32 Hypertension Flashcards

1
Q

Components of BP measurement

A
1 Systolic BP
2 Diastolic BP
3 SV is primary factor of systolic p
4 SVR is major determinant of diastolic p
5 Pure Pressure = sys-dias 
6 Mean Arterial Pressure
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2
Q

Systolic Blood Pressure [SBP]

A

peak pressure during cardiac systole

-the squeezing of heart to pump

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3
Q

Diastolic Blood Pressure [DBP]

A

lowest pressure during cardiac diastole

  • dilating/relaxing part of heart/refilling
  • takes longer than systolic
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4
Q

stroke volume SV

A

amount of blood pumped by Left ventricle per minute

-primary factor influencing systolic pressure

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5
Q

systemic vascular resistance - SVR

A

the force opposing the mvmt of blood w/in the blood vessels

-determined by radius of arteries + degree of vessel compliance

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6
Q

Pulse pressure

A

systolic - diastolic

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7
Q

Mean Arterial Pressure [MAP]

A

calculated average pressure w/in circulatory system throughout the cardiac cycle
MAP=
{ [2x dias] + sys } / 3

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8
Q

Direct measurements of BP

A
  • requires intraarterial catheter + specialized euipt to transduce arterial fluid pulsations into electrl sgnals.
  • catherer commonly placed in RADIAL ARTERY
  • most accurate method to measure BP
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9
Q

where is the catheter usually placed to measure BP?

A

radial artery

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10
Q

Indirect measurement of BP

A
  • commonly via brachial artery w stethoscope + sphygmomanometer or automated oscillometric systm
  • requires careful technique for accuracy
  • auscultation of korotkoff sounds
  • white coat effect
  • elderly auscultatory gap
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11
Q

Auscultation of Korotkoff Sounds

A

-indirect form of measurement of BP
SBP: onset of Korotkoff sounds
DBP: disappearance of Korotkoff sounds

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12
Q

Auscultatory Gap

A
  • occurs in elderly

- period of absent Korotkoff sounds during manual measurement of BP

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13
Q

Cardiac Output [CO]

A

Q=strok vol x heart rate

vol of blood being pumped by heart in 1 minute

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14
Q

Preload

A

end-diastolic volume

-amount of blood returned to heart

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15
Q

Afterload

A

mount of pressure that the heart needs to exert to eject the blood during ventricular contraction

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16
Q

Sympathetic Nervous System [SNS] on BP

A
  • short-term regulator of systemic blood pressure
  • based on epinephrine + norepinephrine
  • incr BP by incr CO + incr in SVR
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17
Q

parasympathetic nervous system on BP

A

slows heart

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18
Q

Renin-Angiotensin-Aldosterone System [RAAS]

A
-important long-term regulator of BP
1 low arterial pressure causes Juxtaglomerular cells to secrete Renin
2 Renin activates ANG  to ANG I
3 ACE activated ANG I into II [PRELOAD]
4 ANG II stim release of ALDOSTERONE
5 reabsorption of Na + H2O> PRELOAD
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19
Q

Angiotensin II

A
  • activated from Angiotensin I by ACE
  • potent vasoconstrictor [AFTERLOAD]
  • stimulates the release of Aldosterone in RAAS
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20
Q

Aldosterone

A

hormone that causes reabsorption of Na

  • causes water to follow
  • PRELOAD
  • release of aldosterone is stimulated by Angiotensin II
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21
Q

Na + H2O retention causes…

A

increase in BLOOD VOLUME>

increase in BLOOD PRESSURE

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22
Q

what it the main outcome of RAAS?

A

pathway leads to INCREASE IN BLOOD PRESSURE

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23
Q

RAAS/long-term syst BP

REGULATION

A

-regulated by neural, hormonal, + renal

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24
Q

increase in xtracellular FLUID VOLUME [PRELOAD]

A

1 increase in CO + SVR
2 elevated BP
-causes kidneys to EXCRETE excess Na + fluid

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25
Q

increase in SERUM SODIUM LVL

A

1 increase osmolality
2 increase ADH secretion
-causes kidneys to REABSORB water + increase PRELOAD

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26
Q

Vasopressin [ADH]

A
  • hormone made by hypothalamus
  • stored in PIT gland
  • causes kidney to conserve/reabsorb H2O
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27
Q

Atrial Natriuretic Peptides [ANP]

A

1 increases GLOMERULAR FILTRATION RATE >
2 increase in H2O + Na EXCRETION
3 results in decrease of PRELOAD

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28
Q

Normal Blood Pressure

A

SBP <120

DBP <80

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29
Q

PRE hypertension

A

SBP 120-139

DBP 80-89

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30
Q

Stage 1 Hypertension

A

SBP 140-159

DBP 90-99

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31
Q

Stage 2 Hypertension

A

SBP >160

DBP >100

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32
Q

Primary Hypertension

A

aka HIGH BLOOD PRESSURE aka silent killer bc organs are damaged before diagnosis is made [END-ORGAN DAMAGE]
-no clear cause

