Sowinski Heart Failure Part 1 Flashcards
Definition of heart failure
-Although heart failure can be readily described as a clinical syndrome….an abnormality of myocardial function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues
-Not a single disease state but the final common pathway for CV diseases
Type of heart failure
-Heart failure with reduced ejection fraction (HFrEF)
-Heart failure with preserved ejection fraction (HFpEF)
How do you define reduced ejection fraction?
EF < 40%
How do you define preserved ejection fraction?
EF > 50%
How do you define mildly reduced ejection fraction?
EF 41-49%
How do you define improved ejection fraction?
EF > 40% after previously having reduced ejection fraction
How is cardiac function impaired in HFrEF?
Systolic dysfunction: Decreased contractility
How is cardiac function impaired in HFpEF?
Diastolic dysfunction: Impairment in ventricular relaxation/filling
What causes HFrEF?
Dilated ventricle
-Ischemic dilated CM (~70% of cases)
-Non-ischemic dilated CM
-HTN, thyroid Dz, Obesity, Stress, Cardiotoxins, Myocarditis, Idiopathic, Tachycardic, Peripartum
Determinants of left-ventricular performance (Stroke Volume)
-Preload
-Myocardial contractility
-Afterload
Beneficial effects of increased preload due to Na/water retention
Optimize stroke volume via Frank-Starling mechanism
Detrimental effects of increased preload due to Na/water retention
-Pulmonary/systemic congestion and edema
-Increased MVO2
Beneficial effects of vasoconstriction
-Maintain BP in face of reduced cardiac output
-Shunt blood from nonessential tissues to the heart
Detrimental effects of vasoconstriction
-Increased MVO2
-Increased afterload decreases SV and further activates the compensatory response
Beneficial effects of tachycardia and increased contractility (SNS activation)
Maintain cardiac output
Detrimental effects of tachycardia and increased contractility (SNS activation)
-Increased MVO2
-Shortened diastolic filling time
-Beta-receptor downregulation and decreased responsiveness
-Ventricular arrhythmias
-Increased risk of myocardial cell death
Beneficial effects of ventricular hypertrophy and remodeling
-Maintain cardiac output
-Reduce myocardial wall stress
-Decrease MVO2
Detrimental effects of ventricular hypertrophy and remodeling
-Diastolic and systolic dysfunction
-Risk of myocardial cell death and ischemia
-Risk of arrhythmias
-Fibrosis
Negative inotropes that can induce heart failure
-Antiarrhythmics (disopyramide, flecainide)
-Beta-blockers (atenolol, propranolol, metoprolol)
-Calcium channel blockers (verapamil, diltiazem)
-Itraconazole
Direct cardiac toxins that can induce heart failure
-Doxorubicin
-Epirubicin
-Daunomycin
-CYP
-Trastuzumab
-Bevacizumab
-5-FU
-Blue cohosh
-Imatinib
-Lapatinib
-Sunitinib
-Ethanol
-Cocaine
-Amphetamines
Drugs that cause sodium/water retention that can induce heart failure
-Glucocorticoids
-Androgens
-Estrogens
-NSAIDs/COX-2 inhibitors
-Rosiglitazone/pioglitazone
-Sodium-containing drugs (carbenicillin DiNa+, ticarcillin DiNa+)
Clinical presentation of heart failure
-Shortness of breath
-Swelling of feet/legs
-Chronic lack of energy
-Difficulty sleeping at night due to breathing problems
-Swollen or tender abdomen with loss of appetite
-Cough with frothy sputum
-Increased urination at night
-Confusion and/or impaired memory
Symptoms of right ventricular failure
-Abdominal pain
-Anorexia
-Nausea
-Bloating
-Constipation
Signs of right ventricular failure
-Peripheral edema
-JVD
-HJR
-Hepatomegaly
-Ascites
Symptoms of left ventricular failure
-DOE
-Orthopnea
-PND
-Tachypnea
-Bendopnea
-Cough
-Hemoptysis
Signs of left ventricular failure
-Rales
-S3 gallop
-Pulmonary edema
-Pleural effusion
-Cheyne-Stokes respiration
Nonspecific symptoms of heart failure
-Exercise intolerance
-Fatigue
-Weakness
-Nocturia
-CNS symptoms
Nonspecific signs of heart failure
-Tachycardia
-Pallor cyanosis
-Cardiomegaly
Major signs/symptoms of pulmonary congestion
-Exertional dyspnea (DOE)
-Orthopnea
-Paroxysmal nocturnal dyspnea (PND)
-Rales
-Pulmonary edema
-Bendopnea
Major signs/symptoms of systemic venous congestion
-Peripheral edema
-Jugular venous distention (JVD)
-Hepatojugular reflex (HJR)
-Hepatomegaly, ascites
Other major non-specific finding inf heart failure
-Fatigue, weakness and exercise intolerance
-Nocturia
-Cardiomegaly
Laboratory assessments for heart failure
-CBC, serum electrolytes, BUN, Cr, TFTs
-Electrocardiogram
-Chest X-ray
Abnormal BNP
> 35 pg/mL
Abnormal NT-proBNP
> 125 pg/mL
How to evaluate LV function and measurements of EF
-Echocardiogram
-Nuclear testing
-Cardiac catheterization
-MRI and CT
How do you describe NYHA class I?
