Juan Carlos Linares Casas

Heart Failure (HF) is the end result of a wide variety of heart diseases. In fact, dysfunction of any part of the heart can cause the heart to fail.

Let's say first of all that Heart Failure syndrome has eluded any attempt at a single definition. Most of them highlight the pathophysiology of Heart Failure, while in practice the term is used to describe the clinical syndrome. We must then define it from both points of view.

Recent guidelines from the American College of Cardiology and the American Heart Association (ACC / AHA), to which we will return later, define heart failure as “a complex syndrome that may be due to any structural or functional disorder of the heart that affects the heart. the ability of the ventricle to fill or empty with blood. ' To refine a little more, they define the main manifestations of the syndrome, such as fatigue or dyspnea and water retention, which can lead to pulmonary congestion and peripheral edema. Therefore, it is clear that, as it is a syndrome, there is a huge variety of diseases that can lead to its appearance. We will see later which are the most frequent, but we already anticipate that it is possible that different causes operate in different populations or that they do so with different intensity,

This pathology is in continuous growth, to the point that we can almost classify it as an epidemic. And this growth is due to multiple factors: longer life expectancy, increased survival, greater therapeutic arsenal available and early recognition.

This is how we can affirm that Heart Failure is a disease of the elderly, since a progressive increase in its incidence is observed accompanying aging. Its prevalence in the US is 1% at age 50 and reaches 9% at age 80; its incidence almost doubles in each decade between the ages of 40 and 80, being 2 new cases per 1000 inhabitants and per year at 50, and rises to 14 cases at 80. It is estimated that in the United States there are about five million people with Heart Failure, and 550,000 new cases are diagnosed per year. In Argentina it is estimated that 500,000 people have some degree of Heart Failure and approximately 25,000 patients die annually from this disease.

It is a progressive condition that affects quality of life and produces high mortality despite the various advances made in its treatment. Survival in patients with HF is 3.2 years in men and 5.4 in women, and survival rates at 5 and 10 years are 35% and 15% for men and 53% and 29% in women.

Advanced cases make up 10% of all patients with this disease, have higher short-term mortality, and involve large costs in health systems.


The etiology is frequently heterogeneous, but ischemic heart disease, arterial hypertension, valvular heart disease and dilated cardiomyopathies are substantially the most frequent causes of Heart Failure.

Coronary heart disease is the cause of HF in 25-49% of cases, and it usually coexists with arterial hypertension, although in recent years a decrease in the prevalence of hypertension and valvular disease has been observed.

In a proportion of cases, the cause of heart failure (idiopathic) cannot be established, and in others it is attributed to systemic diseases such as diabetes, exposure to cardiotoxic agents or inflammatory processes of the myocardium.

In some parts of the world we find other important etiologies: Chagas disease in South America, rheumatic valvular disease in India and South Africa, and endomyocardial fibrosis in Equatorial Africa.

Etiology of Heart Failure in Argentina:
Ischemic: 30%
Hypertension: 21%
Valvular: 17%
Language: 14%
Chagas Disease: 3%
Others: 15%


Triggering causes or precipitating factors can be grouped into:

  • Cardiac:
    • Myocardial infarction: 6%
    • Atrial fibrillation: 28%
  • Treatment related
    • Improper treatment
    • NSAIDs and other drugs
    • Corticosteroids
    • Beta-blockers
  • Non-cardiac: Lung embolism 1%
    • Anemia
    • Acute lung diseases and other infectious processes.
    • Stress 7%
    • Diabetic decompensation

Among them, anemia, infections and tachyarrhythmias stand out.


It is possible to identify other risk groups, in addition to the elderly, such as patients with diabetes, hypertension, obesity, alcoholism and advanced malnutrition.


Myocardial alteration due to functional or structural disorders of myocytes leads to ventricular dysfunction with decreased minute volume. In this circumstance, the body tries to compensate it to maintain cardiac output and blood pressure, through three main mechanisms.

  • Neurohormonal activation
  • Ventricular hypertrophy
  • Ventricular dilation

In general terms and considered schematically, they consist of modifications in the structure and function of the myocardium called “remodeling”, associated with fluid retention, vasoconstriction and cell growth, as a consequence of the activation of the autonomic nervous system (ANS), of the renin- angiotensin-aldosterone (RAA) and the vasopressin system (Fig. 1).


