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NOTES Valvular/Cardiomyopathy/Aneurysm cmj
Module #5: Nursing Care of the Individual with Cardiovascular Disorders”
Valvular Heart Disease, Myopathy, and Aneurysms
Valvular Heart Disease
(link here for audio and visuals of valves)
Etiology/Pathophysiology (general) A&P for valvular diseases
A. Valvular disease: (See text p. 901 fig. 30-7)
1. Include acquired valvular disorders resulting from acute conditions (infective
endocarditis) and chronic conditions (rheumatic heart disease)
2. Causes of valvular heart disease: *Rheumatic heart disease: most common
cause; Damage from acute MI, (papillary muscles that affect valve leaf
function); congenital heart disease: often manifests in adulthood; effects of
aging: changes in heart structure and function
B. Pathophysiology
1. Stenosis; Valve leaflets fuse; unable to open or close completely; or valve
scarred from endocarditis, infarction and calcium deposits > stenosis
a. Results in impedance of forward flow of blood >increased afterload and
later preload)
b. decreased cardiac output from impaired ventricular filling, or ejection
and stroke volume
2. Regurgitation (also called insufficient or incompetent valves); valves do not
close completely allow backflow of blood; due to deformity or erosion of
valve cusps, as from endocarditis, myocardial infarction or cardiac dilation
(enlargement)-annulus or supporting ring of valve stretched, no longer allow
complete closure
3. * Changes due to:
a. Blood volume and pressure dec. in front of involved valve
b. Blood volume and pressure are inc. behind involved valve
c. Higher pressures and compensatory changes to maintain cardiac output
lead > remodeling and hypertrophy of heart muscle
d. Eventually > pulmonary complications or heart failure
e. Increased muscle mass and size > increase myocardial oxygen
consumption >may lead to ischemia and chest pain
f. Murmur: Why do they occur?? (p. 901))
g. Increased risk for infective endocarditis Why?? (p. 901)
RNSG 2432  113
Mitral and Aortic Valvular Disorders
Mitral Stenosis*(use as major example)
Mitral Valve Stenosis
A. Pathophysiology: Narrowed mitral valve obstructing blood flow from left atrium
to left ventricle during diastole; usually caused by *rheumatic heart disease
or bacterial endocarditis; chronic and progressive
B. Common Manifestation/Complications
1. Untreated > *left atrial hypertrophy with pressure reflected backward >
increased pulmonary pressure > pulmonary hypertension
2. Lead to right ventricular dilation and hypertrophy and heart failure
(decreased CO)
3. Asymptomatic or severely impaired
a. *Dyspnea on exertion (DOE): earliest manifestation
b. Cough, hemoptysis, frequent pulmonary infections, paroxysmal nocturnal
dyspnea, orthopnea, weakness, fatigue, palpitations
c. *Progresses to right heart failure: jugular vein distension,
hepatomegaly, ascites, peripheral edema
4. On auscultation of heart sounds: loud S1, split S2, mitral opening snap;
diastolic murmur is low-pitched, rumbling, crescendo-decrescendo heard with
bell in apical region
5. Atrial dysrhythmias especially *atrial fibrillation; may cause mural
thrombi and then emboli to brain, coronary arteries, kidneys, spleen,
extremities (why? p. 902)
6. Women asymptomatic until pregnancy then heart unable to adequately
compensate for circulatory changes.
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests:
a. Electrocardiogram/Holter monitor detect irregular rhythm
b. Chest X-ray: determine left atrium enlargement and lung status
c. Echocardiogram; structure of mitral valve and movement with heart
beat; measure speed and direction of blood flow through heart
e. Transesophageal echocardiogram (TEE);
f. Cardiac catheterization: pressure within heart chambers; structural
defects (Review…what follow-up care post cardiac cath?)
