Congestive Heart Failure: New Symptoms You Should Not Ignore

Healthy Living, General Health
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Chronic heart failure (CHF) rarely develops suddenly. More often, it begins with sensations that seem familiar and do not cause concern. A person becomes fatigued more quickly, and routine activities require pauses and longer recovery. These changes are usually attributed to age, stress, lack of sleep, or decreased physical fitness. In the morning, well-being partially improves, which reinforces the sense that nothing serious is happening.

Because of this “mildness” of symptoms, they are often not associated with the heart for a long time. Fatigue is perceived as normal, shortness of breath as a consequence of excess weight or low activity, and edema as a result of heat, diet, or sedentary work. Symptoms may wax and wane, creating the illusion that the situation can be waited out or compensated for by lifestyle changes or naturopathic supplements.

Historical context

Before the advent of modern medications, chronic heart failure was a condition that was almost impossible to keep under control. Physicians had no tools for reliably managing volume overload and pressure within the circulatory system. Supportive measures-rest, salt restriction, dietary changes-could temporarily reduce the severity of symptoms but did not allow compensation to be maintained.

Attempts to control congestion in the body through diet or “natural” diuretics did not produce a sustainable effect. These approaches did not allow predictable regulation of fluid volume and pressure and did not prevent the progression of congestion. As a result, the course of CHF remained unfavorable: the condition gradually worsened, and frequent causes of death included pulmonary edema, renal decompensation, and infections.

CHF became a manageable long-term condition only with the introduction of effective pharmacological therapy capable of controlling the key mechanisms of congestion. This highlights a key point: neither diet nor natural remedies have ever been independent methods for controlling chronic heart failure. They may complement treatment but cannot replace it.

A return to non-pharmacological approaches in established CHF is not an alternative strategy but, in effect, a return to a period when physicians had no means to control the condition or prolong patients’ lives.

Which symptoms should raise concern and why this is important

Chronic heart failure more often presents not with a single acute symptom, but with a combination of signs that gradually alter usual well-being.

  • The most typical are fatigue and reduced endurance: a person notices that familiar activities become more difficult, fatigue occurs more quickly, more time is needed for recovery, and there is a growing need to rest more often. This is not episodic tiredness, but a persistent sense of reduced capacity compared with a previous level;
  • Shortness of breath initially occurs with exertion-brisk walking, climbing stairs, bending. Over time, it may appear with minimal activity or when lying flat, forcing a change in body position or sleeping with the head elevated. It often remains moderate and is not accompanied by a feeling of suffocation, which makes it easy to underestimate;
  • Edema usually appears in the evening, predominantly in the legs: shoes become tight, the legs feel heavy, and sock marks may remain on the skin. In the morning, swelling often decreases or disappears, creating the impression of a temporary or minor problem.

These symptoms are characterized by a wave-like course: during one period, well-being seems relatively normal; during another, it noticeably worsens without an obvious cause. This alternation is often attributed to weather, fatigue, stress, or daily routine.

At early stages, the body can maintain this state for a long time through internal compensatory mechanisms, creating a false sense of safety. When the heart begins to cope less effectively with pumping blood, tissues receive slightly less than they need. The body perceives this as a threat and tries to preserve circulation at any cost. In response, protective reactions are activated: the kidneys receive a signal to retain salt and water in order to increase blood volume and raise pressure. This temporarily supports blood flow to organs but simultaneously increases fluid retention. The amount of fluid in the body increases, and the weakened heart cannot manage it effectively. As a result, excess fluid begins to accumulate: pressure in the vessels rises, the load on the heart increases, and congestion forms-in the lungs, legs, and other tissues. Thus, a vicious circle sustains itself: the more fluid is retained, the harder it is for the heart to pump it.

As long as compensation is maintained, a person may feel relatively tolerable and continue usual life, which creates an illusion of control. However, this is a temporary balance achieved at the cost of constant strain on the entire system. Compensatory capacity has limits: a person does not feel how much reserve remains, and deterioration often seems sudden, although it develops gradually. Therefore, in chronic heart failure, subjective well-being does not indicate physiological stability: the absence of marked shortness of breath or obvious edema does not mean that the heart and vessels are coping with the load without consequences. It only means that the body is temporarily holding the situation-and for this very reason, even moderate and unstable symptoms require attention and evaluation.

CHF is not a problem of a single organ. Shortness of breath, fatigue, and edema may appear as separate complaints, but in reality they reflect a single process-the progression of congestion and a gradual loss of the circulatory system’s ability to maintain normal balance. The entire circulatory system is involved in this process: the heart works under overload, vessels experience increased pressure, and fluid balance in the body is disrupted. As a result, symptoms appear fragmented and are often underestimated.

