Download CV part 3

Cardiovascular
Part 3
Lisa Pearson, RN MSN
HTN
• Hypertension (HTN): is known as high blood pressure.
• Normal BP range: 120/80-140/90.
• HTN BP readings: greater than 140 systolic or greater
than 90 diastolic.
• Diagnosis is made when the average of at least two or
more readings on different dates is above high normal
range.
• BP is the pressure exerted by blood on the walls of blood
vessels.
HTN
• Factors that impair normal regulation of BP may
lead to HTN.
• Some of these factors include increases in
hormones that cause sodium retention, such as
aldosterone, lead to increased fluid retention.
Changes in kidney function that alter the
excretion of fluid also result in an increase in
overall body fluid that may to HTN.
3 Types of HTN
• There are 3 types of HTN: Primary HTN, Secondary HTN, and
Isolated Systolic HTN.
• Primary HTN (also called essential HTN) is the chronic elevation of
BP from an unknown cause.
• Secondary HTN has a known cause. This type of HTN signals that
there is another problem which is causing HTN to occur. Problems
which cause HTN may include a kidney abnormality, a tumor of the
adrenal gland, or a congenital defect of the aorta. When the causing
condition is treated before permanent structural changes occur, BP
usually returns to normal.
• Isolated Systolic HTN is when the SBP is > 140 but the DBP is < 90.
HTN
• HTN often have no s/s other than elevated BP readings.
• S/S of HTN include: headache, dizziness, blurred vision,
and sometimes a nosebleed.
• Most s/s of HTN stem from long-term damaging effects
on the large and small blood vessels of the heart,
kidneys, brain, and eyes (known as target organ
disease).
• Complications of HTN include: heart failure, heart attack,
stroke, and renal failure.
HTN
• Diagnosis of HTN considers a patient’s risk factors for
HTN, a previous diagnosis of HTN, presence of s/s,
history of kidney or heart disease, and current use of
medications.
• When the average BP is above 140/90, then HTN is
diagnosed.
• Research has shown that the most effective method for
predicting risk for stroke and heart attack are self BP
monitoring twice a day for a week.
HTN Risk Factors
• There are two types of risk factors thought to be responsible for the
development of HTN; although the cause remains unknown.
• The two types of risk factors are non-modifiable and modifiable.
• Non-modifiable is genetic which includes a family history of HTN. It
also includes age, ethnicity, and diabetes. This type of risk factor
can not be changed.
• Modifiable is environmental and can be changed. These include
blood glucose levels, activity levels, smoking, and salt and alcohol
intake. Stop smoking, diet, lose weight, control BS, and exercise can
help control HTN.
Non-Modifiable Risk Factors of HTN
• Family history of HTN: a person should be encouraged to have their
BP checked regularly because the risk of developing HTN is
doubled.
• Age: as people age, plaque is building up in blood vessels which
can lead to HTN development.
• Race/Ethnicity: African-Americans are at the greatest risk of
developing HTN than any other race/ethnicity population.
• Diabetes: many adults with DM also have HTN. A person with a
family history of DM and obesity run a greater risk of developing
HTN.
Modifiable Risk Factors of HTN
• Patients with HTN can use lifestyle modifications to help
control HTN.
• Lose weight
• Diet changes: reduce sodium intake, follow low fat and
low cholesterol diet. Limit caffeine and alcohol
consumption. Include foods rich in K+, magnesium, and
calcium.
• Stop smoking
• Regular exercise
HTN
Therapeutic Interventions
• Teach patient s/s of HTN (headache, dizziness, blurred vision, and
nosebleeds).
• Teach patient how to help alleviate s/s of HTN which include: make
sure the patient has taken BP medication, teach patient to lie down
in a cool, quiet, dim-lit room for 30 minutes and recheck BP. If BP is
still elevated and s/s continue, then patient should contact MD or go
to ER.
• Teach patient, family members, or caregiver how to check BP with a
manual or digital BP cuff. (digital is not always accurate).
• Teach patient to take BP medication as ordered (not just when they
feel like their BP is elevated).
HTN
Therapeutic Interventions
• Goal is to have BP controlled below 140/90.
• If BP medications are being taken, teach the
patient to rise slowly to prevent the effects of
orthostatic hypotension which may result in
dizziness and increase risk of falls.
• Teach to avoid dehydration, especially if patient
is on a diuretic.
HTN
Medications
• There are 8 categories for medications to treat HTN
which include: diuretics, alpha-adrenergic blockers, beta
blockers, calcium channel blockers, angiotensinconverting enzyme (ACE) inhibitors, angiotensin II
antagonists (ARB), central acting agents, adrenergic
neuron blockers (peripherally acting), and vasodilators.
• Anti-hypertensive medications can have unpleasant side
effects and patients should be taught the side effects to
look for and report to the MD if noted (erectile
dysfunction is a side effect of some medications).
HTN
Medications
• Diuretics increase urine output by inhibiting sodium and water
reabsorption by the kidneys. Several types of these medications.
