Congestive Heart Failure, Its Pathophysiology, Symptoms, Diagnosys And Management
Heart failure is a common disease, affecting approximately 5 million people in the United States, and it occurs predominately in the elderly, with almost 80% of cases occurring in patients over the age of 65 with Blacks being disproportionately affected. Congestive heart failure (CHF) is a clinical syndrome that results from any functional or structural cardiac disorder that impairs the ability of the heart to fill with or eject blood. As a result, there is decreased cardiac output and therefore inadequate perfusion of tissues. Heart failure can refer to dysfunction of either the right or left ventricle (LV), but the specific term “congestive” heart failure refers to primary dysfunction of the left ventricle. There are two mechanisms of reduced cardiac output: systolic dysfunction and diastolic dysfunction. Since there is no definitive diagnostic test for heart failure, diagnosis is mostly based on a thorough patient history, physical exam and supported by tests such as chest radiograph, electrocardiogram, and echocardiography. This paper will explore the pathophysiology of CHF, the presenting signs and symptoms, as well as the diagnostic tools and management of this progressive disease.
Chances are if an individual develops congestive heart failure, it was precipitated by coronary artery disease, hypertension, myocardial infarction (MI), cardiomyopathy, valvular heart disease or diabetes. CHF is caused by the added stress of these many diseases that result in an increase in the workload of the heart or subsequent damage to the myocardium. This increase in cardiac workload is the body’s way of compensating to ensure perfusion to vital organs. These compensatory mechanisms that arise in congestive heart failure may be beneficial in the short term but lead to adverse clinical outcomes in the long term. Myocardial infarction is one of the primary causes of CHF. This condition causes impaired pumping action which results in the heart muscle being deprived of oxygen causing cardiac tissue ischemia. If patients suffer from hypertension, the constant increase in peripheral vascular pressure increases the force of contraction needed to pump blood out to the body. Regardless of the precipitating factors, heart failure ensues when these compensatory mechanisms become overwhelmed and can no longer work effectively to perfuse tissues.
Pathophysiology
The determinants of cardiac output include heart rate and stroke volume. According to Brashers (2006), the stroke volume is further determined by the preload (the volume that enters the left ventricle), contractility, and afterload (the impedance of the flow from the left ventricle). The heart is dependent on what is pumped in and what it must pump against. The preload is the volume that the left ventricle is given to send forward, the contractility characterizes the pumping action of the heart muscle itself, and the afterload determines the pressure the heart must work against. There are two types of CHF that effect these mechanisms by decreasing stroke volume: heart failure with reduced ejection fraction (HFrEF), and heart failure with preserved ejection fraction (HFpEF).
Heart failure with reduced ejection fraction (HFrEF) or systolic dysfunction, occurs when the left ventricle loses its ability to contract normally. Therefore, the heart can't pump with enough force to push blood into circulation. This impaired cardiac contractile function develops as a result of a neurohumoral processes initiated by long standing hypertension or coronary artery disease, leading to ischemic cardiomyopathy. The initiating insult results in increased sympathetic nervous system stimulation. This causes increased circulating levels of norepinephrine which bind to beta-1 receptors and result in vasoconstriction. The combined effect has an inotropic effect on the heart causing increases in total peripheral resistance, therefore increasing pumping action of the heart, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to do to perform effectively. This resulting hypertension causes hypoperfusion of the kidneys leading to increased renin production and ultimately an increase in angiotensin II levels. Aldosterone production is stimulated by the increase in angiotensin II and causes enhanced re-absorption of sodium by the kidneys, thus maintaining high blood pressure.
Activation of the renin-angiotensin-aldosterone (RAA) system has similar effects to norepinephrine; in that it temporarily stabilizes circulation by attempting to increase preload by stimulating retention of sodium and water, increasing vasoconstriction (and, thus, afterload), and increasing cardiac contractility. Initially, this response will suffice, over time, however, the enhanced circulatory sodium results in the water retention that is characteristic of decompensated CHF. The latter effect is poor left ventricular contraction and inadequate emptying (decreased ejection fraction) which results in an increased end diastolic volume, causing pulmonary congestion. Furthermore, complex inflammatory pathways are activated by myocyte apoptosis which trigger the secretion of tumor necrosis factor alpha and interleukin-6. These inflammatory cytokines and the maladaptive changes occurring in the surviving myocytes promote cardiac remodeling and hypertrophy. Thus, in the long run, neurohumoral activation perpetuates further maladaptive changes leading to worsening heart failure.
