Heart failure is a common and serious condition where the heart muscle is unable to pump sufficiently. It can have multiple causes and the prevalence increases significantly with age. Prognosis remains poor with high mortality rates. Diagnosis involves evaluating symptoms, signs, and testing like echocardiogram. Management focuses on general measures like diet, exercise, and reducing risk factors as well as specific treatments targeting the underlying cause and physiology of heart failure.
3. Introduction/Epidemiology
Heart failure (HF) is a syndrome with major medical and social impact.
Prevalence increases with age
– 3.8 to 29.4 per 1,000 in the general population
– 80 per 1,000 in persons 65 to 75 years old
– 90 per 1,000 in persons over the age of 75
• Hospitalizations primarily for heart failure have increased from 550,000 to 900,000
per year in the last 10 years.
• HF is the single most common cause of hospital readmissions (within six months -
20 - 44% of the cases)
• HF is the most common cause of death in hospital patients.
Prognosis of HF remains poor, with 1 year and 5 year mortality rates of 24% and
45% among men and 28% and 55% among women, respectively.
Mortality is similar or higher than with many common cancers.
4. Definition
• Inability of the heart to maintain adequate cardiac output
to meet the metabolic demands of the body while still
maintaining normal filling pressures (i.e despite having
adequate atrial filling).
• Structural or functional cardiac disorder
5. Heart Failure
Key Concepts
• Cardiac output (CO) = Stroke Volume (SV) x Heart Rate (HR)
– Becomes insufficient to meet metabolic needs of body
• SV – determined by preload, afterload and myocardial contractility
• Ejection Fraction (EF) (need to understand)
• Classifications HF
– Systolic failure – decrease contractility
– Diastolic failure – decrease filling
– Mixed
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6.
7. Terminology
Congestive Heart Failure: Similar to the preceding but with features
of circulatory congestion such as jugular venous distention, rales,
peripheral edema and ascites.
Compensated Heart Failure: Is used in reference to patients with
chronic heart failure whose symptoms and signs of pulmonary or
peripheral congestion are relieved by therapy, although, the EDV and
EDP often remain elevated and the EF remains reduced.
Systolic Heart Failure: Reflects a decrease in normal emptying
capacity [usually with an EF < 45 %] that is usually associated with a
compensatory increase in diastolic volume.
Diastolic Heart Failure: Is said to be present when the filling of one
or both ventricles is impaired, while the emptying capacity is normal.
8. Advanced Heart Failure:
Severe left ventricular systolic dysfunction i.e., EF 35%.
Diagnostic Criteria for Advanced HF:
A: Major criteria (all required)
• Resting left ventricular ejection fraction < 30 – 35%
• Presence of NYHA functional class III or IV or, if available, peak oxygen
consumption of < 14ml/kg/min on symptom – limited exercise testing.
B: Additional criteria that contribute to the diagnosis
• Trial of standard therapy (ACE inhibitors, digoxin, diuretics) for at least 3
months.
• Noninvasive evidence of pulmonary hypertension indicated by high
velocity of the tricuspid regurgitation (> 2.5 m/sec)
• Hyponatremia with serum sodium < 130 mmol/L in patients not treated
with ACE inhibitors.
• Plasma norepinephrine > 900pg/ml.
9. Etiology of Heart Failure
Most common underlying causes
of HF in adults are:
Hypertension
Peripartum cardiomyopathy
Rheumatic Valvular disease
Idiopathic dilated cardiomyopathy
Cor pulmonale
Pericardial disease: constrictive pericarditis,
cardiac tamponade
Diabetes cardiomyopathy
Alcohol cardiomyopathy
Congenital heart disease
Slightly less common causes include:
Hypertrophic cardiomyopathy
Viral myocarditis
IHD
Toxic: Adriamycin, cyclophosphamide
Endocrine and metabolic disorders: thyroid
disease, acromegaly, pheochromocytoma.
Collagen vascular disease:
Systemic lupus erythematosus, polymyositis,
polyarteritis nodosa.
Tachycardia induced cardiomyopathy
Miscellaneous
Large A-V shunts
Adverse effects of drug therapy (e.g. Non
Steroidal Anti Inflammatory Drugs)
1. Volume overload
◦ a. Regurgitant valves( mitral or
tricuspid valve)
◦ b. High out put states( anemia,
thyrotoxicosis)
2. Pressure overload
◦ a. Systemic hypertension
◦ b. Outflow tract obstruction(aortic
stenosis, ASH)
3. Loss of muscle
◦ a. MI, connective tissue disease, SLE
4. Loss of contractility
◦ a. Poison ,alcohol,cobalt,doxorubicin
◦ b. Infections; viral bacterial
5. Restricted filling
◦ a Mitral stenosis,
◦ b. Pericardial disease, constrictive
pericarditis& pericardial
tamponade.
