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Heart failure

Synonym: congestive cardiac failure, congestive heart failure
German: Herzinsuffizienz

1 Definition

Heart failure is present when the heart is unable to provide the cardiac output needed by the organism at normal end-diastolic ventricular pressure.

According to the WHO, heart failure is defined as reduced physical resilience due to a functional ventricular disorder.

It's a clinical syndrome of different etiology.

2 Causes

2.1 Frequent causes

2.2 Rare causes

In some cases, the cause of congestive heart failure remains unknown.

3 Classification

3.1 ...according to degree of severity

According to its clinical degree of severity, congestive heart failure is divided into 4 NYHA stages:

  • NYHA I: Diagnosed heart disease without symptoms and without impairment of resilience.
  • NYHA II: Mild impairment of resilience. No symptoms when resting, but only upon higher stress.
  • NYHA III: Strong impairment of resilience. No symptoms when resting, but already upon little stress.
  • NYHA IV: Persistent symptoms also when resting.

Furthermore, congestive heart failure can be divided into 4 stages according to the AHA American Heart Association:

  • Stadium A: High risk of heart failure, since factors are present that are strongly associated with the development of congestive heart failure; no structural heart disease, no symptoms of heart failure until now.
  • Stadium B: Structural heart disease that is closely associated with the development of heart failure, no symptoms of congestive heart failure.
  • Stadium C: Earlier or current symptoms of congestive heart failure in structural heart disease.
  • Stadium D: Advanced structural heart disease and severe symptoms of congestive heart failure at rest despite maximum drug therapy (special therapy required, eg. heart transplant, i.v. catecholamines, artificial heart)

A slightly rougher classification can be made:

  • Compensated heart failure: Causes symptoms only under stress
  • Decompensated heart failure: Causes symptoms at rest

3.2 ...according to localization

Depending on the affected part of the heart, you can differentiate between:

3.3 ...according to the disease progression

3.4 ...according to pathophysiology

  • Systolic dysfunction: Reduced ejection fraction
  • Diastolic dysfunction: Reduced relaxation capability of the ventricle, impaired ventricle filling in diastole (eg. due to ventricular stiffness)

4 Pathogenesis

Heart failure develops when the pumping performance is not sufficient anymore to adequatly provide the heart itself and other extracardial organ areas with blood, oxygen and substrates. As compensation, several different adaptation mechanisms are turned on. With them, the maintenance of the required cardiac output temporarily succeeds. In cases of chronic activation, these mechanisms, however, contribute to the progression of heart failure, where a vicious cycle develops.

In most cases, chronic heart failure is caused by a reduction of the contractile heart muscle tissue. In histology, you can see pathological growth of individual heart muscle cells (myocytic hypertrophy) on the one hand, on the other hand, you can see an increased loss of cells (myocytic apoptosis).

5 Compensation mechanisms

5.1 Neuroendocrine activation

5.1.1 Activation of the sympathetic nervous system and catecholamine emission

At the beginning, the activation of the sympathetic nervous system and the release of catecholamines lead to an increase in heart rate and contraction force. With increasing heart failure, the level of noradrenaline rises. At the same time, the number of cardiac beta receptors is reduced (downregulation. Therefore, noradrenaline has a less and less inotropic effect, but it increases the peripheral resistance (afterload).

5.1.2 Activation of the RAA system

The activation of the renin-angiotensin-aldosterone system leads to vasoconstriction via an increased production of angiotensin, and thereby, it increases the preload. This effect is enhanced by aldosterone, which causes the retention of sodium and water.

5.1.3 ADH activation

The activation of ADH (vasopressin) also leads to retention of water, and thereby to an increase of the preload.

In later stages of the disease, these helpful neuroendocrine compensation mechanisms, however, lead to a deterioration of the hemodynamic situation of the heart failure, and thereby, to a "vicious cycle", which needs therapeutic interruption.

5.1.4 Release of the natriuretic peptides

The natriuretic peptides (NP) are the most important antagonists of the renin-angiotensin-aldosterone system (RAAS). With their main function, the reduction of the plasma volume and of the blood pressure, they protect the healthy heart from an excessive volume and pressure load. NPs are released eg. due to high pressure or over-expansion of the atria. Therefore, BNP is a good parameter in heart failure to ensure the diagnosis and estimate prognosis. This value, however, can be increased (obesity with BMI > 30), or decreased (renal failure, COPD, myocarditis) by other factors. Therefore, medical history, clinical symptoms and echocardiographical findings are always to take into consideration for evaluation.

