hypertension

Anmerkungen:

• look for symtoms showing elevated pressure (LVH and retinopathy and bruits) End Tissue Damage: caused by increased workload of heart and arterial damage from elevated pressure and accelerated atherosclersosis hypertension leads to increased afterload (systolic dysfunction, LVH, increased oxygen demand) and arterial damage (accelerated atherosclersosisa dn weakened vessel wall) Heart: LVH and diastolic dysfunction. high afterload/high arterial pressure increases wall tension of LV, hypertrophies.  leasd to increased stiffness of left ventricle (concentric hypertrophy without dilatation) and diastolic dysfunction and pulmonary congestion due to LV filling pressures. look for LV heave or S4. later on, might find systolic dysfunction like reduced CO or pulmonary congestion.  coronary artery disease hypertension induced strokes: can be hemorrhagic (rupture of microaneuryms) or atherothrombotic (portions of plaque break off and embolize) development of aneuryisms like AAA or aortic dissection hypertension induced kidney disease: hyaline arteriosclersosis or fibrinoid necoriss hypertensive retinopathy: hemorrhages, papilledemia, exudates hypertensive crisis: severe elevation of BP: acute insult on top of chronic htn. think headache, blurred vision, confusion, somnolence, coma, damage to eyes

1. overview of high blood pressure

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   • baroreceptor reflex: receptors in aortic arch and carotid sinus sense stretch and deformation of arteries. if pressure rises, baroreceptors stimulated, increase impulses to CNS, use ANS to cause BP to fall to normal level. use CN 9 and 10.  use sympathetic and PS. 
   1. Classification for HTN

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      •    Pre HTN: adult 130-189/ 80-89. not a disease, we don't treat it. But many go to stage 1 in 5 years. Stage 1: 140-159/90 -99. Stage 2: more than 160/100   
   2. Factors affecting BP

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      • Usage of Mean Arterial Pressure  Mean arterial pressure:  diastolic BP +1/3 PP= CO x SVR. part of ohms law.  CO deals with contarctility, SV, HR, plasma volume.all three will increase CO and drive BP up. Think  beta agonist. Ionotropy. SVR: driven mostly by alpha 1 agonists(catecholamines, endothelin, Angiotensin II)    PP: systolic-diastolic Reason why we don't use MAP in clinic. It is misleading MAP of 93=93 120/80MAP of 103: 170/70: Systolic is dangerous!!!!MAP of 127: 180/100 
      • Aging and BP   Pressure on Y , Age on X. Young should have elastic arteires, high aortic compliance, narrow PP In young individual, 50 or less, the aorta can distend/compliance/elastic. Arterioles have high SVR. Can get damaged with hyperperfusion. So flow can't be too quick. High flow causes damage to arteries! When column of blood/pressure higts arteriolar bed, sets up resistance wave , creates diastolic blood  pressure. In old: aorta is less elastic, pulse wave velocity is fast. Comes right back up, no relfected wave in  diastole. Reflected wave comes back in sysole. . Increase in systolic, decerase in diastole.  When you age, systolic keeps going up Diastolic: goes up gradually, at age 60 it plateaus or declines.  Risk of stroke, heart failure, kidney failure Consequences of increase in systole: leads to increase in afterload/myocardial oxygenconsumption Incresae in LVH  Decrease in coronary perfusion pressure because diastoilc is low  
      • Factors affecting BP Age Biostatus of body: salt sensitive Heterogenous Genetics
      • BP= CO x TPR CO= SV x HR TPR: regulators like AG II, catecholamines, direct innervation like alpha 1 or beta 2, local regulators like NO (decrease), endothelin (increase), adenosine (decrease), prostaglandins (decrease), or blood viscositity (hemocrity increases PR) SV influenced by cardiac contractility, VR/preload, resistande the LV must overcome to eject blood into aorta/afterload four systems responsibile: heart: pumping, blood vessel tone: systemic resistance, kidney: intravascular volume, hormones: function of other systems
   3. Key Formulas To Know

