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Chapter 35: Care of Patients with Cardiac Problems
Terms in this set (72)
Also called pump failure; inability of heart to work effectively as a pump
Left-Sided Heart Failure
Formerly known as congestive heart failure-Not all cases involve fluid accumulation
Left-Sided Heart Failure: Typical causes
ØCoronary artery disease
Systolic heart failure (systolic ventricular dysfunction)
-Results when the heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation.
-Preload increases with decreased contractility, and afterload increases as a result of increased peripheral resistance (e.g., hypertension)
-ejection fraction drops to below 40% with ventricular dilation. tissue perfusion diminishes and blood accumulates in the pulmonary vessels.
Diastolic heart failure (heart failure with preserved left ventricular function)
-Occurs when the left ventricle cannot relax adequately during diastole.
-"stiffening" prevents the ventricle from filling with sufficient blood to ensure an adequate cardiac output
-The ventricle becomes less compliant over time because more pressure is needed to move the same amount of volume
Right-Sided Heart Failure: Causes
ØLeft ventricular failure
ØRight ventricular MI
Right ventricle cannot empty completely
-Increased volume and pressure in venous system -peripheral edema
High-output heart failure
-Can occur when cardiac output remains normal or above normal, .
-Caused by increased metabolic needs of hyperkinetic conditions
-Increase CO with HF
ØSympathetic nervous system stimulation
ØOther renin-angiotensin system activation
ØChemical responses (BNP)
Left-Sided Heart Failure: Clinical manifestations
ØAcute confusion (low flow)
Proportional Pulse Pressure
Systolic BP − Diastolic BP/ Systolic BP
Right-Sided Heart Failure: Clinical manifestations
ØJugular vein distention
ØIncreased abdominal girth
ØWeight most reliable indicator of fluid gain/loss
30 - 40 mm/Hg
Indicator of left ventricular function
Correlates with CI
Assessment of Right-Sided Heart Failure: Laboratory
*: sodium, potassium, magnesium, calcium, and chloride,
Hemoglobin and hematocrit
*: performed to identify HF resulting from anemia. If the patient has FVE levels may be low as a result of hemodilution.
*: used for diagnosing HF (in particular, diastolic HF) in patients with acute dyspnea, as therapy is optimized, levels decrease
* (proteinuria/high specific gravity), early indicator of decreased compliance
*: hypoxemia (low blood oxygen level) because oxygen does not diffuse easily through fluid-filled alveoli. Respiratory alkalosis= hyperventilation; respiratory acidosis=CO2 retention. Metabolic acidosis= accumulation of lactic acid.
Assessment of Right-Sided Heart Failure: Imaging
*: can be helpful in diagnosing left ventricular failure. Heart is enlarged (cardiomegaly), representing hypertrophy or dilation
*: Cardiac valvular changes, pericardial effusion, chamber enlargement, and ventricular hypertrophy as well as ejection fraction.
Assessment of Right-Sided Heart Failure: Other
: may show ventricular hypertrophy, dysrhythmias, and any degree of myocardial ischemia, injury, or infarction. Not helpful in determining the presence or extent of HF.
: allows the direct assessment of cardiac function and volume status in acutely ill patients
Pulmonary artery catheter
: PA catheter allows for assessment of cardiac function and fluid volume, PAP/PAWP elevated with left heart failure
Analysis of Right-Sided Heart Failure: Priority problems
ØImpaired gas exchange r/t ventilation/perfusion imbalance
ØDecreased cardiac output r/t altered contractility, preload, afterload, pump failure
ØFatigue/weakness r/t hypoxemia
ØPotential for pulmonary edema r/t left-sided heart failure
Promoting oxygenation and gas exchange
ØMonitor respiratory rate every 1-4 hr
ØAuscultate breath sounds every 4-8 hr
ØPosition in high Fowler's if patient dyspneic ØMaintain oxygen saturation of 90%
Improving Cardiac Output
Improve/increase cardiac pump effectiveness
Drugs Used to Reduce Afterload
-Lisinopril (Prinivil, Zestril), enalapril (Vasotec), fosinopril (Monopril)
- valsartan (Diovan), irbesartan (Avapro), losartan (Cozaar)
: nesiritide (Natrecor) causes natriuresis, or loss of sodium in the renal tubules, as well as vasodilation
Interventions That Reduce Preload
Drugs That Enhance Contractility
ØNesiritide (Natrecor - very expensive)
ØMilrinone (Primacor) phosphodiesterase activity enhances calcium activity
.ØLevosimendan (Simdax) binds to troponin
-Given for patients in acute heart failure to reduce anxiety, decrease preload and afterload, slow respirations, and reduce the pain associated with a myocardial infarction (MI).
