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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 review, case discussion.

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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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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 Center Patient Cases

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Heart Failure: Ask the Expert – Patient Cases

Welcome to the GCVI HF Center’s Ask the Expert – Patient Cases channel! On this channel you will have access to multiple heart failure patient cases published by leading ACC experts. We also encourage you to engage and consult with ACC global experts on cases specific to your practice. Ask the Expert through the online portal below!

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Heart Failure Patient Case Quizzes

• Unrecognized HFpEF in a Type 2 DM Patient – Reducing CV and HF Risk
• Untreated HFrEF/Ischemic Cardiomyopathy in Type 2 DM – How to Optimize Medical Therapy to Improve Heart Failure Outcomes
• Restrictive Cardiomyopathies Series: Advanced HF Therapies in ATTR Cardiac Amyloidosis (Certified Patient Case Study)
• ECG of the Month: Variable QRS Morphologies in Heart Failure 
• Untreated HFrEF/Ischemic Cardiomyopathy in Type 2 DM
• Unrecognized HFpEF in a Type 2 DM Patient

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Case presentation: atrial fibrillation in heart failure

Session: Guidelines in Daily Practice I: atrial fibrillation in heart failure Topic: Acute Heart Failure Speaker: Professor D. Kotecha (Birmingham, GB) Event: Heart Failure 2017 - 4th World Congress on Acute Heart Failure

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About the speaker

Professor Dipak Kotecha

University of Birmingham, Birmingham (United Kingdom of Great Britain & Northern Ireland) 35 presentations 0 follower

4 more presentations in this session

What do the guidelines say.

Speaker: Professor C. Linde (Stockholm, SE)

Gaps in evidence

Speaker: Doctor F. Enseleit (Wiesbaden, DE)

Questions & answers with the audience.

Conclusion and take-home messages.

Speaker: Professor P. Ponikowski (Wroclaw, PL)

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Guidelines in daily practice i: atrial fibrillation in heart failure, about the event, heart failure 2017 - 4th world congress on acute heart failure.

29 April - 2 May 2017

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Congestive Heart Failure

Update Author Editor: Christopher Cox MD, Dalhousie University (2019)

Editor: Moises Gallegos MD MPH, Stanford Department of Emergency Medicine, 

Author: Amy Pound, MD, University Hospitals Case Medical Center, Case Western Reserve University

Last Update: September, 2019

70-year-old female with a history of coronary artery disease, and hypertension presents by ambulance to your emergency department, the morning after Thanksgiving, with progressive shortness of breath. She notes that she has had company all week and as a result she didn’t seek medical care. She has noticed shortness of breath at night and has been resting on at least two pillows. Last night she was unable to sleep and had to stay in her recliner chair until she called the paramedics this morning. She denies chest pain now or at any time this week.  She admits that she failed to follow her low salt diet and states she may have missed some of her medications this week due to the holiday.

Her vital signs are HR 105, BP160/80, RR 32, and SpO2 89% on 100% non-rebreather oxygen mask. (case study continues throughout chapter)

Upon finishing this module, the student will be able to:

• Discuss the classifications of heart failure.
• Identify the signs/symptoms for acute exacerbation of congestive heart failure.
• Describe how congestive heart failure can be diagnosed based on laboratory, chest x-ray, and Point of Care Ultrasound (PoCUS) studies.
• Prioritize and list ED treatment options for acute exacerbations of congestive heart failure.

Introduction

Congestive Heart Failure (CHF) is one of the most common illnesses treated in the Emergency Department. It affects about 2% of the US population or roughly 4.8 million Americans. In patients over the age of 65, it comprises 20% of hospitalizations, making it the most common admitting diagnosis. 

CHF arises when the ventricles fail to maintain forward blood circulation, often when the cardiac demand increases. Precipitating events include cardiac ischemia, dysrhythmias, infection, PE, physical/emotional stress, noncompliance with medication/diet, and volume overload. In this condition, the heart lacks the reserve to compensate for the increased burden within the congested circulatory system.

Classification and Terminology

NYHA CHF Classification

Class I – Ordinary activity not limited by symptoms

Class II – Ordinary activity leads to dyspnea, fatigue, etc

Class III – Marked limitation of ordinary activity

Class IV – Symptoms at rest or with any physical activity

Systolic vs Diastolic Dysfunction

Systolic dysfunction includes a dilated left ventricle with impaired contractility, often caused by ischemia, infarction cardiomyopathy, myocarditis, or dysrhythmias. In diastolic dysfunction the left ventricle remains normal in size, but has an impaired ability to relax. This limits the volume of blood in the ventricle, or preload, and causes increased pressure in the chamber which then reaches the lungs where fluid backs up. One example is infiltrative cardiomyopathy. Diastolic dysfunction has a better prognosis that systolic dysfunction.

High vs Low Output

In low output failure, there is decreased cardiac output secondary to myocardial damage, such as with ischemia, dilated cardiomyopathy, valvular disease, or chronic hypertension. In high output failure, the cardiac output is high or normal, but remains insufficient to supply oxygen demands. High output failure can be found in hyperthyroidism, pregnancy, anemia, AV fistulas, beriberi, or Paget’s disease.

Right vs Left Failure

Right sided failure, or increased pressure and fluid build up in the right ventricle, results in hepatic enlargement, increased jugular venous distention, and dependent peripheral edema of the extremities. Left sided heart failure will cause fluid build up in the left ventricle, resulting in pulmonary congestion.

Initial Actions and Primary Survey

Similar to other patients in the Emergecny Department initial actions include establishing IV access,provding supplimental O2 as needed, and vital sign monitor. These patients may require ECG and CXR

If 100% O2 by non-rebreather fails to increase O2 saturation to at least 95%, noninvasive oxygenation/ventilation (NIPPV) such as CPAP or BiPAP may assist in correcting hypoxia. If there is a failure to improve oxygenation, if the patient cannot tolerate the mask, or has a decline in mental status such that they are unable to protect their airway, then endotracheal intubation is required. The use of NIPPV used early can improve work of breathing as well as oxygenation, however caution should be taken as increased intra-thoracic pressure can reduce preload and worsen hypotension.

Hypotension can be difficult to manage in this patient population secondary to existing fluid overload. Early vasopressor support may be needed. Frequently patients with CHF exacerbation with present with significant hypertension. Nitroglycerin can be a useful medication in helping to reduce preload and reduce progression of pulmonary edema.

Presentation

Typical chief complaints, as in this case, include shortness of breath and peripheral edema.

Case Study, continued

Physical exam:

Your patient is in moderate respiratory distress, sitting forward, and speaking in only three word sentences. 

HEENT: She has no stridor. Jugular venous pressure is elevated to the mandible. (Image 1)

Chest: Her lung sounds are crackles in all lung fields without wheezing.