114  RNSG 2432
2. Medical/medications management: diuretics for LHF/RHF; digitalis/beta
blockers and CCB (calcium channel blockers) to control rate of A-fib;
anticoagulation with A-fib; endocarditis prophylaxis (**understand “why”
there meds are used…)
3. (Percutaneous) Balloon valvuloplasty: does not involve open-heart
surgery- in cath lab; soft, thin tube (catheter) tipped with balloon used to open
mitral valve passageway; catheter guided through blood vessel in arm or
groin to right side of heart then through a small hole created in the septum
and into narrowed mitral valve. Through tiny hole (septal opening) surgeons
reach mitral valve and once in position at mitral valve, a balloon at tip of
catheter is inflated to open mitral valve and improve blood flow. Cannot be
used if valve is both tight and regurgitant or if blood clots in heart chambers
(risk of dislodging clots.)
4. Mitral valve repair- mitral commissurotomy (valvotomy) repair mitral
valve without replacing mitral valve; surgically separating or shaving back
valve leaflets; may also make adjustments to cords that anchor valve
leaflets to heart, to improve valve function. Maybe done through openheart surgery, closed-heart surgery.
RNSG 2432  115
Annuloplasty, also performed to repair or reconstruct mitral valve (also
used with tricuspid valve)
5. Mitral valve replacement. Use mechanical valve or tissue valve from
pig (porcine), cow or human cadaver donor; repair preferred when
possible over valve replacement.
Mechanical and biologic prosthetic disadvantages:
Anticoagulation (due to thromboembolic complications for
mechanical valves)
Porcine valves short life expectancy (7 to 14 years).
*Know nursing implications for each type of valve replacement
(mechanical or biologic). (*see p. 908) Note…same types of
“repairs/replacement” used for various types of valular problems.**
Biological valve
(human)
116  RNSG 2432
Porcine valve
(PIG)
Figure 11: Mitral valve
ring
Figure 12: Tissue
valve
Figure 13: Mechanical
valve
Mitral Regurgitation (Regurgitation, Incompetence, Valve Insufficiency)
A. Pathophysiology: Mitral valve does not close fully; allows blood to flow back
into left atrium during systole; *majority cases due to MI, rheumatic heart
disease (common); degenerative calcification of mitral annulus (older women);
left ventricular hypertrophy and/or MI dilating the mitral annulus or supporting
structures; congenital defects. Greatest risk with MI and left ventricular failure >
rupture of chordae tendineae; > sudden increase in vascular resistance and
pulmonary edema! (Why would pulmonary edema develop?)
B. Common Manifestation/Complications
1. Initially > increased left atrial volume; then dilation of left atrium due to
regurgitation of blood into LA during systole
2. LA dilation and hypertrophy then pulmonary congestion (left-sided heart
failure) then right sided heart failure
3. LV dilation and hypertrophy-to accommodate inc. preload and dec CO
(Why?)
4. Manifestations: asymptomatic to left sided heart failure
a. Fatigue, weakness, exertional dyspnea, orthopnea
b. Like left-sided heart failure (pulmonary congestion, edema) >right sided
heart failure
c. Murmur loud, high-pitched, rumbling, holosystolic; most clear at
apex, palpable thrill; musical quality (*know this one)
C. Therapeutic Interventions/Collaborative Care (see Mitral Valve stenosis)
1. See above diagnostics
2. Medications: depend upon sign/symptoms: antibiotics prior to medical and
dental procedures (WHY??...think endocarditis); may require ACE inhibitors
(prils), inotropes (increase contractility); decrease heart rate and decrease
afterload), diuretics and heart valve repair or replacement. (Think about
effect of each type med)
Mitral Valve Prolapse
A. Pathophysiology: type of mitral insufficiency occurring when one or both mitral
valve cusps “billow” into atrium during ventricular systole; most common in
women aged 14 – 30; cause unclear; ?result from rheumatic heart disease,
ischemic heart disease, inherited connective tissue disorders such as
RNSG 2432  117
Marfans; usually benign; if thickened, mitral leaflets>morbidity and sudden
death. *Most common form of valvular disease in US
B. Common Manifestation/Complications
1. Usually asymptomatic; midsystolic ejection click or murmur; may develop
high-pitched late systolic murmur with development of regurgitation of blood
through valve
2. *Most common symptom: atypical chest pain: left sided or substernal pain
related to fatigue, not exertion (know this)
3. Tachydysrhythmias> palpitations, lightheadedness, syncope with sense of
anxiety
4. Complications; **Increases risk for bacterial endocarditis; with
regurgitation > heart failure > develop thrombi and embolization >transient
ischemic attacks (TIAs); require prophylactic antibiotics (How do
antibiotics prevent?)
