...Cardiogenic shock is often cause by myocardial infarction or commonly known as heart disease. During myocardial infarction, the arteries supplying the heart is blocked or restricted the flow of heart which will lead to cardiogenic shock. There are few more conditions that may cause cardiogenic shock for examples pulmonary embolism (a blockage in one of the pulmonary arteries in lungs), pericardial temponade (pressure on the heart that occurs when blood or fluids builds up in the space between the heart muscle and the outer covering sac of the heart), valve damaged, rupture of the wall of the heart, ventricular fibrillation and also tachycardia. If it is not treated quickly, it may cause...
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...protocol stands right now there are parameters for the administration of three out of the four treatments, these are morphine, nitroglycerin and aspirin. For example, the policy states we are not able to give nitroglycerin if the systolic blood pressure is below 90mm/mg or if the patient has taken any phosphodiesterase medications within 12 hours. However, there are no parameters for the administration of oxygen. Coronary heart disease is the leading cause of death within the US. Oxygen has long been advocated as standard treatment in the management of chest pain and myocardial ischemia, although, for over 60 years the scientific background for this has been questioned (Ripley, Riley, Shome, Awan, McCloskey, Murphy & DeBelder, 2012). Recent studies have shown possible negative reactions with the administration of pure oxygen with patients that were not presenting with hypoxia. The possibility for oxygen toxicity to those with ACS could cause more cardiac tissue injury due to vasoconstriction and decreased cardiac output (Williams, Gandy, & Grayson, 2013). The result of this could be poorer patient outcomes. The American Heart Association (AHA) has also been...
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...According to Urden, Stacy, and Lough (2006), shock is a life-threatening condition that can lead to ineffective tissue perfusion or may further progress to multiple organ dysfunction and death. The different types of shock include hypovolemic shock, cardiogenic shock, anaphylactic shock, neurogenic shock, and septic shock (Urden, Stacy, & Lough, 2006). This essay will analyze septic shock based on the analysis of a presented case study. To further understand this concept, a review of treatment and management of septic shock as used in the writer’s practice setting will be discussed. The writer chooses the “case study one” as an issue of septic shock because Karen’s vital signs, physiological and behavioral symptoms are clear indicators of septic shock. Septic shock is described as the body’s inflammatory response to overwhelming infection (Urden, Stacy & Lough 2006). It is also classified as existence of an infection with hypotension despite fluid replacement along with the presence of tissue perfusion abnormalities (Urden, Stacy & Lough 2006). According to Bench (2004), the diagnostic criteria for septic shock include a heart rate greater than 90 beats per minute, a respiratory rate greater than 20 beats per minutes, an increased white cell count, hypotension, and temperature greater than 38 degrees or less than 36 degrees. Karen met these criteria with an increased temperature of 41 degrees which is usually an indicator of infection, increased heart rate and respiratory...
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...I. Introduction - Shock (Chapter 11) A. Review of anatomy and physiology B. Pathophysiology Initiation | * Decreased tissue oxygenation * Decreased intravascular volume * Decreased Myocardial contractility (cardiogenic ) * Obstruction of blood flow (obstructive) * Decreased vascular tone (distributive) * Septic (mediator release) * Neurogenic (suppression of SNS) | No observable clinical indications Decreased CO may be noted with hemodynamic monitoring | Compensatory | * Neural compensation by SNS * Increased HR and Contractiliy * Vasoconstriction * Redistribution of blood flow from nonessential to essential organs * Bronchodilation * Endocrine Compensation (RAAS, ADH, glucocorticoid release) * Renal reabsorption of sodium, chloride, and water * Vasoconstriction * Glycogenolysis | * Increased HR (EXCEPT NEUROGENIC) * Narrowed pulse pressure * Rapid, deep respirations causing respiratory alkalosis * Thirst * Cool,moist skin * Oliguria * Diminished bowel sounds * Restlessness progressing to confsion * Hyperglycemia * Increased specific gravity and decreased creatinine clearance. | Progressive | * Progressive tissue hypoperfusion * Anaerobic metabolism wih lactic acidosis * Failure of sodium potassium pump * Cellular edema | * Dysrhythmias * Decreased BP with narrowed pulse pressure * Tachypnea * Cold, clammy skin * Anuria * Absent bowel sounds * Lethargy progressing...
