Congestive heart failure positive inotropics: Difference between revisions
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| [[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''']] | |||
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| [[File:Critical_Pathways.gif|88px|link= Congestive heart failure critical pathways]]|| <br> || <br> | |||
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{{Congestive heart failure}} | {{Congestive heart failure}} | ||
{{CMG}}; {{AOEIC}} {{LG}} {{EdzelCo}} | |||
==Overview== | |||
Positive inotropes are agents that increase myocardial contractility, and are used to support cardiac function in conditions such as decompensated [[congestive heart failure]], [[cardiogenic shock]], [[septic shock]], [[myocardial infarction]], [[cardiomyopathy]], etc. Examples of positive inotropes include [[digoxin]], [[dobutamine]], [[dopamine]] and [[phosphodiesterase-III inhibitor]]s like [[amrinone]] and [[milrinone]]. | |||
== | ==Inotropics== | ||
===Pharmacologic Mechanisms=== | |||
#Agents that increase intracellular cAMP | #Agents that increase intracellular cAMP | ||
#*Alpha-adrenergic agonists | #*Alpha-adrenergic agonists | ||
| Line 13: | Line 26: | ||
#*Increased sensitization of the contractile proteins to [[calcium]] | #*Increased sensitization of the contractile proteins to [[calcium]] | ||
#Drugs having multiple mechanisms of action | #Drugs having multiple mechanisms of action | ||
#*Pimobendan | #*[[Pimobendan ]] | ||
#*Vesnarinone | #*[[Vesnarinone]] | ||
==Digoxin== | ===Digoxin=== | ||
* Inhibits Na,K+-ATPase resulting in an increase in intracellular Na+, extracellular Ca2+ exchange increasing the velocity and extent of [[sarcomere]] shortening. | * 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. | * 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. | * 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. | * Mortality has not been shown to be improved with use of [[digoxin]]<ref name="pmid9036306">{{cite journal |author= |title=The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group |journal=[[The New England Journal of Medicine]] |volume=336 |issue=8 |pages=525–33 |year=1997 |month=February |pmid=9036306 |doi=10.1056/NEJM199702203360801 |url=http://dx.doi.org/10.1056/NEJM199702203360801 |accessdate=2012-04-05}}</ref>, 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. | * 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]]. | * 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. | * 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== | ===Dobutamine=== | ||
* Activates beta-1 receptors resulting in enhanced [[cardiac contractility]]. | * Activates beta-1 receptors resulting in enhanced [[cardiac contractility]]. | ||
* Long-term dobutamine infusions are arrhythmogenic and increase mortality. | * Long-term dobutamine infusions are [[arrhythmogenic]] and increase mortality. | ||
* Dobutamine also slightly reduces afterload | * Dobutamine also slightly reduces afterload | ||
==Dopamine== | ===Dopamine=== | ||
Dopamine is associated with a dose dependent mechanism of action: | |||
* '''At low doses: (≤2 µg/kg/min),''' | * '''At low doses: (≤2 µg/kg/min),''' selectively dilate splanchnic and renal arterial beds and increase renal perfusion. | ||
* '''At intermediate doses: (2 to 10 µg/kg/min),''' | * '''At intermediate doses: (2 to 10 µg/kg/min),''' increase norepinephrine secretion and result in increased [[cardiac contractility]], [[heart rate]] and [[systemic vascular resistance]]. | ||
* '''At higher doses: (5 to 20 µg/kg/min),''' direct alpha-adrenergic receptor stimulation increases [[systemic vascular resistance]]. | * '''At higher doses: (5 to 20 µg/kg/min),''' result in direct [[alpha-adrenergic receptor]] stimulation and increases [[systemic vascular resistance]]. | ||
===Milrinone=== | |||
* [[Phosphodiesterase-III inhibitor]] that enhances [[cardiac contractility]] by increasing intracellular [[cyclic adenosine monophosphate]] ([[cAMP]]). | |||
* Potent pulmonary [[vasodilator]] that may benefit some patients with [[pulmonary hypertension]]. | |||
* Unlike dobutamine, [[milrinone]] is beneficial in decompensated heart failure patients who are on [[beta-blocker]] therapy. | |||
* Long term milrinone infusions are [[arrhythmogenic]], and increase mortality. | |||
== 2022 AHA/ACC/HFSA Heart Failure Guideline (DO NOT EDIT) <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>== | |||
=====[[Pharmacological]] [[Treatment]] for Stage C [[HFrEF]]: [[Digoxin]]===== | |||
