Heart Failure as a Possible Complication of a Myocardial Infarction - Essay Example

1. Describe the short and long term effects that a myocardial infarction has on the structure and function of the heart. Myocardial infraction is theterm given to the interruption of blood supply and thereby oxygen supply to a part of the heart, which results in the breakdown of the heart muscles there. This interruption of blood supply and thereby shortage in oxygen supply is normally caused by the collection of vulnerable atherosclerotic plaque, which is a combination of lipids and White Blood Cells, on the walls of the arteries. This plaque only results in ischemia, and will lead to minimal or extensive infraction or death of the myocardial cells in the heart. When this myocardial infraction happens, the structure and the function of the heart undergo sizable changes. Following myocardial infarction, there will ischemic cascade during which the affected cells will die. Then, the leukocytes and the fibroblasts start to migrate into that necrotic region, and so the death tissue gradually remodels into a dense collagenous scar. (Ingels, Daughters and Baan 1996). In addition, the damages that happen in the myocytes and extracellular matrix formation after myocardial infarction, changes the size and the shape of the left ventricle and heart, thus impacting its structure. This process of changes is commonly known as “myocardial remodeling”. (Davis, Davies and Lip 2007). During that process of remodeling, the remaining functioning cells of the heart tries assume a different shape by enlarging itself and this is known as hypertrophy. By attaining this enlarged shape, those muscles will try to counter and manage the loss of synchronicity in the functioning of the muscles. These structural changes happen automatically, so the heart can compensate for the loss of key heart muscles. Thus, the function of the heart also gets reoriented after myocardial infraction, because its efficiency deteriorates due to the inability of the dead myocardial cells to aptly contract and thereby contribute to the heart beat and functioning. Even when the heart cells enlarge to compensate for the dead cells, it may not have the desired effect. That is, the enlarged cells may not be able to contract as forcefully and as effectively as the normal-sized and normal functioning cells. This restricted function will directly hinder the heart’s ability to generate expectant force during each beat or contraction, thus limiting heart’s functioning and its’ pumping of blood for all parts of the body. In addition, the function of the electrical system of the heart, which initiates the signals for a contraction, could also get disturbed because of the changes in the structure of the heart after myocardial infraction. The disturbance will be in the form of irregular heart rhythms, which is known as arrhythmias, which is a serious and restrictive problem, and has to be treated through medication or through permanent pacemaker implantation. The structural changes could also activate “systemic processes causing sequelae in many other organs and tissues, as well as further damage to the heart.” (Davis, Davies and Lip 2007, p.10). Thus, these changes in the structure and the function of the heart happens in the form of a vicious cycle, leading to further deterioration of the heart, causing other serious complications, which includes total heart failure. 2. Heart failure is a possible complication of a myocardial infarction. Describe the signs/symptoms and explain the physiological changes that are causing them. Heart failure can be categorized and arbitrarily divided into Left-sided failure and Right-sided failure, with each exhibiting certain symptoms. However, Left sided forward failure could overlap with the right sided backward failure, and also importantly the right-sided heart failure could be caused by the left-sided heart failure. Thus, as both are interrelated, the patients could present with both sets of symptoms. Person being affected with heart failure could exhibit mainly the symptoms of shortness of breath and swelling, sometimes accompanied by nausea, vomiting, palpitations, etc. Then as a further aggravation of the condition, individuals could also lose their consciousness and also die. The left-sided failure and the resultant problems in the left ventricle and left atrium will lead to congestions in the pulmonary vasculature, which could make the patient experience respiratory problems particularly shortness of breath or dyspnea, and this is the main symptom of this category of heart failure. The patient could have dyspnea during exertion and even at rest. This key symptom of dyspnea happens due to the physiological changes that happen in the left ventricle as well as in the lungs. That is, due to heart