Download CV part 2

Nursing Care of Patients with Occlusive CV
& Cardiac Valvular Disorders
Lisa Pearson, RN MSN
Occlusive CV Disorders
• CV disorders are the leading cause of disability and
death in the US.
• One in three adults has cardiovascular disease (CVD).
• Coronary artery disease (CAD) results from the
progressive buildup of plaque in the coronary arteries.
• Education is important in preventing and treating
occlusive CV diseases.
Occlusive CV Disorders
• Arteriosclerosis: is part of the aging process in which the intimal
lining of the artery wall looses elasticity and weakens. May be called
hardening of the arteries.
• Atherosclerosis: is the formation of plaque (fatty fibrous plaque)
within the arterial wall. Thrombi can also form if the plaque ruptures
through the intimal layer. The lumen becomes increasingly narrow.
Over time, this build-up of plaque becomes calcified and hardened,
causing turbulence that damages cells and increases the build-up
within the vessels. This build-up can break off and lodge in another
vessel or can completely block an artery. Stenosis can occur.
Occlusive CV Disorders
• Arteriosclerosis and atherosclerosis are conditions that may
begin in early childhood and progress without symptoms through
adult life.
• Atherosclerosis is often noted when the patient has symptoms of
ischemic attack (TIA), and peripheral artery disease (PAD).
• Causes: risk factors can be divided into two categories: modifiable
and non-modifiable.
• Non-modifiable: include age, gender, ethnicity, and genetics.
• Modifiable: include diabetes, HTN, smoking, obesity, sedentary
lifestyle, infection, depression, hyperlipidemia, and excessive
alcohol intake.
Occlusive CV Disorders
• Signs and symptoms of atherosclerosis are usually not seen until
later stages of development when occlusion has occurred.
• S/S include: chest pain or dizziness caused by decreased blood
supply and oxygen to the heart.
• Other S/S may include: diaphoresis, SOB, nausea, weakness, and
fatigue. Reduced blood flow in the extremities is reflected by pallor
in the nail beds, a reddish purple color in the lower extremities,
thickened nails, dry skin, or loss of hair on the extremities.
Peripheral pulses may be diminished or absent. Skin temperature in
the extremities is cooler and may lead to capillary refill > 3 seconds.
Sometimes symptoms occur only with exertion or with rest in some
people.
Occlusive CV Disorders
• Atherosclerosis Summary: S/S usually seen in later stages:
Vascular: capillary refill > 3 seconds, diminished peripheral pulses,
dry skin, loss of hair on extremities, pallor in nail beds, thickened
nails, and leg cramps.
Cardiac: chest pain, diaphoresis, dizziness, fatigue, nausea, SOB,
and weakness.
• Diagnostic Tests: cholesterol, triglycerides, and arteriogram
• Therapeutic interventions: low fat, low cholesterol diet, smoking
cessation, increased exercise such as walking 30 minutes daily.
Occlusive CV Disorders
• Smoking causes vasoconstriction, which leads to angina pectoris
(chest pain), and cardiac dysrhythmias. The benefits of smoking
cessation are dramatic and almost immediate.
• LDLs are low-density lipoproteins which increase CAD risks.
• HDLs are high-density lipoproteins which are protective against
CAD.
• Remember: LDLs are Low Down Losers and HDLs are Happy Day
Living!
• Blood glucose levels play a role in atherosclerosis. Elevated BS may
increase risk for CAD.
Occlusive CV Disorders
• Exercise increases HDL levels and may also
lower insulin resistance and help with weight
loss. Over time, exercise also leads to the
development of collateral circulation which
allows blood to flow around occluded sites.
• Medications: lowering lipid levels is the major
treatment for atherosclerosis.
• Complications of atherosclerosis include: CAD,
MI, TIA, and stroke.
Occlusive CV Disorders
• Coronary artery disease (CAD) is a term applied to
obstructed blood flow through the coronary arteries to
the heart muscle.
• Primary cause of CAD is atherosclerosis.
• Acute coronary syndrome (ACS) is the continuum of
coronary artery disease and describes the
manifestations of CAD such as unstable angina and MI.
• If blood flow reduction resulting from CAD is severe and
prolonged, an MI can occur, causing irreversible
damage.
Lipid-Lowering Drugs
• Statins: are first-line drugs to reduce LDLs. The generic name
usually ends in statin such as Lipitor (atorbastatin). Mevacor
(lovastatin); Pravachol (pravastatin); Zocor (simvastatin).
• Statin S/E: impaired liver function, rhabdomyolysis (lethal
breakdown of skeletal muscle). Teach patient to report any muscle
pain immediately to MD. Monitor live function studies. May not be
able to take with grapefruit juice because will alter absorption.
• Fribrates: are used to reduce triglycerides. Examples: Tricor
(fenofibrate); Atromid (clofibrate); Lopid (gemfibrozil).
• Fribrates S/E: heartburn and gallstones. Teach patient to take 30
minutes before morning and evening meal. May increase the effects
of anticoagulants and hypoglycemia.
Lipid-Lowering Drugs
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Bile Acid Sequestrants: loser cholesterol by binding bile acids, so stored
cholesterol is used to make more bile acids. Examples: Colestid (colestipol);
WelChol (colesevelam HCl); and Questran (cholestyramine).
Bile Acid Sequestrants S/E: headache, heartburn, constipation, and gas.
Teach patients to add fruits and vegetables high in fiber to reduce
constipation and other GI effects. May interfere with absorption of digoxin,
thiazides, and beta blockers.
Niacin: prevents conversion of fats into very-low-density lipoproteins
(VLDLs). First anti-lipid agent used. Examples: Niacin (nicotinic acid);
Niaspan (extended-release niacin); Zetia (ezetimibe).
Niacin S/E: gastritis, gout, and flushing. Teach patient to take aspirin 30
minutes prior to taking drug to reduce flushing. Take with liquids (milk) and
meals to avoid GI upset. and to take other drugs 1 hour before or 4 hours
after. Use with diet, exercise, and smoking cessation therapy to lower lipids.
Percutaneous Transluminal Coronary Angioplasty
• PTCA: also called angioplasty, is a minimally invasive procedure
that helps reduce symptoms of CAD.
• It is a non-surgical alternative to CABG (coronary artery bypass
graft).
• Is performed in the catheterization laboratory under local
anesthesia.
• Involves the use of a balloon-tipped catheter to dilate the blocked
coronary artery.
• Patients usually recuperate quickly, usually walking the same day
and returning to work in 2 weeks.
• Works best when lesions are readily accessible, non-calcified, less
than 10 mm, discrete, and smoothly tapered.
• Possible complications include acute vessel closure and late restenosis.
