Heart failure resident survival guide

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For acute heart failure prevention click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahmoud Sakr, M.D. [2]; Ayokunle Olubaniyi, M.B,B.S [3]; Rim Halaby, M.D. [4]

Acute Heart Failure Resident Survival Guide Microchapters
Overview
Classification
Causes
FIRE
Diagnosis
Treatment

Stage A and B
Stage C and D
Diuretic Therapy
Medication Dosages

Do's
Don'ts

Overview

Heart failure is a complex syndrome characterized by inadequate blood ejection or impaired ventricular filling, leading to the inability of the heart to pump blood to meet the metabolic demands of the body. Heart failure is a clinical syndrome for which the diagnosis relies mainly on symptoms and physical examination findings. The main symptoms and signs of heart failure are dyspnea, volume overload (leading to pulmonary edema and/or peripheral edema), fatigue, and exercise intolerance. Acute decompensated heart failure (ADHF) is a life-threatening condition that can occur in the setting of a new onset heart failure or worsening of an existing chronic heart failure. Symptoms of ADHF may include dyspnea secondary to pulmonary edema, peripheral edema, hypotension, and impaired end organ perfusion that can manifest by worsening renal function, altered mental status, and cold clammy extremities. The mainstays of treatment of ADHF are 1) oxygen therapy to improve hypoxia, 2) diuresis to reduce both preload and intravascular volume, and 3) vasodilators to reduce afterload. The goals of treatment for chronic heart failure are to relieve symptoms, decrease hospitalization rate, and decrease morbidity and mortality. Treatment of heart failure includes identification and management of precipitating factors, lifestyle changes, pharmacological therapy, and devices.

Classification

Classification by Severity of Congestive Heart Failure

Shown below is a table comparing American College of Cardiology Foundation/American Heart Association (ACCF/AHA) stages to New York Heart Association (NYHA) classification of severity of heart failure.[1]

ACCF/AHA Stages New York Heart Association (NYHA) Classification
Stage Interpretation Class Interpretation
A At high risk for heart failure (HF) but without structural heart disease or symptoms of HF - -
B Structural heart disease but without signs or symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF
C Structural heart disease with prior or current symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF
II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF
III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF
IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest
D Refractory HF requiring specialized interventions IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest

Classification by Other Factors

Left Ventricular Ejection Fraction (LVEF)

Cardiac Output

  • Low cardiac output
  • High stroke volume with/without cardiac output

Left vs. Right Sided

Backwards vs. Forward

  • Backwards: Congestion, elevated filling pressure
  • Forwards: Low systemic perfusion

Causes

Life Threatening Causes

Acute decompensated heart failure is life threatening and should be treated as such irrespective of the underlying cause.

Common Causes

Click here for the complete list of causes.

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients of severe acute decompensated heart failure in need of immediate intervention.[1]

Boxes in red signify that an urgent management is needed.

Abbreviations: BU: Blood urea nitrogen; COPD: Chronic obstructive pulmonary disease; D5W: 5% dextrose solution in water ; HF: Heart failure; IV: Intravenous; MAP: Mean arterial pressure; Na: Sodium; NSAID: Non steroidal anti-inflammatory drug; SBP: Systolic blood pressure; S3: Third heart sound;

 
 
Identify cardinal findings that increase the pretest probability of acute decompensated heart failure

Dyspnea
Cool extremities
Peripheral edema
Decreased urine output
❑ Past medical history of heart failure
❑ History of orthopnea and paroxysmal nocturnal dyspnea
❑ Pulmonary crepitations/rales/crackles

Third heart sound (S3)
 
 
 
 
 
 
 
 
 
Does the patient have any of the following findings that require hospitalization and urgent management?

❑ Severe decompendated HF:

Hypotension (SBP < 90 mmHg or drop in MAP >30 mmHg) and/or cardiogenic shock
Altered mental status
Cold and clammy extremities
Urine output <0.5mL/kg/hr

Dyspnea at rest manifested by tachypnea or oxygen saturation <90%
Atrial fibrillation with a rapid ventricular response resulting in hypotension

Acute coronary syndrome
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Yes
 
No
 
 
 
 
 
 
 
 
 
 
 
Admit to to a level of care that allows for constant ECG monitoring given the risk of arrhythmia
 
 
 
 
 
 
 
 
 
 
 

Initial stabilization:
❑ Assess the airway
❑ Position the patient upright at an angle of 45 degrees, with legs dangling off the bedside (decrease preload)
❑ Monitor heart rate and blood pressure continuously
❑ Monitor oxygen saturation continuously
❑ If hypoxemia is present (Sa02 < 90% or Pa02 <60 mmHg), administer oxygen with/without noninvasive ventilation
Morphine to decrease symptoms and Afterload (avoid IV morphine, may increase mortality / duration of intubation, generally not advisable, may relieve refractory symptoms)
❑ Secure intravenous access with 18 gauge cannula
❑ Monitor fluid intake and urine output carefully (guide the adjustment of the diuretics dose)