These mechanisms thereby seek to attenuate myocardial dysfunction and compensate for the condition. However, when this cascade presents an exaggerated response and / or is perpetuated over time, both the neurohormonal responses as well as the dilation and hypertrophy contribute through positive feedback cycles to the progressive deterioration of heart failure. They are the so-called damaging vicious circles. The deterioration will be related to a series of interconnected spirals, while considering that the worsening of the underlying etiology also contributes to the clinical and pathophysiological deterioration of the condition.

Neurohormonal factors:

The causal or primary myocardial event produces a drop in minute volume, leading to neurohumoral responses. They are probably an evolutionary vestige of diagrammed mechanisms to sustain blood volume and maintain circulatory homeostasis. This drop in minute volume causes sympathetic activation through the inhibition of baroreceptors located in the aortic arch and in the carotid sinus. The consecutive increase in the plasma concentration of norepinephrine (NA) will produce generalized vasoconstriction, with an increase in heart rate (tachycardia) and myocardial contractility, thus helping to maintain minute volume (Fig. 2).


But when prolonged over time, as already expressed, this sympathetic hyperactivity will certainly be harmful, causing tissue hypoxia, generation of free radicals, increased permeability of the cell membrane, myocardial fibrosis and cellular calcium overload (Fig. 3).


In parallel, the drop in blood pressure in the efferent arteriole of the renal juxtaglomerular apparatus leads to the formation and release of renin in the macula densa. There are two other primary mechanisms that induce the production of this proteolytic enzyme: a) an increase in sympathetic activity, with stimulation of beta 1-adrenoceptors in the kidney, and b) a reduction in the infused sodium that reaches the macula densa. Renin acts on angiotensinogen, a tetrapeptide of hepatic origin, forming angiotensin I, which by the action of the converting enzyme (ACE) is transformed into the octapeptide angiotensin II in endothelial cells, mainly in the lung and vasculature. This peptide fulfills various functions, among which it is worth highlighting: 1) it is a powerful direct arteriolar vasoconstrictor that will increase peripheral resistance, contributing to an increase in blood volume; 2) facilitates the release of NA in sympathetic nerve endings (positive feedback mechanism with the ANS); 3) acts on the adrenal cortex, activating the release of aldosterone and thus generating sodium and water retention, with loss of potassium due to kaliuresis. Aldosterone also intervenes in ventricular remodeling, participating in the production of myocardial fibrosis through the stimulation of collagen production; It should be noted that its release is also stimulated by the hypokalemia that it causes; 4) stimulates thirst; 5) stimulates in the hypothalamus the release of antidiuretic hormone or vasopressin, an important and powerful endogenous vasoconstrictor. 6) is responsible for left ventricular hypertrophy acting directly on myocytes; 7) there is a direct action on fibroblasts, inducing their mitogenesis and consequently the development of fibrosis; 8) stimulates the production of endothelin in the endothelium of blood vessels, the most powerful vasoconstrictor in the body, inotropic and pro-proliferative cell.

Increased blood volume increases venous return and preload, volume, and diastolic filling pressure of the ventricle. In this way, new increases in cardiac output are achieved through the well-known Frank-Starling mechanism, originated in an extracardiac system: increasing the volume at the end of diastole will increase the diastolic length of the myocardial fibers and consequently will have to improve ventricular contraction and systolic output. The expansion of blood volume generated by the renin-angiotensin-aldosterone system reaches figures between 10 and 20% in moderate forms, and between 30 and 50% in severe refractory heart failure. Small increases are enough to obtain appreciable improvements in systolic output. Unfortunately, however,


Hypertrophy and dilation:

Left ventricular dysfunction begins as a myocardial injury or stress, and is generally a gradual process, even in the absence of a new injury. The main manifestation of the progression is a change in the geometry of the left ventricle, consisting of hypertrophy and dilation of the chamber, which becomes more spherical; this process is called cardiac remodeling, as already noted.

