This document summarizes a 41-year-old female patient who presented with shortness of breath. Physical examination and tests revealed an ejection fraction of 15% indicating severe systolic dysfunction. She was diagnosed with dilated cardiomyopathy, likely post-viral. Her medications were optimized and a follow up echo 3 months later showed improved ejection fraction to 37%. The document then reviews heart failure definitions, diagnostic criteria, evaluations, treatments including medications, diet and exercise. It stages heart failure and discusses prevention and management of the condition.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
Possible causes of death (Multiorgan failure)
VT/VF intraoperatively
Acute on chronic Heart failur
Respiratory failure
Acute Liver failure
Acute renal failure
Sepsis with septic shock
Concern for Intestinal infarction
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
Possible causes of death (Multiorgan failure)
VT/VF intraoperatively
Acute on chronic Heart failur
Respiratory failure
Acute Liver failure
Acute renal failure
Sepsis with septic shock
Concern for Intestinal infarction
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INTRODUCTION
Overutilization of Proton pump inhibitors (PPI) in hospitalized patients is a well-recognized problem. In our previous study at St. Luke’s Hospital, we found that the lack of published guidelines for PPI use in non-critically ill patients results in overutilization of PPI in hospitalized patients. We conducted an educational intervention program to address this problem.
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52 Year Old Caucasian Male Presents With A Snake Bite
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This will be used as part of your Personal Professional Portfolio once graded.
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Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
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Heart Failure with Reduced Ejection Fraction
1. Morning Report - 5
March 20, 2017
Khushboo Gandhi, PGY2
Internal Medicine Residency Program, St. Luke’s Hospital
2. 41 yr old
Caucasian
Female
presents
to the ER
with SOB
for a
month
Slowly progressive shortness of breath on exertion
beginning approximately 1 month ago
For the past week short of breath even at rest and
while talking
Paroxysmal nocturnal dyspnea and orthopnea,
uses 4 pillows
Able to sleep only for about 20 minutes at a time for
the past week
3. Review of Systems
Constitutional: Weakness, Fatigue, Decreased activity, No fever, No chills, No sweats.
Eye: No recent visual problem.
ENMT: No decreased hearing, No ear pain, No nasal congestion, No sore throat.
Respiratory: Shortness of breath, Orthopnea, PND, No Cough, No sputum production, No
hemoptysis, No wheezing, No cyanosis, No apnea.
Cardiovascular: Chest pain, No palpitations, No bradycardia, No tachycardia, Left lower extremity
edema on/off
Gastrointestinal: No nausea, No vomiting, No diarrhea, No constipation, No heartburn, No
hematemesis.
Genitourinary: No dysuria, No hematuria.
Hematology/Lymphatics: Negative.
Endocrine: Negative.
Immunologic: Negative.
Musculoskeletal: Shooting pain over left upper sternal border, last for a few seconds to 1-2
minutes, for many years, had evaluation before without any significant findings, following up with
the pain management physician in O’Fallon Missouri who prescribes Norco and nortriptyline for
pain control.
Integumentary: Negative.
Neurologic: Alert and oriented X4. Psychiatric: Negative.
4. Allergies: Aspirin, Morphine
Medications:
Norco 5 mg-325 mg
nortriptyline 25 mg
Past Medical and Surgical history:
Hypertension – not on any medications
2 C-sections
Surgical removal of right ovary complicated by left iliac vein thrombosis s/p stent placement in 2002
Chronic pain syndrome on nortriptyline, follows pain specialist at O'Fallon MO
Family History:
Father is 71, has hypertension, had a stroke at the age of 40. Mother is 77 and healthy, has a
healthy brother and 2 daughters, 16 and 21
Social History:
Smoked ½ pack a day for 20 years, quit 4 years ago. Drinks alcohol socially. Married, lives with her
husband. She works as a data entry clerk.
5. Physical Examination:
Tem: 36.7; Pulse: 99 bpm; BP: 142/105 mm hg; RR: 20; SpO2: 96% on RA
General: Alert and oriented, Mild distress.
