Congestive heart failure acute pharmacotherapy
(Redirected from Acute decompensated heart failure)
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Resident Survival Guide |
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). |
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)'' |
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). |
| 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) " |
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) " |
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)''. |
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)''. |
| 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)'' |
| 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)'' |
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)''. |
| 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)'' |
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): |
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❑ Oxygen is recommended in hypoxic patients with SpO2<90% or PaO2 <60 mmHg |
| 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) |
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❑ 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) |
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❑ 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) |
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❑ 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): |
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❑ 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) |
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❑ 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 |
|---|
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 |
|---|
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)
| |||||||||||||||||||||||
| Improvement of hypoperfusion and organ dysfunction | |||||||||||||||||||||||
| Yes | NO | ||||||||||||||||||||||
Weaning from inotropes/vasopressors and/or mechanical circulatory support
| Mechanical circulatory support(Class IIa)
| ||||||||||||||||||||||
| 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)