Hypertension Flashcards
major forms of CVD
hypertension, atherosclerosis, ischemic heart disease, peripheral vascular disease, heart failure, cerebrovascular disease
leading cause of death in canada
disease of the heart and cerebrovascular disease (24 % combined)
prevalence is ____________
going up in both males and females- more so in males
how many people are actually aware of their condition
65% treated and controlled, 18% unaware, 14% treated but not controlled, 4% aware, not treated
visits to the doctor
hypertension leading cause - by a lot!!
- more than diabetes
hypertension affects >__/5, what %?
more than 1 in 5 people, 22% Canadians over 20 , but since 18% not aware this number is actually much higher
the lifetime risk of developing hypertension in adults 55-65 with normal BP is?
90%
is hypertension the number one reason for taking medication?
yes
one in how many Americans have hypertension
one in 3
how is more at risk of hypertension
males, African-america, than whites, than hispanic, than Japanese, than Chinese
MAP
(mean arterial pressure) =
the average pressure in a patients arteries during one cardiac cycle. better indicator of the perfusion to vital organs than systolic bp.
found by:
cardiac output x peripheral resistance
cardiac output
= stoke volume x heart rate
peripheral resistance
= (length of vessel x viscosity of blood) / radius ^4
what 4 things regulate MAP?
- sympathetic NS
- RAAS
- renal function
- hormones
which hormones are involved in regulating MAP
epinephrine, vasopressin, angiotensin II
explain the big “factors influencing MAP” chart in you own words
the 2 factors influencing MAP are cardiac output and total peripheral resistance.
- CO is determined by HR and stoke volume.
- HR is determined by either PSNS or SNS/epinephrine. stroke volume is determined by SNS/epinephrine or venous return.
- venous return is a big one. it is affected by blood volume (affected by vasopressin and angiotensin II, salt and water balance), respiratory activity, skeletal muscle activity and cardiac-suction effect.
- on the other side, TPR is determined by arteriolar radius ( determined by skeletal muscle activity leading to local metabolic control, and SNS/epinephrine activity and vasopressin/ angiotensin leading to extrinsic vasoconstriction control) and by blood viscosity which is determined by # of RBC
primary HPT vs secondary
primary 95 % of cases- is idiopathic meaning that there is no known cause and secondary is caused by another issue/disease such s renal disease or CVD, endocrine disorders
causes of primary HPT
cause is not know! however many factors are at play –> individual differences in RAAS, in genes responsible for salt retention etc, in lifestyle choices ( stress, smoking, diet, excersise)
hypertensive individuals often secrete / overproduce?
vasopressin and angiotensin ( causes vasoconstriction and fluid retention)
non-modifiable risk factors of HPT
over 60, males, postmenopausal women, ethnicity, family history
modifiable risk factors
smoking, excersise, sodium intake, obesity, poor diet, stress
how does smoking contribute to HPT
interfere with NO–> impairs endothelial vasodilation
how does renal disease contribute to HPT
reduced blood flow, increased angiotensin, vasoconstriction and electrolyte/water retention, increases BV
is hyperinsulinemia associated with HPT
yes but mechanism is unclear
how would adrenal issues contribute to HPT
increase epinephrine and norepinephrine lead to vasoconstriction and increased cardiac output
how is HPT classified?
readings greater than 140/90 mm Hg (inclusive) are considered hypertensive. this does not mean that Bothe umbers have to be here, could be 140/80 and still hypertensive
why is hypertension a silent killer?
asymptomatic
what happens in response to low NaCl- / low ECF volume and low arterial blood pressure
the kidneys secrete renin, which converted circulating ( from the liver) angiotensinogen into angiotensin I, the lungs secrete converting enzyme to change 1 into 2, and angiotensin 2 acts on adrenal cortex to release aldosterone ( conserve Na+– passively water saved swell), and thirst is triggered and vasopressin release ( to reabsorb more water ( aquaporins) ) and acts on arteries to vasoconstriction –> all these in place to save body from harmful low BP
where is vasopressin released from
the posterior pituitary ( made in the hypothalamus)
what organs are affected by hypertension
brain - hemorrhage and stroke
kidney- renal failure and proteinuria
heart- CHD, CHF, LVH
eyes - retinopathy ( damage to the retina)
peripheral vascular disease ( blood circulation disorder)
what is top number reading
systolic
what is bottom number reading
diastolic
normal systolic
90-119
normal diastolic
60-79
stage 1 hypertensive
140-156/ 90-99
stage 2 HPT
160-179/ 100-109
stage 3
> 180/ >110
cerebrovascular diseases
diseases or conditions relating to blood supply to the brain –> stoke, dementia, hemorrhage
ACC stands for?