◦ c. Infiltrative diseases like
amyloidosis.
10. Precipitating Cause of Heart Failure
Arrhythmias especially AF
Infections especially pneumonia
Acute MI/ Angina pectoris or recurrent myocardial ischemia
Alcohol excess
Anemia
Thyrotoxicosis
Pulmonary embolism
Pregnancy
Iatrogenic – postoperative fluid replacement or administration
of steroids or NSAIDs
13. Classification
• Classification of HF has been and may continue to change.
• Change is undoubtedly relate to the difficulties integrating
many simple bedside observations (water retention, scant
and concentrated urine, distended neck veins and enlarged
heart) with some laboratory results.
• Clinical syndrome of heart failure must be distinguished
from other causes of circulatory congestion where the heart
is not the culprit.
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14. Diastolic dysfunction
Normal myocardial contractility
Normal left ventricular volume
Normal EF
Impaired myocardial relaxation
Diminished early diastolic filling
Systolic dysfunction
Absolute or relative impairment of
myocardial contractility.
Low EF.
High output heart failure
Bounding pulse
Wide pulse pressure
Accentuated heart sounds
Peripheral vasodilatation
Increased cardiac output
Increased EF
Moderate four chamber
enlargement
High output states:
Anemia
Pregnancy
Hypothyroidism
Pheochromocytoma
Low cardiac output syndrome
Fatigue
Loss of lean body mass
Prerenal azotemia
Peripheral vasoconstriction
Reduced left or right contractility
Right Heart Failure
Dependent edema
Jugular venous distention
Right atrial enlargement
Right ventricular enlargement
Left heart failure
Dyspnea
Pulmonary vascular congestion
Reduced left-sided contractility
Biventricular failure
Dyspnea
Dependent edema
Jugular venous distention
Pulmonary vascular congestion
Bilateral reduced contractility
15. NYH Association Functional Classification [NYHA]
Class I: Asymptomatic- Patients with cardiac disease but without resulting limitations of
physical activity, i.e., ordinary physical activity does not cause undue fatigue, palpitation,
dyspnea or anginal pain.
Class II: Mild- Patients with cardiac disease resulting in slight limitation of physical activity.
These patients are comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea or anginal pain.
Class III: Moderate - Patients with cardiac disease resulting in marked limitation of physical
activity. These patients are comfortable at rest. Less than ordinary physical activity
causes fatigue, palpitation, dyspnea or anginal pain.
Class IV: Severe - Patients with cardiac disease resulting in inability to carry on any physical
activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome
may be present even at rest. If any physical activity is undertaken, discomfort is
increased.
17. Diagnosis : Framingham Criteria
Major Criteria Minor Criteria
Paroxysmal nocturnal dyspnea Ankle Edema
Orthopnea Nocturnal cough
Tachycardia > 120 bpm Hepatomegaly
Central venous pressure >16 cm of water Pleural effusion
Jugular venous distention
Pulmonary rales
Acute pulmonary edema
Third heart sound
Hepatojugular reflux
Radiographic evidence of cardiomegaly
Major or Minor: Weight loss >4.5 kg during first 5 days of treatment for suspected heart failure
Heart failure is considered to be present if two major or one major plus two minor
criteria were present in the absence of an alternative explanation for the symptoms and
signs.
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20. Evaluation
• History and physical examination
• Laboratory Investigations
– FBC, Serum creatinine/ proteins/lipid profile/cardiac enzymes
– Thyroid function tests (if evidence of thyroid disease, > 65 years or patient
with AF)
– CXR
– Urinalysis (proteinuria and red blood, broad or cellular casts)
– Electrocardiogram (arrhythmias, MI, LVH, various blocks etc)
• Echocardiogram (M – mode, 2D: ventricular and atrial chamber enlargements,
valvular diseases, vegetations, wall motions, thrombus, LVH, pericardial effusion
etc)
• Screening for Infections/ pulmonary embolism
• Cardiac catheterization
• Radionuclide ventriculogram
• Myocardial biopsy
21. Management of Heart Failure
1 - General Measures
2 - Specific Measures
General measures
Other Measures
Diet – reduce salt and eat lot of fresh fruits and vegetables
Stop smoking/ Reduce alcohol intake
Take aerobic exercise
Advice
Counselling – about symptoms and compliance
Social activity and employment
Vaccination (pneumococcal)
Contraception www.medrockets.com
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23. “Eras” or Evolution of Heart Failure Therapy
1700 1960 1990 2000 200?
