Drugs for Hypertension

5L/min

Average CO

Stroke volume

amount of blood pumped per beat

Cardiac preload

pressure in the right side of the heart as blood returns to the heart (direct relationship with stroke volume)

Cardiac afterload

The pressure the heart must pump against to eject blood

The greater the stretch of the ventricles, the greater the contractile force

Sterling’s law of the heart

BP=(HRxSV) x PVR (or) vol

Blood pressure equation

1. heart rate

2. force of contraction

3. blood volume

4. venous return

Cardiac output is determined by [4]

1. viscosity

2. length of the vessel

3. vessel diameter

PVR is determined by: [3]

Pressure within the aterial system when the left ventricle contracts, blood flows into the aorta

Systolic BP

Pressure in the arterial system when the ventricle relaxes and fills

Diastolic BP

1. autonomic nervous system (seconds-minutes)

2. renin-angiotensin system (hours)

3. kideys (days to weeks)

Arterial pressure is regulated by [3]

Rapid or steady state control. It is a rapid response

How does the ANS control BP?

Causes vasoconstriction in arteries and veins and retains water in the kidneys

How does the RAAS help regulate BP? [2]

1. genetics

2. obesity

3. diabetes

4. diet

5. stress

6. atherosclerosis

7. renal artery stenosis

Causes of hypertension [7]

systolic over 140mmHg

Diastolic over 90 mmHg

Hypertension is classified as

when two or more diastolic BP measurements on subsequent visits 1 week apart are greater than 90 or greaeter than 140 systolic

when is hypertension dianosed?

130/80

“normal” BP in people iwth diabetes or renal failure

BP less than 140/90

Goal for hypertension treatment

1. decrease saturated fats

2. stop smoking

3. limit alcohol 1-2 oz/day

4. increase exercise to increase HDL

5. manage diabetes

Lifestyle changes to reduc atherosclerosis [5]

1. stop smoking

2. decrease caffeine

3. decrease stress

4. increase exercise and improve endurance

5. decrease weight

Lifestyle modifications to reduce sympathetic nervous system stimulation [5]

Decrease dietary sodium to 800-2000mg.day

lifestyle change to reduce circulating volume:

INcrease fruits and veg, low fat products

DASH diet:

Reduction of blood volume associated with decreased cardiac output.

reduction of arterial resistance

Action of thiazide diuretics

1. hypokalemia

2. dehydration

3. hyperglycemia

4. hyperuricemia

Adverse effects of thiazide diuretics [4]

peeing out potassium

Why are patients on thiazide diuretics at risk of hypokalemia?

suppresses the influence of sympathetic nervous system on heart, blood vessels, and other structures

Action of sympatholytics-andrenergics:

1. binds to receptors on cardiac, bronchial, and skeletal muscle

2. blocks activation (antagonist) of beta-1 receptors by catecholamines

3. blocks beta receptors in the kidneys to decrease renin

4. decrease heart rate and force of contraction

5. decrease impulse conduction at AV node

Beta blocker MOA

Respiratory conditions (asthma, COPD) because of affinity for beta 2 receptors (can block beta-2 in the lungs, causing bronchoconstriction)

Beta blockers should be used with caution in which patients?

2. reduced heart rate

3. reduced FOC

4. reduced velocity of impulse conducion

5. decreased BP secondary to decreased cardiac output

6. treats angina

7. treats MI

8. decrease incidence of sudden death

Beta blocker therapeutic effects: [6]

reduce oxygen demand

How can beta blockers treat angina?

Decrease infarct size

How do beta blocker treat myocardial infarction?

vasodilation can help relieve symptoms

How do beta blockers treat migraines

Lowers heart rate, especially during a thyroid storm. Catecholamines lead to increase in thyroid hormone, beta blockers can als decrease thyroid hormone a little.

How can beta blockers by used to treat symptoms of hyperthyroidism?

Vasodilation to eye vessels, decrease IOP

how can beta blockers treat glaucoma?