The change in the size of the chamber, which increases the stress on the wall, depresses its mechanical performance and precedes symptoms, usually by months or years, and continues to contribute to their worsening, even after starting treatment (Fig. 5).


a.- Dilation:In work overloads, especially those of volume, the heart is subjected to a progressive and persistent dilation that for a long period can become a useful compensatory mechanism using the Frank-Starling law. But gradually this dilation will become inadequate to maintain stroke volume, for several reasons: 1) because progressive dilation causes disorganization and excessive sliding of the sarcomeres, with greater difficulty for the formation of the binding bridges between actin and myosin; consequently, the sarcomeres will not produce a coordinated contraction or be appropriately elongated as the dilation progresses; 2) as a consequence of Laplace's Law, which establishes that the wall pressure of the ventricle depends directly on the intraventricular pressure and the internal radius of the ventricle and is inversely proportional to the thickness of the wall, a point will be reached where the wall pressure will be at higher levels than normal; This leads to increased oxygen consumption and makes cardiac work less economical, with loss of the efficiency of dilation. We will thus have a dilation that produces more dilation.

b.- Hypertrophy: Hypertrophy, that is, the increase in myocardial mass, constitutes one of the most important compensation mechanisms that dispose of the heart when its function declines. Myocytic hypertrophy is accompanied by an increase in connective tissue, which can increase the diastolic stiffness of the ventricle.

It is not known for sure if ventricular hypertrophy responds to the presence of certain substances or is a direct consequence of the increased burden on the heart. It is supposed to be a myocardial adaptation aimed at reducing wall tension in the face of overload. Neurohormonal activation is involved, of course, as well as intermediate stimuli and reactions with the participation of oncogenes and growth factors, second messengers and effectors, which will cause changes in the myocardium and contractile proteins, leading to structural adaptation modifications or starting point of maladjustment.

There are two models of ventricular hypertrophy depending on the type of overload that causes it. In volume overload (aortic regurgitation, mitral regurgitation), the myocardial mass increases as the ventricular cavity dilates, so that the wall thickness hardly becomes greater. It is the so-called “eccentric hypertrophy”. Conversely, in chronic exposures to pressure overloads - high postloads - such as in aortic valve stenosis or arterial hypertension, the end-diastolic volume does not change, the ventricular cavity does not change, but the wall thickness does. It is known as "concentric hypertrophy".

In the initial stages of hypertrophy there is a proportional increase in muscle mass and capillaries. Thus, the contractile properties of the myocardium are preserved to maintain normal output. An effective mass increase has thus been achieved, while contractility is ensured by increased norepinephrine synthesis at adrenergic endings. So far, the "adaptation" or "compensation" of the heart to overload could be considered appropriate.

At a later stage the inotropism of the hypertrophied myocardium begins to decline. Fibrosis areas develop that alternate with normal areas, thus modifying the geometry of the ventricle and thus causing abnormal inotropism. This coincides with the decrease in intracardiac norepinephrine reserves and a relative inability of the adrenergic terminals to synthesize this transmitter again. In this case, the "compensation" of cardiac output is achieved by increased sympathetic activity of circulating catecholamines and the renin-angiotensin system.

But the myocardial inotropic status continues to deteriorate, perhaps after almost total depletion of its catecholamine stores. Synthesis at adrenergic endings is also null, while the myocardium loses its ability to respond to hormonal stimuli due to a reduction in its beta-receptors. It is then that circulatory compensation cannot be maintained for long; The resting cardiac output will then fall and the filling pressures will increase, with retrograde stasis, giving rise to the clinical and hemodynamic manifestations of heart failure syndrome.


  • Increased parietal stress. Spherical chamber.
  • Hipoperfusión subendocárdica
  • Decreased coronary reserve
  • Dilation that produces more dilation
  • Abnormal myocardial stiffness

Natriuretic Peptides

The atria and ventricles produce hormones that are synthesized and released in response to distention of these chambers, increased extracellular sodium, and tachycardia. These substances have diuretic, natriuretic and vasodilator properties. In addition, they inhibit renin production and are suppressive of cell growth. So far, 4 types have been identified: atrial natriuretic peptides (ANP) and brain (BNP) are of cardiac origin, type C peptide (CNP) is of endothelial origin, and type D peptide has recently been isolated in snakes. The most useful from a clinical point of view are ANP and BNP.

Natriuretic peptides would play an important role in maintaining the compensated state of asymptomatic ventricular dysfunction. They stimulate the accumulation of cyclic GMP, and due to its favoring action on nitric oxide, they can intervene by regulating vascular remodeling.

Patients with heart failure have high levels of ANP, originating mainly in the atria, and BNP in the ventricles, which generally correlate with pulmonary venocapillary pressure and with ventricular ejection fraction. But peptide receptors may be down-regulated in patients with severe heart failure, and there is evidence that the effects of these hormones on diuresis are decreased in this syndrome.

