Transcript Alterations in Cardiovascular Function:

Anti -hypertensive Agents
Wanda Lovitz, APRN
Objectives Anti-Hypertensives Agents
Objectives:
For the antihypertensive agents presented:
Identify the:
1.
2.
3.
4.
5.
Classification
MOA
Indications
Common and serious adverse reactions
Nursing implications
Hypertension Facts
Hypertension affects 1 in 3 Americans
Hypertension is the #1
reason for office visits
RCT show that treating HTN can reduce:
Stroke by 40%
Cardiovascular death by 20%
Heart failure by 50%
American College of Cardiology 1996
HYPERTENSION is a major risk factor for
cardiovascular disease
TheProblem?
Cardiovascular Disease can be Deadly!
• MI (Myocardial infarction)
• Stroke
• Vascular Diseases
• DEATH!
Blood Pressure = Cardiac
Cardiac Factors
• Heart
•
•
Rate
Contractibility
Beta-blockers
• Calcium
channel blockers
• Centrally acting
adrenergics/sympatholytics
Output X PVR
Circulating
Volume
Salt (sodium)
• Aldosterone
•
• ACE
•
inhibitors
Diuretics
Drugs that reduce HR, improve cardiac contractility
or reduce blood volume, will lower BP
Blood Pressure = CO x Peripheral Vascular Resistance
Hormones
Peripheral sympathetic receptors
Drugs
• ACE inhibitors*
• Calcium channel
Drugs
Receptors
Alpha
blockers*
• Angiotensin II blockers
CNS
Beta
Drug Group
Local
Drugs
*Centrally
acting
Peripherally acting
adrenergics/
adrenergics/
sympatholytics
sympatholytics
• BetaDrug Group
blockers*
• Alpha
1blockers
Peripheral Vascular Resistance (PVR) is increased by arteriolar constriction.
So, drugs that promote VASODILATION will decrease PVR and thus decrease BP
*Red = Drugs that alter BOTH CO and PVR
Category
Classification of BP in
AdultsSBP (mmHg)
Normal
DBP (mmHg)
< 120
and < 80
120-139
or 80-89
HTN, stage 1
140-159
or 90-99
HTN, stage 2
> 160
or > 100
Prehypertension
JNC 8 Recommendations (cont)
Regulators of Blood Pressure
1. Sympathetic Nervous System
When the B/P is LOW baroreceptors
in the brain are stimulated which then:
 1. activate beta receptors (B1) in the
heart and
 2. activate vascular alpha 1 receptors in
the vasculature, resulting in
VASOCONSTRICTION
• 2. Renin-angiotensinaldosterone system
(RAAS)
• Can elevate BP when it
is too low
• 3. Kidney
• With low B/P, the GFR falls too,
promoting retention of NA,CL
and water to raise the blood
volume
Diuretics
Thiazide
hydrochlorothiazide/
HCTZ
triamterene/
Dyrenium
Loop
furosemide/
Lasix
PotassiumSparing
spironalactone
Aldactone
triameterene/
Dryenium
Vasodilator/
CENTRALLY acting
sympatholytics
Vasodilator/Periph
erally acting
Sympatholytic
methyldopa/
metoprolol/
Aldomet
Lopressor
indirect alpha 2 agonist
(converted in the brainstem)
alpha2 agonist
Beta-Blockers
“olol”
Vasodilator/Periph
erally acting
Symphatholytic/Al
pha Adrenergic
Blocker
RAAS suppressor ACEI
“prils”
doxasin/
Cardura
captropril/
cozaar/
Cardizem/
Capoten
Losartan
Diltiazem
RAAS
suppressor
CCBs
“pines”
ARBs
amlodipine/
Norvasc
clonidine/
Catapress
Indications for the various
anti-hypertensive agents
from JNC 8 Guidelines
Antihypertensives: Diuretics
Diuretic Agents –
1. Increase urinary output
decreasing CO
2. Decrease Circulating Volume
decreasing CO
3. Decrease arterial resistance
decreasing PVR
Classes of Diuretics
Diuresis = “to urinate thoroughly”
•Potassium-sparing = Mild diuresis
•Thiazide and thiazide-like diuretics =
Mild diuresis
•Loop = Moderate to PROFOUND diuresis
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Diuretics
All of the diuretics lower BP by decreasing