Assess congestion and perfusion:
Congestion at rest (dry vs. wet)
"Wet" suggested by orthopnea, ↑JVP, rales, S3, pedal edema
Low perfusion at rest (warm vs. cold)
"Cold" suggested by narrow pulse pressure, cool extremities, hypotension
The patient is:
❑ Warm and dry, OR
❑ Warm and wet, OR
❑ Cold and dry, OR
❑ Cold and wet

Identify precipitating factor and treat accordingly:
Click on the precipitating factor for more details on the management
Myocardial infarction
Myocarditis
Renal failure
Hypertensive crisis
❑ Non adherence to medications
❑ Worsening Aortic stenosis
❑ Drugs (NSAIDS, thiazides, calcium channel blocker, beta blockers)
❑ Toxins (alcohol, anthracyclines)
Atrial fibrillation

Rate control of atrial fibrillation is the mainstay of arrhythmia therapy. Avoid the use of drugs with negative inotropic effects such as beta blockers and non-dihydropyridine calcium channel blockers e.g., verapamil in the treatment of acute decompensated systolic heart failure
Consider cardioversion if the patient is in cardiogenic shock or if new onset atrial fibrillation is the clear precipitant of the hemodynamic decompensation

COPD
Pulmonary embolism
Anemia
Thyroid abnormalities
❑ Systemic infection

Treat congestion and optimize volume status:
Diuretics
❑ Administer IV loop diuretics as intermittent boluses or continuous infusion (I-B)

❑ If patient is already on loop diuretics: IV dose ≥ home PO dose (I-B); rule of thumb: IV dose = 2.5x equivalent oral daily dose
❑ If patient is not already on loop diuretics, administer IV starting dose:
Furosemide 20 to 40 mg, OR
Torsemide 5 to 10 mg, OR
Bumetanide 0.5 to 1 mg
❑ Adjust dose according to volume status (I-B)
❑ Perform serial assessment of fluid intake and output, vital signs, daily body weight (measured every day, with the same scale, at the same time, after first void) and symptoms
❑ Order daily electrolytes, BUN, creatinine (I-C)

❑ Low sodium diet (<2 g daily)
❑ In case of persistent symptoms:

❑ Increase dose of IV loop diuretics (I-B)- double dose at 2 hour interval up to maximal daily dose
Furosemide maximal dose: 40 to 80 mg
Torsemide maximal dose: 20 to 40 mg
Bumetanide maximal dose: 1 to 2 mg
OR
❑ Add a second diuretics, such as thiazide (I-B)

❑ Consider low dose dopamine infusion for improved diuresis and renal blood flow (IIb-B)
❑ Consider renal replacement therapy/ultrafiltration in obvious volume overload (IIb-B) refractory to higher dose/combination of IV diuretics

Venodilators
❑ Consider IV nitroglycerin, nitroprusside, or nesiritide as add-on to diuretics to relieve dyspnes (IIb-A)

Do not administer vesodilators among patients with hypotension.

Treat low perfusion:
Inotropes (click her for details)

If the total body and intravascular volumes are overloaded and the patient is normotensive, then diuresis alone should be undertaken. If the patient is volume overloaded but hypotensive, then inotropes must be administered in addition to diuretics.

Invasive hemodynamic monitoring:

❑ Consider pulmonary artery catheterization in case of failure to respond to medical therapy, respiratory distress, shock, uncertainty regarding volume status, or increase in creatinine; assess the following parameters:

PCWP
Cardiac output
Systemic vascular resistance

VTE prevention:
Anticoagulation in the absence of contraindications (I-B)

Chronic medical therapy:
❑ Chronic ACE inhibitor: Hold if patient is hemodynamically unstable
❑ Chronic beta blocker:

Hold if patient is hemodynamically unstable and/or in need or inotropes
Decrease dose by ≥ half if patient is in moderate heart failure

❑ DO NOT INITIATE ACE INHIBITORS during an acute decompensation
❑ DO NOT INITIATE BETA BLOCKER during an acute decompensation; initiate beat blockers at a low dose in stable patients following optimization of volume status and D/C IV diuretics and inotropes (I-B)

Monitor laboratory tests:
BUN
Creatinine
Sodium (to detect hyponatremia which carries a poor prognosis), chloride, bicarbonate (to detect contraction alkalosis) and serum potassium (to detect hypokalemia as a result of diuresis and which can precipitate arrhythmias), potassium, magnesium

Management of hyponatremia:
❑ Water restriction

❑ <2 L/day if the Na is < 130 meq/L
❑ < 1 L/day or more if the Na is < 125 meq/L
Keep in min that juices are essentially free water with sugar.
In the hyponatremia patient, drips should not be in D5W.