HENT: Normocephalic, Normal hearing, Oral mucosa is moist, No pharyngeal erythema.
Eye: PERLA, Extraocular movements are intact, Normal conjunctiva, Vision unchanged.
Neck: Supple, Nontender, No lymphadenopathy, No thyromegaly.
Respiratory: Air entry significantly reduced BL, more on right side, Dullness to percussion bibasilar lung,
Respirations are non-labored, Symmetrical chest wall expansion, No chest wall tenderness.
Cardiovascular: Normal rate, Regular rhythm, No murmur, No gallop, Good pulses equal in all extremities,
Normal peripheral perfusion, Left lower extremity is large in diameter compared to right, she relates this to her
history of DVT and stent placement.
Gastrointestinal: Soft, Non-tender, Non-distended, Normal bowel sounds, No organomegaly.
Lymphatics: No lymphadenopathy neck, axilla, groin.
Musculoskeletal: Negative
Integumentary: Warm, Pink, Intact.
Neurologic: Alert, Oriented, Normal sensory, No focal defects, Cranial Nerves II-XII are grossly intact
Cognition and Speech: Oriented, Speech clear and coherent, Functional cognition intact.
Psychiatric: Cooperative, Appropriate mood & affect, Normal judgment, Non-suicidal.
Genitourinary: No Costovertebral Angle tenderness.
10. Echocardiogram
Conclusions:
Moderate left ventricular enlargement.
Severe global left ventricular systolic dysfunction.
The left ventricular ejection fraction is measured at 15%.
No left ventricular thrombus was visualized.
Increased LA pressure, Grade III left ventricular Diastolic Dysfunction.
Mild right ventricular enlargement.
Moderate right ventricular hypokinesis.
There is severe left atrial enlargement.
There is mild right atrial enlargement.
Mild mitral regurgitation.
11. Hospital course
● Probable post-viral dialted cardiomyopathy
● Patient was initially started on Lasix and lisinopril, however she developed
rash over right thigh as a drug reaction
● Medications are switched to spironolactone, hydrochlorothiazide and
losartan
● Losartan was later discontinued due to hypotension - Started on carvedilol
● Venous doppler LE - Negative for DVT BL
● Iron deficency anemia - Started on ferrous sulfate
● Elevated LFTs – secondary to hepatic congestion - Normalized at discharge
12. Cardiac Catheterization post discharge
1. Severe left ventricular enlargement with severe left ventricular systolic
dysfunction with an estimated left ventricular ejection fraction of approximately
15%.
2. Moderately severe elevation of the LVEDP of 25 mmHg.
3. Mild mitral regurgitation.
4. Normal aortic root and ascending aorta.
5. Normal coronary arteries.
Repeat Echo after 3 months
The left ventricular ejection fraction is measured at 37%.
Compared with prior study of 11/9/2016, left ventricular contractility and diastolic
function have improved.
14. Heart Failure with Reduced Ejection Fraction
Definition: Complex clinical syndrome resulting from any structural or functional
myocardial dysfunction that leads to an impaired ability to circulate blood at a rate
sufficient to maintain the metabolic needs of internal organs and peripheral
tissues.
Myocardial dysfunction:
1. Long-standing ischemia due to coronary artery disease
2. Loss of myocardial mass due to prior infarction
3. Long-standing myocardial stress due to suboptimally treated hypertension or
valvular disease
4. Direct long-term toxin exposure (alcohol abuse, illicit substance use, or
chemotherapeutic agents)
5. Fulminant infections (especially viral) can lead to autoimmune myocardial damage
6. Idiopathic cardiomyopathy, usually related to inherited or spontaneous gene
mutations
16. Labs:
● CMP
o Hyponatremia - marker of advanced HF or excessive diuretic use
o Elevated urea and creatinine - signs of renal hypoperfusion
o Abnormal LFT - Congestion of the liver
● TSH
o Hypo or Hyperthyroidism
● CBC
o Anemia and iron deficiency - early treatment improves the outcome
● BNP/NT-proBNP
o BNP levels over 100 pg/mL and NT- proBNP levels > 450 pg/mL in younger patients or > 900
pg/mL in patients older than 50 years are highly sensitive and specific for HF
● Serum cardiac troponins
o Sign of volume overload and elevated left ventricular filling pressures - carry powerful prognostic
information - Use vasodilators, avoid positive intravenous inotropes
17. Diagnostic Studies
1. Electrocardiography - structural alterations - LVH, prior myocardial infarctions,
rhythm or conduction abnormalities.