Heart failure with preserved ejection fraction (HFpEF) or diastolic dysfunction occurs when the left ventricle loses its ability to relax normally. This is due to the muscle becoming stiff resulting in the inability of the heart to properly fill with blood during the resting period between each beat. This inadequate filling of the ventricle results in an inadequate stroke volume. This is common in those patients with prolonged hypertension, valvular disease (aortic stenosis), constrictive pericarditis, hypertrophic cardiomyopathy. Acute myocardial ischemia is also a cause of HFpEF. Resistance to filling increases with age, reflecting cardiac myocyte loss, and increased interstitial collagen deposition; thus, HFpEF is particularly common among the elderly.
Alterations in cardiac morphology and geometry start at the cellular level. In HFpEF, studies show that the cardiac myocyte exhibits an increased diameter with little or no change in myocyte length, corresponding to the increase in left ventricular wall thickness with no change in left ventricular volume. However, the absence of structural cardiac changes does not eliminate the diagnosis of HFpEF. Most experts currently define HFpEF by LV ejection fraction as ≥ 50 percent. Occasionally, there is also an increase in the amount of collagen with a growth in the width and continuity of the fibrotic components of the extracellular matrix. While there is usually more interstitial fibrosis in patients with HFpEF than healthy patients, “the differences are not invariably striking, and many patients may not show marked evidence of fibrosis. ”
According to Borlaug (2019), obesity, metabolic syndrome, and sedentary lifestyle have also been identified as important risk factors for HFpEF. There is a link between insulin resistance and HFpEF that proposes the pro-inflammatory state induced by insulin resistance may also produce changes in the vascular endothelium of the heart. Specifically, by reducing availability of nitric oxide, an important vasodilator and protein kinase G, cardiac myocytes undergo hypertrophic changes. Cardiac macrophages are thought to play an important role in the development of fibrosis as they are increased in HFpEF and release pro-fibrotic cytokines, such as interleukin-10.
The most dominant abnormality in HFpEF exists in the diastolic function (Borlaug, 2019). Diastolic dysfunction is multifactorial, and patients may express diverse combinations of the following: inadequate myocardial relaxation, impaired rate of ventricular filling, increased left atrial pressure, “increased stiffness and decreased distensibility of the ventricle, limited ability to exploit the Frank-Starling mechanism, and increased pulmonary venous pressure. ” In a given patient, these impairments will result in a delay of left ventricular filling to the later part of diastole. This redistribution of filling from early to late diastole makes patients with diastolic dysfunction more sensitive than normal individuals to the effects of tachycardia. An increase in heart rate shortens the duration of diastole which is an important phase of diastolic filling. “Most studies suggest that the rate of left ventricular (LV) pressure decay during isovolumic relaxation is prolonged, increasing LV and left atrial (LA) pressure, especially with elevated heart rates, as during exercise. ” Atrial fibrillation is very common in people with HFpEF, being noted in roughly two-thirds of patients. The presence of atrial fibrillation is associated with decreased exercise capacity, development and worsening of right ventricular dysfunction. In addition to diastolic dysfunction, patients with HFpEF display systolic dysfunction, limitations in systolic reserve, pulmonary hypertension, vascular and endothelial abnormalities, and abnormalities in the periphery. The complex interaction of all of these pathophysiologic mechanisms is what drives symptoms and worsens patient outcomes in HFpEF.
