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Cardiovascular Drugs:

Why We Use What We Use

Carol Jacobson RN, MN


www.cardionursing.com

The job of the


cardiovascular system
is to supply every cell in
the body with enough
O2 and nutrients to
function appropriately.
In order for the CV
system to do its job,
these 4 things have to
be working right:
Heart
Arteries
Veins
Volume

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Determinants of Cardiac Output

CO = HR x SV
Preload

Afterload

Contractility

Venous tone Body Position Intrathoracic


pressure

Blood Volume

Distribution of
blood volume

Atrial Kick

Intrapericardial
pressure

LV Function

PRELOAD

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Conditions That Alter Preload


Hypovolemia

Hemorrhage
Dehydration
Burns
Overdiuresis
Third Spacing

Hypervolemia
Overhydration
CHF
Renal disease

Altered Size of
Vascular Space
Sepsis
Spinal or epidural
anesthesia
Anaphylaxis
Venous dilating drugs
NTG
ACEI, ARBs
Nesiritide

Sympathetic NS
Arteriolar Tone

SVR

Aortic Pressure
& Compliance

Aortic Stenosis
HOCM

AFTERLOAD

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Conditions That Alter Afterload


Vasodilation

Vasoconstriction

Sepsis
Spinal or epidural
anesthesia
Anaphylaxis
Arterial dilating drugs

Nipride
ACEI, ARBs
Nesiritide
Milrinone
Ca++ channel blockers
Antihypertensives

SNS Adrenals

Ventricular
Muscle Mass

Catecholamines

Hypertension
Compensatory
vasoconstriction
Drugs

Neosynephrine
Phenylephrine
Levophed
High-dose dopamine
Epinephrine
Vasopressin

H+ CO2 O2

Metabolic
State

Drugs

CONTRACTILITY

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Conditions That Alter Contractility


Decrease

Increase

Pheocromocytoma
Hyperthyroidism
Positive inotropic drugs

Dobutamine
Dopamine
Levophed
Milrinone
Digoxin

Myocardial infarction
Cardiomyopathy
Ischemia
Hypoxia
Acidosis
Negative inotropic drugs

Beta blockers
Ca++ blockers
Antiarrhythmics
Some chemo agents
Some anesthetics, sedatives

Therapy to Alter CO

CO = HR X SV
Atropine
Epinephrine
Pacing

Beta blockers
Ca++ blockers (diltiazem, verapamil)
Antiarrhythmics
Adenosine
Digoxin

Cardiovascular Nursing Education Associates: www.cardionursing.com

CO = HR X SV
Preload

Afterload

Contractility

Diuretics
Venous Dilators:
NTG
ACEI
ARBs
Nesiritide (Natrecor)
Morphine

Fluids
Blood products

CO = HR X SV
Preload

Afterload

Arterial Dilators:
Nitroprusside (Nipride)
Milrinone (Primacor)
Ca++ blockers
Antihypertensives
ACEI
ARBs
Nesiritide (Natrecor)

Contractility
Vasopressors:
Levophed
Dopamine (high dose)
Epinephrine
Neosynephrine
Vasopressin

Cardiovascular Nursing Education Associates: www.cardionursing.com

CO = HR X SV
Preload

Afterload

Dobutamine
Dopamine
Milrinone
Digoxin

Contractility

Beta blockers
Ca++ blockers
Antiarrhythmics
Chemo agents
Anesthetics
Propofol

O2 Supply --------------O2 Demand


Open arteries

Heart Rate

CO
paO2

Preload

Hb, Hct

Contractility

Afterload

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Balancing O2 Supply & Demand


Demand
Preload
Diuretics
NTG
ACEI
ARBs
SARAs
Nesiritide
Morphine

Afterload

Supply
Contractility

Ca++ blockers Beta blockers


Ca++ blockers
ACEI
ARBs
Arterial dilators
IABP

O2

Drugs to
blood
flow

Open
occluded
coronaries

NTG
Ca++ blockers
ASA
Platelet inhibitors
Anticoagulants
Angiomax

Thrombolytics
PTCA
Stents
Atherectomy
Rotablation
CABG

Parasympathetic:
Slows HR
Slows AV conduction

Sympathetic:
Speeds HR
Speeds AV conduction
Increases contractility

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Sympathetic Nervous System


& Sympathomimetic Drugs
Alpha Receptors
(Arteries & Veins)

Beta Receptors
Isoproterenol

Beta 1
Neosynephrine

(Heart)
Dobutamine

Vasoconstriction

Dopamine
Epinephrine
Levophed

Beta 2
(Arteries, Veins)
(Lungs)

contractility
Vasodilation
heart rate
Bronchodilation
automaticity
conduction velocity
Renin release

