Congestive heart failure acute pharmacotherapy: Difference between revisions

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VisualWikitext

Latest revision as of 16:18, 1 December 2022

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Acute heart failure; AHF; Heart failure; HF; BTB; bridge to bridge; BTD; bridge to decision; BTR; bridge to recovery;

Overview

Acute heart failure can occur in the setting of a new onset heart failure or worsening of an existing chronic heart failure (also known as acute decompensated heart failure, flash pulmonary edema, ADHF). ADHF presents with acute shortness of breath due to the development of pulmonary edema (the rapid accumulation of fluid in the lung). Other signs and symptoms of ADHF include hypotension with impaired and organ perfusion manifested by worsening renal function, altered mentation and cold clammy extremities. ADHF associated with a poor prognosis if not treated aggressively. Like chronic heart failure therapy, the goal is to improve symptoms but unlike chronic therapy the other goals are to improve oxygenation and hemodynamic stability. The mainstays of the acute medical treatment in acute decompensated congestive heart failure include oxygen to improve hypoxia, diuresis to reduce both preload and intravascular volume and vasodilators to reduce afterload. Some of the mainstays of chronic heart failure therapy are not initiated acutely (ACE inhibtors,beta blockers and digoxin).

2022 AHA/ACC/HFSA Heart Failure Guideline Hospitalization of patients with acute heart failure

Assessment of Patients Hospitalized With Decompensated HF

Class I
"1. In patients hospitalized with HF, the severity of congestion and adequacy of perfusion should be assessed to guide triage and initial therapy (Level of Evidence C-LD).
"2. In patients hospitalized with HF, the common precipitating factors and the overall patient trajectory should be assessed to guide appropriate therapy (Level of Evidence C-LD).
"3. For patients admitted with HF, treatment should address reversible factors, establish optimal volume status, and advance GDMT toward targets for outpatient therapy (Level of Evidence C-LD).

^[1]

Maintenance or Optimization of GDMT During Hospitalization

Class I
"1. In patients with HFrEF requiring hospitalization, preexisting GDMT should be continued and optimized to improve outcomes, unless contraindicated (Level of Evidence B-NR)''.
"2. In patients experiencing a mild decrease of renal function or asymptomatic reduction of blood pressure during HF hospitalization, diuresis, and other GDMT should not routinely be discontinued (Level of Evidence B-NR)''.
"3. In patients with HFrEF, GDMT should be initiated during hospitalization after clinical stability is achieved. (Level of Evidence B-NR).
''4. In patients with HFrEF, if discontinuation of GDMT is necessary during hospitalization, it should be reinitiated and further optimized as soon as possible (Level of Evidence B-NR)''

^[1]

Diuretics in Hospitalized Patients: Decongestion Strategy

Class I
"1. Patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to improve symptoms and reduce morbidity (Level of Evidence B-NR)''.
"2. For patients hospitalized with HF, therapy with diuretics and other guideline-directed medications should be titrated with the goal to resolve clinical evidence of congestion to reduce symptoms and rehospitalizations(Level of Evidence B-NR)''.
"3. For patients requiring diuretic treatment during hospitalization for HF, the discharge regimen should include a plan for adjustment of diuretics to decrease rehospitalizations (Level of Evidence B-NR).

^[1]

Class IIa
"4. In patients hospitalized with HF when diuresis is inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: a. higher doses of intravenous loop diuretics or addition of a second diuretic(Level of Evidence: B-NR) "

^[1]

Parenteral Vasodilation Therapy in Patients Hospitalized With HF

Class IIa
"1. In patients who are admitted with decompensated HF, in the absence of systemic hypotension, intravenous nitroglycerin or nitroprusside may be considered as an adjuvant to diuretic therapy for relief of dyspnea(Level of Evidence: B-NR) "

^[1]

VTE Prophylaxis in Hospitalized Patients

Class I
"1. In patients hospitalized with HF, prophylaxis for VTE is recommended to prevent venous thromboembolic disease (Level of Evidence B-R)''.

^[1]

Subcutaneous low-molecular-weight heparin, unfractionated heparin, fondaparinux, or approved DOAC are used for the prevention of clinically symptomatic deep vein thrombosis and pulmonary embolism^[1].

Evaluation and Management of Cardiogenic Shock

Class I
"1. In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance(Level of Evidence B-R)''.

^[1]

Class IIa
" 2. In patients with cardiogenic shock, temporary MCS is reasonable when an end-organ function cannot be maintained by pharmacologic means to support cardiac function (Level of Evidence B-NR)".
'' 3. In patients with cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable(Level of Evidence C-NR)''

^[1]

Class IIb
" 4. In patients presenting with cardiogenic shock, placement of a PA line may be considered to define hemodynamic subsets and appropriate management strategies (Level of Evidence B-NR)".
'' 5. For patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management (Level of Evidence C-LD)''

^[1]

Integration of Care: Transitions and Team-Based Approaches

Class I
"1. n patients with high-risk HF, particularly those with recurrent hospitalizations for HFrEF, referral to multidisciplinary HF disease management programs is recommended to reduce the risk of hospitalization(Level of Evidence B-R)''.
"2. In patients hospitalized with worsening HF, patient-centered discharge instructions with a clear plan for transitional care should be provided before hospital discharge(Level of Evidence B-NR)''.

^[1]

Class IIb
" 3. In patients hospitalized with worsening HF, participation in systems that allow benchmark-ing to performance measures is reasonable to increase use of evidence-based therapy, and to improve quality of care.(Level of Evidence B-NR)".
'' 4. In patients being discharged after hospital-ization for worsening HF, an early follow-up, generally within 7 days of hospital discharge, is reasonable to optimize care and reduce rehospitalization (Level of Evidence B-NR)''

^[1]

2021 ESC Guideline for management of acute heart failure

Abbreviations: AHF: Acute heart failure; LMWH: Low-molecular-weight heparin; PaO2: Partial pressure of oxygen ; SBP: Systolic blood pressure; SpO2: Transcutaneous oxygen saturation;

Recommendations for initial treatment of acute heart failure

Oxygen, ventilation support (Class I, Level of Evidence C):

❑ Oxygen is recommended in hypoxic patients with SpO2<90% or PaO2 <60 mmHg
❑ Intubation is recommended in the presence of progressive respiratory failure in spite of oxygen administration or non-invasive ventilation

Oxygen, ventilation support (Class IIa, Level of Evidence B):

❑ In patients with respiratory distress (respiratory rate >25 breaths/min, SpO2<90%), non-invasive positive pressure ventilation is recommended to decrease respiratory distress and reduce the rate of mechanical endotracheal intubation

Diuretics :(Class I, Level of Evidence C) :

❑ Intravenous loop diuretics are considered for all admitted patients with acute heart failure presented with signs, symptoms of fluid overload

Diuretics : (Class IIa, Level of Evidence B)

❑ In patients with resistant edema who do not respond to an increase in loop diuretic doses, combination of a loop diuretic with thiazide type diuretic should be considered

Vasodilators: (Class IIb, Level of Evidence B)

❑ In order to improve symptoms and reduce congestion in patients with AHF and SBP >110 mmHg, vasodilators may be considered as initial therapy

Inotropic agents : (Class 2b, Level of Evidence C)

❑ Inotropic agents may be considered in patients with SBP <90 mmHg and evidence of hypoperfusion without response to fluid challenge, to improve peripheral perfusion and maintain end-organ function

Inotropic agents (Class III, Level of Evidence C):

❑ Routinely administration of inotropic agents are not recommended , due to safety concerns, unless the patient has symptomatic hypotension and evidence of hypoperfusion

Vasopressors: (ClassIIb, Level of Evidence B)

❑ In patients with cardiogenic shock, a vasopressor, preferably norepinephrine, may be indicated to increase blood pressure and vital organ perfusion

Anticoagulant therapy: (ClassI, Level of Evidence A)

❑ Thromboembolism prophylaxis such as LMWH is recommended in patients not already anticoagulated and no contraindication to anticoagulation, to prevent the risk of deep venous thrombosis and pulmonary embolism

Opiates: (ClassIII, Level of Evidence C)

❑ Opiates is not routinely recommended, unless in selected patients with severe, intractable pain or anxiety

The above table adopted from 2021 ESC Guideline

^[2]

Pre-hospital setting

In the pre-hospital setting, AHF patients should be monitored by pulse oximetry, BP, heart rate, respiratory rate, and a continuous ECG.
Oxygen therapy may be given based on a clinical judgment unless oxygen saturation is <90% in which case it should be administered.
Indication for non-invasive ventilation:
Respiratory distress

Respiratory rate >25 breaths/min
Oxygen saturation <90%

In-hospital management

Specific causes of AHF should be searched including ACS, hypertensive emergency, rapid arrhythmias, severe bradycardia, conduction disturbance, acute valve regurgitation, acute pulmonary embolism, myocarditis, tamponade.
After exclusion of these conditions, which need to be treated, AHF should be managed according to the clinical presentations.

Pre-discharge phase

Oxygen therapy, ventilatory support

In AHF, oxygen should not be used routinely in non-hypoxaemic patients due to vasoconstriction and a reduction in cardiac output.
Oxygen therapy is recommended in patients with AHF SpO2 <90% or PaO2 <60 mmHg to correct hypoxemia.
In chronic obstructive pulmonary disease (COPD), hyper-oxygenation may increase ventilation-perfusion mismatch, suppress ventilation and

lead to hypercapnia.

