18. Failure of the left ventricle to eject its quota of blood Increased workload & end-diastolic volume CO .↑HR .Tingling in the extremities Enlargement of the left ventricle .↓BP . ↓urine output .fatigue .cool, clammy skin Diminished left ventricular function Blood pools in the ventricle & atrium & back up into the pulmonary veins & capillaries .dyspnea on exertion .confusion .dizziness .cyanosis .↓ peripheral pulses .postural hypotension Pulmonary circulation becomes engorged Left Ventricular Failure
19. Capillary pressure rises Sodium & water are pushed into the interstitial space Pulmonary edema .cough .crackles .↑Pco2 .↓PO2 .rapid, weak pulse .orthopnea Impaired gas exchange & hypoxia .tachypnea .confusion .restlessness .pulsus alternans .Pulmonary effusion
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22. ↑ pressure in the pulmonary system ® ventricle become stressed because it’s pumping against greater pulmonary resistance & because vascular pressure has risen & cardiac function has declined Stressed ® ventricular hypertrophies & dilate .↑ HR .cool skin .cyanosis .↓ CO .dyspnea .dysrhythmias Blood pools in the ® ventricle & atrium Engorgement of venous system that extends backward Right Ventricular Failure
23. Venous congestion Sluggish blood flow Enlargegement of liver & spleen Lowered output of the heart’s left side .anorexia .nausea .abdominal pain .palpable liver & spleen .weakness .elevated CVP .jugular vein distension Hepatojugular reflux ↑ capillary pressure
24. Forces excess fluid from the capillaries into the interstitial space .unexplained weight gain .abdominal distension .pitting edema .nocturia .weakness .dyspnea on exertion
25. Cardiac Compensatory Mechanism When cardiac output is not sufficient to meet the metabolic needs of the body, compensatory mechanisms, including neurohormonal responses become activated. These mechanisms initially help to improve contraction and maintain integrity of the circulation, but if continued lead to abnormal cardiac muscle growth and reconfiguration (remodeling) of the heart.
26. Ventricular Dilation - refers to lengthening of the muscle fibers that increases the volume in the heart chambers.
32. Diagnostic Evaluation Echocardiography-two-dimensional with Doppler flow studies – may show ventricular hypertrophy, dilation of chambers, and abnormal wall motion. ECG (resting and exercise) – may show ventricular hypertrophy and ischemia. Chest x-ray may show cardiomegaly, pleural effusion, and vascular congestion. Cardiac catheterization – to rule out CAD. ABG studies may show hypoxemia due to pulmonary vascular congestion. Liver function studies may be altered because of hepatic congestion.
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35. Class III Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain. Class IV Unable to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.
69. Stage A – focuses on eliminating risk factors by initiating therapeutic lifestyle changes and controlling chronic diseases, such as hypertension and diabetes. Beta-adrenergic blockers, ACE inhibitors, and diuretics are useful during this stage. Stage B – treatment is similar to Stage A, with emphasis on use of ACE inhibitors and beta-adrenergic blockers. Stage C – same as A and B, but with closer surveillance and follow up. a. Digoxin is typically added to the treatment plan in the stage.
70. b. Drug classes to be avoided due to worsening of heart failure symptoms include antiarrhythmic agents, calcium channel blockers, NSAIDS. 4. Stage D – may need mechanical circulatory support, continuous inotropic therapy, cardiac transplantation, or palliative care. a. Treatment aimed at decreasing excess body fluid. b. May not tolerate other classes of drugs used in previous stages.
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72. Patients receiving ACE inhibitors should be monitored for hypotension, hypovolemia, hyperkalemia, and alteration in renal function, especially if they are also receiving diuretics. Example: Captopril, enalapril, fosinopril, quinapril, lisinopril, moexipril, and trandolapril. 2. Angiotensin II Receptor Blockers (ARBs) - blocks the effects of angiotensin II at the angiotensin II receptor. - ACE inhibitors and ARBs have similar hemodynamic effects: ↓BP, ↓systemic vascular resistance, improved cardiac output. - used in patients who cannot tolerate ACE inhibitors due to cough or angioedema.
73. 3. Diuretics - eliminate excess body water and decrease ventricular pressures. - a low-sodium diet and fluid restriction complement this therapy. - some diuretics may have slight venodilator properties. 4. Positive Inotropic Agents - increase the heart’s ability to pump more effectively by improving the contractile force of the muscle. a. Digoxin (Lanoxin) may only be effective in severe cases of failure. b. Dopamine (Intropin) improves renal blood flow in low does range.
74. c. Dobutaime (Dobutrex) d. Milrinone (Primacor) and amrinone (Inocor) are potent vasodilators. 5. Vasodilator therapy - decreases the workload of the heart by dilating peripheral vessels. By relaxing capacitance vessels (veins and venules) , vasodilators reduce ventricular filling pressures (preload) and volumes. By relaxing resistance vessels (arterioles), vasodilators can reduce impedance to left ventricular ejection and improve stroke volume. a. Nitrates such as NTG, isosorbide (Isordil), NTG ointment (Nito-Bid) – predominantly dilate systemic veins.
