NOTES Valvular/Cardiomyopathy/Aneurysm and Cardiac Surgery cmj
Module #5: Nursing Care of the Individual with Cardiovascular Disorders” Valvular Heart Disease,
Cardiomyopathy, and Aneurysms
Valvular Heart Disease (click to play “valves)
Click here for Tutorial on Valvular Heart Sounds (more than you need-but NCLEX might include a
heart sound or 2)
A.
Etiology/Pathophysiology Valvular Disease (valve function link) *go to valves
1.
Normal physiology: heart: two atrioventricular valves -Mitral , Tricuspid; two
semilunar valves- Aortic, Pulmonic (Valve movie link)
2.
Types of valvular heart disease- depend on valve or valves affected
3.
Two types of functional alterations- Valvular Stenosis, Regurgitation (See
Fig 37-8 p. 878)
a. Stenosis:
1) Valve orifice - restricted; valve leaflets fuse, unable to open or close
completely due to scarring from endocarditis, calcium deposits,
2) Impending forward blood flow
3) Creates a pressure gradient across open valve
4) Degree of stenosis reflected in pressure gradient differences
5) Results in impedance of forward flow of blood >increased afterload,
later stages have increased preload also)
6) Have decreased cardiac output from impaired ventricular filling,
(decreased ejection and stroke volume)
b. Regurgitation (also called insufficient or incompetent)
1) Incomplete closure of valve leaflets
2) Result in backward flow of blood (inc. preload)
3) Due to deformity or erosion of valve cusps, as from endocarditis,
myocardial infarction or cardiac dilation (enlargement)- annulus
(supporting ring of valve) stretched, no longer allow complete closure
4) Blood volume and pressure decrease. in front of involved valve
5) Blood volume and pressure increased behind involved valve
6) Higher pressures and compensatory changes- needed to maintain
cardiac output lead to remodeling and hypertrophy of heart muscle
7) Eventually > pulmonary complications or heart failure
8) Inc. muscle mass and size > inc. myocardial oxygen consumption >
lead to ischemia and chest pain
4.
Murmurs-“characteristic” of valvular disorders (p. 879 tab. 37-13)
a. Valve disorder interfere with smooth flow of blood through heart
b. Blood flow turbulent; *Force of blood flow through stenotic or regurgitant
valve – inc.risk infective endocarditis-damages endocardium of receiving
chamber.
5.
*Caused by acquired valvular disorders resulting from acute conditions (infective
endocarditis) and chronic conditions (rheumatic heart disease); *Rheumatic
heart disease: *most common cause all types; damage from acute MI, (injury to
papillary muscles that affect valve leaf function); congenital heart disease (often
manifests in adulthood); effects of aging: changes in heart structure and function
6.
*Valvular disorders - in children and adolescents primarily congenital conditions;
adults from degenerative heart disease
RNSG 2432  1
Mitral Valve Stenosis
B.
Etiology/Pathophysiology of Mitral Stenosis
1.
Etiology- Majority adult cases-from rheumatic heart disease, scarring of valve
leaflets and chordae tendineae
2.
Contractures develop-adhesions between commissures of leaflets
3.
Stenotic mitral valve - “fish mouth” shape, thickening and shortening of valve
4.
Develop obstruction:  Left atrial pressure and volume; hypertrophy of
pulmonary vessels; chronic left atrial pressure elevation
5.
Clinical Manifestations/Complications mitral valve stenosis (879, Tab 37-13)
a. Asymptomatic or severely impaired
b. *Dyspnea on exertion (DOE): earliest
c. Cough, hemoptysis, frequent pulmonary infections, paroxysmal nocturnal
dyspnea, orthopnea, weakness, fatigue, palpitations
d. Later-right ventricular dilation and hypertrophy, HF (decreased CO)
e. *If progress to right heart failure: jugular vein distension, hepatomegaly,
ascites, peripheral edema (think why)
f. Chest pain from decreased cardiac output
g. Auscultation: loud S1, split S2, mitral opening snap; diastolic murmur- lowpitched, rumbling, crescendo-decrescendo, bell in apical region
h. Atrial dysrhythmias esp. *atrial fib. may cause emboli to brain, coronary
arteries, kidneys, spleen, extremities (why? p. 879)
i. Hoarseness, seizures, stroke (from emboli)
Mitral Regurgitation (Regurgitation, Incompetence, Valve Insufficiency)
2  RNSG 2432
C.
Etiology/Pathophysiology of Mitral Regurgitation
1.
2.
3.
Valve function depends on intact mitral leaflets, integrity of mitral annulus,
chordae tendineae, papillary muscles, left atrium, left ventricle; any defect can
result in regurgitation
Mitral valve does not close fully; allows blood to flow back into left atrium during
systole; *Great risk with MI and left ventricular failure – lead to rupture of chordae
tendineae; sudden increase in vascular resistance and cause pulmonary
edema! (Why?) * Most cases due to due to MI, chronic rheumatic heart
disease, mitral valve prolapse, ischemic papillary muscle dysfunction, infective
endocarditis
Clinical Manifestations:
a. Asymptomatic for years until development of some degree of left ventricular
failure
b. Initially > inc. left atrial volume; *dilation of left atrium due to regurgitation of
blood into LA during systole
c. LA dilation and hypertrophy then pulmonary congestion (left-sided heart
failure) then right sided heart failure
d. *LV dilation and hypertrophy-due to inc. preload; have *dec. CO (think
why)
e. Symptoms
1) Acute (poorly tolerated) fulminating pulmonary edema, shock etc, new
systolic murmurs
2) Chronic- initial symptoms left ventricular failure; fatigue, palpitations and
dyspnea; S3 sound, holosystolic or pansystolic murmur most clear at
apex; weakness, orthopnea
3) *Think left-sided heart failure (pulmonary congestion, edema) >right
sided heart failure
Mitral Valve Prolapse
D.
Etiology/Pathophysiology of Mitral Valve Prolapse
1.
