Heart Failure an abnormal clinical condition involving impaired cardiac pumping/or filling resulting to diminished cardiac output and cardiac congestion
- Associated with a number of cardiovascular diseases long-s
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Heart Failure an abnormal clinical condition involving impaired cardiac pumping/or filling resulting to diminished cardiac output and cardiac congestion
- Associated with a number of cardiovascular diseases long-standing HTN, CAD, and MI
- HF is primarily a disease of older adults and approximately 1 in every 100 has HF
- African Americans have a higher incidence of HF, develop HF at an earlier age, and experience higher mortality rates related to HF than whites
- HF may be caused by any interference with the normal mechanisms regulating cardiac output (CO)
o CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR) any alteration in these factors can lead to decreased ventricular function and the resultant manifestations of HF
Risk Factors of CHF
- Primary:
o CAD
o Advancing Age
- Other:
o HTN (major contributing factor) risk of HF increases progressively with the severity of hypertension
o DM predisposes an individual to HF
o Smoking
o Obesity
o High serum cholesterol
Pathophysiology
- Pathophysiology of Ventricular Failure
o Systolic Failure most common cause of HF
Results from the inability of the heart to pump blood effectively
Caused by impaired contractile function (MI), increased afterload (HTN), cardiomyopathy, and mechanical abnormalities (valvular heart disease)
LV loses its ability to generate enough pressure to eject blood forward through the aorta over time, the LV becomes dilated,and hypertrophied
Hallmark of systolic dysfunction decreased in LV ejection fraction (the percentage of total ventricular filling volume that is ejected during each ventricular contraction)
o Diastolic Failure inability of the ventricles to relax and fill during diastole
20-40% of pts have diastolic failure with a normal EF and systolic function
Decreased filling of the ventricles will result in decreased SV and CO
Diastolic failure is characterized by high filing pressures due to stiff or noncompliant ventricles and results in venous engorgement in both the pulmonary and systemic vascular systems
Dx of diastolic failure is made based on the presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy, and a normal EF
Usually the result of LV hypertrophy from chronic hypertension (most common), aortic stenosis, or hypertrophic cardiomyopathy
o Mixed Systolic and Diastolic Failure seen in disease states such as dilated cardiomyopathy (DCM)
DCM is a condition in which poor systolic function (weakened muscle function) is further compromised by dilated LV walls that are unable to relax
Pts often have extremely poor EF (< 35%), high pulmonary pressures, and biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity)
Can be caused acutely by an MI or chronically from worsening cardiomyopathy or HTN
Body’s response is low CO to mobilize its compensatory mechanisms to maintain CO and BP
- Compensatory Mechanisms
o The patient with ventricular failure of any type may have low systemic arterial blood pressure (BP), low CO, and poor renal perfusion. Poor exercise tolerance and ventricular dysrhythmias are also common. Whether a patient arrives at this point acutely from an MI or chronically from worsening cardiomyopathy or hypertension, the body's response to this low CO is to mobilize its compensatory mechanisms to maintain CO and BP.
o HF can have an abrupt onset as with acute MI and rapid atrial fibrillation, or it can be an insidious process resulting from slow, progressive changes. The overloaded heart resorts to compensatory mechanisms to try to maintain adequate CO. The main compensatory mechanisms include (1) sympathetic nervous system activation, (2) neurohormonal responses, (3) ventricular dilation, and (4) ventricular hypertrophy.
