Pharmacologic management of left ventricular systolic dysfunction (LVSD) is standard and evidence-based, prescribed based on the patient's stage of heart failure (HF). Let's take a closer look.
Angiotensin-converting enzyme (ACE) inhibitors are the gold standard for treating HF. This class of medication lessens neurohormonal responses and prevents the conversion of angiotensin I to angiotensin II. ACE inhibitors also offload fluid and pressure from the heart and lungs and provide cellular effects that improve heart function over time.
In cases where ACE inhibitors can't be used due to adverse reactions such as a persistent, dry cough (from bradykinin release or angioedema), an angiotensin receptor blocker (ARB), such as candesartan and valsartan, may be used. ARBs block receptors that usually bind with angiotensin II, preventing vasoconstriction and causing balanced vasodilation. Several members of this class of medication have been found effective for treating HF.
Both ACE inhibitors and ARBs have potential adverse reactions. The most notable to watch for include hypotension, hyperkalemia, and pre-renal azotemia. If creatinine rises more than 50% or goes over 3 mg/dL upon initiation or up-titration, the ARB should be discontinued. A note should be placed in the patient's medical record that the agent caused this effect so it isn't retrialed. See Nursing considerations for ACE inhibitors for more important interventions when administering this class of medication.
When an ACE inhibitor or an ARB can't be used, a combination of hydralazine and isosorbide dinitrate may be prescribed to provide the same balanced vasodilatory effect. Hydralazine prevents the tolerance effects of the nitrate, and nitrate enhances the effectiveness of hydralazine. Additionally, a combination of hydralazine and nitrate can augment the protective effects of ACE inhibitors or ARBs and beta-blockers.
Beta-blockers are a powerful class of medication used in the treatment of LVSD. Agents approved for LVSD include carvedilol, metoprolol succinate (long acting), and bisoprolol. Several of these agents have been demonstrated to improve heart function in the long term. Beta-blockers block epinephrine and norepinephrine receptors; blocking these chemicals lowers heart rate, BP, and myocardial oxygen consumption that would otherwise worsen HF. If the patient is euvolemic, a beta-blocker should be initiated and titrated up over time to the target dosage. In the short term (over several weeks) additional diuretic may be needed to combat fluid retention caused by beta-blocker therapy; in the long term, the benefit outweighs the risk. Beta-blockers should be started when patients are stable to diminish progression of the disease, not as rescue therapy when patients are decompensating.
Another class of medication useful in the treatment of LVSD is the aldosterone antagonists, such as spironolactone and eplerenone. Although these agents are potassium-sparing diuretics, they're used to prevent the build up of sodium in the body that leads to fluid retention. These medications compete for aldosterone-dependent sodium-potassium exchange sites in the distal tubule cells, ridding the body of sodium and water while sparing potassium. Aldosterone antagonists are useful when chronic HF causes shortness of breath with minimal exertion or at rest. Be watchful for hyperkalemia and an elevated creatinine level.
A loop diuretic is the diuretic of choice for treating a fluid overloaded HF patient, regardless of type. Furosemide, bumetanide, and torsemide are examples of loop diuretics generally administered in response to fluid overload. High doses can lead to diminished hearing or hearing loss and kidney dysfunction, electrolyte imbalances, volume depletion, and ventricular arrhythmias. Observe for these adverse reactions and notify the healthcare provider if evident. See Administering and monitoring diuretic therapy for more nursing considerations.
When a patient presents with worsening fluid overload, an increased dose of diuretic may be prescribed. But if the overload is moderate to severe, the healthcare provider may order hospital observation or admission for I.V. diuretic therapy and cardiac monitoring. If diuretic response isn't sufficient, the dose can be titrated up or another class of diuretic may be given in conjunction with the loop diuretic to strengthen the effectiveness of diuresis. For decompensated HF, the next choice of diuretic is often a thiazide-like diuretic such as metolazone. A thiazide-like drug should be administered about a half hour before the loop diuretic to achieve the best possible synergy and most potent diuresis.
