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)

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@@ 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 heart failure; AHF; Heart failure; HF; BTB;  bridge to bridge; BTD; bridge to decision; BTR; bridge to recovery;
 ==Overview==
-==Acute Pharmacotherapy==
+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]]).
-The goals of acute pharmacotherapy include:
-* Reduce [[preload]]
-* Reduce [[afterload]]
-* Reduce intravascular volume
-* Improve [[cardiac contractility]]
-The following acute therapies are used in the acute management of heart failure and their mechanism of action are as follows
-*[[Diuretics]] reduces [[preload]] and reduces intravascular volume
-*[[Nitroprusside]] reduces [[afterload]] and reduces [[preload]]
-*[[Nesiritide]] reduces [[afterload]] and reduces [[preload]]
-*[[Milrinone]] increases contractility and reduces [[afterload]]
-*[[Dobutamine]] increases contractility in reduces [[afterload]]
-*[[Dopamine]] increases blood pressure and increases renal perfusion at low doses
-*[[Nitroglycerine]] reduces [[afterload]] and reduces [[preload]]
-==Chronic Pharmacotherapy==
-==Diuretics==
-* Provide symptomatic relief
-* Slows the progression of ventricular remodeling by reducing ventricular filling pressure and wall stress
-* No survival benefit and may cause [[azotemia]], [[hypokalemia]], [[metabolic alkalosis]] and elevation of neurohormones.
-* Although [[thiazide]] [[diuretics]] are effective in mild [[heart failure]] they are usually inadequate for the treatment of severe [[heart failure]].
-* [[Thiazide]] [[diuretics]] have also been associative with [[hyponatremia]].
-* Fluid retention usually responds best to [[furosemide]] (Lasix) and at doses of 10 to 20 mg per day. The patient should be told to return to their physician in the next three to seven days for further assessment including assessment of their [[potassium]] concentration. Weight loss should not exceed 1 to 2 pounds/day.
-* Higher lasix doses are associated with higher mortality, likely as a surrogate of disease severity rather than part of a causal pathway.
-* If there is no response to the initial  dose then it can be increased by at least 50%. The maintenance dose of the [[diuretics]] lower than that required to initiate diuresis.
-* If the patient gains more than two pounds and they are instructed to double the dose of their loop diuretic.
-* Once the baseline weight has been re-established than they can resume their previous status.
-* Intermittent use of [[metolazone]] into dose of 2.5 or 5 mg can be given if the patient is refractory to [[furosemide]] Lasix. [[Metolazone]] should be given in the inpatient setting.
-* The role of [[potassium]] sparing diuretics such as [[spironolactone]] (Aldactone), [[amiloride]], or [[triamterene]] remains the subject of controversy. Spironolactone is currently recommended as third line therapy for congestive heart failure.
-*Extreme caution is necessary when adding a [[potassium]] sparing agent to the regiment that includes [[ACE inhibitor]]s particularly when diabetes or renal disease is present because the patient can become [[hyperkalemic]].
-===Electrolyte replacement===
-*[[ACE inhibitor]]s reduce [[potassium]] excretion, but most patients with good renal function require [[potassium]] supplementation during daily therapy with the diuretics such as [[furosemide]] (Lasix) despite of [[ACE inhibitor]]s therapy.
-* Dietary supplementation is rarely adequate.
-* [[Hypokalemia]] can aggravate [[arrhythmias]] and precipitate [[muscle cramps]].
-*[[Potassium]] levels >6 (particularly when occurs rapidly) can be associated with reduced [[myocardial contractility]].
-*Patients are actually at higher risk of [[hyperkalemia]] and [[hypokalemia]]. The goal is to maintain a [[potassium]] between 3.8 and 4.5 mEq.
-*Unless the [[hypokalemia]] is very severe and at life-threatening level, [[potassium]] should be replaced by oral administration.
-* Potassium should not be administered intravenously at a rate that exceeds 10 mEq per hour.
-* Patients who use [[diuretics]] usually require approximately 20-60 mEq/day of oral [[potassium]].