Patient Presentation
Patients that have CHF usually manifest symptoms differently depending on the extent to which the left and right ventricle are affected. In left ventricular failure, the most common symptoms are dyspnea and fatigue due to increased pulmonary venous pressures, and low cardiac output. Dyspnea upon exertion that is relieved by rest is common. As CHF worsens, dyspnea can occur during rest and at night, sometimes causing a nocturnal cough. Orthopnea is common as CHF advances. Patients with severe left ventricular failure may also appear visibly cyanotic, hypotensive, and confused or agitated because of hypoxia and poor cerebral perfusion. Some of these non-specific symptoms like confusion are more common in the elderly. Non-specific symptoms include cool extemities, postural light-headedness, nocturia, and decreased daytime micturition. In right ventricular failure, peripheral edema and fatigue are common. Additionally, jugular vein distention and hepatosplenomegaly due to fluid accumulation in the peritoneal cavity, and subsequent ascites can occur. The resulting abdominal distention can cause early satiety, and anorexia in some patients.
Diagnostics
CHF must be differentiated from other cardiopulmonary diseases such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, pneumonia, asthma or other primary lung diseases. Then once, these are ruled out, the clinician must uncover the underlying cause of the CHF. The clinical manifestations aforementioned suggest a diagnosis of CHF but are usually not apparent early in the disease. Suspicion for heart failure should be high in patients with a history of myocardial infarction, hypertension, or valvular disorders or murmurs and should be moderate in any patient who is elderly or has diabetes. Therefore, a diagnosis of CHF can be established by performing a thorough physical examination and history. To support a diagnosis of CHF or narrow down causative factors, a chest x-ray, electrocardiogram (EKG), and echocardiography should be completed. A chest x-ray can display if there is pulmonary edema or cardiac hypertrophy present. An EKG is not diagnostic, but an abnormal EKG, especially one showing previous myocardial infarction, left bundle branch block, or an arrhythmia does increase suspicion for CHF and may help pinpoint the cause. A serum brain natriuretic peptide (BNP) level can be drawn however, the BNP level is correlated with the severity of CHF but its role in diagnosis is still unclear. A BNP of >100 supports the diagnosis of CHF but is not specific to CHF. An echocardiograph can illustrate chamber dimensions, valve function, and any ventricular hypertrophy, as well as estimate the ejection fraction and cardiac output.
Management
The primary goal of treatment is to diagnose and to treat the disease that led to the CHF. The treatment plan includes lifestyle modification, and nonpharmacologic therapies like salt and fluid restrictions; daily weights, and physical activity as tolerated. Pharmacologic therapies include the use of diuretics, vasodilators, inotropic agents for symptom relief or ACE inhibitors, angiotensin II receptor blockers (ARBs), and beta-blockers. Use of an implantable defibrillator (ICD) or cardiac resynchronization therapy (CRT) is appropriate for some patients. An ICD is recommended for patients with an otherwise good life expectancy and CRT may relieve symptoms and reduce heart failure hospitalizations for patients who have CHF. Surgery may be appropriate when certain underlying disorders are present. Coronary artery bypass grafting (CABG) to reduce ischemia did not improve overall 5-year survival in a large clinical trial of HF patients with ischemic LV systolic dysfunction; however, “CABG was associated with reduced overall 10-yr mortality and with reduced 10-yr mortality and hospitalizations. ” If CHF is primarily due to a valvular disorder, valve repair or replacement should be considered. Heart transplantation is the treatment of choice for patients less than 60 who have severe, refractory CHF and no other life-threatening conditions and who are highly adherent to management recommendations. Some older patients (about 60 to 70 years) with otherwise good health are also typically considered if they meet other criteria for transplantation. Survival is 85% to 90% at 1 year.
Conclusion
Congestive heart failure involves ventricular dysfunction that ultimately leads to the heart not providing tissues with adequate blood for metabolic needs. CHF is not only an inability of the heart to maintain adequate oxygen delivery; it is also a systemic response attempting to compensate for the inadequacy. These compensatory mechanisms become maladaptive and exacerbate and perpetuate the vicious CHF cycle. In heart failure with reduced ejection fraction (HFrEF), the ventricle contracts poorly and empties inadequately resulting in a low ejection fraction. In heart failure with preserved ejection fraction (HFpEF), ventricular filling is impaired, resulting in increased end-diastolic pressure at rest and/or during exercise; in most cases, the ejection fraction is normal. Unless CHF is promptly and adequately treated, it tends to progress and has a poor prognosis.