CARDIAC OUTPUT
Can ENHANCE the effect of other anti-hypertensive
SOME diuretics also decrease PVR by DILATING
arterioles
This class (diuretics) is the LEAST expensive of all
the anti-hypertensives
Thiazides Diuretics
Prototype Drug
hydrochlorothiazide (HydroDiuril, HCTZ)
MOA
↑ both Na & H2O excretion by the kidneys (less volume = less CO)
WATER FOLLOWS SODIUM
Dilation of arterioles (the
only diuretic to widen the arteries = VASODILATION EFFECT)
Indications/Therapeutic Use
1st line management of mild HTN unrelated to RAAS problems
ENHANCES the effect of other antihypertensive agents
Recommended as 1st line agent
Thiazide Diuretics: Side Effects
•SE: related to the interference with the nephron’s normal
regulatory mechanisms
• Most common: HYPOKALEMIA (low K+)
• Nursing action: monitor serum potassium levels
• Potassium supplements may be given
• Nursing action: encourage foods rich in potassium
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Loop Diuretics
MOA
 Inhibits the kidneys ability to REABSORB SODIUM
 Blocks the reabsorption of sodium in the ascending loop of Henle
 Makes the kidneys put more sodium in the urine
 water follows sodium and more urine is excreted
Causes a decrease in fluid in the blood vessels
so …. (CO)
 Can cause PROFOUND DIURESIS!
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Therapeutic uses for Loop
Diuretics
• Indications
• Acute CHF and pulmonary edema
• Edema associated with renal or liver disease
• HYPERTENSION
Loop Diuretics
• Prototype: furosemide (Lasix):
•
- Most commonly used
•
- More diuretic effect than the thiazides
• PO and Parenteral (IV/IM)
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Side Effects: Loop Diuretics
Common SE:
•Important Nursing
LOW K+
(hypokalemia)
•Monitor K levels closely
Dehydration &
hypotension
Assessment
•Most patients will be
receiving supplements of K
WITH their Lasix dose
•Usually po KCL used to
PREVENT hypokalemia
•May see IV to TREAT
hypokalemia
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Potassium Sparing Diuretic
•spironolactone
Aldactone & triamterene /Dyrenium
•MOA:
• Potassium-sparing diuretics are used to reduce the amount of water in the body
•
•BLOCKS the action of ALDOSTERONE – so, increases sodium excretion while
decreasing potassium excretion
•Unlike the other diuretic medicines, these medicines DO NOT cause the body to
lose potassium –
•Used with thiazides and loop diuretics in the therapy of hypertension
•Helps to counteract potassium loss by thiazide and loop diuretics
spironlactone/Aldactone
a Potassium-sparing diuretic
•Aldactone provides only SMALL degree of diuresis
•Only MODEST hypotensive effect
•Most significant SE = HYPERKALEMIA
Sympatholytics
Sympathetic DEPRESSANTS/SNS Blockers/Anti-adrenergic Agents
These drugs decrease BP by decreasing
*
PVR
 Important Principle
Sympathetic NS VASOCONSTRICTS!
Vasoconstriction = ↑ PVR   BP!
So it you DEPRESS or BLOCK the SNS
....you BP
Key Terms to KNOW
 Adrenergic – SNS stimulated; “Fight or Flight”
Response predominates =VASOCONSTRICTION
 Cholinergic – PSNS stimulated; “Rest and Digest”
Response predominates =VASODILATION
•Therefore…
Therefore…….
Anti-adrenergic or Adrengeric Blocking agents
(symphatolytics or SNS blockers) inhibit or work against SNS activity 
decrease in BP and HR (GOOD!)

 Anti-cholinergic agents inhibit or work against PSNS
anti-cholinergic activity  increase in BP and HR
NOT GOOD if you have hypertension!
