chf case study for nursing students

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This case study involves a 76 year old female named Mary Lou Poppins, who presented to the ED accompanied by her son. She called her son after having symptoms of shortness of breath and confusion. Her past medical history includes hypertension, hyperlipidemia, coronary artery disease, and she was an everyday smoker for 30 years. She reports her home medications are lisinopril, simvastatin, and baby aspirin. Her current lifestyle includes: being a widow of six years, she lives alone, she walks her dog everyday, she drives to her knitting group three days a week, she makes dinner for her grandchildren once a week, she attempts to eat healthy but admits to consuming salty and high fat foods, and she insists on being very independent.

Mary Lou Poppins initial vitals in the emergency department includes a blood pressure of 138/70, heart rate of 108. respiratory rate of 26, temperature 98.9 degrees fahrenheit, and oxygen saturation of 84%. Her initial assessment included alert and oriented to person and place, dyspnea, inspiratory crackles in bilateral lungs, and a cough with pink frothy sputum. Her labs and diagnostics resulted in a BNP of 740 pg/ml, an echocardiogram showing an ejection fraction of 35%, an ECG that read sinus tachycardia, and a chest x-ray that confirmed pulmonary edema.

The Emergency Department physician diagnosed Mary Lou Poppins with left-sided heart failure. The orders included: supplemental oxygen titrated to keep saturation >93%, furosemide IV, enoxaparin subq, and metoprolol PO. Nursing Interventions included: monitoring oxygen saturation, adjusting oxygen route and dosage according to orders, assessing mentation and confusion, obtaining IV access, reassessing vitals, administering medications, and keeping the head of the bed elevated greater than 45 degrees. She was admitted to the telemetry unit for further stabilization, fluid balance monitoring, and oxygen monitoring.

On day one of hospital admission, Mary Lou Poppins required 4L of oxygen via nasal cannula in order to maintain the goal saturation of >93%. Upon assessment, it was determined that she was oriented to person and place. Auscultation of the lungs revealed bilateral crackles throughout, requiring collaboration with respiratory therapy once in the morning, and once in the afternoon. Physical therapy worked with the patient, but she was only able to ambulate for 100 feet. During ambulation, the patient had a decrease of oxygen saturation and dyspnea, requiring her oxygen to be increased to 6L. At the end of the day, strict intake and output monitoring showed an intake of 1200 mL of fluids, with an urinary output of 2L.

On day two of admission, Mary Lou began demonstrating signs of improvement. She only required 2 L of oxygen via nasal cannula with diminished crackles heard upon auscultation. Morning weight showed a weight loss of 1.3 lbs and the patient was oriented to person, place, and sequence of events. During physical therapy, she was able to ambulate 300 feet without required increased oxygen support. Daily fluid intake was 1400 mL with a urinary output of 1900 mL.

On the third and final day of admission, Mary Lou was AOx4 and did not require any type of oxygen support. When physical therapy arrived, the patient was able to ambulate 500 feet, which was close to her pre-hospital status. When the doctor arrived, the patient informed him that she felt so much better and felt confident going home. The doctor placed orders for discharge.

Upon discharge and throughout the patient’s hospital stay, Mary Lou Poppins was educated regarding the disease process of heart failure; symptoms to monitor for and report to her doctor; the importance of daily monitoring of weight, blood pressure, and heart rate; and the importance of adhering to a diet and exercise regime. Education was also provided regarding her medications and the importance of strictly adhering to them in order to prevent exacerbations of heart failure. Smoking cessation was also included in her plan of care. The patient received an informational packet regarding her treatment plan, symptoms to monitor for, and when to call her physician. Upon discharge, the patient was instructed to schedule a follow up appointment with her cardiologist for continued management of her care.

The patient was put in contact with a home health agency to help manage her care. The home health nurse will help to reinforce the information provided to the patient, assess the patient’s home and modify it to meet her physical limitations, and help to create a plan to meet daily dietary and exercise requirements. Regular follow-up appointments were stressed to Mary Lou Poppins in order to assess the progression of her disease. It will be important to monitor her lab values to also assess her disease progression and for any potential side effects associated with her medications. Repeat echocardiograms will be necessary to monitor her ejection fraction; if it does not improve with the treatment plan, an implanted cardiac defibrillator may be necessary to prevent cardiac death.

Open-Ended Questions

• What were the clinical manifestations that Mary Lou Poppins presented with in the ED that suggested the new onset of CHF?
• What factors most likely contributed to the onset of CHF?
• What patient education should Mary Lou Poppins receive on discharge in regards to managing her CHF?

Nursing Case Studies by and for Student Nurses Copyright © by jaimehannans is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License , except where otherwise noted.

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Heart Failure

Learn about the nursing care management of patients with heart failure.

What is Heart Failure?

Heart failure, also known as congestive heart failure, is recognized as a clinical syndrome characterized by signs and symptoms of fluid overload or of inadequate tissue perfusion .

• Heart failure is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients.
• The term heart failure indicates myocardial disease in which there is a problem with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) that may or may not cause pulmonary or systemic congestion.
• Heart failure is most often a progressive, life-long condition that is managed with lifestyle changes and medications to prevent episodes of acute decompensated heart failure.

Classification

Heart failure is classified into two types: left-sided heart failure and right-sided heart failure.

Left-Sided Heart Failure

• Left-sided heart failure or left ventricular failure have different manifestations with right-sided heart failure.
• Pulmonary congestion occurs when the left ventricle cannot effectively pump blood out of the ventricle into the aorta and the systemic circulation.
• Pulmonary venous blood volume and pressure increase, forcing fluid from the pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary interstitial edema and impaired gas exchange .

Right-Sided Heart Failure

• When the right ventricle fails, congestion in the peripheral tissues and the viscera predominates.
• The right side of the heart cannot eject blood and cannot accommodate all the blood that normally returns to it from the venous circulation.
• Increased venous pressure leads to JVD and increased capillary hydrostatic pressure throughout the venous system.