-* Extra [[potassium]] should be given after the patient has noted diuresis or weight change. If patient has lost more than two pounds, the electrolyte's level should be checked every three days.
-=== Loop Diuretics ===
-* Furosemide, bumetanide, ethacrynic acid and torsemide.
-* Inhibit the Na+/K+/2Cl- symporter.
-* Furosemide IV has direct vasodilatory effect.
-* Providing additional blood pressure reduction.
-* Relaxes pre-contracted pulmonary venules: beneficial for treatment of Pulmonary Edema.
-=== Thiazide Diuretics ===
-* Inhibit the Na+/Cl- co transporter in the distal convoluted tube.
-* Recommended for management of mild chronic heart failure.
-=== Potassium Sparing Diuretics ===
-* [[Spironolactone]], [[amiloride]] and [[triamterene]].
-* Inhibit principal cells in the distal convoluted tubule and cortical collecting duct.
-* Inhibits Na reabsorbtion and [[Potassium]] secretion.
-* Their significant side effect is [[hyperkalemia]].
-==Renin-Angiotensin-Aldosterone Axis Inhibitors==
-===Angiotensin converting enzyme inhibitor or ACE Inhibitors===
-* [[ACE Inhibitor]]s ([[Angiotensin converting enzyme inhibitor|ACEI]]) should be considered as first-line therapy for the treatment of patients with clinical heart failure due to reduced left ventricular systolic dysfunction (LVSD), patients with asymptomatic LV dysfunction, and for patients who are at high risk for the development of heart failure due to the presence of coronary, cerebrovascular, or peripheral vascular disease.
-* Treatment should not be deferred in patients with few or no symptoms because of the significant mortality benefit derived from [[Angiotensin converting enzyme inhibitor|ACEI]] therapy.
-* Initial therapy usually consist of 12.5 mg tid of [[captopril]], 2.5 mg bid of [[enalapril]], or 2.5 mg daily lisinopril. The optimal dose is usually established by optimizing the dose every 4 to 6 weeks.
-* ACE inhibitors are rarely adequate for the treatment of congestion without the use of [[diuretics]].
-* 5-10 % patients cannot tolerate [[ACE inhibitors]] because of [[cough]]. [[Cough]] can be a sign of elevated left-sided filling pressures. Sometimes [[cough]] will diminish with the treatment of heart failure. A
-* Renal artery stenosis should be considered if there's a decline in renal function with the initiation of [[ACE inhibitors]].
-===Angiotensin receptor blockers (ARB)===
-* * In the CHARM study [[candesartan]] reduced both hospitalization and mortality.
-===Aldosterone Antagonists===
+== 2022 AHA/ACC/HFSA Heart Failure Guideline Hospitalization of patients with acute heart failure ==
-* [[Spironolactone]] is third line therapy for CHF
-* An important side effect of spironolactone is [[hyperkalemia]]
+=== Assessment of Patients Hospitalized With Decompensated HF ===
+{| 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. 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).
+|-
+| 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).
+|-
+| 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).
+|}
+<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>
+=== Maintenance or Optimization of GDMT During Hospitalization ===
+{| 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" />
-==[[Nitrate]]s==
+=== Diuretics in Hospitalized Patients: Decongestion Strategy ===
+{| 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.''' 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" />
-*[[Nitrate]]s can be added to [[ACE inhibitor]]s to relieve symptoms of congestion.
+=== Parenteral Vasodilation Therapy in Patients Hospitalized With HF ===
-*The addition of a [[nitrate]] and [[ACE inhibitor]] may improve exercised tolerance.
+{| class="wikitable" style="width:80%"
-*The combination of [[hydralazine]] and nitrates is useful when [[ACE inhibitor]]s are not well tolerated.
