NSG210 Hinkle Ch. 25: Management of Patients With Complications From Heart Disease

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 25, pp. 793-816 (textbooks/HINKLE_MS_CH25.pdf, also in textbooks/exam01/). Week 02 reading; on Exam 1 (heart failure was 10 of 34 med-surg questions). Numbering note: the weekly outline assigns Ch. 26 for heart failure, but in the 15th edition heart failure is Ch. 25; the exam01 folder holds Ch. 25. Note: the textbook predates SGLT2 inhibitors as a heart failure pillar; the lecture’s “four pillars” (SGLT2 inhibitor, diuretic, RAAS blocker, beta-blocker) are in nsg210-exam-1-studyguide. See also nsg210-week-02-summary.

Learning Outcomes

1. Recognize the etiology, pathophysiology, and clinical manifestations of the classifications of heart failure.
2. Describe medical management, including recommended pharmacologic treatment, of heart failure.
3. Use the nursing process as a framework for care of the patient with heart failure.
4. Identify other complications of heart disease and their medical and nursing management.

Key terms:

• Ejection fraction (EF): percentage of end-diastolic volume ejected each beat; normal 55-65%
• HFrEF (systolic HF): EF 40% or less
• HFmrEF: EF 40-49%
• HFpEF (diastolic HF): EF 50% or greater, stiff ventricle that cannot fill
• Orthopnea: dyspnea lying flat; paroxysmal nocturnal dyspnea (PND): sudden dyspnea during sleep
• Oliguria: under 0.5 mL/kg/h for at least 6 hours, or under 400 mL/24 h; anuria: under 50 mL/24 h
• Pulsus paradoxus: systolic BP more than 10 mm Hg lower on inspiration than expiration
• Pulseless electrical activity (PEA): electrical activity on ECG without an adequate pulse or BP
• Cardiac resynchronization therapy (CRT): device paces both ventricles to synchronize contraction

I. Heart Failure - Overview

• Clinical syndrome: heart cannot pump enough blood to meet metabolic needs; impaired contraction (systolic) or filling (diastolic)
• Usually chronic and progressive; managed to prevent acute decompensated HF
• About 6 million in the US; 870,000 new cases a year
• Most common reason for hospitalization over age 65
• Over 20% readmitted within 30 days; nearly 50% within 6 months
• More prevalent in African Americans and Hispanics; over age 60 more common in men
• Risks: smoking, obesity, poorly controlled diabetes, metabolic syndrome

A. Causes

• Coronary artery disease and atherosclerosis: primary cause; MI causes necrosis and lost contractility
• Hypertension: increases afterload leads to hypertrophy, then impaired filling and dilation
• Cardiomyopathy: dilated cardiomyopathy most common type (idiopathic, myocarditis, alcohol, chemotherapy)
• Valvular heart disease
• Kidney disease (nearly 30% of chronic HF patients have CKD), atrial fibrillation, hypoxia, acidosis, electrolyte abnormalities

B. Pathophysiology (Fig. 25-1)

• Significant dysfunction usually exists before symptoms appear
• Low cardiac output sensed by baroreceptors leads to sympathetic stimulation (epinephrine, norepinephrine): increased HR and contractility at first, but vasoconstriction of skin, GI tract, kidneys
• Decreased renal perfusion leads to renin release leads to angiotensin I, converted by ACE in the lungs to angiotensin II (potent vasoconstrictor, raises afterload)
• Angiotensin II stimulates aldosterone: sodium and water retention, increased blood volume and preload
• Counterregulation: ANP and BNP released from overstretched chambers cause vasodilation and diuresis but cannot overcome the other mechanisms
• Ventricular dilation and hypertrophy lead to ventricular remodeling; enlarged cells die early (apoptosis)
• Fibrosis and stiffness lead to HFpEF
• “Vicious cycle of heart failure”: low CO triggers mechanisms that make the heart work harder

II. Clinical Manifestations (Chart 25-1)

Cardinal signs: dyspnea, fatigue (limits exercise tolerance), fluid retention (pulmonary and peripheral edema).