During oxygen therapy, acid-base balance and SpO2 should be monitored.
Non-invasive positive pressure ventilation, either continuous positive airway pressure and pressure support, improves respiratory failure, increases oxygenation and pH, and decreases the partial pressure of carbon dioxide (pCO2) and work of breathing and reduce the rate of endotracheal intubation.
Non-invasive positive pressure ventilation indicated to improve gas exchange and reduce the rate of endotracheal intubation in patients with:

Respiratory distress (respiratory rate >25 breaths/min
SpO2 <90%

FiO2 should be increased up to 100%, if needed, based on oxygen saturation level.
Blood pressure should be monitored regularly during non-invasive positive pressure ventilation.
The increase in intrathoracic pressure with non-invasive positive pressure ventilation may lead to reduction in venous return, right and left ventricular preload, cardiac output and BP.
In the setting of RV dysfunction, the increase in pulmonary vascular resistance and RV afterload may be present.
Intubation is indicative if there is progressive respiratory failure despite oxygen administration or non-invasive ventilation.

Diuretics

Intravenous diuretics are mainstay therapy of AHF.
Efficacy of diuretics are due to increase renal excretion of salt and water and reduce of fluid overload and congestion.
There was a greater relief of dyspnoea, change in weight and net fluid loss (with no prognostic role for increases in serum creatinine) in the higher-dose regimen.
High diuretic doses may associate with greater neurohormonal activation and electrolyte disturbance and poor outcomes.
Treatment with diuretic should be started with an initial i.v. dose of furosemide, or equivalent dose of bumetanide or torasemide to 1-2 times the daily oral dose taken by the patient before admission.
If the patient was not on oral diuretics, a starting dose of 20-40 mg of furosemide, or a bolus of 10-20 mg i.v torasemide, can be used.
Furosemide can be given as 2-3 daily boluses or as a continuous infusion.
Due to post-dosing sodium retention, daily single bolus administrations are not recommended.
With continuous infusion, a loading dose may be used to achieve steady-state earlier.
Response to diuretic should be evaluated shortly after the start of diuretic therapy and may be measured by performing spot urine sodium content after 2 or

6 h and/or by measuring the hourly urine output.

A satisfactory diuretic response can be considered as a urine sodium content >50-70 mEq/L at 2 h and/or by a urine output >100-150 mL/h during the first 6 h.
If there is an inadequate diuretic response, the loop diuretic i.v. dose can be doubled, with a further assessment of diuretic response.
If the diuretic response remains insufficient including <100 mL hourly diuresisin spite of doubling loop diuretic dose, concomitant administration of other diuretics such as thiazides or metolazone or acetazolamide , may be considered.
Serum electrolytes and renal function should be carefully monitored.
Low doses of loop diuretics, with frequent doses may be less likely to cause dehydration or increase in serum creatinine.
Oral treatment should be started after congestion relief.
Oral loop diuretics are continued at the lowest dose possible to avoid congestion.
Discharge of hospital with persistent congestion is a major predictor of increased deaths and rehospitalizations.
Appropriate long-term diuretic dose should be established before discharge.

Vasodilators

Intravenous vasodilators, namely nitrates or nitroprusside with the effect of dilating venous and arterial vessels leading to a reduction in venous return to the heart, less congestion, lower afterload, increased stroke volume and consequent relief of symptoms.
Nitrates act mainly on peripheral veins whereas the effect of nitroprusside is dilation of arterial and venule.
vasodilators may be more effective than diuretics when acute pulmonary edema is due to increased afterload and fluid redistribution to the lungs in the absence or with minimal fluid accumulation.
Intravenous vasodilators may be considered to relieve AHF symptoms when SBP is >110 mmHg.
They may be started at low doses and uptitrated to achieve clinical improvement and BP control.
Nitrates are generally administered with an initial bolus followed by continuous infusion or repeated boluses.
Nitroglycerine can be given as 1-2 mg boluses in severely hypertensive patients with acute pulmonary edema.
BP monitoring is needed to avoid hypotension due to an excessive decrease in preload and afterload.
Caution should be exercised in patients with LVH and/or severe aortic stenosis.
Hemodynamic parameters should be monitored in patients with left ventricular systolic dysfunction and aortic stenosis when vasodilators are given.

Inotropes

Inotropes is recommended in patients with low cardiac output and hypotension, left ventricular systolic dysfunction and poor organ perfusion.
Inotropes should be started under monitoring.
Common side effects of inotropes with adrnergic mechanism including sinus tachycardia, increase ventricular rate in patients with AF, induced myocardial ischemia and arrhythmias, and increase mortality.
Levosimendan or type-3-phosphodiesterase inhibitors may be preferred over dobutamine for patients on beta-blockers.
Type-3-phosphodiesterase inhibitors or levosimendan may lead to peripheral vasodilation and hypotension, especially when administrated at high doses.

Vasopressors

Norepinephrin may be preferred in patients with severe hypotension, due to peripheral vasoconstriction, to increase perfusion to vital organs at the expense of an increase in left ventricular afterload.
In patients with advanced HF and cardiogenic shock, a combination of norepinephrine and inotropic agents may be considered.
In some studies, the use of norepinephrine was the first choice, compared with dopamine or epinephrine.
Dopamine was preferred to norepinephrine as a first-line vasopressor therapy in patients with shock.
Use of dopamin was associated with arrhythmic events and with ahigher mortality in patients with cardiogenic shock but not in those with hypovolaemic or septic shock.
Use of epinephrine in comparison with norepinephrine in patients with cardiogenic shock due to acute MI was associated with higher heart rateand lactic acidosis and mortality.

Opiates

Opiates relieve dyspnea and anxiety.
They may be used as sedative agents during non-invasive positive pressure ventilation to improve patient adaptation.
Dose-dependent side effects including nausea, hypotension, bradycardia, and respiratory depression.
Administration of morphine is associated with a higher frequency of mechanical ventilation, prolonged hospitalization, more intensive care unit admissions, and increased mortality.
So, routine use of opiates in AHF is not recommended.
Use of morphine is recommended in selected patients with severe/intractable pain or anxiety or in the setting of palliation.

Digoxin

Digoxin should be considered in patients with AF with a rapid ventricular rate (>110 b.p.m.) despite beta-blockers.
Digoxin can be given in boluses of 0.25-0.5 mg i.v., if not used previously.
In patients with comorbidities (i.e. CKD) or other factors affecting digoxin metabolism (including other drugs) and/or the elderly, the maintenance dose may be difficult to estimate.
Serum concentration of digoxin should be measured.

Thromboembolism prophylaxis

Thromboembolism prophylaxis with heparin, low-molecular weight heparin or another anticoagulant is recommended, unless contraindicated or existing therapy with oral anticoagulants.

Management of acute heart failure

Cardiogenic shock, respiratory failure

NO

Yes

Identifying acute causes

Pharmacologic therapy

Acute Coronary syndrome

Yes

NO

Immediate initiation of specific treatment

Further treatment

The above algorithm adopted from 2021 ESC Guideline

^[2]

Short-term mechanical circulatory support

In patients presenting with cardiogenic shock, short-term MCS may be considered to increase cardiac output and support end-organ perfusion.
Short-term MCS can be used as a bridge to recovery (BTR), bridge to decision (BTD) or bridge to bridge (BTB).
The initial improvements in cardiac output, BP and arterial lactate may be affected by significant complications.
Close monitoring of hemodynamics and lactate as the markers of end-organ damage may improve survival.
Use of The Intra-aortic Balloon Pump in Cardiogenic shock was not associated with the reduced long-term mortality compared with medical therapy.
IABP is not routinely recommended in cardiogenic shock post-MI.
However, it may still be considered in cardiogenic shock, especially if not due to ACS, and refractory to drug therapy, as a BTD, BTR, or BTB.
Patients with cardiogenic shock or cardiac arrest treated with venoarterial VA-ECMO showed favorable outcome.
In cases of fulminant myocarditis and other conditions causing severe cardiogenic shock, VA-ECMO may also be considered.
Depending on the severity of myocardial dysfunction and/or concomitant mitral regurgitation or aortic regurgitation, VA-ECMO may increase LV afterload with an increase in LV end-diastolic pressure and pulmonary congestion.
In these cases, LV unloading such as Impella is considered.

2021 ESC Guideline for management of pulmonary edema

Management of patients with pulmonary edema

Oxygen (Class I) or ventilatory support (Class IIa)

Systolic blood pressure ≥110 mmHg

Yes

NO

Loop diuretics (Class I) and/or vasodilators (Class IIb)

Signs of hypoperfusion

Yes

NO

Loop diuretics (Class I) and inotropes/vasopressors(Class IIb)

Loop diuretics (Class I)

Congestion relief

Yes

NO

Optimized medical therapy

Renal replacement therapy

The above algorithm adopted from 2021 ESC Guideline

Acute pulmonary edema is related to lung congestion.
Clinical characteristics include dyspnea with orthopnea, respiratory failure (hypoxemia-hypercapnia), tachypnea >25 breaths/min, and increased work of breathing.
Treatment including as follows:
Oxygen, given as continuous positive airway pressure, non-invasive positive pressure-ventilation and/or high-flow nasal cannula
Diuretics
Vasodilators if systolic BP (SBP) is high, to reduce LV afterload
In the setting of acute pulmonary edema with low cardiac output state, inotropes, vasopressors, and/or MCS are indicated to restore organ perfusion.

