1.
Management of Heart
Failure in the ED Setting:
An Evidence-Based
Review of the Literature
J Emerg Med, 2018 Sep 26.
doi: 10.1016/j.jemermed.2018.08.002

2.
Why is this topic important?
Acute heart failure (AHF) exacerbation
is a common presentation to the ED, with
the potential to cause significant morbidity
and mortality.
It is important to tailor treatments to the
appropriate type of heart failure.

3.
What does this review
attempt to show?
This review provides an evidence-based
summary of the current ED management
of AHF.

4.
Methods
Searched PubMed and Google Scholar
for articles using the keywords
‘‘heart failure,’’ ‘‘management,’’
‘‘treatment,’’ and ‘‘emergency.’
A total of 129 articles were selected for
inclusion in this narrative review.

5.
Discussion
The primary management of AHF includes
hemodynamic stabilization and
symptom relief.
Initial management should focus on
assessment and management of the
patient’s airway, breathing, and
circulation.

6.
1. Mild AHF Exacerbation
with Systemic Overload
2. Hypertensive AHF with
Pulmonary Edema
3. Hypotensive AHF with
Cardiogenic Shock
4. High-Output Heart Failure

7.
Mild AHF
Exacerbation
with Systemic
Overload

8.
A diuretic (e.g., furosemide) can be
provided at an i.v. dose of 1–2 times the
patient’s known oral dose (furosemide at
20–40 mg i.v. or bumetanide at 1 mg i.v.),
with diuresis typically occurring within 30–
60 min of i.v. administration.
Decisions on bolus or continuous infusion
and high- vs. low-dose strategies remain
controversial.

9.
There is variation in the recommendations
for high- vs. low-dose furosemide.
Patients receiving high-dose furosemide
have demonstrated a trend toward higher
rates of diuresis and improved overall
outcomes, but they also experience
increases in creatinine at greater rates.

10.
Morphine is not recommended, as it is
associated with an increased risk of
mortality and need for ICU admission
when it is given in AHF.

11.
Ultrafiltration (UF) should be reserved
for patients who are refractory to standard
diuretic therapy.
Compared with standard diuresis, UF
controls fluid removal rate and may
remove more total body sodium.

12.
Hypertensive
AHF with
Pulmonary
Edema

13.
The primary focus of treatment for these
patients includes respiratory support with
noninvasive positive pressure
ventilation (NIPPV) and vasodilators
(specifically, nitrates), followed by
diuretics if the patient is systemically
volume overloaded.

14.
NIPPV increases intra-thoracic pressure,
thereby decreasing preload and lowering
pulmonary interstitial fluid, as well as
decreasing the work of breathing.

15.
Nitrates rapidly reduce preload at lower
doses and systemic afterload at higher
doses.
Initial sublingual NTG 0.4 mg per dose.
i.v. NTG should be reserved for cases
where the SBP remains > 160 mmHg
Nitrates are contraindicated in patients
who have recently used
phosphodiesterase-5 inhibitors
(e.g.,sildenafil, vardenafil), who have LV
obstruction, or who are hypotensive.

16.
Bolus doses of i.v. NTG have been
demonstrated to be safe and associated
with improved outcomes.
NTG 0.5-2 mg i.v. bolus every 3 min, with
decreased mortality, rates of intubation,
and need for ICU admission.
Initiating i.v. NTG at doses > 0.1 mg/min
with rapid titration to patient response.

17.
Hypotensive
AHF with
Cardiogenic
Shock

18.
If patients with AHF present with
reduced EF and a low BP, immediate
resuscitation is required with initiation of
inotropic agents.
A small fluid bolus (i.e., 250–500 mL)
is recommended prior to initiating an
inotropic agent.

19.
Norepinephrine may be initially utilized to
increase BP and preload in the presence
of hypotension (similar to septic shock).
It can be used in conjunction with
dobutamine to increase cardiac output.

20.
NIPPV should be considered in patients
with respiratory distress and cardiogenic
shock.
NIPPV may further reduce preload and
afterload, causing acute decompensation.
Endotracheal intubation.

21.
Mechanical circulatory support (MCS)
should be considered in patients with
persistent cardiogenic shock, if immediate
stabilization is required to provide recovery
of the cardiac system, if time is required
for definitive therapy.
IABP, VAD, V-A ECMO.

22.
High-Output
Heart Failure

23.
Disposition

24.
More than 80% of AHF patients are
admitted from the ED.
Several studies suggest that the use of
observation units is safe and reduces
overall costs.

25.
For patients with hemodynamic instability,
significant systemic congestion,
inadequate response to medical therapy,
new-onset AHF, electrolyte disturbances,
elevated BUN or creatinine, ischemia on
ECG, or inability to follow up should be
admitted.

26.
Heart Failure
Risk Scores

27.
Ottawa Heart Failure Risk Scale
History
• Stroke or TIA
• Intubation for
respiratory distress
Examination
• Heart rate ≥ 110
on ED arrival
• Saturation ≤ 90%
on arrival
• Heart rate ≥ 110
during 3-min walk test
(or too ill)
Investigations
• New ischemia on ECG
• BUN ≥ 33 mg/dL
• Serum CO2 ≥ 35 mEq/L
• Troponin I/T meeting
criteria for MI
• NT-proBNP ≥ 5000 ng/L

28.
Emergency Heart Failure
Mortality Risk Grade
• Age
• Systolic BP (triage or initial)
• Heart rate (triage or initial)
• Oxygen saturation (lowest triage or initial)
• Creatinine
• Potassium
• Transportation by EMS
• Positive troponin
• Active malignancy
• On outpatient metolazone

29.
Special
Consideration–
Atrial Fibrillation
with Acute Heart
Failure

30.
If the dysrhythmia is the primary cause of
heart failure with hemodynamic instability,
then the patient should undergo
cardioversion.
If the dysrhythmia is not the primary cause
of the exacerbation, immediate
cardioversion may be associated with
adverse outcomes.
Digoxin can be utilized in patients with
decompensated heart failure, with doses
0.25 mg i.v. at one time, up to a maximum
of 1.5 mg over 1 day.