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...critical care review Transfusion-Related Acute Lung Injury* A Review Mark R. Looney, MD; Michael A. Gropper, MD, PhD, FCCP; and Michael A. Matthay, MD, FCCP Transfusion-related acute lung injury (TRALI) is an underreported complication of transfusion therapy, and it is the third most common cause of transfusion-associated death. TRALI is defined as noncardiogenic pulmonary edema temporally related to transfusion therapy. The diagnosis of TRALI relies on excluding other diagnoses such as sepsis, volume overload, and cardiogenic pulmonary edema. Supportive diagnostic evidence includes identifying neutrophil or human leukocyte antigen (HLA) antibodies in the donor or recipient plasma. All plasma-containing blood products have been implicated in TRALI, with the majority of cases linked to whole blood, packed RBCs, platelets, and fresh-frozen plasma. The pathogenesis of TRALI may be explained by a “two-hit” hypothesis, with the first “hit” being a predisposing inflammatory condition commonly present in the operating room or ICU. The second hit may involve the passive transfer of neutrophil or HLA antibodies from the donor or the transfusion of biologically active lipids from older, cellular blood products. Treatment is supportive, with a prognosis substantially better than most causes of clinical acute lung injury. (CHEST 2004; 126:249 –258) Key words: ARDS; lung injury; pulmonary edema; transfusion; transfusion-related acute lung injury Abbreviations: ALI acute lung injury;...
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...I Got….Myocardial Infarction 1. My initial response was to laugh because it is not a diagnosis that I thought I would ever hear. I am very slender and athletic and my cholesterol levels are all well under control. I do know that to get to the point of an MI, means that I more than likely have arteries full of plaque which ultimately leads to a sudden and extended obstruction of blood supple to myocardial tissue. My brain is already spinning in curiosity of the severity of ischemia in my left ventricle. What is even more scary to me, as a woman, is the higher risk of silent ischemia in women. Silent ischemia doesn’t produce any symptoms when the heart experiences ischemic events. So I guess after the shock wears off, that is when the “oh shit” moment is about to happen. 2. Myocardial Infarction(MI) is also known as a heart attack. MI results when the flow of oxygen rich blood to a myocardium suddenly becomes blocked. If blood flow is not restored quickly, this results in cellular death by necrosis or apoptosis. Acute MI is an important form of Coronary Heart Disease (CHD). MI can occur at any age, but the risk of frequency raises with age progression. It is estimated that MI causes more than 150,000 deaths annually in the US. The American male has a greater than 1 in 5 chance of sustaining an MI or fatal ischemic event before the age of 65. Females that are younger than 45 have a 6 fold lesser risk of MI than men of the same age, however after menopause the rate becomes...
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...Top of Form The ABCDE approach Underlying principles The approach to all deteriorating or critically ill patients is the same. The underlying principles are: Use the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach to assess and treat the patient. Do a complete initial assessment and re-assess regularly. Treat life-threatening problems before moving to the next part of assessment. Assess the effects of treatment. Recognise when you will need extra help. Call for appropriate help early. Use all members of the team. This enables interventions (e.g. assessment, attaching monitors, intravenous access), to be undertaken simultaneously. Communicate effectively - use the Situation, Background, Assessment, Recommendation (SBAR) or Reason, Story, Vital signs, Plan (RSVP) approach. The aim of the initial treatment is to keep the patient alive, and achieve some clinical improvement. This will buy time for further treatment and making a diagnosis. Remember – it can take a few minutes for treatments to work, so wait a short while before reassessing the patient after an intervention. First steps Ensure personal safety. Wear apron and gloves as appropriate. First look at the patient in general to see if the patient appears unwell. If the patient is awake, ask “How are you?”. If the patient appears unconscious or has collapsed, shake him and ask “Are you alright?” If he responds normally he has a patent airway, is breathing...
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...Medication Sheet Medication/Dose/RouteClassificationGeneric/Trade Name | Action | ContraindicationAdverse Effects | Nursing Considerations | Acetaminophen/500mg/ By MouthAntipyretic& Analgesic (nonopioid)Acetaminophen/TylenolCarvedilol/6.25mg/By MouthAlpha- and beta-adrenergic blocker & AntihypertensiveCarvedilol/CoregDocusate Sodium/100mg/By MouthLaxative stool softenersDocusate Sodium/ColaceFurosemide/40mg/By MouthLoop diureticsFurosemide/Lasix | Reduces fever by acting directly on the hypothalamic heat-regulating center to cause vasodilation and sweating, which helps dissipate heat.Carvedilol causes vasodilation by blocking the activity of α-blockers, mainly at alpha-1 receptors. It exerts antihypertensive effect partly by reducing total peripheral resistance and vasodilation. It is used in patients with renal impairment, NIDDM or IDDM.Promotes incorporation of water into stool, resulting in softer fecal mass, may also promote electrolyte and water secretion into the colon. It increases the amount of water and fat absorbed by the feces, softening the stool and making it easier to pass.Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule. Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium. | Contraindicated with allergy to acetaminophen. Use cautiously with impaired hepatic function, chronic alcoholism, pregnancy, lactation. Adverse effects CNS: Headache CV: Chest pain, dyspnea, myocardial...