2. Chest radiography - Cardiomegaly (chronic/acute), Interstitial and perivascular
edema, bronchovascular markings at the bases; Kerley lines, spindle-shaped
linear opacities at the periphery of the lung bases - later stages; Pleural effusions
3. Echocardiography
4. Cardiac magnetic resonance imaging - myocardial structure - noninvasive
Infiltrative cardiomyopathies (eg, sarcoidosis, amyloidosis)
Iron overload cardiomyopathies (eg, hemochromatosis)
Acute myocarditis; Genetic cardiomyopathies (eg, arrhythmogenic right ventricular
cardiomyopathy, left ventricular noncompaction cardiomyopathy)
5. Cardiopulmonary exercise stress testing (CPET) - especially when
advanced therapies are considered
18. 1. Measurements of the peak oxygen consumption (peak VO2) and the slope of
the ratio of ventilation (VE) to carbon dioxide production (VCO2) (VE/VCO2)
2. Peak VO2 levels < 14 mL/kg/min in patients intolerant of β-blockers (12
mL/kg/min in patients on β-blockers) or < 50% predicted - indications - heart
transplantation or left ventricular assist device implantation
6. Cardiac catheterization - CAD is the main cause of systolic HF in the US
Surgical revascularization in ischemic systolic HF - improves cardiovascular
outcomes
7. Endomyocardial biopsy - Suspected fulminant myocarditis, giant cell
myocarditis, sarcoidosis, amyloid heart disease, or hemochromatosis
Routine surveillance for rejection after cardiac transplantation - first 6–12 months
8. Genetic testing - Identification of at-risk individuals - inherited
cardiomyopathies
Hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia
19. Staging System in the Classification of Heart Failure
ACC/AHA Staging Clinical Heart Failure NYHA Functional class
D - Refractory, end-stage
(Marked symptoms despite
maximal therapy)
Yes IIIB–IV
C - Symptomatic HF
(Shortness of breath, fatigue,
reduced exercise tolerance)
Yes I–IIIA
B - Asymptomatic HF
(Prior myocardial infarction,
left ventricular hypertrophy,
valvular disease, etc.)
No None
A - High risk for developing HF
(Hypertension, coronary
disease, diabetes, obesity, etc.)
No None
20. Treatment
A. Prevention
1. Better control of Hypertension and DM
2. CAD and myocardial infarction
3. Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), and most
β-blockers and calcium channel blockers – HTN
B. Nonpharmacologic Treatment
1. Dietary measures
o Low salt diet - 1500 mg/day sodium
o Fluid restriction are 1.5–2 L/day - HF and stage D symptoms
2. Physical activity and exercise training
3. Treatment of sleep-disordered breathing
o CPAP in OSA - Improves EF and symptoms
4. Ultrafiltration
o Reserved for patients with preserved renal function who are not responding adequately to high-
dose diuretic therapy
21. Pharmacologic Treatment: Life-Saving Therapies
● ACE inhibitors
○ 20% increase in survival - systolic HF / left ventricular systolic dysfunction after myocardial
infarction, even in those without symptoms or signs of HF.
○ Highest tolerated ACE inhibitor dose should be achieved - outcome improves with higher doses
○ Maximum survival benefit - use with β-blockers and MRBs - Triple therapy
● ARBs
○ Mortality benefit only in patients with systolic HF who are intolerant of ACE inhibitors
○ Candesartan was the only ARB that showed in clinical trials a 15% reduction in mortality when
added to an ACE inhibitor.
● Angiotensin receptor neprilysin inhibitors (ARNIs)
○ ARB (valsartan) with a neprilysin inhibitor (sacubitril)
○ Superior to ACE inhibitors in improving survival and decreasing the hospitalization rates
Lancet. 2011;378:713–721. N Engl J Med. 2014;371:993–1004.