• Thiazide and thiazide-like diuretics (HCTZ) increase urine output
by promoting sodium, chloride, and water excretion which is most
effective in normal renal function. BS may increase in diabetics.
Causes loss of sodium K+, magnesium, and saved calcium in body.
• Loop diuretics (Lasix) also called non-K+ sparing diuretics act on
ascending loop of Henle in kidney to cause sodium and water loss;
also causes loss of K+, magnesium, and calcium.
• Potassium-sparing diuretics are (Aldactone) are mild diuretics
which can be used as combination therapy; promote sodium and
water excretion and K+ retention by the kidney.
HTN
Medications
• Beta Blockers: (Inderal) (end in –olol) decrease sympathetic
nervous system resulting in decreased BP, heart rate, contractility,
cardiac output, and renin activity. Teach patient not to stop
medication abruptly to avoid rebound HTN, angina, or dysrhythmias.
• Alpha 1 Blockers: (Minipress) block effects of sympathetic nervous
system on smooth muscle of blood vessels resulting in vasodilation
and decreased BP.
• Combined alpha and beta blockers: (Coreg) alpha-adrenergic
receptors causing vasodilation and reduced BP; decrease
sympathetic nervous system resulting in decreased heart rate, and
contractility. Teach not to stop abruptly.
• Central acting alpha 2 blockers: (Catapres) block effects of
sympathetic nervous system. Teach not to stop abruptly.
HTN
Medications
• Angiotension-converting enzyme inhibitors (ACE
inhibitors) (Lotensin, Capoten; ends in –pril) blocks
production of angiotension II, a potent vasoconstrictor;
reduces peripheral arterial resistance and blood
pressure.
• Angiotensin II receptor antagonists (ARB) (Avapro,
Cozaar, Diovan) block angiotension II receptors causing
vasodilation and reduction in blood pressure.
• Aldosterone receptor antagonists (Inspra) blocks
binding of aldosterone at receptor site to reduce sodium
reabsorption and then blood pressure.
HTN
Medications
• Calcium Channel Blockers (Norvasc, Cardizem,
Procardia) prevent movement of extra-cellular calcium
into the cell which vasodilates. Take pulse prior to
administration. May increase blood levels of digoxin.
• Direct vasodilators (Apresoline) relax smooth muscles
of blood vessels causing vasodilation and decreased
blood pressure. May increase heart rate and have
headache.
HTN
Medications
• Nursing interventions for administration of HTN
medications include: ALWAYS check BP prior to
administration (not 30 minutes before but right before). If
BP is low, hold medication and notify MD.
• Check pulse and assess for any s/s of HTN (headache,
dizziness, blurred vision, and nose bleeds).
• Teach patient, family members, caregivers about
medication, S/E, and the importance of taking
medication as ordered.
• Teach patient, family members, caregivers about
checking BP routinely at home with a manual or digital
cuff and to keep a log of BP readings.
HTN
Medications
• Teach patient that he/she may need to take BP
medication prior to any type of surgeries, invasive
procedures, etc.
• Teach importance of patient to rise slowly to avoid
dizziness which could lead to falls.
• Teach S/S of HTN and what to do to help alleviate them
and what to do if no relief.
• Teach appropriate placement of BP cuff and arm should
be at heart level (do not cross legs when checking BP).
Complications of HTN
• Common complications of HTN include CAD,
atherosclerosis, MI, heart failure, stroke, kidney damage,
and eye damage. Elevated BP damages the small
vessels of the heart, brain, kidneys, and retina which
results in a progressive functional impairment of these
organs, known as target-organ disease.
• The severity and duration of the increase in BP
determine the extent of the vascular changes causing
organ damage.
• High BP levels may also result in an increase in the size
of the left ventricle (hypertrophy).
Hypertensive Emergency
• Hypertensive emergency is a severe type of HTN characterized by
elevations in SBP > 180 and DBP > 120.
• This puts a patient at risk for or progression of target-organ
dysfunction (MI, HF, and dissecting aortic aneurysm).
• Persons who are untreated, fail to comply with anti-hypertensive
therapy, or stop their medication abruptly are at risk for hypertensive
emergency.
• These patients require immediate reduction of BP to prevent or limit
damage to target organs (may be admitted to critical care).
• Gradual reduction is desired to prevent decreased blood flow to the
kidneys, heart, and/or brain.
• IV Nipride may be given to quickly reduce BP.
Hypertensive Urgency
• Hypertensive Urgency occurs when there is
severe elevation of BP, as in hypertensive
emergency, but without target-organ dysfunction
progression.
• Patient may experience severe headaches,
nosebleeds, SOB, and anxiety (also dizziness
and blurred vision).
• Can usually be treated with combination oral
medication and scheduled for a follow-up visit
within several days.
Inflammatory and Infectious CV Disorders
• The entire heart or its layers can become
inflamed or infected.
• Rheumatic carditis: entire heart
• Endocarditis, myocarditis, and pericarditis:
layers of heart
• Inflammation and infections of any part of the
heart is very serious and could be fatal.