Cardio: She has normal S1and S2. An S3 is present. There is no murmur.

Abdomen: She has no tenderness, no hepato-splenomegaly, and no masses on exam.

Extremities: She has two plus pitting edema to the level of the tibial plateau. (Image 2)

Neuro: She is awake with no weakness, numbness, speech or vision deficits.

Skin: She is pale with central cyanosis, cool to touch, and diaphoretic.  

Image 1: JVD is measured by the peak of the pressure wave in the internal jugular vein. You can see this vessel is dilated as it exits medially from under the sternocleidomastoid. See black arrow. 

By Ferencga (Own work) [CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 )%5D, via Wikimedia Commons. Notation added by C.Cox 4/2019.

Image 2: Pitting edema    

By James Heilman, MD (Own work) [CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 ) or GFDL ( http://www.gnu.org/copyleft/fdl.html )%5D, via Wikimedia Commons

Diagnostic Testing

POINT OF CARE ULTRASOUND: (POCUS)

For your patient, your attending physician shows you multiple bilateral lung views, and parasternal long axis (PSL) and apical four chamber (a4C) cardiac views, and explains their significance in making a diagnosis of CHF. (Image 3-6).

Image 3: B-lines in right lung field suggesting interstitial edema. Original contribution by author, C. Cox. CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 )

Image 4: B-lines in left lung field suggesting interstitial edema. Original contribution by author, C. Cox. CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0

Image 5: PSL, Dilated Left Ventricle with poor contraction  and poor mitral valve excursion suggesting diminished Ejection Fraction (EF) Original contribution by author, C. Cox. CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0

Image 6: a4C, Dilated Left Ventricle with poor contraction  and Mitral valve with poor excursion suggesting diminished EF Original contribution by author, C. Cox. CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 )

Your attending states that your patient has qualitatively diminished heart function and bilateral interstitial edema. As demonstrated at the bedside, she has B-lines in greater that 2 thoracic quadrants bilaterally which suggests a cardiac source of pulmonary edema. (Sensitivity 97%, Specificity 95%)

Common findings are cardiomegaly and effusions. Chest x-ray (CXR) findings may lag by 12 hours from onset of symptoms, and subsequently CXR findings may persist for several days despite clinical improvement. 1 out of 5 patients admitted for CHF exacerbations showed lack of any pulmonary congestion on CXR.

Cardiomegaly is defined as a cardiothoracic ratio greater than 50% diameter. Patients with diastolic failure may have normal heart size.

Image 7: By Nevit Dilmen (Own work) [GFDL]( http://www.gnu.org/copyleft/fdl.html ) or CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 )%5D, via Wikimedia Commons

Additional CXR findings include:

• Peribronchial cuffing – thickened bronchial walls secondary to edema. Indicated by arrow in above image.
• Perihilar congestion – large hila with indistinct margins suggest pulmonary vasculature edema. Indicated by the two arrows in the image below.

Image 8: By James Heilman, MD (Own work) [CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 ) or GFDL ( http://www.gnu.org/copyleft/fdl.html )%5D, via Wikimedia Commons

• Cephalization – redistribution of blood flow to upper lobes. Only seen on upright films. Circled area in the image below.

Image 9: By James Heilman, MD (Own work) [CC BY-SA 3.0 ( http://creativecommons.org/licenses/by-sa/3.0 ) or GFDL ( http://www.gnu.org/copyleft/fdl.html )%5D, via Wikimedia Commons

• Pleural effusion – meniscus at the angle of the diaphragm. Arrow in above image.
• Kerley B lines – Dilated lymphatic channels. Typically 2 cm in length and horizontal, peripherally located perpendicular to pleura. Black arrowheads in following image are kerley b lines, white arrows are septal lines

Image 10: http://www.radpod.org/2007/03/02/acute-pulmonary-oedema/ Reference: Chapman S, Nakielny R. Aids to Radiological Differential Diagnosis 4th edition. Saunders 2003 Credit: Dr Laughlin Dawes

• Alveolar edema – batwing appearance

The Breathing Not Properly study found BNP (brain natriuretic protein) to be 90% sensitive and 76% specific for the diagnosis of CHF. Release is stimulated by high ventricular filling pressures. It has a diuretic effect, and antihypertensive effect, by increasing the amount of sodium excreted in the urine.

• <100pg/ml: unlikely CHF
• 100-500pg/ml: potentially CHF, although could also be PE, pulmonary HTN, ESRD, cirrhosis, or hormone replacement therapy
• >500pg/ml: most likely CHF

BNP levels may be most useful in tracking acute disease severity when compared to previously known levels. BNP levels may not always correlate with suspicion for CHF exacerbation, however, and clinical judgment should be used to further evaluate these patients.

Other Laboratories

• CBC to check for anemia
• Electrolytes: Na, K, Mg for abnormalities due to fluid overload or renal insufficiency
• Creatinine to check for renal dysfunction
• Troponin I or T to check for acute ischemic event.

May show underlying cardiac ischemia, dysrhythmias, LVH or heart block. A normal ECG has a high negative predictive value for systolic dysfunction.

Echocardiogram with Ejection Fraction

Normal ejection fraction is 55-75%. Patients with severe CHF may have EF less than 20%. Echocardiogram can also be used to visualize ventricular size and any wall abnormalities or valvular pathology, pericardial thickening, tamponade or constrictive pericarditis as additional contributors to CHF.

ED Treatment

In addition to initial actions noted above, treatment depends upon clinical presentation.

Normotensive patients: First give rapid acting nitrates to vasodilate and reduce afterload. These may be given sublingual, IV, or transdermal as nitroglycerin tabs/spray, push/gtt, paste/patch respectively. IV Morphine can be given for chest pain and anxiety, and may increase vasodilation. IV diuretics, such as furosemide, can increase urine output, lessening fluid overload, and may also contribute to vasodilatory effects.

Hypertensive patients: If high dose nitrates fail to control the blood pressure, some experts suggest adding Nitroprusside IV drip for severe, persistent hypertension. Nitroglycerin will have more effect as a venous dilator than arterial dilator. Nitroprusside is a more balanced venous and arterial dilator.

Hypotensive patients: Avoid nitrates, furosemide, and morphine, as they will drop the blood pressure. BiPAP may have similar adverse effect due to decreased preload as intra-thoracic pressure rises. Increased myocardial contractility with norepinephrine, dopamine, dobutamine, amrinone or milrinone may improve vital sign parameters so that some of the other therapies may be used. 

Severe or Chronic low output CHF:  Patients may be on ACE inhibitors or ARB to increase hemodynamic stability and exercise capability. If blood pressure allows, consider continuing this medication. If not already on ACEi or ARB, evidence does not support use in acute exacerbations.

