Week 3 - Hypertension/Hypertensive Crisis Flashcards

1
Q

what is considered HTN

A
  • SBP >140

- or DBP >90

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2
Q

HTN is a risk factor for…

A
  • CAD
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3
Q

BP is determined by

A

CO x SVR

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4
Q

what is cardiac output (CO)

A
  • total blood flow thru the systemic or pulmonary circulation per minute
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5
Q

what is SVR

A
  • systemic vascular resistance

= force opposing the movement of blood within blood vessels

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6
Q

what determines SVR

A
  • radius of arteries & arterioles (vasoconstriction & dilation)
  • a small change in radius of arterioles = major change in SVR
    ex. if SVR is increased but CO remains contstant, BP will increase
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7
Q

what is CO determines by

A
  • stroke volume (amt of blood pumped by the left ventricle per beat) x HR
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8
Q

what are alpha adrenergic receptors located and what do tehy do?

A
  • located in peripheral vasculaure & cause vasoconstriction
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9
Q

where are beta receptors located and what do they do?

A
  • beta 1 = in heart & increase HR, contractility, increased speed of conduction
  • beta 2 = in lungs & cause vasodilation
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10
Q

what role does the RAAS have in BP

A
  • renin secreted if decreased blood flow to kidneys, low BP, sympathetic simultation
    = angio 2= vasoconstriction
    = aldo = keep Na and water

= raised BP

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11
Q

what is isolated systolic HTN

A
  • sustained elevation in SBP >140 but DBP <90
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12
Q

what does isolated systolic HTN result in

A
  • increased pulse pressure (difference between SBP and DBP)
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13
Q

HTN is classified as…

A
  • primary or

- secondary

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14
Q

what is primary HTN

A
  • HTN with an unknown cause
  • thought to be complex interaction between genes and enviro
  • 90-95% of HTN cases
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15
Q

what are contributing factors for primary HTN (12)

A
  • increased SNS activity
  • overproduction of na-retaining hormones & vasoconstrictors
  • obesity
  • increased sodium intake
  • DM
  • excessive alcohol intake
  • advancing age
  • elevated serum lipids
  • more prevalent in males
  • FHx
  • sedentary lifestyle
  • stress
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16
Q

what is secondary HTN

A
  • HTN with a specific cause that can be identified and corrected
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17
Q

what are causes of secondary HTN (7)

A
  • renal disease
  • endocrine disorders
  • neuro disorders
  • sleep apnea
  • meds
  • congential narrowing of aorta
  • pregnancy induced
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18
Q

describe what symptoms of HTN are like

A
  • “silent disease” = frequently asymptomatic until it is severe and target-organ disease has occurred
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19
Q

what is target-organ disease

A
  • when pts with HTN experience a variety of symptoms secondary to effects on blood vessels in various organs and tissues , or to the increased workload of the heart
  • chronic HTN leads to damage of organs
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20
Q

what organs can HTN effects (5)

A
  • heart
  • brain
  • kidneys
  • eyes
  • peripheral vasculature
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21
Q

what symptoms can HTN/target-organ disease cause (6)

A
  • fatigue
  • reduced activity intolerance
  • dizziness
  • palpitations
  • angina
  • dyspnea
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22
Q

what are common complications of HTN caused by

A
  • caused by target organ disease
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23
Q

what complication can occur in the heart due to HTN (4)

A
  • hypertensive heart disease
  • CAD
  • heart failure
  • left ventricular hypertrophy
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24
Q

