Pharmacologic Interventions of Pulmonary Embolism Essay

POWER POINT

TOPIC: Pharmacologic Interventions of Pulmonary embolism using Heparin Drips

This will be done weekly and according to what we will be studying for that week, and will begin Week 2, and end Week 9.

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Each student will be responsible for preparing one presentation on pharmacological management of the disease or pharmacological applications of a drug or group of drugs.Pharmacologic Interventions of Pulmonary Embolism Essay

Each student will clearly write a title for this topic. Examples are ‘Pharmacological Management of Deep Vein Thrombosis and/or Pulmonary Embolisms Using Anticoagulants/Thrombolytics and Nursing Implications’ or ‘Pharmacological Effects of Anti-hypertensive Medications in the Management of Hypertension and Nursing Implications’.
Nursing Implications are the nursing related consequences and what you as the nurse should be looking for in the treatment and care of your patient.
Students must get their title approved by the professor before the deadline shown in your schedule. Unapproved titles will not be accepted
The presentation must identify the Pharmacodynamic properties and actual/potential effects on the patient.
This is worth 20 points.Pharmacologic Interventions of Pulmonary Embolism Essay

Pulmonary embolism (PE) is an acute and potentially fatal condition in which embolic material, usually a thrombus originating from one of the deep veins of the legs or pelvis, blocks one or more pulmonary arteries, causing impaired blood flow and increased pressure to the right cardiac ventricle. Pulmonary embolism and deep vein thrombosis are considered to be two manifestations of the same condition, venous thromboembolism, which is the third most common cardiovascular disorder in industrialized countries [1, 2]. PE is difficult to diagnose because symptoms are non-specific and clinical presentation of patients with suspected PE varies widely from patients who are asymptomatic to those in cardiogenic shock.Pharmacologic Interventions of Pulmonary Embolism Essay

In October 2011 the Interdisciplinary Association for Research in Lung Disease (AIMAR) established a Task Force for diagnosis and treatment of PE with multidisciplinary representation including 3 pulmonologists, 3 internists, 2 emergency care physicians, 1 cardiologist, 1 radiologist and 1 nuclear medicine physician. The members of the Task Force have engaged in interdisciplinary collaborations regarding the diagnostic strategies and treatment of PE. The interdisciplinary organization structure of the present Task Force was designed to support the need of a multidisciplinary approach in the early diagnosis of the disease. The Task Force was asked to structure its recommendations on the diagnosis of PE through a multidisciplinary process that can be dynamically adapted to a rapid changing and increasingly personalized delivery of health care within a structured framework. The Task Force reviewed the literature, and discussed clinical practices in Italy on meetings and conference calls. No attempt was made to grade evidence or recommendations. The present article represents the recommended consensus-based guidelines of the Task Force.Pharmacologic Interventions of Pulmonary Embolism Essay

Epidemiology
Symptomatic venous thromboembolism occurs in 1–2 per 1,000 adults each year, with about a third presenting with PE [1, 2]. The incidence of PE correlates strongly with age, being extremely rare in childhood (5 per 100,000 of the population), but increasing exponentially to nearly 500–600 cases per 100,000 in older (> 75 years) age [1–3]. Overall, men and women are affected equally, but women of reproductive age have slightly higher rates of PE because of the association between the disease and pregnancy, and the increased risk conferred by the use of oral contraceptives [1, 4]. In older age, the incidence of PE is higher in men than in women [2]. PE-related mortality can be as high as 25% if untreated [2], however, with adequate anticoagulant therapy, this rate decreases to about 2–8% in the 3 months following diagnosis [5, 6]. However, the actual figures could be higher than those generally reported because patients who die before diagnosis are usually not included in clinical studies. In the acute phase, i.e. the first month after diagnosis, mortality is influenced by the presence of hemodynamic instability, underlying comorbidities, and immobility [5]. In the long term, i. e. ≥ 1 year after diagnosis, due to comorbidities that are strong predictors of mortality [7] such as malignancy, left-sided congestive heart failure, and chronic lung disease, mortality can reach 24–27%. Malignancy is the most frequent cause of death (35–45%), whereas recurrent PE accounts for 2.5–7.0% [7].Pharmacologic Interventions of Pulmonary Embolism Essay

