Download Congestive Heart Failure - UC Irvine`s Department of Medicine

Congestive Heart
Failure
- Mini-LectureKristopher Huston MD, PGY2
Ali Ashtiani MD, PGY2
Arash Taghavi MD, PGY1
Heart Failure-Definition
 “a complex clinical syndrome that can result from any
structural or functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject blood.”
 HFrEF or Systolic HF
 EF<40%
 Aim of majority of therapies
 HFpEF or Diastolic Failure
 EF>50%
 Exclusion of other noncardiac causes of symptoms
Definition
Classification Systems
NYHA Functional Class
 I: No limitation of physical activity. Ordinary physical activity does
not cause symptoms of HF (fatigue, palpitations, dyspnea or angina)
 II: Comfortable at rest, slight limitation of physical activity
 III: Comfortable at rest. Marked limitation, less than ordinary activity
causes discomfort
 IV: Discomfort at rest
 ACCF/AHA Stages



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A = No structural heart disease, risk factors for HF
B = Structural heart disease, no HF symptoms
C = Structural heart disease, with prior or current HF symptoms
D = Refractory HF requiring frequent interventions
The Major Causes
 CAD (~70% of cases)
 Hypertension
 Valvular disease
 Diabetes Mellitus
 cardiomyopathy and progression of CAD
Less Common Causes
 Myocarditis
 Tachyarrhythmia
 Congenital Heart Defects (HOCM)
 Cardiomyopathy


Stress-induced
Toxins: Drugs (Cocaine, Methamphetamine, Chemotherapy, Radiation), Alcohol
 Pulmonary: OSA
 Rheumatologic: Sarcoidosis, SLE
 Infiltrative: Hemochromatosis, Amyloidosis
 Chronic Disease

DM, HIV, Thyroid Disorders
How patients present
 Clinical Symptoms




Dyspnea (100% sensitivity)
PND
Swelling/Dependent edema
Fatigue, Weight gain
 Risk Factors:
 Obesity, smoking, physical inactivity, lower socioeconomic
status factors.
Physical Exam
 Pulmonary: Respiratory distress, Rales
 Cardiac: Bradycardia/Tachycardia, Displaced PMI,
JVD, S3 gallop rhythm.
 Abdomen: Ascites, Hepato-jugular Reflux
 Extremities: cool, dependent edema, cyanosis, pallor
Diagnosis
 EKG (check for MI, PE, Arrhythmia, LVH)
 CXR
 Pulmonary venous congestion, interstitial edema
 Cardiomegaly, pleural effusions
 Labs
 CBC, CMP, Troponin, ABG, Thyroid function tests
 Echocardiography: evaluate severity, causes,
characterization
 Coronary Angiogram in setting of STEMI/NSTEMI
Diagnosis
 BNP, NT-proBNP
 Equally good sensitivity/specificity in diagnosing CHF
 BNP = < 100 unlikely CHF and > 400 likely CHF
 Increases with age, renal disease/arrhythmia, sepsis, CAD,
Women, African-Americans
 Decreased in obesity
 In acute HF, predictor of mortality and cardiovascular events
when >200.
 Limited evidence in serial monitoring in outpatient setting
 Support clinical decision making
 Establish prognosis and disease severity
Management
 Lifestyle Modification



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Vaccines: Pneumococcal and Flu
Low Sodium (<2-3 g daily)
Alcohol and Tobacco cessation
Medications to avoid
 NSAIDs (reduce GFR, worsen response to diuretics and ACE)
 Recommended to use ASA only for CAD
 Thiazolidinedione (fluid retention), Metformin (increased risk for LA)
 Phosphodiesterases (PDE3 and 4, data for PDE5 is not as convincing)
 MORTALITY REDUCTION!
 ACE-I/ARB, Beta-Blocker, Aldosterone Antagonist, Hydralazine plus
Isosorbide Nitrate
Management
ACE-Inhibitors
 Decrease MORTALITY and hospitalizations
 Initial baseline treatment in all patients with heart
failure, regardless of NYHA class
 Enalapril Initial: 2.5 mg PO BID (Target:10-20 mg BID)
 Captopril Initial: 6.25 mg PO TID (Target: 50-100mg TID)
 Lisinopril Initial: 5 mg PO Daily (Target: 20- 40 mg Daily)
**ARB’s have comparable mortality reduction, used when
ACE-I not tolerated**
Management
Beta-Blockers
 These BB decrease MORTALITY in patients with heart failure who already
are taking an ACE inhibitor and/or a diuretic.
 start low and go slow (double every 2-4 weeks)




