Heart Failure (Dropsy, Hydropsy)Back to top
evidence based guidelines for patients with acute decomp heart failure (Crit Care Med 2008;36(Suppl):S129)
Ejection fraction most important determinant
Pts c APE may still be intravascularly depleted
Always think valvular problem in new CHF
Always think valve thrombosis in CHF with a prosthetic valve
Do not give vasodilators in AS, but yes in MR
***A-Line in CHF c decreased CO (cuff bp more representative of mean than systolic)***
Decline in cardiac output leads to increased sympathetic tone, increased peripheral resistance (afterload), and increased renin/angiotensin/aldosterone axis.
Review: Postgrad Med 103:2, 1998
Retrospective Study: Am J EM 17:6
VPW>70 and CTR>.55 has good correlation with PAOP>18 (Chest 122:6, Dec 2002)
but small heart does not mean no heart failure (Eur J Heart Fail 5:117, March 2003)
High Dose Nitro Drip
Start at 50 mcg/min, can rapidly titrate to 200-400 mcg/min. You must stand at the bedside to use these doses.
Need >120 mcg/min to get sig decreased PCWP(Am J Cardio 2004;93:237)
is very effective, give 0.8 mg over 2 minutes=400 mcg/min for 2 minutes. (Annals EM 1997, 30:382) and (Am J Emerg Med;1995;13(5):612)
Run normal drip setting (10 mcg/min=3cc/hr) at 120 cc/hr for 2 minutes to get same dose.
High dose nitroglycerin for severe decompensated heart failure–2mg at a time (Ann Emerg Med 2007;50:144)
Low nitrates c high lasix vs., the opposite, shows nitrates more effective (Lancet 1998 351:389-393)
BP lowering as long as the patient can mentate, ambulate, and urinate.
Cotter gave isosorbide 3 mg q 5 minutes with good results in his study. This is equivalent to nitro 600 mcg/min. (Lancet 1998 351:9100, 389-393)
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
- Captopril SL (12.5-25 mg) (Current Ther Res 1991 29:2) (Acad Emerg Med 3:3, 1996) (Crit Care Med 23:5, 1995) (Int J Cardio 27:3, p.351)
- Enalapril 1.25-2.5 mg (Circulation 94:6, 1996)
ACEI best (tested SL Captopril) (Sacchetti AM J Emerg Med Oct 1996 17 (6))
Do not help and may cause further decline in the acute phase of APE (J Am Soc Nephrol 4:2, 1993) (Am J Med 96:3, 1994)
Vasoconstrictor Response initially by IV furosemide (Ann Intern Med 1985; 103:1-6)
Worsening of outcome when used in prehospital setting (Chest. 1987; 92:586-593)
Head to head nitrites vs. furosemide (Lancet 1983;i:730-32)
Typically requires high dose diuretics Indirect effects of diuretics may be counterproductive Increase neurohormonal activation 1,2 Reflex vasoconstriction, ↓ cardiac output 1 Worsening of renal function 3 1. Francis GS, et al. Ann Int Med. 1985;103:1-6. 2. Bayliss J, et al. Br Heart J. 1987; 57:17-22. 3. Mehta RL, et al. JAMA. 2002;288:2547-2553
Consider furosemide infusion at 20-40 mg/hr
after the first hour of treatment.
Vasodilatory effect of loop diuretics Vasodilation is mediated through prostaglandins Effect is blunted in patients taking ASA Majority of HF patients take ASA because of concomitant CAD
Jhund PS, et al. J Am Coll Cardiol. 1999;33:572-575
Increases ICU admits (Am J EM 17:6 571-574)
When given in prehospital, results in deterioration and subjective increase in distress (Chest 92:4, 1987)
Not very effective. (J Am Coll Cards 2002, 39:798-803)
Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. SO – JAMA 2002 Mar 27;287(12):1531-40. CONTEXT: Decompensated congestive heart failure (CHF) is the leading hospital discharge diagnosis in patients older than 65 years. OBJECTIVE: To compare the efficacy and safety of intravenous nesiritide, intravenous nitroglycerin, and placebo. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind trial of 489 inpatients with dyspnea at rest from decompensated CHF, including 246 who received pulmonary artery catheterization, that was conducted at 55 community and academic hospitals between October 1999 and July 2000. INTERVENTIONS: Intravenous nesiritide (n = 204), intravenous nitroglycerin (n = 143), or placebo (n = 142) added to standard medications for 3 hours, followed by nesiritide (n = 278) or nitroglycerin (n = 216) added to standard medication for 24 hours. MAIN OUTCOME MEASURES: Change in pulmonary capillary wedge pressure (PCWP) among catheterized patients and patient self-evaluation of dyspnea at 3 hours after initiation of study drug among all patients. Secondary outcomes included comparisons of hemodynamic and clinical effects between nesiritide and nitroglycerin at 24 hours. RESULTS: At 3 hours, the mean (SD) decrease in PCWP from baseline was -5.8 (6.5) mm Hg for nesiritide (vs placebo, P<.001; vs nitroglycerin, P =.03), -3.8 (5.3) mm Hg for nitroglycerin (vs placebo, P =.09), and -2 (4.2) mm Hg for placebo. At 3 hours, nesiritide resulted in improvement in dyspnea compared with placebo (P =.03), but there was no significant difference in dyspnea or global clinical status with nesiritide compared with nitroglycerin. At 24 hours, the reduction in PCWP was greater in the nesiritide group (-8.2 mm Hg) than the nitroglycerin group (-6.3 mm Hg), but patients reported no significant differences in dyspnea and only modest improvement in global clinical status. CONCLUSION: When added to standard care in patients hospitalized with acutely decompensated CHF, nesiritide improves hemodynamic function and some self-reported symptoms more effectively than intravenous nitroglycerin or placebo.