Nephron
Pressure sensitive
cells are located
where the renal
tubule touches the
afferent arteriole
In response to
decreased renal blood
flow (whatever the
cause) renin is released
from these pressure
sensitive cells. Renin
initiates the reninangiotensin-aldosterone
cascade (next slide)

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Renin-Angiotensin System
Renal blood flow
Renin release
Angiotensinogen

Angiotensin I

(converting enzyme)

Angiotensin II
Vasoconstriction

Aldosterone release
Na+ & H2O retention

BP & Organ perfusion

The reason the kidney may not be getting


enough flow is that the LV is unable to
function well enough to adequately
perfuse the kidney. The kidneys response
will be stimulation of renin release via the
juxtaglomerular cells.

The two worst things for


a failing left ventricle are
more pressure to pump
against and more
volume to have to pump
(both are a result of
RAAS stimulation).

More pressure
More Volume

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Renin-Angiotensin System
Renal blood flow
Renin release
Beta Blockers

Angiotensinogen

Angiotensin I

(converting enzyme) ACEI

Angiotensin II
ARBs

Vasoconstriction

Aldosterone release
Aldosterone Blockers

Na+ & H2O retention


BP & Organ perfusion

BP = CO X SVR
Increased Pressure
on baroreceptors
Inhibits vasomotor
center
Stimulates vagus nerve
( heart rate)

Decreased Pressure
on baroreceptors
Stimulates vasomotor
center
Inhibits vagus nerve
( heart rate)

Decreases BP
Increases BP

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Drug Therapy to Decrease BP

BP = CO x SVR
Drugs to SVR
Drugs to CO

Peripheral Alpha Blockers

Diuretics

Centrally Acting Agents

Beta Blockers (olols)

(prazosin, terazosin, etc)


(clonidine, reserpine)

Direct Arterial Dilators

Calcium Channel Blockers


ACE Inhibitors (prils)
ARBs (sartans)

(hydralazine, minoxidil)

ACEI, ARBs
PDE inhibitors (milrinone)
Calcium Channel Blockers

Aldosterone Blockers

(pines)

nitric oxide in vascular tissue


(nitroprusside, nitrates)

Drug Therapy to Increase BP


BP = CO x SVR
Drugs to CO

Drugs to SVR

Inotropes
- Dobutamine
- Dopamine
- Milrinone
- Digoxin

Vasopressors
- Levophed
- Neosynephrine
- Vasopressin
- Epinephrine
- Dopamine (high dose)

Volume

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Pathogenesis of ACS

Plaque rupture

Platelet activation
Platelet aggregation

Drug Sites of Action


Heparin
Angiomax

Plavix
ASA

IIb/IIIa Inhibitors

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IIb-IIIa Inhibitors
Reopro
Integrilin (eptifibatide)
Aggrastat (tirofiban)

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Cardiac Action Potential


Phase I: Early Rapid
Repolarization

Phase 2:
Plateau

Ca++
Phase 0:
Depolarization

K+
Phase 3:
Repolarization

Na+

TP
Phase 4: TRP

Drug Action Sites


Class IV:
Ca++ Blockers

3
Class III:

Class I:
Na+ Channel Blockers0

TP

K+

Channel Blockers

TRP

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Class

Examples

IA

Quinidine
Procainamide (Pronestyl)
Disopyramide (Norpace)

IB

Lidocaine
Mexilitine

IC

Propafenone (Rhythmol)
Flecainide (Tambocor)

II
III

Beta blockers (olols)

IV

Calcium channel blockers:


Verapamil, Diltiazem

Speed Sinus Rate:


Atropine
Epinephrine
Slow Sinus Rate:
Beta blockers
Ca++ blockers
Dig
Antiarrhythmics

Speed AV
Conduction:
Atropine
Epinephrine
Slow AV Conduction:
Beta blockers
Ca++ blockers
Adenosine
Digoxin
Vagal Maneuvers

Amiodarone
Ibutilide (Corvert)
Dofetilide (Tycosin)

Suppress Atrial Arrhythmias:


Procainamide
Flecainide
Propafenone
Sotalol
Amiodarone
Ibutilide
Dofetilide

Slow or Block AP:


Procainamide
Flecainide
Amiodarone
Propafenone
Sotalol
Suppress Ventricular
Rhythms:
Lidocaine
Procainamide
Amiodarone
Sotalol
Magnesium

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I apologize for having to cancel my


presentations at NTI. I had laryngitis and
could barely squeak! Thank you for
understanding, and I hope you enjoyed
the NTI! I look forward to seeing you all
at a future NTI or other conference and
presenting this or other topics live.
I can be reached at:
carol@cardionursing.com

Mount Rainier as seen from my home in Seattle

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