+|-
-*[[Hydralazine]] by itself is only an arterial vasodilator and does not reduced ventricular filling pressures to the same extent that nitrates and [[ACE inhibitor]]s do. In fact when used alone it can stimulate sympathetic tone reflexively. The combination of hydralazine and nitrates has been shown to decrease mortality as well as improve the left ventricular ejection fraction and exercise capacity in patients with [[heart failure]]. However the combination of [[hydralazine]] and [[nitrate]]s has been found to be less effective than [[ACE inhibitor]]s.
+| colspan="1" style="text-align:center; background:LemonChiffon" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class IIa]]
-*The major uses this combination is in those patients who are intolerant of [[ACE inhibitor]]s.
+|-
+| 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" />
-==Anticoagulants==
+=== VTE Prophylaxis in Hospitalized Patients ===
-* The annual incidence of systemic and [[pulmonary embolism]] in patients with [[heart failure]] is 2-5%. This is not that dissimilar from the risk of severe bleeding among patients to its anticoagulants which is 0.8-2.5% per year.
+{| 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 hospitalized with HF, prophylaxis for VTE is recommended to prevent venous thromboembolic disease (Level of Evidence B-R)<nowiki>''</nowiki>.
+|}
+<ref name="pmid35363500" />
-* As a result anticoagulation is not routinely recommended in the current guidelines for the treatment of [[heart failure]]. However among those patients with a [[atrial fibrillation]], a history of emboli, or multiple intracardiac thrombi, or akinesis or dyskinesis detected on echo should be anticoagulated.
+''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" />.''
-* While hospitalized, patients with CHF should receive [[DVT prophylaxis]]
+=== Evaluation and Management of Cardiogenic Shock ===
+{| 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 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" />
-==Beta Blockers==
+=== Integration of Care: Transitions and Team-Based Approaches ===
-*[[Metoprolol]], [[Carvedilol]] and [[Bisoprolol]] have FDA approved labeling for use in congestive heart failure.
+{| class="wikitable" style="width:80%"
-* Blockade of compensatory sympathetic stimulation is associated with arrhythmic, ischemic, remodeling, and apoptotic benefits.
+|-
-* Used as monotherapy or combined with conventional heart failure management, beta-blockers reduce the combined risk of morbidity and mortality.
+| colspan="1" style="text-align:center; background:LightGreen" |[[ACC AHA guidelines classification scheme#Classification of Recommendations|Class I]]
-* Initiate low starting dosing and titrate up to tolerated target doses.
+|-
-* [[Lopressor]] should be used instead of [[atenolol]] in the patient with CHF
+| 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>.
-==Antiarrhythmic Drugs==
+|-
-Antiarrhythmic therapy should be considered as a therapy to prevent [[sudden cardiac death]].  Over 50% of heart failure patients will have asymptomatic non-sustained [[ventricular tachycardia]] and there is no general indication for treatment of this arrhythmia. T here are multiple causes of the for [[sudden cardiac death]] in the patient with congestive heart failure which include not only [[arrhythmic]] causes, but also thrombotic and other causes:
+| 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>.
-*Arrhythmic causes
+|}
-*:[[Ventricular tachycardia]]
-*:[[Ventricular fibrillation]]
-*:[[Bradyarrhythmias]]
-*Thrombotic causes:
+<ref name="pmid35363500" />
-*:[[Acute MI]]
+{| class="wikitable" style="width:80%"
-*:[[Pulmonary embolism]]
+|-
+| 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>
+|}
-*Other causes:
+<ref name="pmid35363500" />
-*:[[Hyperkalemia]]
+==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%
-===Metabolism of Antiarrhythmics in the setting of Congestive Heart Failure===
+===In-hospital management===
-Metabolisms of following anti-arrhythmic drugs are significantly affected in patients with [[congestive heart failure]] and care should be taken regarding their administration:
+*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]].
-#[[Quinidine]]
-#[[Procainamide]]
-#[[Disopyramide]]: Contraindicated in patients with [[heart failure]].
-#[[Moricizine]]
-#[[Lidocaine]]
-#[[Mexiletine]]
-#[[Tocainide]]
-#[[Flecainide]]
-#[[Propafenone]]
-#[[Amiodarone]]
-Patients with congestive heart failure should not be treated with [[dronedarone]].
