NSG210 Exam 2 Reading Outline - Hinkle Ch. 24: Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders
Source: Hinkle & Cheever, Brunner & Suddarth’s Textbook of Medical-Surgical Nursing 15th ed., Chapter 24 (~/Documents/texts/nursing/NSG210/exam02/HINKLE_MS_CH24.pdf). Part of nsg210-exam-2-readings-outline. The weekly outline assigns “Ch. 25” for Week 04 valvular heart disease; this is the chapter that matches the topic. Related raw notes: raw/nsg210_wk04_VavularDisorders.md, raw/nsg210_wk04_UCSMtralRegurgitationB_answers.md.
Learning Outcomes
- Define valvular disorders and describe pathophysiology, manifestations, and management of mitral and aortic disorders.
- Differentiate valve repair and replacement procedures and related care.
- Describe pathophysiology, manifestations, and management of cardiomyopathies.
- Describe infections of the heart.
- Apply the nursing process to cardiomyopathy and pericarditis.
Key Terms
- Annuloplasty - repair of a valve’s outer ring
- Aortic valve - semilunar valve between the left ventricle and aorta
- Autograft - replacement valve from the patient’s own valve (e.g., pulmonic valve moved to aortic position)
- Bioprosthesis (heterograft) - replacement valve from animal tissue
- Cardiomyopathy - disease of the heart muscle
- Chordae tendineae - nondistensible fibrous strands connecting papillary muscles to AV valve leaflets
- Commissurotomy - splitting or separating fused valve leaflets
- Ejection fraction - percentage of end-diastolic volume ejected with each beat
- Homograft (allograft) - replacement valve from a human donor
- Leaflet repair - repair of a valve’s movable flaps
- Mitral valve - AV valve between left atrium and left ventricle
- Orthotopic transplantation - recipient heart removed and donor heart grafted into the same site
- Prolapse - stretching of an AV valve leaflet into the atrium during systole
- Pulmonic valve - semilunar valve between right ventricle and pulmonary artery
- Regurgitation (insufficiency) - backward flow through a valve
- Stenosis - narrowing or obstruction of a valve opening
- Total artificial heart - device replacing both ventricles
- Tricuspid valve - AV valve between right atrium and right ventricle
- Valve replacement - insertion of a mechanical or tissue valve
- Valvuloplasty - repair of a stenosed or regurgitant valve by commissurotomy, annuloplasty, or leaflet repair
- Ventricular assist device - mechanical device supporting a failing ventricle
I. Valvular Disorders - Overview
- Valves open and close in response to pressure changes during systole (contraction) and diastole (relaxation)
- Atrioventricular (AV) valves: tricuspid (3 leaflets, right side) and mitral (2 leaflets, left side); both anchored by chordae tendineae to papillary muscles
- Semilunar valves: pulmonic (RV to pulmonary artery) and aortic (LV to aorta)
- Regurgitation - valve doesn’t close completely, so blood flows backward
- Stenosis - valve doesn’t open completely, so forward flow is reduced
- Any valve can be affected; mitral and aortic disorders cause more symptoms and complications than tricuspid and pulmonic
- Asymptomatic disease may just be monitored; symptomatic disease treated by severity - lifestyle changes, medications, repair or replacement
- Left-sided valve disease can lead to left heart failure and eventually right ventricular failure (Figure 24-2)
II. Mitral Valve Prolapse (MVP)
- Deformity where part of one or both mitral leaflets balloons back into the left atrium during systole; usually no symptoms; rarely progresses to sudden death
- Up to 2.5% of the population; twice as common in women
- Often no clear cause; associated with inherited connective tissue disorders (enlarged leaflets); annulus may dilate; chordae and papillary muscles may elongate or rupture
- Can lead to mitral regurgitation, which can cause heart enlargement, atrial fibrillation, pulmonary hypertension, heart failure
- Manifestations: most never have symptoms; some have fatigue (regardless of rest), shortness of breath, lightheadedness, dizziness, syncope, palpitations, chest pain, anxiety
- Assessment: first and often only sign is a mitral click (systolic click - leaflet ballooning into the atrium); a regurgitation murmur if blood flows back; echocardiography diagnoses and monitors
- Medical management: control symptoms; for arrhythmias eliminate caffeine and alcohol and stop tobacco and electronic nicotine products; some need antiarrhythmics; chest pain rarely needs nitrates, calcium channel blockers, or beta-blockers; prophylactic antibiotics NOT recommended before dental or invasive procedures; severe regurgitation with heart failure may need repair or replacement
- Nursing: teach about the diagnosis and that it may be hereditary (first-degree relatives may be screened with echocardiograms); report new symptoms; read OTC labels (cough medicines may contain alcohol, caffeine, ephedrine, epinephrine that can trigger arrhythmias); explore diet, activity, sleep links to symptoms
- Pregnancy: women with MVP without regurgitation or complications can complete pregnancy without close cardiac monitoring and deliver vaginally
III. Mitral Regurgitation
- Blood flows from the left ventricle back into the left atrium during systole; leaflets don’t close completely because leaflets and chordae are thickened and fibrotic