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33
Q

End-Organ Damage

A

1 renal failure, stroke, heart disease
2 damaged arterial sytm >atherosclerosis >cardiovasc disease
3 incr myocardial work > heart failure
4 glomerular damage > kidney failure
5 affects microcirculation of eyes
6 incr pressure in cerebral vasculature > hemorrhage

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34
Q

Primary Hypertension

subtypes

A

1 Isolated Systolic Hypertension
2 Isolated Diastolic Hypertension
3 Combined

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35
Q

Primary Hypertension

risk factors

A
  • family history
  • age
  • ethnicity
  • genetics
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36
Q

Primary Hypertension

modifiable risk factors

A
  • diet
  • sedentary lifestyle
  • obesity/weight gain
  • metabolic syndrome
  • elevated blood glucose/diabetes
  • elevated total cholesterol
  • alcohol + smoking
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37
Q

Primary Hypertension

treatment

A

lifestyle modifications are first + most important prevention + treatment strategy
-drug therapy affects heart rate, SVR, + stroke volume

38
Q

lifestyle modifications are first + most important prevention + treatment strategy for primary hypertension

A
  • weight loss
  • exercise
  • DASH diet
  • alcohol moderation
  • decreased sodium intake
39
Q

Secondary Hypertension

A

-attributed to specific identifiable pathology or condition

40
Q

most common form of hypertension in infants + children

A

Secondary Hypertension

41
Q

most common cause of childhood secondary hypertension

A

RENAL DISEASE + coarctation of the aorta [AORTIC NARROWING]

-other cause is obstructive sleep apnea

42
Q

maintaining normal BP + tissue perfusion requires ____ +_____ effects

A

systemic factors + local peripheral vascular effects

43
Q

BP is a function of both ___ + ___

A

CO + SVR

44
Q

factors that influence CO

A
renal + fluid vol control
-RAAS
-ANP
cardiac
-HR
-contractility
-conductivity
45
Q

factors that influence SVR

A
LOCAL REGULATION
-vasodilators: prostaglandin + nitric oxide
-vasoconstrictors: endothelin
NEUROHORMONAL
-vasoconstrictors: A-II +norepinephrine
SNS
-vasodilators: b2-adrenrgc
-vasoconstrictors: a1 + a2 adrenrgc
46
Q

under normal conditions, BP may be reduced by the withdrawal of _____ or stimulation of _____

A

withdrawal of SNS
or
stimulation of PNS

47
Q

PNS decreases the HR via the _______ and thereby decreases CO

A

vagus nerve

48
Q

_____ senses changes in BP + send info to vasomotor centers in the brainstem

A

baroreceptors

-found in carotid arteries + arch of aorta

49
Q

Black - risk factor

A
  • highest prevalence of HTN
  • women>men
  • more aggressive HTN>EOD
50
Q

Medication for Blacks

A
Ca channel blockers + diuretics
-best BP control
Renin-inhibiting drugs
-blacks produce less renin so they dont respond well
ACE inhibitors
-higher risk for angioedema
51
Q

Hispanics - risk factors

A
  • less likely to receive treatment for HTN

- lower levels of awareness of HTN + treatments

52
Q

men vs women - risk factor

A

before middle age: men>women
after 64: women>men
—-menopause, estrogen withdrawal, overproduction of pit hormone, wt gain
oral contraceptive: 2-3x more women

53
Q

a1 + a2: location + response

A

a1: heart > incr contractility/+inotropic
a1: vasc smth muscles > vasoconstriction

a2: presynaptic nerve terminals > inhibits norepinephrine release
a2: vasc smth muscles > vasoconstriction

54
Q

b1 + b2: location + response

A

b1: heart > incr contractility/+ inotropic
»>incr HR/+ chronotropic
»>incr speed of conduction/+ dromotropic
b1: juxtaglomerular cells > incr renin production

b2: vasc smth muscles in blood vessells of the heart, lungs, + skeletal muscles > vasodilation

55
Q

baroreceptors are sensitive to ____, and are stimulated by _____

A

sensitive to stretching

stim by an incr in BP

56
Q

smooth muscle of blood vessels has ____ receptors

A

alpha and beta2 adrenergic

57
Q

beta 2 adrenergic mainly acts on ____ to cause ____

A

epinephrine to cause vasodilation

58
Q

during postural changes from lying to standing, there is a transient decrease in BP. How does the normal body adjust?