o Sympathetic Nervous System Activation
Often the first mechanism triggered in low-CO states
Least effective compensatory mechanism
In response to an inadequate stroke volume and CO increased SNS activation resulting in the increased release of catecholamines (epinephrine and norepinephrine) increased HR and contractility and peripheral vasoconstriction
Initially this increase in HR and contractility improves CO over time these factors act in a detrimental fashion by increasing the myocardium's need for oxygen and the workload of the already failing heart the vasoconstriction causes an immediate increase in preload, which may initially increase CO increase in venous return to the heart, which is already volume overloaded, actually worsens ventricular performance
o Neurohormonal Response
Renin-Angiotensin-Aldosterone System (RAAS):
• As the CO falls decreased kidney perfusion release of renin by juxtaglomerular apparatus in the kidneys due to decreased volume which converts angiotensinogen to angiotensin I angiotensin I is then converted to angiotensin II converting enzyme made in the lungs angiotensin II causes the adrenal cortex to release aldosterone resulting in sodium and water retention and increased peripheral vasoconstriction (increases BP)
Anti-diuretic Hormone
• Low CO causes a decrease in cerebral perfusion pressure posterior pituitary secretes ADH (vasopressin) ADH increases water reabsorption in the renal tubules causing water retention and therefore increased blood volume (adding to the pre-existing volume overload)
Endothelin a potent vasoconstrictor produced by the vascular endothelial cells
• Production is stimulated by ADH, catecholamines, and angiotensin II results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy
Proinflammatory cytokines
• Released by cardiac myocytes in response to various forms of cardiac injury (MI)
• Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1) further depress cardiac function by causing cardiac hypertrophy, contractile dysfunction, and myocyte cell death
• Over time, a systemic inflammatory response is also mounted and accounts for the cardiac and skeletal muscle myopathy and fatigue that accompany advanced HF.
Activation of the SNS and the neurohormonal response lead to elevated levels of norepinephrine, angiotensin II, aldosterone, ADH, endothelin, and proinflammatory cytokines.
Together, these factors result in an increase in cardiac workload, myocardial dysfunction, and ventricular remodeling (hypertrophy of the ventricular myocytes) altered geometric shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased oxygen consumption, and impaired contractility
Although the ventricles become larger, they become less effective pumps ventricular remodeling is a risk factor for life-threatening dysrhythmias and sudden cardiac death (SCD)
o Ventricular Dilation enlargement of the chambers of the heart
Occurs when pressure in the heart chambers (usually the LV) is elevated over time
The muscle fibers of the heart stretch in response to the volume of blood in the heart at the end of diastole
The degree of stretch is directly related to the force of the contraction (systole) (this is the Frank-Starling law)
Initially, this increased contraction leads to increased CO and maintenance of arterial BP and perfusion
Dilation starts as an adaptive mechanism to cope with increasing blood volume. Eventually, this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively decreasing CO
o Ventricular Hypertrophy an increase in the muscle mass and cardiac wall thickness in response to overwork and strain
Generally follows persistent or chronic dilation and thus further increases the contractile power of the muscle fibers increase in CO and maintenance of tissue perfusion
Hypertrophic heart muscle has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation (tissue becomes more easily ischemic), and is prone to ventricular dysrhythmias
Types of CHF
• HF is usually manifested by biventricular failure, although one ventricle may precede the other in dysfunction
• Normally the pumping actions of the left and right sides of the heart are synchronized, producing a continuous flow of blood
• However, as a result of pathologic conditions, one side may fail while the other side continues to function normally for a period of time
• Because of the prolonged strain, both sides of the heart will eventually fail, resulting in biventricular failure
- Left-Sided Heart Failure most common form of HF
o Results from LV dysfunction, which prevents normal blood flow and causes blood to back up into the left atrium and into the pulmonary veins
o Increased pulmonary pressure causes fluid extravasation from the pulmonary capillary bed into the interstitium and then alveoli, which is manifested as pulmonary congestion and edema
- Right-Sided Heart Failure
o Causes a backup of blood into the RA and venous circulation results in JVD, hepatomegaly, splenomegaly, vascular congestion of the GI tract, and peripheral edema
o Primary cause of right-sided failure is left-sided failure; left-sided failure results in pulmonary congestion and increased pressure in the blood vessels of the lung (pulmonary HTN) eventually, chronic pulmonary HTN (increased RV afterload) results in right-sided hypertrophy and failure
o Cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease) can also cause right-sided failure
o RV infarction may also cause isolated RV failure
Clinical Manifestations of CHF
- Acute CHF
o Pulmonary edema acute, life-threatening situation in which lung alveoli become filled with serosanguineous fluid (most commonly caused by acute LV failure secondary to CAD)
o Increased RR and Decreased PaO2 increase in the pulmonary venous pressure caused by decreased efficiency of the LV engorgement of the pulmonary vascular system lungs become less compliant, and there is increased resistance in the small airways
Lymphatic system also increases its flow to help maintain a constant volume of the pulmonary extravascular fluid.
