Assignment: Left and Right Congestive Heart Failure

Left-sided congestive heart failure (CHF) occurs when the left ventricle cannot pump adequate blood around the body. Consequently, blood builds up in the pulmonary veins causing pulmonary congestion that manifests with shortness of breath (SOB), difficulties in breathing, and productive cough (Schwinger, 2021). In right-sided CHF, the right ventricle is unable to empty completely. As a result, increased volume and pressure develops in the venous system, and the veins push fluid out of the veins into surrounding tissue, resulting in peripheral edema (Schwinger, 2021). It is caused by left ventricular failure, pulmonary hypertension, or right ventricular myocardial infarction.

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Immune system

In left-and right-sided CHF, the activation of the immune system contributes to increased production and release of various pro-inflammatory cytokines. Alterations of adaptive immunity are crucial for CHF pathophysiology. Patients with chronic ischemic cardiomyopathy have been found to have a systemic expansion of CD4+ and CD8+ T cells, which are found in the failing heart, circulation, and lymphoid organs (Perticone et al., 2019). In addition, CHF patients with reduced or preserved ejection fraction (EF) have different immune-mediated mechanisms of inflammation. Perticone et al. (2019) found a significant elevation of pro-inflammatory cytokines and a parallel reduction of the protective cytokine IL-10 in CHF patients with reduced EF, which reflects an increased activation of toll-like receptors (TLRs).

Neurological System

Low cardiac output (CO) in left-and right-sided CHF causes decreased cerebral perfusion. Cognitive impairment is a very common comorbidity in patients with chronic CHF. Villringer & Laufs (2021) explain that more than 40% of CHF patients show signs of memory impairment, attention deficits, and concentration difficulties. Notably, cognitive impairment in CHF is associated with poor prognosis. The fundamental role of the bi-directional interactions between the heart and the brain is increasingly recognized. Chronically decreased cardiac output causes neurological and cognitive dysfunction. This is because it causes reduced cerebral blood flow and slow metabolism, which causes dementia (Villringer & Laufs, 2021). Furthermore, CHF patients with reduced EF have reduced volumes in the fronto-median brain regions, including the orbito-frontal cortex, cingulate cortex, and precuneus. This affects neurological functions like executive, visuospatial, and delayed recall.

Endocrine System

Dysfunction in the endocrine system is often observed in patients with CHF. Endocrine dysfunction is more prevalent in CHF patients with reduced EF. The reduced cardiac output in left-sided CHF activates carotid, aortic, and cardiac baroreceptors. This results in the activation of different neuroendocrine patterns, including plasma atrial natriuretic peptide, noradrenaline, arginine-vasopressin (AVP), brain natriuretic peptide, endothelin and adenosine release, and activation of the renin-angiotensin-aldosterone system (Lisco et al., 2022). These responses are initially significant to reinstate short-term cardiovascular homeostasis. However, the responses become maladaptive in the long term, resulting in myocardial remodeling and increasing an individual’s susceptibility to arrhythmias.

Hematological system

Anemia occurs in CHF patients and usually has a poor prognosis. Anemia in CHF is usually caused by bone marrow depression due to increased cytokine production, malnutrition, and associated renal disease. The reduced cardiac output in left-sided CHF causes a reduced red blood cell (RBC) volume and an increased plasma volume, which results in reduced hematocrit (Schwinger, 2021). Hemodilution often occurs in edematous, hypervolemic CHF patients. Cytokine activation and inflammation in CHF contribute to anemia because of poor utilization of iron. Furthermore, CHF leads to reduced production of erythropoietin hormone by the kidneys. This occurs when there is reduced cardiac output, causing reduced renal supply and renal hypoxia.

Cardiovascular system

The reduced cardiac output in left-sided CHF causes the heart’s walls to thicken to provide more muscle mass to pump enough blood to meet the body’s requirements. This is a compensatory mechanism that leads to more forceful contractions, which further increase cardiac output. However, the myocardium tends to hypertrophy more rapidly than how the circulation can provide adequate blood supply to the muscle (Liu et al., 2021). A hypertrophied heart is usually oxygen deprived to some extent. The compensatory mechanism results in an increase in the consumption of myocardial oxygen. However, when there is an increased demand for oxygen, and the myocardial reserve gets exhausted, clinical manifestations of heart failure occur.

