Download Cardiovascular Unit

Cardiovascular Unit
By Pat Pence, RN, C, MSN
Heart
Located in mediastinum.
 Base (wider) is superior and under the 2nd
rib.
 Apex (narrow) is inferior and slightly to the
left between 5th and 6th ribs.
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Heart wall
Composed of 3 layers.
 Pericardium: transparent, thin layer, lines
outside of heart, 2 layers that contain serous
fluid to decrease friction.
 Myocardium: middle, thickest and
strongest, actual contracting muscle tissue.
 Endocardium: innermost layer, thin layer of
connective tissue.
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4 Heart chambers
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Right atrium: receives deoxygenated blood from
superior vena cava, inferior vena cava and
coronary sinus.
Right ventricle:pumps blood to lungs via
pulmonary artery.
Left atrium: receives O2 rich blood from lungs via
pulmonary veins.
Left ventricle: PMI, thickest, most muscular,
pumps blood to all parts of body via aorta.
Separated by septum.
4 Heart valves
Heart functions as 2 separate pumps.
 Heart valves keep blood flowing forward
and prevent backflow (regurgitation).
 Tricuspid valve and mitral valve (AV
valves).
 Chordae tendineae and papillary muscles
connect valves to walls of heart and
promote a tight seal to prevent backflow.

Semilunar valves
Pulmonary semilunar valve: between Rt
ventricle and pulmonary artery.
 Aortic semilunar valve: between left
ventricle and aorta.

Coronary blood supply
Heart requires a constant supply of O2 rich
blood and return of O2 poor blood from
tissue to the lungs.
 Rt./Lt. Coronary arteries.
 Coronary vein and coronary sinus.
 Collateral circulation.

Blood vessel pattern
Artery: largest, vessels that carry blood
away from heart; thicker, elastic and muscle
tissue.
 Arteriole: smooth muscle, deliver blood to
tissues; dilate or constrict in response to low
O2/hi CO2, affect BP blood flow.
 Capillary: endothelial cells, allow exchange
of products; no muscle or elastic tissue.

Venules: small amounts of muscle and
connective tissue.
 Veins: larger veins have valves to prevent
backflow of blood; carry blood back to
heart; large diameter, thin walled.

Pulmonary circulation
Deoxygenated blood passes through
pulmonary circulation to receive O2.
 Right ventricle, pulmonary semilunar valve,
pulmonary artery, pulmonary capillaries,
pulmonary veins, left atrium, bicuspid
valve, left ventricle, aortic semilunar valve,
and aorta.
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Systemic circulation
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Refers to blood pumped from lt ventricle to all
parts of body and then to rt atrium.
Aorta: largest artery, main trunk of systemic
arterial circulation.
Vena cava: returns deoxygenated blood to rt
atrium.
Superior vena cava: from head, neck, chest, and
upper extremities.
Inferior vena cava: from parts of body below
diaphragm.
Electrical conduction system
Automaticity: specialized ability to contract
in rhythmic pattern.
 Irritability: excitability or sensitivity.
 Hormones, ion concentration, changes in
body temp. affect the conduction system.
 Depolarization = contraction.
 Repolarization = relaxation (resting state).

Impulse pattern
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Initiated in SA node in Rt. Atrium. “Pacemaker”
of heart. Internodal pathways to atria.
AV node: Rt atrium, slows impulses to allow
atrium to contract and ventricles to fill.
Bundle of His: group of conduction fibers in base
of rt atrium.
Rt. and Lt. Bundle branches in septum.
Perkinje’s fibers: surround ventricles.
Cardiac cycle: systole/diastole
Refers complete heartbeat.
 Systole: = contraction, blood is pumped out
of the ventricles. (depolarization).
 Atria relax to receive blood.
(repolarization).
 AV valves close: S1: first heart sound.
 Ventricles contract in response to electrical
impulse having passed through.

Diastole
Diastole = relaxation, blood enters the
relaxed chambers.
 Ventricles fill.
 Semilunar valves close: S2: 2nd heart
sound.
 Atria contract in response to electrical
impulse.

Stroke volume/cardiac output
Stroke volume: volume of blood ejected
(pumped) during each ventricular
contraction (heartbeat).
 Cardiac output: amount of blood ejected
(pumped) by each ventricle per minute.
 CO = SV X HR.
 Numerous factors affect CO.

