Symptoms of Pulmonary Embolus, Severe Acute Anaphylaxis Treatment, Pre-hospital, and Emergency Treatment, Negative Pressure Pulmonary Oedema - Assignment Example

Medical Essay Name Institutional Affiliation Question 1 Pulmonary embolus (PE) Introduction Pulmonary Embolus refers to an abrupt blockage in an artery in the lung that occurs due to a clot in the blood which travels from the leg to the lung. It practically means an occurrence of a blood clot in one body part, which travels to other parts in the bloodstream (Lang, 2009). Pulmonary Embolus is a condition that could result into a permanent damage to a part of a patient’s lung, primarily due to lack of enough blood flowing to its tissues. Other parts of the body could also undergo the same and could be irreparably damaged. The disease can also ostensibly result into death in particular circumstances where the clots are large and/or numerous. It is in most times caused by the thrombi which come from the lower extremities of the deep venous system. After moving and reaching the lung, the thrombi can form at the main pulmonary artery bifurcation and result into hemodynamic compromise (Bee, Büller, Oudkerk & Wiley, 2009). This disease mainly arises from the calf veins of the body. The venous thrombi however come from the venous valve pockets and other sites of presumed venous stasis. To get to the lungs, thromboemboli usually travels through the heart at its right side (Bee, Büller, Oudkerk & Wiley, 2009). The signs and symptoms of Pulmonary Embolus The disease often presents itself through a sudden feeling of chest pains, breathing problems, and hypoxia. In most patients however, it does not have particularly obvious symptoms at presentation. The symptoms in these particular circumstances could be experienced by sudden catastrophic hemodynamic collapse which could also progress to dyspnea. Individuals with respiratory symptoms that cannot be traced through other diagnosis should particularly be highly suspected of pulmonary embolism. From the forgoing, these symptoms and signs of the disease are usually not very specific and in some severe cases, the disease could cause sudden deaths. Some are usually fatal and in most of these cases, the disease is not clinically diagnosed prior to death (George, 2005). Other symptoms of the disease could also include: coughing and haemoptysis, right heart failures causing dizziness or syncope in severe cases and any other symptoms suggesting a deep vein thrombosis (DVT) Some of the recognizable signs of the disease could include having an elevated jugular venous pressure, pyrexia, pleural rub, a gallop heart rhythm, a systemic hypotension or cardiogenic shock and hypoxia which often causes anxiety, restlessness, agitation and/or impaired consciousness The diagnosis of Pulmonary Embolism The doctors in their evaluation of the existence of the disease would have to first study the health history of a patient before performing the necessary physical examinations. This would help in the determination of the likelihood of the disease occurrence while eliminating other alternative possible causes of the symptoms. The various risk factors should also be analyzed in this process (George, 2005). Some of the physical examinations carried out by the doctors include; checking of one’s blood pressure including the rate at which their heart beats, listening to the patient’s lungs and hearts and checking of their legs for the signs and symptoms of the disease. The initial tests usually carried out in this determination often include: EKG or ECG (electrocardiogram); this is always done to check the heart conditions of the patient. measure Chest x-ray involving taking of various picture of some of the crucial body parts of the patient. Ventilation-perfusion lung scan (VQ scan); used to monitor the air and blood flows in all the areas of the lung. Question 2 Severe acute anaphylaxis treatment Introduction This is a life-threatening condition of systemic allergic reaction that most commonly involve the cutaneous or mucosal, cardiovascular, respiratory, and gastrointestinal systems which occur after contact with an allergy-causing substance. It is a medical emergency that requires immediate recognition and intervention. It needs rapid assessment, diagnosis, and treatment. In most instances, basic equipment and medication should be readily available in a physician’s office (Field, 2009). Pre-hospital (ambulance) and the emergency treatment Pre-hospital patients having the initial symptoms of severe anaphylaxis should get standard interventions including high oxygen flow, cardiac monitoring, and intravenous (IV) access. These measures are very appropriate for patients with a history of serious reactions and those that have been re-exposed to the inciting agent. Such measures are however not very necessary for patients with local reactions (Field, 2009). The disposition of patients having this disease depends on how severe the initial reaction of the patient and his/her response to treatment. Those with less threatening symptoms can undergo observed for a few hours after treatment and then discharged. Those however experiencing very severe anaphylaxis should be admitted or undergo treatment and observation for longer periods in the emergency department (ED) (Stoelting, Hines & Marschall, 2012) Adrenaline is also used as a treatment for anaphylaxis. People who have had an anaphylactic reaction in the past are required to carry an auto-injection device, called an adrenalin pen, containing adrenaline with them. The pen is composed of a pre-filled syringe fitted with a needle to enable the adrenalin to be injected straightway in emergency situations. In the events thus of a severe reaction occurring again, one can carry out the adrenaline injection by himself or by a family member or a present health worker. This reaction can start very suddenly. Its early symptoms usually include breathing difficulties, itchy skin rashes, and swelling of the mouth and throat. If it is not treated straightaway, the reaction can lead to a large fall in blood pressure and unconsciousness. An adrenalin injection helps to relieve these symptoms often by causing blood vessels to narrow, and opening up airways. This is able to stop the blood pressure from dropping and making breathing easier providing sufficient time to allow for emergency services to be sought (Stoelting, Hines & Marschall, 2012). In outpatient management system, the early administration of intramuscular epinephrine for anaphylaxis can lead to improved outcomes such as decreased fatalities, severity of symptoms and biphasic reactions. However, delayed epinephrine administration can on the other hand lead to higher rates of biphasic reactions especially in children (Field, 2009). Question 3 Negative pressure pulmonary oedema Introduction This is a rare complication that accompanies general anesthesia, especially after