PTCA
• With angioplasty, a guide catheter is threaded into the coronary
artery. Then a balloon-tipped catheter is inserted through the
occlusion and inflated and deflated to flatten the plaque until the
vessel opened.
• The symptoms of CAD are usually reduced, but the underlying
progression of atherosclerosis continues.
• Re-occlusion of the artery often occurs within a few months.
• Over time, angioplasty may need to be repeated.
• May be done with or without placement of stents, but it is often more
successful when stents are used.
Angioplasty
Coronary Atherectomy
• Is used to cut and remove plaque from atherosclerotic coronary
arteries. “roto-rooter”
• The catheter has a central rotating blade that shaves off the plaque
and contains it for removal and pathological analysis.
• Calcium channel blockers are given before the procedure to prevent
vasospasms from the vibrating cutter.
• Anti-platelet agent is given after the procedure to prevent clot
formation.
Coronary Artery Stents
• Stents are used to prevent closure of a coronary artery from an
atherosclerotic lesion.
• They may be used to hold the walls of a vessel open.
• Some stents are coated with a drug that’s slowly released to inhibit
further aggregation of fibrin or clots.
• Different types of material are used to make stents such as stainless
steel mesh, self-expanding or balloon expandable, or bioabsorbable
materials.
• Complications with stents include thrombosis, bleeding from anticoagulation, stent occlusion, or coronary artery dissection.
Medication with Stents
• After stent placement, patients are usually started on some type of
anti-platelet or anti-coagulation medication.
• Anti-platelet medications include Aspirin, Plavix, Ticlid, Lovenox
(enoxaparin). Effient (prasugrel).
• Anti-coagulation medications include Coumadin (warfarin) and
Arixtra.
Coronary Artery Bypass Graft
• CABG: coronary artery bypass graft is surgery to bypass an
occluded coronary artery using a donor vein or artery from the leg,
arm, or mammary.
• The donor vein/artery is sutured below the occluded area of the
coronary artery and connected to the aorta.
• The patient may have 1 or more vessels bypassed. (will be
documented as CABG x4 which means 4 vessels were bypassed).
• During the CABG surgery, the patient is placed on a heart-lung
bypass machine which circulates the blood in the body for the heart
and lungs.
• The patient is placed in ICU after the surgery and after a few days,
the patient is moved to a private room.
• Recovery time varies for each patient.
CABG
• After CABG surgery, patients are discharged home with instructions
to follow a specialized diet and exercise program.
• The patient will be on medications which will differ and be tailored to
the patient per the physician.
CABG
Acute Coronary Syndromes
• These are group of conditions that are caused by a lack of oxygen to
the heart muscle.
• These include angina (chest pain) and MI (myocardial
infarction/heart attack).
• There are several different types of angina which include stable
angina, variant angina, unstable angina, and silent ischemia.
Angina Pectoris
• Angina pectoris (chest pain) is a symptom of ischemia and is the
primary symptom of coronary artery disease and heart attack.
• Normally, when the heart needs more oxygen, the coronary arteries
dilate to carry more blood.
• However, with CAD, the narrowed vessels are unable to dilate and
supply the heart with this extra blood and oxygen.
• This inability to supply more blood and oxygen causes myocardial
ischemia and chest pain.
• Chest pain results from the ischemia but usually lasts only for a few
minutes, especially if activity is stopped.
• If adequate blood supply to the myocardium is restored with rest, no
myocardial damage usually occurs.
• Angina is not a disease, it is a symptom of CAD.
• Ischemia results from lack of oxygen and blood flow to the heart
muscle which leads to chest pain or angina.
Angina/Chest Pain
• Signs and symptoms are different in all patients.
• Patients often describe the pain as heaviness, tightness, squeezing,
vise-like, or crushing pain in the center of the chest.
• The pain may radiate down one or both arms, with pain the left arm
being more common.
• The pain may radiate into the shoulder, neck, jaw, or back.
• Patients may also describe heaviness in their arms or feeling of
impending doom.
• During episodes of pain, the patient may be pale, diaphoretic, or
dyspneic.
• The pain is usually brought on by exertion and subsides with rest.
• The pain may be relieved with a vasodilator medication such as
nitroglycerin (NTG).
Angina/Chest Pain
• Episodes of chest pain may increase in frequency and severity over
time.
• If patients do not heed this warning to stop their activity and rest,
they may be at risk for a heart attack or sudden death.
• ANY event that increases oxygen demand can cause an anginal
attack.
• Most often precipitating events include large meals, exercise, cold,
stimulant drugs such as cocaine or amphetamines, and emotional
tension.
• Women often exhibit atypical symptoms that should be recognized
as being cardiac related so that treatment is sought. (nausea ,
indigestion, fatigue, SOB, chest pain, jaw pain, and/or heartburn).
Stable Angina
• Stable angina is chest pain that occurs
with moderate exertion in a pattern that is
familiar to the patient.
• The pain is predictable and can usually be
managed with NTG and rest.
• Pain of stable angina usually subsides
when the activity is stopped.
Variant Angina (Prinzmetal’s Angina)
• Variant Angina or Prinzmetal’s Angina is similar
to the pain in stable angina except it has a
longer duration and may occur at rest.
• The pattern of occurrence is often cyclical, with
the pain presenting about the same time each
day.
• This type of angina is often caused by coronary
artery spasms and usually does not cause
damage to the myocardium.
Unstable Angina
• Unstable Angina occurs in patients with worsening CAD
and is noted by its changing pattern.
• Rest does not decrease the chest pain.
• Pain may even occur when the patient is at rest.
• Episodes of chest pain increase with frequency and
severity placing patient at risk for myocardial damage or
sudden death.
• Symptoms usually occur when an artery is narrowed by
at least 60-70%.
Silent Ischemia
• Many people may have myocardial ischemia
without chest pain or symptoms of angina.
• This is called silent ischemia.
• Ischemia with or without pain usually has the
same prognosis.
• The older adult and people with HTN or DM are
most often noted to have silent ischemia.
Diagnostic Testing for Acute Coronary Syndromes
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ECG/EKG
Stress tests
Echo
Cardiac Catheterizations
Angioplasty
Therapeutic Interventions
• Treatment for angina is directed at relieving and preventing anginal
episodes that could lead to MI.
• Weigh reduction
• Low-fat, low-cholesterol diet
• Stress reduction
• Medications
• Three major groups of medications used for angina are vasodilators,
calcium channel blockers, and beta blockers.
• Patients with unstable angina may be given the Fab Four
medications which include anti-platelets, statins, ACE inhibitors, and
beta blockers.
Vasodilators
• Nitroglycerin (NTG) is the drug of choice for chest pain (angina).