associated clinical conditions
list some ACC and target organ damage (TOD) that can occur from HPT
CVD - coronary artery disease, left ventricle hypertrophy, heart failure cerebrovascular Diseases retinopathy nephropathy peripheral artery disease
TOD
TOD is the structural and functional impairment of major body organs due to elevated blood pressure (BP).
who is at high risk ?
one or more of the following:
- clinical or sub-clinical CVD
- chronic kidney disease
- 10 year global cardiovascular risk >15%
- above the age of 75
who is at moderate to high risk
multiple CV risk factors and 10-year global risk >15%
who is at low risk?
no TOD or cardiovascular risk factors
why do we want to stratify risk ?
based on risk there are different thresholds and targets for treatment
if high risk what BP treatment target are we aiming for?
<120 /NA diastolic
if diabetic patient what BP target are we aiming for?
<130/ <80
if moderate risk what target BP?
<140/ <90
if low res what BP are we aiming for
<140 / <90
how does the threshold for starting antihypertensive therapy change with the risk of patient
the higher the risk, the lower the BP reading to start treatment ( for example, if high risk and patient has BP reading of >130/ NA then we start antihypertensive therapy, but if patient is low risk than we wouldn’t Strat until patient is at reading of >160 /100
how do we measure BP
automated office BP (AOBP)
oscillometric ( electric is preferred) vs non-automated office BP
out of office BP measurements method
ambulatory - relating to or adapted for walking
differences in reading for AOBP and non-AOBP
When using AOBP, a displayed mean SBP ≥135 mmHg or DBP ≥85 mmHg is high (Grade D). ii. When using non-AOBP, a mean systolic BP (SBP) ≥140 mmHg or diastolic BP (DBP) ≥90 mmHg is high,
describe the path of diagnosing HPT
elevated BP reading -> go see doctor–> if mean office BP >180/110 - yup , if no AOBP is >135/85 or non-AOBP >140/80 then tell you to go home and need to take out of office measurements –> bc could be white coat hypertension –> at home if reading is > 135/85 with ABPM, then yes hyper tension, if no than white coat hypertension.
how does diagnosis differ with diabetes?
if AOBP or non-AOBP reading is >130/80 then the patient need to take readings at home ( this is different bc for non-diabetic the range is 135/85
goals of treatment
- reduce the risk of CD and renal disease
- lower BP to clinically appropriate levels
dietary constituents in HPT
high cal/weight/obesity Na K Mg Ca alcohol
___ % of under 55 yr old who have excess weight and a normal BP will develop HPT in the next 4 years
60% !! (direct link btw excess weight and HPT
why is HPT related to obesity
insulin resistance/hyperinsulema
overactivity of the SNS
alterations in RAAS
leptin increases sympathetic activity–> function is preserved even in leptin resistance (meaning resistant to appetite control) individuals; still affects the SNS
most beneficial non-pharm approach to HPT
weight loss, 10kg loss = 5-20 mmHG reduced
10 kg loss =
5-20 mmHg
all overweight patients should aim for a loss of ?
5kg to reduce BP
weight loss could be difficult in patients with?
beta blockers- Beta blockers, also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine
what did high sodium intake do for patients with hypertension
increases risk of CHD death, CVD death and all death
AI for sodium
1500 mg/day for 14-50 yr
1300 for 50-70
1200 for above 70
UL for sodium
2300 mg/day for ALL
average daily intake
3400 mg/day
CHEP recommends
reduce sodium to 2000mg/day
how much is 2000 mg of Na in salt?