failure and resultant damage to the myocardium cells in the left ventricles, the output of the left ventricle gets limited. This leads to left ventricular failure, which directly leads to pulmonary edema and results in shortness of breath. The mechanisms invoked to explain the physiological changes that leads to pulmonary edema includes “direct airway luminal narrowing by interstitial fluid, vagally mediated reflexes and compression of the airways by adjacent congested arteries” (Faffe et al. 1999, p.751). There are also a portion of people, particularly elderly people, who might have “silent” heart failure, exhibiting the symptom of paroxysmal nocturnal dyspnea. Right-sided failure on the other hand causes congestion of systemic capillaries. In that case, there will be generation of excess fluid, which will accumulate particularly in the lower limbs, causing swelling under the skin known as oedema. The physiological changes that causes this symptom is that when the right ventricle fails, it may not be able to move the blood forward into the lungs. So, the blood will back up into the atrium, which cannot accept the incoming blood, resulting in the increase of venous pressure, which leads to congestion. (). That is, when venous pressure increases, it leads to fluid drainage and that will get settled in the lower extremities, particularly ankles due to gravity. However, when the affected person lay down during this process, the fluid could accumulate in the lower back area of the body or the sacral area. The other symptoms of nausea, vomiting, palpitations could be triggered by the massive influx of catecholamines throughout the body from the sympathetic nervous system. That is, the nervous system releases these catecholamines in response to the chest pain (which happens myocardial infraction causes heart failure) and other hemodynamic abnormalities that arise, when heart failure happens. Finally, the loss of consciousness happens because of insufficient cerebral perfusion and also due to the sudden cardiogenic shock. Sudden deaths could occur, when all the symptoms aggravate and cause the development of ventricular fibrillation. 3. Describe the effects of Urinary tract infection on the structure and function of the renal tract. The Urinary Track Infections (UTI) is one of the most common types of infection that affects both the male and female population. It occurs heavily in the anterior and in the interior regions of the reproductive organs, due to the entry of bacteria. Although, other microorganisms like virus, fungi, etc can also cause infections in the renal tract, the main casual agent is the bacterium Escherichia coli or E. coli for short. When the bacterium enters the renal tract, through the reproductive organs, it starts to change the structure and function of the organs in the renal tract or renal tract as a whole. “Pathogens usually enter the urinary tract by ascending from the mucous membranes of the perineal area into the lower urinary tract.” (Priscilla 2008, p.847). Lower urinary tract infection includes the bacteria infecting the bladder, Urethra and even the prostate gland. When the bladder gets infected, it can become inflamed as well as edematous, with the accumulated serous fluid getting evicted through urine, making urine cloudier. When inflammation becomes severe enough, it can induce macroscopic hematuria, which is the presence of Red blood cells in the urine. Likewise when Urethra and prostate gland gets infected, they will also become inflamed leading to appropriate conditions. Lower urinary tract infections could include Urethritis, which is the inflammation of the urethra; then prostatitis, which is the inflammation of the prostate gland and finally cystitis, which is the name given to the inflammation of the urinary bladder. (Priscilla 2008). When these structural changes and further complications occurs, these organs particularly bladder will reorient their functions to flush out the bacteria and importantly to prevent it from ascending into the upper urinary tract organ particularly Kidney. For example, the pathogens that enter and contaminate the urethra could be washed out during the voiding process. The reorientation of functions again happens, with the ureters and its vesicoureteral junction prevents to entry of the pathogen into the kidney. “As the ureter enters the bladder, its distal portion tunnels between the mucosa and muscle layers of the bladder wall,” and so the increased intravesiailar pressure inside the bladder will compresses the ureter, thereby preventing “the backflow of urine toward the kidneys” (Priscilla 2008, p.847). Although, the organs in the lower renal tract will reorient its functions to prevent the spread of infections into the kidney, certain times, it will happen. When it ascends to the kidney, it could infect the functional tissues or parenchyma of both or one of the two kidneys. This UTI of kidney or kidneys are called pyelonephritis and it is the inflammation of the kidney and renal pelvis. Thus, because of pyelonephritis also, the structure of the kidney changes, with inflammation being the key change. “The infection may involve superficial tissues such as the bladder mucosa, or may invade other tissues such as prostate or renal tissues.” (Priscilla 2008, p.847). In that case also, Kidney will accentuate its functions to suppress or eliminate this inflection, with the aid of antibiotics and others supplements. The problem with these structural changes is, it could lead to future complications. 