Propranolol [Inderal]

Nonselective beta blocker prototype

Non selectively blocks beta1 and beta2 receptors. Has the same affinity for beta 1 and 2.

Propranolol MOA

Metoprolol [Lopressor]

Selective beta blocker prototype

Selectively binds to beta-1 receptors. has a higher affinity for beta 1, not saying it NEVER binds to beta-2 (cardioselective).

Sows depolarization, decreases HR and contractility. Decreases CO and decreases BP and oxygen consumption

Metoprolol [Lopressor] MOA

1. decrease glycogenolysis [diabetes]

2. crosses blood brain barrier so CNS stimulation (insomnia and anxiety)

3. bradycardia

4. hypotension

5. has major hepatic first pass effect (50%)

Metoprolol side effects [5]

yup.

Can patients with renal failure take metoprolol?

1. monitor BP

2. watch for S+S of CHF

3. Compliance

nursing considerations for patients on metoprolol [3]

the higher dose, the greater the effect

relative dosing of metoprolol

it decreases the force of contraction, might lead to fluid overload

How can metoprolol lead to congestive heart failure?

dysrhythmias

main use for propranolol

1. hypotension

2. bronchospasm (asthma)

Propranolol side effects [2]

Brady cardia as a side effect (they would already have low HR from electrical condution in the heart at SA and AV node)

why are beta blockers not used in patients with 2nd or 3rd degree heart block?

Can mask the signs of hypoglycemia

why should patients with diabetes use beta blockers with caution?

rebound cardiac excitation (really high tacycardia) with abrupt withdrawal

why is compliance with beta blockers so important?

Nifedipine

Dihydropyridine calcium channel blocker prototype

Verapamil

diltiazem

Non-dihydropyridine calcium channel blocker prototypes [2]

Dihydropyridines

Calcium channel blockers that act mainly on the blood vessels and can lead to reflex tachycardia

Reflex tachycardia

When a medication widens blood vessels. The body detects that they are widened and blood rpessure goes down. Low BP is a stressor and the HPA axis is activated, leading to increased HR and BP

Non-dihydropyridines

Calcium channel blocker group that affects the heart AND blood vessels.

1. Less calcium influx to cells leading to low intracellular calcium

2. reduced action of kinases

3. decreased actin-myosin cross bridging in smooth muscle,

4. can act on heart: (decreased FOC and SV, and Decreased depolarization at SA node so Decreased HR) to decrease BP

5. Blood vessels: leads to vasodilation (Decreased BP)

Calcium channel blocker MOA:

1. binds to calcium ion channels

2. decreased vascular smooth muscle tone leading to

3. vasodilation and

4. decreased PVR

5. to decrease BP because

6. Decreased afterload

7. acts in the myocardium to decrease FOC to

8. decrease BP

9. decreases firing rate at SA and AV node to

10. Decrease HR

Diltiazem MOA

1. hypertension

2. angina pectoris

3. cardiac dysrhythmia

uses for diltiazem [3]

1. flushing

2. headache

3. edema at ankles and feet

4. less constipation (still constipation tho)

Side effects of diltiazem [4]

Digoxin is going to decrease HR too, monitor for bradycardia

digoxin and diltiazem interaction

short half life (3-6 hours) so requires TID dosing

effects begin within minutes, peaks at an hour

diltiazem dosing:

grapefruit juice inhibits metabolism, increases levels

diltiazem and grapefruit juice

1. signs of heart failure and peripheral edema

2. assess BP

3. treat constipation (fluids and laxaties)

4. orthostatic hypotension (don’t get up too fast)

important nursing considerations for calcium channel blockers: [4]

1. HTN

2. Angina pectoria

uses for Nifedipine [2]

Blocks Calcium ion channels on blood vessels, lowers BP by vasodilation

increase HR

Nifedipine action

1. flushing

2. headache

3. dizziness

4. peripheral edema

5. gingival hyperplasia

6. reflex tachycardia

Side effects of Nifedipine

to decrease HR and prevent reflex tachycardia

why might nifedipie by combined with a beta blocker