• Nitrates dilate the coronary arteries to increase oxygen to the
myocardium and dilate peripheral vessels so the heart does not
have to work as hard.
• NTG can be given sublingual, oral, transdermal, IV, or as a lingual
spray.
• NTG may relieve chest pain within 1-2 minutes.
• When giving NTG sublingual, 1 tab may be given every 5 minutes x
3 tabs.
• If chest pain is not relieved after 3rd tablet, then 911 should be
called; however, new guidelines suggest calling 911 if the first tab
does not relieve chest pain after 5 minutes and symptoms of MI are
occurring.
Vasodilators
• NTG tablets used sublingual are stored in a small, dark brown glass
bottle with a screw-top lid.
• The lid should be on tightly and should be stored at room
temperature.
• Patients should replace the medication every 6 months.
• Patients should NEVER carry the bottle in their pockets (chest or
pants) because the tablets could come out, melt, and be absorbed
through the skin.
• Patients who take any type of vasodilator (nitrates) should not take
Viagra, Cialis, or Levitra (for erectile dysfunction) because these
medications dilate blood vessels and may cause a significant drop in
blood pressure if used together.
Vasodilators
• Long-acting nitrates are used to prevent chest pain rather than treat
acute pain, and can be given orally, in ointment, or by transdermal
patches.
• A problem with long-acting nitrates is the development of a tolerance
to the medication.
• To prevent tolerance, the patch or ointment is usually removed at
bedtime and reapplied in the morning, giving the patient an 8-12
hours nitrate-free period.
• Headaches may be experienced with nitrates are first begun.
• This side effect usually subsides after a week or two.
• Another side effect is hypotension due to the vasodilatation of
vessels.
Vasodilators
• Sublingual: NTG, Nitrostat, NitroQuick
S/E: Hypotension, H/A. Contraindicated in head trauma,
hypotension, and uncorrected hypovolemia.
• Oral/Sublingual: Isordil (isosorbide dinitrate), ISMO (isosorbide
monitrate).
S/E: Hypotension, transient flushing of face and neck, dizziness if
standing, orthostatic hypotension, N/V, restlessness.
• Transdermal: NTG: Transderm Nitro, Nitro-Bid, NTG patch (NitroDur and Nitrek).
S/E: Same as oral/sublingual above.
Calcium Channel Blockers
• These drugs dilate main coronary arteries, increasing the myocardial
oxygen supply.
• These drugs are also used to decrease systolic and diastolic blood
pressures and to slow the heart rate.
• Are commonly given in conjunction with other vasodilators and beta
blockers.
• They are slow acting and are ineffective in relieving acute anginal
attacks.
• Side effects are usually mild and include constipation, fluid retention,
headache, and dizziness.
• Many of the calcium channel blocker generic medication names end
with –pine.
Calcium Channel Blockers
• Oral: Cardizem (diltiazem), Norvasc (amlodipine), Procardia
(nifedipine)
• Oral/IV: Verapamil (Calan, Isoptin)
• S/E for all calcium channel blockers include: H/A, peripheral edema,
dysrhythmias, flushing, dizziness, atrioventricular blocks, nausea,
and constipation.
• Nursing considerations with calcium channel blockers: assess apical
pulse and BP. If systolic BP is < 90 or heart rate < 60, call physician.
Grapefruit juice may alter absorption with Norvasc and Cardizem.
Also, Verapamil and Calan are not removed by hemodialysis.
• Procardia (nifedipine) and Verapamil (Calan, Isoptin) are potent
inhibitors of coronary artery spasms and are used to treat variant
(Prinzmetal’s) angina.
Beta Blockers
• Beta blockers decrease heart rate and lower blood pressure.
• Helps decrease workload of the heart to help prevent anginal
attacks.
• Should be used with caution in patients with any degree of heart
failure because it makes heart failure worse.
• Beta blockers are not effective for coronary artery spasms.
• The generic names of these medications usually end with –olol.
Beta Blockers
• Oral: Inderal (propranolol), Tenormin (atenolol).
• Oral/IV: Lopressor,Toprol XL (metoprolol).
• S/E include cold extremities, constipation, diarrhea, diaphoresis,
dizziness, fatigue, and nausea.
• Abrupt withdrawal may result in diaphoresis, palpitations, H/A, and
tremors. Do not stop medication abruptly.
• Hypoglycemia may occur in patients with previously controlled
diabetes.
• Patients should not get up quickly and should avoid salt and alcohol.
• Assess apical pulse and BP. Hold medication and call physician if
heart rate is < 60 or systolic BP < 90.
Angiotensin-Converting Enzyme Inhibitors
• ACEIs: block production of angiotension II, which is a potent
vasoconstrictor.
• This allows reduction of peripheral arterial resistance, which lowers
BP and increases cardiac output.
• Some patients may develop a cough and if this occurs, they should
notify their physician so that the medication can be changed.
• Many of these medication generic names end with –pril.
ACEIs
• Oral: Capoten (captopril); Prinivil, Zestril (lisinopril); Altace (rimipril).
• S/E: persistent cough in 20% of patients. Hyperkalemia may develop
in patients with DM or renal impairment.
• Angioedema, swelling of face and lips may occur.
• Assess baseline BP before each dose.
• Give 1 hour before meals; food delays absorption.
Statins
• Helps lower cholesterol levels and inflammation of artery walls.
• We have already discussed statins.
• Always remember to teach the patient to report any muscle
weakness or muscle pain because these are serious signs and
symptoms of a rare S/E known as rhabdomyolisis.
• Patients should also have their liver function lab work routinely done
to make sure liver is functioning optimally while on statins.
Anti-platelets
• Aspirin, Plavix, and Ticlid are commonly used anti-platelets that help
prevent CV events. Effient 10mg 1 po daily.
• Aspirin is the one most often prescribed and may be used in
combination with another anti-platelet.
• Patients with unstable angina, stent placement, or heart attack are
given anti-platelets.
• S/E include increased risk of bleeding including hemorrhagic stroke.
• Enteric coated Aspirin may be given for daily dosing (Ecotrin).
Myocardial Infarction
• MI or heart attack results in the death of heart muscle and the
affected myocardial cells in the heart are permanently destroyed.
• MI occurs from a partial or complete blockage of a coronary artery,
which decreases the blood supply to the cells of the heart supplied
by the blocked coronary artery.
• The extent of the cardiac damage varies depending on the location
and amount of blockage in the coronary artery.
• When a patient has an MI, part of the heart muscle no longer
functions as it should.
• Cardiac conduction, blood flow, and function can be dramatically
altered by an MI.
• Typically, MI patients are usually men over 40 with atherosclerosis
development; can occur at any age in men or women.