This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (PaO2)
o Severe Tachypnea (interstitial edema) if pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the intertsitial space than the lymphatics can drain interstitial edema tachypnea develops and the patient becomes symptomatic (short of breath out of proportion to activity level)
o Alveolar Edema occurs if the pulmonary venous pressure increases further causing the tight alveoli lining cells to be disrupted and allows a fluid containing RBCs to move in to the alveoli (alveolar edema)
o Increased PaCO2 (Acidemia) as the disruption become worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid accommodated by worsening ABG values
o Agitation
o Cyanosis, pale, clammy, and cold skin skin is clammy and cold from vasoconstriction caused by stimulation of the SNS
o Severe dyspnea, orthopnea has severe dyspnea, as evidenced by the use of accessory muscles of respiration, a respiratory rate greater than 30 breaths per minute, and orthopnea
o Wheezing, coughing
o Frothy, blood tinged sputum
o Crackles, wheezes , rhonchi revealed by auscultation
- Chronic HF characterized as a progressive worsening of ventricular function and chronic neurohormonal activation that result in ventricular remodeling involves changes in the size, shape, and mechanical performance of the ventricle
The clinical manifestations of chronic HF depend on the patient's age, the underlying type and extent of heart disease, and which ventricle is failing to pump effectively
Acronym FACES (fatigue, limitation of activities, chest congestion/cough, edema, and shortness of breath) to help educate patients in identifying HF symptoms
o Fatigue (one of the earliest symptoms of chronic HF ) caused by a decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia
o Dyspnea caused by increased pulmonary pressures secondary to interstitial and alveolar edema
Can occur with mild exertion or at rest
Orthopnea is shortness of breath that occurs when the patient is in a recumbent position
o Paroxysmal Nocturnal Dyspnea (PND) occurs when the patient is asleep; caused by the reabsorption of fluid from dependent body areas when the patient is recumbent
The patient awakens in a panic, has feelings of suffocation, and has a strong desire to seek relief by sitting up
o Dry Cough there are increased pulmonary pressures and fluid accumulation in the lung tissues, the patient may have a persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants
A dry, hacking cough may be the first clinical symptom of HF
o Tachycardia diminished CO increases SNS stimulation, which increases HR
Response may be blocked or reduced in patients taking β-blocker medications.
o Edema fluid overload
May occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion)
The development of dependent edema or a sudden weight gain of more than 3 lb (1.4 kg) in 2 days is often indicative of exacerbated HF
It is important to note that not all lower extremity edema is a result of HF
• Hypoproteinemia, immobility, venous insufficiency, and certain medications can cause peripheral edema
o Nocturia when the person lies down at night, fluid movement from the interstitial spaces back into the circulatory system is enhanced causing renal blood flow and dieresis
The patient may complain of having to void 6 or 7 times during the night.
