32 Hypertension Flashcards
Components of BP measurement
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
Systolic Blood Pressure [SBP]
peak pressure during cardiac systole
-the squeezing of heart to pump
Diastolic Blood Pressure [DBP]
lowest pressure during cardiac diastole
- dilating/relaxing part of heart/refilling
- takes longer than systolic
stroke volume SV
amount of blood pumped by Left ventricle per minute
-primary factor influencing systolic pressure
systemic vascular resistance - SVR
the force opposing the mvmt of blood w/in the blood vessels
-determined by radius of arteries + degree of vessel compliance
Pulse pressure
systolic - diastolic
Mean Arterial Pressure [MAP]
calculated average pressure w/in circulatory system throughout the cardiac cycle
MAP=
{ [2x dias] + sys } / 3
Direct measurements of BP
- 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
where is the catheter usually placed to measure BP?
radial artery
Indirect measurement of BP
- 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
Auscultation of Korotkoff Sounds
-indirect form of measurement of BP
SBP: onset of Korotkoff sounds
DBP: disappearance of Korotkoff sounds
Auscultatory Gap
- occurs in elderly
- period of absent Korotkoff sounds during manual measurement of BP
Cardiac Output [CO]
Q=strok vol x heart rate
vol of blood being pumped by heart in 1 minute
Preload
end-diastolic volume
-amount of blood returned to heart
Afterload
mount of pressure that the heart needs to exert to eject the blood during ventricular contraction
Sympathetic Nervous System [SNS] on BP
- short-term regulator of systemic blood pressure
- based on epinephrine + norepinephrine
- incr BP by incr CO + incr in SVR
parasympathetic nervous system on BP
slows heart
Renin-Angiotensin-Aldosterone System [RAAS]
-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
Angiotensin II
- activated from Angiotensin I by ACE
- potent vasoconstrictor [AFTERLOAD]
- stimulates the release of Aldosterone in RAAS
Aldosterone
hormone that causes reabsorption of Na
- causes water to follow
- PRELOAD
- release of aldosterone is stimulated by Angiotensin II
Na + H2O retention causes…
increase in BLOOD VOLUME>
increase in BLOOD PRESSURE
what it the main outcome of RAAS?
pathway leads to INCREASE IN BLOOD PRESSURE
RAAS/long-term syst BP
REGULATION
-regulated by neural, hormonal, + renal
increase in xtracellular FLUID VOLUME [PRELOAD]
1 increase in CO + SVR
2 elevated BP
-causes kidneys to EXCRETE excess Na + fluid
increase in SERUM SODIUM LVL
1 increase osmolality
2 increase ADH secretion
-causes kidneys to REABSORB water + increase PRELOAD
Vasopressin [ADH]
- hormone made by hypothalamus
- stored in PIT gland
- causes kidney to conserve/reabsorb H2O
Atrial Natriuretic Peptides [ANP]
1 increases GLOMERULAR FILTRATION RATE >
2 increase in H2O + Na EXCRETION
3 results in decrease of PRELOAD
Normal Blood Pressure
SBP <120
DBP <80
PRE hypertension
SBP 120-139
DBP 80-89
Stage 1 Hypertension
SBP 140-159
DBP 90-99
Stage 2 Hypertension
SBP >160
DBP >100
Primary Hypertension
aka HIGH BLOOD PRESSURE aka silent killer bc organs are damaged before diagnosis is made [END-ORGAN DAMAGE]
-no clear cause
End-Organ Damage
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
Primary Hypertension
subtypes
1 Isolated Systolic Hypertension
2 Isolated Diastolic Hypertension
3 Combined
Primary Hypertension
risk factors
- family history
- age
- ethnicity
- genetics
Primary Hypertension
modifiable risk factors
- diet
- sedentary lifestyle
- obesity/weight gain
- metabolic syndrome
- elevated blood glucose/diabetes
- elevated total cholesterol
- alcohol + smoking
Primary Hypertension
treatment
lifestyle modifications are first + most important prevention + treatment strategy
-drug therapy affects heart rate, SVR, + stroke volume
lifestyle modifications are first + most important prevention + treatment strategy for primary hypertension
- weight loss
- exercise
- DASH diet
- alcohol moderation
- decreased sodium intake
Secondary Hypertension
-attributed to specific identifiable pathology or condition
most common form of hypertension in infants + children
Secondary Hypertension
most common cause of childhood secondary hypertension
RENAL DISEASE + coarctation of the aorta [AORTIC NARROWING]
-other cause is obstructive sleep apnea
maintaining normal BP + tissue perfusion requires ____ +_____ effects
systemic factors + local peripheral vascular effects
BP is a function of both ___ + ___
CO + SVR
factors that influence CO
renal + fluid vol control -RAAS -ANP cardiac -HR -contractility -conductivity
factors that influence SVR
LOCAL REGULATION -vasodilators: prostaglandin + nitric oxide -vasoconstrictors: endothelin NEUROHORMONAL -vasoconstrictors: A-II +norepinephrine SNS -vasodilators: b2-adrenrgc -vasoconstrictors: a1 + a2 adrenrgc
