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Ventilation Perfusion Ratio - Essay Example

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The writer of the paper “Ventilation Perfusion Ratio” states that obese individuals would be predisposed to venous thrombosis, pulmonary emboli, pressure sores, oedema so these patients would require careful consideration prior to surgery in order to make a plan…
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Extract of sample "Ventilation Perfusion Ratio"

Running Head: VENTILATION PERFUSION RATIO Ventilation Perfusion Ratio [The Writer’s Name] [The Name of the Institution] Ventilation Perfusion Ratio As far as the definition of Ventilation Perfusion ratio is concerned, it may be termed as “the ratio of alveolar ventilation to simultaneous alveolar capillary blood flow in any part of the lung.” (Biology Online) Exercise constraint is widespread in patients having chronic pulmonary venous hypertension. One hypothesized method is ventilation-perfusion variation derivative to edema formation and vascular congestion. Hypoxemia has not been found in many patients at any phase and negligible shunt or low VA/Q lung units have been observed by the inert gas method. As an alternative, regions with high VA/Q ratio have been revealed towards the end of exercise and instantaneously after exercise. This proved to be the result of a marked relocation of pulmonary blood flow, may be owing to an addition of interstitial edema fluid. The extreme ventilatory consequence to exercise assessed in patients with mitral stenosis might, within part, be illustrated by an uneven division of ventilation and perfusion. Variation in ventilation-perfusion ratio can be measured and observed. Alveolar-arterial O2 grade projected from this ventilation-perfusion ratio dissimilarity has been measured to be almost 4 mm Hg. This proposes that the variation and scalar difference in blood flow between lower and upper parts of the lung in erect person accounts for the entire of the ventilation-perfusion ratio disparity in the ordinary lung. The ventilation and perfusion (V/Q) scan consists of two sequential tests. The perfusion scan shows the distribution of microvascular blood flow in the lungs after IV injection of a radionuclide, and the ventilation scan shows distribution of ventilation in the small airways after inhalation of a radioactive gas or aerosol (Hyers, 2000). V/Q scanning does not require IV contrast and therefore is the imaging modality of choice for patients with major renal impairment, anaphylaxis to IV contrast, and pregnancy (Piazza & Goldhaber, 2006). V/Q scanning is an indirect study of embolism because it shows perfusion abnormality. Defects in tracer uptake when inhaled into the lungs are reported as normal, near normal, or indicating low, moderate, or high probability for PE (Ramzi & Leeper, 2004). Although V/Q scanning is sensitive enough to serve as a screening test, specificity is limited. A low or indeterminate study does not rule out a diagnosis of PE, and further evaluation should be undertaken (Ramzi & Leeper, 2004; Riedel, 2004). A V/Q scan often is not diagnostic in patients with chronic pulmonary disease or pleural effusion (Ebell, 2004). "Congestive heart failure is a pathophysiologic condition in which the heart is unable to generate an adequate cardiac output such that there is inadequate perfusion of tissues, and/or increased diastolic filling pressure of the left ventricle, such that pulmonary capillary pressures are increased" (Denton, 1998). Congestive heart failure is actually a complication of other cardiovascular conditions rather than a disease in itself. It is associated with numerous types of heart disease, particularly with coronary artery disease and long-standing hypertension (Gottschalk, 2003). Any factor that puts a continuous strain on the heart by increasing its work, decreasing its ability to contract and hindering or altering the flow of blood within its chambers can cause congestive heart failure (Scott, 1998). Hypertension is a major contributing factor, increasing the risk of congestive heart failure three times (Scott, 1998). The most common risk factor for the development of congestive heart failure is age (Scott, 1998). Structural changes during aging mainly include some left ventricular wall and septal hypertrophy due to left atrial and ventricle widening, and fibrosis of the cardiac muscle. These structural changes reduce the contracticle ability of the myocardium, the resistance that the ventricles pump against increases, the amount of elasticicity of the myocardium decreases, and the heart rate decreases (Carter, 2002). This results in decreased cardiac output, which in turn means that less cardiac reserve is available in older adults. During exercise the heart is unable to increase the amount of blood that is pumped around. Therefore, oxygen demands are not as well met in an older person when compared with a younger person (Gottschalk, 2003) The work of breathing is determined by the amount of effort required by the lung muscles to move air through the conducting airways and the ease with which the lungs can be inflated (Stein, 1999). During inspiration, the diaphragm and intercostals muscles contract. At expiration, the elastic recoil of the chest wall and lungs allows the chest to return to its normal position (Marieb, 2000). In the elderly, there is an increased work of breathing due to age-related changes to the respiratory system such as kyphosis, decreased muscle strength, decreased elastic recoil, fewer and larger alveoli and stiffer chest wall due to atrophy. These factors lead to an increase in the residual volume, which means decreases in maximum breathing capacity and vital capacity. The results in elderly people are: difficulty in breathing and less effective gas exchange (Denton, 1998). Fatigue is caused by decreased cardiac output, impaired circulation, and decreased oxygenation of the tissues. In congestive heart failure decreased cardiac output produces the sign of diminished organ perfusion, because blood is shunted from non vital organs to maintain perfusion of the heart and brain. The perfusion in the skeletal muscles lead to hypoxic tissue and slowed removal of metabolic waste, which in turn cause the client to tire easily (Ramzi & Leeper, 2004). In addition, muscle ergoreceptor activity is increased in congestive