- Chronic or, less often, acute
- Causes: developed countries - degenerative changes (including MVP) and left ventricular ischemia; developing countries - rheumatic heart disease; also myxomatous changes, infective endocarditis (leaflet perforation, scarring), collagen vascular disease (lupus), cardiomyopathy, ischemic heart disease (functional or secondary MR)
- Pathophysiology: problems with leaflets (shorten, tear), chordae (elongate, shorten, tear), annulus (stretched by heart enlargement or calcified), or papillary muscles (rupture, stretch, displaced, or unable to contract from ischemia)
- Each beat pushes blood back into the left atrium, adding to blood from the lungs
- Left atrium stretches, hypertrophies, then dilates
- Backflow blocks blood coming from the lungs, so the lungs become congested, straining the right ventricle
- During diastole the extra volume fills the left ventricle; volume overload causes hypertrophy, then dilation, then systolic heart failure
- Manifestations: chronic often asymptomatic; acute (e.g., from MI) presents as sudden severe heart failure; dyspnea, fatigue, weakness most common; palpitations, exertional dyspnea, cough from pulmonary congestion
- Assessment: systolic murmur - high-pitched blowing sound at the apex, may radiate to the left axilla; pulse regular or irregular (extrasystoles, atrial fibrillation); echocardiography
- Medical management: heart failure medications for pulmonary congestion; afterload reduction with ACE inhibitors (captopril, lisinopril) or ARBs (losartan, valsartan), hydralazine, beta-blockers (carvedilol, metoprolol); heart failure symptoms are an indication to consider valvuloplasty or valve replacement
IV. Mitral Stenosis
- Reduced flow from the left atrium into the left ventricle; usually caused by rheumatic endocarditis, which thickens leaflets and chordae and fuses the leaflets
- Pathophysiology: normal orifice is about three fingers wide; severe stenosis narrows it to a pencil width
- Left atrium can’t empty; residual volume leads to left atrial hypertrophy and dilation
- Less LV filling, so lower cardiac output
- Backflow into pulmonary veins causes pulmonary congestion
- Right ventricle pumps against high pulmonary pressure, hypertrophies, enlarges, and fails
- Faster heart rate shortens diastole (less time for forward flow), so cardiac output falls further and pulmonary pressure rises
- Manifestations: first symptom often dyspnea on exertion (DOE) from pulmonary venous hypertension; symptoms usually appear after the valve opening is reduced by one-third to one-half; progressive fatigue, decreased exercise tolerance; enlarged left atrium presses on the left bronchus (dry cough, wheezing); severe - hemoptysis, palpitations, orthopnea, PND, repeated respiratory infections; dilated left atrium becomes electrically unstable (atrial arrhythmias)
- Assessment: low-pitched rumbling diastolic murmur at the apex; weak irregular pulse with atrial fibrillation; heart failure signs; echocardiography diagnoses and grades severity; ECG, exercise testing, cardiac catheterization with angiography
- Prevention: prevent and treat bacterial infections; prevent acute rheumatic fever with effective antibiotic treatment of group A strep; secondary prophylaxis for recurrent rheumatic fever with carditis may last 10 or more years (penicillin G IM every 4 weeks, oral penicillin V twice daily, sulfadiazine daily, or erythromycin twice daily)
- Medical management: heart failure treatment; anticoagulation for severe left atrial dilation (atrial thrombi); atrial fibrillation - cardioversion, or rate control (beta-blockers, digoxin, calcium channel blockers) plus anticoagulation; avoid strenuous activity, competitive sports, and pregnancy (all raise heart rate); surgical - valvuloplasty, usually commissurotomy; percutaneous transluminal valvuloplasty or replacement
V. Aortic Regurgitation (Aortic Insufficiency)
- Backward flow from the aorta into the left ventricle during diastole
- Causes: congenital (bicuspid aortic valve), inflammatory lesions, aortic dilation, rheumatic endocarditis, syphilis, dissecting aneurysm, blunt chest trauma, deterioration of a replaced valve
- Pathophysiology: blood flows back into the LV, which dilates, then hypertrophies to eject more blood forcefully, raising systolic BP; arteries compensate with reflex vasodilation, lowering peripheral resistance and diastolic BP
- Manifestations: usually no symptoms at first; awareness of a pounding, forceful heartbeat, especially in the head or neck; visible or palpable carotid or temporal pulsations; later DOE, fatigue, then left ventricular failure (dyspnea, orthopnea, PND)
- Assessment: high-pitched blowing diastolic murmur at the 3rd or 4th intercostal space, left sternal border; widened pulse pressure; water hammer (Corrigan’s) pulse - strikes the finger with a quick, sharp stroke and then collapses; echocardiography (preferably TEE), cardiac MRI, catheterization; echo every 6 months if symptomatic, every 2-5 years if not
- Prevention: prevent and treat bacterial infections; same rheumatic fever prevention as mitral stenosis
