Congestive Heart Failure for the Primary Care Physician

ABSTRACT


INTRODUCTION
Heart failure is the presence of signs and symptoms caused by functional and/or anatomical impairment of ventricular systole and/or blood ejection, clinical signs and symptoms in which the heart cannot satisfy the body's metabolic needs. [1] Approximately 2% of the US population has congestive heart failure, most commonly systolic heart disease with reduced ejection fraction; the data show a higher prevalence in African Americans and Hispanics, which could indicate an etiological trend in certain ethnic groups; the incidence increases proportionally with age, an affectation of up to 10% is observed in individuals older than 60 years. [2. 3. 4] Cardiac output, stroke volume multiplied by heart rate, is determined by three factors: preload, afterload, and ventricular contractility. [1] Heart failure can be reduced ejection fraction (HFrEF, HF systolic) or preserved ejection fraction (HFpEF, HF diastolic). Heart failure with reduced ejection fraction is congestive heart failure with reduced volume, which reduces the ejection fraction; left ventricular ejection fraction is ≤35-40%, heart failure with preserved ejection fraction is congestive heart failure with reduced stroke volume, normal/reduced end-diastolic volume, and preserved ejection fraction (LVEF≥ 40-50%). [1,2] It can also be divided into right or left heart failure, depending on which ventricle has the dysfunction. Right heart failure is caused due to a dysfunction of the right ventricle that produces congestion in peripherin the vena cava and peripheral veins, which leads to an increase in venous hydrostatic pressure and makes peripheral edema, increased pressure jugular vein, ascites, and liver affectation. Left heart failure is caused by left ventricular dysfunction that results in tissue hypoperfusion and increased pulmonary capillary pressure. It can exist in both natures, right or left, which is known as biventricular (or global) heart failure [1,2] Suppose a patient has echocardiographic signs obtained incidentally. If the patient is asymptomatic or stable symptomatic, a chronic compensated HF diagnosis is considered. At the same time, acute deterioration of HF or the onset of severe HF due to a critical heart condition such as myocardial infarction is acute decompensated heart failure. [

CLINICAL FEATURES
Remembering that there are different modalities of heart failure, we can highlight general clinical characteristics such as nocturia, fatigue (see below NYHA classification), tachycardia, arrhythmias, auscultation of cardiac foci shows S3/S4 in gallop, as well as alternating pulse and the presence of cachexia in some patients. [6,7] The classic features of heart failure with systolic dysfunction are symptoms of pulmonary congestion such as breathing difficulty, orthopnea, pulmonary edema, paroxysmal nocturnal dyspnea (characterized by acute nocturnal attacks of cough and dyspnea, caused by reabsorption of peripheral edema during the night, resulting in increased venous return), as well as cardiac asthma with asthma-like symptoms, with dyspnea, wheezing and cough, this as a result of increased pressure in the bronchial arteries, which increase airway compression and bronchospasm. On physical examination, bilateral basilar rales may be found during field auscultation, laterally displaced apical heartbeat, and evidence of peripheral hypoperfusion (coldness, pallor, and decreased pulses) [6,7,8] Diastolic heart failure's clinical features are symptoms of fluid retention and increased central venous pressure, such as peripheral fovea-positive edema resulting from fluid transudation due to increased venous pressure. Appreciate symptoms of hepatic venous congestion such as abdominal pain and jaundice, nausea, and hyporexia/anorexia. During the physical examination, it is possible to see jugular venous distention, Kussmaul's sign, hepatosplenomegaly that can cause cirrhosis, and hepatojugular reflux. [6,8] maintain the glomerular filtration rate. The compensatory mechanism for aldosterone involves renal reabsorption of Na+ and H2O, which increases preload. Brain natriuretic peptide secretion is a hormone secreted by the ventricular myocyte at the time of increased filling and ventricular stretching, which helps to decrease the wedge pressure of the pulmonary capillary. [6,7,8,9] Correct classification of heart failure is essential because its medical treatment is based on it, and a higher success rate depends on it. Although there are different classifications, the most used are the AHA classification (Table 1), which is based on physical and structural changes of the heart, and the NYHA ( There is a structural damage to the heart (heart attack scars, dilation, hypertrophy) and no signs or symptoms of heart failure. Stage C Structural damage to the heart and signs or symptoms of heart failure. Stage D End-stage heart failure. NYHA Classification 1 High-output heart failure or heart failure secondary to organic dysfuction that generate a high-output state, in which cardiac output rises to meet the oxygen-metabolic demands of the tissues. It is caused due to peripheral vasodilation or arteriovenous shunt, causing a decrease in systemic vascular resistance and, thus, an increase in heart rate and stroke volume, which increases cardiac output. [10] The conditions that lead to an increase in cardiac demand and, therefore, a state of high output is varied and can range from physiological such as exercise, pregnancy, and even fever, to secondary to an underlying pathology, such as morbid obesity, cirrhosis in advanced stages, severe anemia, systemic arteriovenous fistulas, Paget's disease, hypothyroidism, vitamin B1 deficiency, sepsis, myeloma, glomerulonephritis, carcinoid heart disease and/or other types of cancer.
[10] Symptoms are almost entirely shared with low-output heart failures, such as dyspnea, tachypnea, tachycardia, peripheral edema, fatigue, low blood pressure, and high-output symptoms such as mid-systolic murmur, S3 gallop, jugular distention with audible buzz, pulsatile tinnitus and binding peripheral pulses. The diagnosis is clinical, although an X-ray or echocardiogram showing cardiomegaly suggests the disease. Treatment is symptom management and hemodynamic stabilization, as well as treatment of the underlying cause. [10]

