Cardiovascular Nursing Part I

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Cardiovascular Nursing Part I

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Title: Cardiovascular Nursing Part I

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Cardiovascular NursingPart I

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Structure

Composed of 3 histologically distinct tissues
Epicardium
Myocardium
Endocardium
Surrounded by fibrous sac
Pericardium

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Endothelial Cell
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Dysfunctional Endothelium
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The Heart

Drives Hgb to the cells
Muscle
Functions as a pump
Mechanical and electrical components
Approx. the size of a clinched fist
Holds about 500 ml of blood
Beats to supply O2 rich blood to the body
100,000 times/day
2,000 gallons of blood/day
Through almost 65,000 miles of blood vessels

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Coronary Arteries
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BLOOD FLOW through the Heart
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The Cardiac Cycle

Refers to complete heart beat
Systole Contraction (pumping)
Closure of Tricuspid and Mitral Valves S1
Heard loudest over Apex (5th ICS)
Diastole Relaxation (filling)
Closure of Pulmonic and Aortic Valves S2
Heard loudest over 2nd ICS (R side)

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The Cardiac Cycle
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Cardiac Concepts

Cardiac output amt. of blood pumped in 1 minute
CO SV x HR
Stroke Volume amt. of blood ejected by the LV
with each contraction (systole)
Ejection Fraction of blood ejected from L.
Ventricle during systole
Preload
Volume of blood in any chamber at end of diastole
Afterload
Amt. of resistance ventricle overcomes to pump
Contractility force of contraction

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Cardiac Functioning
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Hemodynamic Monitoring

Measurement
Systemic and pulmonary blood pressures
Pulmonary Artery Catheter (invasive)
Right Atrial Pressure (RA)
CVP - R. Ventricle pressure
Pulmonary artery pressure
PAWP filling pressure of the LV
Cardiac Output -measured using process called
Thermodilution
Used to monitor patients in shock, Pulmonary
edema, post CABG, anytime for complicated
cardiac, pulmonary, intravascular problems
CVP Central Venous Pressure (invasive)
Measures R. ventricular preload
Arterial Lines (invasive)
Monitors systemic blood pressure
Important to monitor for SS of Infection at
insertion site

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Pulmonary-artery catheter
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Pulmonary Artery Catheter
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Preload (Volume)

The volume of blood in chamber at the end of
diastole, or the degree of myocardial fiber
stretch
? Volume/fluid ? Preload
So, preload can be ? by administering fluids
? Volume/fluid ? Preload
Meds used to decrease preload
Diuretics, (Lasix, Bumex)
Vasodilators (Natrecor)
Nitrates (Nitroglycerin)
Morphine
So, preload can be ? by diuresis

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Altered Preload

Preload can be ?administering fluids
Preload can be ?through diuresis
Signs and symptoms
Fatigue
JVD
Edema/weight gain
Murmurs
CVP - high or low
PAWP high or low

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Afterload (Resistance/pressure)

The pressure or resistance that the ventricle
must overcome to eject blood
Resistance of L. Ventricle pumps against systemic
arterial pressure, and the size of the ventricle
Meds used to decrease afterload Afterload
Reduction
A - ACE Inhibitors
- ARBs
- Alpha Antagonists
B - Beta Blockers
C - Calcium Channel Blockers

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Altered Afterload

?Afterload ?CO
?Afterload ?CO
Signs and Symptoms
Shortness of Breath/dyspnea
Cold, clammy skin
Color changes (pallor/cyanosis)
Prolonged CRT
Decreased peripheral pulses

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Contractility of the Heart

Intracellular calcium causes heart to contract
? contractility? Preload ? Stroke Volume
causing ventricles to empty
Epinephrine Norephinephrine when released by
SNS ? contractility
Meds that ? force of contraction are called
Positive Inotropics
Digoxin (Lanoxin)
Dobutamine (Dobutrex)
Dopamine (no brand)
Milrinone (Primacor)
Epinephrine (brand depends on the route)

Remember Starlings Law?
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Stroke Volume

SV affected by preload, afterload,
contractility
? preload, afterload contractility ? SV
? SV ? Workload of the heart
? Oxygen demand

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Altered Cardiac Output

Related to altered HR/rhythm SV
? CO may mean ? circulating volume
? CO may mean ? circulating volume
? Cardiac Output can be related to the following
Alteration in ECG rhythm ( like A-fib,)
? heart rate
? B/P
? contractility (like CHF)
?SV

