CHAPTER 5 Cardiac and vascular disorders
Cardiovascular assessment: general
Palpation
Pulse assessment to evaluate for decreased tissue perfusion:
• Pulse quality and regularity bilaterally (scale 0 to 4+)
• Edema (scale 0 to 4+): extremities, back, and sacrum
• Evaluate all peripheral pulses to assess for vascular disease.
• Heart sounds to evaluate for contributors to decreased cardiac output (note changes with body positioning and respirations):
Labwork
Blood studies can reveal causes of dysrhythmias or changes in pacing/conduction or HR changes:
• Electrolyte levels: ↑ or ↓ potassium or magnesium
• Complete blood counts: anemia, ↑ white blood cells (WBCs)
CARE PLANS FOR GENERALIZED CARDIOVASCULAR DYSFUNCTIONS
related to decreased cardiac output
1. Determine patient’s physical limitations.
2. Determine causes of fatigue and perceived causes of fatigue.
3. Monitor cardiorespiratory response to activity (tachycardia, other dysrhythmias, tachypnea, dyspnea, diaphoresis, pallor) and hemodynamic response (elevated pulmonary artery pressures [PAPs], central venous pressure [CVP], or no change/little increase in cardiac output) if a pulmonary artery catheter or bioimpedance device is in place.
4. Monitor for chest discomfort during activity.
5. Reduce all causes of discomfort, including those induced by the patient’s environment, such as uncomfortable room temperature or position, thirst/dry mouth, and wrinkled or damp bedding.
Self-care assistance: instrumental activities of daily living (iadls)
1. Determine need for assistance with IADLs including walking, cooking, shopping, housekeeping, transportation, and money management.
2. Provide for methods of contacting support of assistance people (such as lifeline services, emergency response services including readily accessible telephone numbers if patient’s area is not 911 accessible).
3. Determine financial resources and personal preferences for modifying their home to accommodate any disabilities.
related to altered cardiac pump function
1. Palpate and evaluate quality of peripheral pulses, for presence of edema, capillary refill, and skin color and temperature of extremities.
2. Monitor ECG continuously, noting HR and rhythm. Select the most diagnostic lead(s) for monitoring patient. Consider use of ST-segment monitoring if available.
3. Compare current ECG readings with past readings and report abnormal findings that create instability or have the potential to create instability.
4. Use a 12- or 15-lead ECG to diagnose heart rhythm changes, because one or two leads are often insufficient to fully diagnose ECG changes.
5. Provide antidysrhythmic medications as appropriate to abate heart rhythms that prompt hypotension.
6. Provide positive inotropic drugs as appropriate to help increase cardiac output to maintain stable BP.
7. Monitor effects of negative inotropic medications (e.g., beta blockers) carefully, as the decreased myocardial workload may prompt hypotension.
8. Evaluate chest pain for location, radiation, intensity, duration, and precipitating factors. Emphasize to patient the importance of reporting all instances of chest pain and pressure and arm, neck, and jaw pain.
9. Apply oxygen when chest pain is present, according to Advanced Cardiac Life Support (ACLS) guidelines.
10. Monitor pacemaker function as appropriate to insure device is sensing, pacing and capturing appropriately.
11. Auscultate heart tones; be alert for development of new S3 and S4, new “split” sounds, or pericardial friction rubs.
12. Auscultate lungs for rales, crackles, wheezes, rhonchi, pleural friction rubs, or other adventitious sounds indicative of fluid retention.
13. Monitor for diminished level of consciousness, which may signal cerebral perfusion is compromised secondary to decreased cardiac output.
14. Auscultate abdomen and monitor for decreased bowel sounds and/or abdominal distention, which may indicate abdominal perfusion is compromised.
15. Record intake and output, urine output, and daily weight and evaluate for fluid retention, which may indicate renal perfusion is compromised.
16. Note electrolyte values at least daily, monitoring closely for changes in potassium and magnesium, which may prompt dysrhythmias; increased blood urea nitrogen (BUN) or increased creatinine, which may indicate low CO is causing renal insufficiency; and hyperglycemia, which may indicate patient has underlying diabetes.
17. Monitor for increasing activity intolerance, dyspnea, excessive fatigue, and orthopnea, which may all indicate CO is lessening.
18. Keep head of the bed (HOB) elevated if patient is unable to breathe comfortably when flat in bed.
19. Insert urinary catheter if patient is unable to void without markedly increasing activity level, or anuria is noted, as appropriate.
1. Monitor values generated by pulmonary artery catheter to directly assess CO.
2. Assess for further decreases in CO reflected by elevated pulmonary artery occlusive/wedge pressure, elevated CVP, and elevated pulmonary vascular resistance (PVR).
3. Monitor for fluid overload by assessing for elevated systemic vascular resistance (SVR).
4. Monitor the effects of all medications on hemodynamic readings, including effects of positive or negative inotropic agents, antidysrhythmics, and vasodilating or vasoconstricting medications.
related to decreased perfusion to the lungs
Respiratory Status: Ventilation
1. Assess for patent airway; if snoring, crowing, or strained respirations are present, indicative of partial or full airway obstruction, open airway using chin-lift or jaw-thrust.
2. Insert oral or nasopharyngeal airway if patient cannot maintain patent airway; if severely distressed, patient may require endotracheal intubation.