  • ANP (atrial natriuretic peptide) - stimulation of natriuresis
  • BNP (brain natriuretic peptide) - stimulation of natriuresis, in higher concentrations also stimulation of renal blood flow and GFR (glomerular filtration rate)
  • CNP (C-type natriuretic peptide)- regulation of the vaso-tonus (vasodilatation)
  • DNP (dendroaspis natriuretic peptide) - inhibition of the tubular sodium reabsorption
  • Urodilatin - inhibition of the tubular sodium reabsorption

5.2 Remodelling

Remodelling is defined as a number of molecular, biochemical and cellular meachanisms that change structure and function of the heart after its damage.

5.3 Cardiac hypertrophy

  • Acute heart failure leads to a dilatation of the heart.
  • In chronic heart failure, the kind of load plays an important role:
    • Volume load (eg. valvular insufficiency) leads to an eccentric hypertrophy (hypertrophy with dilatation)
    • Pressure load (eg. valvular stenosis) leads to a concentric hypertrophy (hypertrophy without dilatation)

6 Symptoms

The symptoms of heart failure are versatile. These include, among others:

7 Diagnostics

7.1 Physical exam

7.2 Causal diagnostics

  • Coronary artery disease: Diagnostics via stress ECG, stress echocardiography, cardio MRI, coronary angiography (cardiac catheter exam) with the option of dilating possibly detectable vascular constrictions (PTCA, balloon dilatation and possibly stent implantation).
  • Heart valve diseases: Cardiac echo (echocardiography) for the detection and estimation of the degree of severity.
  • Cardiomyopathy (disease of the heart muscles without adequate coronary blood supply): Detection in cardiac stress echo, cardio MRI, and, if required myocardial biopsy. Coronary artery disease possibly has to be excluded in coronary angiography.

7.3 Diagnostics of the secondary symptoms

Diagnostics of an eventual

  • Overhydration (clinical exam: Edemas up to anasarca, ascites)
  • Pulmonary edema (clinical exam: dispnea, bilateral rales; pulmonary X-ray image with signs of congestion?)
  • Cardiac performance insufficiency (clinical exam: blood pressure too low? Limited resilience? Cardiac echo: left-sided ventricular ejection fraction reduced?)
  • Too low oxygen saturation of the blood (blood gas analysis)

7.4 Laboratory diagnostics

Blood tests only are needed to be able to detect causes and complications of heart failure (eg. diabetes mellitus, renal failure or electrolyte disorders) and possible side effects of therapy.

Since the beginning of the 21st century, with the determination of the plasma concentration of the brain natriuretic peptide BNP, or NT-proBNP, a test that can also be useful in daily routine diagnostics of heart failure is available. As per degree of heart failure, the levels are moderately to highly inreased, while normal BNP and NT-proBNP levels in an untreated patient mostly exclude presence of heart failure. The normal range depends on age and gender. The measurement of BNP for differential diagnosis and follow-up of heart failure, meanwhile, has been integrated into the guidelines of the German Cardiac Society and German Pediatric Cardiology Society.

Furthermore, with increasing heart failure, the plasma level of noradrenaline rises, and it correlates with a deterioration of the prognosis.

7.4.1 Recommended lab tests in suspected heart failure

Exam method Reason
blood cell count
  • Anemia can cause or aggravate heart failure
urea and creatinine
  • Hypokalemia: can occur as a consequence of the administration of diuretics
  • Hyponatremia: can occur as a consequence of [diuresis]] and in terminal stage heart failure; prognostic indicator, which predicts a bad outcome; warning of possible intolerance to ACE-inhibitors (overshooting BP drop upon maximum activation of the RAA system)
y-GT (possibly GOT, GPT)
  • Increase can point to secondary liver damage
total protein, albumin
blood tests which can be used for rarer and particular questions:
CK, LDH, troponin
cholesterol, HDL, LDL
  • In patients with CAD, the decrease of the cholesterol level leads to a reduction of the infarcation risk, and thereby, possibly to a deceleration of the progression of heart failure
virus titer

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8 Therapy

8.1 Control and causal therapy of risk factors

8.2 No-medicinal

No-medicinal therapy of heart failure consists of a number of general measures which reduce the work load of the heart, or, respectively, should prevent further damage of the myocardium:

8.3 Medicinal

Medicinal therapy depends on the degree or stage of heart failure. Moreover, the symptoms (eg. edemas) as well as presence of concomitant diseases (eg. hypertension) are important factors for the determination of the exact medication. The most commonly used drug classes are:

  • ACE-inhibitors, drugs of choice from NYHA I, since they reduce overall mortality (up to 25%) and improve prognosis.
  • Aldosterone antagonists, possibly in NYHA III and IV
  • diuretics
  • Beta receptor blockers, in NYHA I after myocardial infarction, and NYHA II-IV (bisoprolol, carvedilol or metoprolol succinate)
  • Cardiac glycosides (only in tachycardic atrial fibrillation, otherwise just reserve drug in therapy-refractory stage NYHA III and IV!)
  • Phosphodiesterase-III-inhibitors such as ISDN or hydralazine in NYHA II to IV and intolerance/contraindication for ACE-inhibitors and AT1-blokcers (in consultation with a cardiologist)

The medicinal intervention in the fluid and electrolyte balance requires daily weight controls of the patient.

8.4 Implantable Cardioverter-Defibrillator (ICD)

An Implantable Cardioverter-Defibrillator (ICD) is indicated in patients with malignant arrhythmia and/or advanced heart failure with an ejection fraction <30%.

8.5 Cardiac Resynchronization (CRT)

Cardiac resynchronization by a biventricular pacemaker system is indicated in patients with an ejection fraction <35 %, maintained sinus rhythm and left bundle branch block.

8.6 Further adjuvant therapies

Surgical ventricular reduction, mechanical support systems

8.7 Heart transplant

This is the last resort when other therapy options fail.

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8.8 Overview

Therapy of heart failure primarily depends on the trigger cause. The following table gives an overview of the potential therapeutic approach.

Causes Possible therapeutic approaches
1. Chronic ischemic heart disease Possibly revascularization
2. LV-remodelling after myocardial infarction Conservative-medicinal
3. Hibernating myocardium (vital myocardium with chronic ischemia) Early revascularization
Hypertension, hypertensive heart disease with hypertrophic LV Medicinal control of hypertension
Cardiomyopathy (CMP)
1. Dilatative Cardiomyopathy (DCM, idiopathisc form) Physical rest, medication, alternative therapies, and consider HTX
2. DCM subsequent to toxic damage due to alcohol, drugs, or medication Strict abstinence from alcohol; strict abstinence from drugs (especially cocaine); revision and possibly change of medication (eg. NSAR, cytostatics, etc.)
3. Hypertrophic CMP with obstruction (HOCM) High-dose medication verapamil; discussion: DDD pacemaker; catheter ablation of the septum hypertrophy or surgical myectomy
4. Hypertrophic CMP without obstruction High-dose verapamil
5. Restrictive CMP, idiopathic form Discussion of HTX
6. CMP in storage diseases (amyloidosis, hemochromatosis) Symptomatic therapy and treatment of the underlying disease, eg. chemotherapy in plasmocytoma, venesection in hemochromatosis
Tachycardic forms
Chronic or acute atrial fibrillation Medicinal normalization of the heart rate; possibly rhythmization (electrical/medicinal)
Typical atrial flutter Catheter-guided HF ablation
Supraventricular tachycardia with reentry mechanism (eg. WPW-syndrome)
Persistent ventricular tachykarda ICD (Implantable Cardioverter Defibrillator), antiarrhythmics, possibly HF ablation
Arrhythmogenic right-sided ventricular cardiomyopathy (ARVCM) Antiarrhythmics; ICD (only rarely leads to heart failure)
Bradycardic forms
Sinus or AV node diseases Possibly DDD(R)-pacemaker
Absolute bradyarrhythmia in chronic atrial fibrillation Revision of the medication; possibly VVI(R) pacemaker implant
Heart valve diseases Surgical valve replacement or valvuloplasty
Inflammatory heart diseases
1. Acute myocarditis Symptomatic
2. Acute endocarditis with hemodynamically relevant valvular dysfunction Surgical sanitation (valve replacement)
3. Acute rheumatic fever Antibiotics
4. Constriktive pericarditis Surgical sanitation pericardectomy
Cardiac involvement in vasculitis and other autoimmune diseases Immunosuppressive therapy of the underlying disease; symptom oriented therapy
Cardiac involvement in endocrine and metabolic diseases Compensation of the hormonal and metabolic factors
Diabetic autonomous neuropathy
Anemia Transfusion and determination of the cause
Renal failure Possibly dialysis

9 Drugs that should be avoided in heart failure

This page was last edited on 1 November 2020, at 22:27.

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