how does HTN contribute to CAD

A
  • the shear stress results in endothelial dysfnxn = impairement in synthesis & release of nitric oxide = promote development and acceleration of atheroscleoris and plaque formation
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25
how does HTN cause LV hypertrophy
- sustained high BP = increased cardiac workload = hypertrophy
26
what does LV hypertrophy leads
- intially, its a compensatory mechanism that strengthens cardiac contraction and increases CO - then increased contractility increases myocardial work and O2 consumption = heart cannot meet demands = HF
27
how does HTN lead to HF
- occurs when the heart's compensatory adaptations are overwhelmed & heart cannot pump enough blood to meet metabolic needs of the body
28
what complication can occur in the brain d/t HTN (2)
- cerebrovascular disease | - hypertensive encephalopathy
29
what is cerebrovascular disease
- group of conditions that effect blood flow to the brain
30
what is the most common cause of cerebrovascular disease
- athersclerosis
31
what is a major risk factor for cerebral atherosclerosis and stroke
- HTN
32
what can atherosclerotic plaques in the carotid artery lead to
- can break off and travel to intracerebral vessels = TIA or stroke
33
when does hypertensive encephalopthy occur
- after a marked rise in BP if the cerebral blood flow cannot be decreased by autoregulation * autoregulation = physiological process that maintains constant cerebral blood flow despite fluctuation in arterial BP*
34
what happens in the brain when arterial BP exceeds the body's ability to autoregulate cerebral blood flow
- cerebral blood vessels suddenly dilate = cerebral edema = increased ICP
35
what complication can occur in the peripheral vasculature d/t HTN
- peripheral vascular disease
36
what is peripheral vascular disease? how does HTN lead to this
- a blood circulation disorder that causes the blood vessels outside of your heart and brain to narrow, block, or spasm - HTN = increased atherosclerosis
37
what is a classic symptom of peripheral vascular disease
- intermittent claudication = ischemic muscle pain precipitated by activity and relieved w rest
38
what complication can occur in the kidneys d/t HTN (2)
- nephrosclerosis | - ESRD
39
how does HTN lead to nephrosclerosis
- direct result of ischemia caused by the narrowed lumen of the intrarenal blood vessels = eventual death of nephrons
40
what is a sign of nephrosclerosis (3)
- microalbuminuria - elevated BUN - elevated creatinine
41
what complication occurs in the eyes d/t HTN
- retinal damage
42
what are signs of retinal damage (3)
- blurred vision - retinal hemorrhage - loss of vision
43
how is HTN diagnosed
- not based on a single elevated BP | - requires severeal elevated BP readings over several weeks
44
what findings can be used to diagnose HTN (6)
- history - physical exam - electrolytes (K+ indicated hyperaldo) - BG (monitor for development of DM) - cholestrol and triglyceride lvls - ECG
45
what does collaborative care of HTN focus on (3)
- risk stratification - lifestyle modifications - meds
46
what lifestyle modifications are included in treatment of HTN (6)
- dietary changes - limitation of alcohol intake - regular physical activity - avoidance of tobacco use - stress management - weight reduction
47
what is emphasized in nutritional therapy for a pt with HTN (6)
emphasize - fruit - veggies - low-fat dairy - fibre - whole grains - protein
48
what is reduced in nutritional therapy for a pt with HTN (5)
- sat fats - cholestrol - sodium - maintain K+, Ca, Mg - calories restriction if overweight
49
why is weight reduction imp for manageemnt of HTn
- obesity = increased incidence of HTN and increased cardio risk - weight reduction = signif effect on lowering BP
50
what weight loss strategies are used for a pt with HTN (3)
- increased physical activity - behavioral intervention - decreased cal, na, fat
51
why is modification of alcohol consumption imp for treatment of HTN
excessive alcohol = strongly associated w HTN
52
what guidelines are used for alcohol consumption
- 2 drinks or fewer per day - should not exceed 14 drinks per week for men - & 9 drinks per week for women
53
what physical activity guidelines are recommended for pts w HTN
- 30-60 min of moderate intensity exercise, 4-7 days per week
54
what benefits does physical activity have for a pt with HTN (3)