- Medical management: avoid physical exertion, competitive sports, isometric exercise if symptomatic or LV function declining; treat arrhythmias and heart failure; control BP with ACE inhibitors and dihydropyridine calcium channel blockers (afterload reduction); beta-blockers used less (slower heart rate may raise BP); sodium restriction if symptomatic
- Treatment of choice: aortic valve replacement or valvuloplasty, ideally before LV failure; surgery recommended for any significant LV dilation (with or without symptoms) and for any symptomatic patient
VI. Aortic Stenosis
- Narrowing of the opening between the left ventricle and aorta; in adults usually degenerative calcification (similar to atherosclerosis); also congenital leaflet malformation (one or two leaflets instead of three) or rheumatic endocarditis (fused commissures, stiff cusps, calcific nodules)
- Pathophysiology: progresses over years to decades; LV contracts more slowly and forcibly to overcome the obstruction; pressure load causes LV hypertrophy; heart failure develops when compensation fails
- Manifestations: many asymptomatic; first symptom often DOE (rising pulmonary venous pressure from a dilating LV); later orthopnea, PND, pulmonary edema; dizziness and syncope (reduced cerebral flow); angina (limited coronary flow, shorter diastole for perfusion, higher oxygen demand of hypertrophied LV); BP normal or low; low pulse pressure (30 mmHg or less)
- Classic triad to remember: angina, syncope, dyspnea on exertion / heart failure
- Assessment: loud, harsh systolic murmur over the aortic area (right 2nd intercostal space), radiates to carotids and apex; low-pitched, crescendo-decrescendo, rough, rasping; S4 may be heard; accentuated by leaning forward during exhalation; palpable thrill at the base and along the carotids; LV hypertrophy on 12-lead ECG or echo; echo every 6-12 months if symptomatic, every 2-5 years if not; left heart catheterization before surgery; stress testing used cautiously in severe AS (risk of VT or VF) and not in symptomatic patients
- Prevention: control risk factors for inflammation - diabetes, hypertension, high cholesterol and triglycerides, tobacco and electronic nicotine
- Medical management: treat arrhythmias and LV failure; definitive treatment is aortic valve replacement - surgical or transcatheter aortic valve replacement (TAVR); balloon valvuloplasty for symptom relief if not a replacement candidate
VII. Valve Murmur Summary
| Disorder | Timing | Sound | Location |
|---|---|---|---|
| Mitral valve prolapse | Systolic | Mitral click; regurgitant murmur if MR | Apex |
| Mitral regurgitation | Systolic | High-pitched, blowing | Apex, radiating to left axilla |
| Mitral stenosis | Diastolic | Low-pitched, rumbling | Apex |
| Aortic regurgitation | Diastolic | High-pitched, blowing | 3rd-4th ICS, left sternal border |
| Aortic stenosis | Systolic | Loud, harsh, crescendo-decrescendo | Right 2nd ICS, radiating to carotids |
Memory aid: stenosis murmurs occur when the valve should be open; regurgitation murmurs occur when the valve should be closed. Mitral and tricuspid are open in diastole and closed in systole; aortic and pulmonic are open in systole and closed in diastole.
VIII. Nursing Management - Valvular Heart Disorders
- Teach diagnosis, progressive nature, treatment plan; report new or changing symptoms
- Teach that bacteria adhere to diseased valves more easily, causing endocarditis; teach infection prevention
- Compare vital signs to prior data; auscultate heart and lungs; palpate peripheral pulses
- Assess for:
- Heart failure - fatigue, DOE, decreased activity tolerance, increased cough, hemoptysis, repeated respiratory infections, orthopnea, PND
- Arrhythmias - pulse strength and rhythm, palpitations, forceful heartbeats
- Dizziness, syncope, weakness, angina
- Medication schedule and teaching (name, dose, actions, adverse effects, interactions)
- Aortic stenosis and nitroglycerin: venous dilation reduces return to the heart, lowering cardiac output and raising risk of syncope and reduced coronary flow; teach to try rest and relaxation before nitroglycerin and to expect side effects
- Heart failure: daily weight, report sudden gain; plan activity and rest
IX. Surgical Management - Valve Repair and Replacement
A. Valvuloplasty (Repair)
- Repair rather than replacement; procedure depends on cause and type of dysfunction
- Open-heart (general anesthesia, cardiopulmonary bypass) or percutaneous (cath lab or hybrid room, no general anesthesia or bypass); TEE at the end to evaluate
Commissurotomy (for fused leaflets, usually mitral stenosis):
- Closed commissurotomy / balloon valvuloplasty (percutaneous transvenous mitral commissurotomy):
- Mitral: catheter from right atrium through the atrial septum into the left atrium, across the mitral valve; balloon (three sections that inflate in stages - ventricle side, atrial side, then the orifice) or two smaller balloons (smaller atrial septal defect, allow some forward flow); inflated 10-30 seconds, repeated
- Used for younger patients or high surgical risk; contraindicated with left atrial or ventricular thrombus, severe aortic root dilation, significant mitral regurgitation, severe calcification
- Complications: some mitral regurgitation in all patients, bleeding at insertion sites, emboli (stroke), rarely left-to-right atrial shunt