3. Position patient to alleviate dyspnea and ensure maximal ventilation—generally in a sitting upright position unless severe hypotension is present.
4. Clear secretions from airway by having patient cough vigorously, or provide nasotracheal, oropharyngeal, or endotracheal tube suctioning as needed.
5. Have patient breathe slowly or manually ventilate with Ambu bag slowly and deeply between coughing or suctioning attempts.
6. Assist with use of incentive spirometer as appropriate.
7. Turn patient every 2 hours if immobile. Encourage patient to turn self, or get out of bed as much as tolerated if able.
8. Provide mucolytic and bronchodilating medications orally, intravenously (IV), or by inhaler, aerosol, or nebulizer as ordered to assist with thinning secretions and relaxing muscles in lower airways.
9. Provide chest physical therapy as appropriate, if other methods of secretion removal are ineffective.
1. Provide humidity in oxygen or bilevel positive airway pressure (BiPAP) device if used for longer than 12 hours to help thin secretions.
2. Administer supplemental oxygen using liter flow and device as ordered.
3. Restrict patient and visitors from smoking while oxygen is in use.
4. Document pulse oximetry with oxygen liter flow in place at time of reading as ordered. Oxygen is a drug; the dose of the drug must be associated with the oxygen saturation reading or the reading is meaningless.
5. Obtain arterial blood gases (ABGs) if patient experiences behavioral changes or respiratory distress to check for hypoxemia or hypercapnia.
6. Monitor for oxygen-induced hypoventilation, especially in patients with chronic obstructive pulmonary disease (COPD).
7. Monitor for changes in chest radiograph and breath sounds indicative of oxygen toxicity and absorption atelectasis in patients receiving higher concentrations of oxygen (greater than FIO2 45%) for longer than 24 hours. The higher the oxygen concentration, the greater is the chance of toxicity.
8. Monitor for skin breakdown where oxygen devices are in contact with skin, such as nares and around edges of mask devices.
9. Provide oxygen therapy during transportation and when patient gets out of bed.
10. If patient is unable to maintain SPO2 reading of greater than 88% off oxygen, consult with respiratory care practitioner and physician about the need for home oxygen therapy.
1. Monitor rate, rhythm, and depth of respirations.
2. Note chest movement for symmetry of chest expansion and signs of increased work of breathing such as use of accessory muscles or retraction of intercostal or supraclavicular muscles. Consider use of BiPAP for impending respiratory failure.
3. Ensure airway is not obstructed by tongue (snoring or choking-type respirations) and monitor breathing patterns. New patterns that impair ventilation should be managed as appropriate for setting.
4. Note that trachea remains midline, as deviation may indicate patient has a tension pneumothorax.
5. Auscultate breath sounds following administration of respiratory medications to assess for improvement.
6. Note changes in oxygen saturation (SaO2), pulse oximetry (SpO2), and end-tidal CO2 (ETCO2) and ABGs as appropriate.
7. Monitor for dyspnea and note causative activities or events.
8. If increased restlessness or unusual somnolence occur, evaluate patient for hypoxemia and hypercapnia as appropriate.
9. Monitor chest radiograph reports as new films become available.
Heart failure
Pathophysiology
HF is a syndrome stemming from impaired cardiac pump function, resulting in systemic perfusion that is inadequate to meet the body’s metabolic demands for energy production. The condition may be divided into systolic or diastolic HF. In systolic HF, there is reduced cardiac contractility, while in diastolic HF, there is impaired cardiac relaxation and abnormal ventricular filling. HF is the leading cause of death in the United States, affecting approximately 5 million patients. One in five patients dies within 1 year of diagnosis. The annual medical cost is over $30 billion. Although much progress has been made in the treatment, the annual mortality rate remains high (5% to 20%). The greatest number of patients die from New York Heart Association (NYHA) Class IV symptoms, including progressive pump failure and congestion. Over half die from sudden cardiac death. Many die from end-organ failure resulting from inadequate perfusion. The kidneys are especially vulnerable. Those with a poor cardiac prognosis typically manifest a higher NYHA HF class, high catecholamine and BNP levels, renal dysfunction, cachexia, valvular regurgitation, ventricular dysrhythmias, lower ejection fraction, hyponatremia, and left ventricular (LV) dilation. Patients with both systolic and diastolic LV dysfunction have a worse prognosis than do patients with either condition alone.
Biventricular failure
Patients who experience both LV and RV MI (a combination often seen with inferior wall MI) experience hemodynamics that are extremely complex to manage. The impaired right ventricle needs volume infusion to promote better expansion, or “more stretch,” of the ventricle, whereas the left ventricle may be unable to accommodate a normal or pre-MI volume and requires volume reduction. Deviation of the intraventricular septum associated with right-sided HF caused by distention of the ventricle can significantly reduce the size of the left ventricle. Ultimately, failure in either side of the heart will affect both sides, because the ventricles are interdependent.
Cardiovascular assessment: heart failure
Goal of system assessment
Evaluate for decreased CO and decreased tissue perfusion initially with General Assessment, p. 418. If patient has developed HF secondary to acute coronary syndrome, see Assessment in Acute Coronary Syndromes, p. 434.