extubation. Negative pressure pulmonary edema (NPPE) is not as common and involves a complication of anesthesia resulting from laryngospasm during extubation. The various risk factors include; male sex and head or neck surgery. It is an example of a noncardiogenic pulmonary edema in which case it can develop even in instances where the heart and lungs are functioning normally (Gregory & Andropoulos, 2012). How the disease develops The disease occurs when there is an upper airway obstruction. This closure experienced in the upper airway marks the first stage for the pathophysiology which develops. Because of this obstruction, a large, negative and intrathoracic pressure is generated as the patient’s effort to breathe increases. This resulting pressure triggers an increase in the left ventricular preload and afterload. The extramural hydrostatic pressure further decreases. This condition changes pulmonary vascular resistance, as opposed to other areas in the body. This results into right ventricle dilation, shift of intraventricular to the left and left ventricular diastolic dysfunction. All these conditions increase the loading conditions in the left heart, and thus enhancing microvascular intramural hydrostatic pressure. A situation now forms where fluids can easily move from different concentrations, and thus into lung interstitium from the capillaries. This condition is not very common though a standard anesthesia provider should be able to identify its signs and symptoms and start the prerequisite treatments (Gregory & Andropoulos, 2012). This disease is dangerous and could potentially be a fatal condition with a multifactorial pathogenesis. Its occurrence is an indication of the obstruction of the upper airway involving the mechanism of the large negative intrathoracic pressures started by forced inspiration against the obstructed airway. Such negative pressures in patients lead to an increase in the volume of the pulmonary vascular and pulmonary capillary transmural pressure thus leading to a risk of disruption of the alveolar–capillary membrane (Litman, 2004). The disease exact incidence is not widely known with an estimated development of eleven percent in patients requiring active intervention for acute upper airway obstruction. Adults are associated with such risk factors as obesity with obstructive sleep apnea and the presence of airway lesions. The young athletes, especially the male, are also usually at risk because they are able to generate significant negative intrapleural pressures. (Litman, 2004). Question 4 Frank-Starling and Laplace laws in relation to the heart The Frank–Starling law of the heart states that an increase in the stroke volume of the heart occurs with an in increase in the end diastolic volume of the heart when all other factors remain constant. The mechanisms stipulate that an increase in the volume of the blood would stretch the wall of the ventricles and cause the heart muscles to contract with more force. It is one of the most important physiological principles for regulation of contractile performance of the heart. Another condition that could also lead to an increase in the stroke volume of the heart is during exercise when the cardiac muscles could contract (Miller, 2010). Laplace laws on the other hand consider the heart as a hollow sphere, comparing it to the heart’s ventricle. According to the Laplace laws, the pressure existing internally in the heart is directly proportional to the tension of the wall, and inversely proportional to the internal radius. An increase in the wall tension in the heart would aid early ejection and as this ejection continues; a decrease in the radius is experienced, which facilitates ejection in systole (Miller, 2010). The pathology of heart failure Heart failure refers to that pathological condition where the heart is not able to pump blood enough blood to sustain the functioning of the body’s metabolizing tissues or can only perform this at elevated filling pressures. Most adults often suffer from heart failure when their left ventricles become unable to fill and eject blood. The degree of diastolic filling abnormalities in several cases dictates the severity of heart failure more than blood ejection. Heart failure in other instances could be as a result of some damage caused to the heart muscles or due to a myocardial infarction. In the instances of myocardial infarction, little or no blood is taken to the muscles of the heart thence starving them of oxygen. This causes the death of such muscles making them not to function normally hence making individuals run at a risk of heart failure (Seifter, Sloane & Ratner, 2005). The contraction of the heart could weaken when the ventricle gets overloaded with blood during a diastole. In a healthy people, according to the laws, such an overload should trigger an increase in muscle contraction in order for the cardiac output to be raised. In cases where the heart fails though, this mechanism fails to work due to the weakened heart muscles that result in its failure to pump an adequate blood amount to the body. The heart rate as a result increases in order to make up for this decreased cardiac output. The failure of the systole and diastole contractions then reduces the stroke volume. Little blood is released as the volume of blood in the ventricle at the end of the systole increases. On the other hand, little blood enters the heart at the end of diastole as the blood volume decreases. The cardiac reserve then reduces to a level that it cannot cope up with the normal and elevated body metabolic demand. This reserve is lowered and could potentially result into heart failure (Mebazaa, 2008). Reference Lang, F. (2009). Encyclopedia of molecular mechanisms of disease. Berlin: Springer. Beek, E. J. R., Büller, H. R., Oudkerk, M., & Wiley InterScience (Online service). (2009). Deep vein thrombosis and pulmonary embolism. Chichester, UK: J. Wiley-Blackwell. George, R. B. (2005). Chest medicine: Essentials of pulmonary and critical care medicine. Philadelphia, PA: Lippincott Williams & Wilkins. Field, J. M., American College of Emergency Physicians., & American Heart Association. (2009). The textbook of emergency cardiovascular care and CPR. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. Stoelting, R. K., Hines, R. L., & Marschall, K. E. (2012). Stoelting's anesthesia and co-existing disease. Philadelphia: Saunders/Elsevier. Gregory, G. A., & Andropoulos, D. B. (2012). Gregory's pediatric anesthesia. Chichester, West Sussex: Wiley-Blackwell. Litman, R. S. (2004). Pediatric anesthesia: The requisites in anesthesiology. St. Louis, Mo: Mosby. Miller, R. D. (2010). Miller's anesthesia. Philadelphia, PA: Churchill Livingstone/Elsevier. Seifter, J., Sloane, D., & Ratner, A. (2005). Concepts in medical physiology. Philadelphia, PA: Lippincott Williams & Wilkins. Mebazaa, A. (2008). Acute heart failure. New York: Springer. Read More