Abnormality mitral valve leaflets and papillary muscle or chordae- allows leaflets
(or mitral valve cusps to “billow” (or prolapse) into atrium during ventricular
systole
2.
*Most common in women aged 14 – 30- *Most common form of valvular
disease in US-cause unclear; ?result from rheumatic heart disease, ischemic
heart disease, inherited connective tissue disorders such as Marfans; *usually
benign; if thickened, mitral leaflets > morbidity and sudden death.
RNSG 2432  3
3.
Clinical manifestations
a. Most asymptomatic for life
b. Murmur from insufficiency- gets more intense through systole
c. *Late or holosystolic murmur; clicks mid to late systole - may be constant
or vary beat to beat; does not alter S1, S2 sounds
d. Dysrhythmias inc. paroxysmal supraventricular tachycardia (PSVT),
ventricular tachycardia (VT)
e. Palpitations
f. Lightheadedness, dizziness
g. May or may not be present with chest pain; if pain occurs, episodes tend to
occur in clusters, especially during stress (*atypical type chest pain)
h. Pain may be accompanied by dyspnea, palpitations, and syncope
i. *Pain does not respond to antianginal treatment (*use B-adrenergic
blocking agents for chest pain and control palpitations)
j. Complications; **Chance for inc. risk for bacterial endocarditis if leads to
regurgitation > heart failure > develop thrombi and embolization
>transient ischemic attacks (TIAs); *require prophylactic antibiotics .
k. *Refer to Teaching Guide for Mitral Valve Prolapse p. 880, Tab. 37-14
Aortic Stenosis
E.
Etiology/Pathophysiology of Aortic Stenosis
1.
Usually discovered in childhood, adolescence, or young adulthood; if seen later
in life usually aortic stenosis from rheumatic fever or senile fibrocalcific
degeneration of a normal valve; More common in males than females- *causes
idiopathic; congenital defect; (often also has mitral valve disease); degenerative
disease (associated with aging); May be asymptomatic for years
2.
*Isolated aortic valve stenosis almost always of nonrheumatic origin
a. Results in obstruction of flow from left ventricle to aorta during systole; effect
= *left ventricular hypertrophy and  myocardial oxygen consumption
due to  myocardial mass
b. *Leads to  CO and pulmonary hypertension
c. *Also-with inc. work of left ventricle >left ventricle hypertrophy > myocardial
ischemia (inc. oxygen consumption) > dec. coronary blood flow (*Why?)
Leads to pulmonary vascular congestion (pulmonary HTN) and edema
d. ** Inc. afterload >reduced CO > LV hypertrophy > incomplete emptying
of LA > pulmonary congestion>RV strain (**Why??)
4  RNSG 2432
3.
Clinical manifestations
a. Syncope, angina, syncope, exertional dyspnea; S (syncopy) A (angina) D
(dyspnea) SAD *Chest pain! =Triad reflects left ventricular failure; have
narrow pulse pressure
b. Poor prognosis if experiencing symptoms and valve obstruction not relieved
c. *Nitroglycerin contraindicated (reduces preload; need preload to allow
(force) stiffened valves to open. *Understand this!
d. Auscultatory findings: normal to soft first heart sound, diminished or absent
second heart sound
e. **Harsh systolic crescendo–decrescendo murmur that ends before
second heart sound; prominent fourth sound; may radiate to carotid
arteries (good NCLEX audio question!)
f. *Untreated leads >pulmonary hypertension and right ventricular failure;
increased risk for sudden cardiac death!
Aortic Regurgitation (Aortic Insufficiency)
F.
Etiology/Pathophysiology of Aortic Regurgitation
1.
Primary disease (congenital), discovered in childhood, adolescence, or young
adulthood; if later found, may result from disease of aortic valve leaflets, aortic
root, or both
2.
May to due to infective endocarditis, trauma, aortic dissection
3.
Chronic aortic regurgitation from rheumatic heart disease, congenital bicuspid
aortic valve, syphilis, chronic rheumatic heart conditions
4.
Physiology- Retrograde blood flow from ascending aorta to left ventricle lead to
volume overload (*Blood flows back into left ventricle from aorta during diastole
= inc. preload-*60% of stroke volume can be regurgitated)
a. Initial- l. ventricle compensate by dilation and hypertrophy; then myocardial
decline in contractility
b. Pulmonary hypertension and R. ventricular failure develop (*inc. diastolic
left ventricular pressure)
5.
Clinical manifestations
a. Acute: sudden cardiovascular collapse, l. ventricle with high aortic “back”
pressure during diastole; weakness, severe dyspnea, chest pain,
hypotension
1) Medical emergency-If *SEVERE Aortic Valve Regurgitation: pulses “water-hammer” or collapsing with abrupt distention during systole and
quick collapse during diastole-**Also wide pulse pressure, “water-hammer” pulse “Water hammer”
(jerky pulse: full, then collapses due to aortic insufficiency (when blood
ejected into the aorta regurgitates back through aortic valve into left
ventricle; Also called Corrigan pulse or cannonball, collapsing, pistolshot, or trip-hammer pulse (Click here for video Corrigan’s pulse)
RNSG 2432  5
2) May have characteristic head bob (Musset’s sign)- shakes whole body
3) Auscultatory- soft or absent S1. presence of S3 and S4 ; soft, highpitched diastolic murmur; systolic ejection click; Austin-Flint murmur
(good one to listen too!)
b. Chronic aortic regurgitation; remains asymptomatic for years: exertional
dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND)
G.
Etiology/Pathophysiology of Tricuspid & Pulmonic Valve Disease
1.
*Uncommon -diseases of tricuspid and pulmonic valve (p. 879, tab 37-13)
2.
Tricuspid stenosis (more frequent than regurgitation) , Rt. atrial output
obstructed; cause right atrial enlargement and elevated systemic venous
pressure
3.