- Aortic balloon valvuloplasty: less effective; restenosis about 50% within 6 months; used for palliation or as a bridge to TAVR; complications include aortic regurgitation, emboli, ventricular perforation, annulus rupture, ventricular arrhythmia, mitral damage, bleeding
- Open commissurotomy: general anesthesia, bypass, direct visualization (can remove thrombus or calcification, repair chordae and papillary muscles); used less now
Annuloplasty (for regurgitation):
- Repair of the annulus (junction of leaflets and heart wall), narrowing the orifice
- Urgent indication: ruptured chordae with severe MR - annuloplasty with chordae resuspension
- Techniques: annuloplasty ring (leaflets sutured to a ring; the ring bears the stress, preventing progressive regurgitation) or folding and tacking tissue with sutures (may degenerate faster)
Leaflet repair:
- Remove excess tissue; plication (tuck and suture); leaflet resection (wedge removed and gap sutured); release short chordae; extend with pericardial patch; patch holes
B. Valve Replacement
- Preferred when anatomy makes repair unlikely to succeed (extensive calcification, severely fibrotic or fused structures); multidisciplinary team decides surgical vs minimally invasive
- Surgical: general anesthesia, bypass, median sternotomy (mitral may use right thoracotomy); minimally invasive options with smaller incisions or robot assistance (less bleeding, pain, infection, scarring, shorter stay)
- Aortic and pulmonic leaflets removed; mitral structures partly left to preserve LV shape; prosthesis sutured to the annulus
- TAVR: cath lab or hybrid room, general anesthesia, no bypass or sternotomy; balloon valvuloplasty then a catheter-delivered tissue valve; now used for intermediate and low-risk patients too
- MitraClip: transcatheter clip joining two leaflets for degenerative MR; fewer symptoms and heart failure admissions
- Surgery abruptly changes intracardiac pressures; all prostheses create mild stenosis
- Stenotic valve replaced - heart failure signs improve in hours to days; regurgitant valve replaced - may take months to recover
- Postop complications: bleeding, thromboembolism, infection, heart failure, hypertension, arrhythmias, hemolysis, mechanical obstruction
C. Types of Replacement Valves
| Type | Source | Durability | Anticoagulation | Typical candidates |
|---|---|---|---|---|
| Mechanical (bileaflet, tilting disc, caged ball) | Synthetic | Most durable | Lifelong (thromboembolism risk) | Younger patients; kidney injury, hypercalcemia, endocarditis, sepsis (don’t deteriorate or infect as easily) |
| Bioprosthesis (heterograft) | Pig, cow, or horse tissue | 7-15 years | Not long-term (not thrombogenic) | Women of childbearing age (avoid anticoagulation risks with menses, placental transfer, delivery); over 70; can’t tolerate anticoagulants |
| Homograft (allograft) | Human cadaver | 10-15 years | Not long-term | Younger patients needing valve root replacement; limited availability, expensive |
| Autograft | Patient’s own pulmonic valve moved to aortic position (Ross procedure, usually with homograft pulmonic replacement) | Over 20 years | Not needed | Children (grows with child), women of childbearing age, young adults, peptic ulcer history, can’t tolerate anticoagulation |
D. Nursing Management - Valvuloplasty and Valve Replacement
- Prepare patient and family, reinforce explanations, psychosocial support
- After percutaneous balloon valvuloplasty: telemetry or ICU; assess for heart failure and emboli; heart sounds at least every 4 hours; care as for post-cardiac catheterization; hospital stay 24-48 hours
- After surgical repair or replacement: ICU; vitals every 5-15 minutes until recovered from anesthesia; IV vasoactive and antiarrhythmic drips weaned; neuro, respiratory, cardiovascular assessments every 1-4 hours; transfer to telemetry in 24-72 hours; discharge in 3-7 days
- Anticoagulation teaching:
- Warfarin target INR usually 2-3.5 for mitral replacement, 1.8-2.2 for aortic replacement (per text)
- Annuloplasty ring or tissue valve: anticoagulation usually for only 3 months unless atrial fibrillation or prior thromboembolism
- Aspirin with warfarin for bioprostheses or high embolic risk
- Frequent follow-up and lab tests
- Prosthetic valves and repair materials raise infective endocarditis risk - teach prevention
- Echocardiogram 3-4 weeks after discharge as a baseline, then every 1-2 years
- Home care checklist (Chart 24-1): name the procedure; diet and activity (walking, breathing exercises; avoid lifting, driving, contact sports as instructed); medications including anticoagulant at the same time daily, lab appointments, avoid injury, report bleeding (gums, petechiae, tarry stools); report fevers, chills, petechiae clusters, malaise, weight loss; tell all providers about the surgery (possible antibiotic prophylaxis); oral hygiene and dental visits; wound care; follow-up; support resources; health promotion
X. Cardiomyopathy
A. Overview
- Disease of the heart muscle associated with cardiac dysfunction
- Types: dilated (DCM), hypertrophic (HCM), restrictive (RCM), arrhythmogenic right ventricular (ARVC/D), unclassified