2021 ESC Guideline for management of cardiogenic shock

Management of patients with cardiogenic shock

Acute coronary syndrome (ACS), mechanical complications

Yes

NO

Emergency PCI or surgical treatment

Identifying and treatment of other specific causes

Oxygen therapy (Class I) or ventilatory support (Class IIa)

Inotropes, vasopressors (Class IIb)
Short-term mechanical circulatory support (Class IIa)

Improvement of hypoperfusion and organ dysfunction

Yes

NO

Weaning from inotropes/vasopressors and/or mechanical circulatory support

Treatment of underlying etiology and medical therapy optimization (Class I )

Mechanical circulatory support(Class IIa)

Renal replacement therapy (Class IIa)

Palliative care

The above algorithm adopted from 2021 ESC Guideline

References

↑ ^1.00 ^1.01 ^1.02 ^1.03 ^1.04 ^1.05 ^1.06 ^1.07 ^1.08 ^1.09 ^1.10 ^1.11 Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 145 (18): e876–e894. doi:10.1161/CIR.0000000000001062. PMID 35363500 Check |pmid= value (help).
↑ ^2.0 ^2.1 McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, Burri H, Butler J, Čelutkienė J, Chioncel O, Cleland J, Coats A, Crespo-Leiro MG, Farmakis D, Gilard M, Heymans S, Hoes AW, Jaarsma T, Jankowska EA, Lainscak M, Lam C, Lyon AR, McMurray J, Mebazaa A, Mindham R, Muneretto C, Francesco Piepoli M, Price S, Rosano G, Ruschitzka F, Kathrine Skibelund A (September 2021). "2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure". Eur Heart J. 42 (36): 3599–3726. doi:10.1093/eurheartj/ehab368. PMID 34447992 Check |pmid= value (help). Vancouver style error: initials (help)

Template:WikiDoc Sources

[pmid35363500-1] 1.00 ^1.01 ^1.02 ^1.03 ^1.04 ^1.05 ^1.06 ^1.07 ^1.08 ^1.09 ^1.10 ^1.11 Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM; et al. (2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 145 (18): e876–e894. doi:10.1161/CIR.0000000000001062. PMID 35363500 Check |pmid= value (help).

[pmid34447992-2] 2.0 ^2.1 McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, Burri H, Butler J, Čelutkienė J, Chioncel O, Cleland J, Coats A, Crespo-Leiro MG, Farmakis D, Gilard M, Heymans S, Hoes AW, Jaarsma T, Jankowska EA, Lainscak M, Lam C, Lyon AR, McMurray J, Mebazaa A, Mindham R, Muneretto C, Francesco Piepoli M, Price S, Rosano G, Ruschitzka F, Kathrine Skibelund A (September 2021). "2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure". Eur Heart J. 42 (36): 3599–3726. doi:10.1093/eurheartj/ehab368. PMID 34447992 Check |pmid= value (help). Vancouver style error: initials (help)

[1]

[2]