• Women who smoke or use oral contraceptives are at greater risk for
MI.
MI S/S
• Chest pain is a classic symptom of MI.
• The pain begins suddenly and continues without relief with rest or
NTG.
• Patient may describe pain in the center of the chest as crushing,
vise-like, or as if an elephant is standing on chest.
• Pain may radiate to the back, one or both arms and shoulders, neck,
or jaw.
• Pain may imitate indigestion or a gallbladder attack with abdominal
pain and vomiting.
• Other classic symptoms include SOB, dizziness, nausea, and
sweating.
MI S/S
• When listening to lung sounds, crackles or wheezing may be heard.
• The pulse may be rapid or irregular, and an extra heart sound (S3 or
S4) may be present which can mean ventricular failure is imminent.
• Many people deny or fail to recognize they are having an MI
because they may relate the pain or symptoms as some they have
experienced in the past with other mild conditions such as
indigestion.
• Many MI patients state that the symptoms they experienced were
not what they expected with an MI.
• Many may wait to seek treatment 2-24 hours.
• The first hour after symptom onset is crucial for seeking the newer
reperfusion treatments that restore blood flow, minimize tissue
damage, and save lives.
Complications of MI
• Dysrhythmias: PVCs, V- tach, V-fib, and heart block.
• Cardiogenic shock: decreased BP, increased HR, diaphoresis (cold,
clammy, gray skin).
• Heart failure/pulmonary edema: dizziness, orthopnea, weight gain,
edema, enlarged liver, jugular venous distention, crackles.
• Emboli: dependent on location of emboli.
• Ventricular aneurysms, rupture of muscles or valves of the heart,
septal rupture, pseudoaneurysm: signs of cardiogenic shock, death.
• Pericarditis (inflammation of the heart muscle): chest pain, increased
with movement, deep inspiration, or cough; pericardial friction rub
(fine grating sound).
Women and MIs
• Heart disease remains the leading cause of death in women in the
U.S.
• African American women are more likely that Caucasian women to
develop heart disease.
• Atypical symptoms reported by women may include: extreme
fatigue, epigastric pain, abdominal pain, jaw pain, indigestion, N/V,
SOB, or cramping in the chest. Discomfort/pain between shoulder
blades.
• More than 50% of women with MI noted symptoms a month before
an acute MI such as unusual fatigue, sleep disturbances, and SOB.
ECG Changes during MI
Treatment of MI
• ECG/EKG
• Lab work including cardiac enzymes (Troponin I, CK, CK-MB, PT,
PTT).
• Thrombolytic or heparin therapy
• Oxygen
• Medication: anti-platelets, statins, ACEIs, and beta blockers may be
used. Analgesics, vasodilators, and thrombolytics.
• Keep patient on bed rest with a bedside commode for BM to
decrease myocardial oxygen demand. Activity is advanced gradually
as tolerated.
• Avoid bumping bed or loud noises which could “scare” patient and
cause irregular heart rhythm.
Treatment of MI
• Blood sugar levels within range of 70-100 helps reduce mortality for
critically ill patients.
• Diet and weight loss
• Smoking cessation
• Check VS as ordered, cardiac monitoring is used continuously, and
follow any physician orders such as medication administration,
preparing patient for any other tests such as heart catheterization,
stents, cardiac surgery, etc.
Medications for MI Treatment
• Anti-platelets: Aspirin (chew is MI symptoms occur) should be given
as soon as ACS or MI is suspected.
• Analgesics: Morphine Sulfate (MSO4) is given slow IV push by RN.
May cause respiratory depression, hypotension, and bradycardia.
Monitor VS for 10 minutes after IV administration. Always check
respirations, heart rate, and BP prior to and after administration.
• Vasodilators: NTG, Isordil, Imdur.
• Thrombolytics: Ativase (alteplase); t-PA (tissue plasminogen
activator); Eminase (anistreplase); Retavase (reteplase); Streptase
(streptokinase). Most effective when given in the first 6 hours of
coronary event. Avoid VP after administration. S/E include bleeding,
stroke, dysrhythmias which may occur when blood flow is reestablished.
Medications for MI Treatment
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Anti-coagulants: heparin IV or SC
Beta Blockers
ACEIs
Statins
Anti- dysrhythmics bolus or infusion: Lidocaine IV. Helps control
depolarization.
Antiemetics
Anxiolytics (control anxiety)
Antacids
Stool softeners
Interventions
• Patient Education
• Cardiac Rehab and Exercise: to improve cardiac function and assist
the patient to return to normal a life as possible.
Peripheral Vascular System
• The peripheral vascular system is venous (veins) and arterial
(arteries).
• Peripheral Vascular Disease (PVD) is most common in older adults
or diabetics.
• PVD is a serious disease in which the nurse must be knowledgeable
in order to help prevent any further complications.
• The nurse will need to be aware of how to distinguish between
venous and arterial disease.
Arterial Thrombosis and Embolism
• Acute arterial occlusions are often sudden and dramatic.
• Most commonly found in the lower extremity; however, occlusions
may occur in the upper extremity.
• A blot clot (thrombi/thrombus) forms and sticks the artery wall due to
arterial injury, sluggish blood flow, or even from plaque formation.
• Arterial blood clots can also be caused from polycythemia (too many
RBCs), dehydration, and repeated arterial needle sticks (frequent
ABGs).
• A blood clot can break off (thrombus) and this clot can travel through
the arterial blood supply and get stuck in a smaller area of the
arterial blood flow.
• If the clot gets stuck, it can cause an occlusion which cuts off blood
supply below the clot.
Arterial Thrombosis and Embolism
• Some causes of arterial embolism include dysrhythmias (atrial
fibrillation), prosthetic heart valves, and rheumatic heart disease.
• Signs and Symptoms of acute arterial occlusion are usually abrupt
with onset (come on in a hurry).
• Six clinical signs of acute arterial occlusion (the 6 Ps) include: pain,
pallor, pulselessness, paresthesia (numbness), paralysis, and
poikilothermia (temperature).
• The patient experiences pain, numbness, and decreased movement
in the extremity, which is pale and without pulses distal to the
occlusion.
• The extremity feels cold because blood provides warmth.
• Treatment must be immediate to prevent ischemia which may
progress to tissue necrosis (death of tissue) and gangrene which
may develop within a few hours.
Arterial Thrombosis and Embolism
• If the patient has a history of chronic arterial insufficiency, the s/s
may be slow because of the development of collateral circulation.
• S/S depend on the artery occluded, the tissue supplied by that
artery, and whether collateral circulation is present.
• Early treatment is needed to protect and save the affected limb.
• Anticoagulant therapy of IV Heparin is the treatment of choice to
prevent further clotting. (Heparin does not effect existing clots).