- Ischemic cardiomyopathy - enlarged heart from coronary artery disease, usually with heart failure
- AHA classification: primary (genetic, nongenetic, acquired - mainly heart muscle) vs secondary (heart involved as part of systemic disease: amyloidosis, sarcoidosis, scleroderma, Fabry disease)
- Pathophysiology of all types ends in impaired cardiac output; low stroke volume triggers the sympathetic nervous system and RAAS, raising vascular resistance and sodium and fluid retention, increasing the heart’s workload; ejection fraction often falls; leads to heart failure
- Concept Mastery Alert: sodium is the key electrolyte - fluid overload is often tied to high sodium intake
B. Types
| Type | Key feature | Details |
|---|---|---|
| Dilated (DCM) | Most common; ventricles dilated without hypertrophy; systolic dysfunction; low ejection fraction | Diminished contractile filaments and myocyte necrosis; more blood left in ventricle, higher end-diastolic pressure, pulmonary and systemic congestion; stretched valves regurgitate; mural thrombi can embolize. Over 75 causes: pregnancy, hypertension, heavy alcohol, viral infection, chemotherapy (doxorubicin, daunorubicin), thyroid disease, persistent tachycardia, Chagas disease; idiopathic 20-30%; familial 30-50% - family history is essential |
| Hypertrophic (HCM) | Autosomal dominant; thickened muscle, especially the septum | Leading cause of sudden death in adolescents and young athletes; disorganized myocytes contract poorly; thickened coronary arterioles cause ischemia, fibrosis, VT/VF; small stiff ventricles fill slowly, so atrial kick is critical; LV outflow tract (LVOT) obstruction from mitral valve moving against the septum in systole (worse with low volume or provocation); screen with ECG, exam, echo; genetic testing and testing of first-degree relatives; annual screening for gene-positive relatives; manage with hydration, beta-blockers, calcium channel blockers; avoid rapid preload changes (hot tubs, saunas, long hot showers); myectomy or alcohol septal ablation if refractory |
| Restrictive (RCM) | Least common; rigid walls, diastolic dysfunction | Filling pressures rise sharply with small volume increases; chamber size and systolic function usually normal; arrhythmias and conduction problems common; symptoms mimic constrictive pericarditis (echo helps differentiate); causes: infiltrative (amyloidosis), storage (hemochromatosis), noninfiltrative (scleroderma), endomyocardial (radiation, anthracyclines); biopsy often needed |
| Arrhythmogenic RV (ARVC/D) | Inherited; myocardium replaced by fibrous and fatty tissue | Starts in the RV, spreads to whole heart (renaming to arrhythmogenic cardiomyopathy); palpitations or syncope at 15-40 years; sudden death may be first sign; ECG: QRS widening, T-wave inversions V1-V3, epsilon wave; genetic testing (negative in up to 50%); ICD for arrhythmias |
| Unclassified | Mixed features | Left ventricular noncompaction, stress-induced (Takotsubo) cardiomyopathy |
C. Clinical Manifestations and Diagnosis
- May be stable and asymptomatic for years; DCM or RCM often first diagnosed when heart failure appears: DOE, fatigue, PND, cough (with exertion or at night), orthopnea, peripheral edema, early satiety, nausea; also chest pain, palpitations, dizziness, syncope with exertion
- Exam: tachycardia, S3 and S4; RCM may have diastolic murmurs; DCM and HCM may have systolic murmurs; later crackles, JVD, pitting edema, hepatomegaly
- Diagnosis: history and ruling out other causes (MI); echocardiogram is one of the most helpful tools; cardiac MRI (HCM, ARVC/D); ECG (arrhythmias, LVH changes); chest x-ray (enlargement, congestion); catheterization, coronary CT, or stress test to rule out CAD; endomyocardial biopsy (especially RCM)
D. Medical Management
- Treat underlying cause; heart failure medications, low-sodium diet, exercise and rest regimen; antiarrhythmics and possibly ICD
- Fluid limit about 2 L/day if congested; but HCM patients must avoid dehydration (may need beta-blockers to prevent LVOT obstruction)
- Anticoagulants no longer routine
- Biventricular pacing (cardiac resynchronization therapy) can raise EF and reverse remodeling in some DCM
- Family history; genetic counseling and testing of first-degree relatives
E. Surgical Management
- LVOT surgery for symptomatic HCM despite medical therapy: septal myectomy (Morrow procedure) - about 1 cm of septum removed below the aortic valve; complications include complete heart block (pacemaker), VSD, inadequate relief; mortality under 1% to 16%
- Heart transplantation:
- For end-stage disease (cardiomyopathy, ischemic disease, valve disease, prior graft rejection, congenital disease); candidates have severe symptoms despite therapy, no other surgical options, and life expectancy under 1-2 years
- UNOS allocates by ABO compatibility, body size, age, severity, wait time, geography
- Orthotopic transplantation - bicaval technique now preferred (fewer AV valve regurgitation, arrhythmia, conduction problems)
- Immunosuppression: corticosteroids (prednisone), calcineurin inhibitors (tacrolimus, cyclosporine), antiproliferatives (mycophenolate, azathioprine, sirolimus); balance rejection against infection and cancer; endomyocardial biopsies to detect rejection