o Skin Changes tissue capillary oxygen extraction is increased causing dusky, cool, and diaphoretic skin
o Behavioral Changes cerebral circulation is impaired secondary to decreased CO restlessness, confusion, and decreased attention span or memory are often observed (may also be secondary to poor gas exchange and worsening HF)
o Chest Pain due to decreased coronary perfusion from decreased CO and increased myocardial work
Complications of CHF
- Pleural Effusion results from increasing pressure in the pleural capillaries a transudation of fluid occurs from these capillaries into the pleural space
- Arrhythmias chronic HF causes enlargement of the chambers of the heart enlargement (stretching of the atrial and ventricular tissues) may cause an alteration in the normal electrical pathway, especially in the atria
- Left Ventricular Thrombus enlarged LV and decreased CO combine to increase the chance of thrombus formation in the LV
o Once a thrombus has formed, it may also decrease left ventricular contractility, decrease CO, and further worsen the patient's perfusion
o The development of emboli from the thrombus also places the patient at risk for stroke
- Hepatomegaly especially associated with RV failure; the liver lobules become congested with venous blood the hepatic congestion leads to impaired liver function eventually leading to death of liver cells, fibrosis, and cirrhosis
- Renal Failure decreased CO that accompanies chronic HF results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure
Classification of Heart Failure
- Functional Classification of CHF based on physical activity related to occurrence of symptoms such as: fatigue, dyspnea, palpitation, anginal pain
Diagnostic Studies diagnosing HF is often difficult since neither patient signs nor symptoms are highly specific, and both may mimic many other medical conditions (e.g., anemia, lung disease)
TABLE 35-6 COLLABORATIVE CARE: Acute Decompensated Heart Failure and Pulmonary Edema
- EF can be measured using echocardiography and/or nuclear imaging studies
- EF can be used to differentiate between systolic and diastolic HF important for early treatment
Collaborative Therapy
- Treat the underlying cause
- High Fowlers Position place the patient with HF in a high Fowler's position with the feet horizontal in the bed or dangling at the bedside position helps decrease venous return because of the pooling of blood in the extremities also increases the thoracic capacity, allowing for improved ventilation
- O2 Therapy / mask or nasal cannula supplemental oxygen helps increase the percentage of oxygen in inspired air
- Cardiac Monitoring / Oximetry electrocardiogram (ECG) and oxygen saturation are monitored on a continuous basis; vital signs and urinary output are assessed at least every hour
- Drug Therapy
o Morphine IV decrease preload and afterload and is frequently used in the treatment of acute HF and pulmonary edema
It dilates both the pulmonary and systemic blood vessels, a goal in decreasing pulmonary pressures and improving the gas exchange
IV morphine decreases oxygen demands, which may be increased as a result of anxiety and subsequent increased musculoskeletal and respiratory activity
When morphine is used, the patient often experiences relief from dyspnea and, consequently, the anxiety that is often associated with dyspnea
Although morphine-related respiratory depression is rare, monitor the patient's respiratory rate
o Diuretic Therapy decreasing venous return (preload) reduces the amount of volume returned to the LV during diastole decreasing intravascular volume with the use of diuretics reduces venous return Loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) can be administered by intravenous (IV) push and act rapidly in the kidneys by decreasing venous return to the LV and thereby reducing preload, the overfilled LV may contract more efficiently and improve CO this increases left ventricular function, decreases pulmonary vascular pressures, and improves gas exchange
o Digitalis positive inotropic agent that increases myocardial contractility and increases myocardial oxygen consumption improves left ventricular function
o Nitroglycerin vasodilator that reduces circulating volume by decreasing preload and also increases coronary artery circulation by dilating the coronary arteries reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply
When titrating IV nitroglycerin, BP is monitored frequently (every 5 to 10 minutes) to avoid symptomatic hypotension
- Daily Weight instructing patients to weigh themselves daily is important for monitoring fluid retention, as well as weight reduction
o Teach patients to weigh themselves at the same time each day, using the same scale and preferably before breakfast, while wearing the same type of clothing this helps ensure valid comparisons from day to day and helps identify early signs of fluid retention
- Sodium Restricted Diet edema associated with chronic HF is often treated by dietary restriction of sodium teach the patient what foods are low and high in sodium and ways to enhance food flavors without the use of salt (e.g., substituting lemon juice and various spices)
• The degree of sodium restriction depends on the severity of the HF and the effectiveness of diuretic therapy diets that are severely restricted in sodium are rarely prescribed because they are unpalatable and patient compliance is poor