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Monitoring Cardiac Output

Outside of a critical care unit when your patient
does not have a PA Catheter, How does the nurse
evaluate the patients CO??
Parameters include
Heart rhythm
Heart Rate
Blood Pressure
Urinary Output
Mental status/LOC
Skin Temperature
?Quality of Pulses

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The Heart

Responds to
Sympathetic System
Parasympathetic System
Renin/Angiotensin System
Baroreceptors and Chemoreceptors

The Sympathetic Nervous System
Adrenergic nerve fiber in the
sympathetic system
Sympathetic nervous system/Adrenergic
system (may be used interchangeably)
Chief neurotransmitters or catecholamine's
Epinephrine, Norepinephrine, Dopamine
Two types of Adrenergic receptor sites
Alpha and Beta

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Sinus Tachycardia

Note differences in P waves

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Parasympathetic Nervous System

Parasympathetic Nervous System
Acetylcholine - Neurotransmitter
Source of Vagal Response if stimulated
Vagus nerve when stimulated, releases
Acetylcholine causing heart to contract while
chambers are empty (after systole)

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Sinus Bradycardia
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Other Controls of the Heart

Baroreceptors
Located in Aortic Arch Carotid Sinus
Triggers enhancement of Parasympathetic Nervous
System
Chemoreceptor's
Located in the Aortic Arch and Carotid Artery
Responds to changes in O2 CO2 and pH of blood
Increases activity

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Renin/Angiotensin/Aldosterone
System

Renin enzyme/hormone kidney
?
Angiotensinogen liver
?
Angiotensin I
?
ACE
?
Angiotensin II
?
Aldosterone adrenal glands
?
Increased water reabsorbed ? Blood Pressure

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Common medications affecting Renin-Aldosterone
system

ACE inhibitors
All the prils
Angiotensin II receptor blockers
End in Sartan
Atacand (Candesartan)
Diovan (Valsartan)
Cozaar (Loesartan)

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Review

Three main systems that affect the
Heart and Blood Pressure
Adrenergic/sympathetic
Cholinergic/parasympathetic
Renal-Angiotensin/Aldosterone

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Assessing Cardiac Status
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Symptoms Cardiovascular Problems

Fatigue
Fluid Retention
Irregular Heart Beat
Dyspnea
Pain
Tenderness in Calf or leg
Leg Pain
Syncope
Changes in sensory or motor function
Table 32-2

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Health HistorySubjective

History of symptoms
Hx chest pain, SOB, anemia
Activity, sleeping, breathing, falls, dizziness,
passing out
Smoking , alcohol other substances
Congenital heart anomalies, HTN, DVT,
claudication, varicosities, edema, cyanosis,
melena
Hx syncopal episodes, CVA, TIAs or previous MI
DIABETES MELLITUS
Medications Including OTC and herbals
Surgery or other treatments
Table 32-4

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Medication History

Tricyclic antidepressants Arrhythmias
Oral Contraceptives Thrombophlebitis
Lithium Arrhythmias
Corticosteroids Na and Fluid retention
Theophylline Tachycardia Arrhythmias
Illegal Drugs Tachycardia and
Arrhythmias
Digoxin Toxicity

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Assessing Cardiac StatusObjective

Vital Signs - BP supine, sitting, standing, Rt
and Left arm, correct cuff size
Auscultation of lungs and heart extra heart
sounds, abnormal heart sounds
Inspect for pallor, cyanosis, edema, JVD, CRT,
Homans Sign
Palpation of pulses, quality and regularity
Review Table 32.5 for complete listing

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Cardiac Changes associated with aging

Myocardial Hypertrophy
?B-Adrenergic receptors
?Responsiveness to
Adrenergic Agonists
?CO, ?HR in response to stress
Stiffening of arterial vessel walls
? B/P, widened pulse pressure
Diminished pedal pulses
Review Table 32-1

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ECG RhythmsOf Gerontological patients
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Geriatric Assesment Findings

Irregular cardiac rhythms can result from
? amplitude of QRS complex
Lengthening PR, QRS, QT intervals
? SA Node cells
Fibrosis of Conduction System

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Sick Sinus Syndrome
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Atrial flutter
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Atrial fibrillation
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Wenckebach
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Assessment of the chest and major vessels