Tricuspid stenosis- almost always in patients with rheumatic mitral stenosis, IV
drug abusers, or patients treated with dopamine agonist (Dostinex) *antiparkinson drug…PS…not sure how/why this effects heart???
4.
Pulmonic stenosis results in right ventricular hypertension and hyper trophy ;
almost always congenital; cause backward flow of blood from right ventricle;
then right ventricle hypertension and hypertrophy
5.
Common Manifestation /Complications: *Result- R sided heart failure-Why!
a. Tricuspid stenosis
1) Right sided failure (peripheral edema, hepatomegaly, etc)
2) Atrial fibrillation, (*atrial dilation-key factor)
3) Diastolic love-pitched murmur decrescendo murmur with inc. intensity
during inspiration
b. Pulmonic stenosis (asymptomatic unless severe)
1) Fatigue. Dyspnea on exertion,; progress to “right sided heart failure”
2) Loud, harsh midsystolic murmur (hear in pulmonic area, second left
intercostal space
H.
Collaborative Care- Valvular disease1.
*Keys- prevent recurrent rheumatic fever and infective endocarditis
(majority valvular due to endocarditis or rheumatic fever) (See p. 865) *Infective
endocarditis –“infection of endocardial surface of heart, contiguous with heart
valves and damages heart valves)
2.
Keys-*Important- valvular dysfunction usually identified by physical exam- *hear
murmur; defects in structure or function of valves interfere with proper cardiac
circulation (have either stenosis or regurgitation)- *effect on preload, afterload,
lead to heart failure, pulmonary hypertension (change in hemodynamics)
a. Close observation for progression of disease
b. *Prophylactic therapy (antibiotics before invasive procedures as dental
cleaning) to prevent valvular infection (*endocarditis)
c. *Manage heart failure (if present): diet, meds, surgical repair/replacement
valves
d. *Treatment depends on valve involved and severity of disease
e. Focus - preventing
1) Exacerbations of heart failure
2) Acute pulmonary edema
3) Thromboembolism
4) Recurrent endocarditis
3.
*Drugs- prevent/manage complications as dysrhythmias, thrombolism, heart
failure
a. *Atrial dysrhythmias most common (esp with mitral stenosis)- treat with
antidysrhythmics meds, digoxin, electrical cardioversion, B-adrenergic
blockers (review p.856, tab 36-8)
b. Anticoagulation (esp if atrial fibrillation present)
6  RNSG 2432
c.
4.
5.
6.
*Prophylactic antibiotics prior to dental work, prevent bacterial
endocarditis.
d. Diuretics, drugs to manage heart failure (if develops)
e. ACE inhibitor; dec. blood pressure, reduce afterload (increase CO)
f. Vasodilator; lower blood pressure; reduce afterload (increase CO)
Diet- low sodium if at risk for heart failure.
Diagnostic tests *Determine type, degree valvular problem
a. Generally based on history; PE; chest X-ray, ECHO, heart cath, EKG, TEE
(p. 881, Tab. 37-15)
b. Echocardiography & TEE (TransEsophageal Echo): identify valve leaflets
abnormalities, myocardial function, chamber size, EF
c. Chest X-ray; for cardiac and blood vessel hypertrophy, calcifications of valve
leaflets and annular openings (review)
d. Electrocardiography; identifies atrial and ventricular hypertrophy, associated
conduction defects or dysrhythmias; most common-*atrial fib; need 12 lead
(review)
e. Cardiac catheterization; assess cardiac contractility; measure pressure
gradients across heart valves, heart chambers, and within pulmonary system
(Heart failure?)
Surgical Interventions- Valvular disease (open & closed procedures)
*recognize, identify each!
a. *Terms associated with repair/replacement of heart valves
1) Annuloplasty-repair of a cardiac valve's outer ring
2) Chordoplasty- repair of the tendinous fibers that connect the free edges
of AV valve leaflets to papillary muscles
3) Commissurotomy- splitting or separating fused cardiac valve leaflets
4) Heterograft- heart valve replacement made of tissue from an animal
heart valve (synonym: *xenograft)- *biologic graft
5) Homograft- heart valve replacement made from a human heart valve*(synonym: allograft)- *biologic graft
6) Leaflet repair- repair of a cardiac valve's movable “flaps” (leaflets)
7) Valve replacement-insertion of a device at site of a malfunctioning heart
valve to restore blood flow in one direction through heart (can use a
biologic or mechanic replacement device)
8) Valvuloplasty- (a general term) repair of a stenosed or regurgitant
cardiac valve by Commissurotomy (valvotomy), Annuloplasty, leaflet
repair, or chordoplasty (or a combination of procedures)- summary of
procedures*
b. Not all types valve disease require surgery
1) Decision by valves involved, pathology, severity, patient condition
2) *Procedure palliative, not curative
3) Closed method (as mitral commissurotomy-valvulotomy)-less precise,
ok is “pure” mitral stenosis
4) Open method, direct vision-need cardiopulmonary bypass (heart lung
machine)
5) *Risks of valve repair without replacement of valve- may not establish
valve competence
6) **Repair valve (replace only if required)
c. *From CABG surgical considerations review - p. 809-810 related to open
heart, cardiopulmonary bypass- need ICU 24-36 hrs; careful monitoring
hemodynamic status including PA catheter, EKG status, may require pacing;
complications include use of coronary pulmonary bypass (CPB) as bleeding,
anemia, fluid and electrolyte imbalance, monitoring for bleeding (chest tube
drainage) READ/review this section …general complications to consider.
d. Percutaneous transluminal balloon valvuloplasty (PTBV) or called
Balloon Valvuloplasty non-invasive; passage of balloon catheter from
RNSG 2432  7
femoral vein through atrial septum to mitral valve or through femoral artery to
aortic valve; balloon inflated to enlarge orifice. *Risks- arterial puncture;
caution to monitor for bleeding at catheter insertion site; systemic emboli;
need to monitor for CO (related to regurgitant valve and changes in
hemodynamic pressure).