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      •    Aortic compliance: change in SV/PP  MAP= diastolic BP +1/3 PP = CO x SVRPP= S-DMyocardialoxygen demand= CO- AV difference= fick equation. Relates to old arteriesCoronaryperfusion pressure= aortic diastolic pressure- LVEDP. Measured with swanz gatzcatheters  
2. Two theories of primary HTN

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   • 90%, the cause is unknown, multiple reasons age of onset 20-50 years family hx normal serum K, normal urinalysis disease of exclusion, look for secondary firstreasons include: excessive HR/sympatheticblood vessels wthat constrict in response to increased sympathetic activity, abnormal regulation of vascular tone by NO, endothelin, ANP, ion channel defects in contractile smooth muscle. kidney retaining excessive Na and water by not regulating renal blood flow appropriately, ion channel defects, bad hormones. 
   • other things that can affect primary HTN: obesity Type 2 DM increases after young adulthood
   1. Pressure Naturesis

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      • normal patient: increase in BP leads to more urine volume nad Na excretion to bring BP back to normal. this doesn't work in kidneys so you need higher pressures to excrete given Na and water load.  could be because of microvascular and tubular injury in kidneys that impairs Na excretion.  could be with hormonal factors critical to alter renal reactions.   OnX axis: blood prsesure in MAP: 0,50,100,150,200 OnY axis; urinary salt exretion: low to high Youeat more salt, pushes more Na out of renal circulation, excrete more salt, comeback to maintain homeostasis D:low BP and low salt excretion: dehydration or drug to lower Na concentration.Low BP, conserve Na to go back towards A.  Normalfollows yellow A to B to C. HighBP: inability to excrete Na to normal ability.  Hypertensive:pressure naturesis curve SHIFTS TO RIGHT!!!!. For any amount of na, pressurehas to be higher!  Saltsensitive or resistance. Salt sensitive is more like HTN.  Thisis why we use diureitcs.  
   2. Impaired Vascular Relaxation Theory

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      •    Too much pressor (increased SVR  via alph1 a, endothelin, AG II) or decreased in vasodilator (too little NO)   Insert catheter into small artery and infuse LNMNIA (an inhibitor of NO synthase). Give different concentrations (1-4 units). Infuse and look at forearm blood flow. With NMNIA, get reduction in blood flow. For those with hypertension, the line is higher than normal. With less NOS generated  or vascular receptiveness to NSO is impaired, if you remove NOS, it has less of an effect.   Vasorelaxation is important in HTN     Increase NO production or receptor: Ras inhibitors, CCB (calcium channel blockers), or vasodilators Doesn't work with diuretics or beta blockers   
3. Reasons for Secondary HTN

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   • definable cause can be cured think age severity onset associated signs and symptoms family hx lab tests: urinarlysis measurement of creatinine and BUN serum K blood glucose for DM serum cholesterol, HDL, tags EKG: for LVH caused by chronic HTN also hyperthyroid or hypothyroid patients have significant hypertension
   • drug causes: oral contraceptives glucocorticoids cyclosproine EPO sympathomimetic drugs NSAIDS ethanol cocaine
   1. Experimental Reasons
      1. Two Kidney 1 clip

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         •    1 kidney is unaffected Other kidney, put a clip on external renal artery, narrows to 90%. Only has 10% of blood flow. Made it ischemic. The animal became massively HTN. Due to Renin: proteolytic enzyme in JGA. When he took the clip off, bp went to normal. Renin went down. Model of AG II or renin dependent hypertension. Better when you take away obstruction/ischemic cause   Other kidney can have fibrinoid necrosis, can also become damaged with 2 years damage. Can lead to 1 kidney 1 clip model. Timing matters.   
      2. One Kidney 1 clip

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         •    Did a nephrectomy and did 90% clip on other healthy kidney. Saw major incrase in BP Saw increase in renin Increased AG II When you take off clip, the BP is still high! This is stenosis of one side! Mixed pathogeniesis volume dependent hypertension because you removed 50% of GFR.   
   2. Kidney