heart failure which results in an increase in sympathetic nervous activity and subsequently high minute ventilation for a given level of exertion. This causes the patient feel tired and exhausted even when they have not exerted themselves very much physically (Resnick, 2004). Fatigue can be made much worse in elderly people by fluid and electrolyte imbalance or anorexia (Hyers, 2000). Peripheral edema is caused by fluid accumulation in the interstitial spaces of the tissues (Hyers, 2000). Left congestive heart failure can result in increase in left ventricular filling pressure that is reflected back into the pulmonary circulation. As pressure in the pulmonary circulation rises, a resistance to right ventricular emptying increases and finally lead to right congestive heart failure. When this happens pressure will rise in the systemic venous circulation and capillaries (Mccance & Huether, 2004). A number of additional factors also may contribute to the development of edema in congestive heart failure. Increased hydrostatic pressure and decreased plasma oncotic pressure contribute to the transudation of fluid out of the capillary bed. Abnormalities of lymphatic drainage related to an elevated central venous pressure and resulting inhibition of thoracic duct drainage also may contribute to the development of peripheral edema (Woods, Frolicher & Motzer, 2000). In right congestive heart failure pressure in the right atrium leads to increased pressure in the capillaries and results in fluid escaping from the capillaries to the interstitial spaces in tissues throughout the body. The most obvious places to observe the fluid accumulation are in the feet and ankles (Stein, 1999). Fluid overload of the congestive heart failure patient is complicated by an age related decrease in kidney function, A fall in creatinine clearance relates with a decrease in the glomerular filtration rate of approximately 50% as one ages from 30 to 90 years. The decrease of glomerular filtration rate affects the ability of the elderly to remove body fluid (Ebell, 2004). According to nursing assessments and client signs and symptoms in relation to his illness, his health condition and his age, the nursing interventions will focus on the following: Proper positioning is crucial. In the upright position, dyspnea is relieved because by gravity abdominal organs fall away from the diaphragm, fluid within the lung seeks the bases (inferior portions) of the lungs, and venous return of blood to the right atrium is decreased. The result is an increased thoracic capacity of the lungs for gas exchange and the dyspnea is relieved (Stein, 1999). Proper positioning aids in lung expansion, allowing air to reach the alveoli, and improve ventiliation and minimize respiratory effort (Stern, 2003). The fatigue that a patient experienced was likely caused by an inadequate oxygen supply to the body's tissues. To decrease the needs of the body for oxygen, both physical and emotional rest should be provided (Carter, 2002). The Nurse should assess to determine the patient’s tolerance level. A patient should be instructed to participate in limited activities with adequate recovery periods in between (Ramzi & Leeper, 2004). Respiratory disorders like asthma confirm that the patient should have to be positioned in an upright position to make certain adequate bilateral ventilation of the lungs. Weight tells us many things if the patient is underweight or overweight we would be concerned about pressure sores and difficult intubations. Malnutrition may be the reason for underweight and then it must be queried whether the patient is fit for surgery as they would have impaired wound healing. Obese individuals would be predisposed to venous thrombosis, pulmonary emboli, pressure sores, oedema so these patients would require careful consideration prior to surgery in order to make a plan. Often one forgets that drugs can have a bearing on the intraoperative experience. Reference Biology Online; Medical Dictionary: Accessed on March 18, 2008 from http://www.biology-online.org/dictionary/Ventilation-perfusion_ratios Carter WD, Brady TM, Keyes JW, Thrall JH, Greenhouse JB, Biello DR et al. Relative accuracy of two diagnostic schemes for detection of pulmonary embolism by ventilation-perfusion scintigraphy. Radiology 2002; 145: 447–51 Denton ER, Barrington SF, Kettle AG, Morrison ID, O’Doherty MJ. The value of the chest radiograph in reporting aerosol ventilation-perfusion scans. Nucl Med Commun 1998; 19: 71–6 Gottschalk A, Sostman HD, Coleman ER, Juni JE, Thrall J, McKisick KA et al. Ventilation-perfusion scintigraphy in the PIOPED study: evaluation of the scintigraphic criteria and interpretation. J Nucl Med 2003; 34: 1119–26 Marieb, E. (2003). Essentials of Human Anatomy and Physiology (7th ed.). San Francisco: Benjamin Cummings. McCance, K., & Huether, S. (2004). Pathophysiology: the biologic basis for disease in adults and children (4th ed.). St Louis: Mosby. Resnick, B. (2004). Encouraging exercise in older adults with congestive heart failure. Geriatric nursing, 25 (4), 204-211 Scott HR, Gillen GJ, Shand J, Bryden F, Milroy R. A structured approach to the interpretation and reporting of ventilation/perfusion scans. Nucl Med Commun 1998; 19: 107–12 Stein PD, Henry JW, Gottschalk A. Mismatched vascular defects. An easy alternative to mismatched segmental equivalent defects for the interpretation of ventilation/ perfusion lung scans in pulmonary embolism. Chest 1999; 104: 1468–72 Stern, S., Behar, S., & Gottlieb, S. (2003). Aging and Diseases of the Heart. Circulation,  14, 108-110. Woods, S. L., Sivarajan Froelicher, E. S., & Underhill Motzer, S. U. (2000). Cardiac nursing (4th ed.). Philadelphia : Lippincott Company. Ebell, M.H. (2004). Suspected pulmonary embolism: Evidence-based diagnostic testing. American Family Physician, 69, 599–601. Piazza, G., & Goldhaber, S.Z. (2006). Acute pulmonary embolism. Part 1: Epidemiology and diagnosis. Circulation, 114, 28–32. Hyers, T.M. (2000). Pulmonary thromboembolism. In H.D. Humes (Ed.), Kelley’s textbook of internal medicine (4th ed., pp. 2531–2536). Philadelphia. Ramzi, D.W., & Leeper, K.V. (2004). DVT and pulmonary embolism: Part 1. Diagnosis. American Family Physician, 69, 2829–2836. Riedel, M. (2004). Diagnosing pulmonary embolism. Postgraduate Medical Journal, 80, 309–319. Read More
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