A. Left-sided heart failure (pulmonary congestion)

• Blood backs up from LV to left atrium to pulmonary veins; fluid forced into interstitium and alveoli
• Dyspnea on exertion, then at rest; orthopnea (sleeps on several pillows or upright); PND
• Cough: dry and hacking at first (mistaken for asthma or COPD); large amounts of frothy, pink or tan sputum signal acute pulmonary edema
• Bibasilar crackles that do not clear with coughing, spreading throughout lung fields as it worsens; falling SpO2
• S3 (“ventricular gallop”)
• Low perfusion: decreased urine output by day, nocturia at night; dizziness, confusion, restlessness, anxiety; pale, cool, clammy skin; tachycardia, palpitations; weak pulses; fatigue and activity intolerance

B. Right-sided heart failure (systemic congestion)

• Right ventricle cannot eject; blood backs up in venous system
• JVD
• Dependent edema (feet, ankles; sacral edema on bed rest); pitting edema obvious after retaining at least 4.5 kg (10 lb) of fluid
• Hepatomegaly and RUQ tenderness; ascites (increased abdominal girth)
• Weight gain
• Anorexia, nausea, abdominal pain from venous engorgement
• Weakness

C. Congestive heart failure

• Left-sided failure can cause right-sided failure; both pulmonary and peripheral congestion

D. Pulmonary edema (acute decompensated HF)

• Acute LV failure; can follow MI or exacerbate chronic HF; “flash” pulmonary edema can develop quickly
• Restlessness, anxiety, sudden breathlessness and sense of suffocation
• Tachypnea, low SpO2, pale to cyanotic skin, cool clammy hands, tachycardia, JVD
• Incessant cough with increasing foamy sputum; progressive confusion
• Emergency

III. Assessment and Diagnostic Findings

NYHA functional classification (Table 25-1):

• I: no limitation; ordinary activity causes no symptoms
• II: slight limitation; comfortable at rest, ordinary activity causes fatigue, palpitations, or dyspnea
• III: marked limitation; comfortable at rest, less than ordinary activity causes symptoms
• IV: symptoms at rest; any activity increases discomfort

ACC/AHA stages (Table 25-2):

• Stage A: high risk, no structural disease or symptoms (hypertension, atherosclerosis, diabetes, metabolic syndrome) - heart healthy lifestyle, risk factor control
• Stage B: structural disease, no symptoms (prior MI, LVH, low EF) - add ACE inhibitor, ARB, or ARNI; beta-blocker; statin
• Stage C: structural disease with current or prior symptoms - add diuretics, aldosterone antagonist, sodium restriction, ICD, CRT
• Stage D: refractory end-stage - fluid restriction, end-of-life care, inotropes, transplant, mechanical support

Diagnostics:

• Echocardiogram: EF, structure, valves; confirms diagnosis
• HFpEF is a diagnosis of exclusion; increasing in older women with hypertension (hypertension is the most common cause); comorbid obesity, CAD, diabetes, AF, hyperlipidemia
• Chest x-ray, 12-lead ECG
• Labs: electrolytes, BUN, creatinine, LFTs, TSH, CBC, BNP, urinalysis
• BNP: key indicator; high levels mean high filling pressure; rising levels suggest acute exacerbation; best with a baseline and a discharge value

IV. Medical Management

Goals: improve cardiac function, reduce symptoms, stabilize and lower hospitalization risk, delay progression and extend life, promote heart-healthy lifestyle.

Lifestyle: restrict sodium, no smoking or secondhand smoke, avoid excess fluid and alcohol, lose weight if needed, regular exercise, recognize symptoms to report.

A. Pharmacologic therapy (Table 25-3)

Cornerstone for HFrEF: diuretic, angiotensin system blocker, beta-blocker. Blockers and beta-blockers improve survival; diuretics improve symptoms only. HFpEF: diuretic (often aldosterone antagonist), possibly angiotensin blocker and beta-blocker for symptoms (no survival benefit shown).