{|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"|<nowiki>"</nowiki>'''1.''' In [[patients]] with [[symptomatic]] [[HFrEF]] despite GDMT (or who are unable to tolerate GDMT), [[digoxin]] might be considered to decrease [[hospitalizations]] for [[HF]]. <ref name="pmid9036306">{{cite journal| author=Digitalis Investigation Group| title=The effect of digoxin on mortality and morbidity in patients with heart failure. | journal=N Engl J Med | year= 1997 | volume= 336 | issue= 8 | pages= 525-33 | pmid=9036306 | doi=10.1056/NEJM199702203360801 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9036306 }} </ref><ref name="pmid16339157">{{cite journal| author=Ahmed A, Rich MW, Love TE, Lloyd-Jones DM, Aban IB, Colucci WS | display-authors=etal| title=Digoxin and reduction in mortality and hospitalization in heart failure: a comprehensive post hoc analysis of the DIG trial. | journal=Eur Heart J | year= 2006 | volume= 27 | issue= 2 | pages= 178-86 | pmid=16339157 | doi=10.1093/eurheartj/ehi687 | pmc=2685167 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16339157 }} </ref> ''([[ACC AHA guidelines classification scheme#Level of Evidence|Level of Evidence: B-R]])'' <nowiki>"</nowiki> | |||
== | |} | ||
* [ | |||
==External Link== | |||
*[https://www.ahajournals.org/doi/epub/10.1161/CIR.0000000000001063.full.pdf 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines]<ref name="pmid35363499">{{cite journal |vauthors=Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, Drazner MH, Dunlay SM, Evers LR, Fang JC, Fedson SE, Fonarow GC, Hayek SS, Hernandez AF, Khazanie P, Kittleson MM, Lee CS, Link MS, Milano CA, Nnacheta LC, Sandhu AT, Stevenson LW, Vardeny O, Vest AR, Yancy CW |title=2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines |journal=Circulation |volume=145 |issue=18 |pages=e895–e1032 |date=May 2022 |pmid=35363499 |doi=10.1161/CIR.0000000000001063 |url=}} </ref> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
[[Category:Cardiology]] | |||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Intensive care medicine]] | |||
[[Category:Medicine]] | |||
[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
[[Category:Up-To-Date cardiology]] | [[Category:Up-To-Date cardiology]] | ||
Latest revision as of 21:15, 22 June 2022
 |
Resident Survival Guide |
| File:Critical Pathways.gif |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2] Edzel Lorraine Co, DMD, MD[3]
Overview
Positive inotropes are agents that increase myocardial contractility, and are used to support cardiac function in conditions such as decompensated congestive heart failure, cardiogenic shock, septic shock, myocardial infarction, cardiomyopathy, etc. Examples of positive inotropes include digoxin, dobutamine, dopamine and phosphodiesterase-III inhibitors like amrinone and milrinone.
Inotropics
Pharmacologic Mechanisms
- Agents that increase intracellular cAMP
- Alpha-adrenergic agonists
- Phosphodiesterase inhibitors
- Agents that affect sarcolemmal ion pumps/channels
- 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
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[1], 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.
- Dobutamine also slightly reduces afterload
Dopamine
Dopamine is associated with a dose dependent mechanism of action:
- At low doses: (≤2 µg/kg/min), selectively dilate splanchnic and renal arterial beds and increase renal perfusion.
- At intermediate doses: (2 to 10 µg/kg/min), increase norepinephrine secretion and result in increased cardiac contractility, heart rate and systemic vascular resistance.
- At higher doses: (5 to 20 µg/kg/min), result in direct alpha-adrenergic receptor stimulation and increases systemic vascular resistance.
Milrinone
- Phosphodiesterase-III inhibitor that enhances cardiac contractility by increasing intracellular cyclic adenosine monophosphate (cAMP).
- Potent pulmonary vasodilator that may benefit some patients with pulmonary hypertension.
- Unlike dobutamine, milrinone is beneficial in decompensated heart failure patients who are on beta-blocker therapy.
- Long term milrinone infusions are arrhythmogenic, and increase mortality.
2022 AHA/ACC/HFSA Heart Failure Guideline (DO NOT EDIT) [2]
Pharmacological Treatment for Stage C HFrEF: Digoxin
| Class IIb |
| "1. In patients with symptomatic HFrEF despite GDMT (or who are unable to tolerate GDMT), digoxin might be considered to decrease hospitalizations for HF. [1][3] (Level of Evidence: B-R) " |
External Link
- 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines[4]
References
- ↑ 1.0 1.1 "The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group". The New England Journal of Medicine. 336 (8): 525–33. 1997. doi:10.1056/NEJM199702203360801. PMID 9036306. Retrieved 2012-04-05. Unknown parameter
|month=ignored (help) - ↑ 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). - ↑ Ahmed A, Rich MW, Love TE, Lloyd-Jones DM, Aban IB, Colucci WS; et al. (2006). "Digoxin and reduction in mortality and hospitalization in heart failure: a comprehensive post hoc analysis of the DIG trial". Eur Heart J. 27 (2): 178–86. doi:10.1093/eurheartj/ehi687. PMC 2685167. PMID 16339157.
- ↑ Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, Drazner MH, Dunlay SM, Evers LR, Fang JC, Fedson SE, Fonarow GC, Hayek SS, Hernandez AF, Khazanie P, Kittleson MM, Lee CS, Link MS, Milano CA, Nnacheta LC, Sandhu AT, Stevenson LW, Vardeny O, Vest AR, Yancy CW (May 2022). "2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". Circulation. 145 (18): e895–e1032. doi:10.1161/CIR.0000000000001063. PMID 35363499 Check
|pmid=value (help).