22. ● MRBs
○ In combination with ACE inhibitors and β-blockers - 15–30% decrease in mortality - 30–40%
decrease in hospitalizations - Eplerenone selective MRB - devoid of the painful gynecomastia
● β-Adrenergic receptor blockers
○ Early deterioration in cardiac function, followed by return to baseline values after 1 month and
an increase in the ejection fraction after 3 months, with further improvement for up to a year.
○ Bisoprolol, Carvedilol, and Metoprolol succinate
○ Highest tolerated β-blocker doses is recommended
○ Carvedilol Vs Metoprolol succinate - Better survival, Incidences of MI, stroke, Afib, DM lower
● Hydralazine-nitrates combination
○ Nitrates - venous, Hydralazine - arterioles
○ African-American Heart Failure Trial (A-HeFT) - 43% improvement in survival and a 33%
decrease in HF hospitalizations, when used in addition to ACE inhibitors, β-blockers, and
spironolactone
○ Genotype - benefits of the therapy evident - homozygous for glutamic acid in position 298
(GLU298GLU) - 80% of African Americans - 40% of Caucasians
J Card Fail. 2009;15:191–198. J Am Coll Cardiol. 2013;62:e147–e239. N Engl J Med. 2011;364:11–21.
23. ● Diuretics and aquaretics
○ Loop diuretics
■ Increase sodium excretion by 20–25%
■ Have to be given twice daily - rebound sodium retention
■ Oral - variable bioavailability (10–100% in patients with HF)
■ Start with twice the home dose
■ Diuretic resistance - Intravenous administration of diuretics (Intermittent bolus or
continuous infusions have the same efficacy); diuretic combinations (eg, loop and
thiazide), or use of intravenous diuretics with low-dose dopamine
○ Tolvaptan
■ vasopressin V2 receptor antagonist
■ Promotes excretion of water without electrolyte loss
■ HF with reduced systolic function, and hyponatremia (serum sodium < 134 mEq/L)
Pharmacologic Treatment: Symptomatic Therapies
24. ● Digoxin
○ Increase in myocardial contraction, reduces the sympathetic outflow, reduces the renal tubular
reabsorption of sodium
○ Reserved in systolic HF patients in sinus rhythm who are still symptomatic despite triple
therapy with ACE inhibitors, β- blockers, and MRBs
○ Systolic HF and atrial fibrillation - decrease the ventricular response
● Digitalis Intoxication
○ Nausea, vomiting, anorexia, malaise, drowsiness, headache, insomnia, altered color vision, or
arrhythmia.
○ Cardiac arrhythmias - PVCs, junctional tachycardia, paroxysmal atrial tachycardia with block,
bidirectional ventricular tachycardia
N Engl J Med. 2011;364;797–805. J Am Coll Cardiol. 2012;59:2145–2153.
25. Other Therapies
● Oral phosphodiesterase-5 inhibitors (sildenafil, tadalafil)
○ Chronic SHF - secondary pulmonary hypertension - improves symptoms
● Antiarrhythmic agents
○ 80% of systolic HF patients - frequent and complex ventricular arrhythmias
○ 50% - frequent nonsustained ventricular tachycardia
○ 35–40% - paroxysmal or persistent atrial fibrillation
○ class III antiarrhythmics (dofetilide and amiodarone) - safe to use
● Amiodarone
○ Afib with RVR in HF patients
○ symptomatic ventricular tachycardia in combination with β-blockers
● Dofetilide
○ Effective in restoring sinus rhythm in patients with systolic HF and atrial fibrillation
● Antithrombotic therapy
○ All patients with systolic HF and atrial fibrillation (even paroxysmal) should be anticoagulated
with warfarin or one of the newer antithrombotic agents in order to prevent strokes.