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...A heart attack occurs when the blood supply to a portion of the heart muscle is severely reduced or stopped. This happens when one of the arteries that supply blood to the heart muscle is blocked by an obstruction. This blockage can be due to a condition called atherosclerosis (a buildup of fatty like substance along the wall of the artery), a blood clot or a coronary vessel spasm along with a total obstruction. If the blood supply to a portion of the heart stops, that area of the heart will no longer receive the oxygen or nutrients needed to carry out its function and will die. If it is a very small part of the heart involved, it will be able to work without it. If a large portion is damaged, irreversible damage will happen which can lead to death. Damage to the heart muscle may be so severe that it may cause abnormal heart rhythm, called arrhythmias. Most people who are of a myocardial infraction or a heart attack do so within a few hours due to a type of arrhythmia. The heart attack victim will complain of pressure, discomfort or a squeezing sensation in the center of the chest. There may be pain radiating to the arms or the neck. There may also be shortness of breath, weakness, fatigue, nausea, vomiting and or indigestion. The pain that occurs is the result of heart tissue ischemia (decreased blood supply). The area that is not receiving enough blood is literally crying out for help. When a person complains of any of the symptoms mentioned, they should be transported...
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...Case Study: Coronary Disease Laura Kwan Past Medical History: - tonsils removed as a child - no regular medication - takes reloads occasionally Family Medical History: - father died of myocardial infarction at age 52 - mother is 73 and in good health Social History: - moderately heavy social drinker - 2-3 beers after work - 5-6 beers per day on weekends - smokes a pack of cigarettes a day - married with two children - finances are stable History of Present Illness: - woke up at 4am with pressure in his chest, described as “worst indigestion I ever had” - sweaty and slightly short of breath - achy, heavy feeling in his right arm - ate pizza before bed (unhealthy) - took four Rolaids initially - didn't bring any relief - sitting made the pressure settle down - he was clammy - pressure on his chest persistently for approximately two hours - put on oxygen mask - nurses concerned about his EKG - EKG showed 1 cm ST elevation on leads V2,3,4,5 with slight ST depression on leads 2,3 and AVF Physical Examination: - heart rate was 110 (high heart rate) - respiratory rate was 22 (high respiratory rate. Should be 16-20) - blood pressure was 160/100 (high bp) - sweaty, pale, and had no obvious jugular venous distention - chest was clear on auscultation - abdomen was unremarkable - skin was slightly sweaty - chest x-ray was normal with normal heart size - lab work was normal Research: Heart Problems - closely linked to diet and lifestyle choices ...
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...Cardiovascular Case Study Mr. Smith is a 56-year-old Caucasian man who is being evaluated in the emergency room with progressively worsening chest pain that began 2 hours ago. The patient describes the pain as pressure in the center of his chest. He rates his pain 7/10. He reports the pain is now radiating down his left arm and through to his back, he is diaphoretic, and complaining of shortness of breath. He denies nausea or vomiting. Mr. Smith reports no previous history of chest pain or pressure. He smoked one pack of cigarettes daily for 13 years but quit smoking last year. He denies a family history of heart disease. Upon initial examination he did not have jugular venous distension, no carotid bruits, normal S1 and S2 with an S3 present. No S4 or murmurs auscultated. Lung sounds clear to auscultation bilaterally, bowel sounds normal, all pulses palpable 2+/4, no edema present. Diagnostic data: BP: 165/98 mmHG HR: 96 bpm RR: 30 breaths/min Temp: 37 C SaO2: 96% with 2L/min O2 per nasal cannula Wt:100 kg A 12-lead ECG was performed in the emergency room showed: Normal Sinus Rhythm (NSR) with frequent premature ventricular contractions. ST segment elevation in Leads 1, aVL, and V2 through V6 (3mm). ST segment depression in Leads III and aVF. Q waves in V2 through V4. The chest X-ray revealed slight cardiomegaly with mild congestive heart failure. An echocardiogram reveals an ejection fraction of 30% and mild mitral valve regurgitation. Mr. Smith’s...