Stroke volume factors
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Preload: volume of blood within ventricles at end
of diastole, comes from veins, before next
contraction. Preload determines the amount of
stretch placed on the myocardium.
Afterload: pressure that ventricles work against
when they contract to eject blood from the heart.
That pressure is located in arteries (peripheral
resistance or arterial BP).
Normal heart overcomes afterload and
maintains CO except when muscles have
been damaged.
 Contractility increased by norepinephrine
and epinephrine.
 Increased preload, afterload and
contractility increase workload and O2
demand on heart.

Inotropic state
Inotropic state = strength of myocardial
contraction unrelated to blood volume.
 Affected by sympathetic stimulation,
metabolic abnormality, hypoxemia,
metabolic acidosis, drugs (epinephrine).

Starling’s law
To a point the heart will pump out all blood
it receives within certain limits.
 The more the fibers are stretched, the
greater their force of contraction.
 If stretched beyond capacity- blood will
accumulate in ventricles and back up into
pulmonary system.

Heart sounds
Produced by closure of valves.
 Lubb: (S1) long duration, low pitch, AV
valves close.
 Dubb: (S2) short duration, sharp sound,
semilunar valves close.
 Murmur: swishing sound, may be normal or
abnormal.

Cardiovascular assessment
Subjective data: past CV problems, health
habits (smoking, diet, activity), current CV
problems.
 History: description of symptoms, when
they occurred, course and duration,
location, precipitating factors, relief
measures.
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Pain
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Character, quality, radiation, associated symptoms.
Rated on pain scale.
Location: *chest, radiated to jaw, left shoulder.
Description: dull, sharp, pressure, squeezing,
crushing, viselike, grinding, radiating.
Precipitating onset.
Pain in extremities or lack of sensation.
Palpitations
Characterized by rapid, irregular, or
pounding heartbeat.
 Associated with dysrhythmias or ischemia.
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Dyspnea
Exertional dyspnea is associated with
decreased cardiac output.
 DOE, DAR, PND, orthopnea.
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Cough
Dry, productive, irritating, spasmodic.
 May be associated with dyspnea.
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Fatigue
Exhaustion/ activity intolerance.
 Associated with decreased cardiac output.
 Depression may associated with fatigue.
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Syncope
Fainting: brief lapse of consciousness.
 Caused by transient cerebral hypoxia.
 Sudden decrease in cardiac output to brain
resulting from dysrhythmia or decreased
pumping action of heart.
 Preceded by lightheadedness.
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Objective data
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Vital signs. LOC.
Lung sounds. Bowel sounds. Sputum.
Heart: Apical pulse, heart sounds, carotid arteries,
systemic with no bruit.
Jugular veins not distended when sitting or
standing.
Extremities: color, temp, moisture, edema, hair
distribution, capillary refill, clubbing, peripheral
pulses, Homan’s sign, turgor.
Cyanosis
Caused by: excess of deoxygenated Hgb in
blood.
 Results from: decreased cardiac output and
poor peripheral perfusion.
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Diaphoresis
Profuse sweating associated with
clamminess.
 Result of decreased cardiac output and poor
peripheral perfusion.
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Edema
Wt. Gain of more than 3lb. In 24 hours.
 Inability of heart to pump efficiently or
accept venous return, causes backflow of
blood and increased blood volume.
 Increased hydrostatic pressure results and
an increase in fluid to interstitial spaces.

Diagnostic Tests
CBC
Determination of RBCs, WBCs, platelets,
Hgb, Hct.
 Low Hgb = decreased O2 carrying capacity
 High WBC = infection or inflammation.
 High RBC = body compensating for chronic
hypoxemia by stimulating RBC production
in bone marrow, leading to secondary
polycythemia.