@@ Line 1: / Line 1: @@
 __NOTOC__
+{| class="infobox" style="float:right;"
+|-
+| [[File:Siren.gif|30px|link= Congestive heart failure resident survival guide]]|| <br> || <br>
+| [[Acute decompensated heart failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
+|}
 {{Congestive heart failure}}
 {{CMG}}
-{{SK}} acute decompensated heart failure, ADHF, flash pulmonary edema
+{{SK}} Acute heart failure; AHF; Heart failure; HF; BTB;  bridge to bridge; BTD; bridge to decision; BTR; bridge to recovery;
 ==Overview==
 Acute heart failure can occur in the setting of a new onset heart failure or worsening of an existing chronic heart failure (also known as [[acute decompensated heart failure]], [[flash pulmonary edema]], [[ADHF]]).  ADHF presents with acute shortness of breath due to the development of [[pulmonary edema]] (the rapid accumulation of [[fluid in the lung]]).  Other signs and symptoms of ADHF include [[hypotension]] with impaired and organ perfusion manifested by [[worsening renal function]], altered mentation and [[cold clammy extremities]].  ADHF associated with a poor prognosis if not treated aggressively.  Like chronic heart failure therapy, the goal is to improve symptoms but unlike chronic therapy the other goals are to improve oxygenation and hemodynamic stability.  The mainstays of the acute medical treatment in acute decompensated [[congestive heart failure]] include [[oxygen]] to improve [[hypoxia]], [[diuresis]] to reduce both [[preload]] and intravascular volume and vasodilators to reduce [[afterload]].  Some of the mainstays of [[chronic heart failure therapy]] are not initiated acutely ([[ACE inhibtors]],[[beta blockers]] and [[digoxin]]).
-==General Recommendations==
-===Hospitalization===
-Hospitalization is required for the management of the patient with ADHF with the following signs, symptoms and laboratory abnormalities: <ref name="pmid20610207">{{cite journal |author=Lindenfeld J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Katz SD, Klapholz M, Moser DK, Rogers JG, Starling RC, Stevenson WG, Tang WH, Teerlink JR, Walsh MN |title=HFSA 2010 Comprehensive Heart Failure Practice Guideline |journal=[[Journal of Cardiac Failure]] |volume=16 |issue=6 |pages=e1–194 |year=2010 |month=June |pmid=20610207 |doi=10.1016/j.cardfail.2010.04.004 |url=http://linkinghub.elsevier.com/retrieve/pii/S1071-9164(10)00173-9 |accessdate=2013-04-29}}</ref>
-*[[Hypotension]] and/or [[cardiogenic shock]]
-*Evidence of poor end organ perfusion such as [[worsening renal function]], [[cold clammy extremities]], [[altered mental status]]
-*[[Hypoxemia]] with an oxygen saturation under 90%
-*[[Atrial fibrillation]] with a rapid ventricular response resulting in [[hypotension]]
-*The possible presence of an [[acute coronary syndrome]] and ongoing myocardial ischemia
-===Telemetry and Monitoring===
-The patient should be admitted to a level of care that allows for constant electrocardiographic monitoring given the risk of arrhythmias and frequent vital signs.
-*The heart rhythm and oxygen saturation should be monitored continuously.
-*Is and Os (intake and output) should be monitored carefully.  A daily target should be established (for example the patient should be one liter negative for the day) and [[diuretic]] dosing should be adjusted to achieve this target.
-*Daily weights should be obtained using the same scale at the same time of the day, usually before the patient has eaten, and after they have first voided in the morning. Often times Is and Os measurements will underestimate insensible losses that occur through the lungs.
-*The [[BUN]] and [[creatinine]], [[serum sodium]](to detect [[hyponatremia]] which carries a poor prognosis), chloride, bicarbonate (to detect [[contraction alkalosis]]) and [[serum potassium]] (to detect [[hypokalemia]] as a result of [[diuresis]] and which can precipitate [[arrhythmias]]) should be monitored daily. Potassium and magnesium should be repeated as needed following [[diuresis]].
-*If the patient is [[hyponatremic]] this does not suggest an inadequate intake of salt, but excess free water ingestion and retention.  In these patients, access to free water should be restricted to <2 li/day if the Na is < 130 meq/li, and < 1 li/day or more if the Na is < 125 meq/li.  It should be borne in mind that juices are essentially free water with sugar.  In the hyponatremia patient, drips should not be in D5W.  Patients with [[congestive heart failure]] should be on a <2 g per day sodium diet.
-===Oxygen===
-Oxygen improves the patient's status if [[hypoxemia]] is present, and the goal is to keep the oxygen saturation above 90%. [[Positive airway pressure|Continuous positive airway pressure]] may be applied using a face mask; this has been shown to improve symptoms more quickly than oxygen therapy alone,<ref>{{cite journal |author=Gray A, Goodacre S, Newby DE, Masson M, Sampson F, Nicholl J |title=Noninvasive ventilation in acute cardiogenic pulmonary edema |journal=N. Engl. J. Med. |volume=359 |issue=2 |pages=142–51 |year=2008 |month=July |pmid=18614781|doi=10.1056/NEJMoa0707992}}</ref> and has been shown to reduce the risk of death.<ref>{{cite journal |author=Peter JV, Moran JL, Phillips-Hughes J, Graham P, Bersten AD |title=Effect of non-invasive positive pressure ventilation (NIPPV) on mortality in patients with acute cardiogenic pulmonary oedema: a meta-analysis |journal=Lancet |volume=367 |issue=9517 |pages=1155–63 |year=2006 |month=April |pmid=16616558|doi=10.1016/S0140-6736(06)68506-1}}</ref><ref>{{cite journal |author=Weng CL |title=Meta-analysis: Noninvasive ventilation in acute cardiogenic pulmonary edema |journal=Ann. Intern. Med. |volume=152 |issue=9 |pages=590–600 |year=2010 |month=May |pmid=20439577 |doi=10.1059/0003-4819-152-9-201005040-00009 |url= |author-separator=, |author2=Zhao YT |author3=Liu QH |display-authors=3 |last4=Fu |first4=CJ |last5=Sun |first5=F |last6=Ma |first6=YL |last7=Chen |first7=YW |last8=He |first8=QY}}</ref> Severe [[respiratory failure]] requires treatment with [[endotracheal intubation]] and [[mechanical ventilation]].
-==Management Considerations==
-The patient's therapy must be tailored to:
-*Whether the patient has acute diastolic or systolic heart failure
-*The patient's intravascular volume status
-*The patient's hemodynamic status
-*The precipitant of the decompensation
-===Systolic Versus Diastolic Heart Failure===
-The management of the patient with acute decompensated heart failure depends upon whether the patient has acute decompensated [[systolic heart failure]] or acute decompensated [[diastolic heart failure]].  Both forms of acute decompensated [[heart failure]] are treated with oxygen and [[vasodilator]] therapy and [[diuresis]].  Importantly, [[inotropic agents]] that increase contractility are not indicated in the patient with acute decompensated [[diastolic heart failure]] while they are important for the patient with acute decompensated systolic heart failure.  While [[beta blocker]] initiation is relatively contraindicated in acute decompensated systolic heart failure, control of [[tachycardia]] is very useful in the patient with [[diastolic heart failure]] to prolong left ventricular filling time. While the initiation of [[ACE inhibitors]] may not be recommended in acute decompensated [[systolic heart failure]], [[ACE inhibition]] may be of benefit in acute decompensated [[diastolic heart failure]].
-===Intravascular Volume Status===
-The aggressiveness of diuresis depends upon the patient's volume status.  If the patient is total body and intravascular volume overloaded in normotensive, then diuresis alone should be undertaken.  If the patient is volume overloaded but [[hypotensive]], then [[inotropes]] must be administered in addition to [[diuretics]].  Vasodilators cannot be administered to these patients.
-===Identification of and Treatment of Underlying Cause of Decompensation===
-Identification of and treatment of precipitants of acute decompensation is a mainstay of therapy. Please see the accompanying chapters for detailed management strategies.
-*[[Hypertension]]: Vasodilators should be administered
-*[[Acute coronary syndrome]]: Antiplatelets, antithrombin, vasodilators, PCI, intra-aortic balloon pump placement should be used to reverse myocardial ischemia
-*[[Valvular heart disease]]: For mitral regurgitation vasodilator therapy should be administered, for mitral stenosis heart rate slowed to prolonged left ventricular filling, for aortic stenosis either balloon vavlotomy, [[TAVR]] or valve replacement may be necessary
-*[[Atrial fibrillation]] can cause acute decompensation of [[heart failure]] due to an increase in heart rate and oxygen demands, and conversely acute decompensation of heart failure can precipitate [[atrial fibrillation]] due to left atrial dilation and increased wall stress.  Thus, [[atrial fibrillation]] and acute decompensated [[heart failure]] are often intimately related, and the successful management of [[atrial fibrillation]] is often critical to the success of reversing the acute decompensation.
-:In the patient with acute decompensated [[heart failure]], rate control of [[atrial fibrillation]] is the mainstay of arrhythmia therapy.  Obviously agents that have a negative inotropic effect such as beta blockers and non-dihydropyridine calcium channel blockers are relatively contraindicated in the management of acute decompensated systolic heart failure.  Intravenous diltiazem does not have a [[negative inotropic]] effect and is often used for rate control.  Short acting [[esmolol]] is sometimes used.  [[Digoxin]] has a very narrow therapeutic/toxic window,  it's onset of action is relatively delayed, and it is often not used.
-:If a patient is in [[cardiogenic shock]], then [[cardioversion]] can be considered in the patient with [[atrial fibrillation]], however in the absence of severe hemodynamic compromise it should be noted that atrial fibrillation will often recur in this setting.  Thus, [[cardioversion]] is not particularly helpful in the absence of profound hemodynamic compromise.  [[Cardioversion]] can also be undertaken if new onset [[atrial fibrillation]] is the clear precipitant of the hemodynamic decompensation.  If the patient is going to be [[cardioverted]], [[unfractionated heparin]] should be administered.