History and risk factors
History of HF, CAD, and MI; familial history of CAD; age greater than 65 years; cigarette smoking; alcohol use; hypercholesterolemia; hypertension; diabetes; obesity; dysrhythmias; weight gain; and decreasing activity tolerance. Fatigue may be the only presenting symptom. Other important data include understanding of and compliance with low-sodium diet, fluid restriction or medications, and a decreased exercise tolerance.
| Left-Sided Heart Failure Pulmonary Edema and Congestion |
Right-Sided Heart Failure Cor Pulmonale and Systemic Congestion |
Biventricular Failure Pulmonary and Systemic Congestion |
| Anxiety, air hunger, tachypnea, nocturnal dyspnea, dyspnea on exertion (DOE), orthopnea, moist cough with frothy sputum, tachycardia, diaphoresis, cyanosis or pallor, insomnia, palpitations, weakness, fatigue, anorexia, and changes in mentation | Fluid retention, peripheral edema, weight gain, decreased urinary output, abdominal tenderness, nausea, vomiting, constipation, and anorexia. Because the edema of heart failure is dependent, patients on bed rest may have edema of the feet, ankles, legs, hands, and/or sacrum. | All signs of both right- and left-sided heart failure, as stated, along with possible signs of cardiogenic shock in acutely ill patients: peripheral cyanosis, fatigue, decreased tissue perfusion, decrease in metabolism, and low urinary output |
| Physical Assessment | ||
| Decreased BP, orthostasis (drop in BP with sitting or standing), tachycardia, dysrhythmias, tachypnea, crackles or bibasilar (or dependent) rales, S3, or summation gallop | Hepatomegaly, splenomegaly, dependent pitting edema, jugular venous distention, positive hepatojugular reflex, and ascites | Hypotension, tachycardia, tachypnea, pulmonary edema, dependent pitting edema, hepatosplenomegaly, distended neck veins, pallor, and cyanosis |
| Monitoring | ||
| Decreased CO/CI, SpO2 and SVO2; elevated PAP, PAWP, SVR; dysrhythmias | Dysrhythmias, elevated RAP and CVP, precipitous drop in SVO2 with minimal activity, and possibly decreased CO/CI, caused by failure of right ventricle to pump adequate blood through the pulmonary vasculature to maintain adequate left ventricular filling volumes for normal cardiac output | Elevated PAP, PAWP, SVR, pulmonary vascular resistance (PVR), RAP, and CVP, decreased CO/CI, dysrhythmias, and decreasing SpO2 and SVO2, despite increasing administered oxygen |
Diagnostic Tests for Acute Heart Failure
| Test | Purpose | Abnormal Findings |
|---|---|---|
| Noninvasive Cardiology | ||
| Electrocardiogram 12-, 15-, or18-lead ECG |
Assess for ischemic heart disease and acute or older myocardial infarction (MI); may reveal atrial and/or ventricular hypertrophy, dysrhythmias such as atrial fibrillation, which may precipitate heart failure by decreasing cardiac output, and dysrhythmias associated with electrolyte imbalance. | Presence of ST-segment depression or T wave inversion (myocardial ischemia), or pathologic Q waves (resolved MI) in 2 contiguous or related leads Contiguous leads indicative of location of ischemia or old MI: V1 and V2: Intraventricular septum V3 and V4: Anterior wall of left ventricle V5 and V6: Lateral wall of left ventricle V7–V9: Posterior wall of left ventricle II, III, AVF: Inferior wall of left ventricle V1, V1R–-V6R: Right ventricle |
| Blood Studies | ||
| Digitalis levels | Digitalis levels are often difficult to manage in heart failure patients, so levels should be done daily if the dosage is being altered. | Chronic heart failure predisposes the patient to digitalis toxicity because of the low cardiac output state, which also causes decreased renal excretion of the drug. |
| Complete blood count (CBC) Hemoglobin (Hgb) Hematocrit (Hct) RBC count (RBCs) WBC count (WBCs) |
Assess for anemia, inflammation, and infection; assists with differential diagnosis of chest discomfort and fluid balance. | May reveal decreased Hgb and Hct levels in the presence of anemia or dilution. |
| Electrolytes Potassium (K+) Magnesium (Mg2+) Calcium (Ca2+) Sodium (Na+) |
Assess for possible causes of dysrhythmias and/or heart failure. | Abnormal levels of K+, Mg2+, or Ca2+ may cause dysrhythmias; elevation of Na+ may indicate dehydration (blood is more coagulable); may reveal hyponatremia (dilutional); and may reveal hypokalemia, which can result from use of diuretics, or hyperkalemia, if glomerular filtration is decreased. Hyperkalemia can also be a side effect of angiotensin-converting enzyme inhibitors (ACEIs) and potassium-sparing diuretics. |
| Coagulation profile Prothrombin time (PT) with international normalized ratio (INR) Partial thromboplastin time (PTT) Fibrinogen D-dimer |
Assess for efficacy of anticoagulation in heart failure patients receiving warfarin therapy; also helps to evaluate for the presence of cardiogenic shock or hypoperfusion. | Decreased PT with low INR promotes clotting and reflects inadequate anticoagulation; elevation promotes bleeding; elevated fibrinogen and D-dimer reflects abnormal clotting is present. |
| B-type natriuretic peptide (BNP) | BNP, a hormone secreted by the ventricles, can be useful in distinguishing dyspnea due to heart failure from dyspnea due to pulmonary causes and in monitoring response to therapy. | Levels >100 pg/ml support the diagnosis of heart failure. However, though the BNP level decreases with effective therapy, it may remain chronically >100, even when the patient is no longer symptomatic. |