- lowers BP - promote relaxation - decrease/control body weight
55
why is avoidance of tobacco products imp for treatment of HTN
- nicotine = vasoconstriction = increased BP
56
what drugs are used in treatment of HTN (5)
- diuretics - adrenergic inhibitors - direct vasodilators - RAAS inhibitors - Ca channel blockers
57
what action do diuretics have in reduction of BP (4)
- promote Na and water excretion - reduce plasma vol - reduce vascular response to catecholamines - decrease Na in arteriolar walls
58
what do adrenergic inhibitors do?
- diminish the sympathetic effects that increase BP - act centrally on vasomotor center - inhibit NE release - block adrenergic receptos on blood vessels --> alpha and beta blockers
59
what do direct vasodilators do
- decrease BP by relaxing vascular smooth muscle & cause arteriolar vasodilation by preventing the movement of extracellular Ca into cells
60
what are 2 examples of direct vasodilators
- nitroglycerin | - nipride
61
what are 3 types of RAAS inhibitors
- ACE-I - ARBs - renin inhibitors
62
describe how layering meds works for treatment of HTN
- start w first drug at low dose, if BP not controlled in several weeks, dosage increased - second drug added (or substituted) if the first drug was ineffective or too many s/e (most pts require at least two meds + lifestyle changes) - third or fourth med may be added but only if the max doses of the first and second drug have been achieved
63
what is step down therapy
- after 1 year of optimum BP control, step down therapy may be tried - number and dose of meds is gradually decreases to the lowest amt required to control BP
64
what is required w step down therapy
- regular follow ups to detect elevations in BP
65
what are potential s/e of diurectis (5)
- hypokalemia - hyperglycemia - hyperuricemia - polyuria - dry mouth
66
what are potential side effects pf ACE-I (3)
- coughing - angioedema - hyperkalemia * may be switched to ARB if experiencing these*
67
what are 2 potential side effects of adrenergic inhibitors
- orthostatic hypotension | - sexual dysfnxn
68
what are 2 potential s/e of vasodilators
- orthostatic hypotension | - tachycardia
69
what is important pt teaching r/t meds (5)
- otrho hypotension --> rise slowly when moving from sitting/laying down to upright position - encourage to discuss s/e with HCP (esp. sexual dysfunction, as the s/e may be decreased by changing to a diff antiHTN drug) - sugarless gum can relieve dry mouth r/t diuretics - take diuretics earlier in day to prevent nocturia - BP highest after waking up & lowest at night = BP meds with 24 hr duration should be taken eary in morning
70
what is a major challenge in management of HTN
- adherence to prescribed treatment plan (meds, diet, exercise, smoking cessation, etc.)
71
what is hypertensive crisis
- severe & abrupt elevation in BP | - DBP > 120
72
who does hypertensive crisis often occur in
- pts with a hx of HTN who have failed to adhere to meds, or have been undermedicated - drug users on cocaine or meth
73
what are S&S of hypertensive crisis (9)
- headache - NV - seizures - confusion - stupor, coma - blurred vision - chest pain - dyspnea - high BP * signs of organ damage)
74
how is hypertensive crisis classified
- degree of organ involvement and rapidity in which the BP must be lowered
75
what do hypertensive emergencies necessitate (3)
- hospitalization - parental admin of antiHTN drugs - intensive care monitoring
76
what is the initial treatment of hypertensive emergency
- decrease MAP by 10-20% in first 1-2 hours with further gradual reduction over 24 hr * drop in BP too far/fast could = decreased cerebral perfusion*
77
what IV drugs are used for hypoternsive crisis (3)
- vasodilators - adrenergic inhibitors - ACE-I
78
what is the most effective parental drug for treatment of hypertensive crisis
- IV sodium nitroprusside (nipride, nitrate)
79
what should you monitor during treatment of hypertensive crisis (6)
- BP and pulse every 2-3 min during initial admin - continual ECG monitoring - hourly urinary output - neuro checks - assess cardiac, renal, pulmonary systems for decompensation r/t elevated BP - pt may be restricted to bed
80
what is the onset of nipride
- seconds to minutes
81
the rate of drug admin is determined how for hypertensive crisis
- titrated according to lvl of BP
82
what should you monitor during HTN crisis (4)
- BP - cardiac monitoring - dysrhythmias - UO --> could be low d/t nitroprusside