The goal of therapy for HF is to cut back on the diuretic when possible and to optimize the agents known to quell the neurohormonal stimulation that triggers HF exacerbation.
Digoxin is the only oral positive inotrope available. It helps to improve the pumping action of the heart while reducing myocardial oxygen demand. It's used in HF patients with shortness of breath on mild exertion or at rest (New York Heart Association Classes III and IV). Studies show digoxin is useful in improving symptoms and preventing rehospitalization. Unfortunately, there's a very narrow therapeutic window with this medication and too much can build up in the bloodstream quickly, especially when kidney dysfunction is present. Watch for bradycardia, nausea, vomiting, or increasing fatigue. See Digoxin use and toxicity in HF for more nursing considerations.
The healthcare provider may ask you to draw a digoxin level from time to time to assess for a therapeutic range. In this case, don't administer the dose on the day blood is to be drawn until after the lab specimen result is available to prevent a falsely high serum level.
Beyond the standard
When HF doesn't respond to standard therapy, more aggressive measures need to be instituted. There are several pharmacologic agents that can be administered I.V. Nesiritide, a natriuretic and balanced vasodilator that acts to offload fluid and pressure from the heart and lungs while diuresing/natriuresing the patient, may be useful when other agents have failed. Hypotension is the most common adverse reaction, and the patient's kidney function should be monitored. Nesiritide requires a separate I.V. site so it doesn't interact with many preservatives found in other I.V. drugs the patient may be receiving.
Other I.V. medications that may be prescribed include milrinone and dobutamine to improve the contractility of the heart and forward blood flow in patients not responding well to other therapy. Milrinone is known as an inodilator because it's a balanced vasodilator and has a positive inotropic effect. It's used 24/7 as a bridge to transplant for some patients. Milrinone can produce thrombocytopenia. Dobutamine is a synthetic catecholamine-like epinephrine used for refractory decompensated HF and often for cardiogenic shock. Long-term use of these agents can increase mortality; in the short term, they do help improve HF symptoms. Both of these agents increase myocardial oxygen demand and arrhythmias, and they both carry the risk of ventricular arrhythmias.
Patient teaching = positive outcomes
It's important that patients have access to medications and understand that every dose of every medication must be taken. Be sure your patient understands that he needs to obtain his refills before running out of each drug. For hospitalized patients, an effective admission assessment question is whether the patient can afford his medications. If not, a case manager should be consulted to provide him with medication assistance applications and to find the most cost-effective ways to obtain medications after discharge.
HF is a chronic, progressive disease that can be controlled when patients are armed with the necessary knowledge to make positive lifestyle decisions for themselves. While medications are essential to control symptoms, it's equally important to ensure appropriate lifestyle modification to prevent frequent HF exacerbations, rehospitalization, and mortality. Patients often believe they develop HF occasionally and get better when they leave the hospital. Nurses are in the perfect position to make sure patients receive as much individualized information as possible before discharge from their care. Providing patients with this knowledge will help optimize outcomes and slow the progression of the disease.
Administering and monitoring diuretic therapy
When nursing care involves diuretic therapy for HF, the nurse needs to administer the medication and monitor the patient's response carefully, as follows:
* Administer the diuretic at a time conducive to the patient's lifestyle; for example, early in the day to avoid nocturia. A second dose can be given 6 to 8 hours after the first dose.
* Give supplementary potassium with thiazide and loop diuretics as prescribed to replace urinary potassium loss.
* Check lab results for electrolyte depletion, especially potassium, magnesium, and sodium, and for electrolyte elevation, especially potassium with potassium-sparing agents (ACE inhibitors and ARBs).
* Monitor daily weights and intake and output to assess diuretic response. Monitor serum blood urea nitrogen and creatinine. Notify the healthcare provider if renal impairment is suspected.
* Assess lung sounds, jugular vein distention, daily weight, and peripheral, abdominal, or sacral edema for improvement after diuresis.
* Monitor for adverse reactions, such as nausea and gastrointestinal distress, vomiting, diarrhea, weakness, headache, fatigue, anxiety or agitation, and cardiac dysrhythmias.
