Veins and Arteries
There are significant pathogenic and clinical presentational symptoms that differ with chronic venous insufficiency (CVI) and deep vein thrombosis (DVT). As a provider, it is important to differentiate between both the pathogenic processes and clinical presentation to provide an accurate diagnosis and plan of care. This paper will review the pathophysiology of CVI and DVT, including thrombosis differentiation. The influence of behavioral factors on the pathophysiology, diagnosis, and treatment will additionally be reviewed.
Pathophysiology
An understanding of the pathophysiology and function of both veins and arteries can help clinicians recognize disease processes such as CVI and DVT. According to Huether and McCance (2012), veins are comprised of a thin layer of endothelium and fibrous tissue that exhibits less recoil than arteries. Changes in the endothelium of the vein 's wall will lead to an "exposed subendothelial wall potentiating prothrombogenic and proinflammatory cytokines" (Huether & McCance, 2012). These cellular changes can lead to opportunities for vasoconstriction, platelet adhesion, and inflammatory processes (Huether & McCance, 2012). Furthermore, the function of blood flow back to the heart can be altered when pathogenic changes occur at the cellular level, and there are changes in muscle contraction. Veins have valves that return circulating blood back to the heart. Muscle activity will support blood return by contracting skeletal muscles in the extremities to assist with blood return (Huether & McCance, 2012). Therefore, individuals who have conditions that alter the vessel endothelium such as hypertension or are inactive are at risk for inefficient blood flow back to the heart or...
... middle of paper ...
...ent who presents with these behavioral factors.
Diagnosis of a DVT involves a physical assessment, doppler, and lab tests (D-dimer) (Huether & McCance, 2012). Treatment would need to include anticoagulation therapy or insertion of a superior vena cava (Huether & McCance, 2012). When behavioral factors such as inactivity, obesity, and smoking are present considerations will need to include risk for the presence of other cardiovascular disease processes.
Summary
When caring for patients who exhibit signs of vein disease, it is important to assess and identify vein disease progression. Furthermore, a detailed history and physical will need to include coexisting behavioral factors that can be modified to help prevent further progression of vein disease. Lastly, providing education related to preventative strategies and signs of thrombi formation are essential.
Qiao T, Liu C and Ran F. (2005) The impact of gastrocnemius muscle cell changes in chronic venous insufficiency. Eur J Vasc Endovase Surg 30; 430-436.
...so discuss making a exercise plan that will work for the patient, and will not cause him/her any pain. If all of the correct measures are taken, and the patient is taking care of themselves, they can prevent more serious complications from occurring. They must know that they are serious complications from one not taking care of themselves, or living a unhealthy life style. It does involve a lifelong commitment to change. Medication will help, but one must also be willing to change.
Many factors can increase the risk of these clots, including prolonged bed rest (such as after surgery), sitting for long periods (such as on a plane), use of birth control pills or hormone replacement therapy, pregnancy, family history of DVT, inflammatory bowel disease, and certain genetic clotting disorders. Compression stockings are also sometimes used in people who have an acute DVT, to prevent a group of symptoms known as post-thrombotic syndrome that includes leg pain and
The arteries have a thick inner layer of muscle and elastic fibres. This means that they can stretch a lot more than the veins that have a thin inner layer, this means that they are more compact.
One of the characteristics of the common disorder, and perhaps the most worrisome for the patients affected, is decreased blood flow in the atria, which is associated with and allows thrombi to form. Embolism from the atria can cause cerebrovascular accidents, which can be devastating to the affected individuals and their families.
Wells, Philip S., Anderson, David R., Rodger, Marc et al (2003). Evaluation of D-Dimer in the Diagnosis of Suspected Deep-Vein Thrombosis. New England Journal of Medicine; 349: 1227-1235.