75. b. Hydralazine (Apresoline) – predominantly affects arterioles; reduces arteriolar tone. c. Prazosin (Minipress) – balanced effects on both arterial and venous circulation. d. Sodium nitroprusside (Nipride) – predominantly affects arterioles. e. Morphine (Duramorph) – decreases venous return, decreases pain and anxiety. 6. Beta-adrenergic blockers - decrease myocardial workload and protect against fatal dysrhythmias by blocking norepinephrine effects of the sympathetic nervous system.
76. a. Metoprolol (Lopressor) are commonly used. b. Carvedilol (Coreg) is a nonselective beta and alpha adrenergic blocker. Patients may actually experience in general malaise for a 2 to 3 week period while they adjust to the medication. 7. Aldosterone Antagonist - decrease sodium retention, sympathetic nervous system activation and cardiac remodeling. a. Spironolactone (Aldactone) is most commonly used.
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79. 4. Cardiac resynchronization therapy or biventricular pacing - helps to restore synchronous ventricular contractions , improves ventricular left ventricle filling, and improves CO. 5. Left ventricular assist device 6. Partial left ventriculectomy (reduction ventriculoplasty or Batista procedure) - a triangular section of the weakened heart muscle is removed to reduce ventricular wall tension. This procedure is not commonly used. 7. Endoventricular circular patch plasty or the Dor procedure - removal of diseased portion of septum or left ventricle
80. 7. Endoventricular circular patch plasty or the Dor procedure - removal of diseased portion of septum or left ventricle with a synthetic or autologous tissue patch, thus providing a more normal shape and size of the heart, which improves hemodynamics. 8. Acorn cardiac support device - a polyester mesh, custom-fitted jacket is surgically placed on the epicardial surface, providing diastolic support. Over time, it decreases or halts remodeling. 9. Heart transplant
81. Complications Intractable or refractory heart failure Cardiac dysrhythmias Myocardial failure and cardiac arrest Digoxin toxicity Pulmonary infarction, pneumonia, and emboli
82. Nursing Diagnoses Decreased cardiac output related to impaired contractility and increased afterload and preload. Impaired gas exchange related to alveolar edema due to elevated ventricular pressures. Excess fluid volume related to sodium and water retention. Activity intolerance related to oxygen supply and demand imbalance.
83. Nursing Interventions Maintaining Adequate Cardiac Output 1. Place patient at physical and emotional rest to reduce work of heart. Provide rest in semi-recumbent position or in armchair in an airconditioned environment – reduces work of heart, increases heart reserve, reduces BP, decreases work of respiratory muscles and oxygen utilization, improves efficiency of heart contraction; recumbency promotes diuresis by improving renal perfusion. Provide bedside commode – to reduce work of getting to bathroom and for defecation.
84. Provide for psychological rest – emotional stress produces vasoconstriction, elevates arterial pressure, and speeds the heart. - promote physical comfort - avoid situations that tend to promote anxiety and agitation - offer careful explanations and answers to the patient’s questions. 2. Evaluate frequently for progression of left-sided heart failure. Take frequent BP readings. Observe for lowering of systolic pressure. Note narrowing of pulse pressure. Note alternating strong and weak pulsations
85. 3. Auscultate heart sounds frequently and monitor cardiac rhythm. 4. Observe for signs and symptoms of reduced peripheral tissue perfusion: cool temperature of skin, facial pallor, poor capillary refill of nail beds. 5. Administer pharmacotherapy as directed. 6. Monitor clinical response of patient with respect to relief of symptoms (lessening dyspnea and orthopnea, decrease in crackles, relief of peripheral edema). NURSING ALERT: WATCH FOR SUDDEN UNEXPECTED HYPOTENSION WHICH CAN CAUSE MYOCARDIAL ISCHEMIA AND DECREASE PERFUSION TO VITAL ORGANS.
86. Improving Oxygenation Raise head of bed 8 to 10 inches (20 to 30 cm) – reduces venous return to heart and lungs; alleviates pulmonary congestion. Support lower arms with pillows – to eliminate pull of their weight on shoulder muscles. Sit orthopneic patient on side of bed with feet supported by a chair, head and arms resting on an over-the-bed table, and lumbosacral area supported with pillows. Auscultate lung fields at least 4 hours for crackles and wheezes in dependent lung fields. Observe for increased rate of respirations (could be indicative of falling arterial pH).
87. Observe for Cheyne-stokes respirations. Position the patient every 2 hours (or encourage the patient to change position frequently) – to help prevent atelectasis and pneumonia. Encourage deep breathing exercises every 1 to 2 hours – to avoid atelectasis. Offer small, frequent feedings – to avoid excessive gastric filling and abdominal distention with subsequent elevation of diaphragm that causes decrease in lung capacity. Administer oxygen as directed. Restoring Fluid Balance 1. Administer prescribed diuretic as ordered.