* Assess for signs of volume depletion, such as postural hypotension, dizziness, and balance problems.
* Monitor for glucose intolerance in patients with and without diabetes who are receiving thiazide diuretics.
* Monitor for potential ototoxicity in patients, especially those with renal failure, who are receiving a loop diuretic.
* Advise patients to avoid prolonged exposure to the sun because of the risk of photosensitivity.
* Monitor for elevated serum uric acid levels and the development of gout.
Digoxin use and toxicity in HF
Digoxin, a cardiac glycoside derived from digitalis, improves cardiac function as follows:
* increases the force of myocardial contraction
* slows cardiac conduction through the arterioventricular (AV) node and slows the ventricular rate in instances of supraventricular dysrhythmias
* increases cardiac output by enhancing the force of ventricular contraction
* promotes diuresis by increasing cardiac output.
The therapeutic level is usually 0.5 to 2.0 ng/mL. Blood samples are usually obtained and analyzed to determine digitalis concentration at least 6 to 10 hours after the last dose. Toxicity may occur despite normal serum levels, and recommended dosages vary considerably.
A serious complication of digoxin therapy is toxicity. Diagnosis of digoxin toxicity is based on the patient's clinical symptoms, which include the following:
* anorexia, nausea, vomiting, fatigue, depression, and malaise (early effects of digitalis toxicity)
* changes in heart rate or rhythm; onset of irregular rhythm
* ECG changes indicating sinoatrial (SA) or AV block, new onset of irregular rhythm indicating ventricular dysrhythmias, or atrial tachycardia with block, junctional tachycardia, and ventricular tachycardia.
Reversal of toxicity
Digoxin toxicity is treated by holding the medication while monitoring the patient's symptoms and serum digoxin level. If the toxicity is severe, digoxin immune FAB may be prescribed. This binds with digoxin and makes it unavailable for use. The digoxin immune FAB dosage is based on the digoxin level and the patient's weight. Serum digoxin values aren't accurate for several days after administration because they don't differentiate between bound and unbound digoxin. Because digoxin immune FAB quickly decreases the amount of available digoxin, an increase in ventricular rate due to atrial fibrillation and worsening of symptoms of HF may ensue shortly after its administration.
Nursing considerations and actions
1. Assess the patient's clinical response to digoxin therapy by evaluating relief of symptoms, such as dyspnea, orthopnea, crackles, hepatomegaly, and peripheral edema.
2. Monitor the patient for factors that increase the risk of toxicity:
* decreased potassium level (hypokalemia), which may be caused by diuretics (Hypokalemia increases the action of digoxin and predisposes patients to digoxin toxicity and dysrhythmias.)
* use of medications that enhance the effects of digoxin, including oral antibiotics and cardiac drugs that slow AV conduction and can further decrease the heart rate
* impaired renal function, particularly in patients age 65 and older. (Because digoxin is eliminated by the kidneys, renal function [serum creatinine] is monitored and doses of digoxin are lowered accordingly.)
3. Before administering digoxin, it's standard nursing practice to assess the apical heart rate. When the patient's rhythm is atrial fibrillation and the heart rate is less than 60, or the rhythm becomes regular, the nurse may withhold the medication and notify the healthcare provider because these signs indicate the development of an AV conduction block. Although withholding digoxin is a common practice, the medication doesn't need to be withheld for a heart rate of less than 60 if the patient is in sinus rhythm because digoxin doesn't affect SA node automaticity. Measuring the PR interval for a patient with cardiac monitoring is more important than the apical pulse in determining whether digoxin should be held.
4. Monitor for gastrointestinal adverse reactions: anorexia, nausea, vomiting, abdominal pain, and distention.
5. Monitor for neurologic adverse reactions: headache, malaise, nightmares, forgetfulness, social withdrawal, depression, agitation, confusion, paranoia, hallucinations, decreased visual acuity, yellow or green halo around objects (especially lights), and "snowy" vision.
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