Risk factors
Pulmonary embolism is currently considered to be the result of an interaction between patient-related and setting-related risk factors. Patient-related predisposing factors are usually permanent, whereas setting-related risk factors are more often temporary. Commonly, more than one risk factor is present, illustrating that PE is a multicausal disease. However, PE can occur in patients without any identifiable predisposing factors.Pharmacologic Interventions of Pulmonary Embolism Essay

Inherited risk factors
Prothrombotic inherited risk factors are associated with either reduced levels of anticoagulant proteins or increased levels or function of coagulation proteins. In the general population, thrombophilic abnormalities vary in prevalence and also in the risk of PE that they convey. Generally, the overall absolute risk of PE is low, regardless of the increased relative risk caused by the presence of a thrombophilic factor [2]. Deficiencies of natural coagulation inhibitors, such as antithrombin, protein C and protein S, are strong risk factors for PE, but these deficiencies are rare and only account for 1% of all cases of PE. Factor V Leiden and prothrombin (factor II) G20210A are the two more common genetic variants that have been consistently found to be associated with PE, but still only explain a small proportion of PE cases. The search for new genetic variants associated with PE is ongoing and, at the present, the impact of identification of new genetic risk factors on the management of individual patients is unclear. More insight into how genetic risk factors are involved in PE may enable personalized risk profiling in selected patients. However, to be applicable in a clinical setting, the assays must be fast, affordable, and able to detect a combination of clinically relevant genetic factors.Pharmacologic Interventions of Pulmonary Embolism Essay

Acquired risk factors
Several acquired risk factors for PE have been identified. The highest risk for PE is conferred by surgery (particularly orthopedic surgery, surgery for cancer, and neurosurgery), history of previous venous thronboembolism, immobility for more than 48 h, hospitalization, infection, and cancer [8–14]. In the Prospective Investigative Study of Acute Pulmonary Embolism Diagnosis (PISA-PED), at least one of these risk factors was present in more than 80% of patients with established PE and in about 70% of those without PE [8]. The risk of developing symptomatic PE is 7 fold higher among patients with cancer than in those without cancer and approximately 10% of all PEs are secondary to a known cancer [11]. In a large population-based study, confirmed symptomatic PEs were diagnosed within 2 yrs in 1.6% of 235,149 cancer cases [11], and metastatic disease at the time of diagnosis was the strongest predictor of PE [11]. All haematological and solid tumour types have been associated with PE but the PE risk varies among the various types of cancer. Blom et al. [11] observed the highest risk of PE adjusted for age and sex among patients with haematological malignancies (odds ratio: 28), lung cancer (odds ratio: 22) and gastrointestinal cancer (odds ratio: 20). Adjusting for age, race and stage, diagnosis of PE was a significant predictor of death during the first year for all cancer types [15]. In patients with PE, the prevalence of concomitant cancer, not known before the diagnosis of PE and discovered by routine investigation at the time of PE diagnosis, varies between 4% and 12% [16]. The risk of occult cancer is increased three- to four-fold in patients with idiopathic PE compared with secondary PE [16]. Considering the high incidence of cancer in the initial months following diagnosis PE, screening for an underlying malignancy may be clinically relevant in selected cases.Pharmacologic Interventions of Pulmonary Embolism Essay

About two-thirds of PE cases occur during pregnancy and one-third post partum. A recent study showed that the risk of PE was increased five-fold during pregnancy and increased 60-fold during the first 3 months following delivery compared with non-pregnant females [17].

Hormone replacement therapy is reported to increase the risk of PE by two- to four-fold [18, 19]. However, at variance with the oral route of administration, transdermal oestrogen does not have a first pass effect through the liver and it has been suggested that this might lead to less risk of thrombosis [18, 19]. Oral contraceptive therapy increases the risk of PE by two- to five-fold [20]. However, since the absolute risk of PE is low in young females, the annual risk in users of oral contraceptives remains low at two to three cases per 10,000 [20]. The risk is highest during the first year of use. The type of progesteron affects the risk of venous thrombosis, with a two fold higher risk for contraceptives containing a third generation (desogestrel and gestodene) than a second generation (levonorgestrel) progestogen [20].Pharmacologic Interventions of Pulmonary Embolism Essay

Other medical disorders associated with increased risk for PE include heart failure, ischemic stroke, acute respiratory failure or intubation, sepsis, acute rheumatic disease, and inflammatory bowel disease [10, 13].