Inspection Thorax
Palpation Thrills,
abnormal pulsation over the chest valve
disorders or aneurysm
Abnormal pulsation over the abdomen aneurysm
Auscultation Bruits, Heart sounds, Murmurs
Auscultate apical heart rate palpate radial
pulse
simultaneously
Difference between the two pulse deficit
possible arrhythmias

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Areas of Auscultation

Aortic
2nd ICS right sternal border
Pulmonic
2nd ICS left sternal border
Tricuspid
4th or 5th ICS left sternal border
Mitral
5th ICS MCL

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Auscultation points
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Auscultation Points
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Physical Assessment

Inspection color, symmetry, presence of obvious
heaves
Auscultation S1, S2, murmurs graded
6-point scale, clicks, friction rub, bruits
Extra Heart Sounds (S3, S4) are not an expected
finding in adults use bell of stethoscope
Table 32-5 description of sounds
Document timing, location, pitch, position,
characteristics
Palpation heaves, thrills, abnormal pulsations,
record PMI location,
Percussion heart borders assessing for
hypertrophy

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Treating Cardiac Problems

Speed up HR
Slow down HR
Control Ectopy
Introduce pacemaker
Permanent, Temporary, AICD
Administer electric shock
Defibrillation
Cardioversion
Do nothing

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Cardiac Medications
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Cardiac Medications

Adrenergics (Agonists Antagonists)
Anticholinergics
Nitrates
Anticoagulants
Anti-Platelets
Low-Molecular Weight Heparin
Cardiac Glycosides
Antiarrhythmics Class IA, IB,IC, II, II, IV and
misc.
Beta Blockers
Calcium Channel Blockers
ACE Inhibitors
Antilipemics
Morphine

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Agonists

Work together
Enhances

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Adrenergic Agonists

Medications that enhance the SNS
Causing ? B/P, ? HR
Dobutamine
Dopamine
Epinephrine
Some Broncho-dilators
Albuterol

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Adrenergics

Epinephrine
Powerful stimulant
Used in Emergency Situations
Given IV, SQ, or by Inhalation

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Adrenergic -Dobutamine

Stimulates Beta I receptors
? Contractility of the heart
? CO, little effect on HR
Short term management of CHF
? Afterload
IV Infusion Only. (mcg/kg/min)
Can cause HTN or hypotension, tachyarrhythmia's
and PVCs
Monitor B/P, HR, EKG Rhythm

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Adrenergic - Dopamine

Small Doses (Renal Dose 2-5 mcg/kg/min) Renal
vasodilation, Effect ?urine output
New Research as published in Nursing Journal 2007
states this is not as effective as once thought
Larger Doses Cardiac Stimulation
?B/P, ?CO
Renal Vasoconstriction w/ doses gt10mcg/kg/min
IV drip titrated (mcg/kg/min)
Can cause arrhythmias and hypertension
Monitor blood pressure, heart rate, pulse
pressure, ECG, PCWP, Monitor urine output
continuously

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Calc. For Dopamine and Dobutamine Infusions

These drugs are ordered mcg/kg/min
Equation
DO- mcg ordered x pt wt. Kg x 60
OH- drug concentration IV infusion rate
(ml/hr)
Example- Order Dopamine to run at 5mcg/kg/min
Pharmacy sends Dopamine 200mg in 250 ml of NS
Pts weight 132 lbs.
What will you set your pump at

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Dopamine Infiltration

Very Serious
Severe vasoconstriction
Tissue necrosis will result if not treated right
away
Antidote Phentolamine (Regitine)
Alpha1 adrenergic blocker
Onset Immediate
Given SubQ
Must observe IV site frequently

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Antagonists

Work Against
Block the effects of either
Sympathetic Nervous System
ParaSympathetic Nervous System

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Adrenergic Antagonists

Meds affecting this system
Adrenergic Inhibitors/Antagonists
Central-acting
Peripheral-acting
Alpha Blockers
Beta Blockers end in LOL
Alpha and Beta Blockers

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Beta Blockers

Medications ending in lol ( like metoprolol)
Compete for adrenergic neruotransmitters
Epinephrine, Norepinephrine, Dopamine
Expected results ?HR, ? B/P, Reduction of
workload of the heart
Side Effects nightmares, depression,
bronchospasms, erectile dysfunction, hypoglycemia
in diabetics
Measuring effectiveness Reduction in angina,
reduction of symptoms associated with ADLs