It is interesting to note the role assigned to natriuretic peptides as prognostic indicators. Elevated BNP would indicate a greater severity of heart failure and is also important for early detection of the syndrome.

Inflammatory cytokines and heart failure.

There is experimental and clinical evidence that, although recent, demonstrates the installation of an immunoinflammatory activation state in heart failure. High levels of various cytokines have been found in the myocardium and in the circulation of patients with this syndrome. These cytokines act on endothelial function, oxidative stress, induction of anemia, apoptosis of myocytes and progressive loss of skeletal muscle mass. Not only the myocardium but several other tissues synthesize these cytokines and perpetuate this continuous and low-grade inflammatory state, in response to the stimulus of hypoxia, mechanical stress, neurohumoral activation, and endotoxins: these include lymphocytes, monocytes, muscle cells striated and endothelial cells. Thus a network of molecules is formed that interact, not only with each other,

This progressive and repetitive state of immuno-inflammatory activation is associated with the progression of left ventricular dysfunction

The action of cytokines on the cardiovascular system consists of a stimulus to inflammation, endothelial dysfunction, intravascular coagulation, uncoupling of the beta-adrenergic stimulus, generation of free radicals, progressive loss of muscle mass and tolerance to effort. A synthesis of these actions can be seen in Table 1.

TABLE 1 - Actions of cytokines on the cardiovascular system
  • Direct toxic action on cardiomyocytes.
  • Stimulation of apoptosis and hypertrophy of myocytes.
  • Direct stimulation on the metalloproteinases of the extracellular matrix.
  • Generation of free radicals in the myocardium.
  • Stimulation of the synthesis of other cytokines
  • Skeletal myopathy: direct stimulation of apoptosis and myofibrillar necrosis.
  • Alteration of intramyocytic calcium metabolism.
  • Promotion of endothelial dysfunction
  • Promotion of synthesis of adhesion molecules and acute phase proteins.

The main cytokines synthesized are: tumor necrosis factor alpha, interleukin-1 and interleukin-6.

The stimulus for the overexpression of tumor necrosis factor (TNF) is the increase in wall tension associated with higher ventricular filling pressure. But there is also extracardiac production, especially in striated muscles, endothelial cells, neutrophils, smooth muscle cells, and fibroblasts.

TNF is a stable trimer, whose actions are explained in Figure 1. It also stimulates the production of fibroblasts and the synthesis of prostaglandin E-2 and superoxide dismutase, in addition to its antiviral and bacterial activity. Initiates a cascade of apoptotic cytotoxic responses through the caspase pathway that could contribute to so-called "cardiac cachexia."

The nuclear factor kappa-beta (NF-kb) is a nuclear transcription factor that regulates many pro-inflammatory substances and that can be activated by multiple stimuli, such as hypoxia, reactive oxygen species, bacterial endotoxins, cytokines and others. There is an overexpression of it in heart failure of different etiologies.

Interleukin-6 (IL-6) is a multifunctional cytokine linked to the progression of myocardial dysfunction, promoting the hypertrophy of cardiomyocytes, the maturation and proliferation of lymphocytes, and stimulates the synthesis of caspases and C-reactive protein . It is also produced by the myocardium and extracardiac tissues.

Interleukin-1 (IL-1) triggers its pro-inflammatory effects through the synthesis of prostaglandins and, perhaps, a direct action on beta-receptor uncoupling. It would also have a negative inotropic effect.

The hepatic production of C-reactive protein (CRP) constitutes a specific and sensitive indicator, with high prognostic correlation, in different inflammatory states, as a result of its property of interfering in practically all stages of the immune-inflammatory response once released into the circulation . High levels of CRP have been observed in decompensated heart failure and not linked to ischemic or infectious events, which allows us to classify it as an independent predictor of survival, low cost and highly sensitive.

Chronic oxidative stress and heart failure.

There is clear evidence of an increase in oxidative stress in chronic heart failure. It is the consequence of an increased production of reactive oxygen species in response to mechanical stress, angiotensin and pro-inflammatory cytokines. Large amounts of superoxide anion are produced, with functional and structural effects on the myocardium. The most prominent action would be the ability of chronic exposure to oxygen free radicals to cause ventricular remodeling. It has been shown that oxidative stress can stimulate apoptosis of myocytes together with a shift towards the fetal phenotype in surviving cells.