Cardiac enzymes
Elevated amounts of enzymes (proteins,
cardiac “markers”) are released into blood
during cardiac muscle cell damage.
 These enzymes are helpful in determining
the degree of myocardial damage and the
timing of onset of damage.
 Some enzymes are more specific to cardiac
muscle tissue.
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Creatine phosphokinase (CPK)
Enzyme found in brain, skeletal muscle, and
myocardium.
 Can be broken down into isoenzymes.
 CPK II (MB) is more specific to cardiac
tissue. Levels > 7.5 ng/ml associated c MI.
 Onset: 3-6 hours; peak 12-18 hours;
duration 3-4 days.
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Lactic dehydrogenase (LDH)
Found in many body tissues (cardiac,
kidneys, RBCs, brain, stomach, skeletal
muscle). Normal < 100 U/L.
 Late indicator of damage.
 Rises in 24-72 hours; peaks in 3-4 days;
returns to normal levels in about 14 days.
 Not as specific as other enzymes.
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Myoglobin
Small O2 binding protein found in cardiac
and skeletal muscle.
 Because it is smaller when compared to
larger enzymes, it is detected earlier.
 1-4 hours after onset. Peak 6-9 hrs.
 Must be done within 1st 18 hrs after onset.
 Normal < 92 men; < 76ng/ml women.
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Troponin
Protein located on cardiac and skeletal
muscle tissue.
 3 forms. Troponin I is more specific; found
exclusively in cardiac tissue.
 Onset 3-6 hours; peaks 14-20 hours; returns
to normal in 5-7 days.
 Elevated levels of Troponin I is diagnostic
of MI. Range 0 - 0.4ng/mL.
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Serum Lipids
Cholesterol: fatty substance coated with 2
types of proteins. LDL or HDL.
 Total cholesterol level is sum of all
cholesterols. Level should be < 200mg/dl.
(nonfasting test).
 Associated with diet high in saturated fat,
cholesterol and calories.
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Hyperlipidemia: elevated levels of any or
all of lipids in plasma.
 Triglycerides: Mixture of fatty acids.
 Normal: 40-190 ng/dl.
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HDL/LDL
HDL and LDL: need to fast 12 hrs.
 High-density lipoprotein: “good
cholesterol”. More protein than fat.
 Removes cholesterol from vessels and
transports to liver for removal.
 Higher the level = less risk of CAD.
 Desirable level = 35 or >.
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LDL
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Low-density lipoprotein: “bad cholesterol”.
Promotes CAD.
Equal amount of fat and protein.
Transports cholesterol from the liver to body
tissues, accumulating in vessel walls.
Level < 160mg/dl (c no risk factors). Higher the
level = greater risk of CAD. Desired level for LDL
depends on the risk factor profile of pt. More risks
= a goal for a lower LDL level. (ex. 100mg/dl)
EKG
A graphic representation of the heart’s
electrical activity reflected by changes in
the electrical potential at the skin surface.
 Recorded as a tracing on a strip of paper.
 “Resting” EKG over < one minute.
 Telemetry: continuous visualization on a
screen (monitor).
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Purposes
Identify rhythm disturbances.
 Provides information about the position of
the heart in the chest and the size of the
chambers.
 Detects electrolyte imbalances.
 Monitors the effectiveness of pacemakers
and cardiotonic meds.
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Holter monitor
“Ambulatory” EKG: a type of portable
EKG which records 12- 48 hours of usual
pt.’s activities with normal stress.
 Pt keeps a diary of activities and symptoms.
 Purposes: determines exercise tolerance
post-MI. Provides more diagnostic
information.
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Inpatient or outpatient basis.
 Detects intermittent arrythmias c ADLs c
associated manifestations of dizziness,
palpitations, chest pain.
 Guages antiarrythmic meds.
 Instruct pt to update diary regularly and
note any symptoms; not to get monitor wet.
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EKG waveforms
P wave: depolarization or contraction of the
atria. SA node fires impulse, delay by AV
node seen as space after P wave.
 QRS complex: ventricles depolarize or
contract, atria repolarize (relax), strong
signal because of greater mass of ventricles.
 T wave: ventricles repolarize or relax.
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Intervals are the length of time it takes the
impulse to travel from one area of heart to
another.
 Cardiac dysrhythmias result of abnormal
pacemaker function.
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Cardiac dysrhythmias
(arrhythmia)
Any cardiac rhythm that deviates from
normal sinus rhythm.
 The result of alteration in the formation of
impulses through the sinoatrial node.
 Results from irritability of myocardial cells
that generate impulses.
 S&S and treatment vary depending on type
and severity.
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Classified according to origin (atrial or
ventricular),
 Mechanism: bradycardia, tachycardia, or
both.
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Normal sinus rhythm
Originates in SA node.
 Characterized by:
 Rate: 60-100 beats/min.
 P waves: precede each QRS complex. (atrial
depolarization)
 P-R interval: interval between atrial and
ventricular repolarization.
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QRS: ventricular depolarization.
 T wave: ventricular repolarization.
 Rhythm: regular.
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Sinus Tachycardia
A rapid regular rhythm.
 Originates in SA node.
 Rate: 100 or >.
 S&S: occasional palpitations, hypotension,
angina.
 Most are asymptomatic.
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Sinus Bradycardia
A slow rhythm.
 Originates in SA node.
 Rate: <60.
 S&S: fatigue, lightheadedness, syncope.
 Some are asymptomatic.
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Atrial fibrillation
A very rapid production of atrial impulses.
 Atria beat chaotically resulting in improper
contraction.
 Rate: 350-600.
 S&S: pulse deficit, palpitations, dyspnea,
angina, lightheadedness, pulmonary edema,
decreased cardiac output.
 May cause emboli or CHF.
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Premature Ventricular
Contractions
PVCs: early ventricular beats that occur in
conjunction with regular rhythm.
 Originates in more than one location in
ventricles.
 S&S: depend on frequency of PVCs and
their effect on ability of heart to pump
effectively.
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Some are asymptomatic.
 Palpitations, weakness, lightheadedness,
decreased cardiac output.
 PVCs that last long enough to cause
ventricular tachycardia may lead to death.
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Ventricular Tachycardia
