A cerebral hemorrhage (also spelled haemorrhage) is a subtype of intracranial hemorrhage that occurs within the brain tissue itself. It is alternatively called intracerebral hemorrhage (ICH). It can be caused by brain trauma‚ or it can occur spontaneously in hemorrhagic stroke. Non-traumatic intracerebral hemorrhage is a spontaneous bleeding into the brain tissue.[1] A cerebral hemorrhage is an intra-axial hemorrhage; that is‚ it occurs within the brain tissue rather than outside of it. The other
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study was conducted by ARDMS- certified sonographers who used an L9-3 linear probe on 284 patients (older than 18 years old) to test three modalities of sonographic imaging to determine if they would help spot an acute DVT during a lower extremity venous duplex. The three modalities used for this test was 2D imaging‚ resolution preset and B-color preset. Other variables/factors included in this study were age‚ sex‚ ethnicity‚ BMI‚ diabetes and hypertension. As a result‚ there were no major differences
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using short acting alpha and beta blocking agents‚ such as labetalol‚ or vasodilators like hydralazine. Angiotensin-converting-enzyme inhibitors and calcium channel blockers are also appropriate choices for blood pressure management in this cohort. Venous vasodilators should not be used‚ for they will increase intracranial pressure. Increased intracranial pressures can be managed by elevating the head of bed to 30 degrees and intravenous sedatives and analgesics. If the patient has a Glasgow Coma Scale
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Sepsis; pathophysiology‚ etiology and treatment Abstract To define the disease known as sepsis‚ briefly discuss its pathophysiology‚ etiology‚ signs‚ symptoms‚ and treatments. Outline protocols for sepsis screening‚ early directed goal therapy‚ and to establish the nurse’s role in the process. Sepsis is a complex disease‚ or response to a disease process that can lead to patient mortality rates up to 60%. Gram negative infectious organisms invade the blood stream‚ and activate a systemic
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Pain and discomfort of the shoulder and entire upper extremity is a significant problem for many people and it can be attributed to a wide variety of causes1. The focus of this paper is to discuss the cause‚ symptoms‚ diagnoses‚ treatment and management of thoracic outlet syndrome (TOS). TOS is caused by a neurovascular compression event that can elicit pain‚ paraesthesia or discomfort in areas varying from the chest to the fingertips2‚3. The ‘thoracic outlet’ is composed of three confined spaces
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Chapter 14: Cardiovascular Physiology Cardiovascular Physiology Chapter 14 " Heart anatomy " Cardiac muscle cells " Autorhythmic cells " Cardiac cycle " Cardiac output " 1 Functions of Circulatory System " Transportation" – Respiration" Transport 02 and C02." – Nutrition" Absorbed digestion products delivered to liver and tissues" – Excretion" Carry metabolic wastes to kidneys" – Hormonal: " Carry hormones to target tissues" 2 The cardiovascular
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contractility is depressed; hypodynamic in late shock Ventricular dilation; decreased ejection fraction Loss of sympathetic responsiveness ● ● ● ● PATHOPHYSIOLOGYCont. CardiovascularCont. ● Hypovolemia due to vascular leakage; central venous pressure may be decreased or increased depending upon fluid resuscitation Compromised nutrient blood flow to organs; decreased organ oxygen extraction ● PATHOPHYSIOLOGYCont. Pulmonary & Renal ● ● ● ● ● ● ● Hyperventilation with respiratory
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list the possible consequences of developing plaques in those areas. Case 2 You have two patients with ulcers on their lower extremities. Patient A has ulcers caused by peripheral artery disease and patient B has ulcers caused by chronic venous insufficiency. 1. Describe the pathophysiology of how each type of ulcer developed. 2. List the signs you expect to see when you examine each patient’s extremities. 3. Why do these ulcers look so different? Case 3 KH is a 67-year-old
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regulated by the control of sodium excretion and extracellular fluid (ECF) volume. When sodium (Na+) is retained water (H2O) retained as well. As a result of Na+ and H2O‚ ECF volume increases which causes an increase in CO and blood pressure by the venous return to the heart and stroke
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perfected this to a point where they can reach a ‘steady state’ in which oxygen supply meets oxygen demand. The arteriovenous oxygen difference‚ or a-vO2 diff‚ is the difference in the oxygen content of the blood between the arterial blood and the venous blood. It is an indication of how much oxygen is removed from the blood in
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