Soap Note
Bettyd2382
Internal Medicine 04: 67-year-old female with shortness of breath and lower-leg swelling User: Beatriz Duque Email: [email protected] Date: October 9, 2020 3:56PM
Learning Objectives
The student should be able to:
Interpret neck vein findings for jugular venous distention (JVD) and abdominal jugular reflex. Identify and translate auscultatory findings of the heart including rate, rhythm, S3/S4, and murmurs. List the major pathologic states that cause dyspnea. Compare the differing etiologies and signs of left-sided vs. right-sided heart failure. Use the staging system for heart failure. Discuss the factors leading to symptomatic exacerbation of HF, including ischemia, arrhythmias, anemia, hypertension, thyroid disorders, non-compliance with medications and dietary restrictions, and use of nonsteroidal anti-inflammatory drugs (NSAIDS). Interpret B-type natriuretic peptide (BNP) results. Propose pharmacologic management of heart failure.
Knowledge
Dyspnea
Definition
A subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. Etiology
Interactions among multiple physiologic, psychologic, social and environmental factors may induce secondary physiological and behavioral responses. Congestive heart failure, asthma, chronic obstructive pulmonary disease (COPD), pneumonia, cardiac ischemia, interstitial lung diseases, and psychogenic causes account for about 85% of all causes of dyspnea. Other important causes of dyspnea to keep in mind while taking history from the patient are anemia, pulmonary embolus, pneumothorax, malignancy, valvular disorders, arrhythmias, metabolic (acidosis), and neuromuscular disorders (e.g., myasthenia gravis, muscular dystrophy). There are more than 30 different causes of dyspnea involving multiple organ systems. The clinical approach to dyspnea depends on the acuteness of the problem.
Orthopnea
Definition
Shortness of breath that begins or increases when the patient lies down. Associated history
Physicians frequently question patients about this by asking in the history if the patient has had to sleep on more than one pillow recently due to shortness of breath when lying flat and if this has helped his/her breathing. Nocturnal cough is a frequent manifestation. Etiology
Orthopnea results from the redistribution of fluid from the splanchnic circulation and lower extremities into the central circulation during recumbency, with a resultant increase in pulmonary capillary pressures which forces fluid into the alveoli leading to pulmonary edema.
Paroxysmal nocturnal dyspnea (PND)
Definition
Acute episodes of shortness of breath at night that awaken the patient from sleep usually one to three hours after the patient lays down. Associated history
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Sitting upright helps in orthopnea but not in PND. Patients usually open a window to get some fresh air and feel better. Etiology
PND is quite specific for congestive heart failure when present, although it is a less commonly reported symptom as many patients may not recall these events after waking up.
Signs of Elevated Right Heart Pressures
Elevated JVP and exaggerated abdominojugular reflux are signs of elevated right heart pressures.
Causes of a Mid-Systolic Murmur at the aortic area
Anemia, fever, thyrotoxicosis, pregnancy (high output states) Aortic sclerosis (valve thickening without outflow obstruction) Aortic stenosis Hypertrophic cardiomyopathy (consider in younger patients).
Other causes of murmurs
Aortic regurgitation is an early diastolic murmur (second left-upper sternal border). Mitral regurgitation is a holosystolic murmur heard well in the mitral area.
Heart Failure (Systolic vs Diastolic; Left vs Right)
Risk factors
In the U.S. and Europe, hypertension and coronary artery disease are the primary risk factors for developing heart failure. Systolic vs diastolic heart failure
Heart failure is a syndrome caused by cardiac dysfunction, generally resulting from myocardial muscle dysfunction or loss and characterized by either left ventricle (LV) dilation or hypertrophy or both. Heart failure can be classified into systolic or diastolic dysfunction:
Systolic heart failure is a clinical syndrome characterized by signs and symptoms of HF and reduced left ventricular ejection fraction (LVEF). Most commonly associated with LV chamber dilation. Diastolic heart failure (also known as Heart Failure with preserved ejection fraction HFpEF) (about one-third of heart failure cases) is a clinical syndrome characterized by signs and symptoms of HF with preserved LVEF, most commonly associated with a nondilated LV chamber. Patients with diastolic heart failure have impaired ventricular relaxation and elevated filling pressures. Prevalence of diastolic heart failure increases with age, if the patient is female, and particularly with hypertension.