A regular or slightly irregular rhythm in
which 3 or more successive premature
ventricular contractions occur.
 Rate: 140-240.
 Life threatening.
 May lead to ventricular fibrillation and
death.
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Ventricular fibrillation
Ventricular muscles are quivering.
 Characterized by rapid and disorganized
ventricular pulsation.
 *Medical emergency.
 S&S: are a result of no cardiac output.
 Loss of consciousness, lack of pulse, loss of
BP and respirations, possible seizures, and
sudden death if untreated within 3 min.
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Cardiac arrest
A sudden cessation of cardiac output and
effective circulation.
 Usually precipitated by ventricular
fibrillation or ventricular asystole.
 Asystole: a life threatening cardiac
conduction characterized by absence of
electrical and mechanical activity in heart.
S&S: lack of pulse and breathing.
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Atrial arrhythmias prevent proper filling of
ventricles and decrease CO.
 Ventricular arrhythmias prevent proper
filling of ventricles, decrease or absent CO.
Life-threatening.
 V Tach is likely to result in V Fib and death.
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Arteriogram
Series of radiographs taken after an
injection of radiopaque dye into a coronary
artery.
 Diagnose vessel occlusion, pooling in
chambers of heart, and congenital
anomalies.
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Stress Test
Exercise EKG.
 Types: Treadmill: walking, then increase
speed and incline until pt reaches a target
HR, has chest pain, fatigue, extreme
dyspnea, vertigo, or claudication (calf pain
c walking, relieved c rest).
 Stationary bicycle.
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MUGA: (multigated acquistion scan) use of
computers with EKG during scanning.
Persantine: pharmacological stress test.
Vasodilator. No caffeine 12 hrs. prior.
Thallium: nuclear agent used during scan.
Purpose: To evaluate CV fitness prior to an
exercise program,
To diagnose exercise induced symptoms and
arrythmias,
To evaluate the effectiveness of meds.
Nursing care: No eating, drinking, or
smoking 2 hours prior.
 Wear comfortable clothes.
 Continue all meds.
 Vitals, monitor.
 The earlier manifestations developed =
more serious the heart disease is.
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Cardiac catheterization
Invasive procedure used to visualize heart
chambers, valves, great vessels, and
coronary arteries in order to determine the
degree of blockage.
 Catheter is inserted through a peripheral
vessel and advanced to heart chambers.
 Dye injected to assist in examining structure
and motion of the heart.
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Measure pressure within heart.
 Measure blood-volume relationship to
cardiac competence.
 Determine valvular defects, arterial
occlusion, or congenital anomalies.
 Blood samples obtained.
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Nursing care
Check for allergy to iodine (used as contrast
medium).
 Consent. NPO. Give sedative as ordered.
 Instruct will feel warmth/fluttering
sensation as catheter is passed.
 Post-procedure: Pressure dressing and 510lb. sandbag used to provide pressure over
site to prevent hemorrhage.
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Supine position 4- 8hrs. Then elevate HOB
30 degrees.
 Inspect site for bleeding and swelling.
 Monitor vital signs, heart and lung sounds,
peripheral pulses, color and sensation.
 Encourage fluids to eliminate dye.
 Monitor I&O, labs.
 Advise pt. to report chest pain.
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Percutaneous transluminal
coronary angioplasty (PTCA)
Invasive surgical procedure performed in
cardiac cath lab.
 Consent required.
 Balloon tipped catheter is guided by
fluoroscopy from the femoral or brachial
artery to the coronary arteries.
 Balloon is inflated intermittently and opens
narrowed vessel to improve blood flow.
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1-2 hour procedure.
 Mild sedative is given.
 Post procedure: monitor catheter insertion
site for hemorrhage.
 Risk for complications.
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Stent Placement
Used to treat abrupt or threatened vessel
occlusion following PTCA.
 Expandable, meshlike structures compress
against vessel wall.
 Potential for thrombus formation: must be
on anticoagulants for 3 months.
 Complications: hemorrhage, injury,
dysrhythmias.
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Risk factors for CV disease
Nonmodifiable: family history,
 Age: > with elderly.
 Sex: men > risk, but incidence increasing in
women.
 Race: African-American males (high BP,
CVA), Hispanics with diabetes, Caucasians
have highest rate of CV disease, higher total
cholesterol levels.
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Modifiable factors
Smoking: 2-3 X > risk than nonsmokers.
More Caucasian women smoke than other
women.
 Hyperlipidemia: diet, exercise, meds.
 Hypertension: BP > 140/90 mm Hg.
 Diabetes mellitus: related to elevated BS
levels, altered lipid metabolism c elevated
cholesterol and triglycerides.
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Obesity: increases workload. Increased
obesity among Americans.
 Sedentary lifestyle: exercise lowers BS
levels, improves ratio of HDL to LDL,
reduces Wt., BP, stress, and improves wellbeing.
 Stress: releases catecholamines, results in
vasoconstriction.
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Oral contraceptives
 Psychosocial factors: Type A personality.
 Asthma: more prone to heart disease; meds
side effects or chronic lung inflammation
damages arteries.
 Homocysteine: elevated levels triple your
risk; amino acid associate with folate
deficiency.
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Dietary Modifications
Total fat intake < 30 % of total calories.
 Saturated fats < 10 % of total calories.
 Sodium under 1g of sodium for every 1,000
calories consumed.
 Cholesterol < 300mg. (eggs, meat, butter,
whole milk)
 Alcohol moderation.
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Polyunsaturated fats lower both LDL and
HDL (corn oil).
 Monounsaturated fats lower only LDL.
(olive oil, canola oil).
 Dietary supplements: Vitamin E,
antioxidant.
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Common cardiac drugs
Adrenergics
 Adrenergic blockers.
 Diuretics.
 Beta-blockers.
 Calcium channel blockers.
 ACE inhibitors.
 Vasodilators.
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Adrenergics
Stimulate the sympathetic nervous system.
 Act on one or more of adrenergic receptor
sites.
 Alpha 1-receptor: increases force of
contraction of heart; vasoconstriction,
increases BP.
 Alpha 2-receptor: inhibits release of
norepinephrine, vasodilator, decreases BP.