-* [[Ventricular Arrhythmias]]: The development of either [[ventricular tachycardia]] or [[ventricular fibrillation]] are life-threatening complications and must be treated promptly with the [[cardioversion]].  Many antiarrhythmic's can be pro-arrhythmic in the patient with heart failure and are contraindicated.  [[Amiodarone]] is the antiarrhythmic of choice for the management of ventricular arrhythmias in the patient with heart failure.  Underlying precipitants of ventricular arrhythmias such as [[hypokalemia]] and [[hypomagnesemia]] should be corrected. It should also be noted that inotropic agents can be proarrhythmic. And
+== 2022 AHA/ACC/HFSA Heart Failure Guideline Hospitalization of patients with acute heart failure ==
-==Specific Therapies==
+=== Assessment of Patients Hospitalized With Decompensated HF ===
-====Diuretics====
+{| class="wikitable" style="width:80%"
-*Usually, but not always, patients with decompensated systolic heart failure are total body and intravascular volume overload and intravenous diuretics are often required in the acute setting.  Even in the absence of volume overload (decompensation due to [[hypertension]] or [[valvular heart disease]]) [[diuresis]] may help the symptoms of [[congestive heart failure]] because "dry lungs work better than wet lungs".  These drugs also cause venodilation in the lung vasculature that also relieves [[shortness of breath]].  While contractility of the heart increases with increasing volumes, this relationship is not preserved past a certain volume.  By reducing volume overload, these drugs optimize the heart's contractility (they keep the patient from falling off the end of the [[Starling curve]]).  Reducing the heart's volume also reduces functional [[mitral regurgitation]] and [[tricuspid regurgitation]].
+|-
-* [[Diuretics]] reduce [[preload]] and reduce intravascular volume.
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
-*Intravenous preparations are preferred because of more predictable absorption. When a patient is extremely fluid overloaded, they can develop intestinal edema as well, which can affect enteral absorption of medications.
+|-
-* The traditional starting dose of [[Lasix]] or [[furosemide]] is 40 mg intravenously. If this does not work, the dose is doubled.  There is insufficient data to suggest a [[Lasix]] drip is superior to boluses of [[Lasix]].<ref name="pmid16034890">{{cite journal |author=Salvador DR, Rey NR, Ramos GC, Punzalan FE |title=Continuous infusion versus bolus injection of loop diuretics in congestive heart failure |journal=[[Cochrane Database of Systematic Reviews (Online)]] |volume= |issue=3 |pages=CD003178 |year=2005 |pmid=16034890 |doi=10.1002/14651858.CD003178.pub3 |url=http://dx.doi.org/10.1002/14651858.CD003178.pub3 |accessdate=2013-04-30}}</ref>  A useful rule of thumb is that the IV dose should be 2.5 times the usual oral dose based upon the trend for superiority of high doses over low doses in the DOSE trial <ref name="pmid21366472">{{cite journal |author=Felker GM, Lee KL, Bull DA, Redfield MM, Stevenson LW, Goldsmith SR, LeWinter MM, Deswal A, Rouleau JL, Ofili EO, Anstrom KJ, Hernandez AF, McNulty SE, Velazquez EJ, Kfoury AG, Chen HH, Givertz MM, Semigran MJ, Bart BA, Mascette AM, Braunwald E, O'Connor CM |title=Diuretic strategies in patients with acute decompensated heart failure |journal=[[The New England Journal of Medicine]] |volume=364 |issue=9 |pages=797–805 |year=2011 |month=March |pmid=21366472 |pmc=3412356 |doi=10.1056/NEJMoa1005419 |url=http://www.nejm.org/doi/abs/10.1056/NEJMoa1005419?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dwww.ncbi.nlm.nih.gov |accessdate=2013-04-30}}</ref>. Usually an effect is seen in 30 minutes.
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1. I'''n patients hospitalized with HF, the severity of congestion and adequacy of perfusion should be assessed to guide triage and initial therapy (Level of Evidence C-LD).
-* [[Torsemide]] is another alternative and it's dose is 10 to 20 mg intravenously.
+|-
-* If high doses of furosemide are inadequate, boluses or continuous infusions of [[bumetanide]] (1 mg intravenously) may be preferred.
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' In patients hospitalized with HF, the common precipitating factors and the overall patient trajectory should be assessed to guide appropriate therapy (Level of Evidence C-LD).
-*These [[loop diuretics]] may be combined with [[thiazide diuretics]] such as oral [[metolazone]], [[hydrochlorothiazide]] (25 to 50 mg twice daily) or intravenous [[chlorothiazide]] (500 to 1000 mg/day) for a synergistic effect.
+|-
-*[[Hypotension]] may result from diuresis if mobilization of fluid from the extra vascular space does not keep pace with fluid leaving the intravascular space through diuresis.   Patients with diastolic dysfunction  and restrictive physiology are also prone to [[hypotension]] due to reductions in [[preload]].
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' For patients admitted with HF, treatment should address reversible factors, establish optimal volume status, and advance GDMT toward targets for outpatient therapy (Level of Evidence C-LD).
-* Typically the BUN and Cr slightly will rise during diuresis.  If the rise in creatinine is minimal, at the patient remains fluid overloaded, then diuresis can continue with careful attention to the renal function.  If the [[creatinine]] rises significantly before the patient is euvolemic, this suggests that there is reduced perfusion to the kidney, and this is associated with a poorer prognosis.  If the [[creatinine]] rises significantly, other [[nephrotoxic drugs]] should be discontinued, and the dosing of the diuretic may need to be reduced.  Despite a rise in the [[creatinine]], continued [[diuresis]] is sometimes required if severe [[pulmonary edema]] persists and consideration should be given to the addition of an inotropic agent.
+|}
-*If further efforts to induce [[diuresis]] are failing and the patient remains volume overloaded, then [[ultrafiltration]] or [[dialysis]] should be considered.
+<ref name="pmid35363500">{{cite journal| author=Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM | display-authors=etal| title=2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: Executive Summary: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. | journal=Circulation | year= 2022 | volume= 145 | issue= 18 | pages= e876-e894 | pmid=35363500 | doi=10.1161/CIR.0000000000001062 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=35363500  }}</ref>
-*In post MI patients with heart failure, an aldosterone antagonist such as [[spironolactone]] or [[eplerenone]] can be added instead of a thiazide diuretic.  Given the risk of [[hyperkalemia]] these agent should only be added if the renal function and [[serum potassium]] can be carefully monitored.
-===Vasodilator Therapy===
+=== Maintenance or Optimization of GDMT During Hospitalization ===
-In the absence of [[hypotension]], the intravenous administration of vasodilators such as [[nitroglycerin]], [[nitroprusside]] and [[nesiritide]] can reduce both [[preload]] and [[afterload]] and can rapidly improve symptoms.  These benefits are observed when the drugs are administered in addition to diuretics or when there is a poor response to diuretics.
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' In patients with HFrEF requiring hospitalization, preexisting GDMT should be continued and optimized to improve outcomes, unless contraindicated (Level of Evidence B-NR)<nowiki>''</nowiki>.
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' In patients experiencing a mild decrease of renal function or asymptomatic reduction of blood pressure during HF hospitalization, diuresis, and other GDMT should not routinely be discontinued (Level of Evidence B-NR)<nowiki>''</nowiki>.
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' In patients with HFrEF, GDMT should be initiated during hospitalization after clinical stability is achieved. (Level of Evidence B-NR).
+|-
+| bgcolor="LightGreen" |<nowiki>''</nowiki>4. In patients with HFrEF, if discontinuation of GDMT is necessary during hospitalization, it should be reinitiated and further optimized as soon as possible (Level of Evidence B-NR)<nowiki>''</nowiki>
+|}
+<ref name="pmid35363500" />
-====Nitroglycerin====
+=== Diuretics in Hospitalized Patients: Decongestion Strategy ===
-*[[Nitroglycerine]] reduces [[afterload]] and reduces [[preload]]. Nitroglycerine is helpful in improving symptoms of dyspnea.  At higher doses, [[nitroglycerin]] also reduces [[afterload]].
+{| class="wikitable" style="width:80%"
-*Unfortunately tolerance or [[tachyphylaxis]] can develop within hours of continuous administration of high-dose nitroglycerin.
+|-
-*The initial dose of intravenous nitroglycerin is 5 to 10 µg per minute and this dose is increased every 3-5 minutes in 5 to 10 µg increments to a maximum dose of 10 to to 200 µg per minute.
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' Patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to improve symptoms and reduce morbidity (Level of Evidence B-NR)<nowiki>''</nowiki>.
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' For patients hospitalized with HF, therapy with diuretics and other guideline-directed medications should be titrated with the goal to resolve clinical evidence of congestion to reduce symptoms and rehospitalizations(Level of Evidence B-NR)<nowiki>''</nowiki>.
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''3.''' For patients requiring diuretic treatment during hospitalization for HF, the discharge regimen should include a plan for adjustment of diuretics to decrease rehospitalizations (Level of Evidence B-NR).
+|}
+<ref name="pmid35363500" />
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]
+|-
+| bgcolor="LemonChiffon" |"4'''.''' In patients hospitalized with HF when diuresis is inadequate to relieve symptoms and signs of congestion, it is reasonable to intensify the diuretic regimen using either: a. higher doses of intravenous loop diuretics or addition of a second diuretic''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B-NR]])'' <nowiki>"</nowiki>
+|}
+<ref name="pmid35363500" />
-====Nitroprusside====
+=== Parenteral Vasodilation Therapy in Patients Hospitalized With HF ===
-*Like nitroglycerin, [[nitroprusside]] is both a [[venodilator]] and arterial [[vasodilator]], but [[nitroprusside]] provides a greater degree of [[afterload]] reduction compared with [[nitroglycerin]].  Thus, clinical scenarios where rapid and potent arterial dilation are acquired may benefit from [[nitroprusside]] as opposed to [[nitroglycerin]], and these include a [[hypertensive emergency]], acute [[mitral regurgitation]], [[ventricular septal rupture]], and [[aortic insufficiency]].