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: See above
2. Treatment depend upon manifestation/complications
Aortic Stenosis
A. Pathophysiology: Cause blood flow to be obstructed from left ventricle into
aorta during systole; more common in males than females: causes idiopathic;
congenital defect; rheumatic damage (often also has mitral valve disease);
degenerative disease (associated with aging)
1. Valve annulus decreases in size, inc. work of left ventricle >left ventricle
hypertrophy >myocardial ischemia (increased oxygen consumption) >
decreased coronary blood flow (Why does this happen?)
2. Pulmonary vascular congestion and edema
118  RNSG 2432
3. ** Inc. afterload >reduced CO> LV hypertroph>incomplete emptying
of LA>pulmonary congestion>RV strain (Why does this happen?? Think
about process!)
B. Common Manifestation/Complications
1. May be asymptomatic for years
2. Classic manifestations: *dyspnea on exertion; angina, syncope; narrow pulse
pressure
3. **Harsh systolic crescendo-decrescendo murmur heard best in second
intercostal space right of sternum with palpable thrill; may radiate to carotid
arteries
4. Untreated leads >pulmonary hypertension and right ventricular failure;
increased risk for sudden cardiac death!
5. S (syncopy) A (angina) D (dyspnea) SAD *Chest pain!
C. Therapeutic Interventions/Collaborative Care
1. Depends upon symptoms: treat for heart failure; use medications including
ACE inhibitors, digitalis, diuretics, vasodilators, beta blockers, anticoagulants,
*prophylactic antibiotics,
2. **Nitroglycerin contraindicated for patients with significant aortic stenosis.
Why? Due to need for preload to allow (force) stiffened valves to open.
Aortic Regurgitation (Aortic insufficiency)
A. Pathophysiology; Allows blood to flow back into left ventricle from aorta during
diastole; mostly due to rheumatic heart disease
1. Other causes: Congenital disorder; infective endocarditis; blunt chest trauma;
aortic aneurysm; syphilis; marfan syndrome; chronic hypertension
2. Leads to increased diastolic left ventricular pressure
3. Get increased preload- 60% of stroke volume can be regurgitated
(*think about this fact! Why??)
4. *Characteristic water hammer (H2O) pulse due to regurgitation of
blood into the LV; wide pulse pressure (Think about “why”…don’t try to
memorize…)
RNSG 2432  119
5. LV dilation and hypertrophy (first high stroke volume then ventricular
hypertrophy compromises cardiac output > lead to pulmonary congestion)
*Read text carefully on this one…! p. 904
B. Common Manifestation/Complications
1. May be asymptomatic for years
2. Complaints of persistent palpitations; throbbing pulse visible in arteries of
neck
3. May have characteric head bob (Musset’s sign)- shakes whole body
4. Dizziness, exercise intolerance, angina, fatigue, paroxysmal nocturnal
dyspnea (angina less frequent)
5. Murmur heard during diastole; “blowing” high-pitched; poss. palpable thrill
and ventricular heave
6. **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 the aortic valve into the left
ventricle). Also called a Corrigan pulse or a cannonball, collapsing, pistolshot, or trip-hammer pulse.
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: as above
2. Treatment depends upon manifestations
Tricuspid and Pulmonic Valve disorders (*right sided-failure)
Tricuspid stenosis
A. Pathophysiology; Rare; Blood flow obstructed from right atrium to right
ventricle; usually due to rheumatic heart disease; occurs with mitral stenosis;
right atrium enlarges, right ventricular stroke volume decreases get *right sided
heart failure.