Surgical Therapies

As a patient’s CHF becomes more advanced, they may need an Automatic Internal Cardiac Defibrillator (AICD), Left Ventricular Assistance Device (LVAD), or heart transplant.

AICD placement

MADIT trial showed that in patients with previous MI, EF < 35%, non-sustained ventricular tachycardia, and inducible ventricular tachycardia unresponsive to procainamide, AICD placement reduced sudden death by 54% at 2 yrs.

MADIT II trial showed that patients with history of MI and EF <30% had a 29% reduction in mortality after AICD placement.

LVAD placement

Patients may receive an LVAD as a temporizing measure until a heart transplant can be performed, or as a definitive treatment alone, if not a transplant candidate. The REMATCH study showed that patients had increased quality of life and had a 52% rate of survival at one year, compared to 25% for medical management only.

Heart transplant

Heart transplant is the only long-term definitive treatment for congestive heart failure. Patients who receive a heart transplant have a 10-year survival rate of 50%.

Pearls and Pitfalls

• Acute exacerbations of CHF can rapidly progress over hours to days, commonly due to a precipitating event, leaving the patient with no reserve to compensate for increased burden on the heart.
• The precipitating event may be an MI! Check an ECG and troponins.
• CXR findings may lag by 12 hrs. Treat clinical symptoms, and use PoCUS of the heart and lungs if available. 
• Most common CXR findings are cardiomegaly and effusions.
• Start with 100% O2 on NRB mask, but use noninvasive CPAP or BiPAP early for increased work of breathing, or intubate when necessary.
• Elevating the head of bed will reduce venous return and decrease preload and improve patient symptoms. In a small group of stable patients who are cognitively intact, placing the legs over the side of the bed may also be helpful in achieving the same physiologic outcomes mentioned previously.
• AVOID nitrates, morphine, and diuretics in hypotensive patients, and be careful with BiPAP these interventions may have a negative effect on blood pressure.
• Patients who present with new heart failure will require thorough inpatient workup to determine if it is a result of ischemic or non-ischemic disease. 

Case Study, conclusion

Your patient was started on BiPAP, received three nitro sprays sublingually, and a nitroglycerin drip was started at 4ug/min IV and was titrated to a systolic blood pressure of 130 mm Hg. She received furosemide 40mg IV and the nurses documented a diuresis of 1500 ml of urine in the next two hours. Her troponin I was normal range, as was her CBC, and CHEM 7. Her BNP was elevated to 1020 pg/ml.  She was monitored on a cardiac monitor until she was transferred to the hospital cardiac step down unit where she was weaned off of BiPAP, transitioned to oral furosemide, had her low salt diet reinstated, and was transferred to a general floor bed. She was discharged on hospital day 4 on furosemide, an ACE inhibitor, a low salt diet, and outpatient follow up with her primary care provider in one week.

• American Heart Association. Classes of heart failure. Available at:  http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp . Accessed: Mar 16, 2016.
• Collins, S.P., Storrow, A.B. Chapter 53: Acute Heart Failure. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Online@ Access Medicine. McGraw-Hill Medical
• PMID: 12135939, McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. Jul 23 2002;106(4):416-22.
• PMID: 16234501, Wang CS, FitzGerald JM, Schulzer M, et al: Does this dyspneic patient in the emergency department have congestive heart failure?. JAMA 2005; 294:1944.
• PMID: 18614781, Gray, A, Goodacre, S, et al. Noninvasive ventilationin acute cardiogenic pulmonary edema. N Engl J Med 2008; 359: 142-151. 
• PMID: 8960472, Moss AJ, Hall WJ, Cannom DS, et: Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996; 335:1933.
• PMID: 11794191, Rose EA, Gelijns AC, Moskowitz AJ, et al: Long-Term Use of a Left Ventricular Assist Device for End-Stage Heart Failure. N Engl J Med 2001; 345:1435-1443.
• PMID: 16387212, Collins SP, Lindsell CJ, Storrow AB et al: Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann Emerg Med. Jan 2006;47(1):13-8.
• PMID: 11911755, Publication Committee for the VMAC Investigators : Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: A randomized controlled trial. JAMA 2002; 287:1531.
• PMID: 18403664, Lichtenstein,D. Meziere, G. Relevance of Lung Ultrasound in the diagnosis of respiratory failure. Chest, 134 (1) (2008), pp. 117-125.
• PMID: 8376698, Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct. 22(4 Suppl A):6A-13A.
• PMID: 30266198, Long B, Koyfman A, Gottlieb M. Management of Heart Failure in the Emergency Department Setting: An Evidence-Based Review of the Literature. J Emerg Med, 55(5), 2018, 635-646.Congestive Heart Failure (CHF) 

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Introduction, case presentation.

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Clinical case: heart failure and ischaemic heart disease

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Giuseppe M C Rosano, Clinical case: heart failure and ischaemic heart disease, European Heart Journal Supplements , Volume 21, Issue Supplement_C, April 2019, Pages C42–C44, https://doi.org/10.1093/eurheartj/suz046

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Patients with ischaemic heart disease that develop heart failure should be treated as per appropriate European Society of Cardiology/Heart Failure Association (ESC/HFA) guidelines.

Glucose control in diabetic patients with heart failure should be more lenient that in patients without cardiovascular disease.

Optimization of cardiac metabolism and control of heart rate should be a priority for the treatment of angina in patients with heart failure of ischaemic origin.

This clinical case refers to an 83-year-old man with moderate chronic obstructive pulmonary disease and shows that implementation of appropriate medical therapy according to the European Society of Cardiology/Heart Failure Association (ESC/HFA) guidelines improves symptoms and quality of life. 1 The case also illustrates that optimization of glucose metabolism with a more lenient glucose control was most probably important in improving the overall clinical status and functional capacity.

The patient has family history of coronary artery disease as his brother had suffered an acute myocardial infarction (AMI) at the age of 64 and his sister had received coronary artery by-pass. He also has a 14-year diagnosis of arterial hypertension, and he is diabetic on oral glucose-lowering agents since 12 years. He smokes 30 cigarettes per day since childhood.

In February 2009, after 2 weeks of angina for moderate efforts, he suffered an acute anterior myocardial infarction. He presented late (after 14 h since symptom onset) at the hospital where he had been treated conservatively and had been discharged on medical therapy: Atenolol 50 mg o.d., Amlodipine 2.5 mg o.d., Aspirin 100 mg o.d., Atorvastatin 20 mg o.d., Metformin 500 mg tds, Gliclazide 30 mg o.d., Salmeterol 50, and Fluticasone 500 mg oral inhalers.

Four weeks after discharge, he underwent a planned electrocardiogram (ECG) stress test that documented silent effort-induced ST-segment depression (1.5 mm in V4–V6) at 50 W.