1) Used for mitral, tricuspid and pulmonic stenosis (*most often for mitral
stenosis); not as often for aortic stenosis
2) Performed in cath lab; best for older patients; fewer complications
3) *Not used if valve both tight and regurgitant or if blood clots in heart
chambers (risk of dislodging clots)
e. Annuloplasty-tightening and suturing the malfunctioning the malfunctioning
valve annulus (ring) to eliminate or markedly reduce regurgitation (often for
mitral valve)8 narrows valve orifice; Need general anesthesia,
cardiopulmonary bypass.
f. Commissurotomy/valvulotomy; requires open heart; direct visualization;
valve visualized, thrombi removed from atria; fused leaflets incised and
calcium debrided from leaflets to widen orifice.
1) Surgical *Most common valvuloplasty- (commissurotomy) --each valve
has leaflets; (*site where leaflets meet called commissure); Can use
closed method, but difficult to remove emboli* ( See p. 882 for Surgical
care pre & post considerations)
2) *Used often for mitral valves (Think about mitral stenosis, risk for a-fib &
why)
8  RNSG 2432
3) Requires use of heart lung machine (open method)
4) For mitral stenosis, involves several procedures, including debriding
calcified valve
g. Ross procedure: use one valve (pulmonic) for another (aortic)
h. *Many innovative procedure to correct valvular problems…view PPT slides
(be aware of innovations, not test on them)
i. Valve Replacement *some patients may need!
1) Valve replacement began 1960s- valve choice determined by many
factors (see p. 882).
2) Need general anesthesia and cardiopulmonary bypass
3) Incision through a median sternotomy (ie, incision through the sternum)
4) *Mitral valve- may approach through right thoracotomy incision. Mitral,
rarely aortic, valve replacements- may use minimally invasive techniques
not require cutting through length of sternum (robot assisted)
5) Hospital stays- little as 3 days; recovery 3 weeks.
6) *Surgery abruptly “corrects” blood flows through heart; complications
unique to valve replacement due to *sudden changes in intracardiac
blood pressures(hemodynamic alterations)
a) Risk for postop complications, as bleeding, thromboembolism,
infection, HF, hypertension, dysrhythmias, hemolysis, and
mechanical obstruction of valve
b) *Types of valves- (p. 882, 883, Tab 37-16) mechanical valve (from
combination metal alloys) or biologic valve from pig (porcine), cow
(Bovine) or human cardiac tissue; repair preferred when possible
over valve replacement.
c) *Mechanical and biologic prosthetic advantages/disadvantages:
Anticoagulation needed- mechanical valves- *thromboembolic
risk; *Biologic valves- short life expectancy (7 to 14 years).;
mechanical longer life- better for younger person usually; *Know
nursing implications/ advantages, disadvantages each type
valve replacement (mechanical or biologic). (*see p.882-883,
Tab 37-16) ; *Both types valve replacement at risk for leakage and
endocarditis. (from text- p 883) **This is important!!
RNSG 2432  9
A & B both mechanical; C biologic (porcine)
I.
Nursing Management for Valvular Disease
1.
Nursing assessment- See p. 883 Tab 37-17; check assess for subjective and
objective date especially abnormal heart sounds (murmurs, clicks, S3, S4 ),
dysrhythmias, peripheral edema, crackles, wheezes, etc.
2.
Nursing Diagnoses (see p. 884, 885 NCP)
a. Activity intolerance
b. Excess fluid volume
c. Decreased cardiac output
d. Ineffective therapeutic regimen management
e. Planning includes patient will have:
1) Normal cardiac function
2) Improved activity tolerance
3) Understanding of the disease process and preventive measures
3.
Nursing Implementation prevention rheumatic valvular disease by
a. Diagnosing and treating streptococcal infection
b. Providing *prophylactic antibiotics for patients with history of rheumatic
heart disease
c. Treating patient with *history of endocarditis with prophylactic Antibiotics
1) Teach when to seek medical treatment
2) Design activity to patient’s limitations
3) Discourage smoking
4) Avoid strenuous activity
5) Auscultatory assessment to monitor effectiveness of medications
6) Medical alert bracelet
7) Teach importance of completing antibiotic regimen, drug side effects
8) Manage anticoagulation therapy-INR (know therapeutic ranges)
9) Follow-up care
d. Appropriate *instructions for patient with valve replacement (know if
mechanical or biologic) *mechanical needs life-long anticoagulants
*important!
1) Instruct re anticoagulant therapy; report excessive bruising, monitoring
for therapeutic levels
2) Good oral hygiene to reduce risk of infective endocarditis (high risk with
valvular disease, valve replacement)
3) Prophylactic antibiotics prior to ANY invasive procedures (including
dental); need to inform all health care professionals of valvular disease
history
4) Wear Medic-Alert bracelet
5) Note-if mechanical valve, will have audible click
4.
Evaluation
a. Demonstration of cardiac tolerance to increased activity
1) Normal BP, HR, and breath sounds
2) No peripheral edema, no fatigue
3) Knowledge of signs and symptoms when to seek health care
4) Knowledge of when to use prophylactic antibiotics
5) Adherence to therapeutic regimen
10  RNSG 2432
Cardiomyopathy
A.
B.
Etiology/Pathophysiology of Cardiomyopathy
1.
Cardiomyopathy (CMP)- group of diseases that directly affect structural or
functional ability of myocardium. (* from wikipedia- “heart muscle disease”
…deterioration of actual function of myocardium for any reason…people with
cardiomyopathy often at risk of arrhythmia or sudden cardiac deathc or both.
Categorized as extrinsic -*most common type, due to cause that originates
outside myocardium itself; includes ischemic, valvular, alcoholic, inflammatory,
hypertensive; or intrinsic focus for this unit, myocardial weakness/alteration not
due to identifiable cause.
a. CMP-classified as primary (those conditions in which etiology of heart
disease unknown) or secondary (cause known but secondary to another
disease process)
b. Cardiomyopathies can lead to cardiomegaly, *HF, *leading cause for
heart transplants
Types cardiomyopathy (Intrinsic)
1.