Inflammatory and Infectious CV Disorders
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Rheumatic Carditis
Infective Endocarditis
Pericarditis
Myocarditis
Inflammatory and Infectious CV Disorders
Rheumatic Carditis
• Rheumatic carditis (entire heart) is a serious
complication stemming from rheumatic fever.
• Rheumatic fever occurs from an upper
respiratory (throat) infection from beta-hemolytic
streptococci.
• Rheumatic fever occurs 2-3 weeks after the
strep infection; however, rheumatic fever does
not occur as much as it did in the past due to
availability of antibiotics.
Rheumatic Carditis
• Rheumatic carditis from rheumatic fever involves all layers of the
heart being inflamed.
• Pericardial layers are covered with an exudate and becomes
thickened; as healing occurs, the pericardial sac can be damaged or
destroyed by fibrosis.
• Myocardial layer of tissue has nodules form that become scar tissue
over time.
• Endocardium, specifically the mitral valve, is the most seriously
affect. Tiny, pinhead-size vegetations from blood and fibrin form on
the valve leaflets which may lead to thickening, fibrosis, and
calcification of the valve leaflets and supporting structures. Stenosis
or regurgitation can occur.
Rheumatic Carditis
• S/S of rheumatic carditis include: tachycardia, heart murmur,
pericardial friction rub, mild to moderate chest pain, heart
enlargement, ECG changes, and evidence of heart failure.
• S/S of rheumatic fever include: fever, polyarthritis, SQ nodules, and
chorea with rapid, uncontrolled movements, rheumatic carditis,
arthralgia, and pneumonitis.
• To help prevent rheumatic carditis/rheumatic fever is to detect and
treat strep infections promptly with PCN (erythromycin for pts
allergic to PCN). Throat culture needs to be performed. Pts may be
treated with antibiotic therapy, anti-inflammatory meds, and possibly
steroids.
• Patient activity may be limited by the MD depending on severity.
Rheumatic Carditis
• As the nurse, you would assess the patient’s
recent history of any illnesses (sore throat, strep
infection, or scarlet fever) including past
episodes of rheumatic fever, heart disease, joint
pain, and any current medications.
• Assess VS and note any tachycardia and/or
fever.
• Assess for murmurs, pericardial friction rub, and
s/s of heart failure.
Infective Endocarditis
• Infective endocarditis is an infection of the endocardium.
• This infection can be fatal related to end-organ failure and other
disease processes even with treatment of antibiotics.
• Develops most commonly from a bacteria or fungi that has attached
to an eroded part of the endocardium where platelets and fibrin
deposits have formed a vegetative lesion.
• Damage to the valve leaflets occur as the vegetations grow.
• As the blood flows through the heart, these vegetations may break
off and become emboli.
• The mitral valve is the valve most commonly infected, with the aortic
valve being second.
Infective Endocarditis
• How does the infection get in the body and end up in the
heart?
• The bacteria or fungi must have a portal of entry into the
bloodstream.
• Portals of entry include: IV drug use, surgery, dental or
invasive procedures, and infections of the skin and GI or
GU tract.
• Because dental disease is thought to be a common
cause of infective endocarditis, oral care is an important
preventative measure. (patients with known heart
problems should take prophylactic antibiotics prior to any
dental work or invasive surgery).
Infective Endocarditis
• S/S include: fever, murmur, splinter
hemorrhages in the distal nail beds, petechiae,
Janeway lesions (small, painless red-blue
lesions on palms and soles), Osler’s nodes
(small, painful nodes on fingers and toes),
nightsweats, fatigue, weight loss, weakness, and
pain in abdomen, joints, muscles, and/or back.
Infective Endocarditis
• Complications of infective endocarditis is vegetative emboli (major
complication) and heart failure.
• If an emboli breaks off and travels out of the heart and affects an
organ then s/s may occur from that organ area.
• Brain emboli may produce changes in LOC or stroke.
• Kidney emboli cause pain the flank area, hematuria, or renal failure.
• Emboli in the spleen may cause abdominal pain.
• Emboli in the small blood vessels can impair circulation in the
extremities.
• Pulmonary emboli result in sudden dyspnea, cough, and chest pain.
• Stenosis or regurgitation of the heart valves may occur.
Infective Endocarditis
• Diagnostic tests for infective endocarditis include positive blood
cultures (do not start antibiotic therapy until after blood cultures are
drawn) and echocardiogram (shows cardiac effects). Also, WBCs
will be elevated with infection.
• The blood cultures will identify which germ is causing the infection.
• Drug to treat the infection depends on germ identified by blood
cultures.
• Antimicrobial antibiotic drugs are used such as PCN, vancomycin,
and amphotericin B are given IV for 4-6 weeks (may have central
line or PICC).
• Surgical repair or replacement for valves may be done.
Pericarditis
• Pericarditis is an acute or chronic inflammation of the
pericardium (sac surrounding the heart).
• The inflammation restricts the heart’s ability to contract
and expand to fill with blood.
• Acute pericarditis may be caused by infections, drug
reactions, connective tissue disorders (lupus, RA,
rheumatic fever), neoplastic disease, post-op cardiac
surgery, post MI, renal disease or uremia, and chest
trauma.
