- 1 Background
- 2 Clinical Features
- 3 Differential Diagnosis
- 4 Evaluation
- 5 Management
- 6 Disposition
- 7 See Also
- 8 External Links
- 9 Video
- 10 References
- Leading cause of death in patients with ACS who reach the hospital alive
- Myocardial infarction
- RV infarction
- Decreased forward flow
- Mechanical obstruction to forward flow
- LV regurgitation
- Chordal rupture
- Aortic Insufficiency
- Assess for signs of CHF
- elevated JVD, pulmonary edema, S3
- Assess for valvular disease (mitral regurgitation, critical aortic stenosis, or aortic regurgitation)
- Assess for end-organ hypoperfusion
- cool/mottled extremities, weak pulses, altered mental status, decreased UOP
- Assess for pulsus paradoxus (cardiac tamponade)
- Biologically active metabolite of proBNP (released from ventricles in response to increased volume/pressure)
- Utility is controversial and may not affect patient centered outcomes
- May be trended to gauge treatment response in acute decompensated CHF
- May have false negative with isolated diastolic dysfunction
- <100 pg/mL: Negative for acute CHF (Sn 90%, NPV 89%)
- 100-500 pg/mL: Indeterminate (Consider differential diagnosis and pre-test probability)
- >500 pg/mL: Positive for acute CHF (Sp 87%, PPV 90%)
- American College of Cardiology, American Heart Association, Heart Failure Society of America guidelines as of May 2017
- BNP should be measured in patients presenting with dyspnea to help diagnose or exclude heart failure
- BNP or nt-pro-BNP should be measured to determine prognosis or disease severity in chronic heart failure
- Baseline BNP, cardiac troponin, or both should be measured upon hospital admission to determine prognosis in patients with acutely decompensated heart failure
- N-terminal proBNP (biologically inert metabolite of proBNP)
- <300 pg/mL → CHF unlikely
- CHF likely in:
- >450 pg/mL in age < 50 years old
- >900 pg/mL in 50-75 years old
- >1800 pg/mL in > 75 years old
Differential Diagnosis (Elevated BNP)
BNP In Obese Patients
- Visceral fat expansion leads to increased clearance of active natriuretic peptides
- Obese patients also frequently treated for hypertension or coronary artery disease which may also contribute to lower BNP levels
- In one study of 204 patients with acute CHF, an inverse relationship between BMI and BNP was noted. The standard cutoff of 100pg/mL resulted in a 20% false-negative rate
- Analysis of a subgroup of patients with documented BMI from the Breathing Not Properly study showed that a lower cutoff was more appropriate to maintain 90% sensitivity in obese and morbidly obese patients (54pg/mL)
Aim for MAP >65
- Consider etiologies (see above) and treat specific one, if present
- Consider small fluid challenge (250-500cc normal saline IV) or fluid removal, depending on estimation of patient's point on Starling curve
- Increase inotropy
- Dobutamine +/- norepinephrine OR dopamine
- Consider calcium chloride 1 g if hypocalcemic or normocalcemic through good PIV or central line
- Consider transfusion if hemoglobin < 10 (be aware of added fluid)
- Consider intubation
- Decreases O2 demand BUT may worsen preload
Increase forward flow
- PCI or thrombolysis
Decrease afterload (with extreme caution in very small, carefully-titrated doses)
- Do not give preload reducers such as nitro
- Patients are flow dependent over stenotic value. Flow proportional to degree of stenosis and afterload.