+{| class="wikitable" style="width:80%"
-*The initial dose of nitroprusside is 5 to 10 µg per minute and this dose is titrated up every five minutes to a maximum dosing of 5 to 400 pg per minute two maintain a [[mean arterial pressure]] ([[MAP]]) of 65 mm Hg or a [[systolic blood pressure]] of 90 mm Hg.
+|-
-*While patients administered intravenous [[nitroglycerin]] can develop [[tachyphylaxis]], patients administered [[nitroprusside]] can develop an accumulation of metabolites including [[cyanide]] or [[thiocyanate]] which can be toxic and even fatal.  Thus, the duration of a [[nitroprusside]] infusion is usually only 24 to 48 hours.
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]
+|-
+| bgcolor="LemonChiffon" |"1'''.''' In patients who are admitted with decompensated HF, in the absence of systemic hypotension, intravenous nitroglycerin or nitroprusside may be considered as an adjuvant to diuretic therapy for relief of dyspnea''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B-NR]])'' <nowiki>"</nowiki>
+|}
+<ref name="pmid35363500" />
-===More Aggressive Pharmacotherapy===
+=== VTE Prophylaxis in Hospitalized Patients ===
-*[[Ionotropes]] may be administered if the patient's circulatory volume is adequate but there is persistent evidence of inadequate end-organ perfusion.
+{| class="wikitable" style="width:80%"
-* [[Milrinone]] increases contractility and reduces [[afterload]]
+|-
-* [[Dobutamine]] increases contractility in reduces [[afterload]]
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
-* [[Dopamine]] increases blood pressure and increases renal perfusion at low doses
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' In patients hospitalized with HF, prophylaxis for VTE is recommended to prevent venous thromboembolic disease (Level of Evidence B-R)<nowiki>''</nowiki>.
+|}
+<ref name="pmid35363500" />
-===ACE Inhibition===
+''Subcutaneous low-molecular-weight heparin, unfractionated heparin, fondaparinux, or approved DOAC are used for the prevention of clinically symptomatic deep vein thrombosis and pulmonary embolism<ref name="pmid35363500" />.''
-*[[ACE inhibition]] can be continued in the setting of acute decompensated [[congestive heart failure]] if the patient is hemodynamically stable without a rising [[creatinine]] or [[hyperkalemia]].  An exception is the patient who chronically has a [[systolic blood pressure]] below 90 mm Hg who may tolerate the continued administration of an ace inhibitor in the decompensated setting.  The half-life of an [[ACE inhibitor]] is relatively long, and this could results in persistent hypotension in the setting of aggressive diuresis.
-*An ACE inhibitor should not be initiated within the first 12 to 24 hours of acute decompensation of [[heart failure]] as these agents may result in prolonged [[hypotension]] and impaired end organ perfusion.  In particular, intravenous [[enalaprilat]] has been associated with poor outcomes among patients with [[acute MI]] and [[heart failure]].<ref name="pmid8076657">{{cite journal |author=Sigurdsson A, Swedberg K |title=Left ventricular remodelling, neurohormonal activation and early treatment with enalapril (CONSENSUS II) following myocardial infarction |journal=[[European Heart Journal]] |volume=15 Suppl B |issue= |pages=14–9; discussion 26–30 |year=1994 |month=May |pmid=8076657 |doi= |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8076657 |accessdate=2013-04-30}}</ref>
-*[[Hyponatremia]] and a low systolic blood pressure are markers of increased activation of the [[renin angiotensin system]],  and are associated with [[hypotension]] following the administration of an [[ACE inhibitor]].
-===Morphine===
+=== Evaluation and Management of Cardiogenic Shock ===
-* [[Morphine]] reduces [[preload]], reduces [[catecholamines]], and reduces the stimulation by stretch receptors in the lung thereby improving symptoms of [[dyspnea]].
+{| class="wikitable" style="width:80%"
-*Nonrandomized observational studies have demonstrated that in the setting of acute decompensated heart failure morphine is associated with an increase in-hospital mortality, increased mechanical ventilation and longer hospital admissions despite adjustment of covariates in multivariate models.
+|-
-*Given the potential hazard identified in these non-randomized observational studies, morphine  administration is generally not recommended in the setting of acute decompensated [[heart failure]].
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' In patients with cardiogenic shock, intravenous inotropic support should be used to maintain systemic perfusion and preserve end-organ performance(Level of Evidence B-R)<nowiki>''</nowiki>.
+|}
+<ref name="pmid35363500" />
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]
+|-
+| bgcolor="LemonChiffon" |" 2'''.''' In patients with cardiogenic shock, temporary MCS is reasonable when an end-organ function cannot be maintained by pharmacologic means to support cardiac function (Level of Evidence B-NR)".
+|-
+| bgcolor="LemonChiffon" |<nowiki>''</nowiki> 3. In patients with cardiogenic shock, management by a multidisciplinary team experienced in shock is reasonable(Level of Evidence C-NR)<nowiki>''</nowiki>
+|}
+<ref name="pmid35363500" />
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]]
+|-
+| bgcolor="LemonChiffon" |" 4'''.''' In patients presenting with cardiogenic shock, placement of a PA line may be considered to define hemodynamic subsets and appropriate management strategies (Level of Evidence B-NR)".
+|-
+| bgcolor="LemonChiffon" |<nowiki>''</nowiki> 5. For patients who are not rapidly responding to initial shock measures, triage to centers that can provide temporary MCS may be considered to optimize management (Level of Evidence C-LD)<nowiki>''</nowiki>
+|}
+<ref name="pmid35363500" />
+=== Integration of Care: Transitions and Team-Based Approaches ===
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''1.''' n patients with high-risk HF, particularly those with recurrent hospitalizations for HFrEF, referral to multidisciplinary HF disease management programs is recommended to reduce the risk of hospitalization(Level of Evidence B-R)<nowiki>''</nowiki>.
+|-
+| bgcolor="LightGreen" |<nowiki>"</nowiki>'''2.''' In patients hospitalized with worsening HF, patient-centered discharge instructions with a clear plan for transitional care should be provided before hospital discharge(Level of Evidence B-NR)<nowiki>''</nowiki>.
+|}
+<ref name="pmid35363500" />
+{| class="wikitable" style="width:80%"
+|-
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIb]]
+|-
+| bgcolor="LemonChiffon" |" 3'''.''' In patients hospitalized with worsening HF, participation in systems that allow benchmark-ing to performance measures is reasonable to increase use of evidence-based therapy, and to improve quality of care.(Level of Evidence B-NR)".
+|-
+| bgcolor="LemonChiffon" |<nowiki>''</nowiki> 4. In patients being discharged after hospital-ization for worsening HF, an early follow-up, generally within 7 days of hospital discharge, is reasonable to optimize care and reduce rehospitalization (Level of Evidence B-NR)<nowiki>''</nowiki>
+|}
+<ref name="pmid35363500" />
+==2021 ESC Guideline for management of [[acute heart failure]]==
+<span style="font-size:85%">'''Abbreviations:'''
+'''AHF:''' [[Acute heart failure]];
+'''LMWH:''' [[Low-molecular-weight heparin]];
+'''PaO2:''' [[Partial pressure of oxygen]] ;
+'''SBP:''' [[Systolic blood pressure]];
+'''SpO2:''' [[Transcutaneous oxygen saturation]];
+</span>
+<br>
+{| style="cellpadding=0; cellspacing= 0; width: 600px;"
+|-
+| style="padding: 0 5px; font-size: 100%; background: #4682B4; color: #FFFFFF;" align=center |'''Recommendations for initial treatment of acute heart failure'''
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''[[Oxygen]], [[ventilation]] support  ([[ 2021 ESC guidelines classification scheme|Class I, Level of Evidence C]]):'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[Oxygen]] is recommended in [[hypoxic]] [[patients]] with  [[SpO2]]<90% or [[PaO2]] <60 mmHg<br>
+❑ [[Intubation]] is recommended in the presence of progressive [[respiratory failure]] in spite of [[oxygen]] administration or non-invasive [[ventilation]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''[[Oxygen]], [[ventilation]] support  ([[ 2021 ESC guidelines classification scheme|Class IIa, Level of Evidence B]]):'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ In [[patients]] with [[respiratory distress]] ([[respiratory rate]] >25 breaths/min, SpO2<90%), [[non-invasive]] [[positive pressure ventilation]] is recommended to decrease [[respiratory distress]] and reduce the rate of mechanical [[endotracheal intubation]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Diuretics]] :([[ESC guidelines classification scheme|Class I, Level of Evidence C]]) :'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ Intravenous [[loop diuretics]] are considered for all admitted [[patients]] with [[acute heart failure]] presented  with [[signs]], [[symptoms]] of [[fluid]] overload<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Diuretics]] : ([[ESC guidelines classification scheme|Class IIa, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ In [[patients]] with resistant [[edema]] who do not respond to an increase in [[loop diuretic]] doses, combination of a [[loop diuretic]] with [[thiazide]] type [[diuretic]] should be considered <br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Vasodilators]]: ([[ESC guidelines classification scheme|Class IIb, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ In order to improve [[symptoms]] and reduce [[congestion]] in  [[patients]] with [[AHF]] and SBP >110 mmHg, [[vasodilators]] may be considered as initial therapy<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Inotropic agents]] : ([[ESC guidelines classification scheme|Class 2b, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[Inotropic]] agents may be considered in [[patients]] with [[SBP]] <90 mmHg and evidence of [[hypoperfusion]] without response to fluid challenge, to improve peripheral