Cardiorenal
Model
Interventions:
Diuretics
Digitalis
Hemodynamic
Model
Interventions:
Vasodilators
Inotropes
Neurohormonal
Model
Interventions:
ACE I
Β Blockers
ARBs
Aldosterone
antagonists
HDZ/Isosorbide
Biomechanical
Model
Interventions:
ICDs
CRT
LVSD
CSD
Personalized
Model
Interventions:
Genomics
Proteomics
Biomarkers
Treatment of Heart Failure
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24. DIGOXIN DOSING
Indications
To control significant tachycardia in Atrial Fibrillation or Atrial Flutter
Positive inotropic effect in Heart failure with or without Atrial Fibrillation
Caution: Digoxin may precipitate VF in WPW with AF. Digoxin is contraindicated in intermittent heart
block, digitalis arrhythmias and hypertrophic obstructive cardiomyopathy.
Dosing
Always check baseline U + E
Commence loading regimen:
Calculate the total loading dose at 10 – 15 micrograms/kg for oral dose (~ 1 – 1.5mg) or 8
– 12 µg/kg for IV dose based on ideal or lean body weight.
Initially give half the calculated loading dose as oral digoxin (~ 0.5mg) or give IV dose if in
severe CHF or with significant nausea e.g. IV digoxin (~ 0.5mg) in normal saline 100ml
over 30 minutes.
Then give a further one quarter of the calculated loading dose at 6 hours oral digoxin (~
0.25 – 0.5mg).
Then give a further one quarter of the calculated loading dose at 12 hours oral digoxin (~
0.25 – 0.5mg).
Establish a maintenance dose of 62.5 - 250 µg/day. Dose reduction is required in the elderly
and patients with a creatinine clearance < 50 ml/min.
Assay digoxin levels in 7 – 12 days (approximate time to reach steady).
Ideally blood samples should be drawn immediately prior to the next dose to avoid the distribution
phase. If this is not possible:
Sample at least 4 hours after the last IV dose for plasma digoxin levels.
Sample at least 6 hours after the last oral dose for plasma digoxin levels.
Adjust to the narrow therapeutic range of 1.2 – 2.6 nanomol/l.
Some patients may require > 3.0 nanomol/l for full chronotropic effect.
25. Diuretics
1. Should be introduced at a low dose and the dose increased according
to the clinical response.
2. Optimize the dose.
3. Consider combination treatment with a loop and thiazide (thiazide –
like) diuretic.
4. Consider combining a low dose of spironolactone with ACE inhibitor
provided that there is no evidence of hyperkalemia.
5. Administer loop diuretics (either as a bolus or a continuous infusion)
intravenously.
Watch out for:
Acute precipitation of gout with high dose thiazides
Hypo/hyperkalemia etc
Painful gynecomastia
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26. ACE Inhibitors
Stop potassium supplements and potassium sparing diuretics.
Omit (or reduce) diuretics for 24 hours before first dose.
Advise patient to sit or lie down for 2 – 4 hours after first dose.
Start low dose.
Review after 1 – 2 weeks to reassess symptoms, blood pressure, renal
chemistry and electrolytes.
Increase dose unless there has been a rise in serum creatinine concentration ( to >
200 mol/l ) or potassium concentration (to > 5.0 mmol/l).
Titrate to maximum tolerated dose, reassessing blood pressure and renal
chemistry with electrolytes after each dose titration.
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27. ACE Inhibitors: High risk patients warranting hospital admission for
start of Treatment
1. Severe HF (NYHA class IV) or decompensated HF.
2. Low systolic blood pressure (< 100 mmHg).
3. Resting tachycardia > 100 beats per minute.
4. Low serum sodium concentration ( < 130 mmol/l).
5. Other vasodilator treatment.
6. Severe chronic obstructive airways disease and pulmonary
disease ( cor pulmonale).
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28. Recommended starting and maintenance dose ranges for
selected ACE Inhibitors and Beta Blockers used in clinical
trials for the Treatment of Heart Failure
Angiotensin converting enzyme inhibitors
Drug Starting dose Maintenance dose
Captopril: 6.25 mg three times daily 25 - 50 mg three times daily
Enalapril: 2.5 mg once daily 10 mg twice daily
Lisinopril: 2.5 mg once daily 5 - 20 mg once daily
Perindopril: 2 mg once daily 4 mg once daily
Ramipril: 1.25 - 2.5 mg once daily 2.5 - 5 mg twice daily
Trandolapril: 1 mg once daily 4 mg once daily
29. Beta Blockers
1. Improvement of left ventricular function.
2. Reduced sympathetic tone.
3. Improve autonomic nervous system balance.
4. Up regulate adrenergic receptors
5. Reduce the risk of arrhythmias.
6. Reduce Ischemia and further infarction.
7. Reduce myocardial fibrosis and apoptosis.
Indication:
Should be considered for all patients with systolic HF who are stable
on optimal doses of a diuretic and ACEI.
