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Acute Heart Failure

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 Introduction
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 It is a syndrome defined as
 the new onset (de novo HF) or
 worsening (acutely decompensated HF) of symptoms
and signs of HF, mostly related to systemic congestion.
 leading to an unplanned hospital admission or an
emergency department visit.
 AHF is the most common cause of hospital
admission in patients > 65 years

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 In-hospital mortality ranges from 4% to 10%.

 Post-discharge 1-year mortality: 25–30% with up to
>45% deaths or readmission rates.
 Compared to patients with acutely decompensated CHF,
 those with new onset HF may have
 a higher in-hospital mortality but
 a lower post-discharge mortality and rehospitalization rates

 Acute decompensated heart failure (ADHF) is the most

common form of AHF, accounting for 5070% of
presentations.
2021 ESC Guidelines
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 Out of 2981 AHF patients, 62% had a history of
chronic HF.
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European J of Heart Fail, Volume: 12, Issue: 3, Pages: 239-248, First published: 15 February 2010, DOI: (10.1093/eurjhf/hfq002)
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 Patients can be categorized based on

 S/S of congestion and/ or hypoperfusion
 Wet: patients with volume/fluid overload (e.g., edema
and JVD), whereas
 Dry: patients with euvolemia

 Warm: patients with adequate CO to perfuse

peripheral tissues (skin will be warm to touch), whereas
 Cool: patients with evidence of hypoperfusion (skin
cool to touch with diminished pulses).
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 Invasive hemodynamic monitoring can be used to

provide objective data for assessing
 volume status (pulmonary capillary wedge pressure
[PCWP]) and
 perfusion (cardiac output)
 A CI < 2.2 L/min/m2 (0.037 L/s/m2) is
 reduced contractility an hypoperfusion
 A PCWP > 15 to 18 mm Hg (2–2.4 kPa)
 elevated LV preload and congestion
 Invasive hemodynamic monitoring is useful to guide
dose titration for vasoactive therapies
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 Common Factors Precipitating HF Hospitalization
With Acute Decompensated HF
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Diagnostic workup of new onset acute heart failure
 Treatment
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Desired Therapeutic Outcomes

 The goals of therapy for AHF are to

a) Correct the underlying precipitating factor(s);

b) Relieve patient symptoms;
c) Improve or normalize hemodynamics;
d) Optimize GDMT; and
e) Educate the patient, reinforcing adherence to
lifestyle modifications and the drug regimen

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 Oral agents such as β-blockers, ACE inhibitors or

ARBs (and possibly an ARNI), and MRAs should
be initiated
 as soon as possible during the hospitalization before
discharging
 They can also acutely contribute to improvement
in hemodynamics in addition to mortality and
prevent readmissions.

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 Pharmacologic Treatment
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 Treatment of AHF targets

 relief of congestion and optimization of CO
 A specific treatment approach depends on
 the patient’s symptoms (congestion vs hypoperfusion)
and
 hemodynamic indices (CI and PCWP)

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 Patients who have significant volume overload often

have
 impaired absorption of oral loop diuretics because of
 intestinal edema or altered transit time
 Therefore, loop diuretics are usually administered via
 IV boluses or continuous IV infusions

 Higher doses may be required for patients with renal

insufficiency due to
 decreased drug delivery to the site of action in the loop of
Henle 04/18/2023
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 Data suggest doses 2.5 times the home oral dose

given intravenously may be
 associated with better diuresis compared
 to simply using the home dose intravenously

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 N Engl J Med 2011; 364:797-805

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 Occasionally, patients with HF do not respond to a

diuretic, defined as
 failure to achieve a negative net fluid balance of at least
500 mL or greater depending on clinical need
 after several increasing bolus doses.