Not that I have anything against the industry or anything, but an interesting twist has twisted in the ‘life after death’ aftemath of the Nesiritide scandal. A study designed and funded by Scios for the purpose of addressing the furor that followed the publication of a provocative meta-analysis in JAMA (2005;293:1900-1905) has now been published in J Emerg Med (2005; 29:243-252). The JAMA SR reported a RR for death, nesiritide compared to control, of 1.7 (95% CI 0.97, 3.1), just missing statistical significance. The JEM study reported an all-cause mortality rate of 5/120 (4%) in the nesiritide group and 1/117 (1%) in the standard care group with a resulting p value of 0.213 (also not significant). Now, as reported in our own ACEP News of February 2006, it turns out that 2 extra deaths, both in the nesiritide group, were first lost, and now found (Funny how things happen). This would convert the death toll to 7/120 nesiritide versus 1/117 in the control. ACEP News reports that both the PI on the study and a Scios spokesman ‘downplayed’ the ‘significance’ of the two additional deaths, emphasizing that one died of CO poisoning and the other in a traffic accident. This raises an interesting issue- all cause versus disease specific mortality. The stakes are a bit high. Whatever the PI and the Scios rep mean by ‘significance’, it is apparently not to do with statistical significance. A quick visit to the useful online free access calculator site (http://members.aol.com/johnp71/ctab2x2.html) reveals that when the new numbers are plugged into a standard formula we have a RR for death, nesiritide compared to control, of 6.8 I(95% CI 1.1, 42). In short, accepting these results, we now have a statistically significant increase in all cause death in patients treated with nesiritide. So the issue is all-cause mortality. Should we reject the deaths of the 2 extra patients in the nesiritide as ‘insignificant’. One might speculate that they were probably not ‘insignificant’ to the patients and their families, particularly considering that one was functional enough to be taking a ride in a car or walking across the street and the other perhaps being poisoned in a car or in a closed space running a fuel driven device. One might also speculate that perhaps one drifted off due to uremic encephalopathy due to after effects of nesiritide (which another SR, published in Circulation, showed worsened renal function) and that the other collapsed from flash pulmonary edema while driving. Speculative certainly. However, the fantasies illustrate why all cause mortality is actually the preferred outcome with respect to adverse effects of drugs. When looking at direct effects of drugs, disease specific mortality may have a case for preference. For example, screening mammography may effectively and significantly lower mortality from breast cancer without altering all cause mortality, simply because most women do not die from breast cancer. However, when the effect is statistically significant and when ‘wild card’ consequences of adverse effects pertain, all cause mortality wins all. Again, this is just for teaching purposes. Purely objective science…. Peter
Another negative nesiritide study (Ann Emerg Med 2008;51:571)
Lancet 356:2126, December 23/30, 2000
Systematic Review (Ann Emerg Ned 2006;48:260)
Eur Heart Journal 2002, 23:1379
In one study (Emerg Med J 2004; 21:155-161) survival to hospital discharge was improved with CPAP (10 mm/Hg) over BiPap (Ipap 15 Epap 5) and conventional therapy.