❑ Optimization of chronic home medications

❑ Persistent hyponatremia and risk of cognitive impairment: vasopressin antagonist for short term (hypervolemic)
 
 
 
 
 

Complete Diagnostic Approach

A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.[1][2]

Abbreviations: ANA: Antinuclear antibody; ARDS: Acute respiratory distress syndrome; BNP: B-type natriuretic peptide; BUN: Blood urea nitrogen; CAD: Coronary artery disease; CBC: Complete blood count; CCB: Calcium channel blocker; CHF: Congestive heart failure; CT: Computed tomography; CXR: Chest X-ray; DM: Diabetes mellitus; ECG: Electrocardiogram; JVP: Jugular venous pressure; HF: Heart failure; HTN: Hypertension; LVEF: Left ventricular ejection fraction; LVH: Left ventricular hypertrophy; MI: Myocardial infarction; MRI: Magnetic resonance imaging; NT-pro BNP: N-terminal pro-brain natriuretic peptide; OCPs: Oral contraceptive pills; PAWP: Pulmonary artery wedge pressure; SBP: Systolic blood pressure; S1: First heart sound; S3: Third heart sound; TSH: Thyroid stimulating hormone

 
 
 
 
 
 
 
Characterize the symptoms:

Symptoms of left-sided fluid accumulation:
Dyspnea

❑ At rest
❑ Exertional

Paroxysmal nocturnal dyspnea
Orthopnea
Cough
Symptoms of right-sided fluid accumulation:
Peripheral edema
❑ Right upper quadrant abdominal discomfort
Bloating
Satiety
Symptoms of reduced cardiac output:
Fatigue
Exercise intolerance
Oliguria
Dizziness
Syncope
Altered mental status
Cyanosis
Anorexia
Abdominal pain (suggestive of mesenteric ischemia)
Symptoms suggestive of precipitating events:
Chest pain (suggestive of myocardial ischemia)
Palpitations (suggestive of arrhythmias)
Fever (suggestive of infection)
Nonspecific symptoms:
Nausea
Weight loss


Obtain a detailed history:
Past medical history

Atrial fibrillation
Cardiomyopathy
Diabetes mellitus
Hypertension
Myocarditis
Previous myocardial infarction
Prior heart failure
Sleep apnea
Thyroid disease
Valvular heart disease

Medication history

❑ Noncompliance with previously prescribed medications for heart failure
❑ Intake of the following drugs:
Alcohol
Beta blockers
Calcium channel blockers like verapamil which can exacerbate CHF or diltiazem which can cause peripheral edema
Chemotherapy drugs - anthracyclines
NSAIDs which should not be given in CHF
Thiazolidinedione

Family history

❑ History of dilated cardiomyopathy
Radiation to the chest

Determine the NYHA classification based on symptoms:
❑ Class I (no symptoms)
❑ Class II (symptoms with ordinary activities)
❑ Class III (symptoms upon minimal activity)
❑ Class IV (symptoms at rest)

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Examine the patient:

General appearance:
❑ Ill-looking
❑ In respiratory distress
❑ In upright sitting position

Vitals:
Temperature

Fever (suggestive of underlying infection)

Pulse

Tachycardia
Narrow pulse pressure (<25% of SBP)

Blood pressure

Hypotension (suggestive of circulatory collapse)
Hypertension

Respiration

Tachypnea (most common symptom)

Pulse oximetry (maintain oxygen sat ≥ 94% unless COPD)

Weight:
❑ Measure weight daily at the same time after the first void
❑ Subtract 'dry weight' from current weight to estimate extent of volume overload and edema

Skin
Cool and clammy (suggestive of hypoperfusion)
Cyanosis (suggestive of severe hypoxemia)
Anasarca
Jaundice (suggestive of liver dysfunction secondary to right-sided fluid overload)

Neck examination:
Jugular vein distention (suggestive of right-sided fluid overload)
❑ Positive hepatojugular reflux (suggestive of right-sided fluid overload)

Respiratory examination
Tachypnea
Wheeze
❑ Dullness at lung bases (suggestive of pleural effusion, may be present in chronic HF secondary to lymphatic compensation)
Crackles/crepitations/rales (suggestive of pleural effusion)
Cheyne-stokes respiration

Cardiovascular examination
❑ Displaced apex beat (suggestive of enlarged left ventricle)
Parasternal heave (suggestive of elevated right ventricular pressure)
S3 (typical) or S4 or both
❑ Soft S1
❑ Pulsus alternans
S4 (suggestive of diastolic dysfunction)
❑ New or changed murmur (suggestive of an underlying valvular heart diseases)

Mitral regurgitation - Holosystolic murmur
Aortic regurgitation - Decrescendo diastolic murmur
Aortic stenosis - Crescendo-decrescendo systolic ejection murmur with ejection click

Abdominal examination
The following findings suggest volume overload and / or poor forward cardiac output:
Hepatojugular reflux
Hepatomegaly
Ascites

Extremity examination
Pedal edema

Neurological examination
Altered mental status
Syncope (suggestive of aortic stenosis or pulmonary embolism)