Left vs right heart failure
Left heart failure (or pump failure) is used clinically in reference to symptoms and signs of elevated pressure and congestion in the pulmonary veins and capillaries. Left ventricular dysfunction can result from nonischemic causes like valvular disorders, arrhythmias, alcohol, chemotherapy, and myocarditis (multifactorial etiology like viral, bacterial, parasitic, autoimmune) as well as illicit drugs, like cocaine, and idiopathic causes. Right heart failure refers to symptoms and signs of elevated pressure and congestion in the systemic veins and capillaries characterized by jugular vein engorgement and hepatic congestion. Right heart failure is most commonly caused by left heart failure.
Neurohumoral Hypothesis of Heart Failure
Neuroendocrine mechanisms are now the targets of several important and successful therapeutic interventions in heart failure and hypertension and have a key role in determining prognosis. ACE inhibitors, beta-adrenergic blockers, and aldosterone antagonists now have a prominent role in the treatment of heart failure, and new, more innovative neuroendocrine-blocking agents are being rapidly developed, adding strong support to the neurohumoral hypothesis. Decreases in blood pressure, stroke volume (pulse pressure), and perfusion (flow) in heart failure are sensed by mechanoreceptors in the LV, carotid sinus, aortic arch, and renal afferent arterioles. Diminished activation of these receptors, as in heart failure, leads to:
Augmentation of sympathetic outflow, resulting in tachycardia and arrhythmias; Activation of the renin-angiotensin-aldosterone system (RAAS), causing myocyte hypertrophy and collagen synthesis, and Nonosmotic release of arginine vasopressin (AVP), which can lead to hyponatremia.
Heightened peripheral vasoconstriction (which causes edema) occurs along with increased blood volume.
Causes of Heart Failure
Hypertension and coronary artery disease (CAD) are the most common causes of heart failure in the U.S. CAD should be considered especially in patients with symptoms or risk factors.
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Amyloid infiltration
Amyloid infiltration classically results in a restrictive cardiomyopathy which is characterized by abnormal diastolic function. The restrictive diseases often present with relatively more right-sided symptoms, such as edema, abdominal discomfort, and ascites, although filling pressures are elevated in both ventricles.
Constrictive pericarditis
Patients with constrictive pericarditis and tamponade may present with dyspnea and signs of right heart failure resulting from impaired ventricular filling. This patient's echo is not consistent with this.
Hemochromatosis Hemochromatosis is an infiltrative disease resulting in abnormal iron deposition in multiple organs and is a rarecause of CHF.
Hyperthyroidism Hyperthyroidism can cause CHF by the mechanism of high output heart failure. The hyperthyroidism wouldneed to be untreated for some time to cause this.
Hypertrophic obstructive cardiomyopathy
Hypertrophic obstructive cardiomyopathy can be inherited in an autosomal dominant fashion or acquired due to disproportionate hypertrophy of the interventricular septum. Findings include a systolic murmur at the left lower sternal border and hypertrophy on the echo.
Viral cardiomyopathy
Viral cardiomyopathy can be caused by various viruses that cause myocarditis. These can lead to an enlarged left ventricle with decreased systolic function. It is one of many causes of a dilated cardiomyopathy. Although possible in this patient, CAD is more likely.
Heart Failure Discharge Criteria
Exacerbating factors are addressed At least near optimal volume status is achieved Transition from intravenous to oral diuretic successfully completed Patient and family education completed, including clear discharge instructions LVEF documented Smoking cessation counseling initiated Near optimal pharmacological therapy achieved, including ACE inhibitor and beta blocker (for patients with reduced LVEF), or intolerance documented Follow-up clinic visit scheduled, usually within seven days.