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Adrenergic System Receptorsand their Effects
release

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Adrenergic meds are often non-discriminating

May affect either receptor

Beta 1
Alpha 1
Alpha 2
Beta 2
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Cholinergic Antagonists(Also referred to as
Anti-cholenergic)

Atropine
Scopolamine
Some Parkinsons drugs

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Anticholinergics

Atropine
Blocks Cholinergic System
Increases Heart Rate
Indications symptomatic Bradycardia, heart block

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ACE Inhibitors

Prils (like Lisinopril)
Remember the Renin/Aldosterone System
Renin enzyme/hormone kidney
Angiotensinogen liver
Angiotensin I
ACE Inhibitors Block from here
Angiotensin II
Aldosterone adrenal glands
Increased water reabsorbed
Increased Blood Pressure

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ACE Inhibitors (contd)

Drug of Choice in Tx. Of CHF
Expected Results
? B/P in hypertensive patients
? Afterload in CHF patients
Side Effects
Dry, Hacking Cough,
Hypotension,
Hyperkalemia (monitor potassium),
Renal insufficiency in high doses (monitor
creatinine)
Therapeutic Results
improves EF (Ejection Fraction),
? activity tolerance

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Cardiac Glycosides

Digoxin
Increases Intracellular Calcium
Positive Inoptropic effect
? Contractility
Negative Chronotropic effect
? Heart Rate
Indications Treatment of CHF, Tachyarrhythmias
(PAT, atrial fibrillation, atrial flutter)
Loading dose may be required
Drugs causing hypokalemia, such as Thiazide
Diuretics, Corticosteroids, Laxatives, Quinidine.
Can increase risk for toxicity

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Cardiac GlycosidesMechanism of Action

Increase myocardial contractility
Change electrical conduction properties of the
heart
Decrease rate of electrical conduction
Prolong the refractory period
Area between SA node and AV node
Result reduced heart rate and improved cardiac
efficiency

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Cardiac GlycosidesAdverse Effects

Digoxin (Lanoxin)
Very narrow therapeutic window
Drug levels must be monitored
Electrolyte levels must be monitored

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Cardiac Glycosides

Digoxin Levels 0.5-2.0
Monitor for 1. ?Potassium, 2.?Magnesium, and 3.
?Calcium levels
Is the patient on Lasix (Furosemide) or other
loop diuretic?
Can easily lead to Toxicity
Many drugs interfere with Digoxin Reglan,
Rifampin, Phenytoin, antacids, antibiotics

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Patients At Risk for Dig Toxicity

Diuretics
Beta blockers
Calcium preparations
Amiodarone (Cordarone)
Cardizem (Diltiazem)
Erythromycin, omeprazole
Verapamil, Quinidine

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S/S of Dig. Toxicity

N/V
Anorexia
Visual disturbances yellow vision
Headaches
Fatigue/Maliase
Arrhythmias (PVCs, A-fib, 1st degree block)
Bradycardia
Treatment for Dig Toxicity
Dig Immune Fab or Digibind

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ST Segment Depression - Dig. toxicity
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Antiarrhythmics

Divided into 4 classes (I,IA,IB,IC,II,III,IV)
Classified based on effect of the conduction
system
Plus a Miscellaneous class
Goal ? symptoms,
?Hemodynamic stability

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Most Common Antiarrhythmics

Lidocaine - PVCs
Monitor for signs of confusion
Onset Peak Immediate
Amiodarone (Cordarone)
Onset 2hr., peak 3-7 hr.
Half-life 13-107 days
Diltiazem (Cardizem) Ca Channel Blocker
IV onset 2-5 min, peak 2-4 hr.
Half life 3.5 -7 hours
Verapamil (Calan) Ca Channel Blocker
Procardia (nifedipine)
Digoxin

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Antiarrhythmics

Miscellaneous Class
Adenosine (Adenocard)
Slows Conduction through AV node
Treats PSVT
Given Rapid IVP, can cause pronounced flushing
and transient arrhythmias or asystole for a few
seconds
Digoxin, and atropine in this class also

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Nursing Implications

Monitor for therapeutic response
Decreased BP in hypertensive patients
Decreased edema
Decreased fatigue
Regular pulse rate
Pulse rate without major irregularities
Improved regularity of rhythm
Improved cardiac output