B. Common Manifestation/Complications:
1. Increased jugular venous distention, ascites, hepatomegaly,
peripheral edema (right sided-failure)
120  RNSG 2432
2. Fatigue, weakness
3. Murmur during diastole, low-pitched, rumbling sound in 4th intercostals
space at left sternal border or xiphoid process; *murmur pre-systolic;
increases with inspiration
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: as above
2. Treatment depends upon manifestations
Tricuspid regurgitation
A. Pathophysiology: Rare; secondary to right ventricular dilation; blood flows back
into right atrium during systole; causes: left ventricular failuare, pulmonary
hypertension; develop right sided heart failure
B. Common Manifestation /Complications:
1. Right sided failure
2. Atrial fibrillation, (*atrial dilation-key factor)
3. Systolic murmur- high-pitched, blowing, heard over tricuspid or xiphoid area;
increases in intensity with inspiration
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: as above
2. Treatment depends upon manifestations
Pulmonic valve disease (rare)
Pulmonic Stenosis
A. Pathophysiology: Obstruction of blood flow from right ventricle into pulmonary
System; usually congenital, also from rheumatic heart disease or cancer
B. Common Manifestation /Complications:
1. Asymptomatic, unless severe
2. Dyspnea on exertion, fatigue progressing to *right sided heart failure
3. Murmur- harsh, crescendo-decrescendo heard in pulmonic area,
second left intercostals space
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: as above
2. Treatment depends upon manifestations
Pulmonic regurgitation (more common than pulmonary stenosis)
A. Pathophysiology: Blood flows back into right ventricle during diastole; dec.
blood flow into pulmonary circulation; due to pulmonary hypertension; also
infective endocarditis, pulmonary artery aneurysm, syphilis
B. Common Manifestation /Complications:
1. Right sided heart failure
2. Murmur- diastolic, high-pitched, decrescendo and blowing, best heard along
left sternal border
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: as above
2. Treatment depends upon manifestations
Therapeutic Interventions/Collaborative Care
*Keys to Management of Valvular Disorders: (regardless of type disease)
RNSG 2432  121
A. *P.E. After diagnosis (usually murmur heard on physical exam)
Keys: defects in structure or function of valves-interfere with proper cardiac
circulation; two major categories: stenosis or regurgitation
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, medications, surgical
repair/replacement damaged valves
B. Diagnostic tests: (major)
1. Echocardiography & TEE (TransEsophageal Echo): Identifies valve leaflets
abnormalities, myocardial function, chamber size, determine ejection fraction
2. Chest X-ray; Identifies cardiac and blood vessel hypertrophy, calcifications of
valve leaflets and annular openings
3. Electrocardiography; identifies atrial and ventricular hypertrophy, associated
conduction defects or dysrhythmias; most common-*atrial fib; 12 lead
4. Cardiac catheterization; assessment of cardiac contractility; measure pressure
gradients across heart valves, heart chambers, and within pulmonary system
C. Medications (*determined by symptoms-treat for heart falure from valve disease)
1. ACE inhibitor; ldec. blood pressure, reduce afterload (increase cardiac
output).
2. Vasodilator; lower blood pressure; reduce afterload (increase cardiac
output).
3. Digitalis; inc. force of heart muscle contraction congestive heart failure
present; treatment of some arrhythmias, esp. atrial fibrillation (control rate)
4. Diuretics: dec.fluid volume (preload); heart failure.
5. Beta-blockers and anti-arrhythmics; Beta-blockers- for variety of
conditions: valvular heart disease, HTN, irregular heart rhythms.
6. Anticoagulants; prevent blood clots -important with *atrial fibrillation, with
*mechanical valves replacement.