Diuretics:

• Smallest dose that controls fluid
• Loop (furosemide): act in ascending loop of Henle; first choice for severe volume overload; IV for exacerbations and pulmonary edema
• Thiazide (metolazone, hydrochlorothiazide): early distal tubule; may add to loop when unresponsive
• Both lose potassium - monitor K+; can cause orthostatic hypotension and kidney injury
• Aldosterone antagonist (spironolactone): potassium sparing; check creatinine and K+ in the first week then every 4 weeks; not given with elevated creatinine
• Need for diuretics falls with fluid under 2000 mL/day and sodium no more than 2 g/day
• Cardiorenal syndrome: prerenal AKI from poor renal flow; diuretic resistant

Administering diuretics (Chart 25-2):

• Check K+, Na+, Mg before giving; check for volume depletion (orthostatic hypotension, dizziness)
• Give early in the day to avoid nocturia
• Monitor urine output, I&O, daily weight, orthostatic BP, electrolytes, creatinine, uric acid (gout)
• Replace K+ (food or supplements) and Mg; watch hyperkalemia with potassium-sparing diuretics
• Assess lung sounds and edema; watch for arrhythmias

ACE inhibitors (lisinopril, enalapril):

• Relieve symptoms, decrease mortality and hospitalization in HFrEF; slow progression; improve exercise tolerance
• Vasodilation and diuresis decrease afterload and preload; decrease aldosterone; retain potassium
• Monitor hypotension, hyperkalemia, renal function (especially with diuretics)
• Patient on loop or thiazide may not need K+ supplements; watch hyperkalemia with spironolactone
• Stop if K+ remains over 5.5 mEq/L or creatinine rises
• Dry persistent cough (bradykinin) - but cough may also mean worsening HF; assess it
• Angioedema in under 1%, more often in African Americans and women; if it affects the airway, stop immediately and give emergency care
• If intolerant: ARB, ARNI, or hydralazine-isosorbide dinitrate

ARBs (valsartan, losartan):

• Block angiotensin II at receptors; alternative to ACE inhibitors; no cough

ARNI (sacubitril-valsartan):

• ARB plus neprilysin inhibitor (neprilysin breaks down natriuretic peptides)
• First-line angiotensin blocker for most symptomatic HFrEF; costlier
• Never give with or within 36 hours of an ACE inhibitor (angioedema)
• Monitor hypotension, renal function, angioedema, hyperkalemia

Beta-blockers (carvedilol, bisoprolol, metoprolol):

• Block sympathetic effects; reduce mortality and morbidity; used even in asymptomatic HFrEF
• Benefit may take weeks to months
• Side effects (dizziness, hypotension, bradycardia, fatigue, depression) most common in the first weeks; start low, titrate slowly every few weeks
• Caution in asthma and bronchospastic disease

Ivabradine:

• Slows SA node rate; adjunct for symptomatic HFrEF with resting HR at least 70 on beta-blockers, or if beta-blockers not tolerated
• Bradycardia, dizziness, fatigue; increased atrial fibrillation risk

Hydralazine and isosorbide dinitrate:

• For patients who cannot take any angiotensin blocker, if systolic BP at least 90
• Nitrate lowers preload; hydralazine lowers afterload
• Hypotension; rare lupus-like reaction

Digoxin:

• Increases contractility, slows AV conduction; reduces symptoms and hospitalization, not mortality
• Smaller doses for renal dysfunction and older adults (renally excreted)
• Toxicity: anorexia, nausea, visual disturbances, confusion, bradycardia
• Hypokalemia increases digoxin effect and toxicity - monitor K+; check digoxin level if renal function changes or toxicity suspected

IV inotropes (for acute decompensated HF with low BP or poor perfusion; ICU; may increase mortality):

• Dopamine: raises BP and contractility; low dose may improve diuresis and renal flow
• Dobutamine: beta-1 agonist; raises contractility and renal perfusion; may cause tachyarrhythmias and ectopy
• Milrinone: phosphodiesterase inhibitor; increases contractility and vasodilates; check BP first (hypovolemia leads to rapid drop); hypotension and ventricular arrhythmias

IV vasodilators: nitroglycerin, nitroprusside, nesiritide - contraindicated if hypotensive; continuous BP monitoring.