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Various Drugs

Anticoagulants
Inhibit the action or formation of clotting
factors
Prevent clot formation
Antiplatelet drugs
Inhibit platelet aggregation
Prevent platelet plugs
Thrombolytic drugs
Lyse (break down) existing clots
Antilipemics

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Anticoagulants

Have no direct effect on a blood clot that is
already formed
Used prophylactically to prevent
Clot formation (thrombus)
An embolus (dislodged clot)

84
AnticoagulantsMechanism of Action

All ultimately prevent clot formation
heparin
Low-molecular-weight heparins
warfarin (Coumadin)

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Anticoagulants Indications

Used to prevent clot formation in certain
settings where clot formation is likely
Myocardial infarction
Unstable angina
Atrial fibrillation
Indwelling devices, such as mechanical heart
valves
Major orthopedic surgery

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Antiplatelet Drugs

Prevent platelet adhesion
Aspirin - (now considered an Anti Thrombetic)
Dipyridamole (Persantine)
Clopidogrel (Plavix) and ticlopidine (Ticlid)
ADP inhibitors
Tirofiban (Aggrastat), eptifibatide (Integrilin)
New class, GP IIb/IIIa inhibitors

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Thrombolytic Drugs

Drugs that break down, or lyse, preformed clots
Patient selection is required
Bleeding is a complication
IV therapy Bolus or drip
Critical monitoring of patient
Monitor for re-perfusion

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Thrombolytic Drugs (contd)

streptokinase (Streptase) older drug
anistreplase (Eminase)
alteplase (t-PA, Activase) newer drug
reteplase (Retavase)
tenecteplase (TNKase)
drotrecogin alfa (Xigris)

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Thrombolytic Drugs Indications

Acute MI most beneficial w/in 1st hour
Can be administered up to 6 hours
Goal in AMI Stop the infarction
Ideally 1st hour
Must within first 6 hours
DVT
Occlusion of shunts or catheters
Pulmonary embolus
Acute ischemic stroke
Table 33-14

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Antilipemics

Drugs used to lower lipid levels

Antilipemic drugs are used as an adjunct to diet
therapy
Drug choice based on the specific lipid profile
of the patient
All reasonable non-drug means of controlling
blood cholesterol levels (e.g., diet, exercise)
should be tried for at least 6 months and found
to fail before drug therapy is considered

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Antilipemics

HMG-CoA reductase inhibitors (HMGs, or statins)
Bile acid sequestrants
Niacin (nicotinic acid)
Fibric acid derivatives
Cholesterol absorption inhibitor
Combination of these drugs
Table 34-6

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Antilipemics HMG-CoA Reductase Inhibitors
(HMGs, or statins)

Most potent LDL reducers
lovastatin (Mevacor)
pravastatin (Pravachol)
simvastatin (Zocor)
atorvastatin (Lipitor)
fluvastatin (Lescol)
Lower the rate of cholesterol production
First-line drug therapy for hypercholesterolemia
New studies showhas anti-inflammatory effect on
the endothelium

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HMG-CoA Reductase Inhibitors (contd)

Adverse effects
Mild, transient GI disturbances
Rash
Headache
Myopathy (muscle pain), possibly leading to a
more serious condition Rhabdomyolsis
Important to ask about muscle pain/tenderness
Monitor for elevations in liver enzymes
CK
levels

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Bile Acid Sequestrants

Also called bile acidbinding resins and
ion-exchange resins
cholestyramine (Questran)
colestipol hydrochloride (Colestid)
colesevelam (Welchol)

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Bile Acid Sequestrants (contd)

Mechanism of action
Prevent resorption of bile acids from small
intestine
Bile acids are necessary for absorption of
cholesterol
May be used along with statins
Should be taken by itself can interfere with
other drugs
Side Effects
GI, gritty taste

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Niacin (Nicotinic Acid)

Vitamin B3
Lipid-lowering properties require much higher
doses than when used as a vitamin
Effective, inexpensive, often used in combination
with other lipid-lowering drugs

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Niacin (Nicotinic Acid) (contd)

Adverse effects
Flushing (due to histamine release) Expected
Side Effect
Pruritus
GI distress

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Fibric Acid Derivatives

Also known as fibrates
gemfibrozil (Lopid)
fenofibrate (Tricor)
Effect
Reduces Triglycerides
?HDL
Side Effects
Mild GI
Enhance anticoagulants