A

vasomotor center is stimulated> SNS response causes periph vasoconstriction> incr venous return to the heart

*if these don’t occur, blood flow to the brain would be inadequate, resulting in dizziness or syncope

59
Q

endothelium-derived vasoactive substances

A

NO: vasodilator
prostaclyn: vasodilator
endothelin [ET]: vasoconstrictor

60
Q

smoking _ diabetes on endothelial cells

A

reduce functional endothelial cells

nicotine in tobacco also causes vasoconstriction

61
Q

renal hormones

A

A-II: vasoconstrictor> incr SVR
»stim adrenal cortex to release aldosterone
Aldosterone: incr ECF> incr CO +SV
Prostaglandin: systemic vasodilator> decr SVR > decr BP
ANP/BNP: oppose ADH + aldosterone

62
Q

endocrine hormones

A

epinephrine: incr HR + contractility> incr CO
—activates b2 to vasodilate
—activates a1 periph arterioles to vasoconstrict (skin + kidneys)
norepinephrine:

63
Q

patho of primary HTN

A

early: incr in blood vol, CO, + SVR

as HTN progresses: SVR rises but CO returns to normal

***persistently incr SVR is the hemodynamic hallmark of HTN

64
Q

patho of primary HTN

A

early: incr in blood vol, CO, + SVR

as HTN progresses: SVR rises but CO returns to normal

***persistently incr SVR is the hemodynamic hallmark of HTN

65
Q

effect of sodium on BP has a strong _____ component

A

genetic

66
Q

high insulin levels

A
  • stim SNS activity
  • impair NO-mediated vasodilation
  • vascular hypertrophy
  • incr renal Na absorption
67
Q

endothelial dysfunction is a marker for ____

A

CVD (incl. HTN)

  • prolonged vasoconstriction
  • O-free radicals> impair bioavailability of NO> impaired vasodilation
68
Q

secondary s/s of HTN vs hypertensive crisis s/s

A

secondary: fatigue, dizzy, palpitations, angina, + dyspnea
hypertensive: dyspnea, severe headache, anxiety, nosebreed

69
Q

why is potassium level important?

A

high levels might indicate hyperaldosteronism, a cause of secondary HTN

70
Q

normal BP on circadian rhythm

A

BP is highest in the AM and lowest in PM

71
Q

nondippers

A

absence of the typical nocturnal fall in BP

-common w HTN

72
Q

reverse dippers

A

incr in nighttime systolic BO

-highest risk for CVD

73
Q

AHA’s life’s simple 7

A
1 manage BP
2 control cholesterol
3 reduce blood sugar
4 get active
5 eat better
6 lose weight
7 stop smoking
74
Q

Na restriction range

A

normal adult: 2300mg/day
HTN: 1500 mg/day

avoid pizza, cured meat, lunch meat, bread products, soup, sandwich, poultry

75
Q

incr levels of ____ + ____ are assoc w lower levels of BP

A

potassium + calcium

76
Q

BP goal range for individual w HTN

A

130/80

77
Q

preferred first line therapy for Stage I HTN

A
  • thiazide diuretic
  • Ca channel blocker
  • ACE inhibitor/ARB
78
Q

how often are follow-ups after anti-HTN therapy has started

A

Qmonthly until goal BP is reached

after, Q3-6months

79
Q

when measuring BP, the arm should be…

A

at heart level.

so if pt. is laying down, raise the arm w a pillow

80
Q

orthostatic BP measurement

A

lie down 5 mins. take BP
stand for 1 min. take BP
stand for 3 min. take BP

81
Q

orthostatic HTN range

A

decr of 20mmHg or more in SBP

or decr of 10mmHg or more in DBP

82
Q

can HTN be cured?

A

no, it is a chronic illness

83
Q

aging on HTN

A

1 loss of elasticity in large arteries fr atherosclerosis
2 incr collagen/stiffness in heart
3 incr periph vasc resistance
4 decr adrenergic receptors
5 blunting baroreceptor reflex
6 decr renal function
7 decr renin response to Na/H2O depletion

84
Q

postprandial drops in BP in adults is highest most significant in _____

A

1 hr after eating

85
Q

160/120

A

hypertensive crisis

-can often be greter than 220/140

86
Q

urgency vs. emergency

A

emergency has presence of target organ damage such as encephalopathy, intracranial or subarachnoid hemorrhage, HF, MI, renal failure, retinopathy

urgency may be assoc w chronic stable complication slike stable angina, chronic HF, prior MI, or cerebrovascular accident w no acute threat

87
Q

goap of hypertensive crisis

A

decrease MAP by no more than 20% or to 110-115mmHg

88
Q

lower BP too quickly can cause

A

decr in cerebral, coronary, or renal perfusion

-rapid decr could cause a stroke, MI or renal failure

89
Q

patients w aortic dissection

BP goals

A

SBP < 100-120 mmHg asap

90
Q

elevated BP in post stroke

A

compensatory response to improve cerebral perfusion

DO NOT USE ANTI-HTN

91
Q

how often to asses a pt with IV of anti-HTN

A

assess BP + HR Q2-3min
monitor ECG for ischemia, MI, or dysrhyttmia
-may be on bed rest