CPAP was just as good as PSV (Intens Care Med 2005;31:807)
New York Heart Association Classification
Class Functional state Symptoms
I No limitation Asymptomatic during usual daily activities
II Slight limitation Mild symptoms (dyspnea, fatigue, or chest pain) with
ordinary daily activities
III Moderate limitation Symptoms noted with minimal activity
IV Severe limitation Symptoms at rest
Common Precipitants Of CHF Decompensation
Dietary indiscretion (salt)
Acute valvular dysfunction
Pulmonary and other infections
Administration of inappropriate medications (e.g., negative inotropes)
Substantial subset of elderly pts presenting with CHF have near-normal LV systolic function and their underlying cause may be dysrhythmia, ischemia, or valvular abnormalities. Early echo should be considered. (Am J Med Sci 323(5), 2002)
decreased ventricular distensibility
Multicenter rct showed better avoidance of intubation and resolution of symptoms (Intensive Care Med (2011) 37:15011509)Back to top
Use cut off of 100 pg/ml. Not much different than cardiomegaly on C-XR
(N Engl J Med 347(3):161, July 18, 2002 manufacturer funded)
B-type Natriuretic Peptide as a Marker for CHF
The symptoms and signs of heart failure are neither sensitive nor specific and considerably overlap those of pulmonary disease. B-type natriuretic peptide (BNP) is a polypeptide secreted by the cardiac ventricles in response to myocyte stretch, resulting from ventricular volume expansion and pressure overload. BNP levels are elevated in patients with left ventricular dysfunction, and the levels correlate with both the severity of symptoms and the prognosis.
In the largest study to date, the Breathing Not Properly Multinational Study, BNP levels were more accurate than any historical or physical finding or laboratory value in identifying heart failure as the cause of dyspnea. The diagnostic accuracy of BNP at a cutoff value of 100 pg/ml was 83%, with a sensitivity of 90% and a specificity of 76% (1,2).
There is a high negative predictive value of a low level of BNP with respect to the diagnosis of heart failure. A BNP level below 100 pg/ml in a patient with acute dyspnea makes the diagnosis of heart failure very unlikely and can help clinicians focus on alternative diagnoses, whereas a level above 500 pg/ml makes the diagnosis of CHF highly likely. For intermediate levels, use of clinical judgment and adjunctive testing are encouraged (4).
It should be noted that in patients with severe renal disease, B-type natriuretic peptide levels are increased. Therefore, higher cutoff values need to be identified for this important patient population.
(1) Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161-167.
(2) McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002;106:416-422.
(3) Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004;350:647-654.
(4) Mark, D. B., Felker, G. M. (2004). B-Type Natriuretic Peptide — A Biomarker for All Seasons?. N Engl J Med 350: 718-720
Comparison of BNP vs. ECHO. (J Am Coll Card 40(10):1794, Nov 20,2002) Use <80 no CHF, >300 CHF, in between grey zone. BNP 12% missed, physical exam 15% miss.
Remember that either ventricle failing will produce BNP so any patient with cor pulmonale from copd will also have elevated bnps.
Anterior Q waves or Left BBB both have specificity of ~90% but lack sensitivity (Ann Emerg Med 41:4, April 2003)
B-type is so named because it was first isolated from porcine brains, mostly secreted from ventricles.
Patients with PE can have levels from 200-300 (Ibid) COPDers with cor pulmonale can have levels of 300-600 (Ibid)
New NEJM study (N Engl J Med 2004 Feb 12)
I use the BNP both to rule in and to rule out CHF. So, in the example of the patient who has chronic lung disease and who has rales that might be “wet” or “dry” and a chest x-ray that shows interstitial markings that could represent fibrosis or fluid (and no priors for comparison, of course): a BNP less than 100 satisfies me that the patient probably does not have CHF, while one greater than 500 (or, better yet, 1,000) strongly suggests that the patient does, indeed, have CHF. Values between 100 and 500 are not very useful. Although our lab reports the results with a cut-off of 100 between normal and abnormal, I consider values between 100 and 500 to be indeterminate.