• A Heparin IV bolus (5000 IU) is given followed by an IV infusion as
ordered which may last several days.
• Patient will have daily PTT (APTT) lab values done to measure
therapeutic levels while on Heparin.
• These lab results will determine whether the Heparin needs to be
increased or decreased. (may be in Heparin sliding scale).
Arterial Thrombosis and Embolism
• Once the patient has been on Heparin IV therapy for 3-7 days,
warfarin (Coumadin) therapy may be ordered.
• Coumadin is an oral anticoagulant and takes 3-5 days to reach
therapeutic levels.
• Both Heparin and Coumadin will be given until the Coumadin
therapeutic level is achieved.
• PT w/ INR (2-3 is therapeutic) is a lab test that determines the
therapeutic effects of Coumadin. (PT w/ INR is ordered daily)
• The results of the PT w/ INR determines if the Coumadin dosage will
need to be increased, decreased, or maintained.
• Coumadin is usually given around 5pm every day so not to interfere
with the PT w/ INR lab results which are usually drawn early in the
morning.
Arterial Thrombosis and Embolism
• S/E of Coumadin include: increased bruising and bleeding.
• Nursing Considerations with Coumadin include: using only an
electric razor to shave, cut nails straight across and gently file nails
(only a nurse should cut nails). Patient should avoid or limit intake of
green, leafy vegetables due to the vitamin K. Patients should have
lab work checked routinely as ordered by MD.
• Patients with severe occlusions, especially if risk of limb loss is
imminent, surgery or thrombolytic agents are used to save the
extremity.
Peripheral Arterial Disease
• Peripheral Arterial Disease (PAD): is a disorder of the arterial
circulation usually caused by chronic, progressive narrowing of
arterial vessels that lead to obstruction or occlusion.
• PAD usually affects the lower extremities.
• Atherosclerosis is the leading cause of occlusive disease.
• PAD is either organic or functional in nature.
• Organic disease is caused by structural changes from plaque or
inflammation in the blood vessels.
• Functional disease is a short-term localized spasm in the blood
vessel (Raynaud’s).
Peripheral Arterial Disease
• As we have learned, arteries carry oxygen-rich blood to the body.
• If at any time the arterial blood flow is slowed or disrupted, damage
or some form of death of tissue may occur. (blood clots)
• Remember, PAD is from narrowing of arteries or spasms of arteries.
• S/S of PAD may not be present or experienced until late in the
disease progression.
• S/S of PAD include: pain in the calves related to activity or exercise
which is called intermittent claudication (common symptom of
occlusive disease).
• As ischemia increases, the muscle develops a cramping-type pain
that subsides when activity is stopped; however, as PAD
progresses, the pain may be present even at rest.
Peripheral Arterial Disease
• S/S of PAD also include: skin color changes such as pale extremity
when leg is elevated.
• If the extremity is in a dependent position (dangling down), it may be
reddish-purple or cyanotic (blue).
• The extremity may be cool to touch, hair loss on the lower calf,
ankle, and foot may be present.
• The skin of the affected extremity may be dry, flaky, scaly, pale, or
mottled.
• Toenails may be thickened.
• Diminished or absent arterial pulses (as the nurse, you should
assess pulses in all extremities).
• Loss of circulation leads to tissue death and gangrene.
Peripheral Arterial Disease
• Treatment of PAD includes medication and diet.
• Surgical interventions such as endarterectomy to remove
atherosclerotic lesions or grafting to bypass the occluded area may
be performed.
• Diet includes low fat, low cholesterol, and low calorie (if patient is
overweight).
• Teach patient to avoid red meats, fried foods, whole milk, and
cheese and foods high in cholesterol such as egg yolks, organ
meats, animal fats, and shellfish.
• Medications such as Trental and Pletal can be ordered for patients
with intermittent claudication because the drugs make red blood
cells more flexible to improve perfusion. These meds should be
taken with food to minimize S/E of GI upset.
Raynaud’s Disease
• Raynaud’s Disease is a the vasoconstriction of small arteries
causing ischemia due to exposure to cold and stress.
• It primarily affects the hands but can also occur in the feet, ears, or
nose.
• Diagnosis is based on patient experiencing intermittent attacks of
ischemia for at least 2 years.
• The disease is characterized by spasms of small arteries in the
digits which prevent arterial blood from perfusing the fingertips and
sometimes the toes.
• The spasms may be unilateral, in one or two digits, but most
commonly occur bilaterally and in all digits.
• May be seen with patients diagnosed with RA, scleroderma, and
lupus.
Raynaud’s Disease
• S/S include vascular spasms of the hands when exposed to cold
resulting in ischemic pain.
• After a few minutes of ischemia, hyperemia occurs which is intense
reddening of the hands from dilation of all the vessels of the hands
and pain becomes more intense at this time.
• Various phases may be experienced such as blanching of the skin,
pain, and reddening of the skin.
• The disease may progress over time with the vessels remaining
constricted and the severe decrease in blood flow can lead to
fingers becoming gangrenous and necrotic.
Raynaud’s Disease
• Teach the patient to keep hands warm by wearing gloves when
going outside, using refrigerator, or working with cold foods.
• Teach patients to avoid smoking, alcohol, and caffeine which may
contribute to vasoconstriction and reduce stress levels.
• Teach patient to place hands in warm water when attack occurs
which may help decrease the vasospasm.
• Vasodilator medication may be ordered such as nifedipine or longacting nitrates.
• REMEMBER: Raynaud’s = Red (digits fingers/toes, ears, nose).
Buerger’s Disease
• Buerger’s Disease is a recurring inflammation of small and medium
arteries and veins of the lower extremities.
• Usually the result of occlusion of the vessels by clot formation.
• Cause is unknown but may be contributed by smoking; encourage
patients to stop smoking.
• The inflammation and irritation of the vessels contribute to the
development of vasospasms which lead to an obstruction in blood
flow.
• The tissues become hypoxic, and the development of ischemic pain
can occur; if left untreated, the ischemia can lead to ulceration and
gangrene.
Buerger’s Disease
• Intermittent claudication and other symptoms of occlusive disease
are common.
• Other symptoms include numbness or decreased sensation and
cool extremities.
• Lower extremities may be red or cyanotic when in a dependent
position, and pulses may be diminished.
• Medication such as calcium channel blockers (Cardizem) promotes
vasodilatation and may help with intermittent claudication.
• As the nurse, careful inspection of the lower extremities for signs of
breakdown is important so early treatment can begin.
• Remember: Buerger’s = RED or BLUE (lower extremities).
Care of Patient with Peripheral Arterial Disorders
• Monitoring peripheral circulation is most important.