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 Diuretic resistance commonly occurs due to

 adaptation of the kidney to chronic inhibition of sodium
reabsorption in the ascending limb of the loop of Henle
 by enhancing sodium reabsorption in the distal
portion of the nephron.
 Therefore,adding a thiazide provides sequential
blockade of sodium reabsorption and enhanced
diuresis.
 Diuretic resistance may also be a result of poor CO
and diminished renal perfusion.
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 Several strategies are used to overcome diuretic resistance

include
 using larger doses,
 converting to IV administration after failing to respond to
oral doses,
 increasing the frequency of administration, or
 using a combination of loop and thiazide diuretic
 An effective strategy for overcoming diuretic resistance is
 combining two diuretics with different sites of action within
the nephron

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 There is little difference in diuretic efficacy whether the

loop diuretic is administered via
 a continuous infusion or intermittent boluses
 A meta-analysis result reported there was no difference
between continuous infusion and bolus of furosemide
for
 all-cause mortality, length of hospital stay and electrolyte
disturbance,
 but continuous infusion was superior to bolus administration
with regard to diuretic effect and reduction in BNP.
Anaesthesia 2018, 73, 238–247
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 Vasodilators
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 Are recommended in addition to diuretic therapy

for relief of dyspnea in patients with
 acutely decompensated HF and not symptomatically
hypotensive
 This class includes
 nitroglycerin, nitroprusside, and nesiritide
 IV vasodilators may be considered to relieve AHF
symptoms when SBP is >110 mmHg.

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 Decrease in SVR and a potential increase in SV and CO

 Also cause venodilation,
 reducing ventricular filling pressures (PCWP) within 24 to
48 hours, and
 potentially reducing myocardial oxygen consumption
(MVO2) and ventricular workload.
 Are contraindicated in patients whose cardiac filling
(and hence CO) depends on
 venous return or intravascular volume, as well as
 in patients who present with cardiogenic shock

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 • Use of IV vasodilators is limited to the relief of dyspnea in the
hospitalized HF patient with intact or high BP
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 Inotropic Agents
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 Positive inotropic agents act via increasing

intracellular
 cyclic adenosine monophosphate (cAMP)
concentrations, which
 increases the rate and extent of calcium influx during
systole, thereby enhancing contractility.
 Phosphodiesterase inhibitors reduce degradation of
cAMP. E.g., milrinone

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 Inotropes are needed for treatment of patients with

 low cardiac output and hypotension
 They should be reserved for patients with
 LV systolic dysfunction, low cardiac output and
 low SBP (e.g. <90 mmHg) resulting in poor vital
organ perfusion
 Starting at low doses and uptitrating them with
close monitoring.

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 Milrinone has both

 positive inotropic and vasodilating properties and as
such is referred to as
 an “inodilator.”
 It is a good option for who are also chronically
receiving β-blockers because
 the inotropic effects are achieved independent of β-
adrenergic receptors.

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 Mechanical, Surgical, and Device Therapies
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 For patients with cardiac failure who do not respond

to standard therapies
1. Percutaneous Mechanical Circulatory Support
(MCS) Devices
 Once in position in aorta, the balloon is programmed
 to inflate during diastole and deflate during systole
 The device is typically useful for short-term
therapy due to its
 invasiveness, need for limb immobilization, and
requirement for anticoagulation.
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2. Ventricular Assist Device (VAD)

 A surgically implanted pump that reduces or replaces the

work of the right, left, or both ventricles.

 Used for short-term support in patients refractory to
pharmacologic therapies,
 As long-term bridge therapy (a temporary transition treatment)
in patients awaiting cardiac transplant.
 as destination therapy for patients who are not appropriate
candidates for transplantation
3. Heart Transplant
 The final option for refractory end-stage HF patients who

have exhausted medical and device therapies.

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 Outcome Evaluation of Acute HF
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 Monitor for rapid relief of symptoms such as dyspnea,

oxygenation, fatigue, JVD, and other markers of congestion or
distress.
 Monitor for adequate perfusion of vital organs through
 assessment of mental status, urine output, CrCl, liver function tests,
serum lactate, a stable HR between 50 and 100 beats/min, and
normal acid–base balance.
 Monitor changes in hemodynamic variables if available.
 PCWP should decrease in volume-overloaded patients to a goal of
less than 18 mm Hg (2.4 kPa).
 CI should increase, with a goal to maintain above 2.2 L/min/m2
(0.037 L/s/m2).
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 Closely monitor BP, renal function, and

intravascular volume status while decreasing
preload with diuretics and vasodilators.
 Because oral therapies can both improve symptoms
and prolong survival,
 optimizing outpatient HF management is a priority
when preparing a patient for hospital discharge.

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