7. *Prophylactic antibiotics *Risk for infective bacterioendocarditis: Antibiotic
prophylaxis prior to dental work
D. Invasive procedures, surgery (*refer to discussion with mitral stenosis)
1. Percutaneous balloon valvuloplasty; See above-under fluoroscopy; divide
fused leaflets of valve and enlarge orifice of valve; treatment of choice for
symptomatic mitral stenosis; treat aortic stenosis in children, young adults;
“bridge to surgery” for older adults who are poor surgical risks
a. Post-procedural care similar to angioplasty
2. Surgery: Repair or replacement of diseased valve-before cardiopulmonary
function is severely compromised (may irequire open heart/bypass)
a. Repair-if risk too great with valve replacement
3. Procedures
a. Valvuloplasty: Reconstruction or repair of heart valve (above)
b. Open commissurotomy : surgical devision of fused valve leaflets to
open stenotic valves (see above)
c. Annuloplasty: (see above) repair narrowed or enlarged or dilated valve
annulus, may use prosthetic ring
d. **Valve replacement/open heart: (see p. 908 tab. 30-9) & above with
mitral
122  RNSG 2432
……………….examples
Ross procedure:use one valve (pulmonic) for another (aortic)
1) Outcome determined by heart function at time of surgery
2) Intraoperative/postoperative care (may need open heart/heart-lung
by-pass) Read p. 907-909; review 821-825 bypass surgery
3) Review characteristics/durability replacement valves-inc. risk of
endocarditis
5) Types prosthetic heart valves: (see Mitral valve * know this)
a) Mechanical valves: Long term durability; Disadvantage:
Lifetime anticoagulation to prevent clot formation on valve
b) Biological tissue valves: Advantages: More normal blood flow;
low risk of thrombus formation; Disadvantages: Less durable
than mechanical: 50% need replacement in 15 years
c) Types: a. Heterografts (pig, calf pericardium); b.
Homografts (from human cadaver or during transplant like Ross
procedure)
4. *Nursing care with valve disease/surgery like open-heart surgery
(*emphasis adequate anticoagulation, prevent endocarditis)
RNSG 2432  123
a. *Preventi rheumatic heart disease- early and adequate treatment of strep
throat (complete course of antibiotics)
b. *Prophylactic antibiotic therapy before invasive procedures for clients with
pre-existing heart disease
5. Nursing Diagnoses: (Ref to text p. 908-910)
a. *Decreased Cardiac Output: medication teaching/diet
b. Risk for Infection *risk for bacterial endocarditis; *instruct to prevent
endocarditis!!
c. Activity Intolerance: Monitor vital signs before and after activities (late
stage dysfunction)
d. Ineffective Protection/risk for injury (thrombus formation); patient
teaching
e. Knowledge deficit (medication, diet, prevention infection, surgery)
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Cardiomyopathy (see p. 912; Tab. 30-9)
A. Pathophysiology: abnormality of heart muscle>functional changes in heart
(systolic and diastolic) *understand differences and effect on
hemodynamics
1. Cause unknown
a. Primary: Idiopathic - cause unknown
b. Secondary: result of other processes- inc. ischemia, infections disease,
exposure to toxins, connective tissue disorders, etc.
c. Mortality higher- older adults, men, and African Americans
2. Three types: dilated, hypertrophic, and restrictive (least common)
*Know key differences each type-p. 912-tab. 30-9)
124  RNSG 2432
Dilated Cardiomyopathy
A. Pathophysiology: Most common (87% cases); cause often unknown; ? related
to alcohol,cocaine abuse, chemotherapeutic drugs, pregnancy, HPT; some cases
genetic
1. All heart chambers dilate; ventricular contraction impaired
2. Decreased cardiac output
3. Extensive interstitial fibrosis (scarring)
B. Common Manifestation /Complications: Manifestations (develop gradually)
1. Same as associated with left and right sided heart failure
2. S3, S4, AV regurgitation murmur
3. Dysrhythmias common: supraventricular tachycardias, atrial fibrillation,
complex ventricular tachycardias; Genetic
* Heart chamber dilate and contraction impaired > decreased EF%
3. Complications: *Sudden death (due to dysrhythmias); Mural thrombi
secondary to dysrhythmias) > multisystem involvement- disease progresses
to right and left heart failure
4. Outcome: Progressive worsening; 50 % mortality within 5 years of
diagnosis; Need transplant!