Dilated
2.
Hypertropic
3.
Restrictive
Dilated Cardiomyopathy
A.
Etiology/Pathophysiology Dilated Cardiomyopathy (p. 885, 885,Tab 37-18 & 37-9)
1.
Characterized by diffuse inflammation, rapid degeneration of myocardial fiberslead to ventricular dilation, impairment of *systolic function, atrial
enlargement, stasis of blood in left ventricle. (What is risk of blood stasis?)
2.
*40% develop HF (right and left sided)
3.
More frequent in African American, men, some genetic relationship; follow
infectious endocarditis, *viral infection
B.
Clinical manifestations (HF)
1.
Develop acutely post infectious process or insidiously over period of time
2.
Symptoms- dec. exercise capacity, fatigue, dyspnea at rest, paroxysmal
nocturnal dyspnea, orthopnea, palpitations, abdominal bloating, nausea,
vomiting, and anorexia
3.
Signs - irregular heart rate with an abnormal S3 and/or S4, (*signs heart failure)
, tachycardia or bradycardia, pulmonary crackles, edema, weak peripheral
pulses, pallor, hepatomegaly, and jugular venous distention.
4.
Heart murmurs and dysrhythmias common.
5.
*Symptoms most often related to heart failure- * Heart chamber dilate and
contraction impaired > dec. EF%; Complications: *Sudden death (due to
dysrhythmias);
RNSG 2432  11
C.
A.
Collaborative Care for Dilated Cardiomyopathy
1.
*Focus- control HF- enhance myocardial contractility and decrease afterload
(drug therapy usually key): goal of therapy -keep the patient at an optimal level
of function and out of hospital
2.
Diagnostic tests
a. Evaluate patient history; r/o other causes HF; maybe biopsy
b. Doppler ECHO (p. 753)
c. Chest X-ray (signs of enlarged heart
d. EKG
e. Lab studies (esp BNP) (know what this is!)
f. Cardiac Catheterization, MUGA, dec EF (p. 754)
3.
Nutritional therapy
a. Low sodium diet
4.
Drug therapy (key)* (p. 831, Tab 35-9 & p. 887) & p. 831-833 (review HF)
a. Nitrates
b. Loop diuretics
c. ACE inhibitors
d. B-Adrenergic Blockers and aldosterone blockers (spironolactone)
e. *Digoxin & other antidysrhythmics (note cautions-see text p. 887)
f. *Anticoagulation (Why?)
g. *Dobutamine, milrinone infusions & diuresis (recall how these drug work to
treat /manage HF)
h. Need to change habits (stop alcohol if a factor)
i. *Maybe immunosuppressive drugs-if autoimmune cause
5.
Surgical/resynchronization therapy
a. Ventricular assist device (VAD)- allow heart to rest and recover from acute
HF or act as bridge to heart transplantation
b. Cardiac resynchronization therapy (CRT) (p. 830) and implantable
cardioverter-defibrillator (p. 857-858) –for some cases
c. If end stage- consider for heart transplant- or destination therapy with
permanent or implantable VAD (p. 837-840-review).
Hypertropic Cardiomyopathy
Etiology/Pathophysiology
1.
Hypertrophic cardiomyopathy (HCM)- asymmetric left ventricular hypertrophy
without ventricular dilation *Also
a. *Four main characteristics of HCM:
1) Massive ventricular hypertrophy
2) Rapid, forceful contraction of the left ventricle
3) Impaired relaxation (diastole)
4) Obstruction to aortic outflow (not present in all patients).
b. End result- impaired ventricular filling as ventricle becomes noncompliant
and unable to relax (diastolic dysfunction);
c. *Most common cause of SCD in otherwise healthy young people.
12  RNSG 2432
B.
C.
A.
B.
C.
Clinical manifestations (p. 888)
1.
Asymptomatic or may have exertional dyspnea, fatigue, angina
2.
*Dyspnea- most common due to sudden elevated left ventricular diastolic
pressure-(obstruct blood flow from ventricle through aorta> dec. cardiac output
> *inc. pulmonary and venous pressures)
3.
Fatigue due to sudden dec. in CO (exercise induced flow obstruction)
4.
Angina from increased left muscle mass or compression of small coronary
arteries
5.
Syncopy due to obstruction of aortic outflow during inc. activity (dec. CO
and circulatory collapse)
6.
*Dysrhythmias > SCD
Collaborative Care for Hypertropic Cardiomyopathy
1.
*Goals of intervention-*improve ventricular filling: reduce ventricular
contractility and relieve left ventricular outflow obstruction.
2.
Diagnostic Studies
a. Assessment: on palpation- “forced” apical, sound heard more laterally
b. S4 heart sound, systolic ejection murmur between apex and sternal border at
fourth intercostals space
c. EKG shows ventricular hypertrophy,
d. *ECHO show left ventricular hypertrophy, wall motion abnormalities
e. Cardiac Catheterization
3.
Drug therapy for HCM
a. *-adrenergic blockers or calcium channel blockers- (negative inotropic
dec. myocardial contractility to decrease obstruction of outflow tract; dec.
rate and inc. ventricular compliance and inc. diastolic filling time and cardiac
output; (avoid vasodilators, digitalis, nitrates **Think WHY??
b. ** Digitalis preparations contraindicated unless used to treat atrial
fibrillation; antidysrhythmics used as needed. (Need to understand why not
use drugs that increase contractility as digitalis?)
4.
Surgical/Other Treatment
a. Cardioverter-defibrillator (ICD)recommended-at risk for SCD
b. Atrioventricular pacing-beneficial for patients with HCM and outflow
obstruction
c. *Ventriculomyotomy and myectomy, (involves incision of hypertrophied
septal muscle and resection of some of the hypertrophied ventricular muscle)
5.