-==Positive Inotropics==
-#Agents that increase intracellular cAMP
-#*Alpha-adrenergic agonists
-#*[[Phosphodiesterase inhibitors]]
-#Agents that affect sarcolemmal ion pumps/channels
-#*[[Digoxin]]
-#Agents that modulate intracellular calcium mechanisms by either:
-#*Release of [[sarcoplasmic reticulum]] [[calcium]] (IP3)
-#*Increased sensitization of the contractile proteins to [[calcium]]
-#Drugs having multiple mechanisms of action
-#*Pimobendan
-#*Vesnarinone
-===== Digoxin =====
-* Inhibits Na,K+-ATPase resulting in an increase in intracellular Na+, extracellular Ca2+ exchange increasing the velocity and extent of [[sarcomere]] shortening.
-* ACC/AHA recommend [[digoxin]] for symptomatic patients with left ventricular systolic dysfunction.
-* Commonly used in patients with [[heart failure]] and [[atrial fibrillation]] to reduce the ventricular response rate.
-* Mortality has not been shown to be improved with use of [[digoxin]], but the use of [[digoxin]] has been associated with a reduction in hospitalization in the RALES study.
-* There is no need to load a CHF patient with [[digoxin]].  For the majority of patients with normal renal function, a daily dose of 0.25 mg of [[digoxin]] is usually adequate.  In the older patient or in those patients with renal impairment, a dose of 0.125 mg per day may be adequate.
-* Drugs that increase the concentration of [[digoxin]] include antibiotics and anticholinergic agents as well as [[amiodarone]], [[quinidine]] and [[verapamil]].
-* In the RALES study, a level of < 1 ng/ml was associated with efficacy.  Levels above 1 ng/ml were not associated with greater efficacy and were associated with higher mortality.
-===== Dobutamine =====
-*Activates beta-1 receptors resulting in enhanced cardiac contractility.
-*Long-term dobutamine infusions are arrhythmogenic and increase mortality.
-=====Dopamine =====
-*Unique dose dependent mechanism of action.
-*At low doses: (≤2 µg/kg/min), selective dilation of splanchnic and renal arterial beds. assists in increasing renal perfusion.
-*At intermediate doses: (2 to 10 µg/kg/min), increased norepinephrine secretion results in increased cardiac contractility, heart rate and peripheral vascular resistance.
-*At higher doses: (5 to 20 µg/kg/min), direct alpha-adrenergic receptor stimulation increases systemic vascular resistance.
-===== Milrinone =====
-*Phosphodiesterase-III inhibitor that enhances contractility by increasing intracellular cyclic adenosine monophosphate (cAMP).
-*Potent pulmonary vasodilatation that benefits pts with pulmonary hypertension.
-*Unlike dobutamine: milrinone is beneficial to decompensated heart failure patients on beta-blocker therapy.
-*Long term milrinone infusions are arrhythmogenic, and increase mortality.
-==Metformin==
-*[[Metformin]] use in [[diabetics]] with [[CHF]] is associated with lower mortality
-==Ca Channel Blockers==
-* Although calcium channel blockers cause [[vasodilation]] their overall benefit is minimized by the fact that they have a [[negative inotropic]] effect and by the reflex activation of the sympathetic nervous system.
-* These agents are not recommended as vasodilators in patients with congestive heart failure, however they may be useful as antihypertensive agents in patients with [[diastolic dysfunction]].
-==Drugs to Avoid in CHF==
-* [[Dronedarone]] should be avoided in patients who were hospitalized with CHF (this is a boxed warning)
-* [[Sotalol]] (has a negative inotropic effect)
-==Biventricular Pacing or Cardiac Resynchronization Therapy (CRT)==
-* Cardiac resynchronization therapy should only be undertaken if the blood pressure is low and if the heart failure medicines have been optimized
-* CRT is indicated for symptomatic patients with NYHA III-IV heart failure and wide QRS complex (>120ms) who are him normal sinus rhythm.