Coreg 3.125 mg PO BID (Target: 25 to 50 mg BID)
Metoprolol Succinate 12.5 mg PO daily (Target: 200 mg daily)
Bisoprolol 1.25 mg PO daily (Target: 5 to 10 mg PO daily)
COMET (2003): NYHA classes II-IV treated with Coreg had greater reduction
in mortality than those treated with metoprolol, although hypotension was
increased in Coreg group
 Relative Contraindications
 Symptomatic Hypotension or pressor requirement
 HR < 60, 2nd or 3rd degree AV block, PAD with ischemia
Management
 Aldosterone receptor antagonist (Spironolactone)
 NYHA Class II-IV, LVEF of 35% or less
 Reduce morbidity and mortality
 Monitor renal function, BMP
 Creatinine 2.5mg/dl or less
 Potassium 5.0 mEq/L or less
 Hydralazine and Isosorbide
 African Americans. NYHA Class III-IV
 Optimal ACE-I and BB
 Reduce morbidity and mortality
Management
 Digoxin
 Symptom relief in absence of arrhythmias
 decreases hospitalization
 Diuretics
 improve the symptoms and exercise tolerance
 Anticoagulation
 In the setting of Afib and additional cardio-embolic risk
factors
Management
 Fish Oil
 Conflicting evidence for this, however, not harmful
 Consider 1g daily supplementation with OTC
 Statins
 No evidence for benefit in CHF
 CCB
 Peripheral vasodilators (Amlodipine, Felodipine) safe to
use in HF
 No benefit, and possible harm, with Diltiazem or
Verapamil like drugs
Management
 ICD
 Primary Prevention
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
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Prior MI (<40 days) and EF <30%
NYHA Class II, EF <35%
Have been on maximal medical therapy > 3 months
Syncope with structural heart disease and sustained VT/VF on EP
study
 Cardiac Resynchronization
 GRADE 1A Indication
 1. SR, QRS > 150 ms, LBBB, EF < 35%, NYHA > III with optimal
therapy
 GRADE 1B Indication
 1. SR, QRS > 150 ms, LBBB, EF < 30%, NYHA > II with ICD placement
Nonpharmalogic Treatment
 Multidisciplinary Approach
 Patient education and instruction
 Appropriate hospital follow-up (within 7 days)
 Management of comorbidities
 Decreases hospitalizations and quality of life
 Moderate Exercise in chronic stable HF
 Decrease mortality
 Improves hospitalizations and quality of life
References

KING, M, KINGERY, J and CASEY, B. “Diagnosis and Evaluation of Heart Failure” Am Fam
Physician. 2012 Jun 15;85(12):1161-1168.

MCCONAGHY, J. “Outpatient Treatment of Systolic Heart Failure” Am Fam Physician. 2004 Dec 1;70(11):21572164.