• Acute pericarditis resolves usually in less than 6 weeks.
Pericarditis
• Chronic pericarditis is the result of fibrous
scarring of the pericardium.
• The heart becomes surrounded by a thickened,
stiff sac that limits the stretching ability of the
heart’s chambers for filling.
• Results from neoplastic disease and metastasis,
radiation, or TB.
Pericarditis
• Echocardiogram results show pericardial
effusions.
• Lab tests may indicate bacterial or viral
infections (WBCs).
• Fluid may be obtained during pericardiocentesis
to examine the cause.
• CT or MRI may show a thickened pericardium.
Pericarditis
• Chest pain is the most common symptom of pericarditis.
The intense, sharp, creaky, grating pain increases with
deep inspiration, coughing, moving the trunk, or lying
flat. Pain may be relieved by sitting up and leaning
forward.
• The classic sign of pericarditis is a pericardial friction rub
(grating, scratchy, high-pitched sound) that is heard
when a rub is present. The rub is a result of friction from
the inflamed pericardial and epicardial layers rubbing
together as the heart fills and contracts.
• Chronic constrictive pericarditis produces s/s of rightsided heart failure.
Pericarditis
• Immediate treatment is required if patient is unstable such as an
emergency pericardiocentesis (fluid removed from pericardial sac
using needle and syringe).
• Once patient is stable, the cause of pericarditis is determined and
treatment is started (antibiotics, bed rest, NSAIDs, steroids, etc.).
• Chronic effusive pericarditis can be treated with a pericardial
window to allow continuous drainage of pericardial fluid into the
pleural space. (created surgically by removing a portion of the outer
pericardial layer).
• Chronic constrictive pericarditis is treated with pericardiectomy,
which is the surgical removal of the entire tough, calcified
pericardium. (It relieves constriction of the heart and allows normal
filling of the ventricles).
Pericarditis
• The most common complication of pericarditis is a pericardial
effusion (build-up of fluid in pericardial space).
• As fluid accumulation grows, cardiac tamponade can occur which is
a life-threatening compression of the heart by fluid accumulated in
the pericaridal sac. Cardiac output drops to compensate, heart rate
increases. BP falls as compensatory mechanisms fail. S/S of
decreased cardiac output, such as restlessness, confusion,
tachycardia, and tachypnea. Jugular vein distention is present from
increased venous pressure, and heart sounds are distant. Cardiac
tamponade requires immediate treatment with pericardiocentesis to
puncture the pericardium with a 16 gauge needle and remove the
excess fluid in the pericardial sac.
Pericarditis
• Nursing care for patients with pericarditis focuses on relieving the
patient’s pain and anxiety and maintaining normal cardiac function.
• Pain is relieved by giving NSAIDs or corticosteroids.
• Patient to be positioned for comfort by sitting up and leaning forward
helps relieve pain.
• Monitor VS and cardiac function.
• Report any s/s of cardiac tamponade or heart failure immediately to
MD.
• Teaching patient about pericarditis and its treatment relieves anxiety
and allows a feeling of control by allowing the patient to make
knowledgeable health-care decisions.
Myocarditis
• Myocarditis is the inflammation of the myocardium and is
a rare condition that most commonly develops following
a viral infection. (also caused by bacteria, parasites,
fungi, medications, lead toxicity, autoimmune factors,
rheumatic fever, lupus, pericarditis, infective
endocarditis, or cardiac transplant rejection)
• Cardiac muscle destruction and necrosis may occur as a
result of myocarditis. (the amount depends on the extent
of damage).
• With cardiac damage, the heart may enlarge; however,
most cases are with few s/s.
Myocarditis
• S/S of myocarditis vary from none to severe.
• S/S include fatigue, fever, pharyngitis, malaise, dyspnea,
palpitations, muscle aches, GI discomfort, and enlarged
lymph nodes may occur early from a viral infection.
• Chest discomfort, pain, or tachycardia may occur about
2 weeks after a viral infection.
• A percutaneous endomyocardial biopsy during the first 6
weeks of inflammation is the preferred diagnostic test.
Myocarditis
Therapeutic Interventions
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Goal is to reduce the heart’s workload.
Bed rest and limited activity.
Oxygen to treat hypoxia.
Treat the cause such as antibiotics for bacterial infections.
No alcohol or smoking.
Treat heart failure with medications.
Myocarditis may make the heart sensitive to digoxin (Lanoxin) by
exhibiting s/s of dig toxicity even with small doses.
• S/S of dig toxicity includes: anorexia, n/v, bradycardia,
dysrhythmias, malaise, seeing green halos around lights, and
dizziness. Antidote for dig is Digibind.
Myocarditis
• Nursing care is aimed at the patient’s
maintenance of normal cardiac function by
monitoring VS, s/s, and administering
medications as ordered.
• Encourage rest periods and teach energy
conservation methods.
• Teach about diagnosis, medications, etc. to help
reduce anxiety.
Cardiac Trauma
Non-Penetrating and Penetrating
• Non-penetrating injuries (contusions) occur from blunt trauma such
as MVA (MVC), CPR or contact sports.