Adjunct medications:

• BP target under 130/80
• IV iron may help iron deficiency; erythropoietin agents not recommended (thromboembolism)
• Anticoagulants with AF or prior thromboembolism; amiodarone for arrhythmias; statins
• Avoid NSAIDs (decrease renal perfusion, especially older adults)

B. Other therapies

• Sodium no more than 2 g/day; avoid excess fluid; omega-3 fatty acids recommended; other supplements not recommended
• Supplemental oxygen as HF progresses
• Sleep apnea in about 61%; sleep study; CPAP for OSA
• Revascularization (PCI, CABG) if CAD
• ICD: EF under 35%, to prevent sudden cardiac death
• CRT (biventricular pacemaker): for prolonged QRS / LBBB causing dyssynchrony; improves CO, reduces mitral regurgitation, slows remodeling; combination CRT-ICD devices
• Ultrafiltration: for diuretic-resistant fluid overload; monitor fluid removed, BP, hemoglobin
• Stage D: transplant, LVAD as bridge or destination therapy

C. Gerontologic considerations

• Age-related increases in systolic BP, wall thickness, fibrosis
• May have atypical symptoms (weakness, somnolence) rather than dyspnea
• Reduced renal function: diuretic resistance and volume sensitivity
• Older men on diuretics: watch for bladder distention from enlarged prostate (bladder scan, palpate)
• Urgency and frequency are hard with arthritis and limited mobility

V. Nursing Process - The Patient With Heart Failure

A. Assessment

• History: dyspnea, fatigue, edema, sleep disruption, number of pillows, abdominal symptoms, mental status, ADLs, understanding of self-care
• Restlessness and anxiety (hypoxia); level of consciousness
• Respiratory rate, depth, effort; crackles at end of inspiration that do not clear with cough; wheezes
• BP (hypo- or hypertension); orthostatic changes
• S3 is an early sign of volume overload; heart rate and rhythm
• JVD: patient at 45 degrees; distention more than 4 cm above the sternal angle is abnormal (right ventricular failure)
• Peripheral pulses 0 (absent) to 3+ (bounding); skin color and temperature
• Edema 0 to 4+; check sacrum and back if in bed
• Abdomen: hepatomegaly, ascites; hepatojugular reflux - pressure on RUQ 30-60 seconds; neck vein rise of more than 1 cm is positive
• I&O (negative balance is usually the goal); watch for oliguria and anuria
• Daily weight: same time, same clothing, same scale; notify provider for gain of 2-3 lb in a day or 5 lb in a week

B. Nursing diagnoses and complications

• Activity intolerance; hypervolemia; anxiety; powerlessness; impaired family management
• Potential complications: pulmonary edema, hypotension and cardiogenic shock, arrhythmias, thromboembolism, pericardial effusion

C. Interventions

Promoting activity tolerance:

• Avoid prolonged inactivity (deconditioning, pressure injury, VTE); bed rest only for acute exacerbation
• Daily walking increased over 6 weeks; alternate activity and rest; no two major activities back to back
• Debilitated patients: 3-5 minutes at a time, 1-4 times a day
• Increase duration, then frequency, then intensity
• Sit to do tasks; small frequent meals; plan activities for peak energy times
• Monitor VS and SpO2 before, during, after activity; HR should return to baseline within 3 minutes
• Cardiac rehab referral
• Exercise guidelines (Chart 25-3): low impact, warm-up, build to 30 minutes, cool-down; avoid extreme heat, cold, humidity; wait 2 hours after a meal; should be able to talk; stop for severe dyspnea, pain, dizziness

Managing fluid volume:

• Give oral diuretics early in the morning
• Lung sounds, daily weight; weight gain almost always means fluid
• Low sodium diet (Chart 25-4): read labels for “salt” and “sodium”; avoid canned, processed, convenience and restaurant foods; additives (sodium alginate, sodium benzoate, disodium phosphate) add sodium; municipal and softened water contain sodium; avoid OTC antacids, cough syrups, laxatives; salt substitutes are high in potassium; flavor with lemon, vinegar, herbs
• Plan fluid restriction through the day; concentrate IV medications
• Positioning: extra pillows, HOB up, recliner; support arms on pillows; acute decompensation - upright with legs dangling decreases venous return and lung congestion
• Frequent position changes to prevent pressure injury in edematous areas

Controlling anxiety:

• Comfort, oxygen during acute event, family presence, relaxation techniques
• Quality and Safety Nursing Alert: avoid restraints in confused or anxious HF patients - resisting increases cardiac workload

Minimizing powerlessness:

• Active listening, decision-making opportunities, identify controllable factors
• Screen for depression (common, increases morbidity and mortality)

Health management and transitions:

• Nonadherence to diet, fluid, medications causes many readmissions; some patients deliberately self-adjust medications (Chart 25-5)
• Effective discharge: patient-centered instructions, provider follow-up within 7 days, phone follow-up within 3 days
• Teach-back method

D. Pulmonary edema - acute management

• Upright, legs dependent (reduces preload)
• Assess airway, breathing, VS; pulse oximetry, cardiac monitor, IV access
• Labs: ABG, electrolytes, BUN, creatinine, CBC, BNP, troponin; chest x-ray or lung ultrasound
• Oxygen: non-rebreather initially; noninvasive positive-pressure ventilation preferred if respiratory failure persists; intubation with PEEP if needed
• Stay with the patient; calm, simple explanations
• IV nitroglycerin or nitroprusside with continuous BP monitoring
• IV furosemide (push or infusion): large diuresis within minutes; watch for hypotension; bedside commode; Foley if needed
• Transition to oral diuretics; monitor I&O, weights, electrolytes, creatinine

Diuretic-related problems:

• Hypokalemia: ventricular arrhythmias, hypotension, muscle weakness; increases digoxin toxicity
• Hypomagnesemia: arrhythmias
• Hyperkalemia (ACE inhibitors, ARBs, spironolactone): bradycardia, arrhythmias
• Hyponatremia: disorientation, weakness, muscle cramps, anorexia
• Volume depletion, hypotension (worse with ACE inhibitors and beta-blockers), rising creatinine, hyperuricemia and gout

E. Patient teaching (Chart 25-6 Home Care Checklist)

• HF is chronic and manageable
• Take medications exactly as prescribed; know orthostatic hypotension precautions
• Weigh daily, same time and clothing
• Sodium no more than 2 g/day; avoid canned and processed foods; fresh or frozen
• Daily activity, increase gradually; balance rest; avoid extremes of heat and cold; air conditioning in heat and humidity
• Avoid tobacco and alcohol
• Report immediately: weight gain of 2-3 lb (0.9-1.4 kg) in a day or 5 lb (2.3 kg) in a week; unusual dyspnea; increased swelling of ankles, feet, abdomen; persistent cough; loss of appetite; restless sleep or more pillows needed; profound fatigue

Continuing care: home health, HF clinics (fewer exacerbations and admissions), telehealth monitoring. End of life: discuss ICD deactivation, VAD, advance directives while the patient can participate.

VI. Other Complications of Heart Disease

A. Cardiogenic shock

• Low CO causes inadequate tissue perfusion; most often after a large acute MI; also end-stage HF, tamponade, PE, cardiomyopathy, arrhythmias; high mortality (see Ch. 11)

B. Thromboembolism

• Atrial fibrillation causes intracardiac thrombi that can embolize to the brain (stroke); mural thrombi with poor contractility; treat with heparin, warfarin
• DVT from immobility: leg pain, swelling, erythema, warmth; can cause PE (see Ch. 26)

C. Pericardial effusion and cardiac tamponade

• Normal pericardial sac holds about 20 mL; slow accumulation may reach 1-2 L before symptoms; rapid accumulation (trauma) causes acute tamponade
• Causes: advanced HF, pericarditis, metastatic cancer, cardiac surgery, trauma
• Rising pressure compresses the heart: decreased venous return and filling, low CO, obstructive shock
• Acute: sudden chest pain, tachypnea, dyspnea, JVD, hypotension, muffled heart sounds, tachycardia
• Pulsus paradoxus: systolic drop of at least 10 mm Hg on inspiration
• Cardinal signs (Fig. 25-4): falling arterial pressure, rising venous pressure (neck veins), distant heart sounds
• Diagnostics: echocardiogram confirms; chest x-ray enlarged silhouette; ECG tachycardia and low voltage
• Pericardiocentesis (echo-guided): continuous ECG and VS; decreased CVP and increased BP mean relief; fluid sent for analysis; complications - coronary artery puncture, myocardial trauma, arrhythmias, pleural laceration, gastric puncture; monitor for recurrence
• Pericardiotomy (pericardial window) for recurrent effusions, often malignant