4. Haematuria and Dysuria are possible signs and symptoms of Urinary tract infection. Describe these signs/symptoms and explain the physiological changes that occur in each one. The term hematuria, or haematuria is used when red blood cells is present in the urine. Haematuria is not considered as a medical condition, but as a symptom of some other deeper problems. Thus, Haematuria when viewed independently does not have or exhibit clear cut symptoms. “Haematuria does not always cause symptoms. It may be a sign of an underlying condition, which may cause symptoms.” (Farrell 2010). That is, Haematuria will result when there are some complications in the renal tract, as it could be a sign that are stone or tumor in any of the organs in the renal tract particularly kidneys, ureters, bladder, prostate as well as urethra. However, one of the commonest causes for Haematuria is UTI, and when WBC is found alongwith RBC, it can be confirmed that a Haematuria is caused by UTI. The physiological changes that happen as part of Haematuria could mainly occur in the renal tract. That is, the “RBCs can be added to the urine at any point along the urinary tract, from the glomerulus through the tubule or through the collecting system, the ureter, the bladder, or the urethra.” (Fleisher and Ludwig 2010, p.310). In that direction, haematuria can categorized as either glomerular or nonglomerular in origin. When the inflammation happens in kidney due to pyelonephritis caused by UTI, there could damage to the glomerular filtration surface. This damage to the glomerular could leak RBCs along with protein. When the non-glomerular area is focused, Haematuria mainly happens if the renal papillae, tubules and interstitium start bleeding due to extreme UTI. Thus, when haematuria happens, there will be physiological changes on the glomerular as well as other areas in the urinary tract, which will lead to blood in the urine. The term dysuria is used to refer to painful and difficult urination, which could be caused by any complications in the renal tract. Like haematuria, dysuria is also not a stand-alone medical condition; instead it is a symptom of other underlying medical problems. Although, sizable diseases or complications in the renal tract and other parts will have dysuria as the symptom, it is most commonly viewed as the key symptom of UTI. In particular, if there is an inflammation in the bladder, urethra and also kidney due to UTI, it will exhibit in the form of dysuria. That is, if the above parts in the renal tract undergo physiological changes gets inflamed due to Urethritis, prostatitis, pyelonephritis and importantly cystitis, dysuria will be the result. “Though it has a broad differential diagnosis, dysuria most often results from inflammation or infection of the bladder and/or the urethra.” (Fine and Saint, p.349). The other physiological change that creates the pain or burning sensation during urination is the stimulation of nerve endings in the bladder and urethra. When the nerve endings are stimulated due to the information inside the bladder or urethra, it will lead to the pain. Importantly, the onset of pain also provides clues about the cause of dysuria. For example, the pain that arises just before the voiding normally indicates bladder irritation or distention, while the pain at the start of urination or voiding indicates about bladder outlet irritation. (Kowalak and Hughes 2002). Thus, the physiological changes of inflammation only leads to dysuria, and at the same time, dysuria leads to further physiological changes including edematous and hyperemic state, in which there will more accumulation of serous fluids and blood fluids (even leading haematuria). References Davis, RC, Davies, MK and Lip, GYH 2007, ABC of Heart Failure, John Wiley & Sons, London. Faffe, DS, Faffe, DS, Chagas, PSC., Medeiros, AS., Saad, EA., Saldiva, PHN., Rocco, PRM and Zin, WA 1999, Pulmonary morphofunctional effects of acute myocardial infarction, European Respiratory Journal, vol. 14, pp. 751-758. Farrell, E 2010, What is haematuria? 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