Hypertension

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ariadne9
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224435
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Hypertension
Updated:
2013-06-20 16:51:54
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BC Nurse Anesthesia NU 494
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HTN
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  1. Normal BP values
    <120 / <80
  2. preHTN values
    120-139 / 80-89
  3. stage 1 htn values
    140-159/ 90-99
  4. stage 2 htn values
    ≥160 / ≥100
  5. What % of ppl with HTN don't know it or are untreated?
    2/3's
  6. What percentage of ppl over age 55 will get HTN?
    90%
  7. What normally happens to BP with advancing age?
    Increases, but not necessarily to an acceptable level
  8. Does SBP or DBP more accurately predict CV complications
    SBP, in the past DBP was emphasized more
  9. What factors influence systemic BP?
    CO and peripheral rx

    • CO= HR X SV
    • Peripheral rx is affected by: circulating regulators (catecholamines, angio II), direct innervation (alpha1 and beta2 receptors), local regulators (NO), blood viscosity (Hct)
  10. What 4 organs have major involvement in BP control?
    Heart (contractility), BV themselves (SVR- tone), kidneys (regulate ECF (IV) volume), endocrine (hormones modulate the 1st 3)
  11. What factors affect SV?
    Venous return, venous tone (afterload), blood volume (renal function), contractility
  12. What is autoregulation of ECF?
    What occurs with increased ECF?
    At what ABP does it occur at?
    • -Autoregulation- local vasculature VC or VD to maintain constant blood flow.
    • -With increased ECF vasoconstriction occurs, this increases TPR, which increases arterial pressure, which leads to increased urine output
    • -Autoreg occurs btw 75-160 mmHg
  13. How does increased ECF directly cause an increase in BP?
    Increased ECF causes increased blood volume, increased preload, which increases CO
  14. How does increased ECF indirectly cause an increase in BP?
    Increased CO (direct effect) increases blood flow to all tissues, some vessels constrict to return blood flow back to normal, autoregulation causes an increase in TPR and an increase in BP
  15. Does auto regulation effect GFR or renal blood flow?
    No, minimal change only.  Autoregulation is impaired in renal disease, so there are much larger changes
  16. What is the effect of salt intake?
    • ECF (plasma) osmolarity increases, this stimulates the thirst center and fluid intake increases.
    • There is an increase in ADH secretion (released by hypothalamus), water pores are inserted, there is increase water reabsorption
  17. What is pressure diuresis?
    • -Increase in arterial pressure causes increased urine output (due to increased GFR)
    • -There is also increased sodium excretion (pressure natriuresis)
  18. In what 3 ways do the kidneys regulate intravascular volume?
    • 1) urine output
    • 2) decreased reabsorption
    • 3) decreased angiotensin II (this further decreases reabsorption)
  19. What occurs with increased volume to decrease renal tubular reabsorption (and thus decrease urine output)?
    • -Increased volume causes increased BP, this causes increased peritubular capillary hydrostatic pressure, increased interstitial hydrostatic pressure, increased urine output
    • -Increased BP means less angiotensin II, less reabsorption, increased UO
  20. What effect does angiotension II have (2 major effects)?  When is it released?
    • -Causes vasoconstriction
    • -Causes decreased excretion of salt water
    • -Stimulates aldosterone which further enhances reabsorption
    • -Released at low BP
  21. Regardless of rx or CO the kidneys can return the BP to normal by decreasing IV volume, T or F?
    T!
  22. Pts with chronic hypertension need a higher blood pressure (and capillary hydrostatic pressure) to excrete a given water and sodium load, why?
    • -In the HTN pt, there are microvascular kidney injuries that impair Na+ excretion
    • -Defective RAAS- hormonal problem
  23. What occurs in stage 1 (acute phase) of volume loading HTN?
    • -There is increased salt and water intake, this increases ECF and blood volume, CO increases (this is the basic cause of HTN)
    • -BP rises, although slower due to baroreflex (BR takes a few days to adapt to new BP and can no longer prevent the rise in BP)
  24. What occurs in stage 2 (secondary changes) in volume loading HTN?
    • -Secondary changes occur over a few weeks
    • -There is an increase in total peripheral rx (TPR) and a decrease in CO (due to autoregulation)
  25. In what situation would volume-loading HTN occur?
    Renal failure- there is an impaired ability of the kidneys to excrete excess ECF