5 g of salt which is just under a tsp
major foods with sodium
breads, processed meats, soups, pasta, tomato dishes
choose foods with less than ___ sodium
120 mg / serving or less than 5%
3000 mg Na
no high Na processed foods and beverages
up to 0.25 tsp to cooking
2000 mg Na diet
no high Na processed foods and beverages, no salt in prepration to foods, limit milk products to 2 cups/day
1000 mg
same as 2000 but no canned, frozen, deli foods, cheese, margarine and no more than 2 servings of bread/day
benefits of reducing sodium intake
found through epidemiological and ecological and intervention studies
- reduce BP
- prevent hypertension
- additive effect with medications
- reduces risk of complications
potassium
inverse relationship between K and BP
- decreased prevalence of HPT with higher K intake
potential mechanism of K intake
- natriuresis
- suppressed renin
- vasodilation
- reduce sympathetic activity and angiotensin II
contributing factors for HPT
smoking (NO), excessive vasopressin, renal disease ( reduced blood flow will secrete more angiotensin II, adrenal disorders, hyperinsulinemia
patients with HPT have an increased risk of TOD such as
heart-> CAD, LVH, HF brain--> stroke, dementia retinopathy nephropathy rest of body -peripheral artery disease
describe hypertension Canada’s stratifying risk system
canada stratifies patients based on cardiovascular risk and then treatment is adjusted based on that risk ( so if a patient is high risk, the S/D threshold is going to be lower to administer medication than someone with hypertension but low risk) as well the BP treatment target is going to be LOWER - really want to minimize the risk
high-risk patients
patients with one or more of the following clinical indications:
- clinical or sub-clinical TOD such as CVD
- Chronic kidney disease
- age: over 75
- estimated 10-year global cardiovascular risk > 15%
- diabetes mellitus
moderate to high risk patients
multiple CVD risk FACTORS and 10 year global risk greater than 15%
low risk
no TOD or cardiovascular risk factors
BP threshold for initiation of antihypertensive therapy for a high risk patient ?
greater than 130 SBP (same as if diabetic)
- want to aim for a treatment target of <120 for high risk and less than 130/80 for diabetic
BP threshold for initiation of antihypertensive therapy for a moderate to high risk patient?
greater than 140 or greater than 90 - aim to be less than 140 and 90
BP threshold for initiation of antihypertensive therapy for a low risk patient
greater than 160 or greater than 100 - aim to be less than 140 and 90
dietary things to consider for HPT
Mg, Na, K, Ca, alcohol, excess calories,
in adults over 55 what has been proven with weight and HPT
direct link excess weight and HPT–> 60% will develop in net 4 years
- caused from insulin res, overactive SNS (leptin activates), RAAS alterations
what does leptin have to do with excess weight and HPT
leptin activates SNS and an over active SNS may need to HPT
most potent no pharmacological approach
weight loss (5-15% loss has significant impact)
all overweight patients should aim for?
weight loss of 5kg to drop SBP to 4.4 and DBP to 3.6mmHG)
first line treatment ?
weight loss and PA and smoking cessation
B-blockers
makes weight loss more challenging ( bc reduce heart weight, (think they block SNS epinephrine on heart ), and may cause weight gain
what may affect salt responders/non-responders
age, severity of HPT, RAAS, potassium, genetics
average sodium intake vs recommended
3.5g vs limit to 2000 mg (less than 1 tsp of salt)
ideally 1500mg
potassium mechanism
surpress’s renin, naturens, vasodialation, reduce SNS
Na/K ATPase in the kidney vs in smooth muscle / everywhere else cells
on the basolateral side of the tubual cells, Na+ is retained and K+ is excreted (think of aldosterone effect), whereas in every where else ( tears are salty) and 3Na is excreted and 2K+ is into cells
excess Na and deficient K (LONG TERM) causes what in muscle cells, leading to impaired contraction and more peripheral resistance = increasing BP
excess Na INHIBITS the pump (normally, 3Na+ out and 2K+ in ), thus causing no Na out and more sodium retained in the cell. when this happens Na+/Ca+ transporter is activated. more Ca into cell! membrane voltage triggers! cause K+ to leave (depolarize), Ca+ triggers contraction! increase BP
amount of K+ should be more than
2300 mg
not recommended to supplement- only if diuretic induced hypokalemia
who is at risk of hypokalemia
RAAS inhibitors
other drugs
kidney disease
calcium and Mg intake in relation to BP
inverse to BP
want moe to lower BP
why calcium intake good to BP
more NA excretion, more sensitivity to NO, less vasoconstrictor production
alcohol on BP
immediate lowering but then increases it next 10-15 hours ( dose-dependent)
- limit to 2 drinks men, 1 women