Underlying causes of chronic heart failure

Chronic heart failure almost never develops on its own. In most cases, it is the consequence of other conditions that place a prolonged overload on the cardiovascular system. CHF is not an independent disease but the result of chronic strain with which the heart and blood vessels eventually fail to cope.

The conditions that most often lead to the development of chronic heart failure include:

  • Long-standing elevated arterial blood pressure;
  • Past heart diseases, including ischemic heart disease and inflammatory processes;
  • Cardiac rhythm disturbances;
  • Lung diseases associated with increased pressure in the pulmonary vessels;
  • Chronic fluid volume overload;
  • Metabolic and endocrine disorders;
  • Age-related changes in combination with persistent stress on the system.

In all of these situations, the underlying mechanism is similar: the load on the heart and blood vessels increases gradually and, at a certain point, begins to exceed the system’s ability to maintain normal blood flow and fluid balance. As a result, conditions develop for congestion and reduced circulatory stability.

Identifying the primary cause is important for prognosis and treatment strategy. However, the search for the cause should not turn into a wait-and-see approach. While diagnostic evaluation and clarification of the underlying condition are ongoing, overload and congestion may persist or increase, even if overall well-being remains relatively tolerable.

Therefore, when chronic heart failure is suspected, the strategy should always be twofold: on the one hand, to determine the causes of the condition’s development, and on the other, to promptly confirm and control the congestion itself. Such an approach helps reduce the risk of complications and preserve the system’s reserve.

Two mechanisms of congestion development and why this matters

Chronic heart failure can present with similar symptoms-shortness of breath, fatigue, and edema-but the internal causes of these sensations can be fundamentally different. Understanding these differences is important not for formal classification, but for assessing how exactly the circulatory system is affected and what kind of support it requires.

At the core of the problem there is always impaired function of the heart as a pump, but it can manifest through two scenarios.

First scenario - impaired contraction (a weak heart) In this case, the heart muscle becomes weak and cannot eject blood into the vessels with sufficient force. Physicians refer to this as a “reduced ejection fraction.” The heart dilates, its walls may thin, and it begins to “miss” part of the required workload.

  • Risk profile: In this variant, congestion often develops rapidly, especially in the lungs (left-sided congestion). This creates a risk of acute conditions, when shortness of breath can suddenly progress to suffocation. This state requires active pharmacological support to help the “weak” pump cope with the blood volume.

Second scenario - impaired relaxation (a stiff heart) This variant is often described as insidious, because on examination the strength of cardiac contraction may appear normal. However, the heart walls become stiff and lose elasticity. The heart ejects blood well but fills poorly, because it cannot fully relax.

  • Risk profile: The patient experiences the same shortness of breath and fatigue as with a weak heart, but diagnosing this problem is more difficult. This type is common in people with long-standing hypertension and excess body weight. Here, congestion develops because blood “backs up” against a heart that cannot accommodate it in the required volume.

The relationship between pulmonary and systemic congestion

In addition to the mechanism of the heart muscle itself, it is important to understand where exactly excess fluid accumulates. This determines which signals the body produces:

  • Congestion in the pulmonary circulation (left-sided): When the left side of the heart cannot cope (regardless of whether due to weakness or stiffness), fluid accumulates in the pulmonary vessels. This manifests primarily as shortness of breath. A characteristic feature is worsening dyspnea in the supine position, when fluid redistributes and interferes with breathing more intensely;
  • Congestion in the systemic circulation (right-sided): It usually develops more slowly and is often a consequence of prolonged pulmonary congestion. Over time, the right side of the heart also begins to fatigue, and fluid “retreats” into the veins of the entire body. This leads to leg edema, a sensation of heaviness in the right upper abdomen, and abdominal enlargement.

Different forms and scenarios do not imply different degrees of severity-they indicate different pathways by which the disease deprives the system of stability. In one case, the risk may be immediate and acute; in another, cumulative and hidden. In both cases, however, lack of control leads to the heart and blood vessels losing their ability to sustain life.

How chronic heart failure is usually treated

Chronic heart failure is a condition that is not treated “once and for all.” The goal of therapy is to control congestion and overload, not to eliminate the diagnosis. If CHF has developed, it is impossible to get rid of it; it can only be kept under control. This is important to understand from the very beginning in order to avoid false expectations.