*: High-ceiling diuretics, such as furosemide (Lasix, Furoside image, Novosemide image), torsemide (Demadex), and bumetanide (Bumex), are most effective for treating fluid volume overload.
*hydrochlorothiazide (HCTZ) (HydroDIURIL, Urozide image) and metolazone (Zaroxolyn), for older adults with mild volume overload. Self-limiting (i.e., diuresis decreases after edema fluid is lost)
Cardiac glycoside (Lanoxin)*
ØReduces heart rate (HR)
ØSlows conduction through atrioventricular node
ØInhibits sympathetic activity
Heart Failure: Other Nonsurgical Options
CPAP -continuous positive airway pressure
: improves obstructive sleep apnea in patients with HF. It also improves cardiac output (CO) and ejection fraction (EF) by decreasing afterload and preload, blood pressure (BP), and dysrhythmias.
CRT - cardiac resynchronization therapy
: Electrical stimulation causes more synchronous ventricular contractions to improve EF, CO, and mean arterial pressure.
replaces damaged genes with normal or modified genes by a series of injections of growth factor into the left ventricle.
Heart Failure: Surgical Management
VADs: Ventricular Assist Devices
: a mechanical pump is implanted to work with the patient's own heart
Heart Failure: Other surgical therapies
Heart reduction: Partial left ventriculectomy (PLV)
*: removing a triangle-shaped section of the weakened heart in the left lateral ventricle to reduce the ventricle's diameter and decrease wall tension
ØEndoventricular circular patch cardioplasty: removes portions of the cardiac septum and left ventricular wall and grafts a circular patch into the opening. Provides a more normal shape to the left ventricle to improve ejection fraction (EF) and cardiac output (CO).
ØAcorn cardiac support device: a polyester mesh jacket that is placed over the ventricles to provide support and to avoid overstretching the myocardial muscle. Reduces hypertrophy, assists with improvement of the EF.
ØMyosplint: Electrical stimulation of several tension pads (splints) on the outside of the ventricle changes it to a more normal shape to improve function.
Preventing or Managing Pulmonary Edema
Assess for early signs (for example, crackles in bases)
ØDyspnea at rest, disorientation, confusion
High Fowler's position
Nitroglycerin: decrease afterload and preload if the patient's systolic blood pressure is above 100
Rapid-acting diuretics: Lasix or Bumex.
IV morphine sulfate: to reduce venous return (preload), decrease anxiety, and reduce the work of breathing
Heart Failure: Community-Based Care
Home care management: signs of heart failure, nutritional status, home environment, meds and O2
Teaching for self-management: (Medication,Activity, Weight, Diet, Symptoms)
Health care resources: home care nurse, ambulatory care clinic, or nurse-led follow-up program, AHA, medical supply companies
Indications for Worsening or Recurrent Heart Failure
Rapid weight gain
Decrease in exercise tolerance
Excessive awakening at night to urinate
Development of dyspnea/angina at rest Increased edema in feet, ankles hand
Mitral stenosis: Etiology
-Usually rheumatic carditis, which can cause valve thickening by fibrosis and calcification. Rheumatic fever is the most common cause of the problem.
-In more developed nations, congenital anomalies affect the majority of patients
Mitral stenosis: Pathophysiology
.-Valve leaflets fuse and become stiff and the chordae tendineae contract and shorten. The valve opening narrows, preventing normal blood flow from the left atrium to the left ventricle.
-Left atrial pressure rises, the left atrium dilates, pulmonary artery pressures increase, and the right ventricle hypertrophies.
Mitral stenosis: Symptoms
Dyspnea on exertion
Paroxysmal nocturnal dyspnea
Neck vein distention
Rumbling, apical diastolic murmur
Mitral regurgitation (insufficiency): Etiology
-"degenerative" due to aging and infective endocarditis
-Other causes include papillary muscle dysfunction or rupture resulting from ischemic heart disease or congenital anomalies.
-Rheumatic heart disease is the number-one cause in developing nations usually coexisting with some degree of mitral stenosis;
Mitral regurgitation (insufficiency): Pathophysiology
-Prevent the mitral valve from closing completely during systole. Incomplete closure of the valve allows the backflow of blood into the left atrium when the left ventricle contracts.
-During diastole, regurgitant output again flows from the left atrium to the left ventricle along with the normal blood flow. The increased volume must be ejected during the next systole.
-To compensate for the increased volume and pressure, the left atrium and ventricle dilate and hypertrophy.