-* 70% of patients receiving synchronous ventricular contraction report significant symptomatic improvements.
-===Implantation of Intracardiac Defibrillator===
-*50% of heart failure patients die of [[sudden cardiac death]].
+{{Family tree/start}}
-*ICDs are indicated for patients with previous myocardial infarction and LVEF <30%, sustained ventricular tachycardia, inducible ventricular tachycardia.
+{{Family tree | | | | A01 | | | |A01= Management of [[acute heart failure]] }}
-*Morbidity/mortality benefit of ICD placement vs. anti-arrhythmic drug therapy is controversial.
+{{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>
-===Ultrafiltration===
-The process of ultrafiltration consists of the production of plasma water from whole blood across a semipermeable membrane (hemofilter) in response to a transmembrane pressure gradient. Possible benefits of ultrafiltration as follow;
-#Provides fluid regulation
-#:*Relieve pulmonary edema
-#:*Reduce ascites and/or peripheral edema
-#:*Hemodynamic stabilization
-#:*Improve oxygenation
-#:*Facilitate blood product replacement without excess volume
-#:*Enable parenteral nutritional support without excess volume
-#Improves solute regulation
-#:*Correct acid-base balance
-#:*Correct serum sodium content
-#:*Eliminate myocardial depressant factors or known toxins
-#:*Correct uremia
-#:*Correct hyperkalemia
-#:*Correct other electrolyte disturbances
-#Helps to establish homeostasis
-#:*Reset water omostat
-#:*Restore diuretic responsiveness
-#:*Reduce neurohormonal activation
-===Cardiac Surgery===
-*Resection of non-viable myocardium
-*Revascularization without resection of non-viable myocardium
-*Dor procedure: Surgical resection of infarcted myocardium and left ventricular reconstruction.
-*Placement of a passive containment device to prevent progressive cardiac dilation ('''Under investigation''')
-===Left Ventricular Assist Devices===
+===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
+|-
+|}
-*LVADs are temporary devices to bridge end stage patients to cardiac transplantation.
-*Current clinical research in implementing permanent portable LVADs is underway, and first studies have promising results.
-===Cardiac Transplantation===
+*[[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]].
-* For patients with end-stage congestive heart failure despite all interventions.
+==2021 ESC Guideline for management of [[cardiogenic shock]]==
-* 80% 1 year survival and 60% 5 year survival.
-* Lifelong immunosuppressive therapy to prevent (or postpone) rejection, increased risk for opportunistic infections and malignancies.
-'''AHA/ACC Guidelines: Indications for heart transplantation'''
+{{Family tree/start}}
-*Any hemodynamic compromise due to heart failure.
+{{Family tree | | | | A01 | | | |A01=Management of [[patients]] with [[cardiogenic shock]] }}
-*Requiring IV inotropic support to maintain adequate organ perfusion.
+{{Family tree | | | | |!| | | | | }}
-*Peak Vo2 <10 ml/kg/min.
+{{Family tree | | | | B01 | | | |B01= [[Acute coronary syndrome]] ([[ACS]]), [[mechanical complications]] }}
-*NYHA Class IV symptoms not amenable to any other intervention.
+{{Family tree | |,|-|-|^|-|-|.| | }}
-*Recurrence of symptomatic ventricular arrhythmias refractory to all therapeutic intervention.
+{{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]] }}
-==Exercise and Daily Activities==
+{{Family tree/end}}
-*Patient should have uninterrupted exercise at least four days a week including a walking program.
+{|
-*Rowing machines usually are too vigorous of exercise.
+! colspan="2" style="background: PapayaWhip;" align="center" + |The above algorithm adopted from 2021 ESC Guideline
-*Patients with heart failure should avoid weightlifting.
+|-
-*The patient should not routinely lift more than 20 pounds.
+|}
-*Patients can continue their sexual activity. Some patients take 2.5 or 5.0 mg of sublingual nitroglycerin before sexual activity.
 ==References==
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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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