Navigating Decompensated Heart Failure: Practical Guidelines

• Heart failure (HF) syndrome is defined by congestion and hypoperfusion . In acute HF (AHF), congestion is the usual condition, with or without variable degrees of compromised perfusion. In turn, congestion, although it can affect both territories, usually predominates in one of them , pulmonary or systemic .
   
• Approximately 50% of patients with AHF have reduced ejection fraction (EF red); the remaining 50%, with preserved ejection fraction (pre-EF), the coexistence of comorbidities is a determining factor in the evolution and prognosis. The prevalence of both conditions depends on the population treated, with pre-EF predominating. in health centers that preferably assist older adults.
   
• The ICA with FE pre . It is characterized by pulmonary congestion, in general, without an obvious drop in perfusion. Mortality from all causes is similar to that of FE network. but with a lower proportion of cardiovascular disease and a higher proportion due to comorbidities; The age is approximately 10 to 15 years older than the other.

Hypertrophic and storage cardiomyopathy (amyloidosis among others) are probable etiologies of decompensated HF with preserved EF.

• In the ICA with FE network. Coronary heart disease predominates, especially a history of myocardial infarction, followed by dilated cardiomyopathy of non-ischemic etiology.
   
• The diagnosis of AHF is clinical, based on symptoms and signs; BNP is useful in confirming hemodynamic failure ; It must be remembered that BNP has lower sensitivity in AHF with pre-EF, in acute mitral insufficiency and in obese patients.
   
• In cardiogenic shock the drop in perfusion is critical, with lactic acidosis and tissue dysfunction; Lesser degrees of hypoperfusion are expressed by systolic blood pressure less than 90 mm Hg, tachycardia, oliguria, and skin coldness. In other words, hypoperfusion is a continuum , from mild, subclinical degrees to definite cardiogenic shock.
   
• The pathophysiological interpretation of AHF is of primary importance for the implementation of the therapeutic strategy, but decisions are primarily based on the adjustment of a few clinical and hemodynamic parameters. 
  - Blood pressure and heart rate. 
  - Signs of congestion, pulmonary and systemic, skin perfusion, diuresis. 
  - Arterial saturation of O2, lactic acid and PH. 
  - FE (by echocardiography). 
  - Hemodynamic variables (central and pulmonary venous pressures, minute volume and mixed venous O2 saturation).

Other parameters such as end-diastole volume and right ventricular EF, or those resulting from the combination of the above, are of secondary value.

ICA may be the consequence of a recently installed process or be the result of decompensation from a chronic pump failure.

The correct interpretation of the condition is essential from the perspective of treatment, prognosis and, above all, in relation to prevention.

Among the associated factors of recent installation we can mention:

• Suspension or reduction of specific treatment for pump failure.
• Acute coronary syndrome.
• Arrhythmias (extreme bradycardia or high-frequency tachycardia).
• Arterial hypertension.
• Excessive use of anti-inflammatories (corticosteroids/NSAIDs).
• Acute myocarditis.
• Infections / anemia / hyperthyroidism - hypothyroidism.

Among the valve defects as the etiology of AHF, endocarditis, rupture of chordae tendineae of the mitral valve, spontaneous or due to endocarditis, and acute thrombosis of valve prostheses should be noted.

Finally, among the differential diagnoses of AHF, pulmonary embolism should be noted, a condition to be considered as a possible etiology in case of sudden respiratory distress.

The use of hemodynamic monitoring varies in different centers, but in general its indication is not systematic and is restricted to the unclear interpretation of the clinical picture on admission or when the response to the instrumented intervention is inadequate.

Doppler ultrasound is key in the diagnosis of valvular defects, pericardial effusion and in the estimation of ventricular function.

In general, there is a good relationship between hemodynamic variables and the ejection fraction estimated in the echocardiogram. However, under certain conditions a mismatch between hemodynamics and Doppler ultrasound is observed , such as in cases with left ventricle without or with minimal dilation, as in pre-EF HF in general and in acute myocarditis, in acute post-transplant rejection, in restrictive cardiomyopathies (hypertrophic, amyloidosis) among others. Since EF is the ratio between systolic volume and end-diastole volume, since the latter is normal, slight decreases in shortening significantly reduce systolic volume and thus cardiac output. Furthermore, lower compliance significantly increases diastolic and pulmonary pressures without dilation of the ventricular chamber.

Although images, Doppler ultrasound, computed tomography and magnetic resonance imaging are essential in the diagnosis of pericardial pathologies , their functional impact sometimes requires hemodynamic recording.

Finally, the coexistence of heart failure with arterial vasodilation secondary to inflammation (infectious or otherwise) defined as mixed failure may be associated with pseudonormal hemodynamic findings in the presence of significant tissue dysfunction.