Mitral regurgitation (insufficiency): Symptoms
Dyspnea on exertion
Neck vein distention
High-pitched holosystolic murmur
Mitral valve prolapse: Etiology
-Variable and has been associated with conditions such as Marfan syndrome and other congenital cardiac defects.
-Also has a familial tendency. Usually, however, no other cardiac abnormality is found.
Mitral valve prolapse: Pathophysiology
-Valvular leaflets enlarge and prolapse into the left atrium during systole.
-Usually benign but may progress to pronounced mitral regurgitation in some patients.
Mitral valve prolapse: Symptoms
Most patients are asymptomatic
Atypical chest pain
Systolic click or a late systolic murmur
Aortic stenosis: Etiology
-Congenital bicuspid or unicuspid aortic valves are the primary causes
-Rheumatic aortic stenosis occurs with rheumatic disease of the mitral valve and develops in young and middle-aged adults.
-Atherosclerosis and degenerative calcification of the aortic valve are the major causative factors in older adults.
-Most common valvular disorder in all countries with aging populations.
Aortic stenosis: Pathophysiology
-The aortic valve orifice narrows and obstructs left ventricular outflow during systole.
-Increased resistance to ejection or afterload results in ventricular hypertrophy.
-As worsens, cardiac output becomes fixed and cannot increase to meet the demands of the body during exertion. Symptoms then develop.
-Eventually the left ventricle fails, blood backs up in the left atrium, and the pulmonary system becomes congested. Right-sided HF can occur late in the disease
Aortic stenosis: Symptoms
Dyspnea on exertion
Syncope on exertion
Paroxysmal nocturnal dyspnea
Harsh, systolic crescendo- decrescendo murmur
Aortic regurgitation (insufficiency): Etiology
-Usually results from nonrheumatic conditions such as infective endocarditis, congenital anatomic aortic valvular abnormalities, hypertension, and Marfan syndrome (a rare, generalized, systemic disease of connective tissue).
Aortic regurgitation (insufficiency): Pathophysiology
-Aortic valve leaflets do not close properly during diastole and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed.
-Allows flow of blood from the aorta back into the left ventricle during diastole.
-Left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies.
Aortic regurgitation (insufficiency): Symptoms
-Remain asymptomatic for many years because of the compensatory mechanisms of the left ventricle. -With progression left ventricular failure occurs causing exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
-Palpitations may be noted with severe disease.
-Nocturnal angina with diaphoresis often occurs.
-On palpation, a"bounding" arterial pulse. The pulse pressure is usually widened, with an elevated systolic pressure and diminished diastolic pressure. -High-pitched, blowing, decrescendo diastolic murmur.
Valvular Heart Disease: Assessment
Sudden illness or slowly developing symptoms over many years
Ask about attacks of rheumatic fever, infective endocarditis; ask about possibility of IV drug abuse
Chest x-ray, ECG, stress test
-Echocardiography to visualize the structure and movement of the heart.
-Transesophageal echocardiography (TEE) or transthoracic echocardiography (TTE) is also performed to assess most cases
Valvular Heart Disease: Nonsurgical Management
ØDiuretics ØBeta blockers ØDigoxin ØOxygen ØNitrates ØVasodilators ØAnticoagulants
Valvular Heart Disease: Surgical Management
: balloon has dilated the orifice and improved leaflet mobility.
Direct or open commissurotomy: removes thrombi from the atria, incises the fused commissures (leaflets), and débrides calcium from the leaflets, widening the orifice.
Mitral valve annuloplasty
: result in an annulus of the appropriate size and in leaflets that can close completely.
: prosthetic (synthetic) and biologic (tissue)
Home care management- aticoagulant therapy, nurse for assistance with incision care, ADLs
Teaching for self-management:
• The disease process and the possibility of heart failure
• Drug therapy, including diuretics, vasodilators, beta blockers, calcium channel blockers, antibiotics, and anticoagulants
• The prophylactic use of antibiotics
• A plan of activity and rest to conserve energy
Health care resources:
The American Heart Association's Mended Hearts, Inc.
-A card to identify the patient as needing prophylactic antibiotics.
-An identification bracelet or necklace that states the name of the drugs the patient is taking should also be worn.
Infective Endocarditis: Pathophysiology
-Microbial INFECTION (e.g., viruses, bacteria, fungi) of the endocardium.
-Most common infective organism is Streptococcus viridans or Staphylococcus aureus.
Infective Endocarditis: Risk factors
ØIV drug abusers
ØValve replacement recipients
ØStructural cardiac defects
Manifestations of Endocarditis
Murmur (newly developed or change in existing)
Arterial embolization: fragments of vegetation (clots) break loose and travel randomly through the circulation.