The American College of Cardiology and American Heart Association have classifications of heart failure.

• Stage A. Patients at high risk for developing left ventricular dysfunction but without structural heart disease or symptoms of heart failure.
• Stage B. Patients with left ventricular dysfunction or structural heart disease that has not developed symptoms of heart failure.
• Stage C. Patients with left ventricular dysfunction or structural heart disease with current or prior symptoms of heart failure.
• Stage D. Patients with refractory end-stage heart failure requiring specialized interventions.

Pathophysiology

Heart failure results from a variety of cardiovascular conditions, including chronic hypertension , coronary artery disease , and valvular disease.

• As HF develops, the body activates neurohormonal compensatory mechanisms.
• Systolic HF results in decreased blood volume being ejected from the ventricle.
• The sympathetic nervous system is then stimulated to release epinephrine and norepinephrine.
• Decrease in renal perfusion causes renin release, and then promotes the formation of angiotensin I .
• Angiotensin I is converted to  angiotensin II by ACE which constricts the blood vessels and stimulates aldosterone release that causes sodium and fluid retention.
• There is a reduction in the contractility of the muscle fibers of the heart as the workload increases.
• Compensation . The heart compensates for the increased workload by increasing the thickness of the heart muscle.

Just like coronary artery disease, the incidence of HF increases with age.

• More than 5 million people in the United States have HF.
• There are 550, 000 cases of HF diagnosed each year according to the American Heart Association.
• HF is most common among people older than 75 years of age .
• HF is now considered epidemic in the United States.
• HF is the most common reason for hospitalization of people older than 65 years of age.
• It is also the second most common reason for visits to the physician’s office.
• The estimated economic burden caused by HF is more than $33 billion annually in direct and indirect costs and is still expected to increase.

Heart failure can affect both women and men, although the mortality is higher among women.

• There are also racial differences; at all ages death rates are higher in African American than in non-Hispanic whites.
• Heart failure is primarily a disease of older adults, affecting 6% to 10% of those older than 65.
• It is also the leading cause of hospitalization in older people .

Systemic diseases are usually one of the most common causes of heart failure.

• Coronary artery disease . Atherosclerosis of the coronary arteries is the primary cause of HF, and coronary artery disease is found in more than 60% of the patients with HF.
• Ischemia . Ischemia deprives heart cells of oxygen and leads to acidosis from the accumulation of lactic acid.
• Cardiomyopathy . HF due to cardiomyopathy is usually chronic and progressive.
• Systemic or pulmonary hypertension . Increase in afterload results from hypertension, which increases the workload of the heart and leads to hypertrophy of myocardial muscle fibers.
• Valvular heart disease . Blood has increasing difficulty moving forward, increasing pressure within the heart and increasing cardiac workload.

Clinical Manifestations

The clinical manifestations produced y the different types of HF are similar and therefore do not assist in differentiating the types of HF. The signs and symptoms can be related to the ventricle affected.

Left-sided HF

• Dyspnea or shortness of breath may be precipitated by minimal to moderate activity.
• Cough . The cough associated with left ventricular failure is initially dry and nonproductive .
• Pulmonary crackles . Bibasilar crackles are detected earlier and as it worsens, crackles can be auscultated across all lung fields.
• Low oxygen saturation levels . Oxygen saturation may decrease because of increased pulmonary pressures.

Right-sided HF

• Enlargement of the liver result from venous engorgement of the liver.
• Accumulation of fluid in the peritoneal cavity may increase pressure on the stomach and intestines and cause gastrointestinal distress.
• Loss of appetite results from venous engorgement and venous stasis within the abdominal organs.

Prevention of heart failure mainly lies in lifestyle management.

• Healthy diet. Avoiding intake of fatty and salty foods greatly improves the cardiovascular health of an individual.
• Engaging in cardiovascular exercises thrice a week could keep the cardiovascular system up and running smoothly.
• Smoking cessation . Nicotine causes vasoconstriction that increases the pressure along the vessels.

Complications

Many potential problems associated with HF therapy relate to the use of diuretics .

• Hypokalemia . Excessive and repeated dieresis can lead to hypokalemia .
• Hyperkalemia . Hyperkalemia may occur with the use of ACE inhibitors , ARBs, or spironolactone.
• Prolonged diuretic therapy might lead to hyponatremia and result in disorientation , fatigue, apprehension, weakness , and muscle cramps.
• Dehydration and hypotension . Volume depletion from excessive fluid loss may lead to dehydration and hypotension .

Assessment and Diagnostic Findings

HF may go undetected until the patient presents with signs and symptoms of pulmonary and peripheral edema.

• ECG : May show hypertrophy, axis deviation, ischemia, and damage patterns. Dysrhythmias and ST-T segment abnormalities may be present.
• Chest x-ray : May show enlarged cardiac shadow or abnormal contour indicating ventricular aneurysm .
• Sonograms (echocardiography, Doppler, and transesophageal echocardiography): May reveal chamber dimensions, valvular function/structure, and ventricular dilation and dysfunction.
• Heart scan (MUGA): Measures cardiac volume, ejection fraction, and wall motion.
• Exercise or pharmacological stress myocardial perfusion: Determines presence of myocardial ischemia and wall motion abnormalities.
• PET scan: Sensitive test for evaluating myocardial ischemia and viability.
• Cardiac catheterization : Assesses pressures, differentiates right- versus left-sided heart failure, and evaluates coronary artery patency.
• Liver enzymes: Elevated in liver congestion/failure.
• Digoxin and other cardiac drug levels: Determines therapeutic range.
• Bleeding and clotting times: Identifies clotting risks and therapeutic range.
• Electrolytes : May be altered due to fluid shifts, renal function, or diuretic therapy.
• Pulse oximetry: Measures oxygen saturation, especially in conjunction with COPD or chronic HF.
• Arterial blood gases ( ABGs ): Reflects respiratory and acid-base status.
• BUN/creatinine: Evaluates renal perfusion and function.
• Serum albumin/transferrin: Indicates protein intake and liver function.
• Complete blood count (CBC): Assesses for anemia , polycythemia, and dilutional changes.
• ESR: Evaluates acute inflammatory reaction.
• Thyroid studies: Determines thyroid activity as a potential precipitator of HF.