C. Therapeutic Interventions/Collaborative Care
1. Drugs: treat heart failure (caution with beta blockers- dec. contractility of
heart); pacemaker
2. Anticoagulants
3. Cardiac transplant; temporary VAD (ventricular assist device)
What is a VAD?
Hypertropic Cardiomyoathy (opens to video clip)
A. Pathophysiology: dec. compliance of left ventricle and hypertrophy of
ventricular muscle mass > impaired ventricular filling and low cardiac output;
1. Half of clients-family history (genetic)
RNSG 2432  125
2. Hypertrophic subaortic stenosis (IHSS): interventricular septal mass
enlarges> obstructs blood flow from ventricle through aorta> dec. cardiac
output > inc. pulmonary and venous pressures
3. Symptoms develop during, after physical activity;
B. Common Manifestation /Complications: *sudden death may be first
symptom: death in young athletes due to sudden inc. in oxygen demand!
1. Manifestations: dyspnea, angina, syncope; fatigue, dizziness, palpitations
2. Harsh crescendo-decrescendo systolic murmur, S4
C. Therapeutic Interventions/Collaborative Care
1. Medications: beta blockers-reduce anginal symptoms; 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;
(no vasodilators, dig, nitrates, and diuretics) Think WHY??
2. Surgery; symptomatic; remove excess muscle (myectomy-identify before
death) from aortic valve outflow tract; implant ICD; pacemaker
Restrictive Cardiomyopathy (least common)
A. Pathophysiology: Ventricular walls become rigid > impair filling during diastole;
causes: myocardial fibrosis, infiltrative processes
1. Dec. in ventricular size occurs with dec. cardiac output
2. Rigid right ventricular walls do not stretch during diastolic filling > creat back
pressure, right heart failure, reduced stroke volume, low cardiac output. (*EF
can be normal due to low volume-do you undrstand why?)
126  RNSG 2432
B. Common Manifestation /Complications: heart failure, dec. tissue perfusion
1. Exertional dyspnea, exercise intolerance; right sided heart failure
2. Audible S3 and S4; emboli formation
3. Contraction and EF normal
4. Prognosis-poor (<3 years survival rate)
C. Therapeutic Interventions/Collaborative Care
1. Drugs: treat heart failure (ACE inhibitors, vasodilators, digitalis);
anticoagulants
2. No surgery; does not correct underlying problem
*Keys to Management of Cardiomyopathy
A. Assessment (as above)
1. Fatgue all types
2. Dilated; weakness, sign of left heart failure, S3 & S4;
Hypertropic: exertional dyspnea, syncope, angina, signs of heart failure S4,
sudden death 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. Hemodynamics
5. Perfusion scan
6. Cardiac cath
7. Myocardial biopsy (Why would this be indicated?)
RNSG 2432  127
C. Medications (*determined by symptoms)
1. No medical therapy to cure/prevent cardiomyopathy; medical regime to treat
symptoms
2. Caution with medication; antiarrhythmic drugs decrease contractility;
may need ICD to override potentially dyrhythmias (What is an ICD?)
3. See specific disease process (if infection cause; 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
Aneurysm
A. Etiology/Pathophysiology (general) Aneurysm> abnormal dilation of blood
vessel at site of weakness or tear in vessel wall under high pressure , often aorta
and peripheral arteries (See p. 995 fig. 33-3)
1. Arterial aneurysms: more common in males over age of 50
2. HTN: major contributing factor; aorta esp. susceptible due to continued
stress; atherosclerosis major risk factor
3. Most asymptomatic; symptoms depend upon pressure of aneurysm on nearby
structures
4. Usually secondary to atherosclerosis. aorta most common
5. Half all aneurysms grearter than *6 cm- rupture within 1 year!
*Monitor!