Nursing interventions for HCM
a. Focus on relieving symptoms
b. Observe for and preventing complications
c. Provide emotional and psychological support.
Restrictive Cardiomyopathy (p. 889)
Etiology/Pathophysiology-Restrictive Cardiomyopathy
1.
*Least common CMP, impairs diastolic filling and stretch; systolic function
unaffected
2.
Ventricular walls do not stretch during diastolic filling; lead to “backwards”
pressure and right heart failure, dec. stroke volume and low cardiac output.
3.
*Can have normal EF (due to restricted diastolic filling)
4.
Specific etiology often unknown; infiltrative processes, myocardial fibrosis,
sarcoidosis
5.
Generally poor prognosis
Clinical Manifestations
1.
Fatigue, exercise intolerance, and dyspnea (heart cannot increase CO by
increasing heart rate without further compromising ventricular filling)
2.
Symptoms of heart failure (right sided)
Collaborative Care for Restrictive Cardiomyopathy
RNSG 2432  13
1.
D.
Diagnostic Studies
a. Chest X-Ray to identify cardiomegaly, left atrial enlargement, pleural
effusions, etc
b. ECG, show esp tachycardia, usually supraventricular dysrhythmias (atrial
fibrillation) or AV block (*why?)
c. ECHO , EMB, CT nuclear imaging to diagnose
2.
Drug therapy
a. Meds- *improve diastolic filling; conventional therapy for management of
dysrhythmias, heart failure (refer to previous treatment modalities as ACE
inhibitors, vasodilators, digitalis); anticoagulants
b. *No specific treatment for restrictive CMP exists- treat (if can identify)
underlying disease process.
3.
Surgical/Other Treatment
Nursing care
1.
Similar to care of patient with HF.
2.
See p. 889, Tab. 37-21 for patient and family teaching guidelines
Summary of Cardiomyopathy (key facts) (Refer also p. 886 Tab 37-18, 19, 20)
A.
Assessment (as above)
1.
Fatigue all types
2.
Dilated; weakness, signs of left heart failure, S3 & S4;
Hypertropic: exertional dyspnea, syncope, angina, signs of heart
failure S4, sudden death may be first sign: syncopy;
Restrictive: dyspnea, right-sided heart failure, S3 & S4, emboli
formation
B.
Diagnostic tests: (same as with valvular disease)
1.
Echo2.
EKG
3.
CXR
4.
Hemodynamic changes
5.
Perfusion scan
6.
Cardiac cath
7.
Myocardial biopsy (Why important?)
C.
Medications (*determined by symptoms)
1.
No medical therapy to cure/prevent cardiomyopathy; medical regime to treat
symptoms/determine type of cardiomyopathy
2.
Caution with medication; antiarrhythmic drugs decrease contractility; are
negative inotropes (*hypertropic-need to dec. contractility)
3.
May need ICD to override potentially dysrhythmias (What is an ICD?)
4.
Dual chamber pacemaker
5.
See specific disease process (if autoimmune cause; maybe immunosuppressive
drugs)
D.
Invasive procedures, surgery:
1.
Vad-bridge to transplant
2.
Heart Transplant (only effective treatment!)
3.
Myoloplasty Hypertrophic (myectomy)- excision of ventricular septum
4.
ICD
5.
Dual chamber pacemaker/Biventricular pacing (Why/how does a pacemaker
help?)
E.
Nursing Diagnoses: (p. 915)
1.
*Decreased Cardiac Output
2.
Fatigue
3.
Ineffective Breathing Pattern
4.
Fear
5.
Ineffective Role Performance
6.
Anticipatory grieving
14  RNSG 2432
F.
Heart Transplant/Open Heart Surgery Click here for (Open Heart Surgery “Practice”
& here to do a Heart Transplant!
1.
Require use of Heart Lung Machine
Aneurysm (Aortic Aneurysm & Aortic Dissection
(click-view UTUBE lecture)
A.
B.
Etiology/Pathophysiology of Aortic Aneurysm
1.
Aneurysms, most common problem of aorta-outpouchings or dilations of arterial
wall
2.
Common problems involving aorta; more frequent in men than women
3.
Incidence  with age
4.
Abdominal aortic aneurysms (AAA)- occur in 4.1% to 14.2% of men; 0.35% to
6.2% of women over 60; cause of 16,000 deaths per year
5.
May involve aortic arch, thoracic aorta, and/or abdominal aorta; *most found in
abdominal aorta below renal arteries
6.
¾ of true aortic aneurysms occur in abdominal aorta; ¼ found in thoracic; may
have aneurysm in more than one location
7.
Growth rate unpredictable
8.
*Larger the aneurysm greater risk of rupture- Half all aneurysms greater
than *6 cm- rupture within 1 year! *Monitor
9.
*Dilated aortic wall becomes lined with thrombi-can embolize: leads to acute
ischemic symptoms in distal branches
10. Atherosclerotic plaques deposit beneath intima; plaque formation thought to
cause degenerative changes in media (middle lining)-lead to loss of elasticity,
weakening, and aortic dilation
11. Male gender and smoking stronger risk factors than hypertension and diabetes
12. Studies suggest strong genetic predisposition
13. Other predisposing factors as degenerative disorders, congenital, familial
tendency etc.; *most common cause-atherosclerosis
Classification-Aneurysms- 2 basic classifications
1.
True
a. Wall of artery forms aneurysm
b. At least one vessel layer still intact
c. Further subdivided into
1) Fusiform-circumferential, relatively uniform in shape
2) Saccular- pouchlike with narrow neck connecting bulge to one side of
arterial wall
RNSG 2432  15
Saccular
Fusiform
False aneurysm (or pseudoaneurysm-not an aneurysm)
a. Disruption of all layers of arterial wall
b. Results in bleeding contained by surrounding structures
c. May result from trauma, infection, post peripheral artery bypass graft surgery
at site of anastomosis, arterial leakage after cannulae removal
Clinical Manifestations
2.
C.
1.
2.