We see then that the mechanisms that govern the heart failure syndrome are not limited to structural and functional damage to the myocardium. They are the expression of an intricate multifactorial process that at different levels causes or contributes to ventricular remodeling.


When a patient goes to the doctor's office with symptoms and signs of congestive heart failure, not only the syndrome but also the cause of it must be identified. In addition to the medical history, physical examination, chest X-ray, and electrocardiogram, an echocardiogram and other non-invasive and invasive procedures will be indicated to determine the etiology of the condition.

It is also important to determine whether the clinical syndrome corresponds to a systolic or diastolic ventricular dysfunction. In most cases it is a systolic dysfunction, which is expressed in a depressed ejection fraction. There are two primitive causes of systolic dysfunction: myocardial damage (such as myocardial infarction) and work overload. As already mentioned, the latter is subdivided into pressure overload (as in arterial hypertension or aortic stenosis) and volume overload (as in mitral and aortic regurgitation).

In other cases, the etiology will be exclusively diastolic, where the symptoms and signs of heart failure present with a normal or almost normal systolic function and are accompanied by evidence of diastolic dysfunction. This includes cases of hypertrophic cardiomyopathy, ventricular hypertrophy of other origins, restrictive cardiomyopathies, pericardial diseases, certain infiltrative processes such as amyloidosis or others that, by causing a decrease in compliance (or an increase in ventricular stiffness), limit or they prevent ventricular filling, which leads to higher diastolic pressures or, what is the same, the reverse: to obtain the same ventricular filling volumes, higher filling pressures are required. The same pressures thus achieve lower diastolic volumes.

It should be emphasized that it is unusual for systolic dysfunction to present in isolation, since it is almost always accompanied by some degree of diastolic abnormalities due to the stiffness of the ventricular chamber. Even in the initial stages of hypertrophy and remodeling, there may be exclusively diastolic dysfunction, which can subsequently evolve to global, systolic and diastolic dysfunction.

It should also be stressed that chronic heart failure is a complex syndrome whose diagnosis, especially in the initial stages, can be classified as difficult. This is how the concept of “asymptomatic ventricular dysfunction” has been definitively incorporated, which implies including a significant group of patients with decreased function but who do not have symptoms.

Thus, in 2001 the American Heart Association and the American College of Cardiology classified heart failure due to its progressive and sometimes insidious nature into 4 stages of evolution, which describe the development and progression of the condition. The first two do not present symptoms of heart failure, encompassing the cases of “asymptomatic ventricular dysfunction” that we have mentioned, different from those with classic and strict insufficiency, which does present with symptoms and signs. Despite this distinction, asymptomatic cases are of fundamental importance for the identification of Heart Failure, due to the risk of developing the symptomatic picture, and that is why they are included in this classification.

The stadiums are:

Stage A : patients at high risk of heart failure, but who still do not present structural alterations or symptoms of Heart Failure. They are hypertensive, coronary, diabetic patients, the use of cardiotoxic drugs or a family history of cardiomyopathies.

Stage B : these patients do not present symptoms of Heart Failure. but they have already altered the geometry of the myocardium, such as concentric hypertrophy or dilation. These are the cases of previous myocardial infarction, systolic dysfunction or asymptomatic valve disease.

Stage C : structural heart disease with previous or current symptoms of Heart Failure. These are patients with known structural heart disease who present dyspnea, fatigue or decreased tolerance to exertion.

Stage D : patients in the final stage of the disease, in Heart Failure. refractory and requiring special treatment interventions, such as mechanical circulatory support, continuous infusion of inotropics, heart transplantation, etc.

Diagnostic difficulties have led to the appearance of different criteria, some based on scores, which seek to delimit a set of clinical characteristics that allow reaching the diagnosis. It is worth mentioning here the criteria of the Framingham Study, which groups the symptoms and signs suggestive of heart failure into major criteria and minor criteria for the recognition of the syndrome:

Major criteria

Minor criteria

  • Paroxysmal nocturnal dyspnea
  • Ortopnea
  • Acute Pulmonary Edema
  • Jugular engorgement
  • Baseline pulmonary rales
  • Cardiomegaly
  • Ventricular gallop rhythm
  • Hepatojugular reflux
  • Malleolar edema
  • Dyspnea on exertion
  • Night cough
  • Hepatomegalia
  • Pleural effusion
  • Tachycardia> 120 bpm

According to these criteria, to establish the definitive diagnosis of heart failure there must be 2 major criteria or one major and two minor.