Diagnostic strategies
The diagnostic pathway of PE is guided by two principles. First, accurate and fast identification of patients with PE is critical because PE is a potentially fatal condition and anticoagulation is associated with the risk of major bleeding. A false diagnosis thus exposes patients to unnecessary risk of death from PE or of bleeding which can also be fatal. Second, the use of individual diagnostic tests in isolation may lead to mismanagement of suspected PE. For these reasons, integrated diagnostic approaches that include a combination of different diagnostic tests are preferred. Because use of a validated diagnostic work-up is associated with a substantially diminished risk of complications [21], implementation of such standardized approaches is highly recommended.Pharmacologic Interventions of Pulmonary Embolism Essay

Clinical probability assessment
In general, the initiating point for any diagnostic approach is the clinical suspicion that should guide the choice of the initial test [22]. Prior to the development of objective testing, the diagnosis of PE was largely based on clinical history and physical examination. Unfortunately, PE cannot be diagnosed or excluded on clinical grounds as symptoms and signs are non-specific [23–25]. However, it has long been recognised that unexplained dyspnoea and/or chest pain are present in about 97% of the patients with proven PE and may be useful to raise the suspicion of PE and to select patients for further diagnostic testing [8]. Therefore, in the diagnostic work-up of PE, the information obtained from the clinical history and a physical examination should be evaluated in conjunction with additional data derived from readily available laboratory tests, such as chest radiography, electrocardiography, and arterial blood gas analysis [26]. The combination of clinical and laboratory data may either increase the clinical suspicion of PE, or suggest alternative diagnoses [26]. Although diagnostic strategies of PE may differ significantly in different clinical contexts and special conditions, the present Task Force recommends that pre-test clinical probability of PE must always be objectively assessed in each patient, while D-dimer measurements should be determined if pre-test probability of pulmonary embolism is low or intermediate. Diagnostic imaging of the chest should be used to assess post-test probability of PE in most patients. Further testing is necessary when the post-test probability of PE is neither sufficiently low nor sufficiently high to permit therapeutic decisions.

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Pre-test clinical probability of pulmonary embolism
A thorough clinical evaluation is the key step in raising the suspicion of the disease and setting up appropriate diagnostic strategies. A recent study [27] has shown that the vast majority of patients with pulmonary embolism has at least one of four symptoms which, in decreasing order of frequency, are: a) sudden onset dyspnoea; b) chest pain; c) fainting (or syncope); d) haemoptysis.Pharmacologic Interventions of Pulmonary Embolism Essay

Acute thromboembolic occlusion of a coronary, cerebral, or peripheral artery mandates definitive prompt intervention to open the vessel and restore downstream blood flow. This paradigm evolved over the 1970s to 1990s as endovascular interventional options were developed and proven with thousands of patient-years of outcome data, such that the standard of care, for example, in ST-segment–elevation myocardial infarction advanced from thrombolytic medications to primary percutaneous coronary intervention. In contrast, management paradigms for acute occlusion of the pulmonary artery—pulmonary embolism (PE)—are less agreed on. Confounding this lack of consensus is the evolution of many mechanical and hybrid pharmacomechanical options. PE management, relative to acute coronary syndrome, is beset by a paucity of clinical and outcome data, with treatment guided generally by expert consensus and case series.1 The goals of this article are to discuss interventional therapies for PE, with reference to how an interventionalist might risk-stratify and select candidate patients, and review emerging data and devices for each type of interventional strategy.Pharmacologic Interventions of Pulmonary Embolism Essay

Pulmonary Embolism: Background
PE is the third most common cause of vascular disease in the United States, trailing myocardial infarction and stroke. The intensity and invasiveness of treatments for PE are generally commensurate with the severity of its hemodynamic, cardiac, and respiratory consequences. However, there is no globally accepted risk-stratification scheme for classifying severity of PE. Three professional society statements—from the American Heart Association,2 American College of Chest Physicians,3 and European Society of Cardiology4—encapsulate contemporary thinking and principles of risk stratification for PE, primarily based on hemodynamic consequences and right ventricular (RV) dysfunction.Pharmacologic Interventions of Pulmonary Embolism Essay