    Primary aldosteronism- excess aldosterone secreted by adrenals, increases rate of water and sodium reabsorption
  26. What 2 factors decrease ECF and blood volume back to normal in the second stage of volume loading HTN?
    • 1) Increased resistance in the arterioles decreases capillary hydrostatic pressure, fluid can now be reabsorbed from ISF back into the blood
    • 2) With increased BP, the kidneys will excrete excess fluid
  27. After weeks of volume loading would there be an increase or decrease in the following: BP, TPR, ECF volume, CO?
    • -BP increased
    • -TPR increased
    • -Almost complete return of ECF volume and CO back to normal
  28. Is the increased TPR found in volume loading HTN because of the HTN of a cause of the HTN?
    Increased total peripheral resistance in volume loading HTN is secondary to the HTN, NOT a cause of it
  29. What are common causes of death from chronic HTN?
    • 1) MI- due to excessive cardiac workload
    • 2) cerebral infarction- damage to cerebral vessels
    • 3) renal failure- prolonged increase in hydrostatic pressures damages kidney blood vessels
  30. What MAP is considered indicative of chronic hypertension?
    • MAP > 110 mmHg
    • Can occur with SBP > 135 and DBP > 90 mmHg
  31. Where is renin stored?
    In the juxtaglomerular cells of the kidney
  32. In what form is renin stored as?
    Stored in inactive form: prorenin
  33. What causes renin release?
    decreased BP
  34. Is renin an enzyme or vasoactive substance?
    It's an enzyme
  35. Where is the juxtaglomerular apparatus?
    In the kidney, near the ascending limb of the loop of Henle where it passes between the afferent and efferent arterioles
  36. What are the 2 parts of the juxtaglomerular apparatus?
    • 1) cells of the macula densa
    • 2) juxtaglomerular cells in walls of afferent and efferent arterioles
  37. BP decreases and the renin angiotensin system is activated, describe what happens.
    • Prorenin splits
    • Renin released
    • Renin converts angiotensinogen to angio 1
    • Lung converts angio 1 to angio 2
  38. What is angiotensin I
    A mild vasoconstrictor
  39. What effects does angiotensin II have?
    • 1) potent vasoconstrictor (increased TPR)
    • 2) decreased excretion of water and salt

    Net effect: increased BP and increased blood volume
  40. Angiotensin II causes both vasoconstriction and decreased excretion of water and salt, which is longer term and more significant?
    It's affect on blood volume
  41. Angiotensin II direct and indirect effect on kidneys to retain salt and water.
    Direct- acts directly on kidneys to cause salt and water retention

    Indirect- causes adrenal glands to secrete aldosterone which increases salt and water reabsorption by the kidney tubules
  42. How does angiotensin cause increased water and salt absorption at a cellular level?
    It causes arteriolar constriction, this decreases renal blood flow, decreases GFR, decreases the pressure in the peritubular capillaries, this favors reabsorption from ISF back into the peritubular capillaries, and hence causes increased water and salt reabsorption
  43. What percent of HTN cases are primary HTN?
    90-95%
  44. What is primary HTN?
    • -There is no identifiable cause for the HTN.
    • -It's a diagnosis of exclusion.
    • -Due to failure of normal homeostatic mechanisms due to acquired defect, possible genetic component
  45. What supports the genetic component of primary HTN?
    -More common in 1st degree relative and identical twins, uneven distribution among racial groups
  46. How can obesity contribute to essential HTN?
    • -Increased CO (more tissue to perfuse, increased metabolic demand)
    • -Increased SNS activity (leptin released from adipose cells stimulates hypothalamus and affect vasomotor center- excitatory effect)
    • -Increased angio II and aldosterone levels (due to increased SNS)
    • -Impaired pressure natriuresis (kidneys won't excrete adequate amts of Na and water unless pressure high)
  47. What is metabolic syndrome?  What are other names for it?
    -HTN, incr. triglyc., decr. HDL, cellular insulin rx, visceral obesity (around the abd)