Yung,, L.M., Laher, I., Chen, Z.Y., Huang, Y. and Leaung , F.P. (2009) Exercise, Vascular Wall and Cardiovascular Diseases. Sports Medicine. Vol. 39, No. 1: 45-63
Coronary heart disease is defined by the hardening of the epicardial coronary arteries. The buildup of plaque in the arteries slowly narrows the coronary artery lumen. In order to better understand the physiology of the disease, it is important to first know the basic anatomy of the human heart. The aorta, located in the superior region of the heart, branches off into two main coronary blood vessels, otherwise known as arteries. The arteries are located on the left and right side of the heart and span its surface. They subsequently branch off into smaller arteries which supply oxygen-rich blood to the entire heart (Texas Heart Institute, 2013). Therefore, the narrowing of these arteries due to plaque buildup significantly impairs blood flow throughout the heart.
Cardiovascular Disease is defined by the American Heart Association as “Heart and blood vessel disease”. Atherosclerosis of the arteries, can lead to hypertension, heart failure, arrhythmias, heart valve problems, myocardial infarctions or a stroke (AHA, 2016). In this paper, all of heart and vessel diseases aforementioned, will be considered cardiovascular disease (CVD). According to
Atkinson, R. P.; & DeLemos, C. (2000). Acute Ischemic Stroke Management. Thrombosis Research. 98:3; 97-111.
This condition can be treated various ways depending on “the type and frequency of arrhythmias, associated symptoms…, and the presence of structural heart disease” (Cleveland Clinic, 2014). Some patients may not need treatment at all, since they show not symptoms, since sometimes this condition can be naturally eliminated over the first year of life, but may still be required to have regular schedule appointments with the physician so the patients can be monitored. If symptoms are prevalent, the different treatment methods include a pacemaker, defibrillator, surgery, and medicine.
Cardiovascular disease is currently the nation’s leading non-communicable cause of morbidity and mortality. According to the American Heart Association, the most common form of cardiovascular disease is coronary artery disease, a condition in which the heart’s blood supply is reduced due to a narrowing of the coronary arteries. These arteries play a significant role in regulating the flow of oxygenated blood to the heart. As blood circulates through the arteries, it exerts a force against the vessel walls, known as blood pressure. To withstand this pressure, elastic fibers interspersed along the artery walls allow the arteries to expand and recoil. Abnormally high blood pressure, however, will cause these muscles to thicken as a result of tears in the damaged artery walls trapping particles that aggregate as plaque. Progressive build-up of plaque ultimately leads to a narrowing of the arteries, subsequently diminishing blood flow to the heart and other body organs. This cascade of events triggered by high blood pressure illustrates why hypertension is one of the most important risk factors for cardiovascular disease. Affecting 1 in every 3 adults in the United States alone, hypertension substantially raises the risk for heart disease in an affected individual who, most likely, does not show any signs or symptoms. In addition to the risks associated with this “silent killer,” comorbidities such as obesity, diabetes, and high cholesterol can drastically worsen health outcomes in hypertensive patients. Given the high prevalence and severe consequences of hypertension if undetected, researching this particular topic will increase our understanding of the causes of hypertension by identifying and narrowing down lead candidates for pot...
In septic patients, increased levels of PAI-1 inhibit plasminogen activator (t-PA), which converts plasminogen to plasmin. Release of fibrin inhibits fibrinolysis by activation of thrombin-activatable fibrinolysis inhibitor (TAFI). In addition, the release of PAF causes platelet aggregation. This combination of inhibition of fibrinolysis, fibrin strand production and platelet aggregation contribute to a state of coagulopathy. This can lead to microcirculatory dysfunction with isolated or multiple organ dysfunction and cell death. Mr Hertz’s coagulation profile showed a fibrinogen level of 5.6 g/L, indicating that coagulopathies were underway in his system.
On these occasions, I rely on my nursing assessment, evaluation, and interventions, collaborative skills, and scientific knowledge to make sound clinical judgments for the benefit of my patients. As a hemodialysis nurse, I will persevere to comply with innovation in nursing practice, EBP, research, and education. I believe growth requires generation of innovative, improved ideas and practices for the betterment of the organization and patient satisfaction. For this reason, I will embrace technological advancements; empower front line staff to embrace change and innovation; and motivate staff to be change agents on the floor with the aim to provide better quality of care for our
A detailed patient history including history of any recent trauma or systemic disease such as renal or cardiovascular problems should be taken. The diagnosis is usually reached by a high clinical suspicion through the history and physical examination.