NOTES Valvular/Cardiomyopathy/Aneurysm and Cardiac Surgery
Module #5: Nursing Care of the Individual with Cardiovascular Disorders” Valvular Heart Disease,
Cardiomyopathy, and Aneurysms
Valvular Heart Disease (click to play))
Click here for Tutorial on Valvular Heart Sounds (great resource for hearing heart sounds!!)
A.
B.
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.
853)
a. Stenosis (constriction or narrowing)
1) Valve orifice - restricted; valve leaflets fuse, unable to open or close completely
due to scarring from endocarditis, calcium deposits,
2) Impend forward blood flow; create pressure gradient across open valve
3) Degree of stenosis reflected in pressure gradient differences
4) Results in impedance of forward flow of blood >inc afterload, later stages >
inc preload also)
5) Dec cardiac output from impaired ventricular filling, (dec ejection and stroke
volume)
b. Regurgitation (insufficiency or incompetence)
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 dec. in front of involved valve; blood volume and
pressure inc behind involved valve
5) Higher pressures and compensatory changes- needed to maintain cardiac
output >lead to remodeling and hypertrophy of heart muscle
6) Eventually > pulmonary complications or heart failure
7) Inc. muscle mass and size > inc. myocardial oxygen consumption > lead to
ischemia and chest pain
4.
Murmurs-“characteristic” of valvular disorders (*p. 853 tab. 37-13) Key
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.
c. *Read chart carefully for key features of commons valvular disorders
5.
*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
Mitral Valve Stenosis
Etiology/Pathophysiology of Mitral Stenosis
1.
Etiology- Majority adult cases-from rheumatic heart disease, scarring 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 & volume; hypertrophy of pulmonary vessels;
chronic left atrial pressure elevation
5.
Clinical Manifestations/Complications mitral valve stenosis (853, Tab 37-13)
a. Asymptomatic or severely impaired
b. *Dyspnea on exertion (DOE): earliest; cough, hemoptysis, frequent pulmonary
infections, paroxysmal nocturnal dyspnea, orthopnea, weakness, fatigue, palpitations
c. Later-right ventricular dilation and hypertrophy, HF (dec CO)
RNSG 2432  1
d.
e.
f.
g.
h.
C.
*If progress to right heart failure: jugular vein distension, hepatomegaly, ascites,
peripheral edema (think why)
Chest pain from dec cardiac output
Auscultation: loud S1, diastolic murmur- low-pitched, rumbling, *bell in apical region
Atrial dysrhythmias esp. *atrial fib. may cause emboli to brain, coronary arteries,
kidneys, spleen, extremities (why? p. 853)
Hoarseness, seizures, stroke (from emboli)
Mitral Regurgitation (Regurgitation, Incompetence, Insufficiency)
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 > regurgitation
Mitral valve does not close fully> blood flows back into left atrium during systole; *Great
risk with MI and left ventricular failure > rupture of chordae tendineae; sudden inc in
vascular resistance > pulmonary edema cardiogenic shock! (Why?) * Most cases due
to due to MI, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary
muscle dysfunction, infective endocarditis- Read carefully p 854.
Clinical Manifestations:
a. If gradual-asymptomatic for years> development some degree of left ventricular
failure; Initially > inc. left atrial volume; *dilation of left atrium due to regurgitation of
blood into LA during systole
b. LA dilation and hypertrophy then pulmonary congestion (left-sided heart failure)
then right sided heart failure
c. *LV dilation and hypertrophy-due to inc. preload >eventually>*dec. CO (WHY?)
why)
d. Symptoms
1) Acute > fulminating pulmonary edema, shock etc, new systolic murmurs; thread
peripheral pulses, cool, clammy extremities, , *New systolic mumur
2) Chronic- initial symptoms left ventricular failure; fatigue, palpitations and
dyspnea, audible S3 sound, holosystolic or pansystolic murmur at apex, radiate
to left axilla most clear at apex; weakness, orthopnea
3) *Think left-sided heart failure (pulmonary congestion, edema) >right sided heart
failure; * Need repair
Mitral Valve Prolapse See Fig 37-10
D.
E.
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 form of valvular disease in US-cause unclear; ? Symptoms vary
between genders; result from rheumatic heart disease, ischemic heart disease, inherited
connective tissue disorders such as Marfans; *usually benign > potential complications
> MR, IE, SCD< HE, cerebral ischemia.