Medical Management

The overall goals of management of HF are to relieve patient symptoms, to improve functional status and quality of life, and to extend survival.

Pharmacologic Therapy

• ACE Inhibitors . ACE inhibitors slow the progression of HF, improve exercise tolerance, decrease the number of hospitalizations for HF, and promote vasodilation and diuresis by decreasing afterload and preload .
• Angiotensin II Receptor Blockers . ARBs block the conversion of angiotensin I at the angiotensin II receptor and cause decreased blood pressure, decreased systemic vascular resistance, and improved cardiac output.
• Beta Blockers . Beta blockers reduce the adverse effects from the constant stimulation of the sympathetic nervous system.
• Diuretics . Diuretics are prescribed to remove excess extracellular fluid by increasing the rate of urine produced in patients with signs and symptoms of fluid overload.
• Calcium Channel Blockers . CCBs cause vasodilation , reducing systemic vascular resistance but contraindicated in patients with systolic HF.

Nutritional Therapy

• Sodium restriction . A low sodium diet of 2 to 3g/day reduces fluid retention and the symptoms of peripheral and pulmonary congestion, and decrease the amount of circulating blood volume, which decreases myocardial work.
• Patient compliance . Patient compliance is important because dietary indiscretions may result in severe exacerbations of HF requiring hospitalizations.

Additional Therapy

• Supplemental Oxygen . The need for supplemental oxygen is based on the degree of pulmonary congestion and resulting hypoxia.
• Cardiac Resynchronization Therapy. CRT involves the use of a biventricular pacemaker to treat electrical conduction defects.
• Ultrafiltration . Ultrafiltration is an alternative intervention for patients with severe fluid overload.
• Cardiac Transplant . For some patients with end-stage heart failure, cardiac transplant is the only option for long term survival.

Nursing Management

Despite advances in the treatment of HF, morbidity and mortality remains high. Nurses have a major impact on outcomes for patients with HF.

For a more comprehensive nursing care management, please visit 18 Heart Failure Nursing Care Plans

Practice Quiz: Heart Failure

Let’s test what you’ve learned from this study guide with this 5-item quiz for heart failure.

1. The most frequent cause of hospitalization for people older than 75 years old is:

A. Angina pectoris B. Heart failure C. Hypertension D. Pulmonary edema

2. The primary cause of heart failure is:

A. Arterial hypertension B. Coronary atherosclerosis C. Myocardial dysfunction D. Valvular dysfunction

3. The dominant function in cardiac failure is:

A. Ascites B. Hepatomegaly C. Inadequate tissue perfusion D. Nocturia

4. On assessment , the nurse knows that a patient who reports no symptoms of heart failure at rest but is symptomatic with increased physical activity would have a heart failure classification of:

A. Stage I B. Stage II C. Stage III D. Stage IV

5. The diagnosis of heart failure is usually confirmed by:

A. Chest x-ray B. Echocardiogram C. Electrocardiogram D. Ventriculogram

Answers and Rationale

1. Answer: B. Heart failure

• B: Heart failure is the most frequent cause of hospitalization for people older than 75 years old.
• A: Angina pectoris also occurs among people more than 75 years of age but it is not the most frequent cause of hospitalization.
• C: Hypertension also occurs among people more than 75 years of age but it is not the most frequent cause of hospitalization.
• D: Pulmonary edema also occurs among people more than 75 years of age but it is not the most frequent cause of hospitalization.

2. Answer: B. Coronary atherosclerosis

• B: Coronary atherosclerosis is the primary cause of heart failure.
• A: Arterial hypertension is not the primary cause of heart failure.
• C: Myocardial dysfunction is not a cause of heart failure.
• D: Valvular dysfunction is not the primary cause of heart failure.

3. Answer C. Inadequate tissue perfusion

• C: Inadequate tissue perfusion is the dominant function as low oxygenation occurs because of this.
• A: Ascites may occur in cardiac failure but is not considered as a dominant function.
• B: Hepatomegaly is present in heart failure but not a dominant function.
• D: Nocturia is not present in heart failure.

4. Answer: A. Stage I

• A: Stage I refer to a patient who reports no symptoms of heart failure at rest but becomes symptomatic with increased physical activity.
• B: Stage II refers to a patient who reports presence of symptoms with increased physical activities.
• C: Stage III refers to a patient who reports presence of symptoms with minimal physical activity.
• D: Stage IV refers to a patient who reports presence of symptoms even during at rest.  

5. Answer: B: Echocardiogram

• B: An echocardiogram is usually performed to confirm the diagnosis of HF, and identify the underlying cause.
• A: Chest x-ray findings are also basis of the diagnosis of HF, but it is not the confirmatory diagnostic test .
• C: ECG is obtained to assist in the diagnosis.
• D: Ventriculogram is not a part of the diagnostic tests for HF.

Posts related to Heart Failure:

• Myocardial Infarction and Heart Failure NCLEX Practice Quiz (70 Items)
• 16+ Heart Failure Nursing Care Plans
• 7 Myocardial Infarction (Heart Attack) Nursing Care Plans

5 thoughts on “Heart Failure”

Great work and keep it up to help nurses. Can you do an app for it on play store or IOS so that we can easily assess it anywhere at any time like medscape did

THANK YOU FOR YOUR WORK, IT HELP US AS NURSES TO BE UPDATED.

