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8 results

  • 4.5 - Fluids, Inotropes and Vasopressors, Vasodilators and Anti-hypertensives

  • from Section 4 - Therapeutic Interventions and Organ Support
  • Edited by Ned Gilbert-Kawai, The Royal Liverpool Hospital, Debashish Dutta, Princess Alexandra Hospital NHS Trust, Harlow, Carl Waldmann, Royal Berkshire Hospital, Reading
  • Book:
    Intensive Care Medicine
    Published online:
    27 July 2023
    Print publication:
    01 December 2021, pp 477-491

  • Summary

    Key Learning Points

    1. 1. Try to avoid high chloride-containing solutions as they worsen peri-operative outcomes and, in particular, can cause acute kidney injury.

    2. 2. There is currently no evidence to support the use of albumin over crystalloids.

    3. 3. Multiple studies have found no evidence of superiority of early goal-directed therapy with dobutamine.

    4. 4. Bicarbonate will denature inotropes if infused together.

    5. 5. Beta-blocker initiation should be used cautiously in the critical care population but may have benefit in the sickest patients.

  • Chapter 15 - Prevention of Stroke by Lowering Blood Pressure

  • from Part V - Prevention
  • Edited by Jeffrey L. Saver, Graeme J. Hankey, University of Western Australia, Perth
  • Book:
    Stroke Prevention and Treatment
    Published online:
    15 December 2020
    Print publication:
    10 December 2020, pp 289-296

  • Summary

    For hypertensive patients without prior stroke, TIA, or other symptomatic vascular disease, anti-hypertensive therapy reducing SBP by 10 mm Hg, is associated with reductions in recurrent stroke (by about one-quarter) and of combined stroke, MI, and vascular death (by about one-fifth). Benefit extends across all ages, race-ethnicities, and pathological stroke subtypes. Combined pharmacological and non-pharmacological therapy to lower blood pressure is indicated in all individuals with SBP> 140 or DBP> 90, and in individuals with SBP 130–139 or DBP 80–89 who have additional vascular risk factors. Non-pharmacological blood pressure lowering is indicated in individuals with SBP 130–139 or DBP 80–89 without important additional vascular risk factors. After an ischaemic stroke or TIA, treatment may be gradually started as early as 24–72 hours after onset. The absolute benefits of antihypertensive therapy increase with greater reductions in BP, and are higher for preventing recurrent stroke than for preventing MI, in both primary and secondary prevention. The degree of BP reduction more greatly influences vascular event prevention than does pharmacological agent class. Nonetheless, unless otherwise indicated, beta-blockers are not a preferred agent, as they show less efficacy for stroke prevention. Calcium channel antagonists, ACE inhibitors, and thiazide diuretics are particularly well-studied.

  • 49 - Disseminated intravascular coagulation and thrombotic thrombocytopenic purpura/hemolytic uremic syndrome

  • from Section 8 - Hematology–oncology emergencies
  • Edited by Kaushal Shah, Jarone Lee, Kamal Medlej, American University of Beirut, Scott D. Weingart
  • Book:
    Practical Emergency Resuscitation and Critical Care
    Published online:
    05 November 2013
    Print publication:
    24 October 2013, pp 330-336

  • Summary

    This chapter discusses the diagnosis, evaluation and management of gastrointestinal bleeding including upper gastrointestinal bleeding (UGIB) and lower gastrointestinal bleeding (LGIB). It describes the special circumstances with regard to aortoenteric fistula, liver disease, and Jehovah's Witnesses. In UGIB, patients typically present with hematemesis, coffee-ground emesis, and/or melena. In LGIB, patients typically present with bright red blood per rectum (BRBPR), also known as hematochezia. Higher severity of disease is indicated by signs of shock such as hypotension, tachycardia, altered mental status (AMS), decreased urine output (UOP), cool skin, syncope, orthostasis. Change in pulse with posture is more sensitive than hypotension, but may be masked by medications (e.g., beta-blockers). Hypotension, tachycardia, and tachypnea can indicate hemorrhagic shock and requires immediate treatment. Massive transfusion protocols are helpful for significant bleeding in order to prevent further coagulopathy due to transfusion of high volume of crystalloid or only red cells.

  • A systematic review of the pharmacological management of aortic root dilation in Marfan syndrome

  • Varsha Thakur, Kathryn N. Rankin, Lisa Hartling, Andrew S. Mackie
  • Journal:
    Cardiology in the Young / Volume 23 / Issue 4 / August 2013
    Published online by Cambridge University Press:
    19 October 2012, pp. 568-581
  • Background

    Marfan syndrome causes aortic dilation leading to dissection and death. This systematic review examined the use of beta-blockers, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blockers in the management of aortic dilation in this disease.