- Denervated heart: resting rate 90-110 bpm; responds only to circulating catecholamines, so exercise needs extended warm-up and cool-down (20-30 minutes to reach target rate); atropine won’t raise the rate; digoxin won’t slow atrial fibrillation; often no angina with ischemia (may present with heart failure, silent MI, sudden death)
- Complications: rejection, infection, cardiac allograft vasculopathy (accelerated atherosclerosis), hypertension (cyclosporine, tacrolimus), osteoporosis, lymphoproliferative disease and skin and lip cancers, weight gain, diabetes, dyslipidemia, kidney failure
- Median survival over 12 years
- Psychosocial: most have better quality of life; some feel indebtedness or guilt toward the donor, which is linked to nonadherence (64% reported nonadherence in one study; older age improved adherence; time since transplant and guilt worsened it)
- Mechanical assist devices:
- Intra-aortic balloon pump - reduces cardiac workload but doesn’t pump for the heart
- Ventricular assist devices (VADs) - support one ventricle (or two for biventricular); pneumatic, electric, axial flow, centrifugal (newer axial and centrifugal pumps are smaller, nonpulsatile, less thrombus); ECMO = VAD plus oxygenator
- Uses: bridge to recovery, bridge to transplant, destination therapy (now about 50% of patients)
- Ethical dilemma: patient request to deactivate an LVAD - autonomy vs nonmaleficence; debated whether it is withdrawal of treatment or euthanasia
- Total artificial heart - replaces both ventricles; SynCardia approved as bridge to transplant
- Complications: bleeding, thromboemboli, hemolysis, infection, kidney injury, right heart failure, multisystem failure, mechanical failure
F. Nursing Process - The Patient With Cardiomyopathy
Assessment:
- Detailed history of symptoms; causes (heavy alcohol, recent illness or pregnancy, family history of sudden death or cardiomyopathy); chest pain details; orthopnea, PND, syncope, exertional dyspnea; number of pillows; weight changes; ADL limits
- ACC/AHA heart failure stages and NYHA functional class
- Diet (sodium, nutrition)
- Psychosocial: role changes, stressors, support systems, emotional status; depression in about 19-21% of heart failure patients
- Physical: vital signs, pulse pressure, pulsus paradoxus, weight, point of maximal impulse (often shifted left), systolic murmur, S3 and S4, crackles, JVD, edema
Nursing diagnoses: impaired cardiac output; risk for impaired cardiac function and tissue perfusion; impaired gas exchange; activity intolerance; anxiety; powerlessness; self-care management.
Potential complications: heart failure, ventricular and atrial arrhythmias, conduction defects, pulmonary or cerebral embolism, valvular dysfunction.
Interventions:
- Improving cardiac output and peripheral flow: rest during symptoms; sitting up with legs down (pools blood, reduces preload); check SpO2 at rest and with activity; oxygen by nasal cannula as needed; medication schedule and reminders (pillbox, link to daily routines); low-sodium food choices; daily weight; compare dyspnea and pillow count; keep warm, reposition often
- Increasing activity tolerance: alternate rest and activity; sit for tasks (chopping, drying hair, shaving); recognize symptoms that call for rest; HCM, ARVC/D, RCM - avoid strenuous activity, isometric exercise, competitive sports
- Reducing anxiety: spiritual, psychological, emotional support; information; realistic hope for those awaiting transplant; anticipatory grieving
- Decreasing powerlessness: identify losses and emotional responses; identify what remains in their control (food, medications); food and weight diary; some manage a self-titrated diuretic
- Home care: medication regimen, symptom monitoring; read nutrition labels; daily weights and symptoms; organize activities; teach family CPR and AED use (arrhythmia risk); women often advised to avoid pregnancy (individualized); build trust for end-of-life discussions; transitional or home care
Home care checklist (Chart 24-4):
- Take medications exactly as prescribed; monitor breathing and edema
- Balance activity and rest; avoid strenuous activity, isometric exercise, competitive sports
- Avoid tobacco and alcohol; manage stress
- Know arrhythmia signs (lightheadedness, dizziness, orthostatic hypotension, racing heart, diaphoresis, confusion); emergency response, CPR, AED
- Daily weight at the same time in the same clothes
- Sodium no more than 2 g/day; read labels; avoid canned and processed foods and added salt
- Daily walking if no unusual fatigue or dyspnea
- Report: weight gain of 2-3 lb in 1 day or 5 lb in 1 week; unusual shortness of breath; increased swelling of ankles, feet, or abdomen; persistent cough; loss of appetite; restless sleep or needing more pillows; profound fatigue
Expected outcomes: improved cardiac function (normal HR and RR, less dyspnea, no weight gain, better peripheral flow), increased activity tolerance, less anxiety, less powerlessness, effective self-care.
XI. Infectious Diseases of the Heart
Named for the layer involved: endocarditis (endocardium), myocarditis (myocardium), pericarditis (pericardium). Diagnosis mainly from symptoms and echocardiography; prevention is ideal; IV antibiotics usually needed once infection develops.