+[[perfusion]] and maintain [[end-organ]] function<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left | '''[[Inotropic]] agents ([[ESC guidelines classification scheme|Class III, Level of Evidence C]]):'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑  Routinely administration of [[inotropic]] agents are not recommended , due to safety concerns, unless the [[patient]] has [[symptomatic hypotension]] and evidence of [[hypoperfusion]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Vasopressors]]: ([[ESC guidelines classification scheme|ClassIIb, Level of Evidence B]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ In [[patients]] with [[cardiogenic shock]], a [[vasopressor]], preferably [[norepinephrine]], may be indicated to increase [[blood pressure]] and vital [[organ]] perfusion<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Anticoagulant therapy]]: ([[ESC guidelines classification scheme|ClassI, Level of Evidence A]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[Thromboembolism prophylaxis]] such as [[LMWH]] is recommended in [[patients]] not already [[anticoagulated]] and no contraindication to [[anticoagulation]], to prevent the risk of [[deep venous thrombosis]] and [[pulmonary embolism]]<br>
+|-
+|style="font-size: 100; padding: 0 5px; background: #B8B8B8" align=left |'''[[Opiates]]: ([[ESC guidelines classification scheme|ClassIII, Level of Evidence C]])'''
+|-
+|style="padding: 0 5px; font-size: 100%; background: #F5F5F5; width: 70%" align=left|
+❑ [[Opiates]] is not routinely recommended, unless in selected [[patients]] with severe, intractable [[pain]] or [[anxiety]]<br>
+|-
+|}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above table adopted from 2021 ESC Guideline
+|-
+|}<ref name="pmid34447992">{{cite journal |vauthors=McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, Burri H, Butler J, Čelutkienė J, Chioncel O, Cleland JGF, Coats AJS, Crespo-Leiro MG, Farmakis D, Gilard M, Heymans S, Hoes AW, Jaarsma T, Jankowska EA, Lainscak M, Lam CSP, Lyon AR, McMurray JJV, Mebazaa A, Mindham R, Muneretto C, Francesco Piepoli M, Price S, Rosano GMC, Ruschitzka F, Kathrine Skibelund A |title=2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure |journal=Eur Heart J |volume=42 |issue=36 |pages=3599–3726 |date=September 2021 |pmid=34447992 |doi=10.1093/eurheartj/ehab368 |url=}}</ref>
+===Pre-hospital setting===
+*In the pre-hospital setting, [[AHF]] [[patients]] should be monitored by [[pulse oximetry]], [[BP]], [[heart rate]], [[respiratory rate]], and a continuous [[ECG]].
+*[[Oxygen]] therapy may be given based on a clinical judgment unless [[oxygen saturation]] is <90% in which case it should be administered.
+* Indication for [[non-invasive ventilation]]:
+*:[[Respiratory distress]]
+*: [[Respiratory rate]] >25 breaths/min
+* [[Oxygen saturation]] <90%
+===In-hospital management===
+*Specific causes of [[AHF]] should be searched including [[ACS]], [[ hypertensive emergency]], rapid [[arrhythmias]], severe [[bradycardia]], [[conduction disturbance]], acute [[valve regurgitation]], acute [[pulmonary embolism]], [[myocarditis]], [[tamponade]].
+* After exclusion of these [[conditions]], which need to be treated, [[AHF]] should be managed according to the [[clinical]] presentations.
+===Pre-discharge phase===
+=== [[Oxygen]] therapy, [[ventilatory]] support===
+*In [[AHF]], [[oxygen]] should not be used routinely in non-[[hypoxaemic]] [[patients]] due to  [[vasoconstriction]] and a reduction in [[cardiac output]].
+* [[Oxygen]] therapy is recommended in [[patients]] with [[AHF]] SpO2 <90% or [[PaO2]] <60 mmHg to correct [[hypoxemia]].
+*In [[chronic obstructive pulmonary disease]] ([[COPD]]), [[hyper-oxygenation]] may increase [[ventilation-perfusion mismatch]], suppress [[ventilation]] and
+lead to [[hypercapnia]].
+* During [[oxygen]] therapy, [[acid-base balance]] and [[SpO2]] should be monitored.
+*[[Non-invasive positive pressure ventilation]], either continuous [[positive airway pressure]] and [[pressure]] support, improves [[respiratory failure]], increases [[oxygenation]] and [[pH]], and decreases the [[partial pressure]] of [[carbon dioxide]] ([[pCO2]]) and work of [[breathing]] and reduce the rate of [[endotracheal intubation]].
+*  [[Non-invasive positive pressure ventilation ]] indicated to improve [[gas exchange]] and reduce the rate of [[endotracheal intubation]] in [[patients]] with:
+:* [[Respiratory distress]] ([[respiratory rate]] >25 breaths/min
+:* [[SpO2]] <90%
+*[[FiO2]] should be increased up to 100%, if needed, based on  [[oxygen saturation]] level.
+*[[Blood pressure]] should be monitored regularly during [[non-invasive positive pressure ventilation]].
+*The increase in intrathoracic pressure with [[non-invasive positive pressure ventilation]] may lead to reduction in  [[venous return]], right and [[left ventricular]] preload, [[cardiac output]] and [[BP]].
+* In the setting of [[RV]] dysfunction, the increase in [[pulmonary vascular resistance]] and [[RV]] afterload may be present.
+* [[Intubation]] is indicative if there is progressive [[respiratory failure]] despite [[oxygen]] administration or [[non-invasive ventilation]].
+=== [[Diuretics]]===
+*Intravenous [[diuretics]] are mainstay therapy of [[AHF]].
+* Efficacy of [[diuretics]] are due to increase [[renal excretion]] of [[salt]] and [[water]] and reduce of [[fluid]] overload and [[congestion]].
+* There was a greater relief of [[dyspnoea]], change in [[weight]] and net [[fluid]] loss (with no prognostic role for increases in serum [[creatinine]]) in the higher-dose regimen.
+*High [[diuretic]] doses may associate with greater [[neurohormonal]] activation and electrolyte disturbance and poor [[outcomes]].
+*  Treatment with [[diuretic]] should be started with an initial i.v. dose of [[furosemide]], or equivalent dose of [[bumetanide]] or [[torasemide]] to 1-2 times the daily oral dose taken by the [[patient]] before [[admission]].
+*If the [[patient]] was not on oral [[diuretics]], a starting dose of 20-40 mg of [[furosemide]], or a bolus of 10-20 mg i.v [[torasemide]], can be used.
+* [[Furosemide]] can be given as 2-3 daily boluses or as a continuous [[infusion]].
+* Due to post-dosing [[sodium]] retention, daily single bolus administrations are not recommended.
+* With continuous [[infusion]], a loading dose may be used to achieve steady-state earlier.
+* Response to [[diuretic]] should be evaluated shortly after the start of [[diuretic]] therapy and may be measured by performing spot urine [[sodium ]] content  after 2 or
+h and/or by measuring the hourly [[urine output]].
+* A satisfactory [[diuretic]] response can be considered as a [[urine sodium]] content >50-70 mEq/L at 2 h and/or by a [[urine output]] >100-150 mL/h during the first 6 h.
+* If there is an inadequate [[diuretic]] response, the [[loop diuretic]] i.v. dose can be doubled, with a further assessment of [[diuretic ]] response.
+* If the [[diuretic]] response remains insufficient including <100 mL hourly [[diuresis]]in spite of doubling [[loop diuretic]] dose,  concomitant administration of other [[diuretics ]] such as  [[thiazides]] or [[metolazone]] or [[acetazolamide]] , may be considered.
+*[[Serum]] [[electrolytes]] and [[renal function]] should be carefully monitored.
+* Low doses of [[loop diuretics]], with frequent doses may be less likely to cause [[dehydration]] or increase in serum [[creatinine]].
+* Oral treatment should be started after [[congestion ]] relief.
+* Oral [[loop diuretics]] are continued at the lowest dose possible to avoid [[congestion]].
+* Discharge of hospital with persistent [[congestion]] is a major predictor of increased deaths and [[rehospitalizations]].
+* Appropriate long-term diuretic dose should be established before discharge.
+===[[Vasodilators]]===
+*Intravenous [[vasodilators]], namely [[nitrates]] or [[nitroprusside]]  with the effect of dilating venous and [[arterial]] [[vessels]] leading to a reduction in [[venous]] return to the [[heart]], less [[congestion]], lower [[afterload]], increased [[stroke volume]] and consequent relief of [[symptoms]].
+*[[Nitrates]] act mainly on [[peripheral veins]] whereas the effect of [[nitroprusside]] is dilation of [[arterial]] and [[venule]].
+* [[vasodilators]]  may be more effective than [[diuretics]] when acute [[pulmonary edema]] is due to increased [[afterload]] and fluid [[redistribution]] to the [[lungs]] in the absence or with minimal fluid accumulation.
+* Intravenous [[vasodilators]] may be considered to relieve AHF [[symptoms ]] when [[SBP]] is >110 mmHg.
+* They may be started at low doses and uptitrated to achieve clinical improvement and [[BP]] control.
+* [[Nitrates]] are generally administered with an initial bolus followed by continuous [[infusion]] or repeated boluses.
+* [[ Nitroglycerine]] can be given as 1-2 mg boluses in severely [[hypertensive]] [[patients]] with acute [[pulmonary edema]].
+* [[BP]] monitoring is needed to avoid [[hypotension]] due to an excessive decrease in [[preload]] and [[afterload]].
+* Caution should be exercised in [[patients]] with [[LVH]] and/or severe [[aortic stenosis]].
+* [[Hemodynamic parameters]] should be monitored in [[patients]] with [[left ventricular]]  [[systolic dysfunction]] and [[aortic stenosis ]] when [[vasodilators]] are given.
+===[[Inotropes]]===
+* [[Inotropes]] is recommended in [[patients]] with low [[cardiac output]] and [[hypotension]], [[left ventricular systolic dysfunction]] and poor [[organ perfusion]].
+* [[Inotropes]] should be started under [[monitoring]].
+* Common side effects of [[inotropes]] with [[adrnergic]] mechanism including [[sinus tachycardia]], increase [[ventricular rate]] in [[patients]] with [[AF]], induced [[myocardial ischemia]] and [[arrhythmias]], and increase [[mortality]].
+* [[Levosimendan]] or [[type-3-phosphodiesterase inhibitors]] may be preferred over [[dobutamine]] for [[patients]] on [[beta-blockers]].
+* [[Type-3-phosphodiesterase inhibitors]] or [[levosimendan]] may lead to [[peripheral vasodilation]] and [[hypotension]], especially when administrated at high doses.
+===[[Vasopressors]]===
+* [[Norepinephrin]] may be preferred in [[patients]] with severe [[hypotension]], due to [[peripheral vasoconstriction]], to increase [[perfusion ]] to vital [[organs]] at the expense of an increase in [[left ventricular]] [[afterload]].
+*In [[patients]] with advanced [[HF]] and [[cardiogenic shock]], a combination of [[norepinephrine]] and [[inotropic]] agents may be considered.
+*  In some studies, the use of [[norepinephrine]] was the first choice, compared with [[dopamine]] or [[epinephrine]].
+*[[Dopamine]] was preferred to  [[norepinephrine]] as a first-line [[vasopressor]] therapy in [[patients]] with [[shock]].