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); Palpitations
e. Lightheadedness, dizziness
f. May or may not be have chest pain; if pain occurs, episodes tend to occur in clusters,
especially during stress (*atypical type chest pain) *use B-adrenergic blockers;
may be accompanied by dyspnea, palpitations, and syncope
g. * Complications; ** inc. risk for bacterial endocarditis if leads to regurgitation >
heart failure > develop thrombi and embolization >transient ischemic attacks
(TIAs); *require prophylactic antibiotics .
h. *Refer to Teaching Guide for Mitral Valve Prolapse p. 855, Tab. 37-14
Aortic Stenosis
Etiology/Pathophysiology of Aortic Stenosis
2  RNSG 2432
1.
2.
3.
F.
G.
Usually congenital; if later in life due to 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
*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; 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
c. ** Inc. afterload >reduced CO > LV hypertrophy > incomplete emptying of LA >
pulmonary congestion>RV strain (**Why??)
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. *No 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 and prominent fourth sound; may radiate to carotid arteries (good
NCLEX audio question!)
e. *Untreated leads >pulmonary hypertension and right ventricular failure; increased
risk for sudden cardiac death!
Aortic Regurgitation (Aortic Insufficiency)
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 & hypertrophy >myocardial dec 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 - “waterhammer”/ collapse with abrupt distention during systole & quick collapse during
diastole-**Also wide pulse pressure, “water-hammer” pulse “Water hammer” (jerky ):
full, then collapses due to aortic insufficiency (when blood ejected into aorta
regurgitates back through aortic valve into left ventricle; Also called Corrigan
pulse or cannonball, collapsing, pistol-shot, or trip-hammer pulse (Click for
video Corrigan’s pulse)
2) May have characteristic head bob (Musset’s sign)- shakes whole body
3) Auscultatory- soft or absent S1. presence of S3 and S4 ; soft, high-pitched
diastolic murmur; systolic ejection click; Austin-Flint murmur ( listen!)
b. Chronic aortic regurgitation; remains asymptomatic for years: exertional dyspnea,
orthopnea, paroxysmal nocturnal dyspnea (PND)
Etiology/Pathophysiology of Tricuspid & Pulmonic Valve Disease
1.
*Uncommon -diseases of tricuspid and pulmonic valve (p. 853, tab 37-13)
2.
Tricuspid stenosis (more frequent than regurgitation) , Rt. atrial output obstructed;> right
atrial enlargement & elevated systemic venous pressure
RNSG 2432  3
3.
4.
5.
H.
Tricuspid stenosis- almost always in patients with rheumatic mitral stenosis, IV drug
abusers, or patients treated with dopamine agonist (Dostinex) *anti-parkinson
drug…PS…not sure how/why this effects heart???
Pulmonic stenosis >right ventricular hypertension and hyper trophy ; almost always
congenital; cause backward flow of blood from right ventricle; then right ventricle
hypertension and hypertrophy
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 low-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, midsystolic murmur ( pulmonic area, second left intercostal space)
Collaborative Care- Valvular disease- (p. 856 Tab 37-15)
1.
*Keys- prevent recurrent rheumatic fever and infective endocarditis (majority valvular
due to endocarditis or rheumatic fever) *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 previous meds)
b. Anticoagulation (esp if atrial fibrillation present)
c. *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)
4.
Diet- low sodium if at risk for heart failure.
5.
Diagnostic tests *Determine type, degree valvular problem
a. Generally based on history; PE;chest X-ray, ECHO, heart cath, EKG, TEE
Echocardiography & TEE (TransEsophageal Echo): identify valve leaflets
abnormalities, myocardial function, chamber size, EF
b. Chest X-ray; for cardiac and blood vessel hypertrophy, calcifications of valve leaflets
and annular openings (review)
c. Electrocardiography; identifies atrial and ventricular hypertrophy, associated
conduction defects or dysrhythmias; most common-*atrial fib; need 12 lead (review)
d. Cardiac catheterization; assess cardiac contractility; measure pressure gradients
across heart valves, heart chambers, and within pulmonary system (Heart failure?)
6.
Surgical Interventions- Valvular disease (open & closed procedures) *recognize,
identify each! **Read information in text on types of valves and valve replacement
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  RNSG 2432
4)
b.
c.
d.
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)
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* 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)
*From CABG surgical considerations review - p. 783-785 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.
Percutaneous transluminal balloon valvuloplasty (PTBV) or called Balloon
Valvuloplasty non-invasive; passage of balloon catheter from 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)
e.
f.
g.
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)
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.