A. Rheumatic Endocarditis
- Acute rheumatic fever (mostly school-age children) can follow group A beta-hemolytic streptococcal pharyngitis
- Rheumatic heart disease signs: new murmur, cardiomegaly, pericarditis, heart failure
- Prevented by prompt, complete antibiotic treatment of strep throat
- Spread by oral and respiratory secretions; risk with malnutrition, crowding, poor hygiene, low income; now mainly a disease of the developing world
- Can cause lifelong mitral stenosis or regurgitation
- Strep pharyngitis signs (Chart 24-5): sudden sore throat, painful swallowing, fever, red swollen tonsils with white patches or pus, palatal petechiae, swollen anterior neck nodes; rapid strep test, then throat culture if negative but suspected (usually not needed in adults); penicillin or amoxicillin; complete the full course
B. Infective Endocarditis
- Microbial infection of the heart’s endothelial surface; rare but deadly (14-22% in-hospital mortality, up to 40% within 1 year)
- Usually older adults or those with prosthetic valves or cardiac devices; staphylococcal right-sided endocarditis common in IV drug users; hospital-acquired with debilitating disease, indwelling catheters, hemodialysis, prolonged IV therapy
- Risk factors (Chart 24-6): prosthetic valves or repair material, implanted devices (pacemaker, ICD), prior endocarditis, certain congenital heart disease, transplant recipients with valvulopathy, IV drug use, body piercing, branding, tattooing, hemodialysis
- Pathophysiology: endocardial injury leads to fibrin and platelet clot; organisms (usually staphylococci or streptococci) invade; vegetations (platelets, fibrin, blood cells, microbes) form and can embolize; new clot hides organisms from defenses; infection erodes valve leaflets, chordae, prosthetic valve attachments, forms abscesses
- Manifestations: insidious onset; primary signs are fever and a heart murmur (fever may be absent in patients on antibiotics or steroids, older adults, those with heart failure or kidney injury; murmur develops in 85%; worsening murmur means progressing damage)
- Petechiae clusters (skin, conjunctiva, mucous membranes)
- Osler nodes - small painful nodules on finger or toe pads
- Janeway lesions - painless flat red or purple macules on palms and soles
- Roth spots - retinal hemorrhages with pale centers
- Splinter hemorrhages - reddish-brown streaks under the nails
- Systemic emboli in 22-50%; up to 65% go to the CNS (embolic stroke, often middle cerebral artery); splenic abscess
- Heart failure is the most frequent complication (valve perforation, chordae rupture, obstruction, prosthetic dehiscence) and an indication for surgery
- Vague complaints (malaise, anorexia, weight loss, cough, back and joint pain) may mimic flu
- Diagnosis: organism in two separate blood cultures plus vegetation on imaging; at least two sets of blood cultures (aerobic and anaerobic) from different sites, at least 2 hours apart over 24 hours, BEFORE any antibiotics; negative cultures don’t rule it out; elevated WBC, anemia, positive rheumatoid factor, elevated ESR or CRP; echocardiography (TEE better for vegetations and perivalvular complications)
- Prevention: antibiotic prophylaxis for high-risk patients before dental procedures involving gums or oral mucosa is “reasonable” (evidence mixed); good oral hygiene and regular dental care; report fever lasting over 7 days; don’t self-medicate or stop antibiotics early; meticulous hand hygiene and aseptic technique with IV lines; remove devices as soon as no longer needed
- Medical management: IV antibiotics for 2-6 weeks at high serum levels (often at home with home health); monitor drug levels and blood cultures; patients feel better but may be confined by IV therapy - need support
- Surgical: for heart failure, intracardiac abscess, recurrent emboli, or failed medical therapy - valve repair or replacement, debridement, abscess closure; most prosthetic valve endocarditis needs repeat replacement
- Nursing: monitor temperature trend (treatment effectiveness; fever may also be drug reaction); give antimicrobials on time; plan rest; hand hygiene; NSAIDs for fever; light linens, fan, tepid baths (stop if shivering); assess heart sounds (new or worse murmur may mean dehiscence, abscess rupture, leaflet or chordae injury); watch for emboli and pulmonary infarction (right-sided); watch for organ damage (stroke, meningitis, heart failure, MI, glomerulonephritis, splenomegaly); assess IV sites daily; teach activity limits, medications, infection signs; high risk for recurrence
C. Myocarditis
- Inflammation of the myocardium; can cause dilation, mural thrombi, cellular infiltration, and muscle fiber degeneration; most mild cases recover fully, some develop cardiomyopathy and heart failure
- Causes: infections (viral - coxsackievirus A and B, HIV, influenza A; bacterial, rickettsial, fungal, parasitic, protozoal - Chagas; spirochetal), immune-related (after rheumatic fever, autoimmune), toxins or drugs
- DCM and HCM may be late effects of myocarditis
- Manifestations: may be asymptomatic; fatigue, dyspnea, syncope, palpitations, chest and upper abdominal discomfort; most commonly flu-like; can cause sudden death or fulminant heart failure
- Diagnosis: often no abnormalities; tachycardia, chest pain; endomyocardial biopsy is definitive; cardiac MRI with contrast increasingly used; arrhythmias or ST-T changes; with structural disease - cardiac enlargement, faint heart sounds (especially S1), friction rub, gallop, systolic murmur; elevated WBC, CRP, ESR