He underwent a coronary angiography (June 2009) and left ventriculography that showed a not dilated left ventricle with apical dyskinesia, normal left ventricular ejection fraction (LVEF, 52%); occlusion of proximal LAD, 60% stenosis of circumflex (CX), and 60% stenosis of distal right coronary artery (RCA). An attempt to cross the occluded left anterior descending (LAD) was unsuccessful.

He was therefore discharged on medical therapy with: Atenolol 50 mg o.d., Atorvastatin 20 mg o.d., Amlodipine 2.5 mg o.d., Perindopril 4 mg o.d., oral isosorbide mono-nitrate (ISMN) 60 mg o.d., Aspirin 100 mg o.d., metformin 850 mg tds, Gliclazide 30 mg o.d., Salmeterol 50 mcg, and Fluticasone 500 mcg b.i.d. oral inhalers.

He had been well for a few months but in March 2010 he started to complain of retrosternal constriction associated to dyspnoea for moderate efforts (New York Heart Association (NYHA) II–III, Canadian Class II).

For this reason, he was prescribed a second coronary angiography that showed progression of atherosclerosis with 80% stenosis on the circumflex (after the I obtuse marginal branch) and distal RCA. The LAD was still occluded.

After consultation with the heart team, CABG was avoided because surgical the risk was deemed too high and the patient underwent palliative percutaneous coronary intervention (PCI) of CX and RCA. It was again attempted to cross the occlusion on the LAD. But this attempt was, again, unsuccessful. Collateral circulation from posterior interventricular artery (PDL) to the LAD was found. The pre-PCI echocardiogram documented moderate left ventricular dysfunction (EF 38%), the pre-discharge echocardiogram documented a LVEF of 34%. Because of the reduced LVEF, atenolol was changed for Bisoprolol (5 mg o.d.).

At follow-up visit in December 2012, the clinical status and the haemodynamic conditions had deteriorated. He complained of worsening effort-induced dyspnoea/angina that now occurred for less than a flight of stairs (NYHA III). On clinical examination clear signs of worsening heart failure were detected ( Table  1 ). His medical therapy was modified to: Bisoprolol 5 mg o.d., Atorvastatin 20 mg o.d., Amlodipine 2.5 mg o.d., Perindopil 5 mg o.d., ISMN 60 mg o.d., Aspirin 100 mg o.d., Metformin 500 mg tds, Furosemide 50 mg o.d., Gliclazide 30 mg o.d., Salmeterol 50 mcg oral inhaler, and Fluticasone 500 mcg oral inhaler. A stress perfusion cardiac scintigraphy was requested and revealed dilated ventricles with LVEF 19%, fixed apical perfusion defect and reversible perfusion defect of the antero-septal wall (ischaemic burden <10%, Figure  1 ). He was admitted, and an ICD was implanted.

Clinical parameters during follow-up visits

Myocardial perfusion scintigraphy and left ventriculography showing dilated left ventricle with left ventricular ejection fraction 19%. Reversible perfusion defects on the antero-septal wall and fixed apical perfusion defect.

In March 2013, he felt slightly better but still complained of effort-induced dyspnoea/angina (NYHA III, Table  1 ). Medical therapy was updated with bisoprolol changed with Nebivolol 5 mg o.d. and perindopril changed to Enalapril 10 mg b.i.d. The switch from bisoprolol to nebivolol was undertaken because of the better tolerability and outcome data with nebivolol in elderly patients with heart failure. Perindopril was switched to enalapril because the first one has no indication for the treatment of heart failure.

In September 2013, the clinical conditions were unchanged, he still complained of effort-induced dyspnoea/angina (NYHA III) and did not notice any change in his exercise capacity. His BNP was 1670. He was referred for a 3-month cycle of cardiac rehabilitation during which his medical therapy was changed to: Nebivolol 5 mg o.d., Ivabradine 5 mg b.i.d., uptitrated in October to 7.5 b.i.d., Trimetazidine 20 mg tds, Furosemide 50 mg, Metolazone 5 mg o.d., K-canrenoate 50 mg, Enalapril 10 mg b.i.d., Clopidogrel 75 mg o.d., Atorvastatin 40 mg o.d., Metformin 500 mg b.i.d., Salmeterol 50 mcg oral inhaler, and Fluticasone 500 mcg oral inhaler.

At the follow-up visit in January 2014, he felt much better and had symptomatically, he no longer complained of angina, nor dyspnoea (NYHA Class II, Table  1 ). Trimetazidine was added because of its benefits in heart failure patients of ischaemic origin and because of its effect on functional capacity. Ivabradine was added to reduce heart rate since it was felt that increasing nebivolol, that was already titrated to an effective dose, would have had led to hypotension.

He missed his follow-up visits in June and October 2014 because he was feeling well and he had decided to spend some time at his house in the south of Italy. In January and June 2015, he was well, asymptomatic (NYHA I–II) and able to attend his daily activities. He did not complain of angina nor dyspnoea and reported no limitations in his daily activities. Unfortunately, in November 2015 he was hit by a moped while on the zebra crossing in Rome and he later died in hospital as a consequence of the trauma.

This case highlights the need of optimizing both the heart failure and the anti-anginal medications in patients with heart failure of ischaemic origin. This patient has improved dramatically after the up-titration of diuretics, the control of heart rate with nebivolol and ivabradine and the additional use of trimetazidine. 1–3 All these drugs have contributed to improve the clinical status together with a more lenient control of glucose metabolism. 4 This is another crucial point to take into account in diabetic patients, especially if elderly, with heart failure in whom aggressive glucose control is detrimental for their functional capacity and long-term prognosis. 5

IRCCS San Raffaele - Ricerca corrente Ministero della Salute 2018.

Conflict of interest : none declared. The authors didn’t receive any financial support in terms of honorarium by Servier for the supplement articles.

Ponikowski P , Voors AA , Anker SD , Bueno H , Cleland JG , Coats AJ , Falk V , González-Juanatey JR , Harjola VP , Jankowska EA , Jessup M , Linde C , Nihoyannopoulos P , Parissis JT , Pieske B , Riley JP , Rosano GM , Ruilope LM , Ruschitzka F , Rutten FH , van der Meer P ; Authors/Task Force Members. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) Developed with the Special Contribution of the Heart Failure Association (HFA) of the ESC . Eur J Heart Fail 2016 ; 18 : 891 – 975 .

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Rosano GM , Vitale C. Metabolic modulation of cardiac metabolism in heart failure . Card Fail Rev 2018 ; 4 : 99 – 103 .

Vitale C , Ilaria S , Rosano GM. Pharmacological interventions effective in improving exercise capacity in heart failure . Card Fail Rev 2018 ; 4 : 1 – 27 .