Nishimura, RA et al. “2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease:
executive summary: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines.” Circulation. 2014 Jun 10;129(23):2440-92. doi: 10.1161/CIR.0000000000000029. Epub
2014 Mar 3.
MKSAP Question 1
A 74-year-old man is evaluated in the emergency department for a 7-day history of
progressive exertional dyspnea associated with a dry cough, increasing orthopnea (from two
to four pillows), and inability to buckle his belt. He has a 20-year history of hypertension
treated with diltiazem.
On physical exam, blood pressure is 162/86 mmHg, pulse rate is irregularly irregular at
84/min, and respiration rate is 18/min. Estimated central venous pressure is 14 cm H2O.
Cardiac examination reveals an irregularly irregular rhythm and an S4. Bibasilar crackles are
heard on auscultation of the lungs. His liver is enlarged 2 cm below the costal margin. His
extremity examination reveals bilateral pitting edema.
Serum electrolyte levels and kidney function tests are normal. Serum B-type natriuretic
peptide level is 2472 pg/mL. ECG shows atrial fibrillation. Echocardiogram shows a left
ventricular ejection fraction of 60%, septal wall thickness of 1.5 cm, and posterior wall
thickness of 1.4 cm. Chest radiograph shows hazy bilateral infiltrates.
Which of the following is the most appropriate next step in management?
(A) B-Blocker
(B) Cardioversion
(C) Furosemide
(D) Spironolactone
Manage heart failure with preserved ejection fraction with diuretics.
Answer: C Furosemide
This patient should be admitted to the hospital and given IV furosemide. His
presentation is characteristic for heart failure with preserved ejection fraction
(HFpEF). He has volume overload manifested by increasing abdominal girth,
increased exertional dyspnea, and progressive orthopnea. His left ventricular
ejection fraction is normal, but he has mild left ventricular hypertrophy and a long
history of hypertension. Additionally, he has a markedly elevated B-type natriuretic
peptide level. The etiology of his acute exacerbation into heart failure is most
likely acute atrial fibrillation, but because he is already on diltiazem and has a
normal heart rate, he may have been in atrial fibrillation for some time and not
noticed it.
In contrast to patients with a reduced ejection fraction, no drugs have been
shown to reduce mortality rates in patients with HFpEF. Instead, guidelines
emphasize controlling blood pressure and volume. Patients with HFpEF are often
volume sensitive, and careful use of diuretics to maintain euvolemia is important.
This patient is not already taking a diuretic, and starting with a low dose of
furosemide is a reasonable approach. Patients with HFpEF should be
encouraged to monitor their weight closely, as small differences in volume can
quickly cause volume overload and subsequent hospital admissions.
B-blocker therapy is relatively contraindicated in this patient with acute
decompensated heart failure as it may exacerbate his heart failure. Once his
heart failure is successfully treated with diuretics, this patient may benefit from Bblocker therapy to manage his heart rate and blood pressure.
Despite the fact that the patient is currently in atrial fibrillation, cardioversion at
this point is incorrect. Because he is hemodynamically stable with good rate
control, there is no indication for immediate cardioversion.
Several small trials have suggested that aldosterone antagonists may improve
diastolic function in patients with HFpEF. However, a recent trial comparing
spironolactone with placebo showed a reduction in heart failure hospitalizations
but no difference in mortality rates or all-cause hospitalizations in patients with
HFpEF, and spironolactone was associated with significant increases in serum
creatinine and potassium levels.
Key point: Patients with HFpEF are often volume sensitive, and careful use
of diuretics to maintain euvolemia is important.
Question 2
A 56-year-old man with heart failure is admitted to the hospital with a 2-week history of
increasing exertional dyspnea and fatigue. He also has type 2 diabetes mellitus. Medications
are metformin, lisinopril, carvedilol, furosemide, metolazone, and digoxin.
On physical examination, blood pressure is 88/60 mmHg, pulse rate is 95/min, and
respiration rate is 20/min. He is somewhat confused and inattentive. Jugular venous
distension is present to the angle of the jaw while sitting. Cardiac examination reveals an S3.
There are bibasilar crackles on pulmonary examination. He has edema to the mid-thighs.
Extremities appear mottled and are cool to the touch.
Serum creatinine level is 3.1 mg/dL; baseline value was 1.1 mg/dL. Serum sodium level is
133 mEq/L. ECG shows no evidence of ischemia. Chest radiograph shows cardiomegaly and
vascular congestion.
In addition to intravenous diuresis, which of the following is the most appropriate
management?
(A) Dobutamine
(B) Intra-aortic balloon pump
(C) Milrinone
(D) Right heart catheterization
Answer: A Dobutamine
This patient should be started on dobutamine for probable cardiogenic shock.
Cardiogenic shock is present when there is systemic hypotension and evidence for
end-organ hypoperfusion, primarily due to inadequate cardiac output. Cardiogenic
shock usually requires treatment intravenous vasoactive medications and, in
severe cases, device-based hemodynamic support.
In this patient, initiating inotropic therapy is reasonable. Both dobutamine and milrinone