under normal conditions, BP may be reduced by the withdrawal of _____ or stimulation of _____
withdrawal of SNS
or
stimulation of PNS
PNS decreases the HR via the _______ and thereby decreases CO
vagus nerve
_____ senses changes in BP + send info to vasomotor centers in the brainstem
baroreceptors
-found in carotid arteries + arch of aorta
Black - risk factor
- highest prevalence of HTN
- women>men
- more aggressive HTN>EOD
Medication for Blacks
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
Hispanics - risk factors
- less likely to receive treatment for HTN
- lower levels of awareness of HTN + treatments
men vs women - risk factor
before middle age: men>women
after 64: women>men
—-menopause, estrogen withdrawal, overproduction of pit hormone, wt gain
oral contraceptive: 2-3x more women
a1 + a2: location + response
a1: heart > incr contractility/+inotropic
a1: vasc smth muscles > vasoconstriction
a2: presynaptic nerve terminals > inhibits norepinephrine release
a2: vasc smth muscles > vasoconstriction
b1 + b2: location + response
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
baroreceptors are sensitive to ____, and are stimulated by _____
sensitive to stretching
stim by an incr in BP
smooth muscle of blood vessels has ____ receptors
alpha and beta2 adrenergic
beta 2 adrenergic mainly acts on ____ to cause ____
epinephrine to cause vasodilation
during postural changes from lying to standing, there is a transient decrease in BP. How does the normal body adjust?
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
endothelium-derived vasoactive substances
NO: vasodilator
prostaclyn: vasodilator
endothelin [ET]: vasoconstrictor
smoking _ diabetes on endothelial cells
reduce functional endothelial cells
nicotine in tobacco also causes vasoconstriction
renal hormones
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
endocrine hormones
epinephrine: incr HR + contractility> incr CO
—activates b2 to vasodilate
—activates a1 periph arterioles to vasoconstrict (skin + kidneys)
norepinephrine:
patho of primary HTN
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
patho of primary HTN
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
effect of sodium on BP has a strong _____ component
genetic
high insulin levels
- stim SNS activity
- impair NO-mediated vasodilation
- vascular hypertrophy
- incr renal Na absorption
endothelial dysfunction is a marker for ____
CVD (incl. HTN)
- prolonged vasoconstriction
- O-free radicals> impair bioavailability of NO> impaired vasodilation
secondary s/s of HTN vs hypertensive crisis s/s
secondary: fatigue, dizzy, palpitations, angina, + dyspnea
hypertensive: dyspnea, severe headache, anxiety, nosebreed
why is potassium level important?
high levels might indicate hyperaldosteronism, a cause of secondary HTN
normal BP on circadian rhythm
BP is highest in the AM and lowest in PM
nondippers
absence of the typical nocturnal fall in BP
-common w HTN
reverse dippers
incr in nighttime systolic BO
-highest risk for CVD
AHA’s life’s simple 7
1 manage BP 2 control cholesterol 3 reduce blood sugar 4 get active 5 eat better 6 lose weight 7 stop smoking
Na restriction range
normal adult: 2300mg/day
HTN: 1500 mg/day
avoid pizza, cured meat, lunch meat, bread products, soup, sandwich, poultry
incr levels of ____ + ____ are assoc w lower levels of BP
potassium + calcium
BP goal range for individual w HTN
130/80
preferred first line therapy for Stage I HTN
- thiazide diuretic
- Ca channel blocker
- ACE inhibitor/ARB
how often are follow-ups after anti-HTN therapy has started
Qmonthly until goal BP is reached
after, Q3-6months
when measuring BP, the arm should be…
at heart level.
so if pt. is laying down, raise the arm w a pillow
orthostatic BP measurement
lie down 5 mins. take BP
stand for 1 min. take BP
stand for 3 min. take BP
orthostatic HTN range
decr of 20mmHg or more in SBP
or decr of 10mmHg or more in DBP
can HTN be cured?
no, it is a chronic illness
aging on HTN
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
postprandial drops in BP in adults is highest most significant in _____
1 hr after eating
160/120
hypertensive crisis
-can often be greter than 220/140
urgency vs. emergency
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
goap of hypertensive crisis
decrease MAP by no more than 20% or to 110-115mmHg
lower BP too quickly can cause
decr in cerebral, coronary, or renal perfusion
-rapid decr could cause a stroke, MI or renal failure
patients w aortic dissection
BP goals
SBP < 100-120 mmHg asap
elevated BP in post stroke
compensatory response to improve cerebral perfusion
DO NOT USE ANTI-HTN
how often to asses a pt with IV of anti-HTN
assess BP + HR Q2-3min
monitor ECG for ischemia, MI, or dysrhyttmia
-may be on bed rest