Most of the clinical manifestations of Heart Failure. They result from the accumulation of fluid behind one of the ventricles. Pulmonary congestion with consequent dyspnea occurs in patients with left heart failure. In right heart failure, venous congestion is systemic, for which edema and visceromegaly may appear. Right insufficiency can be secondary to the left, due to pulmonary hypertension and consecutive right ventricular overload, or primary, as occurs in chronic obstructive pulmonary diseases.

Symptoms and signs

First of all, we must emphasize that the cardinal symptoms of Heart Failure. they are dyspnea on exertion and fatigue, which limit exercise tolerance, and signs of fluid retention such as peripheral edema and pulmonary congestion.

It is usually correctly pointed out that the clinic of Heart Failure. it is best understood by considering hemodynamic abnormalities. A) Increased left ventricular end-diastolic pressure and subsequent left atrial hypertension, especially during exercise, are related to dyspnea in its various forms; B) The reduction in minute volume, especially the lack of increase in minute volume during exercise, is partly related to fatigue and energy deficiency in these patients; C) Elevation of right atrial pressure secondary to pulmonary hypertension is responsible for peripheral venous congestion and lower limb edema that appear during the syndrome.


Dyspnoea : Left atrial hypertension generates chronic pulmonary venocapillary hypertension, leading to pulmonary congestion: the pulmonary vessels become engorged and interstitial edema may occur, reducing lung compliance. These changes cause an increase in the Hering-Breuer reflex, a reflex caused by the changing tension of the alveolus with production of polypnea and rapid and shallow breathing, to which is added the fall in vital capacity and the entry into play of the musculature accessory respiratory system.

The oxygen consumed in the act of breathing increases due to the greater work done by the inspiratory muscles; Added to this is the decrease in oxygen supply due to the drop in minute volume. All this causes the conscious and unpleasant sensation of breathing or dyspnea. According to the magnitude of the effort required to cause dyspnea, there are different degrees of cardiac functional disability, according to the New York Heart Association (NYHA) classification:

Class I : No limitations. Ordinary physical activity does not cause dyspnea, fatigue, or palpitations. Dyspnea appears with excessive or prolonged efforts, or with a sudden onset.

Class II : Slight limitations. We are facing dyspnea from great efforts: walking or climbing stairs quickly, walking uphill or after eating, with cold or headwind, etc.

Class III : Marked limitations. Regular, mild physical activity causes dyspnea. It is the dyspnea of ​​small efforts: when walking one or two blocks or climbing more than one floor of stairs at normal speed.

Class IV : Inability to perform any activity without discomfort. It is dyspnea on minimal exertion or at rest, which increases with physical activity.

The patient with orthopnea, ie, decubitus dyspnea, frequently uses several pillows to sleep; the feeling of suffocation diminishes when sitting up, and some patients find relief by sitting in front of an open window. In advanced cases, the patient cannot rest lying down and must remain seated all night.

The increase in dyspnea that occurs in decubitus is due to greater venous return due to the lack of the action of gravity on the lower limbs, and to greater pulmonary congestion with a decrease in vital capacity and respiratory muscle play.

In bouts of acute dyspnea at night, or paroxysmal nocturnal dyspnea, panting persists despite adopting the positions mentioned above, and coughing may appear. Cardiac asthma is nothing other than dyspnea due to bronchospasm secondary to heart failure itself. It can occur during exertion or spontaneously at night.

Acute pulmonary edema is the most severe form of acute dyspnea and is due to a significant, usually sudden, elevation in pulmonary capillary pressure. It presents with extreme respiratory distress, due to the passage of fluid from the capillary space to the pulmonary alveoli, which is why abundant rales appear - audible even at a distance - in both lung fields and pink expectoration due to the presence of red blood cells. If not treated quickly, it can be fatal.

The classic picture of acute edema is unmistakable: the patient is extremely anxious, sits up in bed, perspires profusely, is pale, cold, and the extremities may appear cyanotic; breathing is rapid and loud (“boiling pot noises”) and is accompanied by pulling, coughing, and pink, “salty” expectoration.

