{"id":5101,"date":"2011-09-06T15:55:28","date_gmt":"2011-09-06T15:55:28","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5101.htm\/"},"modified":"2014-12-28T23:35:21","modified_gmt":"2014-12-29T04:35:21","slug":"heart-failure-acute-pulmonary-edema","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/medical-surgical\/cardiology\/heart-failure-acute-pulmonary-edema.htm\/","title":{"rendered":"Heart Failure"},"content":{"rendered":"

<\/span>Heart Failure (Dropsy, Hydropsy)<\/span><\/h2>\n

<\/span>APE<\/span><\/h2>\n

best review by Hermann<\/a><\/p>\n

\"\"<\/a>\"\"<\/a><\/p>\n

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evidence based guidelines for patients with acute decomp heart failure (Crit Care Med 2008;36(Suppl):S129<\/a>)<\/p>\n

\"\"<\/a>\"\"<\/a>\"\"<\/a>\"\"<\/a><\/p>\n

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Ejection fraction most important determinant<\/p>\n

Pt\u0092s c APE may still be intravascularly depleted<\/p>\n

Always think valvular problem in new CHF<\/p>\n

Always think valve thrombosis in CHF with a prosthetic valve<\/strong><\/p>\n

Do not give vasodilators in AS, but yes in MR<\/p>\n

***A-Line in CHF c decreased CO (cuff bp more representative of mean than systolic)***<\/p>\n

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Decline in cardiac output leads to increased sympathetic tone, increased peripheral resistance (afterload), and increased renin\/angiotensin\/aldosterone axis.<\/p>\n

Review: Postgrad Med 103:2, 1998<\/strong><\/p>\n

Retrospective Study:\u00a0 Am J EM 17:6<\/strong><\/p>\n

<\/span>X-Rays<\/strong><\/span><\/h3>\n

VPW>70 and CTR>.55 has good correlation with PAOP>18 (Chest 122:6, Dec 2002)<\/p>\n

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but small heart does not mean no heart failure (Eur J Heart Fail 5:117, March 2003)<\/p>\n

High Dose Nitro Drip<\/h4>\n

Start at 50 mcg\/min, can rapidly titrate to 200-400 mcg\/min. You must<\/strong> stand at the bedside to use these doses.<\/p>\n

Need >120 mcg\/min to get sig decreased PCWP(Am J Cardio 2004;93:237)<\/p>\n

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Nitro Bolus<\/h4>\n

is very effective, give 0.8 mg over 2 minutes=400 mcg\/min for 2 minutes.\u00a0 (Annals EM 1997, 30:382<\/a>) and (Am J Emerg Med;1995;13(5):612)<\/p>\n

Run normal drip setting (10 mcg\/min=3cc\/hr) at 120 cc\/hr for 2 minutes to get same dose.<\/p>\n

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High dose nitroglycerin for severe decompensated heart failure–2mg at a time (Ann Emerg Med 2007;50:144)<\/p>\n

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Low nitrates c high lasix vs., the opposite, shows nitrates more effective (Lancet 1998 351:389-393)<\/p>\n

BP lowering as long as the patient can mentate, ambulate, and urinate.<\/p>\n

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Cotter gave isosorbide 3 mg q 5 minutes with good results in his study.\u00a0 This is equivalent to nitro 600 mcg\/min. (Lancet 1998 351:9100, 389-393)<\/p>\n