Beta1- receptor: increases HR/force of
contraction, renin secretion and BP.
 Beta 2- receptor: bronchodilation.
 Many of adrenergic drugs stimulate more
than one receptor site.
 Epinephrine: sc or IV, inhalation, topically.
Not po. Used in shock, cardiac arrest.
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Dopamine: to correct hypotension.
 Ephedrine HCL: hypotension. (OTC meds).
 Norepinephrine bitartrate: shock, potent
vasoconstrictor.
 Side effects: hypertension, tachycardia,
palpitations, dysrhythmias, tremors,
dizziness, difficulty urinating, nausea,
vomiting.
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Nursing implications
Monitor vitals and for side effects.
 Monitor urinary output for retention.
 Check IV site for tissue necrosis.
 Offer food to avoid N/V.
 Instruct pt. to read med labels.

Adrenergic Blockers
Stimulate alpha2 receptors , decrease
sympathetic response, decrease epinephrine,
norepinephrine and renin release, resulting
in decreased peripheral vascular resistance.
 (promote vasodilation to decrease BP)
 Minimal effect on CO and renal blood flow.
 Can cause Na/H2O retention. Given c
diuretic.
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Side effects: orthostatic hypotension,
tachycardia, bradycardia, dry mouth,
drowsiness and dizziness.
 Not used as frequently.
 Methyldopa (Aldomet) one of 1st drugs
widely used in controlling hypertension.
 Clonidine: 7 day transdermal patch.