• Direct compression or force is applied to the upper torso.
• Contusions may vary from small bruises to hemorrhage.
• Few or no external injuries.
• May be asymptomatic or have s/s identical to MI.
• Lab results may show elevated CK-MB or Troponin I levels.
• Bleeding may occur in pericardial sac, cardiac tamponade, s/s of
shock. Pericardiocentesis must be performed with shock.
• Bed rest and observation may be ordered.
• Usually no long term effects are noted; however, with severe
trauma, scarring and necrosis of the myocardium may occur.
Cardiac Trauma
Non-Penetrating and Penetrating
• Penetrating traumas may be an external injury to the
chest such as a stab or GSW.
• May be internal injury from invasive lines that penetrate
cardiac muscle (central lines, etc.).
• Complications depends on size, location, and cause of
injury.
• Cardiac tamponade, hemothorax (blood drain in pleural
space), or pneumothorax (air in pleural space).
• S/S of hemorrhage and myocardial ischemia may be
noted.
• Treatment usually requires surgery to repair the damage.
Cardiomyopathy
• Cardiomyopathy is an enlargement of the heart.
• 3 types of cardiac structure and function
abnormalities: dilated, hypertrophic, and
restrictive.
• Consequences of all types can be heart failure,
myocardial ischemia, and MI due to reduced
CO.
• No cure for cardiomyopathy.
Cardiomyopathy
Cardiomyopathy
• Dilated cardiomyopathy: ventricular chambers greatly
enlarge and ventricle walls are thinner which reduces
CO (most frequent type of cardiomyopathy and cause of
HF).
• Contractibility decreases with blood moving slower
through the left ventricle which may lead to clot
formation.
• May be hereditary, may follow infection of myocarditis, or
be caused by chronic alcohol or cocaine use. (also, HIV,
thiamine or zinc deficiencies, infections, or other
causes).
Cardiomyopathy
• Hypertrophic cardiomyopathy: ventricle walls
greatly thicken causing smaller filling areas (may
be asymmetrical).
• Can be hereditary.
• If an enlarged septum obstructs the outflow of
blood through the aortic valve, it is known as
obstructive hypertrophic cardiomyopathy.
• Death occurs suddenly and is likely due to an
abnormal heart rhythm.
Cardiomyopathy
• Restrictive cardiomyopathy: muscle layers are stiff and
resist stretching for filling.
• Is the rarest form of cardiomyopathy.
• Systolic emptying is normal; however, filling is abnormal
because of the stiffness.
• May be caused by infiltrative diseases such as
amyloidosis which causes stiffness.
• Treating underlying cause may help reduce heart
damage.
Cardiomyopathy
• S/S of cardiomyopathy includes varying degrees of HF,
dyspnea on exertion, orthopnea, fatigue, and
occasionally A-fib.
• Cardiomegaly (enlargement of heart) seen on CXR.
• Echocardiogram shows muscle thickness and chamber
size to differentiate between the types.
• ECG changes.
• Cardiac catheterization with angiocardiography may be
useful.
Cardiomyopathy
Therapeutic Interventions
• Treatment is palliative and aimed at managing heart
failure and the underlying cause if known for both dilated
and restrictive.
• In dilated cardiomyopathy, treatment focuses on the
symptoms of HF (ACE inhibitors, beta blockers,
diuretics, and digoxin may be given to increase CO).
• Biventricular pacing and implantable defibrillators may
be used.
• Anticoagulants for prevention of emboli formation.
• Anti-dysrhythmics or cardioversion used for
dysrhythmias.
Cardiomyopathy
Therapeutic Interventions
• For obstructive hypertrophic cardiomyopathy, beta
blockers and calcium channel blockers are given to slow
heart rate to allow more filling time and lessen the
strength of the heart’s contraction.
• Digoxin and vasodilators are avoided because they can
increase the obstruction.
• Strenuous exercise and athletic sports are restricted to
prevent sudden death.
Cardiomyopathy
Therapeutic Interventions
• For hypertrophied muscle, surgery to remove part of the ventricular
septum (myectomy) is done to allow greater outflow of blood ( if
patient is not candidate for surgery septal ablation may be an option
also).
• For severe heart failure, primarily with dilated cardiomyopathy, heart
transplant may be only hope for survival.
• Teach on the importance of medication compliance to prevent HF.
• Emergency phone numbers readily available.
• Family should be taught CPR.
• Hospice and emotional support for terminal patients.
Venous Disorders
Thrombophlebitis
• Thrombophlebitis is the formation of a clot and inflammation within a
vein (clot usually forms first then inflammation occurs).
• Most common disorder of veins (superficial or deep veins), with legs
being most affected.
• DVT is the most serious because PE can result if thrombus
detaches.
• A venous thrombus is made up of platelets, RBCs, WBCs, and
fibrin. Platelets attach to a vein wall and then a tail forms as more
blood cells and fibrin collect. As the tails grows, it drifts in the blood
flowing past it. The turbulence of the blood flow can cause parts of
the drifting thrombus to break off and become emboli that travel to
the lungs.