| Arterial blood gas (ABG) analysis | Assesses for changes in pH and problems with oxygenation | May reveal hypoxemia caused by the decreased oxygen available from fluid-filled alveoli. Decreased pH may be present reflecting hypoperfusion at the cellular level resulting in lactic acidosis. Lactate level may be done in addition to the ABG to assess if shock is ensuing. If the lactate level is more than 4, the patient may be in cardiogenic shock. |
| Hepatic enzymes and serum bilirubin levels | Serum glutamate oxaloacetate transaminase/aspartate aminotransferase (SGOT/AST), serum glutamate pyruvate transaminase/alanine aminotransferase (SGPT/ALT), and serum bilirubin levels may be elevated because of hepatic venous congestion. | Elevation reflects vascular congestion resulting from heart failure that has caused decreased forward blood flow from the liver to the heart. The liver becomes engorged with blood, which results in increased hepatic enzymes and bilirubin. |
| Blood urea nitrogen (BUN) and creatinine levels | Rising BUN and creatinine indicate undesirable renal response to diuretic therapy. | Elevation places patients at higher risk for renal failure secondary to heart disease. |
| Radiology | ||
| Chest radiograph (CXR) | Assesses size of heart, thoracic cage (for fractures), thoracic aorta (for aneurysm) and lungs (pneumonia, pneumothorax); assists with differential diagnosis of chest discomfort and activity intolerance | May reveal pulmonary edema, increased interstitial density, infiltrates, engorged pulmonary vasculature, and cardiomegaly Note: Portable CXR should be done with patient centered on the plate and with head of bed elevated whenever possible. |
| Cardiac magnetic resonance imaging (MRI) | Assesses ventricular size, morphology, function, status of cardiac valves, and circulation | Enlarged heart, remodeled heart, incompetent of stenotic heart valves, narrowed or occluded coronary arteries, which may be the cause of heart failure. |
| Cardiac computed tomography (CT scan) | Assesses ventricular size, morphology, function, status of cardiac valves, and circulation | Enlarged heart, remodeled heart, incompetent of stenotic heart valves, narrowed or occluded coronary arteries; technology is improving in accuracy; may eventually reduce the need for cardiac catheterization. |
| Cardiac ultrasound echocardiography (echo) | Assess for mechanical and structural abnormalities related to effective pumping of blood from both sides of the heart. | May reveal a reduced ejection fraction (ejection fraction <40%), ventricular wall motion disorders, valvular dysfunction, cardiac chamber enlargement, pulmonary hypertension, or other cardiac dysfunction |
| Transesophageal echo | Assess for mechanical and structural abnormalities related to effective pumping of blood from both sides of the heart using a transducer attached to an endoscope. | Same as for echo but can provide enhanced views, particularly of the posterior wall of the heart |
| Cardiac positron emission tomography (PET scan) | Isotopes are used to assess if viable cardiac tissue is present. | Viable tissue has increased uptake of the glucose tracer and decreased uptake of the blood flow tracer (ammonia). |
| Invasive Cardiology | ||
| Coronary angiography/cardiac catheterization | Assesses for presence and extent of CAD, left ventricular function, and valvular disease using a radiopaque catheter inserted through a peripheral vessel and advanced into the heart and coronary arteries | Treatable coronary artery blockages are a major cause of new-onset HF. Low ejection fraction indicates heart failure, stenotic or incompetent heart valves can decrease CO, narrowed or occluded coronary arteries cause chest pain, abnormal pressures in the main coronary arteries indicate impaired circulation, elevated pressures inside the chambers of the heart indicate heart failure, abnormal ventricular wall motion decreases CO, and elevated pulmonary artery pressures indicate heart failure. |
Collaborative management
Care priorities
1. Treat the underlying cause and precipitating factors.
• Diseases/conditions causing left-sided HF: Atherosclerotic heart disease, acute MI (AMI), dysrhythmias, cardiomyopathy, increased circulating volume, systemic hypertension, aortic stenosis, aortic regurgitation, mitral regurgitation, coarctation of the aorta, atrial septal defect, ventricular septal defect, cardiac tamponade, and constrictive pericarditis
• Diseases/conditions causing right-sided HF: Left-sided HF, pulmonary hypertension, atherosclerotic heart disease, AMI, dysrhythmias, pulmonary embolism, fluid overload or excess sodium intake, COPD, mitral stenosis, pulmonary stenosis, and myocardial contusion
• Diseases/conditions causing biventricular failure: Any combination of the diseases that cause either right- or left-sided HF
2. Provide oxygen therapy and support ventilation.
Supplemental oxygen is required to optimize the patient’s oxygen saturation.
Pulse oximetry is done in combination with respiratory assessment, as use of pulse oximetry alone is an inaccurate reflection of efficacy of oxygenation at the cellular level. If patient is tachypneic with increased work of breathing, noninvasive positive pressure ventilation (NiPPV, NPPV, BiPAP) may be used to reduce the work of breathing, and thus relieve additional stress associated with HF (see Acute Respiratory Failure, p. 383, for additional information regarding NiPPV, mechanical ventilation, and oxygen therapy).