Many drugs for cold/flu (OTC) have anti-cholinergic
Should be AVOIDED by patients with HTN
Sympatholytic Drug Classes
1. Beta-adrenergic blockers
aka “beta blockers”
2. Centrally acting alpha2 agonists
3. Alpha-adrenergic blockers
Beta Adrenergic Blockers
•Prototype
•metoprolol (Lopressor)
•beta blockers are all drugs
that end in ‘olol’
MOST COMMON SIDE
EFFECTS
•depression & sedation
•bronchoconstriction
•can exacerbate resp problems in pts
with COPD (bronchoconstriction)
MOA
Blocks
stimulation of
1
beta (myocardial) receptors
Reduces HR and
contractility
Indications/Therapeutic
Uses
Anti-hypertensive
Anti-anginal
Nursing Implications with the beta blockers
 Important to remember that ALL of the beta-blockers
REDUCE HEART RATE as well as blood pressure!
The beta-blockers have a wide variety of
indications/therapeutic uses:
Anti-hypertensive, anti-anginal
 Anti-dysrhythmic
NURSING ALERT
• With ALL beta-blockers (drugs that end in ‘olol’)
• Recognize that these drugs will decrease HR and B/P- no matter WHY
the patient is receiving them
• NURSE JUDGEMNT – HOLD med if HR is less than 60
or B/P is less than 100 systolic
• Know WHY your patient is on a beta-blocker
• for his HTN?
• for his Heart - antiarrhythmic, antianginal?
Centrally Acting Alpha 2 Agonists
Prototype
methyldopa (Aldomet)
MOA:
Stimulates CNS by ACTIVATING inhibitory alpha-adrenergic receptors within the brain
activation of these central alpha receptors produces:
  sympathetic outflow and cause VASODILATION
 PVR
DRUG EFFECTS
 BP & peripheral resistance
 Mild  in HR
Dry mouth
Centrally Acting Alpha 2 Agonists
Methyldopa/ Aldomet
Side Effects
Most frequent: SEDATION & Sexual dysfunction
Serious: hepatic necrosis & hemolytic anemia
Interactions: many drug/drug interactions
Contraindications: active liver disease
Nursing Implications: Centrally Acting Alpha 2 Agonists
•methyldopa/Aldomet
•INITIALLY : Montior BP and HR frequently
• Monitor
temp
“Drug fever” possibly accompanied by
encephalopathy and hepatic function changes
•Teaching
•Do not stop taking suddenly!
• REBOUND HYPERTENSION/HYPERTENSIVE CRISIS
Centrally Acting Alpha 2 Agonist
Clonidine/Catapress
CENTRALLY acting
alpha 2 agonist agent
INDICATION:
Hypertension
SE: : Essentially safe
Drowsiness
Bradycardia and decrease in
Xerostomia (dry mouth)
Rare instances of rebound
hypertension if this drug is
abruptly stopped
•MOA: alpha-adrenergic agonist
•Causes SELECTIVE
ACTIVATION alpha2 receptors
in the CNS
• Decreases sympathetic
outflow to the blood vessels and
heart resulting in VASODILATION
thus decreasing PVR and B/P
•Route: oral or transdermal patch
Alpha Adrenergic Blockers
• doxazosin/Cardura
• MOA: Block CATECHOLAMINES to decrease heart rate and relax
blood vessels
• Decreases CO and PVR
• Indication:
• Hypertension
• BPH (benign prostate hypertrophy) – these drugs relax blood vessels throughout
the body
• Side Effects: Dizziness, Postural hypotension
Calcium Channel Blockers
• These drugs prevent CALCIUM ions from entering muscle cells
• Affect the muscle cells in the heart and around the blood vessels
• Also known as calcium antagonists
• IN THE VASCULAR SMOOTH MUSCLE, CALCIUM
CHANNELS REGULATE CONTRACTION
• If calcium channels are blocked , contraction is prevented, thus
• decreasing the force and rate of myocardial contraction
• relaxes the muscles around the arteries resulting in VASODILATION
•
• CCBs act selectively on peripheral arterioles and arteries
and arterioles of the heart
Calcium Channel Blockers =
“pines”
amlodoPINE/Norvasc
nifedipine/Procardia
nicardipine/Cardene
Plus:
 diltaziem/ Cardizem
VaVasodilator: CCBs
•Know WHY your patient is receiving a CCB
•Antihypertensive effect?
•Anti-anginal?
•Anti-dysrhythmic?