Seferović PM , Petrie MC , Filippatos GS , Anker SD , Rosano G , Bauersachs J , Paulus WJ , Komajda M , Cosentino F , de Boer RA , Farmakis D , Doehner W , Lambrinou E , Lopatin Y , Piepoli MF , Theodorakis MJ , Wiggers H , Lekakis J , Mebazaa A , Mamas MA , Tschöpe C , Hoes AW , Seferović JP , Logue J , McDonagh T , Riley JP , Milinković I , Polovina M , van Veldhuisen DJ , Lainscak M , Maggioni AP , Ruschitzka F , McMurray JJV. Type 2 diabetes mellitus and heart failure: a position statement from the Heart Failure Association of the European Society of Cardiology . Eur J Heart Fail 2018 ; 20 : 853 – 872 .

Vitale C , Spoletini I , Rosano GM. Frailty in heart failure: implications for management . Card Fail Rev 2018 ; 4 : 104 – 106 .

• myocardial ischemia
• cardiac rehabilitation
• heart failure
• older adult

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Heart Failure A Case Study

Oct 29, 2019

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HMD 570 Summer 2014 Final Project Presented by Angela Wolfenberger. Heart Failure A Case Study. Heart Failure Introduction. Definition, Etiology, and Diagnosis Symptoms Risk Factors and Public Health Implications Complicating Factors Nutritional Significances Treatment Algorithm.

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Heart failure.

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HMD 570 Summer 2014 Final Project Presented by Angela Wolfenberger Heart FailureA Case Study

Heart Failure Introduction • Definition, Etiology, and Diagnosis • Symptoms • Risk Factors and Public Health Implications • Complicating Factors • Nutritional Significances • Treatment Algorithm

Heart Failure: Definition Heart Failure (HF) is a chronic, progressive, clinical syndrome wherein the pumping action of the heart is insufficient to meet the metabolic demands of the body. The heart muscle enlarges, stiffens, and weakens, resulting in inefficient filling and pumping. Blood flow is reduced, causing Insufficient perfusion of organs and extremities. Congestive Heart Failure (CHF) is a type of HF with pulmonary and peripheral (abdominal, leg/ankle) edema. CHF and HF are often used interchangeably.

Heart Failure: Definition, cont’d 2 Types of Heart Failure: Diastolic- The heart cannot fill properly during the rest period; preserved Ejection Fraction (EF) Systolic- The weakened ventricle cannot squeeze hard enough to pump fluid properly; Decreased EF Heart Failure generally results in: • Cardiomegaly (enlarged heart) • Increased Heart Rate • Vasoconstriction as the body attempts to compensatefor the weakened heart tissue

Heart Failure: Definition- Stages Stage Definition Stage AEvidence of heart failure risk factors; no heart disease, asymptomatic Stage B Heart disease present (structural changes); asymptomatic Stage C Structural heart disease evident;symptoms present Stage DAdvanced heart disease; progressive HF
 symptoms require aggressive medical therapy Source: The American College of Cardiology and the American Heart Association Stages of Heart Failure

Heart Failure: Etiology What Causes Heart Failure? • Coronary Artery Disease (CAD)- Arteries narrow, decreasing blood flow to heart • Myocardial Infarct (Heart attack)- One or more blocked coronary arteries, heart muscle becomes damaged (cardiomyopathy) • Hypertension(HTN)- High blood pressure weakens heart muscle over time • Abnormal Heart Valves- Valves that don’t open/close properly disrupt blood flow through heart, causing muscle to work harder • Arrhythmias- Abnormal heart rhythms or fibrillations damage heart muscle • Heart Defects- Abnormal heart structure can reduce muscle function • Pulmonary Disease- Fluid in lungs causes pulmonary hypertension, resulting in enlarged left ventricle • Diabetes Mellitus (DM I or II)- High blood sugar weakens the heart muscle • Hypothyroidism- Low thyroid activity increases LDL cholesterol and atherosclerosis • Drugs (ex. Cocaine, alcohol, etc.)-Dugs have various negative effects on the heart muscle

Heart Failure: Diagnosis • How is Heart Failure diagnosed? • Elevated Brain Natriuretic Peptide (BNP) Blood Levels • Dyspnea-Shortness of breath • Cheyne-Stokes Respiration- Periodic breaths • S3 Gallup- Extra heart sounds • Echocardiogram • Ventricular Ejection Fraction (LVEF) <45% • Chest X-ray- Showing Cardiomegaly • Edema-Peripheral (legs/ankles/feet), Abdominal, and Pulmonary • Rales- Fluid sounds in lungs, wheezing, coughing • Hepatomegaly- Fluid retention causes liver swelling • Stasis Dermatitis-Peripheral swelling causes epidermal tissue breakdown *No single test can diagnose heart failure

Heart Failure: Symptoms • What are the Symptoms of HF? • Dyspnea (shortness of breath), especially when supine • Edema (swelling of ankles/legs/feet, abdomen, lungs) • Fatigue • Cough (dry, hacking, unproductive) • Nausea, anorexia • Syncope • Sudden weight gain (>3 lbs./day or 5 lbs./week) • Angina • Elevated heart rate and/or blood pressure • Anxiety, confusion, decreased alertness • Nocturia (need to urinate at night)

Heart Failure Symptoms, cont’d

Heart Failure: Symptoms, cont’d • Stages of HF: • NYHA Class I: Asymptomatic; patient is not short of breath or fatigued with any activity • NYHA Class II: Patient is short of breath or fatigued after moderate activity (such as climbing two flights of stairs, golfing nine holes, or carrying a load of wash up from the basement) • NYHA Class III: Patient is short of breath or fatigued even after very mild exertion (such as walking around the house or up half a flight of stairs) • NYHA Class IV: Patient is exhausted, short of breath, or fatigued at rest (just sitting still or lying in bed). • New York Heart Association Functional Classification (NYHA)

Heart Failure: Risk Factors • CAD (75% of HF is caused by CAD) • HTN (2nd leading cause of HF) • Myocardial Infarct • Diabetes Mellitus (DM I or II) • Some diabetes medications • rosiglitazone [Avandia] • pioglitazone [Actos] • Sleep Apnea- Improper breathing while asleep decrease blood oxygen levels and increases risk of abnormal heart rhythms. • Congenital heart defects, Arrhythmias • Viruses- Someviral infections damage heart muscle. • Alcohol/Drug Use

Heart Failure: Public Health Implications • 5.8 Million Americans suffer from HF • 2.8% of the general population (2010), • Will rise to 3.5% by 2030 • 10% of people >65 years old (2010) • 1 in 5 adults over 40 will suffer from HF in their lifetime • 400,000+ new cases of HF each year in the US • 1 in 5 HF patients die in 1 year, 50% die within 5 years • Major HF risk factors are rising each year: • Diabetes • Obesity • Aging Population • HF costs $24.7 Billion per year (2010), and is projected to escalate to $77.7 Billion by 2030

Heart Failure: Complicating Factors • Kidney Damage/Failure-HF reduces blood flow to kidneys, which can cause kidney failure. Some HF medications can cause kidney damage. • Heart Valve Damage- Valves may not function properly if heart is enlarged, or if the pressure inside the heart is very high. • Liver Damage-HF can cause abdominal edema, putting pressure on the liver, causing scarring. • Stroke-Blood flow in HF through the heart is slower than normal, making blood clots more likely.