• Diuretics: Reduce blood volume and decrease preload. Should be used in conjunction with an ACEI or ARB. A loop diuretic is generally used initially, while a thiazide diuretic is added for patients refractory to the loop diuretic (diuretic resistance or possibly, cardiorenal syndrome) (Table 5-1). Diuretics effectively manage respiratory distress but have not been shown to improve survival. Diuretics may cause azotemia, hypokalemia, metabolic alkalosis, and elevation of neurohormone (e.g., BNP) levels.
• Morphine: Induce vasodilation and decrease venous return, preload, sympathetic tone, anxiety, myocardial oxygen consumption, and pain.
• Inodilators (milrinone and inamrinone): Phosphodiesterase-inhibiting drugs increase contractility of the heart and lower SVR through vasodilation. This allows the failing heart to pump against less pressure (reduced afterload), resulting in increased CO. Milrinone is used for hypotensive patients with low-CO HF and pulmonary hypertension. It is a more potent pulmonary vasodilator than dobutamine. Milrinone is superior to dobutamine for patients on chronic oral beta blocker therapy who develop acute hypotensive HF.
• 
Inotropic agents: Administer digitalis to slow HR, giving the ventricles more time to fill, and to strengthen contractions; administer dopamine or dobutamine to support BP and enhance contractility (see Appendix 6). Digoxin is excreted by the kidneys, so the dose is reduced for those with renal failure. Digoxin may be prescribed for patients with LVSD who remain symptomatic on standard therapy, especially if they develop atrial fibrillation. Dobutamine enhances contractility by directly stimulating cardiac beta1 receptors. IV dobutamine infusions are sometimes used for patients with acute hypotensive HF or shock. The dose of dobutamine should always be titrated to the lowest dose that maintains hemodynamic stability, to minimize adverse events. As with many inotropes, long-term infusions of dobutamine may increase mortality due to lethal dysrhythmias. Chronic dobutamine infusions should be reserved as part of palliative symptom relief and for those who have an implantable cardioverter-defibrillator (ICD) while awaiting heart transplantation. Intermittent outpatient infusions of dobutamine are no longer recommended for routine management of HF. Dopamine and dobutamine are both associated with tachycardia, which can reduce ventricular filling time.
• Aldosterone antagonists: Spironolactone and eplerenone have been approved for patients with HF. Aldosterone inhibition reduces sodium and water retention, endothelial dysfunction, and myocardial fibrosis but may cause hyperkalemia. Serum potassium levels must be closely monitored. These drugs should not be used in patients with a creatinine level higher than 2.5 mg/dl. Data are inconclusive for patients with mild HF. Adding an aldosterone antagonist is reasonable for those with moderately severe to severe symptoms of HF and reduced CO who agree to have both renal function and potassium concentration closely monitored. The RALES trial reported a 30% reduction in mortality and hospitalizations when spironolactone was added to standard therapy for patients with advanced HF. The EPHESUS trial reported a 15% reduction in the risk of death and hospitalization in patients receiving eplerenone with low CO HF with an ejection fraction less than 40% after an MI.
• Vasodilators: Nitrates (oral, topical, or IV) to dilate venous or capacitance vessels, thereby reducing preload and cardiac and pulmonary congestion. Hydralazine will dilate the resistant vessels and reduce afterload, thus increasing forward flow. The combination of hydralazine and nitrate is inferior to an ACEI in improving survival but better than the ACEI in improving hemodynamics. Nitroprusside is used when oral agents, hydralazine, or nitrates are ineffective. Prior to discontinuing nitroprusside infusions, patients should be converted to oral vasodilators (e.g., ACEIs, ARBs, or hydralazine and a nitrate.) Nitroprusside is ideally used only for a short time in patients with advanced renal disease to avoid thiocyanate toxicity, an accumulation of this byproduct of the hepatic metabolism of nitroprusside. Thiocyanate is renally excreted and may not be excreted well in those with severe azotemia or kidney failure. Nitroprusside should also be avoided in patients with acute coronary syndrome because it may cause coronary steal syndrome, which shunts blood away from the ischemic myocardium to better-perfused muscle.
• Cardiac neurohormones: Infusion of BNP/nesiritide is used for patients with cardiorenal syndrome, which is renal insufficiency resulting from reduced renal perfusion due to HF. Nesiritide increases CO by inducing vasodilation without increasing HR or oxygen consumption. The drug helps to regulate vasoconstrictive and sodium-retaining effects of other neurohormones. Nesiritide is administered to patients with acutely decompensated HF as a weight-based bolus followed by continuous IV infusion. It may be initiated in the emergency department and does not require hemodynamic monitoring or frequent titration. Drug tolerance and dysrhythmias are unlikely.
