Hypertension 1 Flashcards
Major forms of cardiovascular disease
Leading causes of death in Canada
Hypertension cost/burden
Hypertension, atherosclerosis, ischemic heart disease, peripheral vascular disease and heart failure
Cancer, diseases of the heart and much less cerebrovascular diseases
Rising trends of hypertension esp in men (many not aware)
Top reason to visit a physician and take medication and antihypertensives are one of the most expensive drugs
What is MAP (equation) and how to calculate its components
General regulators of MAP
Mean Arterial Pressure = CO x peripheral resistance
CO = stroke volume x heart rate = blood pumped out of left ventricle
peripheral resistance = (length of vessel x viscosity of blood)/(r^4)
Vasoconstriction ↑ r, vasodilation ↓ r
Regulators: sympathetic NS, RAAS, renal function and related hormones (epinephrine, vasopressin and angiotensin II)
Elements which influence heart rate and stroke volume
Venous return?
Arteriolar radius and Blood viscosity?
Extrinsic vasoconstriction?
HR: Symp/epinephrine + Parasymp
Stroke volume: Symp/epinephrine + venous return
Venous return: blood volume (Na/H2O), respiratory and skeletal muscle activity, cardiac suction effect
Arteriolar radius: local control, extrinsic vasoconstriction
Blood viscosity: # RBC
Extrinsic vasoconstriction: symp/epinephrine and vasopressin/angiotensin II
RAAS summary: stimulus, organs which produce enzymes, downstream effects
Stimulus: ↓ NaCl/ECF volume or arterial pressure
Liver produces angiotensin
Kidney produces renin
Lungs produce angiotensin-converting enzyme (ACE)
Adrenal cortex produces aldosterone
Angiotensin (renin)–> I (ACE) –> II
Angiotensin II: 1) stimulates vasopressin, 2) thirst, 3) arteriolar vasoconstriction and 4) adrenal stimulation –> aldosterone release –> stim kidney ↑ Na reabsorption (Cl- passive)
- Vasopressin ↑ H2O re-uptake
- Thirst ↑ fluid intake
Causes of HTN
Primary/essential/idiopathic (95%)
- unknown etiology
- environment/genetic interaction
- influenced by diet and behavior
Secondary (5%)
- secondary to another condition (renal, endocrine, neuro)
Both typically are asymptomatic (silent killer)
Modifiable and non-modifiable risk factors of HTN and some mechanisms involved
Modifiable: smoking, sedentary, abdominal obesity, IR, Na intake, diet quality and stress
- Smoking interferes with NO impairing vasodilation
- Excess vasopressin/AngII due to dietary/genetic/kidney/heart disease factors
Non-modifiable: Age> 60 years, men, postmenopausal women, ethnicity, FHx CVD of women <65 yo or men <55 yo
- Renal disease reduces blood flow and ↑ AngII and ↓ blood volume
- Adrenal disorders ↑ E/NE –> vasoconstriction
Target organ damage in associated clinical conditions (ACC)
Increased stress/pressure on vascularization associated with other diseases and can worsen them:
CVD: coronary artery disease, angina, prior MI, left ventricular hypertrophy/dysfunction or heart failure
Cerebrovascular disease: stroke, TIA, hemorrhage and dementia
Retinopathy
Peripheral artery disease
Neuropathy: albuminuria and CKD
How to measure BP
Using a sphygmomanometer in mm Hg
Oscillometric automated office BP (electronic, preferred)
Auscultatory non-automated office BP (mercury, non-automated)
Ambulatory BP measurements to track situations in which BP rises
Basics of the HTN diagnostic algorithm for adults
Suspected elevated BP –> mean office BP
≥ 180/110 –> immediate HTN diagnosis
Diabetes requires 3 day BP measurement, if ≥ 130/80 –> HTN diagnosis
OR general ≥ 135/85 requires more investigation to rule out white coat hypertension (WCH)
High risk HTN individuals and BP threshold for treatment
Moderate risk and BP threshold for treatment
High risk: ≥ 50y + SBP 130-180 mm Hg + CVD/CKD/≥75y/≥15% 10 year CVD risk FRS
- Threshold ≥ 130/NA
- DIabetes threshold ≥ 130/80
Moderate risk: many CVD risk factors + 10-14% CVD FRS score
- Threshold ≥ 140/90
Low risk threshold ≥ 160/100
Components of HTN Therapy Plan
HTN drug categories
Dietary factors of interest in HTN therapy
Goals: ↓ risk of CVD + renal disease and ↓ BP
Includes: PA, weight ↓, nutrition therapy, ↓ alcohol/stress/smoking, pharmacological therapies
HTN Drug categories: loop diuretics, thiazides, carbonic anhydrase inhibitors and K-sparing diuretics
Dietary factors: high kcal/excess weight, Na, K, Ca, Mg and alcohol
Links between obesity and HTN
Weight loss for HTN
In adults <55y direct link between obesity and HTN (esp abdominal obesity)
Causes of HTN associated w/ obesity: IR, overactive sympathetic NS, RAAS alterations, leptin increase with sympathetic activity (effects preserved unlike satiety effects), lowered natriuresis
Weight loss: potent approach for treatment and prevention, ↓ 5-20 mm Hg per 10 kg lost
Note: β-blockers can make weight loss difficult
Na and HTN study results
Responders/non-responders and salt sensitivity
CDRR/UL = 2300mg/d >14y (most exceed)
- 2000 mg/d Na (5g salt) for BP ↓
INTERSALT: for every 100 mmol Na/d –> ↑ in 3-6/0-3 mm Hg SBP/DBP
- increases risk of complications in HTN patients
Modest ↓ in Na –> significant reduction in BP, independent of changing other dietary factors but BP ↓ with DASH diet even w/o changing Na
Na excretion a good indicator of consumption
Non-responders’ BP don’t ↓ with Na ↓ (AKA salt sensitivity)
- genetic, age, HTN severity, restriction intensity, low RAAS renin, high NE
- ↑ K –> ↓ Na sensitivity (reduces negative affects of Na)
Highest sources of Na
Tiers of Na reduction
1/2 tsp = 1150 mg Na
80% processed foods, 10% table salt, 10% naturally occurring in foods
3000: eliminate high Na foods/bev, 1/4 tsp added salt
2000 mg: Eliminate processed/prepared foods, limit milk 2 cups/d and no added salt
1000 mg: All plus omit canned, frozen, deli, cheese, margarine