|Pressor||Initial Dose||Max Dose||Cardiac Effect||BP Effect||Arrhythmias||Special Notes|
|Dobutamine||3-5 mcg/kg/min||5-15 mcg/kg/min (as high as 200) ||Strong ß1 agonist +inotrope +chronotrope, Weak ß2 agonist +weak vasodilatation )||alpha effect minimal||HR variable effects . Also Increase SA and AV node fx||indicated in decompensated systolic HF, Debut Research 1979 Isoproterenol has most Β2 vasodilatory and Β1 HR effects|
|Dopamine||2 mcg/kg/min||20-50 mcg/kg/min||β1 and NorEpi release||α effects if > 20mcg/kg/min||Arrhythmogenic from β1 effects||More adverse events when used in shock compared to Norepi|
|Norepinephrine||0.2 mcg/kg/min||0.2-1.3 mcg/kg/min (5mcg/kg/min) ||mild β1 direct effect||β1 and strong α1,2 effects||Less arrhythmias than Dopamine||Increases MAP with vasoconstriction, increasescoronary perfusion pressure, little β2 effects.|
|Milrinone||50 mcg/kg x 10 min||0.375-75 mcg/kg/min||Direct influx of Ca2+ channels||Smooth muscle vasodilator||PDE Inhibitor which increases Ca2+ uptake by sarcolemma. No venodilatory activity|
|Phenylephrine||100-180 mcg/min then 40-60 mcg/min||0.4-9 mcg/kg/min||Alpha agonist||Long half life|
|Vasopressin||Fixed Dose||0.4 U/min||unknown||increases via ADH peptide||should not be titrated due to ischemic effects|
|Methylene blue||IV bolus 2 mg/kg over 15 min||1-2 mg/kg/hour||Possible increased inotropy, cardiac use of ATP||Inhibits NO mediated peripheral vasodilation||Don't use in G6PD deficiency, ARDS, pulmonary hypertension|
|Medication||IV Dose (mcg/kg/min)||Concentration|
|Norepinephrine (Levophed)||0.1-2 mcg/kg/min||8mg in 500mL D5W|
|Dopamine||2-20 mcg/kg/min||400mg in 250 D5W|
|Dobutamine||2-20 mcg/kg/min||250mg in 250 mg D5W|
|Epinephrine||0.1-1 mcg/kg/min||1mg in 250 D5W|
- Admission, frequently to intensive or higher-level of care
- 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(3):161-167. doi:10.1056/NEJMoa020233.
- Carpenter CR et al. BRAIN NATRIURETIC PEPTIDE IN THE EVALUATION OF EMERGENCY DEPARTMENT DYSPNEA: IS THERE A ROLE? J Emerg Med. 2012 Feb; 42(2): 197–205.
- Yancy CW et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure.
- Januzzi JL, van Kimmenade R, Lainchbury J, et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. Eur Heart J. 2006 Feb. 27(3):330-7.
- Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med. 2005 Feb 17. 352(7):666-75.
- Moe GW, Howlett J, Januzzi JL, Zowall H,. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation. 2007 Jun 19. 115(24):3103-10.
- Clerico A, Giannoni A, Vittorini S, Emdin M. The paradox of low BNP levels in obesity. Heart Fail Rev. 2011;17(1):81-96. doi:10.1007/s10741-011-9249-z.
- Krauser DG, Lloyd-Jones DM, Chae CU, et al. Effect of body mass index on natriuretic peptide levels in patients with acute congestive heart failure: A ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) substudy. Am Heart J. 2005;149(4):744-750. doi:10.1016/j.ahj.2004.07.010.
- Daniels LB, Clopton P, Bhalla V, et al. How obesity affects the cut-points for B-type natriuretic peptide in the diagnosis of acute heart failure. Results from the Breathing Not Properly Multinational Study. Am Heart J. 2006;151(5):999-1005. doi:10.1016/j.ahj.2005.10.011.
- Edmund H. Sonnenblick, M.D., William H. Frishman, M.D., and Thierry H. LeJemtel, M.D. Dobutamine: A New Synthetic Cardioactive Sympathetic Amine
- De Backer Daniel et al. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. NEJM 363(9). 779-789
- Pasin L et al. Methylene blue as a vasopressor: a meta-analysis of randomised trials. Crit Care Resusc. 2013 Mar;15(1):42-8.