Alpha adrenergic blockers
Block alpha adrenergic receptors to promote
vasodilation and decrease BP.
 Benefits: do not affect BS, lipids, or
respiratory function.
 Prazosin HCL (Minipress): selective
 Diuretic added to reduce edema.
 Side effects: hypotension, tachycardia, wt.
Gain, nausea, drowsiness, nasal congestion.

If taken with NTG can cause syncope.
 If taken with other hypertensive drugs or
alcohol can cause hypotension.
 Monitor for fluid retention.
 Encourage pt to decrease salt intake.
 Therapeutic effect takes 4 weeks.
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Beta-adrenergic blockers: decrease HR, BP,
CO, and force of contractions.
 Inderal: nonselective (beta1 and 2): many
side effects- bronchoconstriction.
 Metaprolol (Lopressor) cardioselective.
 Uses: cardiac dysrhythmias, hypertension,
tachycardia, and angina.
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Side effects
Beta-adrenergic blockers: bradycardia,
dizziness, hypotension, HA, mood changes.
 Nursing: Monitor vital signs, assess lung
sounds, instruct to avoid stopping med and
to avoid orthostatic hypotension.

Alpha/beta blockers
Causes vasodilation, decreased HR and
contractility of heart.
 Large doses increase airway resistancedecreased dosage necessary in asthma pts.
 Labetalol HCL (Trandate, Normadyne).
 May cause orthostatic hypotension,
palpitation and syncope.
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Diuretics
Thiazides
 Loop diuretics
 Osmotic diuretics
 Carbonic anhydrase inhibitors
 Potassium-sparing diuretics
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Diuretics
Purpose: to decrease BP and edema.
 Single or combination therapy.
 Produce diuresis by inhibiting Na and H2O
reabsorption in one or more segments of the
renal tubules.
 Diuretics that act closest to the glomeruli
have the greatest effect on Na loss.
 Potassium-wasting or sparing.
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Combination diuretics may promote both
K+ wasting and sparing.
 5 categories: thiazide/thiazide-like
 loop
 osmotic
 carbonic anhydrase inhibitor
 potassium-sparing
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Thiazides
Act on the distal convoluted tubule to
promote Na and H2O excretion and cause
vasodilation to decrease BP.
 Used in pts. c normal renal function.
 Not for immediate treatment.
 Increases BS. Monitor BS.
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Should be taken in am (long half-life) to
avoid nocturia.
 Can elevate lipids and uric acid.
 Can cause hypokalemia and hypocalcemia
(potential for digitalis toxicity).
 HCTZ is usually 1st one in this group
ordered. Inexpensive/ well tolerated.

Nursing implications
Assess vital signs, wt., urine output, labs,
BS, edema.
 Advise to take in am and c food.
 Instruct to include foods rich in K+ or may
need K+ supplement.
 Instruct pt. regarding potential for postural
hypotension.

Loop diuretics
Potent drugs that act on ascending loop of
Henle by inhibiting Cl transport of Na into
circulation.
 No effect on BS.
 Edecrin is most potent and rarely used.
 Bumex is more potent than Lasix.
 Can be used in pts.c renal disease.

Main side effects: fluid and electrolyte
imbalances, high uric acid, elevated lipids.
 Digitalis toxicity can result due to loss of
K+.
 Lasix: PO: onset of action 30-60”; IV- 5”.

Osmotic diuretics
Act by increasing concentration of plasma
and fluid in renal tubules, Na, Cl, K+, and
H2O loss.
 Used: to prevent kidney failure, decrease
ICP and IOP.
 Mannitol: IV potent K+ wasting diuretic
used in emergency.

Uses: to prevent acute renal failure
 decrease cerebral edema
 reduce IOP in narrow-angle glaucoma
 promoted diuresis in chemotherapy pts.

Carbonic anhydrase inhibitors
Act by blocking the action of enzyme
carbonic anhydrase which causes increased
Na, K+, and bicarbonate excretion.
 Potential for metabolic acidosis; high BS,
uric acid, and Ca levels.
 Uses: decrease IOP, for edema, seizures.
 Diamox PO or IV.