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...2008, 12:R36 (doi:10.1186/cc6815) This article is online at: http://ccforum.com/content/12/2/R36 © 2008 Lim et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction To use screening cardiac troponin (cTn) measurements and electrocardiograms (ECGs) to determine the incidence of elevated cTn and of myocardial infarction (MI) in patients admitted to the intensive care unit (ICU), and to assess whether these findings influence prognosis. This is a prospective screening study. Materials and methods We enrolled consecutive patients admitted to a general medical-surgical ICU over two months. All patients underwent systematic screening with cTn measurements and ECGs on ICU admission, then daily for the first week in ICU,...
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...Beta Blockers After Myocardial Infarction Clinical Scenario The acute care nurse practitioner on the cardiology service treats a 67 year-old-male admitted after recovering from an acute ST-Elevation Myocardial Infarction (STEMI). His risk factors include obesity, Type II diabetes mellitus, and family history. Upon exam the patient asks why he has not been started on a beta blocker yet. He explains further that when his brother had a “heart attack” in 2005, he was immediately placed on a beta blocker because the cardiologist reported how beta blockers reduce mortality after myocardial infarction (MI). The patient wants to know if a beta blocker would reduce his chance of mortality? Using the Patient-Intervention-Comparator-Outcome (PICO) format we formulated the following question. In a 67-year-old male with multiple co-morbidities with MI (P), does treatment with a beta blocker (I), compared with no beta blocker or placebo (O), reduce mortality rate (O)? Risk Factors, Incidence and Prevalence of Disease * US incidence rates of cardiovascular disease, including MI, are seen in men more than women (Alexander et al., 2007). This trend is also true in Utah ("Impact of heart," 2007). * The incidence rates of cardiovascular disease increase with age (Alexander et al., 2007). * Risk factors for cardiovascular disease include not eating enough fruits and vegetables, lack of physical exercise, smoking cigarettes and the co-morbidities of diabetes, hypertension, hyperlipidemia...
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...The Role of Technology in Rising Health Care Costs. What should or shouldn’t be done. Neha Para, MPH Student 5453-001 US Health Care System University of Oklahoma Health Sciences Center December 8, 2010 Abstract Health care costs are a longstanding concern to policymakers. For years, health care spending has been rising faster than the rate of economic growth, raising the question of what factors are responsible for rising health care costs. This paper explores published articles that report results from research conducted on technological innovations in health care and its relation to rising health care costs. The cost increases have a significant effect on households, businesses, and government programs. Health care experts indicates the development and diffusion of medical technology as primary factors in explaining the persistent difference between health spending and overall economic growth, with some arguing that new medical technology may account for about one-half or more of real long-term spending growth. Rising health care expenditures lead to the question of whether we are getting value for the money we spend. On an average, increases in medical spending as a result of advances in medical care have provided reasonable value. An alternative viewpoint holds that although new technologies represent medical advances, they are prone to overuse and thereby excess cost. Most of the suggestions to slow the growth in new medical technology in the U.S. focus on...
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...infection control and hospital epidemiology march 2014, vol. 35, no. 3 original article Ventilator-Associated Pneumonia: Overdiagnosis and Treatment Are Common in Medical and Surgical Intensive Care Units Veronique Nussenblatt, MD, MHS;1 Edina Avdic, PharmD, MBA;2 Sean Berenholtz, MD, MHS;3,4 Elizabeth Daugherty, MD, MPH;5 Eric Hadhazy, MS;1 Pamela A. Lipsett, MD, MHPE;3,4 Lisa L. Maragakis, MD, MPH;1 Trish M. Perl, MD, MSc;1 Kathleen Speck, MPH;3 Sandra M. Swoboda, RN, MS;3 Wendy Ziai, MD;3,6 Sara E. Cosgrove, MD, MS1 objective. Diagnosing ventilator-associated pneumonia (VAP) is difficult, and misdiagnosis can lead to unnecessary and prolonged antibiotic treatment. We sought to quantify and characterize unjustified antimicrobial use for VAP and identify risk factors for continuation of antibiotics in patients without VAP after 3 days. methods. Patients suspected of having VAP were identified in 6 adult intensive care units (ICUs) over 1 year. A multidisciplinary adjudication committee determined whether the ICU team’s VAP diagnosis and therapy were justified, using clinical, microbiologic, and radiographic data at diagnosis and on day 3. Outcomes included the proportion of VAP events misdiagnosed as and treated for VAP on days 1 and 3 and risk factors for the continuation of antibiotics in patients without VAP after day 3. results. Two hundred thirty-one events were identified as possible VAP by the ICUs. On day 1, 135 (58.4%) of them were determined to not have VAP...
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