Patients with cardiac disease but without resulting limitations of physical activity (asymptomatic)
How do you describe NYHA class II?
Patients with cardiac disease resulting in slight limitations of physical activity (symptomatic)
How do you describe NYHA class III?
Patients with cardiac disease resulting in limitations of physical activity (symptomatic)
How do you describe NYHA class IV?
Patients with cardiac disease resulting in an inability to carry on any physical activity without discomfort (symptomatic)
How do you describe AHA stage A?
High risk of developing HF. No identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of HF
How do you describe AHA stage B?
Structural heart disease that is strongly associated with HF but NO signs or symptoms of HF
How do you describe AHA stage C?
Current or prior symptoms of HF associated with underlying structural heart disease
How do you describe AHA stage D?
Advanced structural heart disease and marked symptoms of HF at rest despite maximal medical therapy and who require specialized interventions
Examples of heart failure AHA stage A
-Systemic HTN
-CAD
-DM
Examples of heart failure AHA stage B
-LVH or fibrosis
-LV dilation or hypocontractility
-Asymptomatic valvular heart disease
-Previous MI
Examples of heart failure AHA stage C
-Dyspnea or fatigue due to LVSD
-Asymptomatic patients receiving treatment for prior HF symptoms
Examples of heart failure AHA stage D
-Frequently hospitalized for HF and cannot be safely discharged from the hospital
-Patients in the hospital awaiting heart transplantation
-Patients at home receiving continuous intravenous support for symptom relief or being supported with a mechanical circulatory assist device
-Patients in a hospice setting for the management of HF
Types of heart failure
-Heart failure with reduced ejection fraction
-Heart failure with preserved ejection fraction
HFrEF impairment in cardiac function
Systolic dysfunction: decreased contractility
HFpEF impairment in cardiac function
Diastolic dysfunction: impairment in ventricular relaxation/filling
HFrEF definition
HF symptoms with ejection fraction below 40%
HFpEF definition
HF symptoms with ejection fraction greater than 50%
Causes of HFrEF
Dilated ventricle
-Ischemic dilated CM (~70%)
-Non-ischemic dilated CM
-(HTN, thyroid disease, obesity, stress, cardiotoxins, myocarditis, idiopathic, tachycardic, peripartum)
Causes of HFpEF
HTN is most common cause ~60%
Asymptomatic rEF definition
-Asymptomatic LV systolic dysfunction
-No heart failure symptoms with EF < 40%
HFimpEF
Previous symptoms/rEF now improved
HFmrEF
Heart failure with EF 41-49%
Goals of therapy for treatment of rEF and HFrEF
-Slow disease progression
-Reduce symptoms and improve quality of life and prevent/reduce hospitalizations and need for emergency care
-Reduce mortality
Dietary restrictions in patients with HF
-Sodium (2-3 grams/day as possible)
-Alcohol (men no more than 2 drinks/day; women no more than 1 drink/day)
-Fluid intake (< 2 L/day)
Pharmacologic strategies
-Reduce intravascular volume (diuretics, SGLT2i)
-Increase myocardial contractility (positive inotropes)
-Decrease ventricular afterload (ACEIs, vasodilators, SGLT2i)
-Neurohormonal blockade (ARNIs, beta-blockers, ACEIs, ARBs, MRAs, SGLT2is)
GDMT for stage A
-Drug therapies for routine use if atherosclerotic vascular disease is present
-ACEI/ARB
GDMT for stage B
-Drug therapies for routine use if previous MI or asymptomatic rEF
-ACEI/ARB
-Beta-blocker
GDMT for stage C
-ARNI/ACEI/ARB (ARNI preferred)
-GDMT beta-blocker (metoprolol, bisoprolol, carvedilol)
-Aldosterone antagonist (Eplerenone, spironolactone)
-SGLT2i (dapagliflozin/empagliflozin)
-Loop diuretic for volume overload
-ISDN/hydralazine (if black and persistently symptomatic on GDMT; or if ARNI/ACEI/ARB intolerant)
-Ivabradine
-Digoxin
Which HF patients are candidates for diuretic treatment?