    -AKA ins rx syndrome or syndrome X
  48. What percent of americans have metabolic syndrome?
    44%
  49. How does insulin rx play a role in the essential HTN?
    • -Impaired glucose transport into tissues, causes increased BG levels, causes pancreas to release more insulin, elevated insulin rx, HTN due to increased SNS activity
    • -Also causes hypertrophy of tunica media leading to increased vascular rx
  50. Essential HTN is associated with abnormalities in what systems?
    • -Heart
    • -Blood vessels
    • -Kidneys
  51. What abnormalities are associated with the heart in essential HTN?
    -Increased SNS activity, increased HR in stressful situations (whitecoat syndrome), high CO
  52. What abnormalities are associated with the blood vessels in essential HTN?
    • -Contribute to TPR, constrict in response to increased SNS activity
    • -Abnormal regulation of normal vascular tone by local factors (NO, endothelin)
  53. What abnormalities are associated with the kidney in essential HTN?
    • -volume based HTN due to water and salt retention
    • -failure to regulate normal renal blood flow
    • -should have decreased renin production but many have normal or increased renin production
  54. T or F, even with malfunction of BV and heart for example, the kidneys should be able to prevent HTN by brining the BP to normal by ECF elimination?
    T
  55. What are characteristics of primary hypertension (age, severity, onset, family hx)?
    • -Usually diagnosed between the ages of 20-50 yrs
    • -Gradual onset
    • -Family history
    • -K normal
  56. What are characteristics of secondary hypertension (age, severity, onset, family hx)?
    • -Age of onset < 20 or > 50
    • -Dramatic and acute onset
    • -Abnormal K (low)
  57. In looking for clues regarding diagnosis of primary vs. secondary HTN, what would a low K signal?
    Possibility of primary aldosteronism or renovascular causes of secondary HTN
  58. What are causes of secondary HTN?
    • -chronic renal dz
    • -primary aldosteronism
    • -renovascular dz
    • -pheochromocytoma
    • -coarctation of aorta
    • -Cushing's syndrome
  59. What are some exogenous causes of HTN?
    • -Meds (OCP, glucocorticoids, erythropoitin)
    • -ETOH
    • -coke
  60. What would one look at for clues regarding cause of HTN?
    • -H+P
    • -Labs (u/a, BUN/Cr, K, glucose, chol)
    • -EKG (LVH could determine chronicity of HTN)
  61. How can pheochromocytoma cause secondary HTN?
    What percent of pt's with HTN have this?
    • -Catechol secreting tumors usually in adrenal medulla
    • -Release both NE and epi to cause HTN tachycardia (usually sustained)
    • -0.2% of HTN its
  62. Characteristics of pheochromocytoma pt with HTN?
    • -Severe throbbing headache, profuse diaphoresis, palpitations
    • -An attack of the ANS!!!
    • -Wt loss
    • -Episodic HTN (non sustained) in 1/3 of its
  63. How can excess ACTH cause secondary HTN? IE what other diseases can it cause?
    • -Primary aldosteronism increase in mineralocorticoids (aldosterone) 
    • -Cushing's syndrome increase in glucocorticoids (cortisol)
  64. How can primary aldosteronism cause secondary HTN?
    What percent of HTN pts have this?
    • -adrenal adenoma (Conn syndrome)
    • -bilateral hyperplasia
    • -increased blood volume and reabsorption of Na+ (K+ excretion), hence decreased K is a clue!!
    • -10-15%
  65. How can Cushing's syndrome cause secondary HTN?
    What percent of HTN pts have this?
    • -Excess cortisol secretion by adrenal cortex
    • -Cortisol stimulates RAAS pathway and expands blood volume
    • -0.1%
  66. How can hyperthyroidism cause secondary HTN?
    What percent of hyperthyroid pts have HTN?
    -SNS stimulation and cardiac hyperactivity

    -1/3 have HTN
  67. How can hypothyroidism cause secondary HTN?
    What percent of hypothyroid pts have HTN?
    • -Increased TPR, DBP HTN
    • -1/4
  68. How can renovascular disease cause secondary HTN?
    What percent of HTN pts have this?
    • -Or renal stenosis
    • -1 or both renal arteries
    • -usually due to arteriosclerosis, or external compression, emboli, or vasculitis
    • -Decreased renal blood flow, decreased renal perfusion pressures, increased renin secretion, increased angio 2, increased aldosterone, VC
    • -1%
  69. How can renal parenchymal disease cause secondary HTN?
    What percent of HTN pts have this?
    • -Increased intravascular volume damages nephrons and they can't excrete water and Na+
    • -Can progress to ESRD
    • -Excessive renin secretion can cause renal cell damage
    • -2-4%
  70. How can coarctation of the aorta cause secondary HTN?
    What percent of HTN pts have this?
    • -Congenital aortic narrowing, just distal to left SC artery origin
    • -Narrowing is beyond arterial branches to head and arms but before renal arteries
    • -High pressure proximal of coarctation stiffens the aortic arch, accelerates artherosclerosis, and blunts the BR response to increased BP
    • -0.1%
  71. What's a major clue to aortic coarctation as a cause of HTN?
    BP higher in arms than in legs
  72. What symptoms can identify HTN?
    • -Most pts are symptomatic
    • -Flushing, diaphoresis, blurred vision
  73. What are the major organs affected by HTN?
    • -Heart
    • -Brain
    • -Aortic and peripheral vascular system
    • -Kidneys
    • -Retina
  74. How does HTN cause damage to the blood vessels?
    • -Weakened vessel walls can accelerate artherosclerosis
    • -Smooth muscle hypertrophy due to BV breakdown
    • -Fatigue of elastic fibers
    • -Disruption of normal protective mechanisms like NO
    • -plaque can rupture or embolize and occlude distal vessels
  75. Do young ppl usually have DBP HTN or SBP HTN?
    DBP