Great work keep it up sir. Almighty God blessing you in everything of life.

This is an excellent resource for nurses! However, I think nurses would benefit from an update in the medication section to include angiotensin receptor neprilysin inhibitors (ARNI: sacubitril/valsartan), mineralocorticoid receptor antagonists (MRAs: spironolactone, eplerenone), and sodium-glucose co-transporter-2 inhibitors (SGLT2I: dapagliflozin, empagliflozin). The 2022 AHA/ACC/HFSA Guidelines for Heart Failure Management recommends quadruple therapy (ARNI, BB, MRA, SGLT2I) up-titrated to target or maximally tolerated doses for patients diagnosed with heart failure with a reduced ejection fraction to reverse, stabilize, or slow disease progression. These medications are also used in patients with heart failure and preserved ejection fraction.

Hi Keysha, thank you for sharing this. I’ll add your suggestions and the 2022 AHA/ACC/HFSA Guidelines on our next update for this care plan.

Leave a Comment Cancel reply

Heart Failure Case Study (45 min)

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What initial nursing assessments need to be performed for Mr. Jones?

• Full set vital signs
• Heart sounds
• Lung Sounds

What diagnostic tests do you anticipate being ordered by the provider?

• Chest X-ray
• 12-lead EKG
• Echocardiogram
• Cardiac Enzymes

Upon further assessment, the patient has crackles bilaterally and tachycardia. A chest X-ray shows cardiomegaly and bilateral pulmonary edema. An ECG revealed atrial fibrillation. His vital signs were as follows:

BP 150/72 mmHg Urine Yellow and Cloudy

HR 102-123 bpm and irregular BUN 17 mg/dL

RR 24-32 bpm Cr 1.2 mg/dL

Temp 37.3°C H/H 11.8 g/dL / 36.2%

Ht 175 cm LDH 705 U/L

Wt 79 kg ** BNP 843 pg/mL

Mr. Jones was admitted to the cardiac telemetry unit.

Mr. Jones states that this weight is approximately 3 kg more than it was 3 days ago.

What is the significance of Mr. Jones' weight gain?

• 1 kg weight gain is equal to 1 liter of weight gain. This means Mr. Jones has gained 3 liters of fluid (as volume excess) in just 3 days.
• This likely means that there is a new onset or exacerbation of heart failure

What medications do you anticipate the provider ordering for Mr. Jones? Why?

• Diuretics – he is volume overloaded and it is affected his lungs. Diuretics can help relieve fluid retention by promoting excretion of water from the kidneys.
• Beta-Blockers – his blood pressure is high and his heart rate is fast. The beta-blocker can help slow this down and relieve some of the workload of his heart

About three hours after admission to the telemetry unit, Mr. Jones’s skin becomes cool and clammy. His respirations are labored and he is complaining of abdominal pain. Upon physical examination, Mr. Jones is diaphoretic and gasping for air, with jugular venous distension, bilateral crackles, and an expiratory wheeze.  His SpO 2 is 88% on room air and it was noted that his urine output had been approximately 20 mL/hr since admission. His BP is 190/100 mmHg, HR 130 bpm and irregular, RR 43 bpm.

What nursing interventions should you perform right away for Mr. Jones?

• Place into High Fowler’s position 
• Apply oxygen
• Administer any PRN medications available for blood pressure (like hydralazine or metoprolol) if criteria are met
• Notify the provider

Describe what is happening to Mr. Jones physiologically.

• Because his heart cannot pump blood efficiently to the body, the blood is backing up into the lungs. This causes pulmonary edema. His pulmonary edema is so severe that he is struggling to breathe and struggling to oxygenate appropriately.
• His heart is trying to work extra hard to compensate for the low cardiac output, that’s why his blood pressure and heart rate are so elevated. This is perpetuated by the RAAS.
• We also see that his kidneys are not being perfused as his urine output has decreased

What medications should be given to decrease Mr. Jones’s preload? Improve his contractility? Decrease his afterload?

• Preload – diuretics (furosemide, bumetanide, spironolactione), ACE inhibitors (captopril, enalapril), ARB’s (losartan, valsartan), ARNI’s (sacubitril/valsartan)
• Contractility – Inotropes (dobutamine), cardiac glycosides (digoxin)
• Afterload – Beta Blockers (metoprolol, carvedilol), vasodilators (hydralazine, nitrates)

What is the expected outcome of administration of Furosemide? Digoxin?

• Furosemide – should see increase in urine output and decrease in respiratory symptoms – may also see a decrease in any peripheral edema
• Digoxin – decrease heart rate and increase the force of contraction – should see evidence of improved peripheral perfusion.

Melander, S. (2004). Case studies in critical care nursing: A guide for application and review, 3 rd ed. Philadelphia, PA: Saunders Elsevier.

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Chapter 5:  10 Real Cases on Acute Heart Failure Syndrome: Diagnosis, Management, and Follow-Up

Swathi Roy; Gayathri Kamalakkannan

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Case 1: Diagnosis and Management of New-Onset Heart Failure With Reduced Ejection Fraction

A 54-year-old woman presented to the telemetry floor with shortness of breath (SOB) for 4 months that progressed to an extent that she was unable to perform daily activities. She also used 3 pillows to sleep and often woke up from sleep due to difficulty catching her breath. Her medical history included hypertension, dyslipidemia, diabetes mellitus, and history of triple bypass surgery 4 years ago. Her current home medications included aspirin, atorvastatin, amlodipine, and metformin. No significant social or family history was noted. Her vital signs were stable. Physical examination showed bilateral diffuse crackles in lungs, elevated jugular venous pressure, and 2+ pitting lower extremity edema. ECG showed normal sinus rhythm with left ventricular hypertrophy. Chest x-ray showed vascular congestion. Laboratory results showed a pro-B-type natriuretic peptide (pro-BNP) level of 874 pg/mL and troponin level of 0.22 ng/mL. Thyroid panel was normal. An echocardiogram demonstrated systolic dysfunction, mild mitral regurgitation, a dilated left atrium, and an ejection fraction (EF) of 33%. How would you manage this case?