D. Cardiac arrest

• Causes: ventricular fibrillation, progressive bradycardia, asystole, PEA (for example from hypovolemia); associated with MI, massive PE, hyperkalemia, hypothermia, hypoxia, overdose
• Immediate loss of consciousness, pulse, BP; gasping; pupils dilate within a minute; pallor, cyanosis

CPR sequence:

1. Recognize arrest (responsiveness, breathing)
2. Activate emergency response
3. High-quality CPR: no carotid pulse leads to compressions
4. Rhythm analysis and defibrillation within 2 minutes for VF or pulseless VT, then resume compressions

• Compressions on a firm surface, heel of hand on lower half of sternum, 2 inches (5 cm) deep, 100 per minute, full recoil, minimal interruptions; switch compressors every 2 minutes
• Rescue breathing with bag-valve mask by providers after compressions; head-tilt/chin-lift; 100% oxygen
• Advanced airway: confirm placement (breath sounds, chest rise, CO2 detector); then 1 breath every 6 seconds (10 per minute) without pausing compressions
• Defibrillation is treatment of choice for VF and pulseless VT; resume compressions immediately after shock
• Family presence supported; no adverse effects shown
• Post-resuscitation: 12-lead ECG, continuous monitoring, treat precipitating causes; targeted temperature management 32-36 degrees C for at least 24 hours in comatose patients; avoid fever

High-Yield Numbers

• EF: normal 55-65%; HFrEF 40% or less; HFmrEF 40-49%; HFpEF 50% or more; ICD if EF under 35%
• Readmission: over 20% within 30 days, nearly 50% within 6 months
• Pitting edema after at least 10 lb (4.5 kg) fluid retained
• Report weight gain of 2-3 lb in 1 day or 5 lb in 1 week
• Sodium no more than 2 g/day; fluid under 2000 mL/day
• Stop ACE inhibitor if K+ stays over 5.5 mEq/L
• No ARNI within 36 hours of an ACE inhibitor
• Ivabradine if resting HR at least 70; hydralazine-isosorbide if systolic BP at least 90
• BP target under 130/80
• JVD more than 4 cm above the sternal angle at 45 degrees; hepatojugular reflux over 1 cm
• Oliguria under 0.5 mL/kg/h for 6 hours or under 400 mL/24 h; anuria under 50 mL/24 h
• HR back to baseline within 3 minutes after activity; walking program built over 6 weeks
• Discharge follow-up: provider within 7 days, phone call within 3 days
• Pulsus paradoxus: 10 mm Hg or more; normal pericardial fluid 20 mL
• CPR: 100 per minute, 2 inches, switch every 2 minutes; defibrillate within 2 minutes; 1 breath every 6 seconds with advanced airway; TTM 32-36 degrees C for 24 hours
• ACLS drugs: epinephrine 1 mg every 3-5 minutes; amiodarone 300 mg then 150 mg; atropine 0.5 mg up to 3 mg; magnesium 1-2 g for torsades

Priority Nursing Actions and Red Flags

• Pulmonary edema (frothy pink sputum, crackles throughout, severe dyspnea, falling SpO2, anxiety): sit upright with legs dependent, oxygen, IV loop diuretic, stay with patient
• Rapid weight gain, new orthopnea or PND, increasing edema: worsening HF
• Before diuretics: check K+, Na+, Mg and orthostatic BP
• Hypokalemia with digoxin: toxicity risk (nausea, visual changes, bradycardia, confusion)
• ACE inhibitor angioedema affecting the airway: stop drug, emergency care
• Beta-blockers: expect fatigue and dizziness early; do not stop abruptly without provider; caution in asthma
• Do not restrain an anxious or confused HF patient
• Older men on diuretics: check for urinary retention
• Avoid NSAIDs in HF
• Tamponade: hypotension, JVD, muffled heart sounds, pulsus paradoxus - prepare for pericardiocentesis
• Milrinone: check BP and volume status before giving

Medications

Related

• nsg210-exam-1-studyguide - heart failure four pillars from lecture
• nsg210-week-02-summary
• nsg210-hinkle-ch21-cardiovascular-assessment
• nsg210-acls-algorithms
• INDEX