Determine status of congestion and perfusion based on physical exam:
Congestion at rest (dry vs. wet)

"Wet" suggested by orthopnea, ↑JVP, positive hepatojugular reflux, abnormal valsalva response, rales, dullness upon percussion in bases, S3, peripheral edema, hepatomegaly, ascites, jaundice

Low perfusion at rest (warm vs. cold)

"Cold" suggested by narrow pulse pressure, cool extremities, hypotension, soft S1, pulsus alternans, decreased urinary output

The patient is:
❑ Warm and dry, OR
❑ Warm and wet, OR
❑ Cold and dry, OR
❑ Cold and wet

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Order tests:

Routine (Class I, level of evidence C)

CBC (rule out anemia)
Troponin
❑ Elevated in myocardial ischemia and acute cardiogenic pulmonary edema, particularly if creatinine clearance (CrCl) is reduced
Troponin T ≥ 0.1 ng/mL (associated with poor survival)[3]
Electrolytes
Sodium: hyponatremia may occur due to fluid overlaod
Serum calcium
Serum magnesium can be lowered by diuresis
Serum bicarbonate: to monitor contraction alkalosis with diuresis
BUN, creatinine: may be elevated due to poor renal perfusion
Urinalysis
Fasting blood sugar
Fasting lipid profile
Liver function tests: can be elevated secondary to peripheral hypoperfusion
TSH

BNP or NT-pro BNP (if diagnosis is uncertain)
Heart failure is unlikely if:[4][5]

BNP ≤ 100 pg/mL, or
NT-pro BNP ≤ 300 pg/mL

Chest X-ray (Class I, level of evidence C)

Cardiomegaly (cardiothoracic ratio >50%)
❑ Cardiogenic pulmonary edema
Kerley B lines
Peribronchial cuffing
Cephalization
Chest X-ray findings in a patient with acute heart failure

ECG (to help identify the cause of heart failure)

Low QRS voltage (suggestive of infiltrative or dilated cardiomyopathy)
Arrhythmia (atrial fibrillation carries a poor prognosis and requires slowing of the heart rate to improve filling & cardiac output)
Poor R wave progression (suggestive of a prior MI)
Left ventricular hypertrophy (consistent with a history of hypertension)
Left bundle branch block (LBBB) due to prior MI, may result in dysynchrony)
Left atrial enlargement (due to valvular disease or hypertension)
❑ Non-specific ST segment and T wave changes may suggest ischemia

❑ 2-D echocardiography with Doppler
(Class I, level of evidence C)

❑ Assess chambers size, wall thickness, wall motion, and valve function
❑ Assess ejection fraction

Radionuclide ventriculography or MRI

❑ To assess LVEF and volume when echocardiography is inadequate
❑ To assess myocardial infiltrative processes or scar burden (MRI)

Coronary angiography looking for CAD
❑ Comprehensive metabolic panel if no evidence of CAD on coronary angiography
❑ Consider pulmonary artery catheterization in case of failure to respond to medical therapy, respiratory distress, shock, uncertainty regarding volume status, or increase in creatinine; assess the following parameters:

PCWP
Cardiac output
Systemic vascular resistance

Order additional tests to rule out other etiologies:
ANA and rheumatoid factor (for rheumatologic diseases)
❑ Diagnostic tests for hemochromatosis and pheochromocytoma
Endomyocardial biopsy (when myocarditis is suspected)

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Consider alternative diagnoses:

Alternative diagnosesFeatures
Acute asthmaWheeze
❑ Reversal of symptoms following
administration of bronchodilators
COPD❑ Increased cough
❑ Increased dyspnea
❑ Increased sputum production
ARDS❑ Severe hypoxia
❑ Bilateral opacities on chest X-ray
PCWP < 15 mmHg
PneumoniaFever, cough, sputum
Consolidation on chest X-ray
Pulmonary embolismPleuritic chest pain, cough, S4
❑ Risk factors: trauma, immobilization, smoking, OCPs
❑ Clot in pulmonary artery on CT pulmonary angiography
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Assess the stage of heart failure using the ACCF/AHA staging system to guide chronic therapy
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stage C

Patients with structural heart disease
This refers to patients with the following:

❑ Previous MI
❑ LV remodeling* (including LVH + low EF)
❑ Asymptomatic valvular disease

AND

Signs or symptoms of heart failure

*LV remodeling refers to the changes in size, shape and function of the heart resulting from cardiac load or injury
 
Stage D

Refractory heart failure

❑ Marked symptoms at rest
❑ Recurrent hospitalizations
 
 
 

Prevention of Heart Failure in Stage A and B

Shown below is an algorithm depicting the management of stage A and B heart failure.[1]

Abbreviations: ACE I: Angiotensin converting enzyme inhibitor; ACS: Acute coronary syndrome; CVD: Cardiovascular disease; DM: Diabetes mellitus; EF: Ejection fraction; HF: Heart failure; HTN: Hypertension; ICD: Implantable cardioverter defibrillator; MI: Myocardial infarction; PAD: Peripheral artery disease