In this case, a patient with known history of coronary artery disease presented with worsening of shortness of breath with lower extremity edema and jugular venous distension along with crackles in the lung. The sign and symptoms along with labs and imaging findings point to diagnosis of heart failure with reduced EF (HFrEF). She should be treated with diuretics and guideline-directed medical therapy for congestive heart failure (CHF). Telemetry monitoring for arrythmia should be performed, especially with structural heart disease. Electrolyte and urine output monitoring should be continued.

In the initial evaluation of patients who present with signs and symptoms of heart failure, pro-BNP level measurement may be used as both a diagnostic and prognostic tool. Based on left ventricular EF (LVEF), heart failure is classified into heart failure with preserved EF (HFpEF) if LVEF is >50%, HFrEF if LVEF is <40%, and heart failure with mid-range EF (HFmEF) if LVEF is 40% to 50%. All patients with symptomatic heart failure should be started on an angiotensin-converting enzyme (ACE) inhibitor (or angiotensin receptor blocker if ACE inhibitor is not tolerated) and β-blocker, as appropriate. In addition, in patients with New York Heart Association functional classes II through IV, an aldosterone antagonist should be prescribed. In African American patients, hydralazine and nitrates should be added. Recent recommendations also recommend starting an angiotensin receptor-neprilysin inhibitor (ARNI) in patients who are symptomatic on ACE inhibitors.

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5: Case Study #4- Heart Failure (HF)

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• Page ID 9899
• 5.1: Learning Objectives
• 5.2: Patient- Meryl Smith
• 5.3: In the Supermarket
• 5.4: Emergency Room
• 5.5: Day 0- Medical Ward
• 5.6: Day 1- Medical Ward
• 5.7: Day 2- Medical Ward
• 5.8: Day 3- Medical Ward

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Congestive Heart Failure (CHF) Nursing Diagnosis and Care Plan

Last updated on February 20th, 2023 at 08:45 am

CHF can affect either both sides of the heart or just one side. The three types of CHF are biventricular, left-sided, and right-sided heart failure. In left-sided heart failure, the left ventricle becomes enlarged (hypertrophy) and becomes dilated together with the left atrium in order to compensate for the increased pressure.

Right-sided heart failure usually happens after left-sided heart failure. Pooling of blood in the left heart chambers causes an increase in pressure, impairing the normal blood drainage from the lungs to the left atrium.

The pressure in the pulmonary veins increases, causing the right ventricle to compensate by pumping more vigorously.

In time, the cardiac muscles of the right chambers wear down, causing right-sided heart failure. Failure of both sides of the heart is called biventricular heart failure.

Congestion is one of the common features of heart failure, thus the term “congestive heart failure” is still used by many medical professionals.

Signs and Symptoms of Heart Failure

• Dyspnea ( shortness of breath ) upon exertion or lying down
• Jugular vein distention (JVD)
• Fatigue and reduced ability to exercise
• Peripheral edema (swelling of limbs, ankles, and feet)
• Pulmonary edema
• Ascites (swelling of the abdominal cavity)
• Irregular and/or rapid heartbeat
• Cough and wheezing – may come with white or blood-tinged sputum
• Nausea and lack of appetite
• Decreased level of alertness and concentration
• Increased urinary frequency at night
• Chest pain if the HF is caused by myocardial infarction (heart attack)

Causes of Heart Failure

• Myocardial Infarction (heart attack) and Coronary Artery Disease (CAD). These are the most common causes of heart failure. Fat buildup on the arterial walls leads to the reduction of blood flow, resulting to cardiac arrest.
• Hypertension . Having a high blood pressure causes the heart to work harder than normal in order to facilitate the blood circulation throughout the body. This makes the cardiac muscles stiffer and/or weaker, leading to heart failure.
• Alcohol, tobacco, and drug abuse. The toxic effects of alcohol, nicotine, and drugs (e.g. cocaine) may lead to the damage of the cardiac muscles known as cardiomyopathy .
• Congenital heart defects. Faulty heart chambers or valves at birth can directly affect the functionality of the heart.
• Other heart conditions. Viral infections such as COVID-19 may cause inflammation of the cardiac muscles known as myocarditis .
• Chronic diseases. HIV , diabetes , arrythmias, and thyroid problems may lead to heart failure.
• Certain medications. Non-steroidal inflammatory drugs (NSAIDS) , several anaesthesia drugs, chemotherapy agents, and some antihypertensives puts a person at a higher risk for heart problems which may eventually lead to heart failure.

Complications of Heart Failure

• Kidney damage. A reduction of blood flow from the heart to the kidneys may result to reduce capacity of the kidneys to remove toxic waste. If left untreated, this may lead to kidney failure which may require the patient to undergo dialysis .
• Liver damage. Fluid build up may result to an increased pressure to the liver . If left untreated, this may result to liver damage known as scarring.
• Other cardiac issues. Heart failure may result to faulty heart valves and arrythmias if there is an increased pressure in the heart or enlargement of the heart.