Heart failure (HF) is a syndrome characterized by high mortality, frequent hospitalization, reduced quality of life, and a complex therapeutic regimen. Knowledge about HF is accumulating so rapidly that individual clinicians may be unable to readily and adequately synthesize new information into effective strategies of care for patients with this syndrome. Trial data, though valuable, often do not give direction for individual patient management. These characteristics make HF an ideal candidate for practice guidelines.
Prognosis of Symptomatic Heart Failure
Despite many recent advances in the evaluation and management of HF, the development of symptomatic HF still carries a poor prognosis. In large trials, patients with signs or symptoms of CHF have a 5-10 fold higher incidence of death than cohorts without clinical CHF.
Clinical Skills
Physical Exam for Dyspnea
Vitals Pay specific attention to pulse, respiratory rate, and oxygen saturation.
General appearance
Helps to assess the severity of dyspnea, observing for any signs of breathlessness as the patient walks to the exam table. Accessory muscle use can indicate increased work of breathing.
Cardiovascular Elevated jugular venous pressure (JVP, an indication of pressure or volume overload), murmurs (may besuggestive of particular etiology, i.e., critical aortic stenosis), S3 (CHF), or S4.
Respiratory Wheezes or rhonchi (more suggestive for chronic obstructive pulmonary disease), and crackles (more suggestivefor pulmonary edema or interstitial lung disease).
Abdominal Hepatomegaly and an exaggerated abdominojugular reflux (would be suggestive of right heart failure).Abdominal pathology (distension, inflammation) can also cause shortness of breath.
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Extremities Examine for edema and clubbing of the digits.
Cardiovascular Exam
Visit this Easy Auscultation page to hear an S3 Heart Sound.
Measuring abdominojugular reflux
Have the patient in the supine position so that the top of the jugular venous pulsation is seen in the right side of the neck. Encourage the patient to relax and breathe normally. Apply firm steady pressure (25 to 30 mm Hg) to the midabdomen for 30 seconds. The test is positive if there is a sustained (≥ 10-second) 4-cm rise in the venous pressure.
Management
Recommended Management for Patients with Heart Failure
Salt and fluid restriction
Advise the patient to restrict salt intake to 2 grams/day and fluid intake to 1.5 to 2.0 L/day. Check weight daily
Also recommend that patients with fluid retention or renal dysfunction monitor volume status by checking their weight each morning. Adherence to medications / maintain up-to-date immunization status
Encourage patients to adhere to medication regimens to optimize risk-factor control and keep their immunizations up-to-date, especially influenza and pneumococcal vaccines. Risk factor control
Link to American Heart Association (AHA) Patient Education Materials: http://www.heart.org/en/health-topics/consumer- healthcare/order-american-heart-association-educational-brochures Exercise training
Regular physical activity and a moderate-intensity exercise program are recommended for patients with less severe heart failure AFTER their symptoms have stabilized and they are euvolemic. Referral to a cardiac rehabilitation program can also be considered
Assessing Heart Failure: Functional & Volume Status
After heart failure has been diagnosed, the patient's functional capacity and volume status should be assessed. Functional status
The New York Heart Association (NYHA) functional classification
Class I No symptoms
Class II Symptoms with ordinary activity
Class III Symptoms with less than ordinary activity
Class IV Symptoms at rest or with any minimal activity
Volume status
The volume status can be assessed clinically using orthostatic blood pressure changes, weight, JVP, and presence of edema in dependent areas, with or without crackles. Mrs. Rivers qualifies for NYHA class II.
Medications for Systolic Heart Failure
Medications for Systolic Heart Failure Shown to Decrease Mortality
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Medication Mechanism Adverse Effects Comments
ACE inhibitors
Captopril, Enalapril, Lisinopril, Ramipril
Reduce afterload, sympathetic activation and ventricular remodeling
Hypotension
Azotemia
Hyperkalemia
Angioedema
Non- productive cough (due to bradykinins)
Contraindications: Patients with hypotension, volume depletion
May cause hypotension with first dose.
ARBs
Losartan
Valsartan
Same as ACE inhibitors
Hypotension
Azotemia
Hyperkalemia
For patients intolerant to ACE-I or as adjunct to ACE-I and beta blockers.