DIAGNOSIS
Although many times the diagnosis can be made clinically, the most common differential diagnoses, such as COPD or pneumonia, can cause diagnostic confusion, so laboratory studies must be performed (CBC, blood chemistry with creatinine, sodium, glucose, liver chemistry, CRP, lipid profile, thyroid profile), cardiac biomarkers, electrocardiogram, chest x-ray, and echocardiogram, to establish a precise diagnosis, once the diagnosis of heart failure is confirmed, the underlying cause should be investigated (consider coronary angiography, imaging chest, and advanced cardiac imaging), and identification of modifiable risks (hypertension, coronary artery disease). [1,12] Once the laboratory studies have been requested, the findings are variable. Anemia or infection should be sought in the blood count based on hemoglobin levels or white formula levels; elevated creatinine would indicate renal changes, being important for the cardiorenal syndrome, hyponatremia is an indicator of poor prognosis, and fasting glucose as an indicator of risk factors such as diabetes. Altered liver chemistry could indicate hepatic venous congestion. Inflammatory markers such as elevated CRP indicate an infection or acute inflammation. The patient's lipid profile should be investigated and subsequently corrected as necessary. The thyroid profile is important due to the nature of its alterations. [1,12,13,14] Cardiac biomarkers should be requested in patients with suspected heart failure, brain natriuretic peptide (BNP) or brain natriuretic peptide N-terminal prohormone (NT-proBNP), it is indicated to request to establish the diagnosis of heart failure together with echocardiography, in addition to the evaluation of the prognosis, probability of diagnosis (Table 3), and the severity of the disease (taking the difference between their admission levels and their levels before discharge). [14. 15, 16, 17, 18] Peptide biomarkers, the diagnostic probability for heart failure.18  TREATMENT The initial treatment for uncomplicated congestive heart failure begins with modifying the patient's lifestyle; these changes reduce the risk factors associated with the progression of heart failure and other cardiometabolic comorbidities such as diabetes mellitus and hypertension. These lifestyle changes will be specific to each case. However, in general terms, we can mention that aerobic exercise, smoking cessation, alcoholism, drug use, and weight loss are essential to reduce the progression of the disease. Should consider states of immunosuppression in patients with comorbid conditions, requiring immunization with pneumococcal and seasonal influenza vaccines, adapting to each case depending on national epidemiological recommendations. [1,15,21,26] It is important to make the patient understand the pathophysiological bases of their disease, which makes the treatment efficacy and, therefore, their quality of life substantially improve; salt restriction ranges from <3g/day to <1.5g/day, Depending on the stage where the patient is, foods rich in potassium should be avoided during the administration of aldosterone antagonists, and fluids should be limited to 1.5-2 L per day in patients with stage D, who present with edema and/or hyponatremia. The patient must control and recognize the symptoms from daily weight control; if there is an increase of >2kg in less than three days, the patient must return to the doctor to evaluate the use of diuretics. The patient must be able to recognize symptoms of worsening heart failure, such as increased dyspnea at lower exertion than before, and must recognize new symptoms suggestive of medication side effects. It is recommended to carry a copy of the medical records and avoid destinations with limited medical attention. [1,26,27] Furthermore, in the case of significant atherosclerosis, revascularization should be considered. In the case of anemia, specific treatment for each type of anemia should be given to all patients with NYHA class II and III symptoms. [1,27,28,29,30] Most antiarrhythmic agents should be avoided, as well as potassium channel blockers, except amlodipine (simultaneous use of calcium channel blockers with betablockers can cause complete heart block), thiazolidinediones, and anesthetics. Inhaled antidepressants should also be avoided, and due to the increased incidence of depression in patients of all age groups in recent years, careful selection of antidepressants should be made. [1,15,26,29,31] Pharmacological treatment for heart failure is based on the stage of the disease in which the patient is present (Table 5), adding additional therapies to the treatment as symptoms worsen. The recommendations call for gradual initiation of all medications, starting with the lowest recommended dose and slowly increasing the dose, with each visit, up to the target dose. [1,8,15,26,29,32,33] Initial pharmacological treatment of heart failure. [8,15]  For all patients with fluid retention and volume overload, thiazides, as a synergistic effect, do not use as ba as treatment.
Evaluate the dose according to weight, volume, and hemodynamic stability with periodic review of serum electrolytes.