Diagnostic Tests for Heart Failure

• Physical examination – crackles heard upon auscultation, signs of edema upon inspection
• Blood tests – CBC, biochemistry, N-terminal pro-B-type natriuretic peptide (NT-proBNP)
• Imaging – Chest X-Ray, Echocardiogram, CT scan, MRI, coronary angiogram (insertion of a catheter and injecting a dye for visualization)
• Electrocardiogram
• Stress test – letting the patient walk on a treadmill while attached to an ECG machine
• Myocardial biopsy – insertion of a biopsy cord in a vein in the neck or groin to take heart muscle tissue samples

Treatment for Heart Failure

• Medications. Several medications are used in combination to treat heart failure. These include:
• Angiotensin-converting enzyme ( ACE ) inhibitors – promotes vasodilation of the blood vessels, lowering the pressure and improving the blood flow (e.g. lisinopril and enalapril).
• Beta blockers – reduces heart rate and blood pressure (e.g. bisoprolol and carvedilol).
• Angiotensin II receptor blockers – similar to ACE inhibitors and can be used if the patient does not tolerate ACE inhibitors (e.g. losartan and valsartan).
• Digitalis or digoxin – improves the contraction of heart muscles, regulate heart rhythm and reduces heartbeat.
• Inotropes – to improve the function of the heart to pump blood in severe heart failure.
• Diuretics – to facilitate elimination of excess fluid in the body through urination (e.g. furosemide and spironolactone).
• Inotropes. These are intravenous medications used in people with severe heart failure in the hospital to improve heart pumping function and maintain blood pressure.

2. Surgical interventions. These include coronary bypass surgery, heart valve repair or replacement, and heart transplant. It may also involve the insertion of medical devices such as implantable cardioverter-defibrillators (ICDs), cardiac resynchronization therapy (CRT), and ventricular assist devices (VADs).

3. Lifestyle changes. A crucial part of the treatment plan for a patient with heart failure is to change several habits that are linked to the disease. These include smoking cessation, blood pressure control, diabetes management, dietary changes, stress management, exercise and increase in physical activity.

CHF Nursing Diagnosis

Chf nursing care plan 1.

Nursing Diagnosis: Decreased Cardiac Output related to increased preload and afterload and impaired contractility as evidenced by irregular heartbeat, heart rate of 128, dyspnea upon exertion, and fatigue.

Desired outcome: The patient will be able to maintain adequate cardiac output.

CHF Nursing Care Plan 2

Nursing Diagnosis: Impaired Gas Exchange related to alveolar edema due to elevated ventricular pressures as evidenced by shortness of breath, SpO2 level of 85%, and crackles upon auscultation.

Desired Outcome: The patient will have improved oxygenation and will not show any signs of respiratory distress.

CHF Nursing Care Plan 3

Nursing Diagnosis: Deficient Knowledge related to new diagnosis of Congestive Heart Failure as evidenced by patient’s verbalization of “I want to know more about my new diagnosis and care”

Desired Outcome: At the end of the health teaching session, the patient will be able to demonstrate sufficient knowledge of congestive heart failure and its management.

CHF Nursing Care Plan 4

Nursing Diagnosis: Activity intolerance related to imbalance between oxygen supply and demand as evidenced by fatigue, overwhelming lack of energy, verbalization of tiredness, generalized weakness, and shortness of breath upon exertion

Desired Outcome: The patient will demonstration active participation in necessary and desired activities and demonstrate increase in activity levels.

CHF Nursing Care Plan 5

Nursing Diagnosis: Excess Fluid Volume related to decreased cardiac output and increased glomerular filtration rate (GFR) as evidenced by S3 heart sound, blood pressure level of 190/85, orthopnea, pitting edema of the ankles, and weight gain

Desired Outcome: The patient will demonstrate a balanced input and output, and stabilized fluid volume

CHF Nursing Care Plan 6

Nursing Diagnosis: Acute Pain related to decreased myocardial blood flow as evidenced by  pain score of 10 out of 10, verbalization of pressure-like/ squeezing chest pain (angina), guarding sign on the chest, blood pressure level of 180/90, respiratory rate of 29 cpm, and restlessness

Desired Outcome: The patient will demonstrate relief of pain as evidenced by a pain score of 0 out of 10, stable vital signs, and absence of restlessness.

CHF Nursing Care Plan 7

Nursing Diagnosis: Ineffective Breathing Pattern related to pulmonary congestion secondary to CHF as evidenced by shortness of breath, SpO2 level of 85%, cough, respiratory rate of 25 bpm, and frothy sputum

Desired Outcome: The patient will achieve effective breathing pattern as evidenced by normal respiratory rate, oxygen saturation within target range, and verbalize ease of breathing.

With proper use of the nursing process, a patient can benefit from various nursing interventions to assess, monitor, and manage heart failure and promote client safety and wellbeing.

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020).  Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018).  Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020).  Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier.  Buy on Amazon

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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Case study: 33-year-old female presents with chronic sob and cough.

Sandeep Sharma ; Muhammad F. Hashmi ; Deepa Rawat .

Affiliations

Last Update: February 20, 2023 .

• Case Presentation

History of Present Illness:  A 33-year-old white female presents after admission to the general medical/surgical hospital ward with a chief complaint of shortness of breath on exertion. She reports that she was seen for similar symptoms previously at her primary care physician’s office six months ago. At that time, she was diagnosed with acute bronchitis and treated with bronchodilators, empiric antibiotics, and a short course oral steroid taper. This management did not improve her symptoms, and she has gradually worsened over six months. She reports a 20-pound (9 kg) intentional weight loss over the past year. She denies camping, spelunking, or hunting activities. She denies any sick contacts. A brief review of systems is negative for fever, night sweats, palpitations, chest pain, nausea, vomiting, diarrhea, constipation, abdominal pain, neural sensation changes, muscular changes, and increased bruising or bleeding. She admits a cough, shortness of breath, and shortness of breath on exertion.

Social History: Her tobacco use is 33 pack-years; however, she quit smoking shortly prior to the onset of symptoms, six months ago. She denies alcohol and illicit drug use. She is in a married, monogamous relationship and has three children aged 15 months to 5 years. She is employed in a cookie bakery. She has two pet doves. She traveled to Mexico for a one-week vacation one year ago.

Allergies:  No known medicine, food, or environmental allergies.