This point refers to the guideline recommendation to maintain the treatment of chronic HF in the decompensated phase of HF.

The treatment in question is:

• Neurohormonal blockade
• Beta blocking
• Spironolactone blockade
• SGLT2 inhibitors

The basis for this recommendation is the finding in observational studies that demonstrated that the prognosis of AHF was substantially better when treatment was not discontinued.

It should be noted that a statistical bias is likely in these retrospective analyses: many of the patients in whom treatment was discontinued could have had a worse hemodynamic condition with arterial hypotension or requirement for inotropes. In other words, perhaps continuity generated a favorable population selection associated with a better prognosis.

Beyond this consideration, in principle "chronic treatment" should be maintained, or failing that, reduced as much as possible.

Unlike chronic HF, in AHF the evidence is limited and fragmentary. In general, they are based on expert recommendations, personal and institutional experiences, as well as pathophysiological interpretations.

Treatment with vasodilator drugs , with a predominant venous/arterial effect, outside the setting of severe arterial hypertension, is not relevant .

Drugs with an exclusively vasoconstrictive effect (vasopressin, for example) have no indication in cardiogenic shock associated with increased systemic resistance since, although they can sustain blood pressure, they significantly reduce cardiac output . Its widespread use in intensive care is a consequence of the fact that hypotension in this setting, in most cases, is associated with extreme vasodilation and high minute volume typical of the infectious condition.

However, in the context of the coronary unit it is preferable to treat hypotension with drugs with a double effect, vasconstrictor and inotropic .

Cases with mixed shock , contractile failure associated with arteriolar vasodilation constitute a particular situation. Examples of these conditions are the conjunction of sepsis with deterioration of cardiac function or the postoperative period of cardiovascular surgery. However, even in these cases and as a general rule, vasoconstrictor drugs without a contractile effect should not be used in patients with cardiac output less than 5 l/min or its corresponding cardiac index.

It is the central strategy in the ICA. In fact, the response to diuretic treatment usually induces a negative balance that is associated with a significant and immediate relief of pulmonary and systemic signs of congestion. Non-invasive ventilatory assistance complements pharmacological intervention.

But in certain cases, if the response is intense, intravascular contraction may occur as the volume of the interstitial space is not recovered simultaneously. The vena cava that allows estimating the central venous pressure (> 20 mm suggests central venous pressure > 15 mm Hg) will be collapsed in these cases (< 5 mm).

It is a relative and transient hypovolemia that can induce renal failure with hypotension and elevation of creatinine in the presence of interstitial, pulmonary and systemic congestion ("time window"). If the condition is not interpreted correctly, the negative balance can be limited without having reached the condition of euvolemia, with the consequence of considering other differential diagnoses as the cause of the condition, for example, lung disease among others.

The strategy should be aimed at slowing the negative balance to allow recovery of intravascular volume.

The above considerations apply to ultrafiltration . Given the lack of response to diuretic treatment (fursemide and its combination with other diuretics), this procedure is a precise indication, but it must be extended over time with a differential strategy with respect to chronic dialysis.

The failure of the right ventricle (RV) expressed by dilation and reduction of the ejection fraction is due, in most cases, to the elevation of its afterload (pulmonary hypertension), a common condition in AHF, with negative balance being the strategy. usual.

The exception is RV infarction with dilation and genuine contractile failure in the presence of clear lungs. In this case, maintaining a high preload improves hypotension and the rest of the hemodynamic variables until function is recovered.

A similar scenario is pulmonary embolism with hemodynamic decompensation in which it is also required to increase the RV volume.

Now, heart transplantation is a particular scenario as a certain increase in pulmonary resistance (due to chronic heart failure of the left ventricle) coexists with RV of normal dimensions, not adapted to this pressure overload. Under these conditions, expansion should not reach a very high right atrial pressure since this may be associated with RV claudication with greater hemodynamic deterioration. Therefore, central venous pressure must be maintained in a range that does not exceed 15-16 mm Hg since overdistention of the ventricular chamber can lead to a drop in contraction due to high afterload (descending phase of the Starling curve). That is the basis for maintaining the heart rate in a range close to 120 in the immediate postoperative period of the heart transplant.

Lung embolism with hemodynamic failure is a similar condition, acute overload with non-dilated RV in which, as mentioned above, a high preload must be maintained, but in a limited range.

Sometimes the associated condition prompts the following question, for example: is the AHF a consequence of the arrhythmia or does the arrhythmia trigger pump failure? A similar approach occurs with myocardial ischemia. The probable temporal sequence does not always allow us to clarify the question.

Of greater importance is to consider this scenario as a process of reverse causality or positive feedback in which the initial trigger and its consequence interact, not only to perpetuate the condition but also as a trigger for future decompensations.