Beta blockers
Carvedilol,
Metoprolol succinate (long-acting)
Bisoprolol
Reduces effects of sympathetic activity and sudden death
Bradycardia
Heart block
Symptomatic hypotension
Contraindications: Patients with asthma who have active bronchospasm
Effect is dose-dependent.
Indicated to control blood pressure, decrease heart rate, and counter effects of increased sympathetic activity. Recommended in class I and II heart failure, as it decreases mortality by 30%. Start at a low dose after the patient is euvolemic and titrate up the dose every two weeks until the maximal effective dose is reached.
Aldosterone blockers
Spironolactone
Eplerenone
Counteracts the effects of aldosterone (sodium retention, potassium wasting, myocardial hypertrophy, fibrosis, and endothelial dysfunction.
Severe hyperkalemia
Spironolactone
Can cause painful gynecomastia
Contraindications: Patients with creatinine > 2.5 mg/dL
Avoid in patients with serum creatinine above 2.5 mg/dl and potassium more than 5 mEq/L.
.
Recommended in patients with NYHA class II - IV HF and who have LVEF of 35% or less.
Hydralazine & Nitrates
Hydralazine reduces afterload.
Isosorbide dinitrate reduces both preload and afterload.
Mortality decreased (in African Americans). Recommended for patients intolerant to ACE-I or in addition to standard heart failure therapy in African American patients.
Sacubitril & Valsartan
Sacubitril is a neprilysin inhibitor which inhibits degradation of natriuretic peptides and Valsartan inhibits angiotensin (ARB)
Hypotension
Angioedema
Angiotensin receptor blocker adverse effects
This combination underwent a randomized trial against enalapril and demonstrated a significant decrease in death from cardiovascular causes, any cause of death and hospitalizations for heart failure compared to the control group treated with enalapril. In 2019 the medication cost was approximately $6000 per year.
Medications for Systolic Heart Failure Not Proven to Decrease Mortality
Medication Mechanism Adverse Effects Comment
Digoxin In patients with sinus rhythm, improves myocardialcontractility.
Nausea
Diarrhea
Vision changes
Arrhythmias
Lower digoxin levels are as effective as high levels.
Added for continued symptoms and recurrent hospitalizations.
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Diuretics
Loop and Thiazide
Enhance excretion of sodium and water. Block sodium reabsorption at specific sites in renal tubule.
Electrolyte and volume depletion
Azotemia
Indicated if evidence of fluid overload.
Monitor for electrolyte imbalances, hypotension, and azotemia.
Ivabradine inhibits current in the SA node, slowing sinus ratewithout effecting contractility
Sinus bradycardia
Visual side effects
decreased initial hospitalization for CHF but did not alter mortality
Note: All of the above medications used for systolic heart failure decrease morbidity.
Precipitants of Acute Decompensating Heart Failure
Studies have shown that about 40-50% of acute heart failure (AHF) cases have no precipitants. Acute coronary syndrome should be ruled out with ECG and cardiac biomarkers. Atrial arrhythmias, especially atrial fibrillation with a rapid ventricular rate, are more common than ventricular arrhythmias. Evaluate patients for infections like pneumonia, UTI, or sepsis syndromes. NSAIDs can increase risk of hospitalization by nearly tenfold. Acute valvular regurgitation (post MI, endocarditis) can cause acute heart failure. Severe anemia and thyrotoxicosis can cause high output failure and decompensated heart failure. Heart failure is one of four most common conditions that bring patients into a hospital for medical treatment. The Joint Commission for the Accreditation of Healthcare Organizations (JCAHO) has established the following quality measures that, when adhered to, have been shown to help patients recover more quickly with fewer complications or lasting effects:
Prescribing ACE inhibitors or ARBs for left ventricular dysfunction Giving advice on quitting smoking Giving discharge instructions about managing their diet, weight, and medications. Left ventricular function assessment
Device Therapies for Heart Failure
Implantable cardioverter defibrillators (ICDs)
The most common cause of sudden death in patients with heart failure is arrhythmia, including ventricular tachyarrhythmia and bradyarrhythmia. Prophylactic implantation of ICDs demonstrated a survival benefit in patients with ischemic cardiomyopathy (with asymptomatic nonsustained ventricular tachycardia, prior MI and LVEF less than or equal to 30%) and nonischemic cardiomyopathy (LVEF less than or equal to 35%). Biventricular pacemakers
Patients with heart failure who have severe symptoms (NYHA class III or IV) and evidence of ventricular dyssynchrony (left ventricular enlargement and QRS prolongation > 120 ms) benefit from biventricular pacemakers for cardiac resynchronization therapy. Randomized trials involving patients with severe heart failure showed that cardiac-resynchronization therapy resulted in a reduction in symptoms and improved functional capacity, a reduction in the number of hospitalizations for worsening heart failure, and increased survival. Both of these devices are very expensive due to hospital cost, the device itself, and need for surgical implantation. Costs vary around the world but are generally between $50,000 and $90,000.