Dyspnea, a cardinal symptom of left ventricular failure, does not usually appear in isolated right insufficiency, since there is no pulmonary congestion. In fact, when a patient with left ventricular failure - which is the most common cause of right failure - develops right claudication, the more severe forms of dyspnea (paroxysmal nocturnal dyspnea and lung edema) tend to decrease in intensity and frequency, since that the inability of the right ventricle to increase its minute volume prevents fluid overload in the lung.

Fatigue : as said, it expresses the drop in minute volume. It occurs with exertion in the early stages - such as dyspnea - and becomes permanent and at rest in the later stages of the condition.

Nocturia : The increase in urinary volume at night expresses the reabsorption of hidden or visible edema, with a consecutive increase in renal perfusion and minute volume.

Oliguria : occurs due to the water retention that occurs in right ventricular failure, and its magnitude depends on the severity of it. It is a sign of courage.

Epigastralgia, right upper quadrant pain, anorexia and meteorism : these are expressions of abdominal congestion and congestive hepatomegaly that are observed when right insufficiency generates abdominal congestion and systemic venous hypertension.

Other symptoms : the cough can be an expression of left ventricular failure, especially if it occurs with the prone position. It often lasts for much of the night and can be revealed by the presence of interstitial edema on chest radiography.

There may be restlessness and difficulty falling asleep , due to the lung congestion itself, and sleep is often interrupted by the need to urinate.

In some cases there may be profuse sweating because the heat is not adequately dissipated by cutaneous vasoconstriction.

Signs :

Mildly or moderately affected patients usually appear normal. However, they may manifest dyspnea with exertion (when removing clothes, for example) or when decubitus. Advanced cases show rest anxiety and dyspnea.

The pulse is usually fast and the blood pressure is low, while in severe cases the lower limbs may be pale and cold.

In addition to the signs of the causative disease, the signs that accompany HF are:

  1. Downward and outwardly displaced apex beat as an expression of cardiomegaly at the expense of the left ventricle. Right ventricular enlargement is recognized by palpation of a vigorous beat along the left stenal border.
  2. Third noise (R3): it is very specific and of great value as a sign of altered left ventricular compliance. When accompanied by tachycardia, it sets up a R3 gallop rhythm or ventricular gallop rhythm.
  3. Fourth noise (R4) or atrial gallop is less specific, usually accompanies pressure overloads and originates as a consequence of a forceful atrial contraction, which must overcome the resistance exerted by a rigid ventricle.
  4. Edema, one of the major criteria for diagnosis, does not always correlate with the level of venous pressure. In general, it is symmetrical and is located in sloping areas. For this reason, in outpatients it appears first on the dorsum of the foot and in the ankle region, particularly at the end of the day, while in the patient on bed rest it is usually located in the sacral region. In long-standing cases it can evolve to anasarca.
    Water retention can initially manifest itself as an increase in body weight. The appearance of pretibial edema at the end of the day does not become apparent until 4-5 liters of fluid accumulate. Loss of this volume by the action of a vigorous diuretic within 24-48 hours is indicative of heart failure.
  5. Jugular engorgement: it is a very important sign that indicates the presence of systemic venous hypertension. In normal conditions the jugular strain should not exceed 4 cm above the sternal angle. When right ventricular failure is mild, engorgement may be normal, although it rises with sustained compression of the periumbilical region (hepatojugular reflux) for one minute.
  6. Stasis rales are produced as a consequence of the transudation of capillary content to the alveoli and correspond, therefore, to heart failure of - at least - moderate severity.
    These are moist, crackling, symmetrical rales that are heard during inspiration and are not modified by coughing. They are detected mainly on the dorsum and lung bases, although they are sometimes more diffuse, as in acute pulmonary edema. In cases of bronchospasm wheezing is usually added.
  7. Stasis hepatomegaly: usually precedes the installation of edema. If it is recent or of rapid installation, palpation of the hepatic margin is painful, not the same in chronic cases.
    If venous hypertension is severe and prolonged, splenomegaly may also occur. In the late stages, jaundice and increased transaminases and direct bilirubin may be added.
  8. Alternating pulse: consists of the alternation of a vigorous and weak heart contraction, which can be detected using the sphygmomanometer. It is seen above all in HF secondary to arterial hypertension and aortic stenosis, although it can also be seen in other etiologies.
  9. In the later stages of heart failure, a state of cachexia may occur. Increased catabolism, protein-losing enteropathy, decreased intake due to poor appetite, mental depression, drug toxicity, and cellular hypoxia contribute to it.