Thoracic aorta aneurysms often asymptomatic
a. *Most common manifestation-deep diffuse chest pain
b. Pain may extend to interscapular area
*Aortic Aneurysm- Ascending aorta/aortic arch
a. *Produce angina, hoarseness if presses on superior vena cava; decreased
venous return-cause distended neck veins, edema of head and arms
b. *Abdominal aortic aneurysms (AAA)- often asymptomatic; frequently
detected on physical exam
1) *Pulsatile mass in periumbilical area
2) Bruit may be auscultated when examined for unrelated problem (i.e.,
CT scan, abdominal x-ray)
3) May mimic pain associated with abdominal or back disorders
4) *May spontaneously embolize plaque causing “blue toe syndrome”,
patchy mottling of feet/toes with presence of palpable pedal pulses
c. Complications
1) *Rupture- life-threatening complication related to untreated aneurysm
2) *Posterior rupture; Bleeding may be tamponaded by surrounding
structures, thus preventing exsanguination and death; severe pain;
may/may not have back/flank ecchymosis
3) *Anterior rupture; Massive hemorrhage, most do not survive long
enough to get to the hospital
16  RNSG 2432
D.
Collaborative Care for Aortic Aneurysm
1.
Goal- Prevent rupture of aneurysm
a. Early detection/treatment imperative
b. Once detected studies done to determine size and location
c. If carotid and/or coronary artery obstructions present, may need to be
corrected before repair
d. **Small aneurysm (<4 cm)-conservative therapy used
e. Risk factor modification key1) ↓ Blood pressure- follow with ultrasound, MRI, CT scan monitoring q 6
months
2) *5.5 cm =threshold for repair; intervention at <5.5 cm in women with
AAA(High risk for rupture)
*Rupture Triad- 3 key features for AAA (abdominal aortic aneurysm)
2.
3.
4.
Pulsating Hematoma > Back Pain > Hypotension (untreated >
death!)
f. Surgical intervention may occur earlier in younger, low risk patients,
patients with rapidly expanding aneurysm, symptomatic patient, high rupture
risk; older, high risk patients-endovascular repair may be treatment of choice
Drug Therapy-*Key control blood pressure; (*but avoid direct arterial
vasodilators (as hydrazaline) due to effect on arterial wall.)
Diagnostic Studies
a. X-rays-Chest - Demonstrate mediastinal silhouette and any abnormal
widening of thoracic aorta; abdomen -may show calcification within wall of
AAA
b. ECG -to rule out MI
c. Echocardiography- assists in diagnosis of aortic valve insufficiency, related to
ascending aortic dilation
d. Ultrasonography-useful in screening for aneurysms, monitor aneurysm size
e. CT scan- most accurate test to determine anterior to posterior length; crosssectional diameter; presence of thrombus in aneurysm
f. MRI-diagnose and assess location and severity
g. Angiography- anatomic mapping of aortic system using contrast; not reliable
method of determining diameter or length; can provide accurate info about
involvement of intestinal, renal or distal vessels
Surgical Therapy
a. If ruptured, emergent surgical intervention- *33%-94% mortality with
ruptured AAAs *Important to understand
b. Pre-op: Hydration: Electrolyte, coagulation, hematocrit stabilized
c. *Surgical Technique- (See p. 896, Fig 38-4)- (open procedure)
1) Incising diseased segment of aorta
2) Removing intraluminal thrombus or plaque
3) Inserting synthetic graft-Dacron or polytetrafluoroethylene (PTFE)
4) Suturing native aortic wall around graft, act as protective cover
RNSG 2432  17
5.
d. Autotransfusion-reduces need for blood transfusion during surgery
e. *All AAA resections require cross-clamping of aorta proximal and distal
to aneurysm, can be completed in 30-45 minutes, clamps removed and blood
flow restored to lower extremities
1) If extends above renal arteries or if cross clamp must be applied above
renal arteries- adequate renal perfusion after clamp removal should be
ascertained before closure of incision. *Check peripheral pulses before
and after procedure!
2) *Risk of postop renal complications  significantly when repair
above renal arteries
f. Endovascular graft procedure- minimally invasive (See p. 896, fig 38-5)involves placement of sutureless aortic graft into abdominal aorta
inside aneurysm; done through femoral artery cutdown
1) Graft- constructed from Dacron cylinder surface supported with rings of
flexible wire delivered through sheath to predetermined point. deployed,
against vessel wall by balloon inflation.
2) Anchored to vessel by series of small hooks. (Stent)
3) Blood then flows through graft prevent expansion of aneurysm;
aneurysm wall begin to shrink over time
4) Benefits graft- less anesthesia and operative time, smaller operative
blood loss;  morbidity and mortality; more rapid resumption of physical
activity; shortened hospital stay; etc
5) Potential complications (graft) aneurysm growth, aneurysm rupture;
*perigraft leaks (most common complication); aortic dissection,
bleeding; graft dislocation and embolization, etc.
g. *New approach-percutaneous femoral access
1) Advantages: shorter operative time; shorter anesthesia time; reduction in
use of general anesthesia; reduced complications
Nursing Management
a. Assessment
1) Thorough history and physical exam
2) Watch for signs of cardiac, pulmonary, cerebral, lower extremity vascular
problems
3) Establish baseline data to compare postoperatively incl peripheral
pulses, neurological status.