Past Medical History: Hypertension

Past Surgical History: Cholecystectomy

Medications: Lisinopril 10 mg by mouth every day

Physical Exam:

Vitals: Temperature, 97.8 F; heart rate 88; respiratory rate, 22; blood pressure 130/86; body mass index, 28

General: She is well appearing but anxious, a pleasant female lying on a hospital stretcher. She is conversing freely, with respiratory distress causing her to stop mid-sentence.

Respiratory: She has diffuse rales and mild wheezing; tachypneic.

Cardiovascular: She has a regular rate and rhythm with no murmurs, rubs, or gallops.

Gastrointestinal: Bowel sounds X4. No bruits or pulsatile mass.

• Initial Evaluation

Laboratory Studies:  Initial work-up from the emergency department revealed pancytopenia with a platelet count of 74,000 per mm3; hemoglobin, 8.3 g per and mild transaminase elevation, AST 90 and ALT 112. Blood cultures were drawn and currently negative for bacterial growth or Gram staining.

Chest X-ray

Impression:  Mild interstitial pneumonitis

• Differential Diagnosis
• Aspiration pneumonitis and pneumonia
• Bacterial pneumonia
• Immunodeficiency state and Pneumocystis jiroveci pneumonia
• Carcinoid lung tumors
• Tuberculosis
• Viral pneumonia
• Chlamydial pneumonia
• Coccidioidomycosis and valley fever
• Recurrent Legionella pneumonia
• Mediastinal cysts
• Mediastinal lymphoma
• Recurrent mycoplasma infection
• Pancoast syndrome
• Pneumococcal infection
• Sarcoidosis
• Small cell lung cancer
• Aspergillosis
• Blastomycosis
• Histoplasmosis
• Actinomycosis
• Confirmatory Evaluation

CT of the chest was performed to further the pulmonary diagnosis; it showed a diffuse centrilobular micronodular pattern without focal consolidation.

On finding pulmonary consolidation on the CT of the chest, a pulmonary consultation was obtained. Further history was taken, which revealed that she has two pet doves. As this was her third day of broad-spectrum antibiotics for a bacterial infection and she was not getting better, it was decided to perform diagnostic bronchoscopy of the lungs with bronchoalveolar lavage to look for any atypical or rare infections and to rule out malignancy (Image 1).

Bronchoalveolar lavage returned with a fluid that was cloudy and muddy in appearance. There was no bleeding. Cytology showed Histoplasma capsulatum .

Based on the bronchoscopic findings, a diagnosis of acute pulmonary histoplasmosis in an immunocompetent patient was made.

Pulmonary histoplasmosis in asymptomatic patients is self-resolving and requires no treatment. However, once symptoms develop, such as in our above patient, a decision to treat needs to be made. In mild, tolerable cases, no treatment other than close monitoring is necessary. However, once symptoms progress to moderate or severe, or if they are prolonged for greater than four weeks, treatment with itraconazole is indicated. The anticipated duration is 6 to 12 weeks total. The response should be monitored with a chest x-ray. Furthermore, observation for recurrence is necessary for several years following the diagnosis. If the illness is determined to be severe or does not respond to itraconazole, amphotericin B should be initiated for a minimum of 2 weeks, but up to 1 year. Cotreatment with methylprednisolone is indicated to improve pulmonary compliance and reduce inflammation, thus improving work of respiration. [1] [2] [3]

Histoplasmosis, also known as Darling disease, Ohio valley disease, reticuloendotheliosis, caver's disease, and spelunker's lung, is a disease caused by the dimorphic fungi  Histoplasma capsulatum native to the Ohio, Missouri, and Mississippi River valleys of the United States. The two phases of Histoplasma are the mycelial phase and the yeast phase.

Etiology/Pathophysiology 

Histoplasmosis is caused by inhaling the microconidia of  Histoplasma  spp. fungus into the lungs. The mycelial phase is present at ambient temperature in the environment, and upon exposure to 37 C, such as in a host’s lungs, it changes into budding yeast cells. This transition is an important determinant in the establishment of infection. Inhalation from soil is a major route of transmission leading to infection. Human-to-human transmission has not been reported. Infected individuals may harbor many yeast-forming colonies chronically, which remain viable for years after initial inoculation. The finding that individuals who have moved or traveled from endemic to non-endemic areas may exhibit a reactivated infection after many months to years supports this long-term viability. However, the precise mechanism of reactivation in chronic carriers remains unknown.

Infection ranges from an asymptomatic illness to a life-threatening disease, depending on the host’s immunological status, fungal inoculum size, and other factors. Histoplasma  spp. have grown particularly well in organic matter enriched with bird or bat excrement, leading to the association that spelunking in bat-feces-rich caves increases the risk of infection. Likewise, ownership of pet birds increases the rate of inoculation. In our case, the patient did travel outside of Nebraska within the last year and owned two birds; these are her primary increased risk factors. [4]

Non-immunocompromised patients present with a self-limited respiratory infection. However, the infection in immunocompromised hosts disseminated histoplasmosis progresses very aggressively. Within a few days, histoplasmosis can reach a fatality rate of 100% if not treated aggressively and appropriately. Pulmonary histoplasmosis may progress to a systemic infection. Like its pulmonary counterpart, the disseminated infection is related to exposure to soil containing infectious yeast. The disseminated disease progresses more slowly in immunocompetent hosts compared to immunocompromised hosts. However, if the infection is not treated, fatality rates are similar. The pathophysiology for disseminated disease is that once inhaled, Histoplasma yeast are ingested by macrophages. The macrophages travel into the lymphatic system where the disease, if not contained, spreads to different organs in a linear fashion following the lymphatic system and ultimately into the systemic circulation. Once this occurs, a full spectrum of disease is possible. Inside the macrophage, this fungus is contained in a phagosome. It requires thiamine for continued development and growth and will consume systemic thiamine. In immunocompetent hosts, strong cellular immunity, including macrophages, epithelial, and lymphocytes, surround the yeast buds to keep infection localized. Eventually, it will become calcified as granulomatous tissue. In immunocompromised hosts, the organisms disseminate to the reticuloendothelial system, leading to progressive disseminated histoplasmosis. [5] [6]