• 
ACEIs (benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, perindopril, quinapril, ramipril, trandolapril): ACEIs affect the renin-angiotensin system by inhibiting the conversion of circulating angiotensin I into angiotensin II. They reduce remodeling, and both preload and afterload, to decrease the work of the ventricles while resulting in increased CO and systemic perfusion/oxygenation. Vasodilation and neurohormonal modulation with ACEIs reduce mortality and HF symptoms while improving exercise tolerance and LV ejection fraction. Emergency department visits and hospitalizations are also decreased. All patients with LVSD should be treated with an ACEI unless they have a contraindication or intolerance. ACEIs should be used in combination with beta blockers in most HF patients, particularly those with a prior MI, regardless of CO or ejection fraction. These drugs help prevent HF in patients at high risk with atherosclerosis, diabetes mellitus, or hypertension with other cardiovascular risk factors. ACEI dose should be titrated to the maximum tolerated; however, 10% to 20% of patients are ACEI intolerant. The most troubling side effect from ACEIs is cough, which may prompt a change to an angiotensin II receptor blocker (ARB) or a combination of hydralazine and a nitrate.
| Type of Diuretic | Generic Name and Initial Dose | Usage Information |
| Loop | Furosemide (Lasix) 20 mg | Given PO or IV; PO dosage is doubled for the equivalent effect of IV dosing. |
| Bumetanide (Bumex) 0.5 mg | PO and IV dosing result in the same effects from the same dosage. | |
| Torsemide (Demadex) 10–20 mg | Given PO or IV. Has strongest PO effects of all loop diuretics. | |
| Ethacrynic Acid (Edecrin) 50 mg | Given IV to patients who are allergic to furosemide, or other loop diuretics | |
| Thiazide | Hydrochlorothiazide (HCTZ) 12.5 mg | Given PO mainly to manage hypertension; can easily lead to hypokalemia, hyponatremia, and dehydration |
| Metolazone (Zaroxolyn) 2.5 mg | Given PO; should be given 30 minutes before furosemide if used together; has high incidence of hypokalemia |
The majority of patients who cough on ACEIs are doing so because of HF rather than intolerance to the ACEI. Cough may disappear with increased diuresis. Development of either angioedema or acute renal failure requires that the drug be stopped immediately.• AT1 receptor antagonist (candesartan, eposartan, irbesartan, olmesartan, losartan, telmisartan): Have effects similar to ACEIs but have not proved to reduce mortality. AT1 receptor-blocking agents are used in patients who are ACEI intolerant. These drugs were not found to be superior to ACEIs in improving mortality, but they generally have fewer side effects. ARBs are recommended as second-line therapy in patients who are intolerant to ACEIs because of cough or angioedema. ARBs help to prevent HF in high-risk patients with atherosclerosis, diabetes mellitus, and hypertension. ARBs should not be substituted for ACEIs in patients with hyperkalemia or renal dysfunction, as they are associated with similar complications.
• 
Beta adrenergic blocking agents (acebutolol, atenolol, betaxolol, bisoprolol, carteolol, carvedilol, esmolol, labetalol, metoprolol, nadolol, oxprenolol, propanolol, penbutolol, sotalol, pindolol, timolol): Not all beta adrenergic blockers are approved for use in managing HF. Only three (carvedilol, metoprolol succinate [Toprol XL], and bisoprolol) have improved survival. All stable patients with current or prior symptoms of HF and reduced ejection fraction should receive a beta blocker unless contraindicated. These drugs block the effects of circulating catecholamines released during HF. Catecholamines cause peripheral vasoconstriction, increased resistance to ventricular ejection, increased HR, and increased myocardial oxygen consumption and may precipitate myocardial ischemia and ventricular dysrhythmias. Beta blockers reduce contractility, resulting in decreased myocardial oxygen consumption and demand. Historically, reduction in contractility was the main reason many physicians hesitated to prescribe beta blockers to HF patients. Diabetes mellitus, COPD, and peripheral arterial disease do not contraindicate the use of beta blockers; however, patients with severe bronchospasm and hypotension may not tolerate these drugs. The combination of ACEI, diuretics, and beta blockers administered together may cause hypotension. Spacing the drug administration times by at least 2 hours usually relieves this effect.
4. Manage acute pulmonary edema; include the following immediate interventions.
• Monitoring for signs and symptoms of acute respiratory failure
• Titrating supplemental oxygen to maintain adequate oxygenation
• Providing NiPPV for patients with increased work of breathing
• Elevating HOB as needed to promote oxygenation
• If NiPPV is unsuccessful, consider endotracheal (ET) intubation with mechanical ventilation (see Acute Respiratory Failure, p. 383).
• 
Diuretic therapy: In severely ill patients, furosemide or bumetanide may be used as continuous IV infusion to assist with constant fluid removal. Patients with renal impairment/failure may require infusions of appropriate diuretics or ultrafiltration if other efforts to remove fluid fail.
• Pharmacologic therapy, including continuous IV infusions of inotropic agents, vasodilators, beta blockers, and IV morphine. If cardiogenic shock ensues, vasopressors and intra-aortic balloon pumping (IABP) may also be necessary. If the person has evidence of renal insufficiency or failure, ACEI dosage may be reduced or the drug discontinued.