Even when well-being improves, the heart and the vascular system retain a tendency toward recurrent fluid retention. Therefore, treatment is aimed at maintaining fluid balance and load within limits at which the body can function stably, without decompensation.

Lifestyle plays a role in maintaining this balance, but it is not an independent treatment. Salt restriction and dietary control can complement drug therapy but cannot replace it. Control of fluid intake volume is of critical importance: when fluid intake is excessive, even properly selected medications will not be able to prevent the progression of congestion.

For this reason, therapy for CHF is most often long-term and frequently lifelong. This does not mean constant poor well-being. With adequate treatment, many patients remain stable for years and lead their usual lives. However, this stability is the result of control, not a sign that the problem has disappeared.

The treatment strategy is built around regular monitoring. The therapy regimen is individualized and may change over time: doses, combinations of medications, and monitoring schedules are adjusted. Such changes reflect the dynamic nature of the condition rather than treatment failure.

It is important to understand why discontinuation of therapy almost always leads to the return of congestion. While treatment maintains balance, fluid retention may be minimal and barely noticeable. After control is stopped, congestion begins to increase again-sometimes slowly, sometimes more rapidly-often creating an illusion of well-being until a noticeable deterioration occurs.

Thus, in chronic heart failure, treatment is not a temporary measure “for bad days,” but a way to maintain system stability and prevent loss of compensation and the severe consequences of uncontrolled congestion.

How chronic heart failure is confirmed or excluded

Symptoms alone are not sufficient to make a definitive conclusion about the presence of chronic heart failure. Fatigue, shortness of breath, and edema occur in a wide range of conditions-from lung and thyroid diseases to anemia or medication side effects. In CHF, symptoms may remain moderate and unstable, especially at the stage of compensation, which makes reliance on subjective well-being unreliable.

To confirm or exclude the diagnosis, objective methods are used that allow assessment of the cardiovascular system’s ability to cope with load and identification of signs of congestion. The physician considers complaints and physical examination findings; however, instrumental and laboratory studies play the key role.

Diagnostic evaluations

Basic tests without which it is impossible to confirm or exclude CHF:

  • Echocardiography - the primary diagnostic method. It allows assessment of ejection fraction (an indicator of what percentage of blood the heart ejects with each contraction), determination of cardiac chamber size, and identification of objective signs of overload;
  • BNP or NT-proBNP - specific laboratory markers of cardiac overload (natriuretic peptides). This is the “gold standard” blood test that helps confirm the presence of congestion or exclude CHF if values are within the normal range;
  • Electrocardiogram - identifies rhythm disturbances, signs of myocardial overload, or evidence of prior oxygen deprivation of heart tissue (ischemia);
  • Chest X-ray - used for visual assessment of fluid congestion in the lungs and changes in heart size.

Examinations that may be additionally useful

These tests do not directly confirm CHF, but are critically important for assessing disease severity, risks, and appropriate therapy selection:

  • Creatinine and eGFR (estimated glomerular filtration rate) - necessary for monitoring kidney function, which is critical when prescribing medications and managing therapy;
  • Sodium and potassium - allow assessment of water-electrolyte balance, which is often disturbed with fluid congestion and diuretic use;
  • Complete blood count - to identify anemia, which may mimic symptoms of CHF or significantly worsen its course;
  • TSH (thyroid-stimulating hormone) - to exclude thyroid disorders that may provoke heart failure.

Taken together, it is precisely this combination of data that allows clinicians not to guess based on symptoms, but to objectively confirm or exclude chronic heart failure and determine whether further monitoring and specific treatment are required.

How the condition is monitored after diagnosis

After the diagnosis is confirmed, chronic heart failure ceases to be a question of “whether it is present” and becomes a question of whether compensation is being maintained. In this context, monitoring is not a one-time check, but an ongoing assessment of how well the system is coping with the current load.

From the physician’s side, monitoring involves observing the condition over time. Exercise tolerance, signs of congestion, examination findings and laboratory results, and their changes over time are assessed. Particular attention is paid to kidney function, total body fluid volume, and response to therapy. Decisions are made based on the overall combination of parameters rather than on a single isolated result.

From the patient’s side, monitoring appears simpler but is of key importance. The patient is the first to notice increasing fatigue, changes in breathing, the appearance or progression of edema, reduced endurance, and a general sense of instability. One of the simplest self-monitoring methods in CHF is daily morning weighing. A gain of more than 1.5-2 kg over 2-3 days is a sign of hidden fluid retention even before visible edema appears and often allows treatment to be adjusted earlier than laboratory values change.