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. 857 for Surgical care pre & post
considerations)
2) *Used often for mitral valves (Think about mitral stenosis, risk for a-fib & why)
3) Requires use of heart lung machine (open method)
4) For mitral stenosis, several procedures, including debriding calcified valve
Ross procedure: use one valve (pulmonic) for another (aortic)
RNSG 2432  5
*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.
Need general anesthesia and cardiopulmonary bypass
2) Incision through a median sternotomy
3) *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)
4) Hospital stays- little as 3 days; recovery 3 weeks.
5) *Surgery abruptly “corrects” blood flows through heart; complications unique to
valve replacement due to *sudden changes in intracardiac blood
pressures(hemodynamic alterations)
a) Risk postop complications, as bleeding, thromboembolism, infection, HF,
hypertension, dysrhythmias, hemolysis, and mechanical obstruction of valve
b) *Types of valves- (p. 858, Tab 37-16) mechanical valve (from combination
metal alloys) or biologic valve from pig (porcine), cow (Bovine) or human
cardiac tissue; repair preferred if possible
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 857-858) ; *Both types valve replacement at risk for
leakage and endocarditis. *This is important!! Look at valves in text
book
Nursing Management for Valvular Disease
1.
Nursing assessment- See p. 848 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. 859)
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
h.
I.
6  RNSG 2432
4.
5) Note-if mechanical valve, will have audible click
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
Cardiomyopathy
A.
B.
A.
B.
C.
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
Etiology/Pathophysiology Dilated Cardiomyopathy (p. 859-60,Tab 37-18 & 37-19)
1.
Characterized by diffuse inflammation, rapid degeneration of myocardial fibers- lead 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
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 > contraction
impaired > dec. EF%; Complications: *Sudden death (due to dysrhythmias);
Collaborative Care for Dilated Cardiomyopathy
1.
*Focus- control HF- enhance myocardial contractility and dec afterload (drug therapy
usually key): goal of therapy -keep patient at optimal level of function; out of hospital
RNSG 2432  7
2.
3.
4.
5.
A.
B.
C.
Diagnostic tests
a. Evaluate patient history; r/o other causes HF; maybe biopsy
b. Doppler ECHO (p. 730); Chest X-ray (signs of enlarged heart
c. EKG; Lab studies (esp BNP) (know what this is!)
d. Cardiac Catheterization, MUGA, dec EF (p. 731-732)
Nutritional therapy
a. Low sodium diet
Drug therapy (key)* (p. 805, Tab 35-) (review HF)
a. Nitrates; Loop diuretics; ACE inhibitors
b. B-Adrenergic Blockers and aldosterone blockers (spironolactone)
c. *Digoxin & other antidysrhythmics (note cautions-see text p. 887)
d. *Anticoagulation (Why?)
e. *Dobutamine, milrinone infusions & diuresis (recall how these drug work to treat
/manage HF)
f. Need to change habits (stop alcohol if a factor)
g. *Maybe immunosuppressive drugs-if autoimmune cause (explain)
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. 835) and implantable cardioverterdefibrillator (p. 834) –for some cases
c. If end stage- consider for heart transplant- or destination therapy with permanent or
implantable VAD (p. 1697-1698; 814-815 -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 SCD in otherwise healthy young people.
Clinical manifestations (p. 861-862)
1.
Asymptomatic or may have exertional dyspnea, fatigue, angina
2.
*Dyspnea- 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 inc left muscle mass or compression of small coronary arteries
5.
Syncopy due to obstruction of aortic outflow during inc. activity (dec CO> circulatory
collapse) ; *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 dec obstruction of outflow tract; dec. rate and inc.
ventricular compliance and inc. diastolic filling time and CO; (avoid vasodilators,
digitalis, nitrates **Think WHY??
8  RNSG 2432
b.
A.
B.
C.
D.
** 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. 862-863)
Etiology/Pathophysiology-Restrictive Cardiomyopathy
1.
*Least common CMP, impairs diastolic filling/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 inc heart rate
without further compromising ventricular filling)
2.
Symptoms of heart failure (right sided)
Collaborative Care for Restrictive Cardiomyopathy
1.
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. 863, Tab. 37-21 for patient and family teaching guidelines
Summary of Cardiomyopathy (key facts) (Refer also p. Tab 37-18, 19, 20,21)
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 risk
B.
Diagnostic tests: (same as with valvular disease)
1.
Echo; EKG; CXR
2.
Hemodynamic changes
3.
Perfusion scan; Cardiac cath
4.
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)
RNSG 2432  9
D.
E.
F.
A.
B.
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?)
Nursing Diagnoses:
1.
*Decreased Cardiac Output
2.
Fatigue
3.
Ineffective Breathing Pattern
4.