are used to increase cardiac output; however, in the setting of kidney dysfunction,
dobutamine would be the appropriate choice because milrinone is metabolized by the
kidneys. Also, milrinone is a vasodilator, which could exacerbate his hypotension.
Mechanical therapy for cardiogenic shock should be considered in patients with endorgan dysfunction that does not rapidly show signs of improvement (within the first 1224 hours) with IV vasoactive medications and correction of volume overload. It is
premature to consider mechanical therapy for this patient.
Right heart catheterization can be helpful to guide therapy if volume status or cardiac
output is uncertain. However, it has not been shown to improve outcomes in patients
hospitalized with heart failure. Placement of a right heart catheter is not necessary prior
to initiating inotropic therapy.
Question 3
A 66-year-old woman is evaluated prior to discharge. She has ischemic cardiomyopathy and was admitted
to the hospital 5 days ago for worsening symptoms of heart failure. She skipped taking her diuretics during
a recent business trip. Today, she feels well and is able to walk around the ward twice without any
symptoms.
This was her first hospitalization in 3 years, although she has skipped her diuretics during other business
trips without apparent ill effect. She had an implantable cardioverter-defibrillator placed 3 years ago. An
echocardiogram 1 month ago showed a left ventricular ejection fraction of 15% (stable for the past 6 years).
Medications are captopril, metoprolol succinate, digoxin, furosemide, and spironolactone.
On physical examination, blood pressure is 110/72 mmHg, pulse rate is 56/min, and respiration rate is
14/min. She has no jugular venous distension and no S3. Lungs are clear, and she has no edema. ECG
shows sinus rhythm, a QRS interval of 90 ms, and Q waves in V1 through V4. There are no changes
compared with the admission ECG recorded 3 years ago.
Which of the following is the most appropriate management?
(A) Discharge and schedule follow-up within 7 days
(B) Measure B-type natriuretic peptide
(C) Obtain echocardiography prior to discharge
(D) Upgrade to biventricular implantable cardioverter-defibrillator
Answer: A Discharge and schedule follow-up within 7 days
This patient should be discharged home, with a follow-up appointment
scheduled within 7 days. She has had one heart failure hospitalization in
the past 3 years and her nonadherence with her diuretic medication was
the most likely cause of the admission.
With any heart failure hospitalization, it is important to reassess several
factors before discharge. First, patients must be adequately diuresed
prior to discharge. It is important to know that measuring a serum BNP
level will not help with that assessment. Patients should be examined for
flat neck veins, resolution of peripheral or abdominal edema (if possible),
and resolution of the signs and symptoms of acute heart failure. Second,
patients should be on appropriate medical therapy for their stage of heart
failure. For this patient, appropriate medications include ACE inhibitor or
ARB, B-blocker, aldosterone antagonist, and an adequate dosage of
diuretic to prevent readmission. Third, it has been demonstrated that a
patient seen within 1 week after discharge is associated with a
reduction of future heart failure hospitalizations.
An echocardiogram performed 1 month ago demonstrated that the
patient’s left ventricular function is stable. There is no suggestion of
ischemia or change in valvular function as a precipitant of this
hospitalization. If this patient had not had an echocardiogram in at least 6
months, it would be reasonable to repeat the echo.
Patients are candidates for a biventricular pacemaker if they have all of
the following indications: on guideline-directed medical therapy, a
reduced ejection fraction (<35%), a wide QRS interval (>150 ms) or a left
bundle branch block, and New York Heart Association functional class III
or IV symptoms. This patient has a narrow QRS interval and therefore
would not be a candidate for upgrading to a biventricular implantable
cardioverter-defibrillator.
Key point: patients hospitalized for heart failure who are scheduled
for a follow-up appointment within 1 week after discharge have a
reduced risk of future heart failure hospitalization.
Question 4
A 77-year-old man with a 5-year history of idiopathic cardiomyopathy is evaluated for
progressive exertional fatigue and dyspnea. He has recently stopped carrying groceries in
from the car because of his exertional dyspnea. He had an implantable cardioverterdefibrillator placed 3 years ago. Medical history is also significant for hypertension.
Medications are lisinopril 40 mg/d; metoprolol succinate 25 mg/d; furosemide 40 mg/d; and
spironolactone 25 mg/d.
On physical examination, blood pressure is 94/60 mmHg and pulse rate is 70/min. Estimated
central venous pressure is 5 cm H2O. There is no edema.
Serum electrolyte levels and kidney function are normal. ECG shows normal sinus rhythm, a
PR interval of 210 ms, QRS duration of 160 ms, and a new left bundle branch block. His left
ventricular ejection fraction 3 months ago was 25%.
Which of the following is the most appropriate next step in management?
(A) Cardiac resynchronization therapy
(B) Dobutamine therapy
(C) Increase furosemide dose
(D) Left ventricular assist device placement
Manage heart failure with cardiac resynchronization therapy
Answer: A Cardiac resynchronization