Potassium-sparing diuretics
Mild diuretic that is weaker than thiazides
and loop diuretics.
 K+ supplements should NOT be used.
 Act in collecting tubules and interfere c
NaK+ pump controlled by aldosterone.
 More effective if used c K+ wasting diuretic
(Aldactone and HCTZ).

Nursing implications
Side effects: hyperkalemia.
 Should not be taken c ACE inhibitor
because both spare K+.
 Instruct pt. to avoid foods rich in K+.
 Monitor for hyperkalemia: labs, EKG, vital
signs, nausea, diarrhea, ABD cramps.

Vasodilators
Potent antihypertensive drugs that cause
vasodilation.
 Peripheral edema results due to Na/H2O
retention: given c diuretic.
 Reflex tachycardia results due to
vasodilation: given c beta blocker.

Diazoxide (Hyperstat) and Sodium
nitroprusside (Nipride, Nitropress) used in
hypertensive emergency.
 Hydralazine HCL (Apresoline) used for
hypertension.

ACE Inhibitors
Act by inhibiting angiotensin-converting
enzyme,
 Inhibits formation of angiotensin II
(prevents vasoconstriction)
 Blocks release of aldosterone (Na retaining
hormone) resulting in Na and H2O
excretion.
 Used to treat hypertension or CHF.

African-Americans and elderly need a
diuretic added to achieve therapeutic
response.
 10 different drugs in this category.
 1st drug Captopril (Capoten).
 Most drugs end in “pril”.

Side effects: hypotension and hyperkalemia.
 Nursing implications: Should not be given c
Potassium-sparing diuretics or salt
substitutes containing potassium.
 Captopril is given 20” to 1 hr ac.

Angiotensin II blockers
New drugs similar to ACE inhibitors.
 Block angiotensin II from receptors.
 Cause vasodilation and decreased peripheral
resistance.
 Losartan (Cozaar).
 Can cause angioedema.
 Not as effective c African-Americans.

Calcium channel blockers
Decrease calcium levels and promote
vasodilation = decreased BP.
 Better BP response in African-Americans.
 Verapamil (Calan), Diltiazem (Cardizem),
Nifedipine (Procardia).
 Side effects: dizziness, bradycardia,
hypotension, HA.

Cardiac glycosides
3 effect on heart:
 1. Positive inotropic action (increases
myocardial contraction, CO).
 2. Negative chronotropic action (decreases
HR).
 3. Negative dromotropic action (decreases
conduction of heart cells).

Used to treat CHF, atrial flutter or atrial
fibrillation.
 Nursing: Check apical pulse for 1”. HOLD
if <60.
 Potassium-wasting diuretics and cortisone c
digoxin can result in hypokalemia and
digoxin toxicity.

Digitoxin (potent cardiac glycoside c long
half-life) vs Digoxin.
 Ensure that correct drug is given.
 Check serum digoxin levels.
 Normal level = 0.5- 2.0 ng/mL.
 Check serum K+ levels.

Instruct pt. to eat foods rich in K+.
 Monitor for signs of digoxin toxicity:
anorexia, nausea, vomiting, bradycardia,
cardiac dysrhythmias, visual disturbances.
 Monitor response to med: decreased HR,
decreased rales.
 Teach pt to take pulse and when to call MD.

Antianginal drugs
Nitrates
 Beta blockers
 Calcium channel blockers

Increase blood flow by increasing O2 flow
or decreasing O2 demand.
 Nitrates: relax coronary arteries and dilates
veins.
 Beta blockers: decreases HR/contractility to
decrease O2 demand.
 Calcium channel blockers: relax coronary
arteries, dilates arterioles, decrease
HR/contractility.

Nitrates
Nitroglycerin (NTG): 1st drug to treat
angina.
 Must be given SL, ointment, patch, IV.
 Give NTG 1 tab (0.4mg or gr1/150) SL q 5”
up to 3 doses until chest pain relieved. Call
MD if pain not relieved by the 3rd dose.
 Monitor BP and pulse.
 May have stinging/biting sensation.