    Older pts more likely to have isolated SBP HTN
  76. How does SBP vary throughout the lifespan?
    DBP?
    • -SBP rises throughout life
    • -DBP rises until age 50, then declines
  77. What mechanisms are responsible for HTN in young ppl?
    • -Increased CO, normal TPR
    • -Called hyperkinetic phase of essential HTN
  78. What mechanisms are responsible for HTN in older ppl?
    • -Increased resistance due to hypertrophy of the blood vessels
    • -CO has less of an effect
  79. What is the hyperkinetic phase of EH?
    • -Increased CO causes HTN
    • -TPR is normal
    • -Seen in young ppl
  80. What is the major cardiac effect of HTN?
    LVH and diastolic dysfunction
  81. What type of hypertrophy develops with LVH?
    -Concentric due to increased wall tension in the LV
  82. Describe the changes in cardiac muscle that cause concentric hypertrophy
    -New sarcomeres are added in parallel

    -The wall becomes thicker, the wall radius does not change, diastolic function is impaired
  83. What is the strongest predictor of cardiac morbidity?
    LVH, the degree of hypertrophy correlates with CHF, MI, sudden cardiac death, and arrythmias
  84. Does chronic pressure or volume overload cause concentric hypertrophy?
    Pressure
  85. Does chronic pressure or volume overload cause eccentric hypertrophy?
    Volume
  86. Describe the changes in cardiac muscle that cause eccentric hypertrophy
    • New sarcomeres are added in series
    • Dilation occurs
    • Radius increases
  87. How can HTN cause CHF?
    • Increase myocardial wall tension causes: 
    • -LVH
    • or
    • -Increases myocardial O2 demand causing coronary insufficiency, and infarction or arrythmias
    • both lead to CHF
  88. What changes in SV, EDV, EDP, and filling (compliance) are seen with diastolic dysfunction?
    • -Decreased SV
    • -Increased EDP
    • -Decreased EDV
    • -Filling is impaired (decreased compliance)
  89. What percent of pts who die from transmural MI have HTN?
    65%
  90. What post MI complications does HTN put ppl at risk for?
    CHF, ventricular wall rupture, LV aneurysm
  91. What factor regarding HTN is mostly closely linked to CVAs?
    magnitude of SBP
  92. What do you need to consider when managing the HD status of a patient who is chronically hypertensive in terms of cerebral perfusion pressure?
    Pt will need higher perfusion pressure to maintain cerebral blood flow.  Should try to maintain them near their normal BP.  
  93. Explain why HTN is a major cause of CAD.
    There is a combination of accelerated artherosclerosis in the coronary arteries, decreased O2 supply but increased O2 demand due to thick wall
  94. T or F, LVH is compensatory at first, but later is unable to balance against continued HTN.  The continued high BP leads to decreased ability of the LV to contract, and systolic function decreases.
    T
  95. What effects can HTN have on the aortic and peripheral arteries?
    • -plaque formation
    • -aneurysm
    • -aortic dissection
  96. What are the most common sites for plaque formation?
    Aorta and major arteries to LE, neck, and brain
  97. How does HTN contribute to aortic dissection?
    • -Causes degenerative changes to the wall due to increased BP
    • -Tears can occur as the wall is exposed to high pressure
    • -Mortality rate is >90% unless surgically treated
  98. What effects can HTN have on the kidneys?
    • -nephrosclerosis
    • -fibrinoid necrosis
  99. What's the only place where direct visualization of systemic arteries can be seen on PE?
    Retina
  100. What effect can HTN have on the retina?
    -Hypertensive retinopathy
  101. What can papiledema be a sign of?
    • Increased BP
    • -Increased BP, cerebral autoregulation fails, high ICP, causes optic disc swelling, and papiledema 
  102. What clinical s/sx can be seen with hypertensive retinopathy?
    • -Can be an asymptomatic clinical marker of severity and duration of HTN
    • -Hemorrhage of small retinal vessels from acute malignant HTN