Heart Failure: Nutritional Significance • Restrict Sodium Intake to <2000mg/day (about 1 teaspoon) • Sodium causes fluid retention and increased blood pressure • Restrict Fat Intake, Especially Saturated Fats (if hyperlipidemia is involved) • 30% of daily Kcal should come from fats, >10% from Sat fats • Modify Fluid Intake- • Restrict fluids to <1.5 Liters, because of fluid retention/edema • Consume Adequate Protein • 1.12-1.37g protein/kg of weight per day may be necessary to prevent cachexia (wasting) in HF • Micronutrients- Some HF medications cause accumulation or depletion of essential minerals like K, Mg, and/or Ca • Taking a daily Multi-vitamin/Multi-mineral supplement may ameliorate the effect of medications

Heart Failure: Drug Therapy Algorithm

Heart Failure Case Study:Joseph Himm • Patient Information • Patient History • Symptoms • Risk Factors • Diet (24-hour Recall) • Lab Values

HF Case Study:Joseph Himm, Patient Information • Age: 79 years • Height: 65” • Weight: 209 lbs. • BMI: 34.8, obese (class I) • Normal weight range (BMI 18.5—24.9) is 110 to 149 lbs. • Blood Pressure: 119/71 mmHg (without medication: 220/170 mmHg or higher) • Pulse: 60 bpm • LVEF: 27% (normal=55-70%, HF<45%) • Diagnosis: NYHA Class III Heart Failure • Medications: Lasix (120mg/d), Nitroglycerin (.4mg/prn), Carvedilol (25mg/d), Allopurinol (300mg/d), Ramipril (5 mg/d), Plavix (75 mg/d), Isocitrate (90 mg/d) • Caucasian • Physical Activity: No exercise tolerance

HF Case Study: Joseph Himm, Patient History Mr. Himm was diagnosed with HTN in 1972, and has taken medication to control his blood pressure since that time. Mr. Himm suffered an MI in 1982, and another in 1994. He also suffered a CVA (stroke) in 1997, and another in 1999. He has suffered many TIAs (transient ischemic attacks). Mr. Himm had coronary bypass surgery (CABG) with 4 bypasses, (5th blockage could not be bypassed) in 2002, with Carotid Endarterectomy (CEA) at the same time. He had an Implantable Cardioverter Defibrillator (ICD) implanted in 2012. He has had multiple heart catheterizations over the years. Mr. Himm was an athlete in his youth, but has led a sedentary lifestyle for the last 45 years. Mr. Himm was counseled about the DASH diet (Dietary Approaches to Stop Hypertension) by his cardiologist upon his initial HTN diagnosis. He stopped cooking with added salt and adding salt to cooked foods at that time (as did his wife). His diet is otherwise uncontrolled, and he has weighed in excess of 200 lbs. for 15+years. Mr. Himm has difficulty with ADLs (dressing, shaving) because of CVA damage, so he leaves the house infrequently. He sits and watches television for the large part of each day. He also does not like to leave the house because of urinary incontinence fears from his Lasix (diuretic). Mr. Himm has had difficulty sleeping for many years, and takes naps throughout the day and night. He does not sleep for more than 2-3 hours at a time. Mr. Himm’s father died of MI in 1945, at age 45 years.

HF Case Study: Joseph Himm,Symptoms • Angina upon rising and with any effort (stairs, walking, lifting, etc.) • Dyspnea with any physical activity (limits activity due to dyspnea and angina) • Edema in legs, ankles, feet, and abdomen • Stasis Dermatitis in lower legs • Nocturia (2x/night) • Bradycardia (pacemaker controlled) • Memory and Speech deficit, occasional confusion, and anxiety • Bowel Movements loose, 3-4x/day • Sleep Apnea

HF Case Study: Joseph Himm,Risk Factors • Age- Mr. Himm’s HF risk is exacerbated by his advanced age (79 years). 8% of men in this age group have HF. • Obesity- Mr. Himm’s BMI is 34.8. Some of his weight can be attributed to water retention, but his wife states that his weight does not decrease more than 2-3 pounds when he takes Lasix. • Unhealthy diet- Mr. Himm consumes many processed foods at meals and snacks, which have high saturated fat and salt content. He consumes few vegetable-especially green leafy vegetables. He consumes too little fiber. • Genetic Predisposition- Mr. Himm’s father died at age 45 from CVD (cardiovascular disease). • Anxiety- Mr. Himm suffers from anxiety and mental confusion. The stress puts significant strain on his heart, and he occasionally forgets to take his medications. • LVEF- Mr. Himm is in danger of sudden cardiac death from ventricular fibrillation due to his low ejection fraction (27%).

HF Case Study: Joseph Himm,Diet- 24 Hour Recall

HF Case Study: Joseph Himm, Diet- 24 Hour Recall, cont’d Analysis

HF Case Study: Joseph Himm, Diet- 24 Hour Recall, cont’d Analysis, cont’d • Kcal- 2161 Empty Calories- 839 Kcal • Sat Fat- 66g (limit 22g) PRO- 84g (AI for HF 75.68g) • CHO- 215g (AI 100g) • Fiber- 16g (target 25g) • Ca- 1283mg (RDA 1200mg) Vit. C -43mg (RDA 90mg) • K-2035mg (AI 4700mg) Vit. D-15ug (RDA 20ug) • Mg-252mg (RDA 420mg) Vit. K- 43ug (AI 120ug) • Na- 2475mg (AI 1200mg)Vit. E- 8mg (RDA15mg) Mr. Himm consumed adequate amounts of other vitamins and minerals

HF Case Study: Joseph Himm,Significant Lab Values

EAL: Guidelines and Supporting Evidence Relevance to Mr. Himm

EAL Guidelines

EAL Guidelines Mr. Himm has adequate blood levels of Mg, Ca, and K, so the correlating guidelines do not apply at this time. His blood chemistry should be monitored and guidelines Implemented as necessary (if serum levels fall). Mr. Himm does not consume alcohol, so the corresponding guideline does not apply. Mr. Himm does not like taking a lot of pills, So additional bionutrient therapy (per guidelines) is not supported at this time.