Side effects: HA (most common), dizziness
or faintness.
 Nitrobid ointment not used as much due to
effect lasts only 6-8hrs.
 Transderm Nitro patch applied daily. Rotate
sites.
 Tylenol can be given for HA.
 Taper dose of ointment and patch.

Other nitrates
Isosorbide dinitrate (Isordil): PO, SL,
chewable, SR forms. Flushing may occur.
 Isosorbide mononitrate (Imdur): PO, SR.
 Tolerance to nitrates may develop. SR
Imdur form provides continued delivery and
decreases tolerance.

Nursing implications.
Have pt sit or lie down when giving initial
dose and when giving NTG.
 Monitor vital signs.
 Give sip of water prior to NTG to enhance
absorption.
 Instruct pt when to call MD.

Drugs for Circulatory disorders
Anticoagulants/antiplatelets
 Thrombolytics
 Antilipemics
 Peripheral vasodilators

Anticoagulants
Used to inhibit new clot formation in veins.
 Do NOT dissolve clots already formed.
 Heparin: binds c antithrombin III,
inactivates thrombin, inhibits conversion of
fibrinogen to fibrin.
 Must be given subcut for prophylaxis, IV to
treat acute thrombosis.

Monitor PTT.
 Monitor for bleeding.
 Protamine sulfate IV is antidote.
 Side effects: itching and burning.

Low molecular weight heparins
Lower risk of bleeding. Protamine sulfate is
antidote.
 More stable response. Can be started inpt.
and taught to give injections at home.
 PTT not needed.
 Binds to antithrombin III.
 Enoxaparin (Lovenox), dalteparin
(Fragmin).

Given subcut BID in ABD.
 Prefilled syringes.
 Instruct pt not to take other antiplatelet
drugs (ASA).

Coumadin
Long term oral anticoagulant.
 Inhibit hepatic synthesis of Vit K and
affecting clotting factors.
 Warfarin (Coumadin) most commonly used
form.
 Monitor PT/INR. (INR 2-3)
 Monitor for bleeding. (Vit K/blood or
platelets are given as antidote).

Antiplatelets
Prevents thrombosis in arteries by
suppressing platelet aggregation.
 Used to prevent MI or CVA.
 ASA, dipyridamole (Persantine), ticlopidine
(Ticlid).
 DC ASA one week prior to any surgery.

Thrombolytics
Used to dissolve clots by converting
plasminogen to plasma.
 Reduces tissue necrosis caused by blocked
artery.
 Used to treat coronary artery thrombi, DVT,
pulmonary embolism.
 5 drugs: ex. Streptokinase.

Must by given IV and within 4-6 hrs.
 Side effects: hemorrhage, allergic reaction.
 Contraindications: recent bleeding (CVA,
trauma, taking anticoagulants or ASA) and
severe hypertension.
 Antidote: aminocaproic acid (Amicar).
 Labs: CBC, PT, EKG. Monitor vitals and
for signs of bleeding.

Antilipemics
Lower abnormal lipid blood levels when
diet, exercise and smoking cessation are
ineffective.
 Resins: bind c bile acids in intestine.
Cholestyramine (Questran); Colestipol
(Colestid). Powder mixed c water or juice.
Side effects: constipation, peptic ulcer.
 Fibric acid derivatives: gemfibrozil (Lopid).

Nicotinic acid (Niacin, Vit B2): very
effective but has many side effects
(flushing, GI). Requires large doses. Careful
monitoring.
 Statins: inhibit enzyme HMG CoA
reductase in cholesterol synthesis in liver.
 Reduces cholesterol within 2 weeks.
 Names end in “statin”.

Ex: Lovastatin (Mevacor), atorvastatin
(Lipitor), simvastatin (Zocor), pravastatin
(Pravachol).
 Statins are contraindicated in liver disease.
 Nursing implications for all antilipemics:
 Give c water/meals. Monitor liver enzymes,
lipid levels, vital signs. Instruct pt. drug
therapy is lifetime commitment. Not a
replacement for diet/exercise.

Peripheral vasodilators
Increase blood flow to extremities and
promote vasodilation.
 Used in peripheral vascular disease.
 Ex. Vasodilan.
 Side effects: tachycardia, hypotension,
flushing, HA dizziness, GI.

Nursing implications
Assess vital signs and circulation to
extremities.
 Instruct pt. not to smoke, drink alcohol, or
use ASA like drugs without MD approval.
 Take med with meals.