- Management: treat cause (e.g., penicillin for strep); bed rest to reduce workload and damage; young patients limit activity and athletics for 6 months or until heart size and function normalize; increase activity slowly; treat heart failure and arrhythmias; NSAIDs should NOT be used for pain (linked to more cardiac injury and viral replication)
- Nursing: watch tachycardia and fever resolve; assess for heart failure and arrhythmias; continuous monitoring with arrhythmias
- Safety Alert: patients with myocarditis are sensitive to digitalis - watch for toxicity (new arrhythmia, anorexia, nausea, vomiting, headache, malaise) and notify provider
- Anti-embolism stockings and exercises (venous and mural thrombi); pharmacologic prophylaxis for some
D. Pericarditis
- Inflammation of the pericardium (sac around the heart); 5% of ER visits for chest pain; acute, chronic, or recurrent; infectious or noninfectious
- Causes (Chart 24-7): idiopathic; viral (most common infectious cause); bacterial (rare, usually TB), fungal, parasitic; autoimmune (lupus, rheumatic fever, rheumatoid arthritis, scleroderma); drug reactions; adjacent disease (MI, dissecting aneurysm, pneumonia); cancer (lung or breast metastasis, mesothelioma); chest radiation (peaks 5-9 months after); trauma or cardiac procedures (surgery, catheterization, pacemaker); uremia, myxedema; Dressler syndrome (10 days to 2 months after MI); after cardiac surgery
- Pathophysiology: fluid accumulates (pericardial effusion), compressing the heart (cardiac tamponade); repeated or prolonged episodes thicken, scar, or calcify the pericardium (constrictive pericarditis), restricting filling, lowering cardiac output, raising venous pressure (edema, hepatic failure)
- Manifestations: chest pain is the most characteristic symptom (also under the clavicle, neck, left trapezius); fairly constant; worse with deep inspiration, lying down, turning; relieved by sitting up and leaning forward
- Pericardial friction rub - most characteristic sign; creaky or scratchy; best at the left lower sternal border
- Mild fever, elevated WBC, anemia, elevated ESR or CRP, nonproductive cough, hiccups, dyspnea, splinting, tachycardia, heart failure signs with constriction or tamponade
- Diagnosis: history and symptoms; echocardiogram (effusion, tamponade, guide pericardiocentesis); CT (size and location of effusion); cardiac MRI (inflammation, adhesions); biopsy occasionally; 12-lead ECG - concave ST elevation in many or all leads with no reciprocal changes, PR depression, atrial arrhythmias
- Medical management: find the cause, relieve symptoms, watch for tamponade; bed rest until fever, pain, and rub subside if cardiac output impaired; NSAIDs (aspirin, indomethacin, ibuprofen); corticosteroids if NSAIDs contraindicated (kidney disease); colchicine added for severe cases; pericardiocentesis (rare) for diagnosis or relief - fluid for culture and cytology; pericardial window for continuous drainage; pericardiectomy for constriction
- Nursing: pain management, positioning, support; reassure that the pain isn’t a heart attack; forward-leaning or sitting position; restrict activity until pain and fever subside, then increase gradually, resuming restrictions if symptoms return; immune-healthy lifestyle; watch for tamponade and heart failure
Nursing process - the patient with pericarditis:
- Assessment: evaluate pain in various positions and with breathing, breath-holding, spine and arm movement, coughing, swallowing to distinguish from MI pain
- Quality and Safety Alert: a pericardial friction rub is diagnostic; creaky or scratchy, louder at end of exhalation; listen with the diaphragm pressed firmly at the left sternal edge, 4th intercostal space; best heard sitting and leaning forward; if unsure whether it’s pleural, have the patient hold their breath - a pericardial rub continues
- Monitor temperature (abrupt fever onset possible)
- Nursing diagnoses: acute pain; lack of knowledge of diagnosis and self-care
- Potential complications: pericardial effusion, cardiac tamponade
- Relieving pain: rest; sitting upright leaning forward (chair rest); restrict activity until pain subsides; monitor medication responses; watch GI effects of NSAIDs and colchicine; resume rest if pain and rub return
- Teaching: cause, medications, positioning and breathing techniques; when to follow up (relapse, tamponade symptoms - lightheadedness, orthostasis, tachycardia)
- Cardiac tamponade (monitoring and managing):
- Early: shortness of breath, chest tightness, dizziness, increasing restlessness
- Pulsus paradoxus - systolic BP falls 10 mmHg or more during inspiration
- Narrowing pulse pressure (systolic falls, diastolic stable)
- Tachycardia; low ECG voltage or electrical alternans (QRS heights alternate)
- Heart sounds distant to inaudible
- JVD and rising central venous pressure
- Beck triad - hypotension, muffled heart sounds, elevated jugular venous pressure (severe tamponade)
- Notify provider immediately; prepare for echocardiography and pericardiocentesis; stay with the patient and reduce anxiety
- Home care: remind about health promotion and screening
- Expected outcomes: pain-free ADLs, normal temperature, no rub; understands cause and treatment; normal BP, strong heart sounds, no JVD
Critical Thinking Exercises (end of chapter)
- 67-year-old with prosthetic aortic valve, fever, malaise, painful finger-pad nodules (Osler nodes) - suspect infective endocarditis; obtain blood cultures before antibiotics
- 57-year-old newly diagnosed with cardiomyopathy (ankle swelling, dyspnea at 20 feet) - education priorities and team roles
- 47-year-old with HCM who fainted on a hot day - dehydration lowers preload, worsening LVOT obstruction and causing syncope; prioritized ED assessment