Symptoms of infection typically begin to show within three to17 days. Immunocompetent individuals often have clinically silent manifestations with no apparent ill effects. The acute phase of infection presents as nonspecific respiratory symptoms, including cough and flu. A chest x-ray is read as normal in 40% to 70% of cases. Chronic infection can resemble tuberculosis with granulomatous changes or cavitation. The disseminated illness can lead to hepatosplenomegaly, adrenal enlargement, and lymphadenopathy. The infected sites usually calcify as they heal. Histoplasmosis is one of the most common causes of mediastinitis. Presentation of the disease may vary as any other organ in the body may be affected by the disseminated infection. [7]

The clinical presentation of the disease has a wide-spectrum presentation which makes diagnosis difficult. The mild pulmonary illness may appear as a flu-like illness. The severe form includes chronic pulmonary manifestation, which may occur in the presence of underlying lung disease. The disseminated form is characterized by the spread of the organism to extrapulmonary sites with proportional findings on imaging or laboratory studies. The Gold standard for establishing the diagnosis of histoplasmosis is through culturing the organism. However, diagnosis can be established by histological analysis of samples containing the organism taken from infected organs. It can be diagnosed by antigen detection in blood or urine, PCR, or enzyme-linked immunosorbent assay. The diagnosis also can be made by testing for antibodies again the fungus. [8]

Pulmonary histoplasmosis in asymptomatic patients is self-resolving and requires no treatment. However, once symptoms develop, such as in our above patient, a decision to treat needs to be made. In mild, tolerable cases, no treatment other than close monitoring is necessary. However, once symptoms progress to moderate or severe or if they are prolonged for greater than four weeks, treatment with itraconazole is indicated. The anticipated duration is 6 to 12 weeks. The patient's response should be monitored with a chest x-ray. Furthermore, observation for recurrence is necessary for several years following the diagnosis. If the illness is determined to be severe or does not respond to itraconazole, amphotericin B should be initiated for a minimum of 2 weeks, but up to 1 year. Cotreatment with methylprednisolone is indicated to improve pulmonary compliance and reduce inflammation, thus improving the work of respiration.

The disseminated disease requires similar systemic antifungal therapy to pulmonary infection. Additionally, procedural intervention may be necessary, depending on the site of dissemination, to include thoracentesis, pericardiocentesis, or abdominocentesis. Ocular involvement requires steroid treatment additions and necessitates ophthalmology consultation. In pericarditis patients, antifungals are contraindicated because the subsequent inflammatory reaction from therapy would worsen pericarditis.

Patients may necessitate intensive care unit placement dependent on their respiratory status, as they may pose a risk for rapid decompensation. Should this occur, respiratory support is necessary, including non-invasive BiPAP or invasive mechanical intubation. Surgical interventions are rarely warranted; however, bronchoscopy is useful as both a diagnostic measure to collect sputum samples from the lung and therapeutic to clear excess secretions from the alveoli. Patients are at risk for developing a coexistent bacterial infection, and appropriate antibiotics should be considered after 2 to 4 months of known infection if symptoms are still present. [9]

Prognosis 

If not treated appropriately and in a timely fashion, the disease can be fatal, and complications will arise, such as recurrent pneumonia leading to respiratory failure, superior vena cava syndrome, fibrosing mediastinitis, pulmonary vessel obstruction leading to pulmonary hypertension and right-sided heart failure, and progressive fibrosis of lymph nodes. Acute pulmonary histoplasmosis usually has a good outcome on symptomatic therapy alone, with 90% of patients being asymptomatic. Disseminated histoplasmosis, if untreated, results in death within 2 to 24 months. Overall, there is a relapse rate of 50% in acute disseminated histoplasmosis. In chronic treatment, however, this relapse rate decreases to 10% to 20%. Death is imminent without treatment.

• Pearls of Wisdom

While illnesses such as pneumonia are more prevalent, it is important to keep in mind that more rare diseases are always possible. Keeping in mind that every infiltrates on a chest X-ray or chest CT is not guaranteed to be simple pneumonia. Key information to remember is that if the patient is not improving under optimal therapy for a condition, the working diagnosis is either wrong or the treatment modality chosen by the physician is wrong and should be adjusted. When this occurs, it is essential to collect a more detailed history and refer the patient for appropriate consultation with a pulmonologist or infectious disease specialist. Doing so, in this case, yielded workup with bronchoalveolar lavage and microscopic evaluation. Microscopy is invaluable for definitively diagnosing a pulmonary consolidation as exemplified here where the results showed small, budding, intracellular yeast in tissue sized 2 to 5 microns that were readily apparent on hematoxylin and eosin staining and minimal, normal flora bacterial growth. 

• Enhancing Healthcare Team Outcomes

This case demonstrates how all interprofessional healthcare team members need to be involved in arriving at a correct diagnosis. Clinicians, specialists, nurses, pharmacists, laboratory technicians all bear responsibility for carrying out the duties pertaining to their particular discipline and sharing any findings with all team members. An incorrect diagnosis will almost inevitably lead to incorrect treatment, so coordinated activity, open communication, and empowerment to voice concerns are all part of the dynamic that needs to drive such cases so patients will attain the best possible outcomes.

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Histoplasma Contributed by Sandeep Sharma, MD

Disclosure: Sandeep Sharma declares no relevant financial relationships with ineligible companies.

Disclosure: Muhammad Hashmi declares no relevant financial relationships with ineligible companies.

Disclosure: Deepa Rawat declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Sharma S, Hashmi MF, Rawat D. Case Study: 33-Year-Old Female Presents with Chronic SOB and Cough. [Updated 2023 Feb 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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