5. Initiate a low-calorie (if weight control is necessary) and low-sodium diet.
• Extra salt and water are held in the circulatory system, causing increased strain on the heart. Limiting sodium (Table 5-2) will reduce the amount of fluid retained by the body. In addition, fluids may be limited to 1500 to 2000 ml/day.
| Foods High in Sodium* | Foods Low in Sodium |
|---|---|
| Beans and frankfurters | Bread |
| Bouillon cubes | Cereal (dry or hot); read labels |
| Canned or packaged soups | Fresh fish, chicken, turkey, veal, beef, and lamb |
| Canned, smoked, or salted meats; salted fish | |
| Dill pickles | Fresh fruits and vegetables |
| Fried chicken dinners and other fast foods | Fresh or dried herbs |
| Monosodium glutamate (e.g., Accent) | Gelatin desserts |
| Olives | Oil, salt-free margarine |
| Packaged snack foods | Peanut butter |
| Pancake or waffle mix | Tabasco sauce |
| Processed cheese | Low-salt tuna packed in water |
| Seasoned salts (e.g., celery, onion, garlic) | |
| Sauerkraut | |
| Soy sauce | |
| Vegetables in brine or cans | |
| Additional suggestions | |
| Do not add table salt to foods. | Do not buy convenience foods; remember that fresh is best. |
| Season with fresh or dried herbs. | Read all labels for salt, sodium, or sodium chloride content. |
| Avoid salts or powders that contain salt. | |
* Many of these foods now are available in low-salt or salt-free versions.
6. Initiate device or electronic therapy.
• Cardiac resynchronization therapy: Consider biventricular pacing, wherein a third electrode is implanted in a left cardiac vein via the coronary sinus so that the right and left ventricles are activated simultaneously. Relief of symptoms is achieved in approximately 70% of patients because of improved ventricular contraction and reduction of mitral regurgitation. Multiple clinical trials have shown the benefit of cardiac resynchronization therapy (CRT) for those with severe symptomatic HF with a wide QRS complex.
• ICD: Approximately 50% of patients with HF die of sudden death. Implanting an ICD may improve survival in some of these patients. ICD therapy has been superior to antiarrhythmic drug therapy in preventing sudden death. Cardiac resynchronization therapy can be combined with an ICD as a single device if the patient meets the requirements for both therapies.
• LV assist devices (LVADs): Some patients with cardiogenic shock unresponsive to intra-aortic balloon counterpulsation and IV inotrope therapy may be referred for mechanical circulatory support. At present, LVADs are most often used as a bridge to cardiac transplantation in patients who are appropriate candidates. The inflow cannula of an LVAD is connected to the apex of the left ventricle. Blood is pumped by the device via the outflow cannula to the aorta. Complications include stroke, infection, coagulopathy with bleeding, multiple organ dysfunction syndrome (MODS), and prosthetic valve insufficiency. LVADs have been used as permanent implants (destination therapy), and advances in technology have allowed for more widespread implementation.
• Ventricular reconstruction surgery: Ventricular remodeling surgery, or a Dor procedure, is used to manage HF secondary to ischemic cardiomyopathy. There are several components to the procedure including coronary artery bypass grafting (CABG), mitral and tricuspid valve repair, resection of LV scar or aneurysm, reshaping the left ventricle from the remodeled spherical shape back to an elliptical shape, and epicardial LV pacing lead placement. Candidates for this procedure have CAD, severe ischemia or hibernating myocardium, LV dysfunction with akinetic or dyskinetic ventricular segments, and mitral or tricuspid regurgitation.
• Cardiac transplantation: Replacing the heart is a procedure of limited availability done on patients with little disease outside of end-stage HF with severely functional impairment despite optimal medical management. Patients are not transplant candidates if they have significant comorbidities, pulmonary hypertension, active infection, significant psychosocial issues, or history of medical noncompliance. Survival following a heart transplant is about 85% at 1 year. Survival declines by an additional 4% annually. Complications include rejection of the transplanted heart, infection, transplant-related CAD, and malignancy. Following cardiac transplantation, patients must maintain lifelong immunosuppression to prevent rejection, which places them at high risk for opportunistic infections and malignancies.
CARE PLANS FOR HEART FAILURE
related to compromised regulatory mechanism secondary to decreased cardiac output
Fluid Overload Severity; Fluid Balance; Electrolyte and Acid-Base Balance
1. Auscultate lung fields for presence of crackles and rhonchi or other adventitious sounds.
2. Monitor input and output (I&O) closely. Report positive fluid state or decrease in urine output to less than 0.5 ml/kg/hr.
3. Weigh patient daily; report increases in weight. An acute gain in weight of 1 kg can signal a 1-L gain in fluid.
4. Note changes from baseline assessment to detect worsening of HF, such as increased pedal edema, increased jugular venous distention, development of S3 heart sound or new murmur, and dysrhythmias.
5. Monitor hemodynamic status every 1 to 2 hours and on an as-needed basis. Note response to drug therapy as well as indicators of the need for more aggressive therapy, including increasing PAWP and SVR and decreasing CO.
6. Administer diuretics, positive inotropes, inodilators, beta blockers, and vasodilators as prescribed. (See Appendix 6 for more information about inotropic and vasoactive drugs.)
7. Watch for signs and symptoms of renal insufficiency.
8. Limit oral fluids as prescribed, and offer patient ice chips or frozen juice pops to decrease thirst and relieve discomfort of dry mouth.
Invasive Hemodynamic Monitoring; Medication Management; Nutrition Counseling; Surveillance; Teaching: Disease Process; Hemodialysis Therapy
Cardiac Pump Effectiveness; Circulation Status
Cardiac care: acute hemodynamic regulation
1. Monitor cardiac rhythm and rate continuously.
2. Monitor CO, CI, pulmonary and systemic vascular pressures, and other hemodynamic values at least hourly, as appropriate. Implement continuous CO and SvO2 monitoring if available.