Studies
Evaluation of Dyspnea and Edema
Echocardiogram Indications for doing an echocardiogram are if the patient: 1. Is symptomatic with a murmur 2. Has acontinuous murmur 3. Has a diastolic murmur 4. Has a murmur with an intensity > 3/6
ECG An ECG helps to look for ischemic changes, ventricular hypertrophy, signs of old infarction, arrhythmias, andconduction abnormalities.
Chest x-ray
A chest x-ray is useful to look for:
cardiomegaly
pulmonary vascular congestion (CHF)
interstitial edema or fibrosis (interstitial lung disease)
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hyperinflation (COPD)
Hampton's hump or Westermark's sign (pulmonary embolism)
consolidation (pneumonia)
pneumothorax
pleural effusions CBC Use a CBC to check for anemia.
Basic metabolic panel
Use a basic metabolic panel to check for electrolyte abnormalities and renal function, including signs of volume depletion.
BNP
A BNP assay improves the accuracy of diagnosis of acute heart failure in patients presenting with dyspnea. This test is most useful in settings of dyspnea when the pretest probability is intermediate for heart failure. BNP level has a high negative predictive value for the diagnosis of heart failure.
B-type natriuretic peptide is a 32-amino-acid polypeptide secreted by the cardiac ventricles in response to ventricular volume expansion and pressure overload. The prohormone is cleaved to generate the active hormone (BNP) and an N-terminal biologically inactive fragment (NTproBNP). Both are then released into the blood stream in a 1:1 ratio. Both BNP and NTproBNP can be used in the diagnosis of CHF.
Patients with BNP <100 pg/mL are unlikely to have heart failure and patients with BNP >500 pg/mL are more likely to have heart failure. For patients with B-type natriuretic peptide levels between 100 and 500 pg per milliliter, use of clinical judgment as well as possible further diagnostic testing to rule out stable base-line left ventricular dysfunction and other conditions as the real cause of acute dyspnea is recommended.
BNP is generally higher in females and in patients with renal failure, acute coronary syndrome, or myocardial infarction. Levels of BNP correlate with severity of heart failure symptoms and prognosis, including risk for rehospitalization and mortality. (Mueller C, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Eng J Med. 2004; 350: 647-54.)
BNP can also be elevated when there is right heart strain due either to pulmonary embolism, COPD, or other causes of right heart failure. (Mueller C, Laule-Kilian K, Frana B, et al. Use of B-type natriuretic peptide in the management of acute dyspnea in patients with pulmonary disease. American Heart Journal. 2006; 151: 471- 477)
A TSH level is also useful. Severe hypothyroidism can cause congestive heart failure and hyperthyroidism can cause high output heart failure. Also, don't forget to do a urine analysis to look for proteinuria and liver panel to check for hypoalbuminemia. Tests not indicated at this time
An ABG (arterial blood gas) is not needed urgently if the patient's oxygen saturation is in the normal range and she is alert as well as relatively stable. Pulmonary function tests (PFTs) are used to identify obstructive or restrictive lung disease and D-dimer with venous ultrasound is used to rule out deep vein thrombosis and pulmonary embolism. These tests can be done later if the initial workup is not conclusive.