Splenic infarction: sudden abdominal PAIN and radiation to the left shoulder can occur.
Neurologic changes: Emboli to the central nervous system cause either transient ischemic attacks (TIAs) or a stroke
Petechiae (pinpoint red spots)
Splinter hemorrhages: black longitudinal lines or small red streaks on distal third of the nail bed
Endocarditis: Diagnostic Assessment
Positive blood cultures: Slow-growing organisms may take 3 weeks and require a specialized medium to isolate. Low hemoglobin and hematocrit levels may also be present.
New regurgitant murmur
Evidence of endocardial involvement by echocardiography
Endocarditis: Nonsurgical Management.
ØAntimicrobials: usually given IV, with the course of treatment lasting 4 to 6 weeks for most cases, one of the penicillins or cephalosporins.
ØActivities balanced with adequate rest
Endocarditis: Surgical Management.
ØRemoval of infected valve (either biologic or prosthetic)
ØRepair or removal of congenital shunts
ØRepair of injured valves and chordae tendineae
ØDraining of abscesses in heart or elsewhere
-Inflammation or alteration of the pericardium (the membranous sac that encloses the heart).
-The problem may be fibrous, serous, hemorrhagic, purulent, or neoplastic.
Assessment of Pericarditis
Substernal precordial pain
ØRadiating to left side of neck, shoulder, or back
ØGrating, oppressive pain, aggravated by breathing, coughing, swallowing
ØPain worsened by supine position; relieved by sitting up and leaning forward
Pericardial friction rub: scratchy, high-pitched sound
ØAntibiotics for bacterial form
Pericardiectomy: for chronic constrictive pericarditis (surgical excision of the pericardium)
-Occurs when the space between the parietal and visceral layers of the pericardium fills with fluid.
-Puts the patient at risk for
or (excessive fluid within the pericardial cavity)
Small volumes (20 to 50 mL) of fluid accumulate rapidly in the pericardium and cause a sudden decrease in cardiac output (CO)
Cardiac tamponade findings
ØJugular venous distention
ØParadoxical pulse (systolic blood pressure 10 mm Hg or more higher on expiration than on inspiration)
ØIncreased heart rate, dyspnea, and fatigue
ØMuffled heart sounds
Acute Cardiac Tamponade: Emergency Care
Increased fluid volume (manage the decreased CO)
: demonstrates compression of the heart, with all pressures (right atrial, pulmonary artery, and wedge) being similar and elevated (plateau pressures).
: all available pericardial fluid is withdrawn using catheter
: removing a portion of the pericardium to permit excessive pericardial fluid to drain into the pleural space
: removal of the toughened encasing pericardium
Rheumatic Carditis: Pathophysiology
-Sensitivity response from upper respiratory tract infection with group A beta-hemolytic streptococci
Inflammation in all layers of heart
-Formation of Aschoff bodies (nodules that are replaced by scar tissue)
-Impaired contractile function of myocardium, thickening of pericardium, valvular damage
Rheumatic Carditis: Clinical Manifestations
Cardiomegaly (enlarged heart)
New or changed murmur
Pericardial friction rub
Changes in ECG (prolonged PR interval)
Indications of heart failure
Existing streptococcal infection
Subacute or chronic disease of cardiac muscle
Restrictive cardiomyopathy-relaxation or filling
Arrhythmogenic right ventricular cardiomyopathy- genetic, rt. Ventricular dysplasia = arrhythmias
-Most commonly seen.
-Involves extensive damage to the myofibrils and interference with myocardial metabolism.
-Wall thickness is normal, but both ventricles are dilated (left ventricle is usually worse) and systolic function is impaired.
-Asymmetric ventricular hypertrophy and disarray of the myocardial fibers.
-Left ventricular hypertrophy leads to a stiff left ventricle, which results in diastolic filling abnormalities.
-Obstruction in the left ventricular outflow tract is seen in most patients
Dilated cardiomyopathy (DCM)
Toxin exposure avoidance
Cardiomyopathy: Nonsurgical Management
Drug therapy: increase cardiac output
Toxin exposure avoidance (e.g. alcohol)
Surgical Management: Depends on cardiomyopathy type
Implantable cardiac defibrillators
arrhythmogenic right ventricular cardiomyopathy
*: excising a portion of the hypertrophied ventricular septum to create a wider outflow tract
Percutaneous alcohol septal ablation
*: Absolute alcohol is injected into a target septal branch of the left anterior descending coronary artery to produce a small septal infarction.
*: for patients with severe DCM and may be considered for restrictive cardiomyopathy.
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