Atrial fibrillation is the most common cardiac arrhythmia that is associated with a reduced quality of life and an increased number of adverse outcomes such as stroke‚ heart failure‚ increased number of hospitalizations and mortality. Prevalence in developed countries is currently 1.5-2% of the general population‚ with the incidence steadily rising. Hence‚ prevalence is estimated to at least double in the next 50 year as the population ages. It has become a big deal for the health care system in
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Case Study #2 Ambar Alvarez California State University – San Marcos NURS 312 Pharmacology and Pathophysiology Alham Abuatiq. PhD. MSN.RN July 30‚ 2017 Case Study# 2 1. Heart failure (HF) is a syndrome that involves dysfunction of the cardiac muscle‚ it occurs with “any of disorders that damage or overwork the heart muscle” (Karch‚ 2017 p.751). Some of the disorders that may lead to HF are: coronary artery disease‚ cardiomyopathy‚ hypertension‚ and valvular heart disease (Karch‚ 2017).
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Chapter 11 ARDS INTRODUCTION Acute respiratory distress syndrome (ARDS) - lung inflammation seen at the level of the alveolar capillary membrane with increased vascular permeability. ARDS results in: bilateral pulmonary edema and atelectasis despite no evidence of left heart failure (e.g.‚ normal pulmonary capillary wedge pressure (PCWP). ARDS is present when the ALI results in such severe hypoxia that at the PaO2/FIO2 ratio is 200 mm Hg or less. Approximately 10% to 15% of intensive care
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Outline 1. Component 2. Pathophysiology - 3 p.m. Causes & Risk Factors 4. Clinical manifestations - 5. Diagnostic Procedures - 6. 7. Prevention of the ailment. How to differentiate gradual MI changes in ECG? Management 10. MI location ................................................................................................................ Component 1. STEMI ( cells dead ) 2. NSTEMI ( cells dead ) 3. Angina ( Un stable : Un completed thrombus ) ..........................................
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Case Study 130 You are a nurse on an inpatient psychiatric unit. J.M.‚ a 23-year-old woman‚ was admitted to the psychiatric unit last night after assessment and treatment at a local hospital emergency department (ED) for “blacking out at school.” She has been given a preliminary diagnosis of anorexia nervosa. As you begin to assess her‚ you notice that she has very loose clothing‚ she is wrapped in a blanket‚ and her extremities are very thin. She tells you‚ “I don’t know why I’m here. They’re making
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Acute Systemic Anaphylaxis Anaphylaxis is a systemic allergic reaction involving the respiratory and/or the cardiovascular system; it has a rapid onset with the possibility of causing death. However‚ less severe reaction may be also defined as “anaphylaxis” if there is a high index of suspicion for allergic reaction in the setting of previously diagnosed allergy (Sanchez et al. 1999; Simons et al. 2007; Tang and Liew‚ 2008). It was observed by Simons (2006) that anaphylaxis is a disease of modern
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factors are recorded in the consensus paper from the WSACS (1). However‚ this long list is difficult to apply by the critical care nurse at the bedside. More than one study has identified the high BMI‚ abdominal surgery‚ liver dysfunction/ ascites‚ hypotension/vasoactive therapy‚ respiratory failure and excessive fluid balance as risk factors of IAH in the mixed ICU populations. However‚ the precise prediction of IAH development in the mixed ICU populations remains difficult. Because of the tremendous
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But‚ they prevents the formation of the Ang-2 from Ang-1 by inhibiting ACE. 6. Angiotensin-2 type-1 receptor (AT1R) plays a vital role in the controlling of the blood pressure and blood volume in the cardio vascular system. If we knockout AT1R hypotension will occurs due to the increased levels of the angiotensin-1. 7. EDTA is type of chelating agent. EDTA blocks the activity of the ACE1. However‚ EDTA has no effect on the renin activity. The renin activity was blocked the specific renin
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Electrolyte | Hypo | Cause | Clinical Manifestations | Hyper | Cause | Clinical Manifestations | Sodium (Na+) | <125 meq/L | * Inadequate intake * Hypoaldesteronism * Excessive diuretic therapy * Furosemide * Ethacrinic acid * Thiazides | * Extracellular volume contraction and hypovolemia (but may not if water excess) * Increased intracellular water; edema * Brain cell swelling‚ irritability‚ depression‚ confusion * Systemic cellular edema‚ including weakness‚ anorexia
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Patient’s Initials: M.N.M Age: 41 years old Sex: Male Civil Status: Married Medical Diagnosis: CKD Secondary to Uremic Encephalopathy‚ Hypertensive Nephrosclerosis vs. Gouty Neuropathy Attending Physician: Dr. Valdez‚ Dr. Manzon‚ Dr. Ocampo‚ Dr. Concepcion I. CHIEF COMPLAINT - General body weakness - Drowsiness - Pain on knees II. NURSING HISTORY The patient‚ MNM‚ has hypertension for 21 years‚ he’s not taking any medications until year 2008 when he was prescribed Nifedipine
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