Patient Oriented Evidence on BNP
Less than 100 no CHF, >500 definitely CHF, in between use clinical judgment
Knowing the level of B-type natriuretic peptide during initial evaluation in the emergency department is associated with more rapid initiation of appropriate treatment, less needfor hospitalization and intensive care, a shorter length ofstay, and lower costs. The next question is whether the BNPcan replace other tests like the chest x ray or echocardiogramfor some patients. (Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriureticpeptide in the evaluation and management of acute dyspnea. NEngl J Med 2004;350: 647-54) and POEM (BMJ 2004;328 (29 May))
There us a delay of several hours after onset of symptoms before excess BNP is produced
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Data Synthesis Many features increased the probability of heart failure, with the best feature for each category being the presence of (1) past history of heart failure (positive LR = 5.8; 95% confidence interval [CI], 4.1-8.0); (2) the symptom of paroxysmal nocturnal dyspnea (positive LR = 2.6; 95% CI, 1.5-4.5); (3) the sign of the third heart sound (S3) gallop (positive LR = 11; 95% CI, 4.9-25.0); (4) the chest radiograph showing pulmonary venous congestion (positive LR = 12.0; 95% CI, 6.8-21.0); and (5) electrocardiogram showing atrial fibrillation (positive LR = 3.8; 95% CI, 1.7-8.8). The features that best decreased the probability of heart failure were the absence of (1) past history of heart failure (negative LR = 0.45; 95% CI, 0.38-0.53); (2) the symptom of dyspnea on exertion (negative LR = 0.48; 95% CI, 0.35-0.67); (3) rales (negative LR = 0.51; 95% CI, 0.37-0.70); (4) the chest radiograph showing cardiomegaly (negative LR = 0.33; 95% CI, 0.23-0.48); and (5) any electrocardiogram abnormality (negative LR = 0.64; 95% CI, 0.47-0.88). A low serum BNP proved to be the most useful test (serum B-type natriuretic peptide <100 pg/mL; negative LR = 0.11; 95% CI, 0.07-0.16). Conclusions For dyspneic adult emergency department patients, a directed history, physical examination, chest radiograph, and electrocardiography should be performed. If the suspicion of heart failure remains, obtaining a serum BNP level may be helpful, especially for excluding heart failure.Back to top
Hypomagnesemia very common in CHF and can cause dysrhythmia. Check Mg or empirically replace if there are dysrhythmias (Eur J Heart Failure 4:167 2002)
yes you can get APE just from swimming (Annals EM 41:2, 2003)
Unilateral Pulmonary Edema Common teaching states that a unilateral alveolar or interstitial infiltrate is most likely a result of pneumonia, and not pulmonary edema. However, unilateral pulmonary edema has been well documented, and can result from a myriad of causes. Described causes of unilateral pulmonary edema include congestive heart failure (1), severe mitral valve insufficiency (2), upper airway obstruction (3), pulmonary artery compression from aortic dissection (4,5), pulmonary venous obstruction from mediastinal fibrosis (6) neurogenic pulmonary edema (7), and amiodarone-related (8) and heroin-related (9) pulmonary edema. Thus, even if the pulmonary opacities are unilateral – and even though radiology may read the x-ray as exhibiting llikely pneumonia – if the clinical manifestation is compatible with pulmonary edema and not with pneumonia, early and aggressive treatment should be initiated for pulmonary edema. References: (1) Nitzan O, et al. Unilateral pulmonary edema: a rare presentation of congestive heart failure Am J Med Sci 2004;327:362364. (2) Legriel S, et al. Unilateral pulmonary edema related to massive mitral insufficiency Am J Emerg Med 2006;24: 372. (3) Morisaki H, et al. Unilateral pulmonary edema following acute subglottic edema J Clin Anesth 1990;2: 4244. (4) McTigue C, et al. Unilateral pulmonary edema associated with pulmonary arterial compression Australas Radiol 1988;32: 390393. (5) Takahashi M, et al. Unilateral pulmonary edema related to pulmonary artery compression resulting from acute dissecting aortic aneurysm Am Heart J 1993;126: 12251227. (6) Routsi C, et al. Unilateral pulmonary edema due to pulmonary venous obstruction from fibrosing mediastinitis Int J Cardiol 2006;108: 418421. (7) Perrin C, et al. Unilateral neurogenic pulmonary edema. A case report Rev Pneumol Clin 2004;60(1):4345. (8) Herndon JC, et al. Postoperative unilateral pulmonary edema: possible amiodarone pulmonary toxicity Anesthesiology 1992;76: 308312. (9) Sporer KA, Dorn E. Heroin-related noncardiogenic pulmonary edema: a case series Chest 2001;120: 16281632.
Morphine screws up decomp heart fx patients (EMJ 2008;25:205)
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Neurogenic Pulmonary Edema
(CHEST March 2012 vol. 141 no. 3 793-795)
phentolamine may fix neurogenic APE
Phlebotomy-It is somewhat ridiculous but some folks still think it is a good idea
Clin Nephrol. 1997 Jan;47(1):47-9. Phlebotomy for pulmonary edema in dialysis patients. Eiser AR, Lieber JJ, Neff MS. Source Department of Ambulatory Care, Elmhurst Hospital Center, NY, USA.Back to top