It is important to understand that in chronic heart failure, a single “normal” result does not mean safety. Parameters may temporarily appear acceptable in the setting of compensation, while the situation itself is already beginning to change; therefore, isolated tests have limited value without assessment of trends.

Monitoring in CHF is built precisely on changes over time. What matters is not so much individual numbers as their direction: whether stability is maintained, whether load is increasing, and whether reserve is decreasing. Loss of compensation rarely occurs abruptly-more often it begins with small shifts that, if recognized in time, allow serious deterioration to be prevented.

Post-diagnostic monitoring is a collaborative effort between physician and patient, aimed at maintaining compensation and preventing its loss.

Pharmacological treatment of chronic heart failure

Chronic heart failure is controlled through a combination of several groups of medications. The modern standard of treatment is based on the simultaneous use of multiple drugs, each of which targets its own part of the “vicious circle.”

Main groups of medications:

  • ACE inhibitors / ARBs / ARNIs (enalapril, ramipril / losartan, valsartan / sacubitril-valsartan) - these agents protect the heart from hormonal overload, reduce pressure in the vessels, and slow the wear of the heart muscle. The ARNI group is considered the most modern and effective;
  • Beta-blockers (metoprolol, bisoprolol, carvedilol) - they protect the heart from excessive influence of stress hormones, making it work more efficiently. This allows the heart muscle to preserve its functional reserve for longer;
  • Aldosterone antagonists (spironolactone, eplerenone) - block a hormone that causes the body to retain salt and water, and also prevent replacement of normal heart muscle with connective tissue;
  • SGLT2 inhibitors (gliflozins) (dapagliflozin, empagliflozin) - a modern class of medications that has fundamentally changed the prognosis in CHF. They help the kidneys excrete excess sodium and glucose, reducing pressure within the cardiac chambers and protecting the kidneys from damage;
  • Diuretics (furosemide, torsemide) - used to control fluid congestion. Unlike the previous groups, they do not treat the underlying cause of the disease, but they effectively reduce edema and relieve breathing, improving quality of life “here and now.”

This combination makes it possible to address the problem systemically: not only removing excess fluid, but also unloading the heart itself and preventing further disease progression.

Features of treatment in Canada

In Canadian medical practice today, a “four pillars” strategy is used. This means that the physician aims to prescribe not one, but four different medications as early as possible, each protecting the circulatory system from a different angle.

The mandatory standard in Canada now includes the use of new-generation drugs-SGLT2 inhibitors. They help the kidneys excrete excess salt and protect the heart from wear. In addition, instead of older agents, a modern combination drug from the ARNI group (angiotensin receptor-neprilysin inhibitor) is often prescribed.

The Canadian strategy is aimed at titrating all medications to effective doses as quickly as possible and preventing the return of congestion. This approach does not refer to waiting for a specialist appointment - it refers to what is done once you have finally reached that visit. Therefore, always seek care at the earliest symptoms in order to initiate therapy before compensation is lost.

Supportive measures in chronic heart failure alongside pharmacological therapy

With established pharmacological therapy for chronic heart failure, supportive non-pharmacological methods may be used. They do not affect the mechanism of CHF and do not control congestion, but may be applied in stable patients as an addition to primary treatment.

Lifestyle modifications

  • Regular moderate physical activity without worsening shortness of breath or pronounced fatigue;
  • A stable sleep schedule as a factor supporting blood pressure and heart rhythm;
  • Maintenance of muscle mass as a reserve of endurance in chronic heart failure.

Nutrition and fluid control

  • Adequate protein intake to prevent loss of muscle mass, with adjustment of amount when kidney function is reduced;
  • Limitation of salt intake through avoidance of processed foods and ready-made meals;
  • Control of the amount of fluid consumed, guided by changes in body weight and the appearance of edema.

Natural agents with the highest level of evidence

  • Omega-3 fatty acids (EPA/DHA) in moderate doses as support for vascular function and overall cardiovascular health;
  • Coenzyme Q10 as support for energy levels;
  • Magnesium, taking into account increased losses with diuretic use and with mandatory dose adjustment when kidney function is reduced;
  • Thiamine (vitamin B1) with long-term diuretic use;
  • Taurine as additional support of water-electrolyte balance.

Hibiscus (Hibiscus)

  • May contribute to a moderate reduction in blood pressure;
  • Exerts a mild relaxing effect on blood vessels;
  • Has a mild diuretic effect;
  • May be used as additional antioxidant support in stable patients;
  • Requires caution in cases of low blood pressure and when antihypertensive therapy has already been prescribed.