Start with low dose and titrate upwards with doubling of dose every 2 –
4 weeks.
30. Beta Blockers
Bisoprolol 1.25 mg once daily 10 mg once daily
Carvedilol 3.125 mg twice daily 25 mg twice daily
Metoprolol tartrate 5 mg three times daily 50 mg three times daily
Metoprolol succinate CR 12.5-25 mg once daily 200 mg once daily
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31. Potassium Sparing Diuretics
Most beneficial in patient with:
1. Severe HF or NHYA class III or IV.
2. Ejection of fraction of < 35 percent.
3. Serum creatinine of < 221 mol/l.
4. Potassium level of < 5.0 mmol/l.
Start with low dose i.e., 25 mg to maximum of 100 mg per day.
Usual maintenance dose: 25 – 100 mg/day.
Measure serum potassium and creatinine within 5 – 7 days.
Watch out for signs of adverse effects.
Can be combined with digoxin/ACEI/ blocker/diuretic.
32. Antithrombotic and Antiarrhythmic Treatment
Antithrombotic Treatment:
Incidence of stroke and thromboembolism is significantly higher in patients with
chronic HF associated with atrial and left ventricular dilatation.
Incidence can be reduced by long term treatment with warfarin and aspirin.
Antiarrhythmic Treatment:
Chronic HF and AF:
Role of digoxin in restoration of VR.
Amiodarone s long term success rate of cardioversion.
Chronic HF and Ventricular arrhythmias:
Amiodarone effective but long term benefit not significant on survival.
Largely due neutral effect.
33. Devices and Surgery
I. Revascularization (percutaneous transluminal coronary
angioplasty – PTCA).
II. Coronary artery bypass graft – CABG.
III. Valve replacement ( or repair).
IV. Pacemaker or implantable cardiodefibrillator (ICD).
V. Ventricular assist devices (IVCD)/CRT.
VI. Intra – aortic balloon pumping and mechanical devices:
Indications:
1. Possibility of spontaneous recovery – myocarditis
2. Bridge to surgery –(ruptured mitral papillary muscle,
postinfarction ventricular septal defect) or patient awaiting
transplantation.
34. Cardiac Transplantation
Indications
1. End stage HF.
2. Rarely , restrictive cardiomyopathy
3. Congenital HD (combined heart – lung transplantation required).
Absolute Contraindications
1. Recent malignancy (other than basal cell and squamous cell carcinoma
of the skin).
2. Active infection ( including HIV, Hepatitis B, Hepatitis C with liver
disease).
3. Significant pulmonary vascular resistance.
Relative Contraindications
1. Recent pulmonary embolism.
2. Symptomatic peripheral vascular disease.
3. Obesity.
4. Severe renal impairment.
5. Psychosocial problems – lack of social support, poor compliance,
psychiatric illness.
6. Age ( > 60 – 65 years).
35. Complications of Heart Failure
• Arrhythmias – AF, VT, VF and bradyarrhythmias
• Thromboembolism – stroke, peripheral embolism, deep
veins thrombosis; pulmonary embolism
• Gastrointestinal – hepatic congestion and dysfunction,
malabsorption/ cardiac cirrhosis
• Musculoskeletal – wasting of muscle
• Respiratory – pulmonary congestion, respiratory muscle
weakness, pulmonary hypertension (rare)
36. Bad prognostic factors in CHF
1. High NYHA functional class
2. Reduced LVEF
3. Low peak oxygen consumption with maximal exercise (%
predicted value)
4. Third heart sound
5. Increased pulmonary artery capillary wedge pressure
6. Reduced cardiac index
7. Comorbidity – diabetes mellitus, CRF, etc
8. Reduced sodium concentration
9. Raised plasma catecholamines and natriuretic peptide
concentrations
37. Conditions Indicating that referral to a Specialist Is
Necessary
1. Diagnosis is in doubt or when specialist investigation and
management may help.
2. Significant murmurs and valvular heart disease.
3. Arrhythmias – for example AF.
4. Secondary causes – thyroid disease
5. Severe left ventricular impairment – EF < 25%
6. Pre – existing (or developing) metabolic abnormalities – hyponatremia of <
130 mmol/L and/ or renal failure.
7. Severe associated vascular disease – ACE inhibitors in patients with
renovascular disease.
8. Relative hypotension (SBP < 100 mmHg before starting ACE inhibitors)
9. Poor response to treatment.
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