 
 
What is the stage of heart failure (HF)?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stage A
At high risk for HF but without structural heart disease or symptoms of HF
 
Stage B
Structural heart disease but without signs or symptoms of HF
 
 
 
 
 
 
 
 
 
 
 
 
 
 

❑ Encourage healthy lifestyle and exercise
❑ Treat hypertension ( I-A)
❑ Treat dyslipidemia (I-A)
❑ Control obesity (I-C)
❑ Treat DM (I-C)
❑ Avoid tobacco (I-C)
❑ Avoid cardiotoxic agents (I-C)

❑ Administer ACE-I if HTN, DM, CVD, PAD
 

❑ Encourage healthy lifestyle and exercise
❑ Treat hypertension (I-A)
❑ Treat dyslipidemia (I-A)
❑ Control obesity (I-C)
❑ Treat DM (I-C)
❑ Avoid tobacco (I-C)

❑ Avoid cardiotoxic agents (I-C)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

Consider additional measures in selected patients: ❑ Administer ACE-I if history of MI or ACS and reduced EF to prevent symptoms and reduce mortality (I-A), in all decreased EF to prevent symptoms (I-A)
❑ Administer beta-blockers if history of MI or ACS and reduced EF to reduce mortality (I-B), in all reduced EF to prevent symptoms (I-C)
❑ Administer statins if history of MI or ACS to prevent symptoms (I-A)

❑ Consider ICD placement to prevent sudden death if asymptomatic ischemic cardiomyopathy, > 40 days post-MI, LVEF ≤30%, on adequate medical therapy, and good 1 year survival
 
 
 

Treatment of Heart Failure in Stage C and D

Shown below is an algorithm depicting the management of stage C and D heart failure.[1]

Abbreviations: ACE I: Angiotensin converting enzyme inhibitor; ARB: Angiotensin II receptor blocker; ACS: Acute coronary syndrome; BID: Twice a day; BNP: Brain natriuretic peptide; CRT: Cardiac resynchronization therapy CVD: Cardiovascular disease; DM: Diabetes mellitus; EF: Ejection fraction; GDMT: Guideline determined medial therapy; GFR: Glomerular filtration rate; HF: Heart failure; HFrEF: Heart failure reduced ejectoon fraction; HFpEF: Heart failure preserved ejection fraction; HTN: Hypertension; ICD: Implantable cardioverter defibrillator; LVEF: Left ventricular ejection fraction; MCS: Mechanical circulatory support; NYHA: New York Heart Association; MI: Myocardial infarction; PAD: Peripheral artery disease; TID: Three times a day

 
 
 
 
What is the stage of heart failure (HF)?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stage C HFrEF
Structural heart disease with prior or current symptoms of HF and reduced ejection fraction
 
Stage C HFpEF
Structural heart disease with prior or current symptoms of HF and preserved ejection fraction
 
Stage D
Refractory HF requiring specialized interventions
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  • Exercise training (I-A)
  • Education for self-care (I-B)
  • Sodium restriction if symptomatic (IIa-C)
  • Cardiac rehabilitation in patients clinically stable (IIa-B)
  • Treatment of HTN, dyslipidemia, obesity, DM
  • Avoid tobacco (I-C)
  • Avoid cardiotoxic agents

Medical therapy:

Starting dose:
Furosemide 20 to 40 mg, OR
Torsemide 10 to 20 mg, OR
Bumetanide 0.5 to 1 mg
Monitor volume status and adjust dose
No response: double oral diuretics dose rather than administer BID
No or minimal response despite maximal diuretic dose: Administer diuretics BID or TID
 
  • Exercise training (I-A)
  • Education for self-care (I-B)
  • Sodium restriction if symptomatic (IIa-C)
  • Cardiac rehabilitation in patients clinically stable (IIa-B)
  • Treatment of HTN, dyslipidemia, obesity, DM
  • Avoid tobacco (I-C)
  • Avoid cardiotoxic agents

  • Routine drugs:

    PLUS

    Starting dose:
    Furosemide 20 to 40 mg, OR
    Torsemide 10 to 20 mg, OR
    Bumetanide 0.5 to 1 mg
    Monitor volume status and adjust dose
    No response: double oral diuretics dose rather than administer BID
    No or minimal response despite maximal diuretic dose: Administer diuretics BID or TID

    PLUS

    • Aldosterone antagonist
      • NYHA class II with prior history of cardiovascular hospitalization or high BNP OR NYHA class III-IV, AND LVEF <=35%, AND estimated GFR >30 mL/min/1.73 m2, K+< 5 mEq/L (decrease mortality by 34%) (I-A)
      • LVEF ≥40% AND symptoms of HF or DM (I-B)

    Add-on drugs in selected patients:

    • Persistent symptoms AND African American AND NYHA class III-IV already on ACE-I and beta blockers: Hydralazine nitrate (decrease mortality by 43%) (I-A)
    • Contraindications to ACE-I or ARB (IIa-B)
    • Digitalis: to decrease hospitalizations (IIa-B)
    • NYHA class II–IV symptoms and HFrEF or HFpEF: Omega-3 polyunsaturated fatty acid supplementation (IIa-B)
     

    Fluid restriction:

    • Restriction to 1.5 to 2 L/d particularly in case of hyponatremia (IIa-C)

    Inotropes

    • Temporary inotropes: in case of cardiogenic shock to maintain perfusion, awaiting definitive therapy or resolution of acute precipitating event (I-C), OR
    • Continuous inotropes:

    Mechanical circulatory support (MCS)

    • Temporary MCS in HFrEF awaiting definitive therapy or resolution of acute precipitating event (I-B)
    • Temporary MCS HFrEF with severe hemodynamic compromise, as a bridge therapy to recovery or decision (I-B)
    • Durable MCS to prolong survival in selected patients (LVEF <25% and NYHA class III–IV functional status despite GDMT, including, when indicated, CRT, with either high predicted 1- to 2-year mortality, or dependence on continuous parenteral inotropic support, multidisciplinary team) (I-B)

    Cardiac transplantation

    • Refractory to medical therapy, device, and surgery (I-C)
     


    Medications

    Drug Class Drug Daily dose Maximum daily dose
    Loop diuretics Furosemide
    (duration of action: 6 to 8 h)
    PO dose for chronic heart failure: 20 to 40 mg once or twice

    IV dose for acute heart failure:

    Initial dose given slowly (1 to 2 minutes)
    ❑ If patient is already on loop diuretics: IV dose ≥ home PO dose (rule of thumb: IV dose = 2.5x equivalent oral daily dose)
    ❑ If patient is not already on loop diuretics, administer IV starting dose of 20 to 40 mg
    Continuous IV infusion:

    Initial IV bolus administered slowly over 1 to 2 minutes, then continuous IV infusion rate of 10-40 mg/h|| 600 mg

    Bumetanide
    (duration of action: 4 to 6 h)
    PO dose for chronic heart failure: 0.5 to 1.0 mg once or twice 10 mg
    Torsemide
    (duration of action: 12 to 16 h)
    PO dose for chronic heart failure: 10 to 20 mg once 200 mg
    Thiazide diuretics Chlorothiazide
    (duration of action: 6 to 12 h)
    PO: 250 to 500 mg once or twice 1000 mg
    Hydrochlorothiazide
    (duration of action: 6 to 12 h)
    PO: 25 mg once or twice 200 mg
    Metolazone
    (duration of action: 12 to 24 h)
    PO: 2.5 mg once 20 mg
    K+- sparing diuretic Amiloride
    (duration of action: 24 h)
    PO: 5 mg once 20 mg
    Spironolactone
    (duration of action: 1 to 3 h)
    PO: 12.5 to 25.0 mg once 50 mg
    Triamterene
    (duration of action: 7 to 9 h)
    PO: 50 to 75 mg twice 200 mg
    ACE inhibitors Enalapril 2.5 mg twice 10 to 20 mg twice
    Lisinopril 2.5 to 5 mg once 20 to 40 mg once
    Ramipril 1.25 to 2.5 mg once 10 mg once
    ARBs Candesartan 4 to 8 mg once 32 mg once
    Losartan 25 to 50 mg once 50 to 150 mg once
    Valsartan 20 to 40 mg twice 160 mg twice
    Beta blockers Bisoprolol 1.25 mg once 10 mg once
    Carvedilol 3.125 mg twice 50 mg twice
    Carvedilol CR 10 mg once 80 mg once
    Metoprolol succinate extended release 12.5 to 25.0 mg once 200 mg once
    Aldosterone antagonists Spironolactone 12.5 to 25.0 mg once 25 mg once or twice
    Eplerenone 25 mg once 50 mg once
    Inotropes Dopamine 5 to 10 mcg/kg/min, OR
    10 to 15 mcg/kg/min
    Dobutamine 2.5 to 5 mcg/kg/min, OR
    5 to 20 mcg/kg/min
    Milrinone 0.125 to 0.75 mcg/kg/min
    Vasodilators Nitroglycerin 5 to 10 mcg/min, increase dose by 5-10mcg/min
    every 3-5 mins as tolerated
    Max is 400mcg/min
    Nitroprusside 5 to 10 mcg/min, increase dose by 5-10mcg/min
    every 5 mins as tolerated
    Max is 400mcg/min
    Nesiritide 2 mcg/kg bolus; then 0.01 mcg/kg/minute continuous infusion Max of 0.03 mcg/kg/minute
    Hydralazine and isosorbide dinitrate Fixed-dose combination 37.5 mg hydralazine/20 mg isosorbide dinitrate 3 times daily 75 mg hydralazine/40 mg isosorbide dinitrate 3 times daily
    Individual doses Hydralazine: 25 to 50 mg 3 or 4 times daily
    Isosorbide dinitrate: 20 to 30 mg 3 or 4 times daily
    Hydralazine: 300 mg daily in divided doses
    Isosorbide dinitrate: 120 mg daily in divided doses
    Digoxin