Signs of Heart Failure on Chest X-Ray
A mnemonic to look for signs of heart failure on the CXR is ChECK, which stands for: Cephalization (dilation of the pulmonary vessels radiating upward from the hilum due to fluid overload). Effusions (look for blunting of the costophrenic angles). Cardiomegaly (heart shadows occupying >50% of the thoracic diameter). Kerley B lines (horizontal, peripheral white markings, especially at the bases). See images displaying CHF on x-ray.
Clinical Reasoning
Differential of Dyspnea with Lower Extremity Edema
Congestive heart failure
Congestive heart failure can cause dyspnea, orthopnea, and LE edema and is a leading diagnosis. Dyspnea is one of the cardinal manifestations of CHF (systolic or diastolic). Orthopnea is relatively specific for CHF but can also occur with other pulmonary pathology (COPD, pleural effusions). The cause of edema in CHF is increased hydrostatic pressure. Note that it is important to recognize that CHF is a clinical syndrome, and that there are many possible causes of CHF.
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Pulmonary embolism
Pulmonary embolism should remain on the differential, with the caveat that bilateral (rather than unilateral) LE edema is less commonly seen in PE/DVT.
Angina Angina can present as dyspnea, in the absence of classic chest pressure or pain (this is referred to as an "anginalequivalent") or can lead to CHF in the setting of ischemic heart disease and/or myocardial infarction.
Interstitial lung disease Cough and dyspnea are prominent symptoms of interstitial lung disease.
Pulmonary hypertension
Pulmonary hypertension can cause dyspnea along with symptoms of right-sided heart failure. The cause of lower extremity edema in COPD or obstructive sleep apnea results from right heart failure due to pulmonary hypertension. Hypoxia is a major stimulus for pulmonary hypertension.
Chronic kidney disease
Chronic kidney disease can cause volume overload producing many of these symptoms. Another cause of edema in nephrotic syndrome (and cirrhosis) is decreased oncotic pressure from hypoproteinemia. Long-standing hypertension can be a cause for renal failure. At present we don't see any other uremic symptoms (pericardial rub, lethargy, nausea, pruritus), which makes this a little less likely, but possible.
Differential of Dyspnea, Elevated JVP, Systolic Murmur, S3, Crackles, Hepatomegaly, & Lower Extremity Edema
Most Likely Diagnoses
Congestive heart failure
Congestive heart failure is a common syndrome with many causes and is often associated with both elevated right heart and left heart filling pressures. Crackles and an S3 heart sound are signs of elevated left heart pressures.
S3 is specific but not sensitive for left ventricular dysfunction. S3 results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which is the most common cause of an S3 heart sound. This may be a normal physiologic finding in patients less than age 40.
In CHF, crackles are coarse or fine and mostly occur in the early inspiratory phase of the cycle.
Leg edema, elevated JVP, and hepatomegaly are all physical exam findings consistent with elevated right- heart pressures and may result from cardiac or pulmonary causes.
Jugular venous distention has 55-65% sensitivity and 74-80% specificity for increased right-heart filling pressure based on a review of 11 studies (JAMA. June, 1997; 277: 1712) in Evidence Based Medicine, Jan/Feb, 1998; 3(1): 22.)
Pulmonary hypertension
Pulmonary hypertension is a pulmonary condition that can lead to elevated right heart pressures and physical exam findings seen here including leg edema, elevated JVP, and hepatomegaly.
It should still be in consideration, however it does not explain the signs of elevated left heart pressures seen here, including the presence of crackles and an S3 heart sound.
Valvular heart disease
Dyspnea, a heart murmur, and signs of both left and right-sided heart failure can all be seen in valvular heart disease with secondary heart failure.
Less Likely Diagnoses
Pulmonary embolism
While tachycardia does occur in 81% of patients with pulmonary embolism, pulmonary embolism, the absence of risk factors, a history of prior deep venous thrombosis or pulmonary embolism, and the presence of signs of left- sided heart failure point away from this diagnosis.
Pulmonary embolism does not typically cause left-sided heart failure.