Nutrition Care ProcessSubjectiveObjectiveAssessmentPlan Joseph Himm

SOAP: Joseph Himm • S: Mr. Himm reports long Hx of HTN, and CAD, with multiple coronary artery bypass, carotid endarterectomy, 2 MIs and 3 CVAs. Patient suffers dyspnea with walking, stairs, lifting, etc. Patient consume high fat, high energy, high salt diet (per 24-hour recall). He reports taking his medications sporadically in the past, but regularly now that he feels poorly (fatigue, angina, edema, dyspnea). Patient has been obese for approx. 15 years and tolerates no physical activity. Patient suffers anxiety, periodic mental confusion, slow speech, and muscle weakness (from previous CVAs). Father died at age 45 of MI (1945). • O:Age: 79 years, Ht: 65” Wt.: 209# BMI: 34.8 BMI Class: Obese, Class I Dx: Cardiomyopathy (425.1), Edema (782.3), Stable Angina (412.9), Carotid Stenosis (433.1), Heart Failure (428.0) BP (unmedicated): 220/170, BP (medicated): 119/71 Pulse: 60 (with pacemaker working 3-7%). Medications: Lasix (120mg/d), Nitroglycerin (.4mg/prn), Carvedilol (25mg/d), Allopurinol (300mg/d), Ramipril (5 mg/d), Plavix (75 mg/d), Isocitrate (90 mg/d)

SOAP, cont’d: Joseph Himm • A:NI-1.3 Excessive Energy Intake related to Kcal/ fat/CHO consumption above TEE as evidenced by BMI of 34.8 (obese, class I) and 24 hour diet recall NB-2.1 Physical Inactivity related to sedentary lifestyle and heart failure as evidenced by exercise intolerance, excessive TV. watching, and obese BMI. NB-1.1 Food-and Nutrition-Related Knowledge Deficit related to excessive in take of saturated fat and salt as evidenced by24-hour food recall, edema, and adiposity whilst claiming to follow a DASH dietary pattern. • P: Intervention ND-1 Meals and Snacks.Pt. to follow DASH dietary pattern to decrease salt and saturated fat intake and increase fruit and vegetable intake. Pt. to receive printout of DASH guidelines to post in kitchen E-1 Nutrition Education.Pt. will learn to read labels to avoid processed foods with high salt and saturated fat content. Use cognitive behavior theory to instruct Pt. to prepare and include fruits and vegetables in meals and snacks Monitor/Evaluate: F-1.1 Energy Intake. Pt. will keep food log. BE-1.1 Beliefs/Attitudes. Monitor actual fat/salt/energy/vegetable intake vs. Pt. perceived intake S-1.4 Weight/Weight ChangeFollow up with Pt. weight/BMI S2.3Creatinine. Monitor Pt. Lab Values to ensure diet maximizes HF/renal outcomes.

Treatment Plan: Joseph Himm After our initial 45-minute consultation, Mr. Himm will embark on a lifestyle modification plan to include healthy eating (and keeping a food diary), body weight/BMI reduction and increased Physical Activity. Dietary changes will include: (5-10 servings/day) of fruits and vegetables (emphasis on variety and color), daily multivitamin to maintain to comply with recommendation for Folate, Thiamin, B6, B12, Ca, Mg, and Potassium (K). Lab values will be monitored on subsequent visits to ensure adequate intake. Diet will consist of low-Na, Low-fat DASH style dietary pattern to lower BP and ameliorate HTN, lower edema, and maintain cardiovascular integrity. The diet will include 1.12g/kg/day of Protein, <30% Fat with <10% Sat Fat,<100-130g CHO, <2000mg Na, and <1.4-1.9L of fluids. Fiber levels will be monitored and adjusted as necessary due to Mr. Himm’s report of frequent, loose stools. Mr. Himm’s therapeutic prescriptions and lab values will be monitored to ensure no or food/nutrient-drug interactions. For example, Mr. Himm’s diuretics lower serum Potassium while his ACE-inhibitors raise serum Potassium levels. Kcal content of food will be adjusted and monitored to support weight loss while conserving muscle and preserving body composition as indicated for HF. I will suggest that Mr. Himm attempt to decrease TV. watching while increasing physical activity as recommended by his physician for his ability. I will schedule at least 3 monthly 30 minute follow-up visits to evaluate Mr. Himm’s food/nutrient intake based on his Food Diary, and lab values (to include Creatinine/BUN, eGFR, serum mineral levels, serum lipids, glucose, etc.), and to monitor and support his continued healthy diet and physically active lifestyle.

Sample Menu: Joseph Himm

EAL: Lessons Learned I have thoroughly enjoyed becoming familiar with the Evidence Analysis Library this Semester. I love to research topics of interest, especially in nutrition and preventive medicine. The EAL is a handy reference for current knowledge about common health conditions and their nutrition implications. I now feel comfortable looking up guidelines for dietary treatments, and feel confident that the material that I am reading comes from thoughtful analysis of peer-reviewed literature. I especially appreciate the information about the quality and amount of research behind each guideline, together with the ratings and grades. I also feel that the knowledge I glean from the EAL will help me with interview questions when I apply for internships next year. The EAL also helps the practitioner understand the importance of motivational interviewing. There were many guidelines for Heart Failure that I was unsure whether they were applicable until I spoke at length with the subject (Mr. Himm). I asked him questions, then I read through the EAL guidelines, and I thought of many more questions to ask. This helped me gain a far deeper understanding of his diagnosis, symptoms, etc. The news media is filled with “sound bytes” and fad diet “factoids” with little, if any, scientific basis. The EAL helps me separate fact from fiction quickly and efficiently, which will not only be of great use in my future practice, but is very informative for me as a dietetics student, since I constantly field questions from friends and family concerning nutrition “information” in the media. Finally, I am studying dietetics as a second career. I am am following my passion while, hopefully, contributing to society. My first career has provided me with enough disposable income that I can pursue whatever field of dietetics I desire without worrying about supporting my family with the income. I think that I would enjoy participating in the analysis for future EAL topics, as I love scouring peer-reviewed articles for information about interesting topics. What an exciting way to contribute to the future of the profession!