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Cholesterol Absorption Inhibitor

ezetimibe (Zetia)
Inhibits absorption of cholesterol and related
sterols from the small intestine
Results in reduced total cholesterol, LDL,
triglyceride levels
Also increases HDL levels
Works well when taken with a statin drug
Natural Lipid Lowering Agents pg. 796

100
Laboratory Testing

CBC
BMP
CK
TROPONIN
PT, INR
PTT/APTT
BNP
BUN, Creatinine
Table 32-7

K
Magnesium
Cholesterol
Triglycerides
Sed rate

101
Creatine Kinase

CK
Enzymes specific to cells of brain, myocardial,
and skeletal muscle
CK-MM
CK-BB
CK-MB
CK-MB index
Ratio of CK-MB to total CK
More definitive for diagnosing an MI
If CK-MB and the Index are both elevated highly
suggestive of an MI

102
TROPONIN

Troponin protein released with injury of
myocardial cells
Two types I T
Troponin I (begins to rise as early as 1 hour
post pain) _ Lewis textbook
lt0.4 normal baseline (Lewis)
These values vary greatly depending on the
reference you use and laboratory equipment.

103
Cardiac Enzyme Chart
104
Lipid Testing

Cholesterol Goals
Total Cholesterol 140 - lt200Good
HDL (Good) lt35low Not Good
gt60Great
LDL (Bad) Keep lt 160
Triglycerides 40-190 Good
Factors effecting test

105
Lipo Protein Testing

New Lipid testing
Enzyme promotes vascular inflammation
? levels (Lp-PLA) associated with CAD
Called the PLAC Test

106
Prothrombin Time (PT)

Normal value 10-14 seconds
Prothrombin is a protein produced by the liver
and is used in the clotting of blood
Used to monitor clotting and Coumadin therapy
An INR (International Normalized Ratio) is based
on the PT.

107
International Normalized Ratio (INR)

This is the ratio of a patients PT to normalized
PT. The results can be consistently replicated
from one lab to the next.
Normal INR 1
Most anticoagulation ( chronic A-Fib)
INR2-3
Valvular replacement or cardiovascular
prosthesis, DVT therapy
INR3-4

108
PTT/APTT (Activated Partial Thromboplastin Time)

Normal APTT 30--45 seconds
Used to monitor Heparin therapy
Values should be 1.5-2 times normal for
anticoagulation

109
B type Natriuretic Peptide (BNP)

lt100pg/ml Normal
Brain Natriuretic Peptide
(Cardiac)
Increases in CHF
Related to reduction in Na ions, the bodys
attempt to control fluid overload in the lungs

110
Other Labs

BUN ( may be decreased in CHF),
Creatinine interpreted in conjuction with BUN
(10/1 approx)
Serum Potassium lt3.5 or gt5.0 critical values
Serum Magnesium 1.3-2.1
CRP C Reactive Protein

111
Other Diagnostics

CXR
ECG
Holter Monitor
Stress Test
Echocardiogram
TEE
Cardiac Catheterization
EPS

112
CHEST X-RAY (CXR)

A CXR can be used to assess the size, shape, and
position of the heart.
Calcification of great vessels
Pericardial effusion
Placement of central lines
Pleural effusion, CHF

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114
Electrocardiogram (EKG/ECG)

Noninvasive, painless
Telemetry or 12 lead
Can identify arrhythmias
Different leads can assist in detection of
location of MI

115
Holter Monitor

24 hour to 30 day monitoring of EKG
Inform patient to keep a daily diary of activity
and/or chest pain
Do not shower or remove monitor

116
Stress Test

Goal_________________
Exercise or Pharmacologic
Adenosine, Dobutamine, Persantine
With or without Nuclear Imaging using
Radioisotopes Thallium, Cardiolite, Myoview
Consent
Typically NPO
Check about administration of cardiac meds and
caffeine
Monitor for chest pain ECG changes may
indicate ischemia
ST Segment Depression

117
Echocardiography

Noninvasive
Painless
Used to assess structure of heart, especially
valves

118
Echocardiography
119
Trans-esophageal Echocardiography (TEE)

Patient usually NPO
Consent required
Transducer placed in esophagus to assess
structure of heart
Assess post procedure
Gag reflex
Possible complications Esophageal perforation,
Vaso-vagal response, arrhythmias, Hypoxia

120
TEE
121
Cardiac Catheterization