Thrombophlebitis
• Three factors, Virchow’s triangle, are involved in the formation of a
thrombus: stasis of blood flow, damage to the lining of the vein wall,
and increased blood coagulation.
• Venous stasis occurs when blood flow is reduced, veins are dilated,
muscle contractions are decreased, or vein valves are faulty.
• Damage to vein wall can provide site for thrombus formation (IV and
VP can cause trauma to vein, IV catheter in place longer than 48-72
hours increase risk of inflammation and thrombus).
• Increased coagulation of the blood promotes thrombus formation
(patients on anticoagulants who stop medication abruptly). Smoking,
oral contraceptive use, and estrogen therapy may also increase
blood coagulation.
Thrombophlebitis
• Dehydration (common in elderly) should be
avoided to reduce thrombus risk.
• Immobility should be avoided. Encourage
position changes and ambulation.
• Turn q2h, active or passive ROM, post-op early
ambulation, use of TED hose, SCD hose, , deep
breathing, and avoid smoking (vasoconstriction).
Thrombophlebitis
Medications
• Lovenox SQ is more effective for orthopedic patients.
(platelet level needs monitored). Antidote is Protamine
sulfate.
• Heparin SQ may be given post-op (platelets monitored to
help detect heparin induced thrombocytopenia). Antidote
is Protamine sulfate.
• Coumadin can be used in high-risk patients (PT w/
INR…INR normal therapeutic range is 2-3). Antidote is
vitamin K.
• Before administration of anticoagulants, lab values must
be assessed to ensure patient safety (check results
before all doses).
Thrombophlebitis
• Up to 50% of patients have no symptoms with thrombophlebitis in
the legs, for others, the symptoms vary according to the size and
location of the thrombus.
• For some patients, a PE is the only evidence of a DVT.
• Superficial veins may have redness, warmth, swelling, and
tenderness in the area around the site of the thrombus. The vein
feels like a firm cord, which is referred to as induration. Common
cause in arm is IV therapy. (leg is commonly saphenous vein usually
due to varicosity).
• Deep veins may have swelling, edema, pain, warmth, venous
distention, and tenderness with palpation of calf in affected leg.
Positive Homan’s sign is present in less than 50% and is not specific
to DVT (once DVT is positively diagnosed, avoid Homan’s sign
assessment due to possible dislodgement of clot).
Thrombophlebitis
Therapeutic Interventions
• Ultrasound is the primary test used.
• Goals of treatment are to relieve pain and prevent PE, thrombus
enlargement, and further thrombus development.
• Superficial thrombophlebitis is treated with warm, moist heat,
analgesics, NSAIDs, and compression stockings.
• DVT may be treated in hospital or home (depending on patient), SC
heparin or Lovenox, oral anticoagulants, bed rest with leg elevation
above heart level for 5-7 days, warm, moist heat, and elastic
stockings on affected leg.
• Daily measurements of bilateral legs to monitor swelling.
• Lab work.
• Assess for s/s of PE such as dyspnea, tachycardia, tachypnea,
blood-tinged sputum, chest pain, or changes in LOC (call MD
ASAP).
Anticoagulants
• Educate the patient on these medications (use, s/e, what to avoid,
and what to report to MD).
• To prevent injury: wear shoes or slippers with rubber soles (no bare
feet or socks).
• Use electric razor to shave and use a soft toothbrush.
• S/S of bleeding to report to MD: easy bruising, nosebleeds, bleeding
that does not stop, blood in urine, blood in sputum, blood in stools,
or black stools.
• Avoid use of aspirin/NSAIDs because they further prolong clotting.
• Have lab work done as ordered which the results may cause change
in medication dosage.
Heart Failure
• Heart Failure (aka: CHF congestive heart failure) is the inability of
the heart to effectively pump enough blood to meet the body’s
oxygen and nutrient needs.
• S/S vary and include SOB with or without exertion, fatigue, edema to
legs, ankles, arms, face, and even abdomen (fluid volume overload).
• Causes are varied and may include CAD (most often), MI,
cardiomyopathy, heart valve problems, and HTN (any heart problem
can lead to HF).
• In the elderly, most common cause is cardiac ischemia.
• Readmission rates to hospitals soon after discharge for HF are high
and pose a challenge for health-care providers.
Heart Failure
• The heart is divided into two separate pumping
systems but usually work together to ensure
equal amounts of blood enter and leave the
heart.
• HF can be right-sided, left-sided, or biventricular
heart failure.
• The ventricle is the area of the heart’s pumping
system that commonly fails with the left ventricle
typically the one to weaken first because it has
the greatest workload.
Left-Sided Heart Failure
• A certain amount of force must be exerted by the left
ventricle for blood to enter the aorta through the aortic
valve (force is called afterload).
• The pressure within the aorta and arteries influences the
force needed to open the aortic valve to pump blood into
the aorta (this is called peripheral vascular resistance
PVR).
• HTN is one of the major causes of left-sided heart
failure.
• Other causes include aortic stenosis, cardiomyopathy,
coarctation of the aorta, heart muscle infections, MI, and
mitral valve regurgitation.