• Assess pulses, capillary refill, temperature, color, and presence of
edema.
• Report absent pulses IMMEDIATELY!
• Shiny and hairless skin points to chronic diminished blood flow.
• Assess for any skin lesions and ulcerations and report any findings
ASAP!
• DO NOT EVER: compress an arterial wound because the
compression will further impede circulation! (ACE wraps, UNNA
boots, etc.)
Arterial Ulcers
Arterial Ulcers
Arterial Ulcers
Arterial Ulcers
Aneurysms
• An aneurysm is a bulging, ballooning, or dilation at a weakened
point of an artery (time bomb).
• Cause is unknown, but anything that weakens the artery wall or
causes loss of elasticity in the artery can cause an aneurysm.
• Risk factors include: HTN, atherosclerosis, smoking, trauma, and
congenital abnormalities and also may be linked to heredity.
• May occur at any part of the body; however, abdominal aortic
aneurysm (AAA) is most common.
• AAA are often silent if less than 4 cm.
• Most people do not know they have AAA.
• Survival improves with elective surgery rather than emergency
surgery.
Aneurysms
A- Fusiform (entire circumference is dilated)
B- Saccular (one side is dilated)
C- Dissecting (tear in the inner layer causes a cavity to form between layers
and fill with blood)
Aneurysms
• S/S are few if any; however, as the AAA grows, symptoms may
develop such as back or flank pain which is the classic symptom.
• The pain is caused by the aneurysm pressing against nerves of the
vertebrae.
• Patient may complain of abdominal pain, feeling of fullness, or
nausea caused by pressure on the intestines.
• Position change may temporarily relieve symptoms.
• May be a pulsating mass in the abdomen which is found on routine
physical or x-ray.
Aneurysms
• Severe, sudden back, flank, or abdominal pain and a pulsating
abdominal mass can indicate that the aneurysm may be about to
rupture.
• With rupture, the patient’s BP may drop and signs of shock may be
present; immediate surgery is needed with the mortality rate very
high.
Aneurysms
Therapeutic Interventions
• Treatment includes medication to maintain lower BP (HTN or higher
BP may contribute to rupture).
• MD will monitor aneurysm periodically; aneurysm larger than 5 cm
requires surgical repair.
• Nursing should carefully monitor patients such as VS.
• Teach patients importance of taking medications to control BP,
stress control measures, and avoid lifting heavy objects before and
after surgery.
Varicose Veins
Varicose Veins
Spider Veins
Spider Veins
Varicose Veins
• Varicose veins are elongated, twisted-like,
dilated veins.
• Exact cause is unknown; however, a
person may have a family history.
• Varicose veins are classified into primary
and secondary varicosities.
Primary Varicose Veins
• Primary varicosities are believed to be caused
by a structural defect in the vessel wall.
• The defect causes vein dilation and may lead to
incompetent venous valves (valves help prevent
blood from refluxing).
• Any reflux can lead to further dilation of vessel.
• Superficial veins are the vessels most often
involved in primary varicosities.
Secondary Varicose Veins
• Secondary varicosities are caused by an
acquired or congenital pathological condition of
the deep venous system.
• The superficial veins and the collateral veins
dilate which results in decreased blood return to
the heart.
• If the blood is not returned adequately from the
legs to the heart, the blood will pool (stasis) in
the deep venous system and cause blood to be
pushed out into the collateral veins.
Causes of Varicose Veins
• Family history of defects in the walls of the
vessels.
• Prolonged standing
• Pregnancy
• Obesity
• Incompetent valves with the veins can lead to
blockage of blood flow which leads to dilated
veins.
S/S of Varicose Veins
• Most common is the disfigurement of the lower
extremity with primary varicosities.
• Dull pain after prolonged standing (may be
relieved with walking or elevation) and the pain
may be more severe with secondary varicosities.
• Edema
• Ulceration
Varicose Veins
Therapeutic Interventions
• Primary goals are to improve circulation, relieve pain, and avoid
complications.
• Treatment is usually not indicated if the problem is only cosmetic.
• Reduction of factors that contribute to varicose veins (avoid standing
for long periods, not cross legs too long).
• Wear elastic compression stockings (support hose, Jobe stockings).
• May have injection sclerotherapy or laser treatment to treat
superficial veins.
• Radiofrequency ablation stripping of the veins to remove
incompetent valves.
Venous Insufficiency
• Chronic condition from damaged or aging valves
which causes poor blood return to the heart and
leads to pooling of blood in the lower extremities
and can lead to venous stasis ulcers.
• Venous stasis ulcers are the end result of
chronic venous insufficiency.
• These types of ulcers can be compressed.
Venous Stasis Ulcers
Venous Stasis Ulcers
Venous Stasis Ulcers
Venous Stasis Ulcers
• With these types of ulcers, there may be edema and a brownish
discoloration of the leg and foot with the surrounding skin hardened
and leathery in appearance.
• The brownish color is caused by the release of RBCs into the tissue
when veins rupture. (iron in the RBCs cause the color and does not
go away).
• Stasis ulcers develop from the increased pressure and rupture of
small veins.
• Signs of skin breakdown are most commonly seen at the medial
malleolus of the ankle.
• The types of ulcers are difficult to cure and can affect the patient’s
quality of life. (BS must maintain 180 or < for any type of effective
wound healing to occur for any type of wound).
Treatment of Venous Stasis Ulcers
• Focus is to decrease edema and heal the skin ulcers.
• Compression wraps (elastic stockings, UNNA boots, ACE wraps,
Profore) are used to decrease edema).
• When using a compression wrap, always start wrapping from toes
up the leg.
• Do not wrap too tight around top of leg which may impede
circulation.
• May re-wrap BID, QD, QOD, or even 1-2 x week depending on
dressing ordered.
Treatment of Venous Stasis Ulcers
• Elevate legs and feet at or above level of heart to help
decrease edema and promote blood return to the heart
(prop on pillows from knee to ankle…recliners are not
appropriate).
• Avoid dependent position for too long (sitting, standing,
crossing legs) and avoid too tight clothing (knee highs).
• May culture wounds (clean first with NS, collect culture,
then dress wound). Collect culture before antibiotics
begin.
• May have skin grafting if ulcers are severe or do not
heal.
Nursing Considerations for Venous Disorders
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•
•
•
•
•
Assess legs, feet, toes, etc.
Assess pulses
Assess for edema
Assess BS
Assess pain
Assess for any contributing factors
Vascular Surgery
• Embolectomy-removal of embolus.
• Thrombectomy- removal of thrombus.
• Endarterectomy- removal of arteriosclerotic plaques
(usually carotid artery but can be done on peripheral
arteries).