128  RNSG 2432
6. True aneurysms: Due to gradual weakening of arterial wall: effects of
atherosclerosis and HTN affect all 3 layers vessel wall
a. Fusiform: spindle-shaped and tapered at both ends
b. Circumferential: involving entire diameter of vessel. large, grow slowly
c. Saccular: shaped like small out-pouchings (sacs)
d. Berry: type of saccular aneurysm caused by congenital weakness in tunica
media
7. False aneurysms (traumatic aneurysms); caused by traumatic break in
vessel wall rather than weakening (saccular or berry shaped); may follow
heart cath
8. Dissecting aneurysm
a. Develop where break or tear in tunica intima and media allow blood to
dissect layers of vessel wall
b. Blood contained by adventitia forming longitudinal or saccular aneurysm
Examples
Most fusiform; 98% below the renal artery
Saccular
RNSG 2432  129
Location, size, stability
determines s & s and
management
Aortic Aneurysm (thoracic and abdominal)
Thoracic
A. Pathophysiology: Thoracic: frequently asymptomatic, may have substernal,
neck or back pain; account for 10% of aortic aneurysms result from HTN,
arteriosclerosis, trauma, tertiary syphilis, Marfan syndrome Other symptoms
depend on location and structures they compress
B. Common Manifestation /Complications: Varyby location, size, growth rate
and pressure on adjacent structures
1. Substernal, neck, or back pain
2. Dyspnea, stridor, cough, difficult swallowing, hoarseness, edema of face
and neck, distended neck veins
3. Frequently asymptomatic; rupture first sign!
130  RNSG 2432
Location
thoracic
aneurysm
90% below
renal
arteries
C. Therapeutic Interventions/Collaborative Care (See below)
Abdominal aortic aneurysm (AAA) (includes images)
A. Pathophysiology: Aneurysm in abdominal aorta, >* 90% develop below
renal arteries where aorta branches form iliac arteries; associated with
arteriosclerosis, HTN, increasing age (> 70), smoking
B. Common Manifestation /Complications:
1. Most asymptomatic; pulsating mass in mid/upper abdomen-bruit over
mass found on exam
2. **Pain constant or intermittent, in mid abdominal region or lower
back; severity increases with size and closeness to impending rupture; pain
intensity correlates to size and severity Danger signal!
3. *Emboli in lower extremities, if aneurysm contains thrombi > break off
4. Rupture> hemorrhage, hypovolemic shock; survival rate 10 – 20% of
clients experiencing rupture of AAA; Best to rupture posterior…why?
Think about this one>allow tamponade and slow bleed!
5. Popliteal/femoral aneurysms
a. From arteriosclerosis, males and usually bilateral; may rupture
b. Popliteal aneurysms: asymptomatic or intermittent claudication
(cramping or pain in leg brought on by exercise and relieved by rest), rest
pain, numbness, pulsating mass behind knee
c. Femoral aneurysms: pulsating mass in femoral area
6. Aortic dissection
(includes images)
Aortic dissection occurs when
blood enters the wall of
aorta, separating its layers,
and creating a blood filled
cavity.
a. Life threatening emergency-can occur anywhere along aorta inc.
ascending, descending aorta
b. Predisposing factors: HTN, older males, Marfan syndrome, aortitis,
coarctation of aorta
RNSG 2432  131
c. Manifestations:
1) *Sudden, excruciating pain often with ripping, tearing
sensation
2) Chest or back pain
3) Syncope, dyspnea, weakness
4) *If dissection occludes blood flow: rapidly falling or
undetectable BP, no peripheral pulses….Death!