Bibliography: • Academy of Nutrition and Dietetics Evidence Analysis Library. (2008). Heart Failure Guideline. Retrieved July 24, 2014 from http://www.andeal.org/topic.cfm?menu=5289&cat=3249 • Academy of Nutrition and Dietetics Evidence Analysis Library. (2008). Hypertension Guideline. Retrieved July 27, 2014 from http://andevidencelibrary.com/topic.cfm?cat=3248 • American Heart Association (2014). Heart Failure, Retrieved July 24 from http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/About-Heart-Failure_UCM_002044_Article.jsp • Amirkalali, B., Hosseini, S., Heshmat, R., & Larijani, B. (2008). Comparison of harris benedict and Mifflin-ST Jeor equations with indirect calorimetry in evaluating resting energy expenditure. Indian journal of medical sciences, 62, 283. doi: 10.4103/0019-5359.42024 • Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., IzzoJr, J. L., ... & National High Blood Pressure Education Program Coordinating Committee. (2003). The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report. Jama, 289, 2560-2571. doi:10.1001/jama.289.19.2560 • Institute of Medicine (2014). Dietary Reference Intakes,, Retrieved July 28, 2014 from http://www.iom.edu/Activities/Nutrition/SummaryDRIs/~/media/Files/Activity%20Files/ Nutrition/DRIs/5_Summary%20Table%20Tables%201-4.pdf • Mayo Clinic (2014). Heart Failure, Retrieved July 24, 2014 from http://www.mayoclinic.org/diseases-conditions/heart-failure/basics/definition/con-20029801. • National Heart, Lung, and Blood Institute (2014). Heart Failure. Retrieved July 24, 2014 from http://www.nhlbi.nih.gov/health/health-topics/topics/hf/ • Shamsham, F., & Mitchell, J. (2000). Essentials of the diagnosis of heart failure. American Family Physician, 61(5), 1319-1330. • USDA (2014). SuperTracker. Retrieved July 28, 2014 from https://www.supertracker.usda.gov/foodtracker.aspx

Addendum: Patient Education Materials: Allegheny Gen’l Hospital, Pittsburgh, PA.

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Heart Failure

Definition:. A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the bodyIt is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent . Etiology. It is a common end point for many d

1.81k views • 44 slides

Heart Failure. Susan Schayes, MD, MPH Program Director Emory Family Medicine Residency Program Adapted from Dr. Joel Felner and Dr. Eddie Needham. Objectives. Define Heart Failure Know the 5 year mortality rate for heart failure

3.29k views • 120 slides

Heart Failure. Jerri Lamar. Learning Objectives. Understand classification of heart failure, along with the signs and symptoms. Identify heart failure stages for the development of diagnosis, intervention and patient-centered goals. Definitions.

722 views • 18 slides

A french heart failure management program : A comparative study

F Dany,P Virot,C Daragon,F Dalmay,PM Preux and all Icarlim network members. A french heart failure management program : A comparative study . BACKROUND *Multidisciplinary systems for Heart Failure pts : grade A recommendations (ESC 2010) *Systems heterogeneity...

230 views • 11 slides

Steering Failure Case Study

Steering Failure Case Study. MS Basel Australia. At about 0937 [ on 1 November 2010, the Liberian container ship MSC Basel grounded in Moreton Bay, while departing the port of Brisbane.

344 views • 15 slides

Heart Failure. Research By: Dr. Ritta Baena Visual Effects By: John Baena. The Function of the Heart. The heart is a pump that pumps blood to the whole body. The heart is divided into a right side and left side.

1.6k views • 20 slides

Lori Baker, RN BSN. Cardiovascular Disorders. Heart Failure. TERMS. Cardiac Output Heart rate x stroke volume That is, amount of volume with each beat multiplied by the number of beats 5L/min Compensatory mechanisms. Compensatory Mechanisms.

490 views • 19 slides

HEART FAILURE

HEART FAILURE. TEAM MEMBERSHIP CARDIOLOGY, CARDIOVASCULAR SURGERY, MEDICINE, NURSING, QRM, CCE, MEDICAL RECORDS PROJECT COORDINATORS CARMEN BARC, RN, BSN CAROL KEELER, RN, MS.

425 views • 15 slides

Heart Failure. Objectives . Describe congestive heart failure Explain the pathophysiology of congestive heart failure Describe nursing interventions in caring for clients with congestive heart failure. Heart Failure.

818 views • 25 slides

Case Study Congestive Heart Failure

Case Study Congestive Heart Failure. By: Ellinor Lagerberg. Reason for study. Gain knowledge about CHF (congestive heart failure) and its etiology. To understand how nutrition education is applied in acute care for patients with CHF.

7.14k views • 36 slides

Congestive Heart Failure Case Study

Congestive Heart Failure Case Study. Congestive Heart Failure. Congestive Heart Failure. Congestive Heart Failure. Impaired cardiac pumping Ventricular dysfunction Heart remodeling Reduced exercise tolerance Diminished quality of life Shortened life expectancy Associated with CAD and HTN.

3.36k views • 35 slides

Heart failure

Heart failure. Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University. General Consideration. Study objectives. • Discuss the possible causes of heart failure.

1.25k views • 54 slides

Heart Failure. Definintion:. “Defined as a pathophysiological state in which an abnormality of cardiac function is the cause of the heart to pump blood at a rate that is not able to keep up with the needs of the body.”. Heart Failure. 5 million Americans with heart failure today

868 views • 53 slides

Heart Failure Clinical Reasoning Case Study

Heart Failure Clinical Reasoning Case Study. Keith Rischer, RN, MA, CEN, CCRN. Review of Terms…. Pre-load primarily venous blood return to RA Right and left side of heart filling pressure (atria&gt;ventricles) Pressure/Stretch in ventricles end diastole Stroke volume

1k views • 41 slides

Heart failure. Dr. Wael H. Mansy, MD Assistant Professor College of Pharmacy King Saud University 2009. General Consideration. Study objectives. • Discuss the possible causes of heart failure.

789 views • 34 slides

Clinical Case Study: Acute Onset Heart Failure

Clinical Case Study: Acute Onset Heart Failure. Amy Lofley Case study #2. Objectives. Overview of Acute Heart Failure Physiology Pathophysiology Treatment Multidisciplinary team. Case Study Medical Hx Nutrition Assessment Nutrition Intervention Prognosis Conclusion.

886 views • 28 slides

Heart Failure. Renin inhibitors. Inotropic agents.  CO.  Renin. -Blockers. ACE .  Sympathetic activity.  Angiotensin II. ARBs. Vasoconstriction.  Aldosterone. Vasodilators. Spironolactone.  Cardiac filling. Na + , water retention. Cardiac remodeling. Diuretics.

299 views • 19 slides

570 views • 41 slides

Heart failure. Laszlo L. Tornoci Inst. Pathophysiology Semmelweis University. Definition.

2.05k views • 49 slides

heart failure Get the Best Cardiologist in Mahbubnagar | Heart Failure Cardiologist - Our cardiologists and cardiac hospitals offer the best service for Heart Failure at the lowest costs in Mahbubnagar. https://abhayapradahospitals.com/cardiology/ Contact us 1-3-148,Near shetty complex, Newtown,Rajendra Nagar, MahbubNagar-509001 ud83dudcde Phone : 919908828591,08542-253999 ud83dudce9 Email : [email protected]

4 views • 4 slides

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Heart Clinical Case

Heart clinical case presentation, free google slides theme and powerpoint template.

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