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Hypertension

Outline

A. Definition
    1. no definite point at which HTN begins but the Amer. Heart Assoc.
        considers 140/90 the dividing line

    2. Classification according to NHLB (National Heart, Lung, and Blood
        Institute) for adults 18 and older

3. normal blood pressure in other age groups
        a. neonates - 1 year = 60/40
        b. 3- 4 years of age=  70/50
        c. 7 years of age =       100/70
        d. teens to adult =       130/80

    4. tends to rise into old age. Isolated systolic hypertension =
        rise in systolic pressure while diastolic pressure remains within
        normal limits. This is most common form of HTN in elderly.

    5. BP = C.O. x TPR
        a. C.O. = cardiac output
        b. TPR = total peripheral resistance

B. Control of Blood Pressure
    1.baroreceptors- located in the walls of blood vessels and the heart,
        Carotid and aortic baroreceptors respond to changes in the stretch
        of the blood vessel by signaling the brain to change heart rate and
        vascular smooth muscle tone

    2. chemoreceptors- located in carotid bodies and aortic bodies,
        sensitive to changes in oxygen, carbon dioxide and hydrogen ion
         content. although mainly concerned with regulating ventilation,
        can signal vasomotor center in brain to induce widespread
         vasoconstriction

    3. Autonomic control
        a. SNS  (Sympathetic Nervous System) (Adrenergic), with
             epinephrine as neurotransmitter, has three sets of receptors
            1. alpha receptors- when stimulated cause peripheral
                 vasoconstriction  
            2. beta 1 receptors - when stimulated cause: increase in
                heart rate, i.e. have a positive chronotropic effect, an
                increase in force of contraction of ventricle, i.e.
                have a positive inotropic effect and an increase in rate
                of conduction of electrical impulse over AV node, i.e.
                a positive dromotropic effect

            3. beta 2 receptors - when stimulated cause bronchodilation

        b. N.B. PNS (Parasympathetic Nervous System), (Cholinergic), with
   acetylcholine as main neurotransmitter,  can slow heart rate

    4. Central Nervous System Response - CNS Ischemic Response
        when ischemia occurs in vasomotor center of brain, vasomotor
         neurons can cause massive vasoconstriction, raising BP to levels of
         270 mm HG for as long as 10 minutes

    5. Renin Angiotensin System

1. Juxtaglomerular Apparatus Cells (JGA) located in kidney responds to decreased blood     pressure, decreased sodium or SNS stimulation to release renin 2. in blood renin combines with angitensinogen to form Angiotensin I 3. in lungs angiotensin converting enzyme (ACE) converts Angiotensin I to Angiotensin II 4. Angiotensin II is a strong constrictor of arterioles and also constricts veins, stimulates      adrenal gland to secrete aldosterone. 5. Aldosterone acts on tubules to increase reabsorption of Na+ . Level of Na+ in      intravascular fluid compartment rises, causing fluid to be pulled from extracellular      and intracellular fluid compartments, expanding volume of intravascular compartment

    6. release of vasopressin (antidiuretic hormone)   

C.Secondary HTN (due to another disease condition)
    1. occurs in about 10% of adults
    2. renal Causes- nephritis, inflammatory disease, renal vascular,
         parenchymal disease

    3. increased levels of adrenocorticosteroids, e.g. primary aldosteronism,
        Cushing disease

    4. pheochromocytoma

    5. CNS disease, e.g. brain tumor

    6. coarctation of the aorta

D. Essential HTN (idiopathic)
    1 Risk Factors
        a. Family history

        b.age related changes

        c. race - more prevalent in African Americans then whites
            a salt thrifty gene sometimes linked to HTN in blacks, this
            gene does not allow for increased renal excretion of sodium in
             response to increased salt intake

        d. excessive salt intake- controversial

        e. obesity

        f. hyperinsulinemia

        g. excess alcohol consumption (3 or more drinks per day)

        h. decreased potassium intake (potassium helps eliminate sodium), also potassium can dampen vasoconstrictor responses mediated by norepinephrine

        i. stress

        j. oral contraceptive drugs - mild increase in many woman, overt
            HTN in 5%, greatest in those >35 and who smoke

E. Malignant HTN
    1. develops in a small number of people with secondary HTN.
    2. accelerated and potentially fatal form of disease
    3. highest incidence in African American men, women with toxemia of
        pregnancy and persons with renal and collagen disease
    4. sudden marked elevations in BP, diastolic as high as 120 mm Hg

F. Target Organ Damage
    a. HTN major risk factor for atherosclerosis, increase in CVA, MI
PVD, retinopathy
    b. hypertrophy of left ventricle
    c. nephrosclerosis

Discussion  

    HTN is often called the "silent killer" because it seldom produces symptoms.It is usually picked up during screening procedures.If symptoms are present they might include headache (usually on arising and felt in the back of the head or neck) Nocturia may be an early sign of renal damage. Orthostatic hypotension is defined as a transient fall in BP upon moving from a supine to an upright posture. It occurs in everyone but usually doesn't last more than a few cardiac cycles before reflex mechanisms (mediated by baroreceptors) corrects it. It is clinically significant in those cases where there is a drop of 20 mm Hg or more in systolic or or 10 mm Hg or more in diastolic pressure. Symptoms may occur. These symptoms can include lightheadedness (dizziness), or syncope (fainting).  The causes of clinically significant orthostatic hypotension include: reduced blood volume, drug induced hypotension (e.g. antihypertensive drugs, antiparkinsonian drugs, antipsychotic drugs, calcium channel blockers, tricyclic antidepressant drugs, vasodilator drugs), aging, prolonged bed rest, disorders of autonomic nervous system or it may just be idiopathic.  

Clinically  

     A variety of drugs are available which can be used in the treatment of HTN. Diuretics work by decreasing circulating volume and thus decreasing C.O. Adrenergic inhibitors ( beta blockers such as Inderal), can decrease BP via their negative inotropic and negative chronotropic effects. Vasodilator drugs can reverse the effects of vasoconstriction which increases total peripheral resistance. Calcium channel blockers have a negative inotropic effect on the heart. Angiotensin Converting Enzyme Inhibitors   (ACE Inhibitors) work by blocking the conversion of Angiotensin I to Angiotensin II, thus preventing the effects of Angiotensin II, i.e. vasoconstriction and aldosterone release with subsequent Na+ re-absorption and expansion of intravascular fluid compartment.
    For some reason beta blockers and ACE inhibitors are not as effective in blacks as in whites.  A beta blocker would be contraindicated in someone with asthma or COPD because it blocks both beta 1 and beta 2 receptors. Blocking beta 2 receptors in those with respiratory problems could exacerbate their condition.