Chest X-ray: allows to appreciate the size and configuration of the cardiac silhouette and the presence or absence of pulmonary congestion, beyond the eventual pulmonary etiology of a picture of right insufficiency.

As in Heart Failure. There is usually cardiomegaly, the cardiothoracic index is, in general, increased, while pulmonary congestion is detected before its clinical manifestations appear. When the venocapillary pressure rises above normal (12 mm Hg.) The pulmonary veins distend and when it reaches the oncotic pressure of the plasma (25-30 mm Hg.), The capillary fluid transudates into the interstitial space.

Due to the effect of hydrostatic pressure, the veins of the lower lobes will be more prominent than the apical ones in standing. But when pulmonary hypertension occurs, the superior veins appear distended in relation to the basal veins. The increase in pulmonary pressure will manifest itself with the dilation of the hilar shadows.

The radiological translation of interstitial edema is the darkening of the hilar shadows and, in particular, the blurring and loss of definition of arteries and veins. With the accumulation of fluid in the lung pericapillary tissue, the interlobular septa of the pulmonary periphery, located perpendicular to the pleural surface, become visible, especially at the bases. They then appear as well-defined, horizontal and peripheral linear densities, with a length of 1 to 3 cm. These are Kerley's B lines. The longest lines that extend from the hilum to the periphery in the middle and upper regions of the lungs (Kerley's A lines) correspond to interlobar connections existing at this level.

On the other hand, alveolar edema is recognized without difficulty, since it determines the appearance of the characteristic image "in butterfly wings", constituted by confluent exudates in the pulmonary hila.

Effacement of the costophrenic or costovertebral angles suggests the presence of a pleural effusion or an elevation of the corresponding hemidiaphragm.

Electrocardiogram :

There are no specific data on heart failure, but signs of underlying heart disease appear. It may show left ventricular hypertrophy, rhythm disturbances, conduction disturbances, or evidence of coronary artery disease.

Echocardiography and Doppler:

These methods have revolutionized the assessment of heart failure because they are risk-free, even during pregnancy and can provide the diagnosis in most common cases. That is why the exact diagnosis of Heart Failure. It is more important today than ever, due to the availability of treatments that can improve the prognosis, not only in the classic clinical forms but also in patients with asymptomatic left ventricular dysfunction. An echocardiogram is recommended in all patients with suspected asymptomatic dysfunction to confirm or rule out the diagnosis.

Echocardiography and Doppler are the most useful diagnostic methods, as they are capable of determining alterations in ventricular geometry, chamber dilation, wall thicknesses, systolic and diastolic functions, valvular, pericardial or right chamber alterations. The information obtained with the Doppler echocardiogram is not only qualitative but also quantitative, being able to determine the ejection fraction, thickness, volumes, and degree of valve insufficiency.

Despite its limitations, the ejection fraction calculated with echocardiography is an important predictor of mortality in this syndrome: many studies have concluded that patients with reduced EF have a higher annual mortality than those with normal or subnormal values.

The study of ventricular morphology by echo is also valuable, inasmuch as as the ventricle dilates, it loses its normal shape and tends, as already mentioned, to sphericity. Since a more spherical ventricle is associated with greater wall tension and greater depression in contractility, monitoring of these variables is of considerable clinical importance.

It has also become very common to evaluate ventricular diastolic properties in heart failure. The presence of a restrictive pattern of transmitral flow determined by Doppler is a non-invasive marker of severe symptoms and decreased exercise tolerance, which is associated with higher mortality. In the restrictive pattern, most of the ventricular filling is done early, showing a predominant E wave, with late filling

To very small. The Doppler, as already mentioned, also makes it possible to evaluate the presence and severity of possible valve conditions responsible for the condition.

Laboratory exams:

The most frequent manifestations are the following:
1.- Urinalysis may show a discrete proteinuria, not greater than 0.75 g / 24 hours. Urine density may increase during sodium and water retention phases and decrease during periods of diuresis. The uremia may rise slightly (prerenal uremia).
2.- The ionogram is normal, although sodium restriction, diuretic treatment and the inability to excrete water can lead to dilution hyponatremia. Prolonged administration of diuretics can cause hypokalaemia.
3.- Hepatic dysfunction is manifested by a slight increase in bilirubin, GOT and LDH. In prolonged cases, hypoalbuminaemia may occur.