All HF patients with signs/symptoms of fluid retention (SYMPTOMATIC)
Effects of diuretics on HF patients
-Reduce hospitalizations but do not have an impact on mortality or natural progression of HF
-Reduce symptoms associated with fluid overload, improve exercise tolerance and improve QOL
How do you determine dosing of diuretics?
-Lowest dose that maintains euvolemia
-Weight is good indicator of fluid status
Short term benefits of diuretics
Reduce fluid retention via . . . decreased edema, pulmonary congestion and JVD by reducing preload and cardiac filling pressure
Long term benefits of diuretics
Reduced daily symptoms and improve ability to exercise
Diuretic mechanism of action
Increase sodium and water excretion by reducing sodium reabsorption at a variety of sites in the nephron
Which diuretics are most often used in HF patients?
Loop diuretics
Loop diuretics clinical pearls
-Enhancing renal release of prostaglandins (increases renal blood flow and enhancing venous capacitance)
-Blocked by NSAIDS
-Patients with impaired renal function may require higher doses
-Furosemide has erratic bioavailability, torsemide may have an advantage in some patients
Initial dose of oral furosemide
20-40 mg QD or BID
Max dose of furosemide
160 mg QD or BID
Initial dose of oral bumetanide
0.5-1 mg QD or BID
Max dose of bumetanide
2 mg QD or BID
Initial dose of oral torsemide
10-20 mg QD
Max dose of torsemide
80 mg QD
Initial dose of oral ethacrynic acid
25-50 mg QD or BID
IV equivalent doses of the loop diuretics
F 40 mg = B 1 mg = T 20 mg = E 50 mg
Loop diuretics mechanism of action
Potent diuretics block Na and Cl reabsorption in the ascending limb of the LOH
Thiazide diuretics mechanism of action
Relatively weak agents, block Na and Cl reabsorption in the DCT
When are thiazide diuretics recommended to be used?
-May be used in patients with mild HF and small amounts of fluid retention
-HCTZ and MTZ are frequently used in combination with loop diuretics in patients who become resistant to single drug therapy
Initial dose of hydrochlorothiazide
25 mg/day
Max dose of hydrochlorothiazide
100 mg/day
Initial dose of metolazone
2.5 mg/day
Max dose of metolazone
10 mg/day
Adverse effects of thiazide and loop diuretics
-Decrease in magnesium
-Decrease in potassium
-Volume depletion, decreased renal function, pre-renal azotemia
-Decreased sodium
-Postural hypotension
-Increased uric acid
-Increase in calcium (thiazide)
-Decrease in calcium (loop)
Loop diuretics initiation
-Initiate at low-doses, then double and titrate
-Dosage adjustments based on weights and symptoms
-If fluid overload, reduce weight 1-2 pounds/day
-Patients should report if there is weight gain
-Hypotension and increased SeCr or BUN/Cr ratio may be indicative of volume depletion
-Dose adjustments may be required during ACEI/ARB/ARNI and/or beta-blocker titration
When to monitor after initiation of loop diuretics
1-2 weeks and increase
What to monitor in patient after initiation of loop diuretics
-Fluid intake and urinary output; body weight; S/S of congestion, JVD
-Blood pressure
-Serum electrolytes (especially K and Mg)
-Replace K (4 mEq/L or more) and Mg (2 mEq/L or more) as necessary
-Renal function