• Vascular Bypasses and Grafts- uses a vein to bypass an
occluded arterial area.
• Stents
• Angioplasty
Aortic-Femoral Bypass
Complications of Vascular Surgery
• Bleeding and hemorrhage
• Drainage is expected (small with venous and large with
arterial)
• Drains are used (J-P drains) to prevent swelling, pooling,
and hematomas.
• Apply manual pressure if bleeding/hemorrhage occurs
and notify MD ASAP.
• Re-occlusion is a risk due to thrombi/emboli.
Post-Op Care
• Neurovascular checks Q1-4 hours (capillary refill, pulses,
numbness, pain, temp. of skin, color, etc.). Loss of pulse
may indicate occlusion (may use doppler for pulses).
• Assess incision for hematoma, bruising, drainage,
redness, etc.
• Assess abdominal girth (tape measure all around
abdomen); increase in size may indicate abdominal
hemorrhage.
• Report any abdominal changes ASAP to MD.
• Monitor lab work (CBC, INR, etc.)
• I/O
Lymphatic System
• The lymphatic system returns fluid from other
tissues in the body to the bloodstream.
• It is a pump less system with one-way valves
that return fluid to the heart.
• Any interruption in the flow of lymph results in
edema.
Lymphangitis
• This is a bacterial infection of the lymphatic channels usually in the
arms or legs commonly caused by staphylococcus or streptococcus
bacteria.
• The infection can cause sepsis and be fatal.
• S/S include painful red streaks in the extremity, fever and chills may
be noted, and lymph nodes in the area of infection may be enlarged
and painful.
• Treatment is with a broad-spectrum antibiotic, use of heat on the
extremity, and elevation may help improve circulation.
• Pneumatic pressure devices may be used to help alleviate
congestion.
Lymphangitis
Lymphatic Disorders
Lymphatic Disorders
Pneumatic Pressure Device
Chapter 23
• Nursing Care of Patients
with Cardiac Valvular
Disorders
Opening of stenosed and insufficient valves
compared to a normal valve
Valvular Disorders
• There are four valves in the heart: tricuspid, pulmonic, mitral
(bicuspid), and aortic.
• Chordae tendineae and papillary muscles are attachment structures
for both the mitral and tricuspid valves and they ensure the valves
close tightly. (pulmonic and aortic valves do not have these).
• Damage to any of the four valves or their surrounding structures can
result in abnormal valvular function.
• Valves on the left side of the heart (mitral and aortic) are the most
commonly affected.
• Blood flow in the heart can be hindered if the valve is narrowed, or
stenosed, and does not open completely.
• If the valve does not close completely, blood backs up (regurgitation
or insufficiency.
• Abnormal blood flow increases workload of heart and increases
pressure in the affected heart chamber.
Five Valvular Disorders
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•
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Mitral Valve Prolapse
Mitral Stenosis
Mitral Regurgitation
Aortic Stenosis
Aortic Regurgitation
Mitral Valve Prolapse
• Normally when the left ventricle contracts, the mitral valve is closed.
• With mitral valve prolapse (MVP), one or both of the flaps of the
mitral valve bulges backward into the left atrium when the left
ventricle contracts.
• The bulging of one or both of the flaps of the mitral valve is caused
from a defect in the chordae tendineae (which secures the valve to
the heart wall) or one of the valve flaps is too large.
• If the mitral valve flaps do not fit together, then mitral regurgitation
can occur.
• MVP cause is unknown; however, it can be related to heredity,
infections that damaged the mitral valve, ischemic heart disease, or
cardiomyopathy.
• MVP is the most common form of valvular heart disease.
Mitral Valve Prolapse
• The degree of MVP may be mild or have a severity
range from a murmur to chordae tendineae rupture with
mitral regurgitation.
• S/S of MVP: may be none or if s/s do occur, they may
include atypical chest pain not related to exertion,
dysrhythmias such as PVCs causing palpitations,
dizziness, or syncope, fatigue, dyspnea, or anxiety.
• Emboli and infective endocarditis with mitral regurgitation
are concerns.
Cardiac Valvular Disorders
Diagnostic Tests
• History and physical exam
• ECG: may be normal; however, may have
inverted T wave
• Chest X-Ray (CXR)
• Echo: will show any prolapse or regurgitation
• Cardiac Catheterization: can also detect bulging
flaps
Mitral Valve Prolapse
Interventions
• No treatment unless symptoms are present.
• Severity of s/s determine treatment.
• Healthy lifestyle with good diet, exercise, stress management, and
avoidance of stimulants and caffeine can help prevent s/s.
• Medications: beta blockers for rapid heart rate and relief of chest
pain.
• Medications: anti-dysrhythmics
• Surgical repair or replacement of valve may be done for severe
cases.
• Prophylactic antibiotic therapy before any surgeries and/or dental
care to help prevent endocarditis.
• Medications: aspirin or anti-coagulants may be ordered to help
prevent emboli.
Mitral Valve Prolapse
Stenosis versus Regurgitation
• Stenosis: a valve that does not OPEN fully (stenosed/narrowed)
which does not allow a chamber to empty normally causing blood to
build up in that chamber.
• Example of stenosis: mitral stenosis does not allow the left atrium to
empty easily, so blood builds up in the left atrium.
• Regurgitation: (insufficient/insufficiency): a valve that does not
CLOSE fully allows blood to flow back into the chamber that
emptied. Blood builds up in that chamber as a result.
• Example of regurgitation: mitral insufficiency allows blood to
backflow from the left ventricle into the left atrium after the left atrium
has emptied, so blood builds up in the left atrium.
Mitral Valve Stenosis and Mitral Valve
Regurgitation
Aortic Valve Regurgitation and Aortic Valve
Stenosis
Mitral Stenosis
• Mitral stenosis results from thickening of the mitral valve flaps and
shortening of the chordae tendineae, causing narrowing of the valve
opening.
• This narrowed opening obstructs blood flow from the left atrium into
the left ventricle.
• As a result of the obstructed blood flow, the blood volume in the left
atrium increases, pressure increases, and the left atrium enlarges.
• With the left atrium having a higher blood volume, the excess blood
volume begins to back-up into the pulmonary circulation (lungs), and
continues to back-up into the right ventricle causing the right
ventricle to enlarge.
• Eventually, the right ventricle begins to fail and the snowball effect
happens…reduced blood volume delivered to lungs, left side of
heart, and results in decreased cardiac output.
Mitral Stenosis
• Older patients with mitral stenosis usually have calcification and
fibrosis of the mitral valve flaps.
• Major cause of mitral stenosis is rheumatic fever (may take 40 years
to develop s/s after).
