and compliance of resistance
    arteries are also important determinants of
    arterial pressure.
   In hypertensive patients, structural, mechanical,
    or functional changes may reduce lumen
    diameter of small arteries and arterioles
   Hypertensive patients have stiffer arteries, and
    arteriosclerotic patients may have particularly
    high systolic blood pressures and wide pulse
    pressures as a consequence of decreased
    vascular compliance due to structural changes in
    the vascular wall.
   Primary (Essential) Hypertension
     95% of case with no cause of hypertension
     most often the result of complex interactions
      between multiple genetic and environmental
     The onset is usually between ages 25 and 55 years
   Sympathetic nervous system hyperactivity
     tachycardia and an elevated cardiac output
   Abnormal cardiovascular or renal
   Renin–angiotensin system activity
   Defect in Natriuresis
   Intracellular sodium and calcium
   Exacerbating factor
     Obesity
     Sodium Intake
     Alcohol
     Cigarette smoking
     Excercise
   Suspected in patients who had hypertension
    at young age
   Causes include genetic syndromes, renal
    disease, renal vascular hypertension, primary
    hyperaldosteronism, Cushing syndrome,
    pheochromocytoma, coarctation of the
    aorta, hypertension associated with
    pregnancy, estrogen use, hypercalcemia and
 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.
 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

 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.
 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.
Blood Pressure    Systolic BP   Diastolic BP
classification     (mmHg)        (mmHg)
Normal               <120         and <80

Prehypertension    120-139       or 80-89

Stage 1            140-159       or 90-99
Stage 2             >/=160       or >/=100
                          Average Percent Reduction
Stroke incidence :              35–40%

Myocardial infarction :          20–25%

Heart failure :                  50%
In stage 1 HTN and additional CVD risk factors, achieving
a sustained 12 mmHg reduction in SBP over 10 years will
       prevent 1 death for every 11 patients treated.
Evaluation of patients with documented HTN has three objectives:

1.   Assess lifestyle and identify other CV risk factors or concomitant
     disorders that affects prognosis and guides treatment.

2.   Reveal identifiable causes of high BP.

3.   Assess the presence or absence of target organ damage and
   Hypertension*
   Cigarette smoking
   Obesity* (BMI >30 kg/m2)
   Physical inactivity
   Dyslipidemia*
   Diabetes mellitus*
   Microalbuminuria or estimated GFR <60 ml/min
   Age (older than 55 for men, 65 for women)
   Family history of premature CVD
    (men under age 55 or women under age 65)
*Components of the metabolic syndrome.
 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
 Heart
  • Left ventricular hypertrophy
  • Angina or prior myocardial infarction
  • Prior coronary revascularization
  • Heart failure

 Brain
  • Stroke or transient ischemic attack
 Chronic kidney disease
 Peripheral arterial disease
 Retinopathy
 Routine Tests
  • Electrocardiogram
  • Urinalysis
  • Blood glucose, and hematocrit
  • Serum potassium, creatinine, or the corresponding estimated GFR,
                and calcium
  • Lipid profile, after 9- to 12-hour fast, that includes high-density and
                low-density lipoprotein cholesterol, and triglycerides
 Optional tests
  • Measurement of urinary albumin excretion or albumin/creatinine ratio

 More extensive testing for identifiable causes is not generally indicated
  unless BP control is not achieved
                  Goals of Therapy
   to reduce cardiovascular and renal morbidity
    and mortality
   treating SBP and DBP to targets that are
    <140/90 mmHg is associated with a decrease
    in CVD complications
   in patients with hypertension and diabetes or
    renal disease, the BP goal is <130/80 mmHg
     Lifestyle changes beneficial in reducing weight
   Decrease time in sedentary behaviors such as
    watching television, playing video games, or
    spending time online
   Increase physical activity such as walking, biking,
    aerobic dancing, tennis, soccer, basketball, etc
   Decrease portion sizes for meals and snacks.
   Reduce portion sizes or frequency of consumption
    of calorie-containing beverages
Modification   Recommendation      Approx. SBP
Adopt DASH     Consume a diet     8–14 mmHg
eating plan    rich in fruits,
               vegetables, and
               low fat dairy
               products with a
               reduced content
               of saturated and
               total fat
Modification   Recommendation    Approx. SBP
Dietary        Reduce dietary    2–8 mmHg
sodium         sodium intake to
reduction      no more than 100
               mmol per day (2.4
               g sodium or 6 g
               sodium chloride)
Modification   Recommendation    Approx. SBP
Physical       Engage in regular 4–9 mmHg
activity       aerobic physical
               activity such as
               brisk walking (at
               least 30 min per
               day, most days of
               the week)
Modification   Recommendation   Approx. SBP
Moderation of No >2 drinks (24 2–4 mmHg
Alcohol       oz beer, 10 oz
consumption   wine, 3 oz 80-
              proof whiskey) per
              day (men), no >1
              drink per day in
              women and lighter
              weight persons
120-139 mmHg    140-159 mmHg     >160 mmHg S
S or 80-89      S or 90-99       or >100 mmHg
mmHg D          mmHg D           D
Lifestyle       Thiazide-type    2-drug
Modifications   diuretics for    combination for
                most. May        most (usually
                consider ACEI,   thiazidetype
                ARB, BB, CCB,    diuretic and
                or combination   ACEI, or ARB,
                                 or BB, or CCB)

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