This patient with symptomatic heart failure and a reduced left ventricular ejection
fraction with evidence of significant conduction system disease should undergo
placement of a biventricular pacemaker (cardiac resynchronization therapy [CRT]). He
has progressive heart failure symptoms while on appropriate medical therapy and has
New York Heart Association functional class III symptoms. With his EF less than 35%
and left bundle branch block (LBBB), he is a candidate for a biventricular pacemaker,
which has been demonstrated to reduce mortality and symptoms in patients with NYHA
functional class III and IV heart failure by improving cardiac hemodynamics.
The 2013 American College of Cardiology Foundation/ American Heart Association/
Heart Rhythm Society guideline recommends CRT therapy in patients with an ejection
fraction of 35% or below, NYHA functional class III or IV symptoms on guidelinedirected medical therapy, and LBBB with QRS duration greater than or equal to 150
ms. This patient already has an implantable cardioverter-defibrillator. Now that he has
developed a LBBB and an increase in symptoms, it is reasonable to proceed with
placement of a biventricular pacemaker as well.
Inotropic therapy, such as dobutamine, is reserved for patients with end-stage
heart failure, either as a bridge to transplantation or for palliative care. Although
this patient has progressive symptoms, he has not reached this stage yet, and
has no indication for inotropic therapy.
The patient has no evidence of volume overload on examination and a borderline
low blood pressure; therefore, increasing his diuretic dose would not be expected
to improve his symptoms and may worsen them by lowering his cardiac filling
pressures and cardiac output.
The patient is fairly symptomatic but has not yet had optimal therapy, as he has
an indication for CRT and has not yet received it. Left ventricular assist devices
(LVAD) are reserved for patients with end-stage refractory heart failure as a
bridge to heart transplantation or as destination therapy in selected patients who
are not candidates for transplantation. However, prior to being considered for
either an LVAD or heart transplantation, a patient must be on optimal medical
therapy.
Key point: Cardiac resynchronization therapy is recommended in patients
with an EF of 35% or below, NYHA functional class III or IV symptoms on
guideline-directed medical therapy, and LBBB or QRS duration of 150 ms or
greater.
Question 5
A 72-year-old woman is evaluated for progressive heart failure symptoms. She has 10-year history of
nonischemic heart failure. She currently experiences exertional dyspnea with climbing one flight of stairs,
which she was able to do without shortness of breath 3 months ago. Medical history is significant for
hypertension, and her medications are lisinopril, carvedilol, furosemide, digoxin, and spironolactone. The
patient is black.
On physical examination, blood pressure is 134/72 mmHg and pulse rate is 66/min. BMI is 35. She has no
jugular venous distension. Cardiac examination reveals a grade 1/6 holosystolic murmur but is otherwise
normal. There is no lower extremity edema. The remainder of her examination is unremarkable.
Laboratory studies are significant for normal electrolyte levels and a serum creatinine level of 1.5 mg/dL.
ECG shows normal sinus rhythm, a QRS duration of 110 ms, and nonspecific ST-T wave changes.
Echocardiogram shows a left ventricular ejection fraction of 38% and trace mitral regurgitation.
Which of the following is the most appropriate treatment?
(A) Add hydralazine and isosorbide dinitrate
(B) Add losartan
(C) Add warfarin
(D) Cardiac resynchronization therapy
Treat a black patient with heart failure with hydralazine and isosorbide dinitrate
in addition to usual therapy.
Answer: A Add hydralazine and isosorbide dinitrate
This patient should have hydralazine and isosorbide dinitrate added
to her medication regimen for the treatment of her heart failure. She
has New York Heart Association functional class III heart failure and is
black. Hydralazine and isosorbide dinitrate have been demonstrated
to improve symptoms and reduce mortality in patients who are black
and who are already on maximal therapy with NYHA class III or IV
heart failure symptoms. Adverse effects of this therapy include
peripheral edema and headaches, but this regimen should be
attempted in these patients.
Optimal therapy for patients with heart failure includes treatment with
an ACE inhibitor, B-blocker, and an aldosterone antagonist. The
addition of an angiotensin receptor blocker, such as losartan, to this
combination is generally not recommended, primarily because of
concern for hyperkalemia. Additionally, no benefit to this treatment
regimen has been documented.
In patients with heart failure, warfarin treatment is appropriate
only for those with another indication, such as atrial fibrillation
meeting CHADS-VASc criteria, but not heart failure alone. The
routine treatment of patients with heart failure with warfarin is
not indicated.
Cardiac resynchronization therapy (CRT) may be an effective
therapy in patients with heart failure and a prolonged QRS
duration indicating dyssynchrony. Because this patient does
not have evidence of dyssynchrony or an ejection fraction of
35% or less, she is not a candidate for treatment.
Key point: Hydralazine and isosorbide dinitrate improve
symptoms and reduce mortality in patients with NYHA
class III or IV heart failure symptoms who are black and
are already on maximal therapy.