Isosorbide and Hydralazine isosorbide Hydralazine
Patients who do not tolerate ACE inhibitors or ACEs used in Afrodescendants.
Separate dosage of both drugs and monitor volume depletion and hypotension.
Stage D Additional measures to the treatment above: For patients with Stage D Heart Failure, invasive intervention or a palliative care approach should be considered. Continuous intravenous inotropic support should be considered a bridge before heart transplantation or mechanical circulatory support. The use of Digoxin should be considered in patients with HFrFE with persistent symptoms and refractory to first-line treatment; renal function should be closely monitored. [1,8,15,26,29,30,31] To consider the use of cyclic nucleotide-modulated hyperpolarization-activated channel blockers (ivabradine), all of the following must be present:  NYHA class II-III  HFrEF <35%  Sinus rhythm with HR >70bpm at rest with the maximum tolerated dose of B-Blockers. Patients who present arrhythmias such as ventricular tachycardia or fibrillation, in combination with heart failure, can cause symptomatic worsening and increase the risk of sudden cardiac death; these patients are candidates for Corresponding Author: Aranza Vazquez Ruvalcaba invasive interventions, devices with a pacemaker, and/or defibrillator functions. [34,35] The implantable cardioversion defibrillator works by administering an electrical shock, restoring sinus rhythm if an arrhythmia such as ventricular fibrillation or ventricular tachycardia is detected. [34,35,36,37,38] The indications for its placement are for patients who previously presented sustained ventricular tachycardia or cardiac arrest secondary to ventricular fibrillation or tachycardia, as well as patients with HFrEF with expected survival > one year if they receive medical treatment for 3-6 months and still comply with any of the following criteria:  Stage B with ischemic cardiomyopathy if LVEF is >30%  Stage C with dilated cardiomyopathy or ischemic heart disease with LVEF >35% and NYHA class II-III symptoms [34,35,36,37,38] In patients with end-stage heart failure, heart transplantation is the only cure. Unfortunately, most patients are not candidates. Patients accepted for transplantation generally require bridge measures, such as inotropic and/or mechanical circulatory support. Any patient with end-stage heart failure who is not a transplant candidate should be referred for palliative care. [1,8,37,38] COMPLICATIONS Decompensated heart failure is the worsening of heart failure symptoms. It is the most common cause of hospitalization for heart failure complications and one of the most common causes of hospitalization in older adults. Multiple causes can trigger pre-existing acute cardiac decompensation, but It can also occur in patients without a history of a heart condition. The diagnosis is based on typical clinical features as well as imaging findings. Management can be complicated because multiple comorbidities often accompany it. Most patients require treatment with diuretics, vasodilators, respiratory support, medications for underlying heart failure, and careful fluid management. [39,40,41] Other common complications are:  Cardiorenal syndrome  Cardiac arrhythmias  Cardiogenic shock  Cerebrovascular accident (Usually due to thromboembolism)  Cardiac cirrhosis (right CHF)  venous stasis CARDIORENAL SYNDROME It is a complex syndrome in which renal function is progressively diminished as a result of significant cardiac dysfunction; it occurs in 30% of patients with acute decompensated heart failure; its pathophysiology depends on which side of the heart the dysfunction is, in the case of systolic dysfunction, cardiac output is decreased, causing renal hypoperfusion, which would cause prerenal renal failure; in the case of diastolic dysfunction, it causes systemic venous and renal venous congestion, which decreases the gradient of transglomerular pressure, a decrease in glomerular filtration rate and consequently a decrease in renal function. The AHA has classified it into five types: Type I: Acute cardiorenal síndrome is when the heart failure leads to acute kidney injury.  Type II: Chronic cardiorenal syndrome. Chronic heart failure leads to chronic kidney disease.  Type III: Acute renocardiac syndrome. Acute kidney injury leads to acute heart failure.  Type IV: Chronic renocardiac syndrome. Chronic kidney disease leads to chronic heart failure.  Type V: Secondary SRC. Systemic disease leads to kidney and heart failure. Suspicion of cardiorenal syndrome is classically made when a patient with heart failure presents with decreased glomerular filtration rate and increased creatinine that cannot be explained by underlying kidney disease. The treatment is to treat heart failure and nephroprotective measures. The prognosis depends on laboratory levels; in the case of creatinine >3mg/dl, it is associated with a poor prognosis. [1,15,39,40,41]

PROGNOSIS
The prognosis in patients with heart failure is poor unless the cause is corrected. However, it depends mainly on the patient, the type and severity of heart disease, medication regimens, and lifestyle changes. The of patients with preserved EF is better than those with decreased EF, and worse prognostic factors are elevated BNP, hyponatremia, systolic BP <120mmHg, diabetes, anemia, weight loss or low weight, S3, use implantable cardioverter-defibrillator and frequent hospitalizations for heart failure. [1,42] 1-year survival according to NYHA stage:  Class I: 95%  Class II: 85%  Class III: 85%  Class IV: 35%

CONCLUSION
Heart Failure is an important public health problem, so the therapeutic approach must be multidisciplinary to impact all phases of the syndrome positively; that is why currently, the world trend is toward creating Heart Failure Clinics that are defined as specialized services for timely diagnosis and treatment of HF but also develop advanced research and educational programs to treat patients comprehensively.

BIBLIOGRAPHY
I. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, et al. (2013). ACCF/AHA guideline for managing heart failure: a report of the American College of Cardiology