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The Feasibility of Treating Severe Acute Congestive Heart Failure With Bolus Intravenous Nitroglycerin Zalenski RJ, Levy P, Compton S, Delgado G, Welch R, Waselewsky D\/Wayne State University, Detroit Receiving Hospital, Detroit, MI Study objectives: Bolus intravenous nitroglycerin is a potential innovation for the management of severe acute decompensated heart failure (ADHF) but has undergone limited clinical evaluation. Although previous studies have demonstrated improved outcomes, the effect of adding bolus intravenous nitroglycerin to standard American Heart Association (AHA) treatment of severe ADHF has not been defined. Our primary objective is to evaluate the feasibility of using this novel therapeutic approach in the management of severe ADHF. Secondary objectives include an assessment of the safety and efficacy of bolus intravenous nitroglycerin. Methods: This study was designed as an unblinded pilot intervention trial of the addition of bolus intravenous nitroglycerin to standard AHA treatment for ADHF. The eligible study population included all adult patients (age $18 years) presenting to the emergency department of Detroit Receiving Hospital (Detroit, MI: annual census ;85,000) or Sinai-Grace Hospital (Detroit, MI: annual census ;62,000) with a clinical diagnosis of acute cardiogenic pulmonary edema. The prespecified goal was to enroll 30 patients. The main inclusion criterion was a systolic blood pressure of 160 mm Hg or greater or a mean arterial pressure of 120 mm Hg or greater. Patients with a suspected or proven right ventricular infarction, known or suspected pregnancy, or a history of intolerance to nitroglycerin and those requiring immediate intubation or cardiopulmonary resuscitation were excluded. The study was approved by the institutional review board of Wayne State University, and written informed consent was obtained from all patients (or proxy) before initiation of the protocol. On enrollment, baseline hemodynamic values and a serum brain natriuretic peptide level were obtained. Initial treatment of all patients consisted of 100% oxygen (by nonrebreather), 3 doses of sublingual nitroglycerin (0.4 mg), and intravenous furosemide (60 to 100 mg). Administration of morphine sulfate (3 to 5 mg) was permitted but not encouraged. Patients without improvement were then started on the intervention protocol, which included initiation of a nitroglycerin infusion (0.3 to 0.5 mg\/kg per minute) with concurrent administration of a dose of bolus intravenous nitroglycerin (2 mg). Titration of the infusion (#400 mg\/min) and repeated dosing of bolus intravenous nitroglycerin (2 mg) was allowed every 3 to 5 minutes, up to a total of 10 doses, at the discretion of the treating physician. Ventilatory assistance with endotracheal intubation or biphasic positive airway pressure and administration of additional pharmacologic therapy was permitted at any point at the discretion of the treating physician. The primary efficacy endpoint was rate of endotracheal intubation. Secondary efficacy endpoints included the need for ICU admission and total hospital length of stay. Primary safety endpoints included the incidence of cardiac or neurovascular complications and symptomatic hypotension. Descriptive statistics are provided. Results: Twenty-eight patients were enrolled. Mean age was 61.57 years (615.01 years); 89.3% were black and 64.3% were men; 89.3% had a history of heart failure, 92.9% had hypertension, and 35.7% had coronary artery disease; 76.5% were noted with New York Heart Association heart failure classification III or IV, and the median brain natriuretic peptide level was 1,849 pg\/mL. Baseline vital signs (mean6SD) were as follows: mean arterial pressure 155.11 mm Hg (623.49 mm Hg); pulse rate 114.93 beats\/min (624.85 beats\/min), and respiratory rate 31.07 breaths\/min (66.77 breaths\/min). Mean protocol intervention time was 18.21 minutes (614.97 minutes). Symptom improvement was reported in 24 patients (85.7%). Mean dosing of bolus intravenous nitroglycerin was 6.50 mg (63.47 mg). Mean nitroglycerin infusion rate was 38.82 mg\/min (628.04 mg\/min), and mean intravenous furosemide was 85.00 mg (624.11 mg). Other administered medications included morphine (11 patients), angiotensin-converting enzyme inhibitors (10 patients), and b-blockers (3 patients). Patients were monitored for a mean period of 75.46 minutes (669.84). During this time, significant reductions from baseline vital signs were noted (mean D [95% confidence interval (CI)]: pulse ANNALS OF EMERGENCY MEDICINE 4 4 : 4 OCTOBER 2004<\/p>\n

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ACEI<\/h4>\n