26. ● Statins
○ only be used in patients with systolic HF and clinical coronary artery disease
● Omega-3 polyunsaturated fatty acids
○ 10% decrease in cardiovascular mortality and 7% decrease in risk for cardiovascular
hospitalizations
● Intravenous iron therapy
○ Iron deficiency - quite frequent in patients with systolic HF
○ Studies - improvements in symptoms, exercise capacity, and quality of life with intravenous
ferric carboxymaltose
○ Intravenous iron therapy - should be used for all patients with systolic HF who are iron
deficient even in the absence of anemia (ferritin level < 100 mcg/L or 100–299 mcg/L if the
transferrin saturation is < 20%)
● Ivabradine
○ Specific inhibitor of the If current in the sinoatrial node, resulting in heart rate reduction - does
not modify myocardial contractility and intracardiac conduction
○ SHIFT trial - decrease in mortality and hospital admissions due to HF with ivabradine.
■ loses efficacy in patients using greater than 50% target doses of β-blockers
N Engl J Med. 2012;366:1859–1869; Eur Heart J. 2015;36:657–668; JAMA. 2013;309:1268–1277; Lancet. 2010;376:875–885.
27. Specific Therapies in Hospitalized Patients
Volume overloaded
● Vasodilators - decrease the filling pressures and improve dyspnea
○ Intravenous sodium nitroprusside, nitroglycerin, or nesiritide
■ frequent titration need - intensive care setting
○ Nesiritide (recombinant BNP) - vasodilator, natriuretic, and diuretic effects
■ does not require titration - telemetry units - only marginally improve symptoms in patients
with decompensated systolic HF
Very low cardiac output (“cold” profile)
● Intravenous inotropes - dobutamine and milrinone
○ Augments cardiac contractility + vasodilator effects
○ Myocardial injury - can precipitate fatal ventricular arrhythmias
○ USE
■ Bridge to mechanical circulatory support or transplant
■ Patients with palliative home hospice
N Engl J Med. 2011;365:32–43; J Am Coll Cardiol. 2014;63:2069–2078.
28. Electrical Treatment
● Implantable cardioverter-defibrillators (ICDs)
○ Prevention of sudden cardiac death - EF < 35%
● CRT - cardiac resynchronization therapy
○ HF patients with intraventricular conduction abnormalities (eg, left bundle branch block)
○ Ejection fraction, decreases ventricular volumes, improves HF symptoms, improves exercise
tolerance, and decreases the hospitalization rate for HF, as well as cardiovascular and all-
cause mortality
○ Benefits - New York Heart Association functional class I– IV
○ More evident - sinus rhythm, with a left bundle branch block pattern, QRS duration greater
than 150 ms, and an ejection fraction below 35%
● Baroreflex activation therapy
○ Implantable device - stimulate the carotid baroreceptors
○ Centrally mediated reduction in sympathetic outflow and increased parasympathetic activity
○ Improvements in functional status, quality of life, and exercise capacity NYHA III
○ BeAT-HF [Better Effectiveness After Transition–Heart Failure]
JACC Heart Fail. 2015;3:487–496; Am Heart J. 2012;163:954–962; Lancet. 2011;378:722–730; JACC Heart Fail. 2015;3:565–572
29. Surgical Treatment
● Surgical Treatment of Ischemic Heart Failure (STICH) trial
○ 19% decrease in cardiovascular mortality and a 15% decrease in cardiovascular
hospitalizations in patients undergoing CABG in addition to optimal medical therapy when
compared to optimal medical therapy alone
○ Ischemic systolic HF - evaluate for surgical or percutaneous revascularization
● Advanced surgical options
○ Patients with advanced systolic HF who are not amenable to conventional pharmacologic,
electrical, or surgical therapies should be considered
○ Cardiac transplantation
○ Left ventricular assist device
■ Bridge to recovery - acute myocarditis or postpartum cardiomyopathy
■ Bridge to transplant
■ Destination therapy
■ Thoratec HeartMate II and HeartWare HVAD
■ ROADMAP - Better survival than optimal medical management - NYHA IIIB/IV not
dependent on inotropes
Circulation. 2012;125:3191–3200; N Engl J Med. 2016;374(16):1511–1520; N Engl J Med. 2011;364:1607–1616.