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      • no matter how high the CO or TPR, renal excretion has capacity to return BP to normal by reducing intravascular volume.    Afferentarteriole goes into glomerular. Capillary space is where blood is and filteredinto urinary space. Filtration fraction: amount of solute comes in and filteredout. Other side is efferent arteriole: less solute, goes into systemic.  EFFis affected by AG II. Most important constrictor.  
      •    Decrease in renal blood flow (bleeding, gastroenteritistics, dehydration, post op, drugs) . Decrease in afferent flow. JGA senses this on afferent side. Stimulate system to maintain homeostasis, increases renin, starts cascade, increases BP and really increases AG II( production on EFF, increases BP!!! Increases BP in glomerular space, improves filtration fraction   
      •    If renal blood flow decreased due to obstruction aorta or renal artery, real decraese in renal blood flow, increase in renin. Leads to increase in AG II. If you give a drug, ACE inhibitor or AG receptor blocker. You take away AG II on efferent side. You decrease blood prsesure in glomerular space, decrease filtration feraction.  Renal unction goes down. K up, urea up, creatinine up.   Is reversible and identifiable.   Think bruit!   
      • chronic renal disease: increased creatinie or abnormal urinalysis renal parenchymal disease: injury leads to elevated BP through increased intravascular volume. damaged nephrons are unable to excrete normal amounts of Na and water, leads to rise in intravascular volume, elevated CO, increased BP renovascular: abdominal bruit, sudden onset, decreased serum K
      1. Renal Artery Diseases

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         • stenosis of one or both renal arteries.   Fibromusculardisease: overgrowth of media or intima (congenital). Looks like lumps andbumps. Can cause occlusion of flow.  Canbe fixed. discrete regions of proliferation. usually in yhoung women Atherosclerosis:renal artery. Plaque growing. Harder to fix. extensive plaque formation from renal artery or in aorta near renal artery. most in elderly men.  elevated BP due to reduced renal blood flow to affected kidney, responds to lower perfusion pressure by secreting renin, does AG I to AG II by ACE, leads to vasoconstriction and increased aldosterone. renal hypertension is diagnosed by abdominal bruit or unexplained hypokalemia. treatment: ACE inhibitors in those with unilateral renal artery disease don't use in bilateral stenotic lesions.    
   3. Too much aldosterone

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      •    Hyperaldosteronism: most common case of secondary HTN! think decreased serum KAdrenaladenoma. Not cancer. Less than 3 cm in diameter. Nodularor non nodular hyperplasia: gland looks big or lumpy. Bilateral. Idiopathic:don't see other patterns on imaging.   
   4. Pheochromocytoma

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      • catecholamine secreting tumor of neuroendocrine cell in adrenal medulla measure plasma catecholamine levels or urine catecholamines /metabolites treat with alpha receptor blocker and beta blocker and surgical resection   Pheocytomatoma:adrenal medulla. Makes catecholamines. Palpitations, flushing, headaches,paraoxyms of palpitations, diaphoresis, headacheweight lossepisode BP rises,   
   5. Cushing Syndrome

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      • cushinoid appearance: central obesity, hirsutism, rounded face, proximal muscle weakness disorder of gluococorticoid excess due to pituitary ACTH secreting adenoma or peripheral ACTH secreting tumor or adrenal cortisol secreting adenoma use 24 hour urine collection for measurement of cortisool or by dexamethasone test
   6. coarctation of aorta

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      • congenital narrowing of aorta distal to origin or left subclavian artery. causes BP higher near aortic arch. causes hypertensionn because of RAAS and because high blood pressure before the coarctation stiffen the aortic arch and blunt the normal baroreceptor response.  see: inadequate blood flow to legs/left arm (claudication or fatigue or weak femoral pulse) midsystolic murmor indentatio of aorta on CXR do angioplasty of surgery to correct stenosis. 
4. Clinical Examples(attach conference)

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   • Hypertension Q
5. TREATMENT

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   • non pharm: weight reduction, exercise, diet, salt restriction, alcohol reduction, stop smoking