- Cardioversion
- Endotracheal Intubation / Mechanical Ventilation
Nursing Therapeutics/ Plan of Care
Acute CHF
- Goal improve LV function by decreasing intravascular volume, decreasing venous return (preload), decreasing afterload, improving gas exchange and oxygenation, decreasing CO2, and reducing anxiety
o Use of diuretics
o Position patient in high flower position
o IV nitroglycerin
o IV nitroprusside drug of choice for pt. with pulmonary edema
o A potent IV vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion
o Complications of IV sodium nitroprusside include (1) hypotension and (2) thiocyanate toxicity, which can develop after 48 hours of use
o Patients receiving sodium nitroprusside must have their BP monitored frequently (every 5 to 10 minutes) while the drug is titrated
o Morphine administration
o O2 administration
o Digitalis administration
o Decrease Intravascular Volume reduces venous return to the LV, reducing preload, allowing the overfilled LV to contract more efficiently and improve CO increases LV function, decreases pulmonary vascular pressures, and improves gas exchange
Use of diuretics loop
o Decrease Venous Return decreasing preload reduces the amount of volume returned to the LV during diastole use high-fowler’s with feet horizontal or hanging at bedside (causes pooling and decreases venous return
IV nitroglycerin (vasodilator used to reduce circulating volume by decreasing preload and lso increasing coronary artery circulation by dilating the coronary arteries)
o Decrease Afterload (the amount of work the LV has to produce to eject blood into the systemic circulation) if afterload is reduced, the CO of the LV improves and thereby decreases pulmonary congestion
IV sodium nitroprusside (Nipride) is a potent vasodilator that reduces preload and afterload drug of choice for patient with pulmonary edema because of its rapid onset of action and potent effects on the vascular system by reducing both preload and afterload, myocardial contraction improves, increasing CO and reducing pulmonary congestion.
Morphine sulfate dilates both the pulmonary and systemic blood vessels reducing preload and afterload
o Improve Gas Exchange and Oxygenation morphine, oxygen
o Improve Cardiac Function digitalis
o Reduce Anxiety morphine
Chronic CHF
- Goal treat underlying cause, maximize CO, provide treatment to alleviate symptoms
o Administer O2 in a person with HF, oxygen saturation of the blood is reduced because the blood is not adequately oxygenated in the lungs
Administration of oxygen improves saturation and assists greatly in meeting tissue oxygen needs
Thus oxygen therapy helps relieve dyspnea and fatigue
o Monitor O2 by ABG or pulse ox optimally either pulse oximetry or arterial blood gases (ABGs) are used to monitor the effectiveness of oxygen therapy
- Allow physical and emotional rest allows the patient to conserve energy and decreases the need for additional oxygen
o The degree of rest recommended depends on the severity of HF
o A patient with severe HF may be on bed rest with limited activity
o A patient with mild to moderate HF can be ambulatory with restriction of strenuous activity
o The patient should be instructed to participate in prescribed activities with adequate recovery periods
o A structured exercise program, such as cardiac rehabilitation, should be offered to all patients with chronic HF
- Drug Therapy
o ACE Inhibitor ACE inhibitors are the primary drug of choice for blocking the RAAS system in HF patients with systolic dysfunction.14 Examples of ACE inhibitors are listed in Table 35-8. Other examples of ACE inhibitors are discussed in Chapter 33 and listed in Table 33-8. The conversion of angiotensin I to the potent vasoconstrictor angiotensin II requires the presence of ACE (see Chapter 45, Fig. 45-4). ACE inhibitors act by blocking this enzyme, resulting in decreased levels of angiotensin II. As a result, plasma aldosterone levels are also reduced. Thus ACE inhibitors are considered neurohormonal blocking agents. As neurohormonal blockers, ACE inhibitors also decrease the development of ventricular remodeling by inhibiting ventricular hypertrophy. Because CO is dependent on afterload in chronic HF, the reduction in SVR seen with the use of ACE inhibitors produces a significant increase in CO. Though the use of ACE inhibitors may decrease BP, tissue perfusion is maintained or increased as a result of improved CO and diuresis is enhanced by the suppression of aldosterone. Major side effects of ACE inhibitors include symptomatic hypotension, intractable cough, hyperkalemia, angioedema (allergic reaction involving edema of the face and airways), and renal insufficiency (when ACE inhibitors are used in high doses). Aging and baseline renal insufficiency slow the metabolism of ACE inhibitors and may therefore lead to increased serum drug levels. Carefully monitor patients taking ACE inhibitors for potential adverse effects. For example, a cough is frequently attributed to ACE inhibitors when, in fact, it is a common symptom of an exacerbation of HF. It is imperative that the exact cause of cough and/or other intolerances be verified before discontinuing ACE inhibitor therapy.
