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Flashcards in 2cardiovascular HTN Deck (24):
1

What are some risk factors of HTN?

-Increasing age
>50yrs SBP and Pulse Pressure* are better predictors of complications than DBP
-Physical inactivity
-Excessive alcohol consumption
-Smoking
-DM
-Ethnicity

2

What is the goal of treating HTN?

reduce associated morbidity and mortality from CV events

3

Current clinical guidelines

Goal BP Values Most patients, including diabetes and/or CKD and the elderly:
less than 140/90 mm Hg

Frail elderly or high risk:
less than 150/90 mm Hg

*2017 ACC/AHA: <130/80 new goal
Normal: <120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;

4

Hypertensive crisis

Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage.

5

Mean Arterial Pressure (MAP)

During a cardiac cycle, two thirds of the time is spent in diastole and one third in systole.
MAP is calculated by using the following equation:
MAP=(SBPx1/3)+(DBPx2/3)

*MAP should not be below 60

6

What is the major determinant of SBP?

Cardiac output

7

What determines DBP?

Total peripheral resistance(TPR)

8

Cardiac output equations?

CO = HR x SV
BP = CO x TPR
BP = HR x SV x TPR

9

What are the two main causes of elevated BP?

Elevated BP can result from increased cardiac output and/or increased total peripheral resistance.

10

Increased cardiac output

-Increased cardiac preload:
Increased fluid volume from excess sodium intake or renal sodium retention (from reduced number of nephrons or decreased glomerular filtration)
-Venous constriction:
Excess stimulation of the renin–angiotensin–aldosterone system (RAAS)
Sympathetic nervous system over activity

11

Increased peripheral resistance

-Functional vascular constriction:
Excess stimulation of the RAAS
Sympathetic nervous system overactivity
Genetic alterations of cell membranes
Endothelial-derived factors
-Structural vascular hypertrophy:
Excess stimulation of the RAAS
Sympathetic nervous system overactivity
Genetic alterations of cell membranes
Endothelial-derived factors
Hyperinsulinemia resulting from the metabolic syndrome

12

What are the Antihypertensive groups?

1. RAAS
Angiotensin Converting Enzyme Inhibitors
Angiotensin II Receptor Blockers
2. Sympathetic Antagonists/Agonists
β Blockers (Beta blockers)
α1 Blockers (Alpha 1 Blockers)
Central α2 agonists (Alpha 2 Agonists)
3. Calcium Channel Blockers
4. Diuretics (thiazide)
5. Aldosterone antagonists
6. Direct vasodilators

13

Agents that block production or action of angiotensin

Reduce peripheral vascular resistance and (potentially) blood volume

14

Sympatholytic (sympathoplegic) agents

Lower blood pressure by reducing peripheral vascular resistance by inhibiting cardiac function increasing venous pooling in capacitance vessels.
The latter two effects reduce cardiac output

15

Calcium channel blockers

Inhibits calcium influx leading to coronary and peripheral vasodilation

16

Diuretics

lower blood pressure by depleting the body of sodium and reducing blood volume and perhaps by other mechanisms.

17

Aldosterone antagonists

Inhibits aldosterone resulting in inhibition of sodium and water retention and inhibiting vasoconstriction

18

Direct vasodilators

Reduce pressure by relaxing vascular smooth muscle thus dilating resistance vessels and increasing capacitance to varying degrees

19

RAAS sites of action of antihypertensive drugs

slide 17

20

Site of action of diuretics:Proximal Convoluted Tubule (PCT)

-Major site for sodium chloride and sodium bicarbonate reabsorption.
-Responsible for 60–70% of the total reabsorption of sodium.

21

Acetazolamide

Carbonic anhydrase inhibitor
Clinical app: Glaucoma, mountain sickness
PK: Diuresis is self-limiting effects in glaucoma and mountain sickness persist
Possible metabolic acidosis
ex: Dorzolamide, brinzolamide: topical carbonic anhydrase inhibitors for glaucoma only

22

Diuretics types and prototypes

Loop: Furosemide(Lasik)

Thiazide: Chlorthalidone, (better in the distal), Hydrochlorothiazide(HCTZ)

Potassium sparing: Amiloride(w/wo HCTZ), Triamterene

Aldosterone antagonists: Spironolactone w/wo HCTZ

23

What is the overall mechanism of diuretics?

-Blocks the reabsorption of sodium and chloride
-Water follows due to the osmotic pressure within the nephron created by the ions
-Diuresis results in decreased plasma and stroke volume
-Site of action varies along the nephron

24

Thick ascending limb of the loop of henle (TAL)

-pumps sodium, potassium, and chloride out
-a major site of calcium and magnesium re-absorption
**responsible for the re-absorption of 20-30% of sodium