From this interpretation, the strategy must be directed not only to the treatment of AHF but also to resolving the associated factor even when it is considered as a secondary actor.

Supraventricular arrhythmia, particularly atrial fibrillation (AF), is a common complication of AHF secondary to myocardial disease regardless of its origin, primary, ischemic or valvular. In turn, tachemocardiopathy is a contractile deficit secondary to the high heart rate of a certain period of evolution, without a structural basis and with ad integrum recovery of function some time after the rhythm has normalized.

In other words, it is concluded that these are two entities with their own identity, each one with a particular strategy: compensation of the ICA with subsequent focus on the arrhythmia as an etiological treatment of contractile failure in the case of tachycardiomyopathy, or compensation and probable secondary approach to the arrhythmia considered as a complication of pump failure.

Sometimes the differential diagnosis based on the temporal sequence as mentioned is difficult, so it is preferable to conclude that it is a continuum between contractile failure and heart rate with a positive feedback mechanism as the underlying condition.

From this perspective, rhythm control is a fundamental component of HF treatment. If the superiority of rhythm control over rate control has not yet been conclusively demonstrated, this is probably because the randomized trials included an adverse selection of the population that included patients with long-standing arrhythmias. The constant progress of ablation techniques places this procedure as the systematic indication to consider in the near future.

Circulatory assistance with extracorporeal membrane oxygenation (ECMO) is the procedure of choice in our setting for the temporary mechanical support of severe pump failure with cardiogenic shock. In fact, other equipment is difficult to implement in our environment due to the high cost for the health system.

Although it is a practice that requires high specialization, the cardiologist in particular and the intensive therapist in general have a central participation in the indication of the procedure and in the monitoring of clinical variables that must be precisely adjusted for its success.

In circulatory failure, ECMO is with veno-arterial connection , usually femoro-femoral (possibly veno-axillary) that allows biventricular assistance.

Two aspects are of primary importance for the success of the intervention.

The first refers to cerebral oxygenation. With some degree of residual contractile function, cerebral perfusion may depend on left ventricular contraction. In these circumstances and if there was respiratory distress as an associated condition, the perfusion would be with partially saturated blood (Harlequin Syndrome), with consequent neurological damage. It is essential to monitor the saturation in the right arm, expression of the blood ejected by the left ventricle (and with it the cerebral saturation) since the saturation of the left arm can receive retrograde perfusion from the ECMO with optimal saturation through the oxygenating membrane. .

This complication could occur if by mistake, in the case of veno-arterial ECMO with residual LV function, the respirator is programmed with "protective ventilation" because it is a patient with associated respiratory pathology when considering that saturation is ensured by the equipment.

The second condition refers to the unloading of the left ventricle . ECMO with return of blood to the arterial circuit increases ventricular afterload, making it impossible to reduce chamber volume and relieve pulmonary congestion, negative conditions for recovery from myocardial and respiratory damage in cases where the indication is medical assistance. transient pending hemodynamic recovery.

This situation is diagnosed by monitoring pulmonary capillary pressure and LV volume by echocardiogram.

One possible strategy is the counterpulsation balloon , although its effectiveness is limited. More effective is the drainage of the left chambers (atrium or ventricle) using a second arterial cannula, a maneuver that increases the complexity but can reverse a limiting condition in the effectiveness of ECMO.

Although the probable cause for early readmission is the severity of HF , it is not infrequently due to the fact that at hospital discharge the patient is partially compensated as the state of euvolemia has not been reached.

Furthermore, a significant percentage of cases require the administration of post-compensation diuretics , even in conditions of euvolemia at discharge, especially in patients with several previous hospitalization episodes.

However, perhaps the most frequent cause is, we would say, administrative.

Observational studies have shown that readmission in the first 15 days after hospital discharge due to an episode of AHF is strongly associated with delay in the first outpatient consultation .

The cause may be linked to:

• Suspension of discharge medication when the instructions are not correctly interpreted by the patient and/or family members.
   
• Polypharmacy with probable interactions resulting from the new indications with non-cardiological medication.
   
• Non-availability of treatment due to failures in the Health system.

The strategy does not require an outpatient clinic specialized in HF as an essential condition. It is necessary to have a systematically scheduled consultation upon discharge  with a professional who has all the information regarding the AHF episode and who can eventually interact with the doctor who assisted you during hospitalization. In this consultation you must:

• Consolidate and/or adjust medical indications upon discharge; Not infrequently, it is necessary to increase the doses of neurohormonal blockade and beta blockade or reduce the dose of diuretics.
   
• Clarify doubts regarding subsequent follow-up.

After this first consultation, the patient can be referred to his or her family doctor or eventually to a HF specialist.

The strategy is as simple as offering accessibility to maintain continuity of treatment. The problem is that simple is sometimes difficult to implement.