Once again: all of the measures listed above are permissible only as an adjunct to pharmacological treatment and cannot be considered a means of controlling chronic heart failure or preventing its progression.

When you need to go to the hospital urgently

In chronic heart failure, the most dangerous thing is missing the moment of loss of compensation. Before this point, the condition may appear tolerable or relatively stable, but after decompensation, emergency medical care is often required. It is important to know the signs at which waiting and attempts to “observe” the situation become risky.

Signs of loss of compensation include changes indicating that the body is no longer coping with the load:

  • Shortness of breath at rest or a sharp increase in dyspnea with minimal activity;
  • Inability to lie flat due to a sensation of air hunger;
  • Rapidly increasing edema or a sharp gain in body weight over a short period;
  • A feeling of suffocation or “flooding” of the chest;
  • Marked weakness, dizziness, or presyncope;
  • Sudden or irregular heartbeat that does not resolve;
  • Pain or severe pressure in the chest;
  • Confusion, pronounced drowsiness, or a general feeling that “something is wrong.”

In these situations, waiting for spontaneous improvement in these situations is unsafe. In chronic heart failure, such symptoms more often indicate that balance has already been disrupted, and delay increases the risk of serious complications.

It is especially important to seek urgent care if symptoms are progressing rather than remaining stable. Progression is a key sign that compensatory capacity has been exhausted, and the earlier medical intervention begins, the higher the chance of quickly regaining control of the situation.

What happens if chronic heart failure is not treated

If chronic heart failure is not controlled, the condition rarely remains stable. More often, it follows a pattern of gradual deterioration with periods of relative well-being and recurrent decompensations, frequently ending in emergency medical care or hospitalization.

Decompensation means that the body is no longer able to maintain fluid and load balance. Symptoms intensify: shortness of breath increases, pronounced edema appears, weakness develops, and routine activities become difficult. Each such episode is not merely a temporary worsening, but a loss of part of the compensatory reserve and an increased risk of subsequent decompensations.

Over time, uncontrolled CHF involves other organs. The lungs suffer from chronic congestion and elevated pressure, leading to worsening dyspnea and reduced exercise tolerance. The kidneys function under conditions of impaired blood flow and fluctuations in fluid volume, which may worsen renal function and complicate treatment. Blood vessels remain under constant overload, increasing the risk of cardiovascular complications.

It is precisely because of this cumulative nature of changes that CHF is often referred to as a “time bomb.” It can appear tolerable for a long time, creating an illusion of stability, while changes gradually accumulate within the system and eventually lead to abrupt decompensation.

It is important to understand that in the absence of treatment, the body is forced to compensate on its own, using a limited reserve. When this reserve is exhausted, the consequences become evident and require far greater intervention than early control measures.

Control of chronic heart failure is necessary not for short-term improvement in well-being, but to prevent recurrent decompensations, organ damage, and loss of system stability in the future.

Can one live a long time with chronic heart failure

The short answer is yes-one can live a long time with chronic heart failure if the condition is identified and kept under control. It is precisely treatment and regular monitoring that have made CHF a chronic, rather than a fatal, condition.

It is important to understand that such a “long life” does not occur on its own. It is possible only when congestion and load are maintained within acceptable limits. As long as control is maintained, many people preserve relatively stable well-being and functional capacity for years.

At the same time, the chronic nature of CHF does not imply safety. It is not a static state, but a process capable of slow progression. When control weakens-due to discontinuation of therapy, infections, overload, or dehydration-the risk of decompensation increases again.

The danger of the chronic form lies in its outward “tolerability”: the absence of acute symptoms creates an illusion of well-being, while stability persists only as long as control is in place.

Therefore, the main conclusion is simple: people live a long time with chronic heart failure not despite treatment, but because of it. The earlier the condition is identified and placed under monitoring, the greater the chance of preserving stability, quality of life, and system reserve for years to come.

Conclusion

Chronic heart failure is a condition that does not resolve on its own and does not disappear even when symptoms lessen. Its course depends not on how it feels on a given day, but on whether congestion and load are kept under control over time.

Modern therapy has made it possible to live with chronic heart failure for many years, but this stability is always the result of ongoing treatment and monitoring. When control is maintained, the system functions within a compensated range. When it is lost, the risk of decompensation, organ damage, and emergency situations rises sharply.

For this reason, chronic heart failure requires a long-term approach: early recognition, objective confirmation of the diagnosis, consistent pharmacological treatment, regular follow-up, and timely response to early signs of instability. It is this strategy-not isolated interventions or temporary measures-that preserves compensation, reduces complications, and maintains quality of life over time.