4) Monitor for indications of rupture: diaphoresis, paleness, weakness,
tachycardia, hypotension, *abdominal, back, groin or periumbilical pain;
changes in level of consciousness; pulsating abdominal mass5) *If rupture imminent/prepare for immediate surgery
18  RNSG 2432
b. Nursing Diagnosis
1) Risk for Ineffective Tissue Perfusion
2) Risk for Injury
3) Anxiety
4) Pain
5) Knowledge Deficit
c. Planning: Overall goals include
1) Normal tissue perfusion
2) Intact motor and sensory function
3) No complications related to surgical repair
d. Nursing Implementation
1) Health Promotion
2) Alert for opportunities to teach health promotion to patients and their
families
3) Encourage patient to reduce cardiovascular risk factors; these measures
help ensure graft patency after surgery
4) Acute Intervention
a) Patient/family teaching
b) Providing support for patient/family
c) Careful assessment of all body systems
d) *Pre-op teaching-Explanation of disease process, planned surgical
procedures, Preop routines, etc. (see text); explain Post-op careICU monitoring, Arterial line, Central venous pressure (CVP) or
pulmonary artery (PA) Catheter, mechanical ventilation, urinary
catheter, Nasogastric tube, ECG, Pulse oximetry, pain medication
e) *Post-op- *Maintain graft patency, *normal blood pressure; CVP or
PA pressure monitoring; *urinary output monitoring important;
avoid severe hypertension (disrupt graft integrity); drug therapy may
be indicated; cardiovascular status; continuous ECG monitoring;
electrolyte monitoring; arterial blood gas monitoring; oxygen
administration; observations for infection, need for antibiotic
administration; etc (See p. 897) GI status: Nasogastric tube,
abdominal assessment, passing of flatus is key sign of returning
bowel function, *Peripheral perfusion status: pulse assessment,
mark pedal pulse location with felt tip pen; assessment;
temperature, color, capillary refill time, etc, Monitoring CVP/PA
pressure, Blood urea nitrogen/Creatinine etc
f) Note- Lower extremity pulse may be absent for short period of time
post procedure due to vasospasm, hypothermia; however, caution,
could be due to occlusion!! Immediate action needed, Read p, 898.
5) Home Care/Ambulatory care
a) instructed to gradually increase activities
b) No heavy lifting
c) Educate on signs and symptoms of complications: Infection;
Neurovascular changes
e. Evaluation: Expected Outcomes:
1) Patent arterial graft with: adequate distal perfusion
2) Adequate urine output
3) Normal body temperature
4) No signs of infection
Aortic Dissection- misnamed “dissecting aneurysm”
A.
Etiology/Pathophysiology of Aortic Dissection
1. Develops when a break or tear in tunica intima and media allows blood to dissect
layers of vessel wall ; creates “false” lumen in vessel wall
RNSG 2432  19
Aortic Dissection
2. Blood contained by adventitia forming longitudinal or saccular aneurysm
a. *Not really “aneurysm”; most often in thoracic area
b. Affects men more often than women; especially in 4th-7th decades of life
c. *Acute and life threatening; mortality rate 90% if not surgically treated
3. With contraction of heart; ↑ pressure on damaged area and further ↑ dissection
a. *May occlude major branches of aorta
b. Lead to loss of blood supply to brain, abdominal organs, kidneys, spinal cord,
and extremities
4. Cause uncertain
a. Due to destruction of medial layer elastic fibers
b. Most common in older individually with chronic hypertension
c. Marfan’s syndrome  incidence (Marfan’ syndrome & Michael Phelps)
d. *Blunt trauma can precipitate
B.
Clinical Manifestations
1.
*Depend on location of intimal tear and extent of dissection
2.
Pain sudden, severe pain, in anterior part of chest or pain that radiates down
spine to abdomen or legs; “ripping, or tearing” sensation, may mimic MI
a. As dissection progresses, pain may be above and below diaphragm; develop
cardiovascular, neurologic and respiratory signs- *aortic arch involvedneurologic deficiencies may be present (Why??)
b. Complications: cardiac tamponade- life-threatening due to blood escaping
from dissection in pericardial sac (review manifestations); hemorrhage into
mediastinal, pleural or abdominal cavity; rupture and exsanguinations/death;
and occlusion of arterial supply to vital organs.
C.
Collaborative Care- Initial goal - ↓ BP and myocardial contractility to
dec. pulsing forces within aorta (prevent inc. of dissection)
1.
Diagnostic Studies (see aortic aneurysm) (p. 900, Tab. 38-1)
a. Health history and physical exam
b. ECG
c. Echocardiogram- shows left ventricular hypertrophy (systemic HTN)
d. Chest x-ray- may show widening of mediastinal silhouette and left pleural
effusion
e. Transesophageal echocardiogram-show dissections closest to aortic root
f. MRI or multi-detector row CT scan (reflect severity of dissection)
g. Angiography-assess extent of dissection
2.
Drug therapy
a. (Acute risk)- IV administration β-adrenergic blocker as Esmolol (Brevibloc);
give other hypertensive agents as calcium channel blockers, sodium
20  RNSG 2432
D.
E.
nitroprusside, angiotensin-converting enzyme (ACE inhibitors) *Think why,
how these drugs are used.
b. Conservative therapy-no symptoms-*keep BP low; monitor; success of
treatment judged by relief of pain
Surgical/Emergency Treatment
1.
Emergency surgery-ascending aorta involved and symptoms present.
a. Surgical therapy- If drug therapy ineffective or complications of aortic
dissection present as heart failure, leaking dissection, occlusion of an artery
b. Surgery-delay-allow edema to decrease; permit clotting of blood
c. Surgery- involve resection of aortic segment and replacement with synthetic
graft material; extent of replacement depends on extent of dissection. *Even
with prompt surgical intervention, 30-day mortality very high- (10%28%)
Nursing Management
1.
Pre-op- Maintain adequate circulation, prevent extension of dissection-SemiFowler’s position, quiet environment, reduced anxiety; control pain with opioids
and tranquilizers as ordered; continuous IV administration of antihypertensive
agents; continuous ECG and intraarterial pressure monitoring; observation of
changes in quality of peripheral pulses; frequent vital signs
2.
Postop *See aneurysm post-op care (discussed earlier)
3.
Discharge teaching (See Aneurysm) * Therapeutic regimen-a Antihypertensive
drugs and side effects; If pain returns or symptoms progress, instruct patient to
seek immediate help
Open Heart-FYI see PPT for review & Cardiomyopathy section
RNSG 2432  21