Fear
5.
Ineffective Role Performance
6.
Anticipatory grieving
Heart Transplant/Open Heart Surgery *Review from Mod 4 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 p. 867-873
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; *Larger the aneurysm greater risk of rupture- Half all
aneurysms greater than *6 cm- rupture within 1 year! *Monitor
8.
*Dilated aortic wall becomes lined with thrombi-can embolize: leads to acute ischemic
symptoms in distal branches
9.
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
10.
Male gender and smoking stronger risk factors than hypertension and diabetes
11.
Studies suggest strong genetic predisposition
12.
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; At least one vessel layer still intact
b. Further subdivided into p. 868 – Fig 38-3
1) Fusiform-circumferential, relatively uniform in shape
2) Saccular- pouchlike with narrow neck connecting bulge to one side of arterial
wall
Saccular
Fusiform
False aneurysm (or pseudoaneurysm-not an aneurysm)
a. Disruption of all layers of arterial wall > bleeding contained by surrounding structures
b. May result from trauma, infection, post peripheral artery bypass graft surgery at site of
anastomosis, arterial leakage after cannulae removal
Clinical Manifestations
1.
Thoracic aorta aneurysms often asymptomatic *p. 868
a. *Most common manifestation-deep diffuse chest pain; dysphagia
b. Pain may extend to interscapular area
2.
*Aortic Aneurysm- Ascending aorta/aortic arch
2.
C.
10  RNSG 2432
a.
D.
*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) : may mimic pain associated with abdominal or back disorders
3) *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; Bleed may be tamponade by surrounding structures, thus
prevent exsanguinations/ death; severe pain; may/may not have back/flank
ecchymosis (Grey Turner’s sign)
3) *Anterior rupture; Massive hemorrhage, most not survive to get to the hospital
Collaborative Care for Aortic Aneurysm
1.
Goal- Prevent rupture of aneurysm
a. Early detection/treatment imperative; thenstudies done to determine size and location
b. If carotid and/or coronary artery obstructions present, may need to corrected before
repair
c. **Small aneurysm (<5 cm)-conservative therapy used
d. 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)
Pulsating Hematoma > Back Pain > Hypotension (untreated > death!)
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; Echocardiography- assists in diagnosis of aortic valve
insufficiency, related to ascending aortic dilation
c. Ultrasonography-useful in screening for aneurysms, monitor aneurysm size
d. CT scan- most accurate test to determine anterior to posterior length; cross-sectional
diameter; presence of thrombus in aneurysm; MRI-diagnose and assess location and
severity; Angiography- anatomic mapping of aortic system using contrast; not reliable
method of determining diameter or length; provide accurate info about involvement of
intestinal, renal or distal vessels
e.
2.
3.
4.
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. 869, 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  11
d.
e.
5.
Autotransfusion-reduces need for blood transfusion during surgery
*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. 870, 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
b.
c.
d.
12  RNSG 2432
Nursing Diagnosis
1) Risk for Ineffective Tissue Perfusion
2) Risk for Injury
3) Anxiety
4) Pain
5) Knowledge Deficit
Planning: Overall goals include
1) Normal tissue perfusion
2) Intact motor and sensory function
3) No complications related to surgical repair
Nursing Implementation
1) Health Promotion
2)
3)
e.
Alert for opportunities to teach health promotion to patients and their families
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 care- ICU
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.870-871) 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, .
5) Home Care/Ambulatory care
a) instructed to gradually increase activities; No heavy lifting
b) Educate on signs and symptoms of complications: Infection; Neurovascular
changes
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 p. 872- fig 38-6
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
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 >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
RNSG 2432  13
B.
C.
D.
E.
c. Marfan’s syndrome  incidence (Marfan’ syndrome & Michael Phelps)
d. *Blunt trauma can precipitate
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 involved-neurologic
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.
Collaborative Care- Initial goal - ↓ BP and myocardial contractility to
dec. pulsing forces within aorta (prevent inc. of dissection)
1.
Diagnostic Studies (see aortic disection) (p. 873, Tab. 38-1)
a. Health history and physical exam; ECG
b. Echocardiogram- shows left ventricular hypertrophy (systemic HTN)
c. Chest x-ray- may show widening of mediastinal silhouette and left pleural effusion
d. Transesophageal echocardiogram-show dissections closest to aortic root
e. MRI or multi-detector row CT scan (reflect severity of dissection)
f. 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 nitroprusside,
angiotensin-converting enzyme (ACE inhibitors) *Think why 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; 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-Semi-Fowler’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
14  RNSG 2432