+* Use of [[dopamin]] was associated with [[arrhythmic]] events and with ahigher [[mortality]] in [[patients]] with [[cardiogenic shock]] but not in those with [[hypovolaemic]] or [[septic shock]].
+* Use of [[epinephrine]] in comparison  with [[norepinephrine]] in [[patients]] with [[cardiogenic shock]] due to acute [[MI]] was associated with higher [[heart rate]]and [[lactic acidosis]] and [[mortality]].
+===[[Opiates]]===
+*[[Opiates]] relieve [[dyspnea]] and [[anxiety]].
+*They may be used as sedative agents during [[non-invasive positive pressure ventilation]] to improve [[patient]] adaptation.
+*Dose-dependent side effects including [[nausea]], [[hypotension]], [[bradycardia]], and [[respiratory depression]].
+* Administration of [[morphine]]  is associated with a higher frequency of [[mechanical ventilation]], prolonged [[hospitalization]], more [[intensive care unit admissions]], and increased [[mortality]].
+*So, routine use of [[opiates]] in [[AHF]] is not recommended.
+* Use of [[morphine]] is recommended in selected [[patients]] with severe/intractable [[pain]] or [[anxiety]] or in the setting of [[palliation]].
+===[[ Digoxin]]===
+*[[Digoxin]] should be considered in patients with [[AF]] with a rapid [[ventricular rate ]] (>110 b.p.m.) despite [[beta-blockers]].
+* [[Digoxin]] can be given in boluses of 0.25-0.5 mg i.v., if not used previously.
+* In [[patients]] with comorbidities (i.e. [[CKD]]) or other factors affecting [[digoxin]] metabolism (including other drugs) and/or the [[elderly]], the maintenance dose may be difficult to estimate.
+* [[Serum]] concentration of [[digoxin]] should be measured.
+===[[Thromboembolism]] prophylaxis===
+*[[Thromboembolism]] prophylaxis with [[heparin]],  [[low-molecular weight heparin]] or another [[anticoagulant]] is recommended, unless contraindicated or existing therapy with oral [[anticoagulants]].
+{{Family tree/start}}
+{{Family tree | | | | A01 | | | |A01= Management of [[acute heart failure]] }}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | B01 | | | |B01= [[Cardiogenic shock]], [[respiratory failure]]}}
+{{Family tree | |,|-|-|^|-|-|.| | }}
+{{Family tree | C01 | | | | C02 |C01= NO| C02= Yes}}
+{{Family tree | |!| | | | | |!| | | | | | | | | | | |}}
+{{Family tree |  G1 | | | |  F2 | | | | | | | | | | |F2=
+ [[Pharmacologic therapy]]
+* [[Ventilatory support]]
+* [[Mechanical circulatory support]]| G1= Identifying acute causes}}
+{{Family tree | |!| | | | | | | | | | | | | | | | | | }}
+{{Family tree |  G2 | | | | | | | | | | | | | | | |G2=
+[[Acute Coronary syndrome]]
+*[[Hypertension]] emergency
+*[[Arrhythmia]]
+*[[Mechanical]] causea
+*[[Pulmonary embolism]]
+*[[Infections]]
+*[[Tamponade]]}}
+{{Family tree |,|^|-|-|.| | | | | | | | | | | | | | |}}
+{{Family tree | Z1| | Z2| | | | | | | | | Z2=NO| |Z1= Yes}}
+{{Family tree | |!| | |!| | | | | | | | | | | | | | | }}
+{{Family tree | P1| |C  | | | | | | | | | | P1= Immediate initiation of specific treatment |C= Further treatment | | | | }}
+{{Family tree/end}}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above algorithm adopted from 2021 ESC Guideline
+|-
+|}<ref name="pmid34447992">{{cite journal |vauthors=McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, Burri H, Butler J, Čelutkienė J, Chioncel O, Cleland JGF, Coats AJS, Crespo-Leiro MG, Farmakis D, Gilard M, Heymans S, Hoes AW, Jaarsma T, Jankowska EA, Lainscak M, Lam CSP, Lyon AR, McMurray JJV, Mebazaa A, Mindham R, Muneretto C, Francesco Piepoli M, Price S, Rosano GMC, Ruschitzka F, Kathrine Skibelund A |title=2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure |journal=Eur Heart J |volume=42 |issue=36 |pages=3599–3726 |date=September 2021 |pmid=34447992 |doi=10.1093/eurheartj/ehab368 |url=}}</ref>
+===Short-term [[mechanical circulatory support]]===
+*In [[patients]] presenting with [[cardiogenic shock]], short-term [[MCS]] may be considered to increase [[cardiac output]] and support end-organ [[perfusion]].
+*Short-term [[MCS]] can be used as a  [[bridge to recovery]] ([[BTR]]), [[bridge to decision]] (BTD) or [[bridge to bridge]] ([[BTB]]).
+*The initial improvements in [[cardiac output]], [[BP]] and [[arterial]] [[lactate]] may be affected by significant [[complications]].
+*Close monitoring of [[hemodynamics]] and [[lactate]] as the markers of [[end-organ damage]] may improve [[survival]].
+* Use of The [[Intra-aortic Balloon Pump]] in [[Cardiogenic shock]] was not associated with the reduced long-term [[mortality]] compared with [[medical therapy]].
+* [[IABP]] is not routinely recommended in [[cardiogenic shock]] post-[[MI]].
+* However, it may still be considered in [[cardiogenic shock]], especially if not due to [[ACS]], and refractory to drug therapy, as a BTD, [[BTR]], or [[BTB]].
+*  [[Patients]] with [[cardiogenic shock]] or [[cardiac arrest]] treated with [[venoarterial ]] [[VA-ECMO]] showed favorable [[outcome]].
+* In cases of [[fulminant myocarditis]] and other [[conditions]] causing severe [[cardiogenic shock]], [[VA-ECMO]] may also be considered.
+* Depending on the severity of [[myocardial dysfunction]] and/or concomitant [[mitral regurgitation]] or [[aortic regurgitation]], [[VA-ECMO]] may increase [[LV]] afterload with an increase in [[LV end-diastolic pressure]] and [[pulmonary congestion]].
+* In these cases, [[LV unloading]] such as [[Impella]] is considered.
+==2021 ESC Guideline for management of [[pulmonary edema]]==
+{{Family tree/start}}
+{{Family tree | | | | A01 | | | |A01= Management of [[patients]] with [[pulmonary edema]]}}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | A01 | | | |A01= [[Oxygen]] (Class I) or [[ventilatory support]] (Class IIa)}}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | B01 | | | |B01= [[Systolic blood pressure]] ≥110 mmHg}}
+{{Family tree | |,|-|-|^|-|-|.| | }}
+{{Family tree | C01 | | | | C02 |C01= Yes| C02= NO}}
+{{Family tree | |!| | | | | |!| | }}
+{{Family tree |  A6 | | | | | A7| | |A6= [[Loop diuretics]] (Class I) and/or [[vasodilators]] (Class IIb)|A7=[[Signs]] of [[hypoperfusion]] }}
+{{Family tree | |:| | | | |,|-|^|-|.| | | |}}
+{{Family tree | |:| | | | | A8| |A9 | | |A8=Yes|A9=NO}}
+{{Family tree | |:| | | | |!| | | |!| | | }}
+{{Family tree | |:| | | | |A10| |A11| |A10=[[Loop diuretics]] (Class I) and [[inotropes]]/[[vasopressors]](Class IIb)|A11=[[Loop diuretics]] (Class I)}}
+{{Family tree | |`|-|-|-|-|v|-|-|-|'| | | | }}
+{{Family tree | | | | | | | A12 | | | A12=[[Congestion]] relief}}
+{{Family tree | | | | | |,|-|^|-|.| | |}}
+{{Family tree | | | | | |A13| |A14| | |A13=Yes|A14=NO}}
+{{Family tree | | | | | |!| | | |!| |}}
+{{Family tree | | | | | |A15| |A16| | A15= Optimized [[medical therapy]]| A16= [[Renal replacement therapy]]
+*[[ Mechanical circulatory support]]
+* [[Palliative therapy]]}}
+{{Family tree/end}}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above algorithm adopted from 2021 ESC Guideline
+|-
+|}
+*[[Acute pulmonary edema]] is related to [[lung]] [[congestion]].
+* Clinical characteristics include  [[dyspnea]] with [[orthopnea]], [[respiratory failure]] ([[hypoxemia]]-[[hypercapnia]]), [[tachypnea]] >25 breaths/min, and increased work of [[breathing]].
+*Treatment including as follows:
+* [[Oxygen]], given as [[continuous positive airway pressure]], non-invasive positive pressure-[[ventilation]] and/or high-flow nasal cannula
+* [[Diuretics]]
+*[[Vasodilators]]  if [[systolic BP]] ([[SBP]]) is high, to reduce [[LV]] [[afterload]]
+*:: In the setting of [[acute pulmonary edema]] with low [[cardiac output]] state, [[inotropes]], [[vasopressors]], and/or [[MCS]] are indicated to restore [[organ]] [[perfusion]].
+==2021 ESC Guideline for management of [[cardiogenic shock]]==
+{{Family tree/start}}
+{{Family tree | | | | A01 | | | |A01=Management of [[patients]] with [[cardiogenic shock]] }}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | B01 | | | |B01= [[Acute coronary syndrome]] ([[ACS]]), [[mechanical complications]] }}
+{{Family tree | |,|-|-|^|-|-|.| | }}
+{{Family tree | C01 | | | | C02 |C01=Yes| C02= NO}}
+{{Family tree | |!| | | | | |!| | }}
+{{Family tree |   A5| | | |  A6 | | | A5=[[Emergency PCI]] or [[surgical]] treatment|A6=Identifying and treatment of other specific causes}}
+{{Family tree | | |`|-|v|-|-|'| | }}
+{{Family tree | | | | |A7 | | | | | A7=[[Oxygen]] therapy (Class I) or [[ventilatory]] support (Class IIa)
+* [[Inotropes]], [[vasopressors]] (Class IIb)
+* Short-term [[mechanical circulatory support]] (Class IIa)}}
+{{Family tree | | | | |!| | | | | }}
+{{Family tree | | | | |A8 | | | | | A8=Improvement of [[hypoperfusion]] and [[organ]] dysfunction}}
+{{Family tree | | |,|-|^|-|.| | | }}
+{{Family tree | | | A9| |A10| | | | A9=Yes|A10=NO}}
+{{Family tree | | | |!| | |!| | | }}
+{{Family tree | | A11 | |A12| | | |A11=Weaning from [[inotropes]]/[[vasopressors]] and/or [[mechanical circulatory support]]
+*Treatment of underlying etiology and [[medical therapy]] optimization (Class I )|A12=[[Mechanical circulatory support]](Class IIa)
+*[[Renal replacement therapy]] (Class IIa)
+*[[Palliative care]] }}
+{{Family tree/end}}
+{|
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above algorithm adopted from 2021 ESC Guideline
+|-
+|}
 ==References==
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+[[Category:Cardiology]]
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+[[Category:Medicine]]
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 [[Category:Up-To-Date cardiology]]
-[[Category:Primary care]]

Congestive heart failure acute pharmacotherapy: Difference between revisions

Latest revision as of 16:18, 1 December 2022

Overview

2022 AHA/ACC/HFSA Heart Failure Guideline Hospitalization of patients with acute heart failure

Assessment of Patients Hospitalized With Decompensated HF

Maintenance or Optimization of GDMT During Hospitalization

Diuretics in Hospitalized Patients: Decongestion Strategy

Parenteral Vasodilation Therapy in Patients Hospitalized With HF

VTE Prophylaxis in Hospitalized Patients

Evaluation and Management of Cardiogenic Shock

Integration of Care: Transitions and Team-Based Approaches

2021 ESC Guideline for management of acute heart failure

Pre-hospital setting

In-hospital management

Pre-discharge phase

Oxygen therapy, ventilatory support

Diuretics

Vasodilators

Inotropes

Vasopressors

Opiates

Digoxin

Thromboembolism prophylaxis

Short-term mechanical circulatory support

2021 ESC Guideline for management of pulmonary edema

2021 ESC Guideline for management of cardiogenic shock

References

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