    Methods

    We searched four databases – Medline, EMBASE, Web of Science, and The Cochrane Central Register of Controlled Trials – two conference proceedings, references of retrieved articles, and a web-based trial registry. The primary outcome was mortality. The secondary outcomes were aortic dissection, need for elective surgical repair, change in aortic dilation, and adverse events. Two reviewers selected studies, abstracted data, and assessed study quality. Meta-analyses were not performed because of study heterogeneity.

    Results

    A total of 18 studies were included – 12 completed and six in progress. Of the completed studies, three before-and-after treatment, one prospective cohort, three retrospective cohorts, and two randomised control trials examined beta-blockers; one randomised and one non-randomised trial examined angiotensin-converting enzyme inhibitors; and one retrospective cohort study examined angiotensin II receptor blockers. Studies in progress are all randomised trials. Mortality was not impacted by drug therapy, although studies were underpowered with respect to this outcome. All drug classes were associated with a decrease in the rate of aortic dilation (angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers >beta-blockers); none had an impact on other secondary outcomes.

    Conclusions

    On the basis of existing evidence, beta-blockers, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blockers slow the progression of aortic dilation in Marfan syndrome. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers may have more effect than beta-blockers; however, more methodologically rigorous studies currently in progress are needed to evaluate the impact of drug therapy on clinical outcomes.

  • Neuropathy – phantom limb pain

  • from Chief complaints and diagnoses
  • Edited by Stephen H. Thomas
  • Book:
    Emergency Department Analgesia
    Published online:
    18 December 2009
    Print publication:
    25 September 2008, pp 301-305

  • Summary

    The ED physician frequently encounters patients with migraine headache (MH). The ergot alkaloids, available in myriad formulations, are among the oldest drugs used for MH. Clinicians noted that MH pain was often alleviated before the real analgesic was administered by prompting interest in the use of antiemetics as stand-alone therapy. Like the antiemetics, the triptans are useful in myriad benign headache syndromes. Clinical trial evidence from the ED demonstrates sumatriptan's equal efficacy in migraine, probable migraine, and tension-type headaches. Controlled trials demonstrate efficacy of multiple NSAIDs for MH pain. Among those drugs performing better than placebo are aspirin, ibuprofen, tolfenamic acid, diclofenac, and naproxen. Despite their non-specific mechanism of action, opioids are frequently used for MH. Prophylactic medications that may have ED utility in the earliest stages of migraine include the beta-blockers (e.g. metoprolol, propranolol) and the calcium channel blockers.

  • Fibromyalgia

  • from Chief complaints and diagnoses
  • Edited by Stephen H. Thomas
  • Book:
    Emergency Department Analgesia
    Published online:
    18 December 2009
    Print publication:
    25 September 2008, pp 204-212

  • Summary

    The extensive use of short-term oxygen therapy in acute coronary syndrome (ACS), with rarely reported adverse effects and frequent cases of anecdotal benefit, supports oxygen administration as benign intervention for cardiac patients with pain and subnormal peripheral pulse oximetry. The pain of ACS is effectively decreased by beta-blockers. Though their exact analgesia mechanism is not known, there are several possible routes by which beta-blockers could reduce pain. Nitrates dilate the epicardial coronary arteries, their collaterals, and peripheral vessels, thus improving coronary perfusion and potentiating a favorable ratio of subendocardial-to-epicardial flow. Opioids have long been a part of the ACS treatment armamentarium. Due to its properties as a pulmonary venodilator and anxiolytic, morphine has been the analgesic of choice for ACS pain. Intravenous benzodiazepines should be used for patients with cocaine-associated cardiac chest pain. In this population, the risk of vasospasm from beta-blockers is such that these agents should be avoided.

  • 12 - Prevention of coronary heart disease in women

  • from Part III - Disease prevention
  • Edited by Jo Ann Rosenfeld, The Johns Hopkins University
  • Book:
    Women's Health in Mid-Life
    Published online:
    21 August 2009
    Print publication:
    25 March 2004, pp 209-224

  • Summary

    Cardiovascular disease (CVD) is the major cause of death in women in the USA and in the UK. The actual value of the risk factors is used to predict coronary heart disease (CHD) risk more accurately. Primary prevention should focus on the major risk factors of passive and active smoking, systolic and diastolic hypertension, elevated serum total and low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, diabetes, physical inactivity, and obesity. The pillars of secondary prevention are antiplatelet therapy, beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), statins, cardiac rehabilitation, a Mediterranean diet, and folic acid. Future heart attacks are prevented by the prevention of atherosclerosis or plaque formation in the coronary arteries and by the stabilization and regression of existing plaque through lifestyle modification and medication. Women must take personal preventive action to prevent CHD death and disability by working to prevent plaque formation, and promote stabilization of existing atherosclerotic disease.