• S/S of mitral stenosis includes: none (asymptomatic), a click or lowpitched murmur may be heard, pulmonary symptoms (SOB,
crackles, etc.), exertional dyspnea, cough, hemoptysis (bloody
mucous), fatigue, palpitations from atrial flutter/atrial fibrillation, and
chest pain.
• If the right ventricle fails, symptoms related to heart failure are seen.
Mitral Stenosis
Therapeutic Interventions
• Prophylactic antibiotic therapy to prevent
endocarditis.
• Anticoagulants for a-fib to prevent emboli.
• Digitalis and diuretics given for heart failure.
• Valvuloplasty: balloon used to dilate the
stenosed valve.
• Surgical treatment to repair or replace the valve.
Mitral Regurgitation
• Mitral regurgitation, or insufficiency, is the incomplete closure of the
mitral valve leaflets which allows backflow of blood into the left
atrium with each contraction of the left ventricle.
• The extra blood backflow into the left atrium causes the left atrium to
enlarge, the blood begins to backup into the lungs, and eventually
into the right ventricle causing the right ventricle to enlarge (same as
mitral stenosis).
• Major cause of mitral regurgitation is rheumatic heart disease.
• Other causes include endocarditis, rupture or dysfunction of the
chordae tendineae or papillary muscle, MVP, cardiomyopathy,
calcification, or congenital defects.
Mitral Regurgitation
• S/S of mitral regurgitation include: none
(asymptomatic), murmur, exertional dyspnea,
fatigue, palpitations, irregular pulse due to a-fib,
weakness as cardiac output decreases if left
ventricle fails.
• Pulmonary edema and shock may occur if acute
mitral regurgitation develops due to papillary
muscle rupture following MI.
Mitral Regurgitation
Therapeutic Interventions
• Without symptoms, no general medical treatment is
used.
• Prophylactic antibiotic therapy to prevent infectious
endocarditis.
• ACE inhibitors to reduce afterload.
• Digitalis, calcium channel blockers, or beta blockers for
a-fib with rapid heart rate.
• Anticoagulants to prevent emboli.
• Diuretics for s/s of heart failure.
• Surgery for mitral valve repair or replacement.
Aortic Stenosis
• Aortic stenosis is when blood flow from the left ventricle
going into the aorta is obstructed through the stenosed
(narrowed) aortic valve.
• The stenosis of the aortic valve is caused from
thickening, scarring, calcifications, or fusing of the
valve’s flaps.
• The left ventricle begins to contract more forcefully to get
the blood out of the left ventricle and into the aorta.
• The left ventricle, with chronic stenosis, hypertrophies
(mass increases) because of excessive blood volume to
maintain cardiac output, but leads to decreased cardiac
output.
Aortic Stenosis
• The major causes of aortic stenosis are congenital
defects or rheumatic heart disease and calcification of
the aortic valve.
• S/S of aortic stenosis may take years to develop.
• Angina (chest pain) is a primary symptom that occurs
due to the increased oxygen needs of the hypertrophied
myocardium (chest pain in younger patients indicates
severe obstruction).
• Other s/s includes: murmur, syncope from dysrhythmias
or decreased cardiac output, and s/s of heart failure.
• Orthopnea, dyspnea on exertion, and fatigue are
indicators of left ventricular failure.
Aortic Stenosis
Therapeutic Interventions
• Treatment of choice is aortic valve replacement
because of increased risk of sudden death.
• Prophylactic antibiotic therapy.
• Heart failure symptoms are treated carefully.
• Medications that reduce the contractility of the
heart and subsequently cardiac output are
avoided to prevent further failure.
Aortic Regurgitation
• Aortic regurgitation is the backflow of blood from the aorta into the
left ventricle due to aortic valve cusps not closing completely.
• The aortic valve cusps may be scarred, thickened, or shortened
causing the valve not to close completely.
• The left ventricle hypertrophies due increased blood volume leading
to eventual left ventricular failure, decreased cardiac output, and
pulmonary edema.
• Rheumatic heart disease is the usual cause of aortic regurgitation.
• Other causes include congenital defects, syphilis, severe
hypertension, and RA.
• Acute causes may be endocarditis or aortic dissection.
Aortic Regurgitation
• S/S of aortic regurgitation include: none (asymptomatic)
for years.
• Initially, the patient may report feeling a forceful heart
beat which is more pronounced lying down.
• Other s/s include: murmur, Corrigan’s pulse (palpated
carotid pulse is forceful and then quickly collapses),
chest pain is atypical and often happens at rest or at
night along with diaphoresis due to less oxygen to the
myocardium.
Aortic Regurgitation
Therapeutic Interventions
• Surgical valve replacement is treatment of
choice.
• Digitalis, diuretics, ACE inhibitors (vasodilator
therapy), and Procardia may be used on some
patients to reduce SBP and cardiac workload
until surgery is done.
• Prophylactic antibiotic therapy.
Patient Education
Valvular Disorders
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•
•
•
•
•
•
Patient education is a crucial role in nursing care.
Educate patients on valvular disorder in terms they will understand.
Teach patients health maintenance (diet, exercise, meds, etc.).
Teach early recognition of s/s so medical care can be sought.
Include family and caregivers in teaching.
Medication teaching is a critical part of the teaching.
Anticoagulant medications (Coumadin) requires patients to avoid
certain foods, periodic lab work, safety with certain equipment, and
s/s of complications to report to MD.
• Prophylactic antibiotic therapy to help prevent endocarditis.
Cardiac Valve Surgery
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•
•
•
•
•
There are several different types of valves used to replace the
valves of the heart.
The types of valves are mechanical or biological.
There are 3 types of mechanical valves: caged ball, monoleaflet,
and bileaflet.
Mechanical valves are durable but create turbulent blood flow which
can lead to clot formation, requiring lifelong anticoagulant therapy.
There are 3 sources for biological valves: porcine (pig), bovine
(cow), and allograft (human donor: which are in limited availability
because they require a donor).
Biological valves do not require lifelong anticoagulant therapy
because they have a very low incidence of thrombus formation;
however, they do not last as long as a mechanical valve.
Cardiac Valve Surgery
Cardiac Valve Surgery
• Cultural considerations need to observed with
valve replacement.
• The pig (porcine) is considered a dirty animal to
religious Jewish and Muslims; only bovine (cow),
synthetic (mechanical), human valves should be
used for these patients.
• The cow is considered sacred among Hindus;
only porcine, synthetic, or human valves should
be used for these patients.
Cardiac Valve Surgery
Complications
• Tissue valves can have degenerative changes and calcification can
occur which may lead to valve failure.
• Mechanical valves most common complication is thrombus
formation.
• Anemia
• Endocarditis
• Embolism from thrombus formation.