•Major Nursing Considerations:
• Take BP & HR prior to administration
•
•Monitor weights and I & O 
•CCBs can cause FLUID RETENTION
•Note: Serum calcium levels are NOT affected by the CCBs
Blood Pressure = CO x Peripheral Vascular Resistance
Hormones
Drug Groups
• ACE inhibitors*
• Calcium channel
blockers*
• Angiotensin II
Peripheral sympathetic
receptors
Drugs
Receptors
Alpha
Beta
Drug Group
blockers
Drug Group
CNS
Centrally
acting
adrenergics
*
• Beta-blockers*
• Alpha 1-blockers
*
Drugs that alter both CO and PVR
Local
Drugs
Peripherally
acting
adrenergics
• RAAS activated when:
 Loss of blood volume
 Drop in BP
• Decreased renal perfusion  release of renin  conversion of
angiotensinogen to angiotensin I  converted to angiotensin II by
angiotensin-converting enzyme (ACE)
ACEI & ARBs
RAAS Suppressants
ACEI (angiotension converting enzymes INHIBITORS)
ARBs (angiotension RECEPTOR BLOCKERS)
MOA: These drugs basically lower BP by
→DECREASING
peripheral vascular RESISTANCE (PVR)
less pressure in the pipes or vessels less “stiff”
•Also DECREASES circulating VOLUME (CO) by inhibiting
aldosterone reabsorption
Review of Angiotension actions
1. Vasoconstriction
2. Release of ALDOSTERONE
3. Alteration of cardiac and vascular structure
• HYPERTROPHY
• REMODELING
ACEIs: VASODILATE to decrease CO
MOA:
•BLOCKS angiotension converting enzyme (ACE) from converting
angiotensin I to angiotensin II
•Angiotensin I is a weak vasoconstrictor
•Antiotensin II is a very powerful vasoconstrictor
•Also, angiotension stimulates release of aldosterone and
ADH resulting in increase blood volume (CO)
So...if we block angiotenisin II = CO
ACE “inhibitors” decrease BP by BOTH vasodilating and decreasing volume
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Angiotensin-Converting Enzyme Inhibitor (ACEI)
RAAS Suppressant
Prototype
 captopril (Capoten)
 One of the most widely prescribed classes of anti-hypertensives
MOA
 Blocks conversion of angiotensin I to vasoconstricting angiotensin II
 Directly
decreases the amount of antiotension II
 result is a decrease in systemic vasoconstriction and
 Result is VASODILATION
→
Causing decreased BP by decreasing PVR
Nursing Implications:
ACEI/RASS Suppresssant: captopril/Capoten
Initial dosing
•Monitor for significant BP drop 1-3 hours following first dose!
•First dose hypotension  VASODILATION EFFECT
•May require volume expansion
•Stop diuretic therapy 1 week prior to initiating therapy
•Monitor BP & HR closely during initial dose adjustment period!
•Long term
•Periodic monitoring of: BUN/creatinine, serum K+ levels
•Teaching
•Similar to beta blockers
SE: ACE Inhibitors
•SE: Related to the effects of vasodilation & alterations in
blood flow
• headache; GI irritation; RENAL INSUFFICIENCY (transient increases in
creatinine & BUN levels); dry, nonproductive, PERSISTENT COUGH;
angioedema; & fatigue
•Commonly Rx ACEI: captopril/Capoten;
Lisinopril, Zesteril , & enalapril (Vasotec)
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RAAS Suppressant/Angiotensin RECEPTOR BLOCKER
(ARBs)
MOA
•Blocks the action of angiotension II from the RECEPTOR SITES
on the blood vessels
•Effectively decreases the action of angiotensin II
•Result is vasodilation
•Also blocks aldosterone and ADH release
•Examples: cozaar/
Losartan
ACTION OF ARBS
SE: Angiotensin Receptor Blocking (ARBs)
Side/Adverse Effects
Well tolerated
Possible
Angioedema
Renal failure
Fetal harm
Nursing Implications
See ACE Inhibitor (captopril)
DOES NOT ACTIVATE IN LUNGS THEREFORE NO COUGH!
Not 1st line therapy
Often replaces ACEI Rx
Cultural Considerations
for Drug Therapy – African Americans
Most responsive to single-drug therapy (as opposed to
combination drug regimens)
More responsive to diuretics, calcium channel blockers &
alpha-adrenergic blockers
Less responsive to ACE inhibitors & beta-blockers
Screening very important because of increased incidence &
to detect early in order to prevent end-target-organ damage
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The End