    • -Blurred vision from optic nerve ischemia
  103. Recommended Na+ intake
    2.3- 2.5 g / day
  104. What lifestyle changes can decrease BP
    • -weight reduction
    • -exercise
    • -diet
    • -decreased ETOH
    • -smoking cessation
    • -relaxation therapy
  105. Chronic ETOH use is associated with HTN and medication resistance, T or F?
    T
  106. Why is sodium rx to reduce BP controversial?
    Because the kidneys should excrete excess sodium, however some ppl are salt sensitive and others are not
  107. What occurs in ppl who are "salt sensitive"?
    • -Their BP increases with an increase in Na+ intake
    • -this is opposed to ppl who are not salt sensitive where an increase in Na+ intake does NOT cause increased BP
  108. Is salt sensitivity an all or nothing phenomenon?
    No, it's a continuum
  109. What factors are associated with increased salt sensitivity?
    • -African american race
    • -age > 50 yo, salt sensitivity increases with age
  110. Are Mg and Ca deficiency associated with HTN?
    Yes, uncertain MOA
  111. Is chronic caffeine use associated with HTN?  What about right after drinking 2 cups of coffee?
    • -Chronically there is no increase in BP.
    • -After 2 cups of coffee there is a transient increase in BP by 5-15 mmHg
  112. Do we use loop diuretics to treat HTN?
    No, they are too potent and short acting
  113. What classes of drugs are used to treat HTN?
    • -Diuretics
    • -Sympatholytics
    • -Vasodilators
    • -RAAS antagonists (ACEIs and ARBs)
  114. What types of HTNive pts benefit from diuretic therapy?
    -Elderly, african americans, and salt sensitive ppl
  115. What are examples of sympatholytics used to treat HTN?
    BB, alpha blockers, and alpha2 agonists
  116. How do BB decrease BP?
    • -Decrease CO, HR, and contractility
    • -Decrease renin and angiotensin II, decreased rx
  117. What's an example of an alpha 2 (??? alpha 1) blocker?  Who would benefit from this?
    • -alpha 1 has minimal cardiac effects
    • -Prazosin
    • Men with HTN and BPH
  118. What are examples of alpha 2 agonists and how do they work?
    • -Clonidine and methyldopa
    • -Decrease SNS outflow to the heart, BV, and kidneys
  119. What are examples of rapidly acting mechanisms of BP control?  How long does it take for them to work?
    • -Baroreceptor, CNS ischemic response, chemoreceptor mechanism
    • -Secs to mins
  120. What are examples of intermediate acting mechanisms of BP control?  How long does it take for them to work?
    • -RAAS
    • -Stress-relaxation of vasculature (with increased BP blood vessels stretch to buffer pressure back to normal)
    • -Fluid shift (to and from ISF to readjust blood volume PRN)
    • -Mins to hours
  121. What are examples of long acting mechanisms of BP control?  How long does it take for them to work?
    • -renal blood volume control can return BP almost back to normal if kidneys are working properly
    • -also involves RAAS and aldosterone
    • -days to yrs
  122. In our pre-anesthesia evaluation, what factors are we looking at regarding HTN?
    • -adequacy of control
    • -end organ damage
    • -current anti-hypertensives
  123. What can we expect in terms of intraop BP in a poorly controlled HTN pt?
    Hypotension
  124. What can we expect in terms of intraop BP in the general HTN pt?
    Labile BP
  125. How might we control intraop HTN?
    • -Increase anesthetic depth
    • -Esmolol or labetalol
  126. How might we control intraop hypotension?
    • -IVF
    • -Neo
    • -Ephedrine
  127. What effect does spinal anesthesia have on BP?
    Hypotension due to SNS blockade
  128. What's a benefit of using clonidine?
    It also causes sedation
  129. How can we blunt the response to laryngoscopy?
    • 1) IV lido or LTA lido (squirt onto VC), dose is 1.5 mg / kg, do NOT do both due to risk of toxic dose
    • 2) Front load with opiates before induction, this will also decrease the amount of induction agent needed.  

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