3. Monitor neurologic status to assess for adequate cerebral perfusion.
4. Monitor renal function (BUN and creatinine) daily, as appropriate.
5. Monitor liver studies (SGOT/AST, SGPT/ALT, and/or bilirubin), as appropriate.
6. Monitor the other determinants of oxygen delivery, including level of Hgb and oxygen saturation.
7. Refrain from taking rectal temperatures, to prevent bradycardias.
8. Control tachycardia as soon as possible with beta blockers or other appropriate measures as determined by the physician and ACLS guidelines.
9. Obtain 12/15/18-lead ECG to assess new dysrhythmias or profound instability.
10. IABP may be necessary; prepare needed equipment for insertion of the balloon catheter and implementation of pumping.
11. If patient has atrial fibrillation, ensure that patient has been receiving appropriate anticoagulants or antiplatelet agents to prevent thrombus formation.
Cardiac Care: Acute; Circulatory Care: Mechanical Assist Device; Hemodynamic Regulation; Shock Management: Cardiac; Neurologic Monitoring; Medication Management; Dysrhythmia Management
Respiratory Status: Gas Exchange; Mechanical Ventilation Response: Adult
1. Monitor respiratory rate, rhythm, and character every 1 to 2 hours. Be alert to RR greater than 20 breaths/min, irregular rhythm, use of accessory muscles of respiration, or cough.
2. Auscultate breath sounds, noting presence of crackles, wheezes, and other adventitious sounds.
3. Provide supplemental oxygen as prescribed and titrate to SpO2.
4. Monitor SpO2 for decreases to less than 92%.
5. Assess ABG findings; note changes in response to oxygen supplementation or treatment of altered hemodynamics.
6. Suction patient’s secretions as needed.
7. Establish a protocol for deep breathing, coughing, and turning every 2 hours.
8. Place patient in semi-Fowler’s or high Fowler’s position to maximize chest excursion.
9. If mechanical ventilation is necessary, monitor ventilator settings, ET tube function and position, and respiratory status.
Airway Management; Anxiety Reduction; Cardiac Care: Acute; Medication Management; Oxygen Therapy; Respiratory Monitoring
Activity Tolerance; Energy Conservation
1. 
Maintain prescribed activity level, and teach patient the rationale for activity limitation.
2. Organize nursing care so that periods of activity are interspersed with extended periods of uninterrupted rest.
3. To help prevent complications of immobility, assist patient with active/passive range-of-motion (ROM) exercises, as appropriate. Encourage patient to do as much as possible within prescribed activity allowances.
4. Note patient’s physiologic response to activity, including BP, HR, RR, and heart rhythm. Signs of activity intolerance include chest pain, increasing SOB, excessive fatigue, increased dysrhythmias, palpitations, HR response greater than 120 bpm, SBP greater than 20 mm Hg from baseline or greater than 160 mm Hg, and ST-segment changes. If activity intolerance is noted, instruct patient to stop the activity and rest.
5. Administer medications as prescribed, and note their effect on patient’s activity tolerance.
6. As needed to help prevent muscle loss and wasting, refer patient to physical therapy department.
Activity Therapy; Energy Management; Teaching: Prescribed Activity/Exercise; Dysrhythmia Management; Pain Management; Medication Management
Knowledge: Cardiac Disease Management
1. Teach patient the physiologic process of HF, discussing in terms appropriate to the patient how fluid volume increases because of poor heart function.
2. Teach the patient about the adverse effects of smoking and how smoking cessation may benefit him or her. Provide information about smoking cessation classes and nicotine patches and medications prescribed to help people stop smoking, such as varenicline and bupropion.
3. Teach patient about the importance of a low-sodium diet to help reduce volume overload. Provide patient with a list of foods that are high and low in sodium. Teach patient how to read and evaluate food labels.
4. Teach patient the signs and symptoms of fluid volume excess that necessitate medical attention: irregular or slow pulse, increased SOB, orthopnea, decreased exercise tolerance, and steady weight gain (≥1 kg/day for 2 successive days).
5. Advise patient about the need to keep a journal of daily weight. Explain that an increase of ≥1 kg/day on 2 successive days of normal eating necessitates notification of physician.
6. If patient is taking digitalis, teach the technique for measuring pulse rate. Provide parameters for withholding digitalis (usually for pulse rate less than 60/min) and notifying the physician.
7. Teach patient how to manage any advanced therapy that is used, biventricular pacemaker or internal cardiac defibrillator used for CRT, ventricular assist device (VAD), or heart transplant.
8. 
Instruct patient regarding the prescribed activity progression after hospital discharge, signs of activity intolerance that signal the need for rest, and use of prophylactic nitroglycerin (NTG) to reduce congestion of the heart and lungs. General activity guidelines are as follows:
| Week | Distance Walked | Time |
|---|---|---|
| 1–2 | ¼ mi | Leisurely; twice daily |
| 2–3 | ½ mi | 15 min |
| 3–4 | 1 mi | 30 min |
| 4–5 | 1½ mi | 30 min |
| 5–6 | 2 mi | 40 min |