o Diuretic Therapy Diuretics are used to mobilize edematous fluid, reduce pulmonary venous pressure, and reduce preload (see Table 33-8). If excess extracellular fluid is excreted, blood volume returning to the heart can be reduced and cardiac function improved. Diuretics act on the kidney by promoting excretion of sodium and water. Many varieties of diuretics are available. Thiazide diuretics (e.g., hydrochlorothiazide [HydroDIURIL]) are often the first choice in chronic HF because of their convenience, safety, low cost, and effectiveness. They are particularly useful in treating edema secondary to HF and in controlling hypertension. The thiazides inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. Loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) are potent diuretics. These drugs act on the ascending loop of Henle to promote sodium, chloride, and water excretion. Problems in using loop diuretics include reduction in serum potassium levels, ototoxicity, and possible allergic reaction in the patient who is sensitive to sulfa-type drugs.
o Inotropic drugs Digitalis preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action). They also decrease the conduction speed within the myocardium and slow the HR (chronotropic action). These actions allow for more complete emptying of the ventricles, thus diminishing the volume remaining in the ventricles during diastole. CO increases because of an increased stroke volume from improved contractility. Because digitalis requires a loading dose and time to work, it is not recommended for the initial treatment of acute HF.
o Vasodilators Nitrates cause vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates can be used in combination with hydralazine (Apresoline) for chronic HF management in patients who cannot tolerate ACE inhibitors or ARBs. Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries. One specific deterrent to the use of nitrates in HF is nitrate tolerance. In addition, men with HF may experience erectile dysfunction and as a result take an erectile agent (e.g., sildenafil [Viagra]). Erectile agents are contraindicated in patients taking nitrates as together they could precipitate symptomatic hypotension.
o Beta Blockers β-Adrenergic blockers directly block the negative effects of the SNS on the failing heart, such as increased HR. Because β-blockers can reduce myocardial contractility, care must be taken to start gradually, increasing the dosage slowly every 2 weeks as tolerated by the patient. Major adverse effects include edema, worsening of HF, hypotension, fatigue, and bradycardia.
- Dietary Therapy
o Sodium restriction (2 gm sodium diet) avoid/limit milk, cheese, bread, cereal, canned foods
o Diet education & Weight management diet education and weight management are critical to the patient's control of chronic HF diet and weight management recommendations must be individualized and culturally sensitive if the necessary changes are to be made
o Fluid restriction ( if there is renal insuffieciency) Fluid restrictions are not commonly prescribed for the patient with mild to moderate HF. Diuretic therapy, ACE inhibitors, and digitalis preparations act as effective diuretics to promote fluid excretion. However, in moderate to severe HF and renal insufficiency, fluid restrictions are usually implemented. Helping patients deal with thirst as a side effect of the medications is important. To deal with the thirst, suggest ice chips, gum, hard candy, or ice pops.
Ambulatory Home Care
o Teach pt the physiologic changes of CHF
o Encourage to take medications regularly
o Teach pt to take his/her own pulse to know under what circumstances drugs should be withheld and a health care provider consulted
o Alert on sign and symptoms of hypo/hyperkalemia if diuretics that deplete or spare potassium are being used
o Discuss energy saving and energy efficient behaviors
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