Patients with acute PE may present on a spectrum from sudden cardiac arrest or death at one extreme to incidental clots without hemodynamic insult or cardiopulmonary dysfunction (Figure).2 Some 40% of patients inhabit the latter low-risk category and suffer minimal PE-related mortality or morbidity.5 Accordingly, conservative management with anticoagulation alone is standard (though surveillance may be considered in subsegmental PE with low risk for clot recurrence and no proximal deep vein leg thrombosis).3,6 In contrast, patients who present as survivors of cardiac arrest, or with shock or hypotension, classified as high-risk (or massive) PE, require prompt debulking and reperfusion therapy to positively impact the elevated mortality and morbidity. The exact epidemiology of severe PE is likely unknown because the fraction of out-of-hospital fatalities attributable to PE versus other etiologies (myocardial infarction or acute aortic syndromes) remains difficult to quantify.Pharmacologic Interventions of Pulmonary Embolism Essay

Figure.
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Figure. Risk stratification of PE. Patients with PE are risk stratified based on hemodynamic consequences and indicia, including biomarker and imaging evidence of RVS. The highest-risk patients with PE have acute deterioration because of PE, including cardiac arrest or cardiogenic shock. Other phenotypes that convey higher-risk PEs include paradoxical bradycardia, ventricular tachycardia, and relative hypotension (SBP<90 mm Hg). Normotensive patients with PE may be stratified to an intermediate risk by elevated cardiac biomarkers (troponin and natriuretic peptides) or CT or echocardiographic evidence of RVS (right ventricular dilatation, interventricular septal bowing, and on echocardiography, right ventricular systolic dysfunction). Low risk is defined by absences of hemodynamic sequelae, biomarker elevation, and RVS, and low scores on prognostic indices. CT indicates computed tomography; PE, pulmonary embolism; RVS, right ventricular strain; SBP, systolic blood pressure; and sPESI, simplified pulmonary embolism severity index.

The majority of patients with PE fall between these extremes, and various parameters have been devised to assess risk in this normotensive subgroup (Figure).6,7 Radiographic measures of clot burden by computed tomography (CT) have not correlated with mortality and outcomes.8,9 Most stratification systems use a composite of factors to assess overall RV strain (RVS).2,4 Biomarkers provide evidence of myocardial necrosis or RVS by troponin or natriuretic peptides, respectively. Echocardiography assesses RV dilatation, global and local RV systolic dysfunction, tricuspid regurgitation, and interventricular septal bowing.2,10 CT scanning, commonly performed for diagnosing PE, can provide data on some RVS parameters, particularly RV dilatation and septal geometry.11 Certain electrocardiographic changes, for example, T wave inversions in early precordial leads, may constitute RVS.2,12 Patients with PE who are normotensive but manifest at least one factor indicating RVS are considered to have an intermediate-risk PE (submassive in American Heart Association Scientific Statement). After the PEITHO trial (Pulmonary Embolism Thrombolysis),13 updated European Society of Cardiology guidelines delineated an intermediate–high-risk category: normotensive patients with acute PE with both biomarker and imaging evidence of RVS, distinguished from intermediate–low-risk with either the biomarker or imaging element (Figure). Although guidelines focus on results of biomarker and imaging testing for risk stratification in intermediate PE, because there is not a consensus algorithm, clinicians often integrate additional information, including degree of tachycardia, rest and exertional hypoxemia, and preexisting cardiopulmonary reserve, to judge where on the wide spectrum an intermediate-risk PE patient truly fits.6,14 Imaging studies for risk stratification moreover may reveal thrombus-in-transit in the right heart, which does not fit clearly within this risk stratification and yet may require prompt intervention.15 There is a paucity of data on thrombus-in-transit and, therefore, controversy on whether thrombolysis or percutaneous or surgical embolectomy is appropriate therapy Pharmacologic Interventions of Pulmonary Embolism Essay