    Loading dose: PO- 10 to 15 mcg/kg (half the total loading dose initially, then 1/4th the loading dose every 6 to 8 hours two times), OR
    IV- 8 to 12 mcg/kg (half the total loading dose initially, then 1/4th the loading dose every 6 to 8 hours two times)
    Maintenance dose: PO- 3.4 to 5.1 mcg/kg/day once daily, OR
    IV- 2.4 to 3.6 mcg/kh/day once daily
    Drugs that increase the concentration of digoxin include amiodarone, quinidine and verapamil||

    Do's

    Acute Decompensated Heart Failure

    • Differentiate systolic and diastolic heart failure among patients with ADHF in order to guide therapy:
      • Inotropic agents that increase contractility are not indicated as important for the patient with acute decompensated systolic heart failure.
      • While beta blocker initiation is relatively contraindicated in acute decompensated systolic heart failure, control of tachycardia is very useful in the patient with diastolic heart failure to prolong left ventricular filling time.
      • While the initiation of ACE inhibitors may not be recommended in acute decompensated systolic heart failure, ACE inhibition may be of benefit in acute decompensated diastolic heart failure.
    • Rely on the patient's volume status to guide the aggressiveness of diuresis in ADHF.
    • Continue chronic medications during acute decompensation in the following conditions:
    • Digoxin decreases hospitalization but not mortality in the RALES study. It can be used in CHF & afib to reduce the ventricular response. In the RALES study, a level of < 1 ng/ml was associated with efficacy. Levels > 1 ng/ml not associated with greater efficacy and associated with higher mortality. No need to load a CHF patient with dig. For majority of patients with normal Cr, a daily dose of 0.25 mg of digoxin is usually adequate. In the older patient or in those patients with renal impairment, a dose of 0.125 mg per day may be adequate. Drugs that increase the concentration of digoxin include amiodarone, quinidine and verapamil. [6][7][8][9][10][11][12]
    • DVT prophylaxis unless contraindicated.[13][14]
    • Consider adding another diuretic (e.g. metolazone or thiazides) for worsening congestion despite high doses of loop diuretics.[15][16]
    • Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or active titration of heart failure medications.
    • Convert all IV diuretic to oral forms in anticipation of discharge.
    • Schedule an early follow-up visit (within 7 to 14 days) and early telephone follow-up (within 3 days) of hospital discharge .[17][18]