Left-Sided Heart Failure
• Left-sided heart failure is when blood backs up from the
left ventricle into the left atrium and then into the four
pulmonary veins and lungs.
• Excessive fluid in the lungs causes alveolar edema and
reduces gas exchange.
• S/S include SOB and cyanosis because of decreased
oxygenation.
• Severe fluid build-up leads to pulmonary edema which
requires immediate treatment.
• Remember Left = Lung! (s/s are respiratory related).
Right-Sided Heart Failure
• The major cause of right-sided heart failure is left-sided heart failure.
• When the left-side fails, fluid backs up into the lungs and pulmonary
pressure is increased.
• The right ventricle continually pumps blood against this increased
fluid and pressure in the pulmonary artery and lungs and over time
this additional strain eventually causes the right ventricle to fail.
• Conditions causing right-sided HF increase the work of the right
ventricle; these conditions are disorders that increase pulmonary
pressures such as emphysema or congenital heart defects; restrict
the outflow of blood from the right ventricle as in pulmonary valve
stenosis; and allow left atrial blood to flow into the right atrium which
increases blood volume in the right ventricle as in septal defects.
Right-Sided Heart Failure
• When the right ventricle hypertrophies or fails because of increased
pulmonary pressures, it is referred to as cor pulmonale.
• When the right ventricle fails, it does not empty normally and there is
a backward build-up of blood in the systemic blood vessels.
• As blood backs up from the right ventricle, right atrial and systemic
venous blood volume increases.
• The backed up blood begins to push back into the systemic blood
flow which causes the jugular neck veins to become visibly
distended and can be seen when a person is in a 45-degree upright
position.
• Edema may occur in the peripheral tissues, and the abdominal
organs can become engorged.
Right-Sided Heart Failure
• S/S of right-sided HF includes: jugular vein distention visible with
patient in 45-degree upright position, edema in feet, ankles, lower
legs, possibly thighs, abdomen, occasionally arms and face. Weight
gain.
• With these patients, nursing care would include weigh patient every
day at about the same time with the same amount of clothing.
Report any weight gain of 2 or more pounds in a 24 hr period or over
a week’s time to MD, this could be s/s of hidden fluid. Measure
abdominal girth. Assess edema and measure. Elevate edematous
extremities at or above heart level for at least 20 minutes several
times a day. Take medications as ordered by MD. I/O.
Pulmonary Edema
(Acute Heart Failure)
• Pulmonary edema (acute HF), is severe fluid congestion in the
alveoli of the lungs and is life threatening.
• May occur in an acute event such as MI or when the heart is
severely stressed, causing the left ventricle to fail.
• Complications include dysrhythmias and cardiac arrest.
• Pulmonary edema develops when the increase of blood and fluids
accumulates in the lungs and the blood and fluids are pushed by the
pressure into the alveoli resulting in the alveoli and airways
becoming filled with fluid which reduces gas exchange and oxygen
levels.
• Basically, it is like the patient is drowning in his/her own fluids.
Pulmonary Edema
(Acute Heart Failure)
• Pink, frothy sputum is a classic symptom of
pulmonary edema caused by the increased lung
congestion and pressures that allow leaking of
fluid into the alveoli.
• S/S of pulmonary edema includes: rapid
respirations with accessory muscle use, severe
dyspnea, orthopnea, crackles and wheezes,
coughing, pink, frothy sputum, anxiety,
restlessness, pale skin, pale mucous
membranes, and clammy/cold skin.
Pulmonary Edema
(Acute Heart Failure)
• To diagnose pulmonary edema, the MD will order a CXR
which may reveal congestion in the pulmonary system.
• Also to diagnose pulmonary edema, the MD may order
ABGs (arterial blood gases) and the results will show a
decrease in PaO2 that continues as the edema worsens
and an increase in PaCO2 which = respiratory acidosis
(pH = 7.35).
• If the patient has a line for hemodynamic monitoring, the
pulmonary artery catheter will show elevated pulmonary
pressures and decreased CO.
Pulmonary Edema
(Acute Heart Failure)
Therapeutic Interventions
• Immediate treatment is necessary to prevent patients from drowning
in their own secretions.
• The goal is to reduce the workload of the left ventricle so CO will
improve and to reduce patient’s anxiety and treat underlying cause.
• Position the patient in an upright (Fowler’s) position to help make
breathing easier (lungs expand better in this position).
• O2 administered usually by mask to give higher amounts.
• Patient may need to be intubated and placed on ventilator.
• Meds given IV to reduce anxiety, relax airways, and increase
peripheral blood pooling to decrease preload (morphine), reduce
fluid congestion, strengthen heart contractions, reduce arterial
pressure and sodium and water retention to relieve dyspnea.
Chronic Heart Failure
• Chronic HF is just what the name implies…it is an ongoing battle for
the patient…it is progressive and s/s may worsen over time.
• S/S of chronic HF depend on patient’s age, underlying cause, and
severity of the heart disease, and the ventricle that is failing.