Interstitial lung disease
Interstitial lung disease is suggested by the presence of bilateral crackles however does not typically cause the signs of elevated left and right-heart pressures seen here.
The frequency of crackles in interstitial lung disease depends on the etiology.
It is very common in patients with interstitial pulmonary fibrosis (late inspiratory, fine crackles).
References
American Thoracic Society. Dyspnea: Mechanisms, assessment, and management: A consensus statement. Am J Respir Crit Care Med.
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1999;159(1):321-40. DOI: 10.1164/ajrccm.159.1.ats898
Digitalis Investigation Group. The Effect of Digoxin on Mortality and Morbidity in Patients with Heart Failure. N Engl J Med. 1997;336(8):525-33. DOI: 10.1056/NEJM199702203360801
Discover Echo. How Much Does An Echocardiogram Cost: Updated 2018 ECHO TEST COST. https://www.discoverecho.com/echocardiogram-cost. Accessed December 17, 2018.
Fang J, O'Gara P. "The History and Physical Examination: An Evidence-Based Approach." Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. St. Louis, MO: WB Saunders, 2007.
Fuster F, Walsh R, Harrington R. Hurst's The Heart. 13th Ed. New York, NY:McGraw-Hill; 2010
Fuster V, Walsh R, Harrington, R, et al. Hurst's The Heart. 13th edition. McGraw-Hill: New York. 2010
Heart Failure Society of America, Lindenfeld J, et al. Executive Summary: HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010;16(6):475-539.
McMurray JJ, Packer M, Desai AS, et al. Angiotensin–Neprilysin Inhibition versus Enalapril in Heart Failure. N Engl J Med. 2014;371(11):993-1004. DOI: 10.1056/NEJMoa1409077
McMurry JJ. Clinical practice, systolic heart failure, N Engl J Med. 2010;362(3):228-38. DOI: 10.1056/NEJMcp0909392
Pfeffer, MA. Heart Failure and Hypertension, Importance of Prevention. Med Clin North Am. 2017;101(1):19-28. DOI: 10.1016/j.mcna.2016.08.012
Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med. 1999;341(10):709-17. DOI: 10.1056/NEJM199909023411001
Poole-Wilson PA, Swedberg K, Cleland JG, et al. Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomized controlled trial. Lancet. 2003;362(9377):7-13. DOI: 10.1016/S0140-6736(03)13800-7
SOLVD Investigators, Yusuf S, Pitt B, Davis CE, et al. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med. 1992;327(10):685-91. DOI: 10.1056/NEJM199209033271003
Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): a randomized placebo-controlled study. Lancet. 2010;376(9744):875-85. DOI: 10.1016/S0140-6736(10)61198-1
Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol.. 2013;62(16):e147-239. DOI: 10.1016/j.jacc.2013.05.019
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- Internal Medicine 04: 67-year-old female with shortness of breath and lower-leg swelling
- Learning Objectives
- Knowledge
- Dyspnea
- Orthopnea
- Paroxysmal nocturnal dyspnea (PND)
- Signs of Elevated Right Heart Pressures
- Causes of a Mid-Systolic Murmur at the aortic area
- Heart Failure (Systolic vs Diastolic; Left vs Right)
- Neurohumoral Hypothesis of Heart Failure
- Causes of Heart Failure
- Heart Failure Discharge Criteria
- Prognosis of Symptomatic Heart Failure
- Clinical Skills
- Physical Exam for Dyspnea
- Cardiovascular Exam
- Measuring abdominojugular reflux
- Management
- Recommended Management for Patients with Heart Failure
- Assessing Heart Failure: Functional & Volume Status
- Medications for Systolic Heart Failure
- Precipitants of Acute Decompensating Heart Failure
- Device Therapies for Heart Failure
- Studies
- Evaluation of Dyspnea and Edema
- Signs of Heart Failure on Chest X-Ray
- Clinical Reasoning
- Differential of Dyspnea with Lower Extremity Edema
- Differential of Dyspnea, Elevated JVP, Systolic Murmur, S3, Crackles, Hepatomegaly, & Lower Extremity Edema
- References