Pulmonary system

When the heart cannot pump efficiently, blood backs up into the pulmonary vein. This results in pressure building up in the pulmonary vein, and fluid is pushed into the alveoli in the lungs. The fluid in the alveoli hinders normal oxygen movement through the lungs. Consequently, pulmonary edema develops, which is an abnormal buildup of fluid in the lungs and causes shortness of breath (Dobbe et al., 2019). Pulmonary edema that develops in acute decompensated heart failure is caused by dysregulation of pulmonary fluid homeostasis and the forces that maintain an equilibrium of fluid movement into the alveolar space (Dobbe et al., 2019). Furthermore, fluid in the alveoli disrupts surfactant function and increases surface tension, which often contributes to more edema formation and atelectasis with impaired gas exchange.

Renal/Urinary system

CHF is a significant risk factor for renal disease. Low cardiac output in left CHF results in decreased blood flow to the kidneys, and the kidneys experience a reduced supply of oxygenated blood. Also, when the heart cannot pump efficiently, it becomes congested with blood that, causes pressure build up in the inferior venacava, which is connected to the kidneys (Schwinger, 2021). This further leads to congestion of blood in the kidneys, and they start failing. Reduced renal supply results in the hormone system, which regulates blood pressure, going into overdrive to increase blood supply to the kidneys. Consequently, the heart is forced to pump against the higher pressure in the arteries and eventually fails from the high workload. Blood supply to the kidneys then reduces, resulting in progressive renal failure.

Digestive System

Patients with CHF present with common GI manifestations like anorexia, early satiety, and abdominal pain. Patients with advanced CHF often present with ascites, protein-losing enteropathy (PLE), and cachexia. These symptoms are associated with poor perfusion of abdominal organs and edema. Ascites is a pathologic condition characterized by fluid collection within the abdominal cavity (Trongtorsak et al., 2022). Right-sided CHF causes high pressure in the blood vessels of the liver and low levels of albumin. The venous return is obstructed in CHF, which causes an expansion of venous volume, higher hydrostatic pressure, and, eventually, fluid filtration into the peritoneal cavity. Cardiac cachexia is a catabolic state characterized by unintentional and non-edematous weight loss of more than 7.5% of premorbid body weight over six months (Trongtorsak et al., 2022). Cardiac cachexia is related to left ventricular systolic function, poor survival independently of functional capacity, or peak oxygen consumption

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References

Dobbe, L., Rahman, R., Elmassry, M., Paz, P., & Nugent, K. (2019). Cardiogenic pulmonary edema. The American Journal of the Medical Sciences, 358(6), 389-397. https://doi.org/10.1016/j.amjms.2019.09.011

Lisco, G., Giagulli, V. A., Iovino, M., Zupo, R., Guastamacchia, E., De Pergola, G., Iacoviello, M., & Triggiani, V. (2022). Endocrine system dysfunction and chronic heart failure: a clinical perspective. Endocrine, 75(2), 360–376. https://doi.org/10.1007/s12020-021-02912-w

Liu, Y., Chen, X., & Zhang, H. G. (2021). Cardiac Hypertrophy: From Compensation to Decompensation and Pharmacological Interventions. Frontiers in Pharmacology, 12, 665936. https://doi.org/10.3389/fphar.2021.665936

Perticone, M., Zito, R., Miceli, S., Pinto, A., Suraci, E., Greco, M., … & Perticone, F. (2019). Immunity, inflammation and heart failure: their role on cardiac function and iron status. Frontiers in Immunology, 10, 2315. https://doi.org/10.3389/fimmu.2019.02315

Schwinger, R. H. G. (2021). Pathophysiology of heart failure. Cardiovascular diagnosis and therapy, 11(1), 263–276. https://doi.org/10.21037/cdt-20-302

Trongtorsak, A., Kittipibul, V., Antala, D., Meng, Q., & Puwanant, S. (2022). Heart Failure-Related Ascites With Low Serum-Ascites Albumin Gradient: Diagnostic Clues From Triphasic Abdominal Computed Tomography. Cureus, 14(1), e21251. https://doi.org/10.7759/cureus.21251

Villringer, A., & Laufs, U. (2021). Heart failure, cognition, and brain damage. European Heart Journal, 42(16), 1579-1581. https://doi.org/10.1093/eurheartj/ehab061