• Fatigue and weakness are the earliest s/s of HF due to decreased
amount of O2. Fatigue may worsen throughout the day with activity.
• A failing left ventricle produces prominent respiratory effects with
dyspnea being a common symptom of left-sided HF due to
pulmonary congestion.
• Exertional dyspnea is SOB that increases with activity.
Chronic Heart Failure
• Orthopnea is dyspnea that increases when lying flat. Patient may
need 2 or more pillows for rest. May document “2 pillow orthopnea.”
The reason orthopnea occurs is because when the patient is up
ambulating or sitting up during the day, fluids accumulate usually in
lower extremities; when the patient is in a lying position, the
accumulated fluids begin to shift back to the heart and all this extra
fluid overwhelms the heart and lungs causing orthopnea.
• With the excessive fluid being shifted from lower legs to heart and
lungs, the fluid also will cause increased urination when lying down.
The patient should elevate legs at or above heart level 30 minutes
prior to bedtime so they can void prior to sleep.
• Nocturia is an increase of urine output at night, up to 6 x or more
voids during night. This up and down to restroom can fatigue patient.
Chronic Heart Failure
• Paroxysmal nocturnal dyspnea (PND) is sudden
SOB that occurs after lying flat for a time. It is a
result from excess fluid accumulation in the
lungs. The sleeping person awakens with
feelings of suffocation and anxiety. Relief is by
sitting upright for a short time, which reduces the
amount of fluid returning to the heart.
Chronic Heart Failure
• A chronic, dry cough is common in HF. It
increases when lying down from increased
irritation of the lung mucosa. This irritation is due
to the increase in pulmonary congestion that
occurs when gravity no longer keeps fluid in the
legs and more fluid returns to the heart and
lungs.
Chronic Heart Failure
• Pulmonary congestion causes abnormal lung
sounds/breath sounds such as crackles and
wheezes.
• These indicate presence of increased fluid in
lungs.
• Crackles are produced from fluid build-up in the
alveoli because of increased pressure in
pulmonary capillaries.
• Wheezes occur from bronchiolar constriction
caused by the increased fluid.
Chronic Heart Failure
• Tachycardia occurs because of the sympathetic
nervous system trying to compensate for
decreased CO by releasing epinephrine and nor
epinephrine.
• Normally, an increased HR would help by
increasing amount of blood ejected from the
heart (i.e. exercise); however, with a HF patient,
the heart is already failing so an increased HR
requires more O2 which is difficult for the
already failing heart to supply.
Chronic Heart Failure
• Patients may experience chest pain caused from
ischemia which a result of decreased O2 to heart
muscle.
• Cheyne-Stokes respiration is a breathing pattern of
shallow respirations building to deep breaths followed by
a period of apnea. The apneic period occurs because
deep breathing causes CO2 levels to drop to a level that
does not stimulate the respiratory center. Apnea may
last up to 30 seconds and then is followed by the shallow
to deeper respiratory pattern as CO2 rises again.
• Edema occurs because of fluid backing up in the lungs
and/or body.
Chronic Heart Failure
• Cyanosis: the skin, nailbeds, or mucous membranes
may appear blue, or cyanotic, from decreased O2 in the
blood.
• Cyanosis is a late sign of HF and is associated primary
with left-sided HF.
• Altered mental status is caused by decreased amount of
O2 to brain. Patient may be confused, restless,
insomnia, and impaired memory may occur as well as
decrease in LOC.
• Malnutrition occurs due to altered mental status,
dyspnea, and fatigue interfering with ability to eat.
Chronic Heart Failure
Complications
• Complications of HF include liver and spleen
enlargement from fluid congestion.
• Pleural effusion, a leakage of fluid from the
capillaries of the lung into the pleural space, can
occur.
• Thrombosis and emboli can occur due to poor
emptying of the ventricles, which leads to stasis
of blood.
Chronic Heart Failure
Therapeutic Interventions
• The overall goal of medical treatment of chronic HF is to improve the
heart’s pumping ability and decrease the heart’s O2 demands.
• Treatment focuses on indentifying and correcting the underlying
cause, increasing the strength of the heart’s contractions,
maintaining optimum water and sodium balance, and decreasing
heart’s workload.
• O2 therapy is used
• Activity may be limited or worked around many rest periods.
• Diet is restricted in sodium and occasionally, fluids may be
restricted.
• Medications of ACE inhibitors, ARBs, diuretics, beta blockers, and
possibly digoxin are used to control symptoms (K+ supplements,
anticoagulants, and anti-dysrhythmics may also be used in some).
Medications
• Always check K+ levels before giving a K+ wasting diuretic such as
Lasix or before giving a K+ supplement. Do not give medication if K+
level is low. Do not give supplement if K+ level is high.
• Always check dig level before giving Digoxin (Lanoxin). Hold
medication is level is high and call MD. Know your s/s of dig toxicity
and the antidote of Digibind.
• Always check PT w/ INR, platelets, and/or PTT before giving any
anticoagulants. Know your antidotes for the appropriate
anticoagulant.
• Always know S/E what nursing considerations are needed for all
medications before administration.