Stroke Volume of the Heart - Essay Example

Unit Title Assignment Title Student’s Name Student number Name of lecturer Table of Contents Table of Contents 2 Stroke volume of the heart 3 Introduction 3 Frank-Starling and Laplace laws 3 How the laws relates to the underlying pathology of heart failure 5 Conclusion 6 The mode of transmission and signs and symptoms diseases 6 Introduction 6 a)Measles 6 b)Mumps 7 c)Pertussis 7 d)Chicken Pox 8 Conclusion 8 References 10 Stroke volume of the heart Introduction Cardiac out is the volume of blood that the heart pumps in one minute, and it dependents on the heart contractility, preload, heart rate and afterload. It is equal to product of the heart rate and the stroke volume. Frank-Starling and Laplace laws Frank-Starling law of the heart describes the mechanism between the volume of blood in the ventricles at the end of diastole and the stroke volume that results. As the ventricle in diastole stretch, the resulting volume increases. The heart controls its own stroke volume by responding to a contractile force. The heart controls the pressure at the ventricles and the output varies with preload. Thus, a decrease in preload results in a decrease in end-diastole volume, stroke volume and peak pressure (Gradwell & Rainford, 2016). The stroke volume is controlled by the preload (end-diastolic volume), the cardiac contractility and afterload (arterial blood pressure). According to Frank-starling law, the contraction energy depends on the preliminary length of cardiac muscle fiber. Both the heart rate and the venous return affect the end-diastolic volume at the ventricle and the length of cardiac muscle fibers at the beginning of the ventricular systole. An increase in the venous return results in an increase in the end-diastolic volume, but as the heart rate increase the time required for diastolic filling is reduced. Frank-Starling mechanism assist the heart is responding to changes due to preload and matches the left and right outputs of the heart (Gradwell and Rainford, 2016). Overstretching or understretching of myofibrils produce less than optimal contraction (Dennison & Farrell, 2016). In afterload, the ventricle must have enough pressure needed to open the semilunar valve. Afterload affects the load volume such that as the stroke volume decreases with increase in the afterload as shown in figure 1 below. Figure 1: The relationship between the stroke volume and afterload (Dennison & Farrell, 2016) Low systolic pressure results in the heart contracting to a smaller volume at the end of the systole, resulting in improved stroke (Dennison & Farrell, 2016). Contractility is the velocity and the force of blood ejection from the ventricle and is independent of preload and afterload. According to Laplace’s law, contractility affects the cardiac output and stroke volume as shown in the figure below. Figure 2: Relationship between stroke volume and contractility (Dennison & Farrell, 2016). Laplace’s law states that the contractile force generated in the chamber is dependent on the thickness of the wall and the radius of the chamber; thus the thicker the walls and the smaller that radius, the greater the contraction force. Myocardial oxygen consumption also increases with increase in contractility (Dennison & Farrell, 2016). How the laws relates to the underlying pathology of heart failure When the ventricle is normal, the cardiac output increases when the filling pressure increase. In case of systolic dysfunction, the cardiac out can be maintained through compensation mechanisms. If the left ventricle fail and there is a drop in the cardiac output, the protective mechanism cease to function. Left ventricular hypertrophy (LVH) develops which at first unload the muscle fibers and thus reduce the stress on the wall as defined by Laplace law. With time, LVH may damage the ventricular relaxation and filling, which facilitate myocardial ischemia. Frank-starling curve plots wedge pressure or left ventricular end-diastolic pressure against the cardiac output or the stroke volume as shown in the figure 4 below. When the heart is functioning normally, an increase in LV leads to an increase in the cardiac output or contractility. The relationship is poor in LV systolic dysfunction, as there is a smaller increase in cardiac output for an increase in volume (Garibaldi, 2010). Figure 3: Frank-starling pressure – volume relationship in normal, mild and severe depressed function of LV (Garibaldi, 2010) Finally, the ventricle dilates, which further increase the stress on the wall and reduces the shortening of myocardial fiber at the expense of reduction of the stroke volume (Garibaldi, 2010). Conclusion The interpretation of the cardiac output may not be simple when looked at a glance. The relationship between the cardiac output and other components may be complex, but it is important in the understanding of the physiological processes that is important in illness and in understanding effects that various interventions can have on the cardiac output. The mode of transmission and signs and symptoms diseases Introduction Infection in the body is caused by diseases causing organisms such as viruses and bacteria. Infectious diseases