    Chronic Heart Failure

    Don'ts

    References

    1. 1.0 1.1 1.2 1.3 1.4 Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE, Drazner MH; et al. (2013). "2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines". Circulation. 128 (16): 1810–52. doi:10.1161/CIR.0b013e31829e8807. PMID 23741057.
    2. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG; et al. (2009). "2009 Focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation". J Am Coll Cardiol. 53 (15): e1–e90. doi:10.1016/j.jacc.2008.11.013. PMID 19358937.
    3. Perna, ER.; Macín, SM.; Parras, JI.; Pantich, R.; Farías, EF.; Badaracco, JR.; Jantus, E.; Medina, F.; Brizuela, M. (2002). "Cardiac troponin T levels are associated with poor short- and long-term prognosis in patients with acute cardiogenic pulmonary edema". Am Heart J. 143 (5): 814–20. PMID 12040342. Unknown parameter |month= ignored (help)
    4. McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K; et al. (2012). "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC". Eur Heart J. 33 (14): 1787–847. doi:10.1093/eurheartj/ehs104. PMID 22611136.
    5. Fuat A, Murphy JJ, Hungin AP, Curry J, Mehrzad AA, Hetherington A; et al. (2006). "The diagnostic accuracy and utility of a B-type natriuretic peptide test in a community population of patients with suspected heart failure". Br J Gen Pract. 56 (526): 327–33. PMC 1837840. PMID 16638247.
    6. The Captopril-Digoxin Multicenter Research Group. Comparative effects of therapy with captopril and digoxin in patients with mild to moderate heart failure. JAMA. 1988;259:539–44.
    7. Dobbs SM, Kenyon WI, Dobbs RJ. Maintenance digoxin after an episode of heart failure: placebo-controlled trial in outpatients. Br Med J. 1977;1:749–52
    8. Lee DC, Johnson RA, Bingham JB, et al. Heart failure in outpatients: a randomized trial of digoxin versus placebo. N Engl J Med. 1982;306: 699–705.
    9. Guyatt GH, Sullivan MJ, Fallen EL, et al. A controlled trial of digoxin in congestive heart failure. Am J Cardiol. 1988;61:371–5.
    10. . DiBianco R, Shabetai R, Kostuk W, et al. A comparison of oral milrinone, digoxin, and their combination in the treatment of patients with chronic heart failure. N Engl J Med. 1989;320:677–83.
    11. Uretsky BF, Young JB, Shahidi FE, et al., for the PROVED Investigative Group. Randomized study assessing the effect of digoxin withdrawal in patients with mild to moderate chronic congestive heart failure: results of the PROVED trial. J Am Coll Cardiol. 1993;22:955–62.
    12. Packer M, Gheorghiade M, Young JB, et al. Withdrawal of digoxin from patients with chronic heart failure treated with angiotensin-convertingenzyme inhibitors. RADIANCE Study. N Engl J Med. 1993;329:1–7.
    13. Alikhan R, Cohen AT, Combe S, Samama MM, Desjardins L, Eldor A; et al. (2003). "Prevention of venous thromboembolism in medical patients with enoxaparin: a subgroup analysis of the MEDENOX study". Blood Coagul Fibrinolysis. 14 (4): 341–6. PMID 12945875.
    14. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ, American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel (2012). "Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): 7S–47S. doi:10.1378/chest.1412S3. PMC 3278060. PMID 22315257.
    15. Grosskopf I, Rabinovitz M, Rosenfeld JB (1986). "Combination of furosemide and metolazone in the treatment of severe congestive heart failure". Isr J Med Sci. 22 (11): 787–90. PMID 3793436.
    16. Rosenberg J, Gustafsson F, Galatius S, Hildebrandt PR (2005). "Combination therapy with metolazone and loop diuretics in outpatients with refractory heart failure: an observational study and review of the literature". Cardiovasc Drugs Ther. 19 (4): 301–6. doi:10.1007/s10557-005-3350-2. PMID 16189620.
    17. Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ, Horwitz RI (2000). "Predictors of readmission among elderly survivors of admission with heart failure". Am Heart J. 139 (1 Pt 1): 72–7. PMID 10618565.
    18. Hernandez AF, Greiner MA, Fonarow GC, Hammill BG, Heidenreich PA, Yancy CW; et al. (2010). "Relationship between early physician follow-up and 30-day readmission among Medicare beneficiaries hospitalized for heart failure". JAMA. 303 (17): 1716–22. doi:10.1001/jama.2010.533. PMID 20442387.
    19. Heerdink ER, Leufkens HG, Herings RM, et al. NSAIDs associated with increased risk of congestive heart failure in elderly patients taking diuretics. Arch Intern Med. 1998;158:1108–12.
    20. . Herchuelz A, Derenne F, Deger F, et al. Interaction between nonsteroidal anti-inflammatory drugs and loop diuretics: modulation by sodiumbalance. J Pharmacol Exp Ther. 1989;248:1175–81.
    21. Gottlieb SS, Robinson S, Krichten CM, et al. Renal response to indomethacin in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol. 1992;70:890–3
    22. Bank AJ, Kubo SH, Rector TS, et al. Local forearm vasodilation with intra-arterial administration of enalaprilat in humans. Clin Pharmacol Ther. 1991;50:314–21.
    23. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med. 1989;321:406–12.
    24. The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227–33.
    25. Pratt CM, Eaton T, Francis M, et al. The inverse relationship between baseline left ventricular ejection fraction and outcome of antiarrhythmic therapy: a dangerous imbalance in the risk-benefit ratio. Am Heart J. 1989;118:433–40.
    26. Cuffe MS, Califf RM, Adams KF, Benza R, Bourge R, Colucci WS, Massie BM, O'Connor CM, Pina I, Quigg R, Silver MA, Gheorghiade M (2002). "Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial". JAMA : the Journal of the American Medical Association. 287 (12): 1541–7. PMID 11911756. Retrieved 2012-04-06. Unknown parameter |month= ignored (help)
    27. Juurlink DN, Mamdani MM, Lee DS, Kopp A, Austin PC, Laupacis A; et al. (2004). "Rates of hyperkalemia after publication of the Randomized Aldactone Evaluation Study". N Engl J Med. 351 (6): 543–51. doi:10.1056/NEJMoa040135. PMID 15295047.
    28. Bozkurt B, Agoston I, Knowlton AA (2003). "Complications of inappropriate use of spironolactone in heart failure: when an old medicine spirals out of new guidelines". J Am Coll Cardiol. 41 (2): 211–4. PMID 12535810.
    29. Horwich TB, MacLellan WR, Fonarow GC (2004). "Statin therapy is associated with improved survival in ischemic and non-ischemic heart failure". J Am Coll Cardiol. 43 (4): 642–8. doi:10.1016/j.jacc.2003.07.049. PMID 14975476.
    30. Gissi-HF Investigators. Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG; et al. (2008). "Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial". Lancet. 372 (9645): 1231–9. doi:10.1016/S0140-6736(08)61240-4. PMID 18757089.

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