PharmacologyChapter 25

Drugs for HypertensionHypertension

Prehypertension Stage 1 Hypertension

Stage 2 HypertensionLong-term Consequences of

Untreated Hypertension

3 Factors Responsible for Creating High Blood Pressure

Cardiac Output

Peripheral Resistance Blood Volume

sustained systolic BP >140 mmHgor

diastolic BP >90-99 mmHg

140 to 159 mmHg/ 90-99 mmHg 120 to 139 mmHg/ 80-89 mmHg

Heart, Brain, Kidneys, Retina >160 mmHg/ >100 mmHg

Volume of blood pumped per minute

Determined by stroke volume (amt of blood pumped by contraction of ventricles) and

heart rate

SV * HR = CO

1. Cardiac Output2. Peripheral Resistance

3. Blood Volume

total amount of blood in the vascular systemfriction in the arteries as blood flows through

the vascular system

3 Factors Influencing Blood Pressure

4 Lifestyle Changes to Manage Hypertension

5 Primary Antihypertensive Agents

3 Secondary Antihypertensive Agents

Alpha 1 – Adrenergic Antagonists

Alpha 2 – Adrenergic Agonists

Direct-Acting Vasodilators ABC(D)’s of Hypertension

ACE Inhibitors Effect Beta-Blockers Effect

1. Personal habits – Diet/exercise2. Genetics

3. Environmental Factors4. Lose Weight

1. Central and autonomic nervous systems

2. Emotions3. Endocrine System

1. Alpha 1 – Adrenergic Antagonists2. Alpha 2 – Adrenergic Agonists3. Direct-Acting Vasodilators

1. Diuretics2. Angiotensin-Converting Enzyme

(ACE) Inhibitors3. Angiotensin II Receptor Blockers4. Beta-Adrenergic Antagonists5. Calcium Channel Blockers

decrease the outflow of sympathetic nerve impulses, thereby causing the vessels to dilate

block the sympathetic receptors in the arterioles, thereby causing the vessels to dilate

ACE InhibitorsBeta-BlockersCalcium Channel BlockersCardiac GlycosidesDiuretics

directly affect vascular smooth muscle, which lowers blood pressure

used for hypertensive crisis

prevent sympathetic stimulation of the heart, thereby reducing HR and contractility, and

decreases rate of AV conduction

In Short: Lowers heart rate

blocks the conversion of angiotensin I to angiotensin II

This causes vasodilation and decreases peripheral vascular resistance (PVR), which

leads to decreased BP

Also blocks aldosterone, leading to decrease in sodium and water retention

Calcium Channel Blockers Effect

Cardiac Glycosides Effect

Diuretics Effect Preload

AfterloadCalcium Channel Blocker

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Angiotensin-Converting Enzyme (ACE) Inhibitor

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Alpha Adrenergic Antagonist/Blocker

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Direct Vasodilator-prototype-

nifedipine (Procardia XL) Class

increases cardiac output by increasing the force of contraction. This causes the heart to

beat more forcefully, but slower

ACE inhibitors have replaced these

causes smooth muscle in arterioles to relax (dilate), thus decreasing BP

ability of the heart to stretch before entering the heart

lowers blood volume by acting on the kidney

First line medication for hypertension

nifedipine (Procardia XL)

refers to peripheral resistance

PVR increase afterload and increases workload of the heart

doxazosin (Cardura) enalapril (Vasotec)

Therapeutic: antihypertensive and angina treatment

Pharmacologic: Calcium Channel Blocker

hydralazine (Apresoline)

enalapril (Vasotec) Class doxazosin (Cardura) Class

hydrazaline (Apresoline) Classnifedipine (Procardia XL) MOA

and Use

enalapril (Vasotec) MOA and Use

doxazosin (Cardura) MOA and Use

hydrazaline (Apresoline) MOA and Use

nifedipine (Procardia XL) Adverse Effects

enalapril (Vasotec) Adverse Effects

doxazosin (Cardura) Adverse Effects

Therapeutic: drug for hypertension and BPH

Pharmacologic: Alpha 1 adrenergic blocker

Therapeutic: drug for hypertension and heart failure

Pharmacologic: ACE inhibitor

MOA: blocks calcium channels into myocardial and vascular smooth muscle,

including coronary arteriesThis results in less oxygen utilization by heart

and increase cardiac output -> fall in BP

Use: HTN and variant or vasospastic angina; occasionally for Raynauds and

cardiomyopathy

Therapeutic: drug for hypertension and heart failure

Pharmacologic: Direct Acting Vasodilator

MOA: Inhibits sympathetic activation in arterioles, causing vasodilation

Leads to fall in BP and relaxation of smooth muscle around prostate gland

Use: hypertension, BPH

MOST FREQUENTLY PRESCRIBED ACE INHIBITOR FOR HTN

MOA: reduces angiotensin II and aldosterone levels to produce a significant reduction in

blood pressure

Use: hypertension and heart failure

H/A, dizziness, peripheral edema, flushing

Tachycardia

MOA: direct vasodilation of arterial smooth muscle, no effect on veins

Use: hypertension and heart failure

dizziness, dyspnea, asthenia, H/A, hypotension, orthostatic hypotension,

somnolence

hyperkalemia, orthostatic hypotension, H/A, dizziness

Life threatening: angioedema, neutropenia, agranulocytosis

hydralazine (Apresoline) Adverse Effects

H/A, reflex tachycardia, palpitations, hypotension, flushing, N/D

Usually pts also receive a beta-adrenergic blocker to counteract reflex tachycardia

sodium and fluid retention