are communicable and can be transferred from one person to the other. It is critical to understand the signs and symptoms of diseases and their mode of transmission in order to control them. Diseases that include measles, chickenpox, pertussis and mumps are discussed below. a) Measles This is an extremely contagious viral disease. It is caused by morbilli-virus. It has an acute onset with conjunctivitis, prodrimal fever, cough, coryza, and Koplik’s spots on the mucosa of the throat and mouth. Red macular blotchy rash appeasr on the face between 3 to 7 days, and it spread to other parts of the body, lasting for more 4 to 7 days. The erythema change to brown colour and begins to peel off. It is more severe in adults and babies than in old children. Infections can be mild to moderate. Complications include diarrhoea, ear infections, encephalitis and pneumonia. When it is not treated, the disease may cause blood clotting abnormalities, blindness, infertility and dehydration. It can be fatal in children with vitamin A deficiency and malnourished children (Nelson & Williams, 2014). The disease can be transmitted through direct contact with throat and nasal secretions or droplet spread of an infected person or by contact with contaminated fomites. The incubation period is between 7 to 18 days, but usually takes 14 days for rash to appear (Nelson & Williams, 2014). b) Mumps This is a disease caused by virus and usually occurs during spring and winter. Mumps in children can be identified from fever plus tenderness and swelling of salivary glands, normally parotid. The signs and symptoms in males include painful complication; may have inflammation of testicles, but will not result in sterility (Caroline, 2010). The mode of transmission includes direct contact or droplet spread of saliva of an infected person. The period for incubation is between 12 and 26 days. The communicable period takes 9 days after the swelling of salivary glands (Caroline, 2010). c) Pertussis It is caused by borditella pertussis bacteria. It is an acute infection of respiratory system that involves trachea-bronchial tree. There is insidious onset at catarrhal stage with slight fever, irritating cough and malaise that eventually becomes paroxysmal within 1 to 2 weeks (University of Maryland, 2008). At this stage the intensity of the cough increases and ends with a characteristic inspiratory whoop. The new stage can last for 2 to 3 months, specifically when pneumonia develops. The mucous secretions are usually clear and tenacious, and there is vomiting after coughing (Nelson & Williams, 2014). The methods of transmission include direct contact with droplet spread and secretions. It can easily be spread in the intimate confines of the home. The incubation period is between 6 to 20 days, and is extremely contagious at early catarrhal stage, until 3 weeks after the onset paroxysmal stage (University of Maryland, 2008; Nelson & Williams, 2014). d) Chicken Pox It is a highly contagious viral disease which usually affects children. At early stages, there is slight fever and skin rushes and skin eruption that is maculopapular for some hours and vesicular for 3 to 4 days, which finally crusts over leaving granular scabs like as shown in figure 4 below. Figure 4: Rash produced by chicken box (Caroline, 2010). The rashes come in crops, starting from covered areas to uncovered areas of the body. In adults, the virus can cause herpes roster, when the chicken box virus reside in the ganglion of the nerve. If the person becomes stressed later, lesions can appear in the affected area of the nerve. The disease is very painful (Caroline, 2010). Varicella virus is transmitted through direct contact of the respiratory secretions, vesicle fluid or droplets of an individual affected by chickenpox. The virus can also be transmitted by contact with articles contaminated by the fluid. Chickenpox has an incubation period of between 10 and 21 days. Chickenpox can be communicated 1 to 2 days before the rash appear and continue for 5 days after the first vesicles become clear. An individual how may have had chickenpox may develop shingles later (Caroline, 2010). Conclusion Disease infections have minor to major complications. Signs and symptoms of chickenpox, measles, pertusis and mumps have been discussed. Some disease infection may become silent, but they may appear again after a long time. For example, an individual how may have had chickenpox may develop shingles later. References Caroline, N. L. (2010). Nancy caroline's emergency care in the streets. Place of publication not identified: Jones & Bartlett Learning. Dennison, R., & Farrell, K. (2016). Pass PCCN!, St. Louis, Missouri: Elsevier. Gradwell D. and Rainford D. J., (2016). Ernsting's Aviation and Space Medicine 5E, CRC Press Garibaldi, B. T. (2010). Patient encounters. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. Nelson, K. E., & Williams, C. M. (2014). Infectious disease epidemiology: Theory and practice. Burlington, Mass: Jones & Bartlett Learning. University of Maryland, (2008). The Effect of Pertussis Toxin on the Innate Immune Response to Bordetella Pertussis Infection in Mice, University of Maryland, Baltimore, ProQuest Read More