Running head: HEART FAILURE AND INFLAMMATION

Heart Failure Pathophysiology and Inflammation Lee Toledo Guilford Technical Community College

HEART FAILURE AND INFLAMMATION Heart failure is a condition characterized by the ineffective filling and pumping of blood of the lower chambers of the heartthe right and left ventricles; this leads to insufficiency supply of nutrients and oxygen to fulfill the body cells metabolic requirements. Heart failure is the outcome of other underlying diseases or disorders such as cardiomyopathies, rheumatic fever, hypertension, anemia, infection, and infarction of the myocardium. Contingent on these condi-

tions, heart failure can be classified into the following: left or right sided failure, systolic or diastolic failure, low or high output failure, and chronic or acute failure (North Carolina ConceptBased Learning Editorial Board [NCCBLEB], 2011, p.1404-1407). This paper will focus in systolic heart failure. Cardiac output influences the operation of the heart as a pump. Cardiac output is the amount of blood forced out from the ventricles per minute; it is controlled depending in oxygen demand by the body where if its consumption is elevated due to exercise as an example, it will lead to increased cardiac outputthis is also referred as cardiac reserve. Cardiac output is the result of stroke volume (amount of blood pumped out in each heartbeat) and heart rate. Stroke volume is influenced by the factors of preload, afterload, and myocardial contractility; heart failure begins when there are abnormalities within these which affect cardiac output. Although compensatory mechanisms exists to regulate cardiac output (Frank-Starling mechanism, sympathetic nervous system stimulation, renin angiotensin system, and myocardial hypertrophy), these eventually lead to further heart failure (NCCBLEB, 2011, p.1405). In systolic heart failure, impaired blood movement out of the ventricles generates mainly due to decreased myocardial contractility caused by cardiomyopathies, myocardium ischemia or infarction, or hypertension (Grossman & Porth, 2014, p.870). For instance, in hypertension, where the resistance in the peripheral vascular system has been increased due to elevated blood

HEART FAILURE AND INFLAMMATION viscosity and volume (sodium and water retention) or decreased vessel diameter (fatty deposits or plaque in vessels) (NCCBLEB, 2011, p1422-1423), elevates the afterloadthe strength required to open the semilunar valves and move blood into the main arteries. This leads to high

myocardial workload and incomplete emptying. In order to overcome it, the cardiac muscle cells enlarge by augmenting their contracting proteins actin and myosin in a process called hypertrophy and the ventricles dilate to accept the surplus of fluid from the elevated blood volume. Although this helps to contract more efficiently, it will eventually result in ventricular wall degeneration and impaired contractility if the hypertension is not corrected. Moreover, the elevated blood volume increases preloadthe filling of the ventricles with venous return during relaxationwhich is the compensatory mechanism of Frank-Starling taking place; however, if overstretching of the muscle occurs, it will result in further impaired contraction. All these will eventually lead to insufficient supply to the myocardium leading to ischemia or infarction (NCCBLEB, 2011, p.1405-1406). The manifestations of systolic heart failure will be consistent with left sided heart failure being pulmonary congestion or edema interfering with gas exchange, shortness of breath, crackles, productive cough, pale skin, cyanosis, fatigue, anemia, and irregular heartbeat (Grossman & Porth, 2014, p.877). The client I look up in EPIC during clinic was admitted to the hospital due to shortness of breath. She was diagnosed with systolic heart failure. She had a history of essential or primary hypertension. Some of her symptoms according to her records were crackles, productive cough, anemia, and fatigue. The anemia may be the result of the accumulation of blood in the lungs where red blood cells have moved into the alveoli as well as malnutrition due to lack of appetite caused by the fatigue and depression (Grossman & Porth, 2014, p.877); her laboratories showed low red blood cells and hemoglobin. Some of her diagnostics, especially a chest CT scan showed enlarged heart, diffused vascular congestion, and bi-

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basilar atelectasis or collapsed lungs bases. Additionally, she had an acute myocardial infarction that led to a complete atrioventricular block.

HEART FAILURE AND INFLAMMATION Inflammation It is a body reaction to tissue injury with the objective to remove the agents causing the

injury and to repair the injured tissue. It is the first stage to tissue healing and is characterized by the movement of fluid, blood cells and other agents to the site of injury in order to destroy and remove the injurious factor along with the damaged tissue and fluid (exudate) through the process of phagocytosisa process called debridement. Inflammation is characterized by pain, swelling, redness, and heat. It can be classified into acute or chronic inflammation. Acute inflammation refers when there has been an injury that eventually will resolve whereas chronic inflammation refers to an acute injury that has continued for extended period of time evolving to chronic or a chronic autoimmune disease like lupus where inflammation may endure for several years with symptoms evolving to worse (NCCBLEB, 2011, p.886). Inflammation occurs in three stages being these vascular and cellular responses, production of exudate, and reparation. During the vascular and cellular response, chemical agents such as prostaglandins, histamines, and kinins are released by the damaged cells. These agents produce vasodilation which results in increased blood delivery to the injury site; this is called hyperemia and is the sign of redness and heat in the area. Increased vasodilation leads to increased vascular selective permeability that allows leukocytes, fluid, and proteins to leak into the area. Specifically, the process of margination and emigration occurs with leukocytes where they accumulate in the vessel lining and move through the vessel respectively into the damaged tissue (NCCBLEB, 2011, p.886). The endothelial cells lining the blood vessels are in charge of that selective permeability and additionally contribute in the release of agents that induce the inflammation response and growth factors that induce tissue repair. By the same token, they release antiplatelet, antithrombotic, vasodilators and vasoconstrictors in order to control vessel pa-

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tency and blood flow to the area (Grossman & Porth, 2014, p.310).The leaking of leukocytes and fluid develops the signs of swelling or edema and pain caused by the irritation of nerve endings. The migration of leukocytes from the vascular system stimulates the production of more leukocytes in the bone marrow. The exudate results in the escaped fluid from the vascular system, dead tissue, and dead phagocytic cells. The reparative or regeneration stage is characterized by the repair of damaged tissue or substitution of it with fibrous tissue (NCCBLEB, 2011, p.886).

HEART FAILURE AND INFLAMMATION References Grossman, S., & Porth, C. (2014). Porth\. (9th ed.). Philadelphia, PA: Wolters Kluwer Health|Lippincott Williams & Wilkins. North Carolina Concept Based Learning Editorial Board [NCCBLEB]. (2011). Nursing: A concept-based approach to learning. Upper Saddle River, NJ: Pearson Education, Inc.