88. 2. Give diuretic early in the morning. – nighttime diuresis disturbs sleep. 3. Keep input and output record – patient may lose large volume of fluid after a single dose of diuretic. 4. Weigh patient daily – to determine if edema is being controlled: weight loss should not exceed 1 to 2 lb (0.5 to 1 kg)/day. 5. Assess for signs of hypovolemia caused by diuretic therapy – thirst, decreased urine output, orthostatic hypotension, weak, thready pulse, increased serum osmolality, and increased urine specific gravity. 6. Be alert for signs of hypokalemia, which may cause weakness of cardiac contractions and may precipitate digoxin toxicity in the form of dysrhythmias, anorexia, nausea & vomiting, paresthesias, & confusion.
89. 7. Give potassium supplements as prescribed. 8. Be aware of disorders that may be worsened by diuretic therapy including hyperuricemia, gout, volume depletion, hyponatremia, magnesium depletion, hyperglycemia, and diabetes mellitus. 9. Watch for signs for bladder distention in elderly male patients with prostatic hyperplasia. 10. Administer IV fluids carefully through an intermittent access device to prevent fluid overload. 11. Monitor for pitting edema of lower extremities and sacral area. Use convoluted foam mattress and sheepskin to prevent pressure ulcers. (poor blood flow and edema increase susceptibility). 12. Observe for the complications of bedrest – pressure ulcers, phlebothrombosis, pulmonary embolism.
90. 13. Be alert to complaints of right upper quadrant abdominal pain, poor appetite, nausea, and abdominal distention (may indicate hepatic and visceral engorgement). 14. Monitor patient’s diet. Diet may be limited in sodium – to prevent control or eliminate edema; may also be limited in calories. 15. Caution patients to avoid added salt in food and foods with high sodium content. Improving Activity Tolerance Increase patient’s activities gradually. Alter or modify patient’s activities – to keep within the limits of his cardiac reserve. a. Assist patient with self-care activities early in the day (fatigue sets in as day progresses).
91. b. Be alert to complaints of chest pain or skeletal pain during or after activities. 2. Observe the pulse, symptoms, and behavioral response to increased activity. a. Monitor patient’s, symptoms, and behavioral response to increased activities. b. Allow heart rate to decrease to preactivity level before initiating a new activity Note time lapse between cessation of activity and decrease in heart rate (decreased stroke volume causes immediate rise in heart rate.) Document time lapse and revise patient care plan as appropriate (progressive increase in time lapse maybe indicative of increased life-sided-heart failure).
92. Relieve nighttime anxiety & provide for rest and sleep-patients with heart failure have a tendency to be restless at night because of cerebral hypoxia with superimposed nitrogen retention. Give appropriate sedation to relieve insomnia and restlessness.
93. Patient Education and Health Maintenance Explain the disease process; the term failure have terrifying implications. Explain the pumping action of the heart- to move blood through the body to provide nutrients and aid in the removal of waste material. Explain the difference between heart attack and heart failure. Teach the signs & symptoms of recurrence. Watch for Gain weight Swelling of ankles, feet, or abdomen Persistent cough Tiredness, loss of appetite Frequent urination at night
94. Review medication regimen Label all medications Give written instructions. Make sure the patient has a check-off system that will show that he has taken medications. Teach the patient to take and record pulse rate and BP. Inform the patient of adverse drug effects. If the patient is taking oral potassium solution, it maybe diluted with juice and taken after a meal. Tell the patient to weight self daily and log weight if on diuretic therapy.
95. Review activity program. Instruct the patient as follows: Increase walking and other activities gradually, provided they do not cause fatigue & dyspnea. In general continue, at whatever activity level can be maintained without the appearance of symptoms. Avoid excesses in eating and drinking. Undertake a weight reduction program until optimal weight is reached. Avoid extremes in heat and cold, which, increase the work of the heart, air conditioning may be essential in a hot, humid environment.
96. Restrict sodium as directed. 1. Teach restricted sodium diet and the DASH (Dietary Approaches to Stop Hypertension) diet. 2. Give patient a written diet plan with lists of permitted and restricted food. 3. Advise patient to look at all labels to ascertain sodium content. 4. Teach patient to rinse the mouth well after using tooth cleansers and mouthwashes – some of these contain large amounts of sodium. 5. Teach patient that sodium is present in cough remedies, laxatives, pain relievers, estrogens, and other drugs.
97. EVALUATION: EXPECTED OUTCOMES Normal BP and heart rate Respiratory rate 16 to 20, ABG levels within normal limits, no signs of crackles of wheezes in lung field. Weight decrease of 2.2 lb daily, no pitting edema of lower extremities and sacral area. Heart rate within normal limits, rests between activities.