Rupture
Triad
Back Pain
Hypotension
Pulsating hematoma
Keys to Management of Thoracic and Abdominal aneurysm
A. Assessment
1. Thoracic: most often asymptomatic, rupture first sign; signs and symptoms
2. Abdominal-also asymptomatic until rupture; report “heartbeat” in abdomen
when lying down; pulsating abdominal mass; moderate to severe abdominal
or lumbar pain (impending rupture!); claudication; systolic bruit
3. **Dissecting aneurysm sudden, severe persistent pain: tearing or ripping;
pallor, sweating, and tachycardia, initial BP higher in one arm than other,
syncopy and paralysis of lower extremities
B. Diagnostic tests: Establish diagnosis and determine size and location of
aneurysm *Most diagnosed as part of regular work-up
1. Chest xray: visualize thoracic aneurysm
2. Abdominal ultrasonography: diagnose abdominal aneurysm
3. Transesophageal echocardiography (TEE): visualize thoracic/dissecting
aneurysm
4. Contrast-enhanced CT or MRI: precise measurement of aneurysm
5. Angiography: visualize precise size and location of aneurysm
C. Medications *Understand treatment goals!
1. If asymptomatic, low risk for rupture; (aortic aneurysms)- treat long-term
with beta-blockers, calcium channel blockers, vasodilators and other
antihypertensive drugs to control heart rate and blood pressure; also
niacin, mevacor, statins (due to atherosclerosis); treat medically if less
than 5 cm! Must repair if rupture; base ilne eval. of pulses!
2. Clients with dissection
a. *Control heart rate and blood pressure, prevent rupture, stabilize
before aneurysm repaired surgically
b. IV beta-blockers and sodium nitroprusside (Nipride); constant monitoring
(hemodynamic) (Why Nipride…dec. afterload/preload; vasodilate & dec.
cardiac workload; reduce stress on aneurysm site…understand this)
3. Post surgical correction: usually treated with anticoagulant therapy
initially heparin, long term with oral anticoagulants or low-dose aspirin
132  RNSG 2432
D. Invasive procedures, surgery: *Usually repaired if >5cm
1. Indications of rupture/impending(surgery mandatory for rupture); hematoma
into scrotum, perineum, flank or penis indicate retroperitoneal aneurysm;
anterior rupture of aorta into peritoneal cavity means death! *Critical to
evaluate peripheral pulses prior to surgery and after! Why??
a. Symptomatic or rapidly expanding aneurysms
1). Thoracic: >6 cm diameter
2) Abdominal: >5 cm diameter
b. Depends on client’s operative risk factors; area and degree of dissections
2. Types of procedures
a. Open surgical procedure: abd incision, cross clamp aorta, aneuysm
opened and plaque removed, graft suture in place
1) Aneurysm excised, replaced with synthetic fabric graft
2) Thoracic repair more complex, may utilize cardiopulmonary bypass
RNSG 2432  133
b. Endovascular stent grafts (above) usually placed through femoral
artery (opt high risk patients)
1) Stent, metal sheath covered with polyester fabric placed
percutaneously under fluoroscopy
2) Need continuous monitoring of location of graft afterward
3. Post-op complications: Check urine output/peripheral pulses hourly for
24 hours- (when to call Dr.)…Note peripheral pulses may be absent
for 4-12 hours post surgery; should not have leg pain or pale, cool
extremity…report tachycardia or decrease BP
a. Graft occlusion
b. Hypovolemia/renal failure (make sure urine at least 30 cc/hr)
c. respiratory distress
d. Cardiac dysrhythmias
e. Paralytic ileus
f. Paraplegia/paralysis
E. Nursing Diagnoses: (Read p. 998-999)
1. Risk for Ineffective Tissue Perfusion
a. Monitoring manifestations of dissection or rupture in pre-operative client
b. Monitoring for manifestations of arterial thrombosis
2. Risk for Injury: conti. monitoring of adeq. arterial perfusion, renal perfusion
3. Anxiety
4. Pain
5. Knowledge deficit: Education *important- manifestations of increasing size,
dissection, or rupture/need to seek immediate medical attention; control
hypertension, smoking cessation
Education for clients who have had surgical repair include post-operative
recovery, anticoagulation, meeting nutritional needs
Prevention: Prevent atherosclerosis
Treat and control hypertension
Diet- low cholesterol, low sodium and no stimulants
Careful follow-up if less than 5cm. It can grow .5cm /year
134  RNSG 2432