Cardiogenic shock classification: Difference between revisions

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==Overview==
==Overview==
'''Cardiogenic shock''' is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|cardiac failure]], in the presence of adequate [[intravascular]] volume, typically followed by [[hypotension]], which leads to insufficient ability to meet [[oxygen]] and [[nutrient]] demands of [[organs]] and other peripheral tissues.<ref>{{Cite book  | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages =  }}</ref> It may range from mild to severe [[hypoperfusion]] and may be defined in terms of [[hemodynamic]] parameters, which according to most studies, means a state in which [[systolic blood pressure]] is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right [[ventricular]] filling pressures that does not respond to isolated fluid administration, is secondary to [[heart failure|cardiac failure]] and occurs with signs of [[hypoperfusion]] ([[oliguria]], [[cool extremities]], [[cyanosis]] and [[altered mental status]]) or a [[cardiac index]] of < 2.2 L/min/m² (on [[inotropic]], [[vasopressor]] or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg. There are different causes explaining the development of cardiogenic shock, these may be grouped into two major categories: ''intrinsic'' and ''compressive''.<ref>{{cite book | last = Hochman | first = Judith | title = Cardiogenic shock | publisher = Wiley-Blackwell | location = Chichester, West Sussex, UK Hoboken, NJ | year = 2009 | isbn = 1405179260  }}</ref><ref name="GoldbergGore1991">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Gore|first2=Joel M.|last3=Alpert|first3=Joseph S.|last4=Osganian|first4=Voula|last5=de Groot|first5=Jacques|last6=Bade|first6=Jurgen|last7=Chen|first7=Zuoyao|last8=Frid|first8=David|last9=Dalen|first9=James E.|title=Cardiogenic Shock after Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=325|issue=16|year=1991|pages=1117–1122|issn=0028-4793|doi=10.1056/NEJM199110173251601}}</ref><ref name="GoldbergSamad1999">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Samad|first2=Navid A.|last3=Yarzebski|first3=Jorge|last4=Gurwitz|first4=Jerry|last5=Bigelow|first5=Carol|last6=Gore|first6=Joel M.|title=Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=340|issue=15|year=1999|pages=1162–1168|issn=0028-4793|doi=10.1056/NEJM199904153401504}}</ref><ref>{{Cite journal  | last1 = Menon | first1 = V. | last2 = Slater | first2 = JN. | last3 = White | first3 = HD. | last4 = Sleeper | first4 = LA. | last5 = Cocke | first5 = T. | last6 = Hochman | first6 = JS. | title = Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry. | journal = Am J Med | volume = 108 | issue = 5 | pages = 374-80 | month = Apr | year = 2000 | doi =  | PMID = 10759093 }}</ref><ref name="Hasdai-1999">{{Cite journal  | last1 = Hasdai | first1 = D. | last2 = Holmes | first2 = DR. | last3 = Califf | first3 = RM. | last4 = Thompson | first4 = TD. | last5 = Hochman | first5 = JS. | last6 = Pfisterer | first6 = M. | last7 = Topol | first7 = EJ. | title = Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. | journal = Am Heart J | volume = 138 | issue = 1 Pt 1 | pages = 21-31 | month = Jul | year = 1999 | doi =  | PMID = 10385759 }}</ref><ref name="Fincke-2004">{{Cite journal  | last1 = Fincke | first1 = R. | last2 = Hochman | first2 = JS. | last3 = Lowe | first3 = AM. | last4 = Menon | first4 = V. | last5 = Slater | first5 = JN. | last6 = Webb | first6 = JG. | last7 = LeJemtel | first7 = TH. | last8 = Cotter | first8 = G. | title = Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. | journal = J Am Coll Cardiol | volume = 44 | issue = 2 | pages = 340-8 | month = Jul | year = 2004 | doi = 10.1016/j.jacc.2004.03.060 | PMID = 15261929 }}</ref><ref name="DzavikCotter2007">{{cite journal|last1=Dzavik|first1=V.|last2=Cotter|first2=G.|last3=Reynolds|first3=H. R.|last4=Alexander|first4=J. H.|last5=Ramanathan|first5=K.|last6=Stebbins|first6=A. L.|last7=Hathaway|first7=D.|last8=Farkouh|first8=M. E.|last9=Ohman|first9=E. M.|last10=Baran|first10=D. A.|last11=Prondzinsky|first11=R.|last12=Panza|first12=J. A.|last13=Cantor|first13=W. J.|last14=Vered|first14=Z.|last15=Buller|first15=C. E.|last16=Kleiman|first16=N. S.|last17=Webb|first17=J. G.|last18=Holmes|first18=D. R.|last19=Parrillo|first19=J. E.|last20=Hazen|first20=S. L.|last21=Gross|first21=S. S.|last22=Harrington|first22=R. A.|last23=Hochman|first23=J. S.|title=Effect of nitric oxide synthase inhibition on haemodynamics and outcome of patients with persistent cardiogenic shock complicating acute myocardial infarction: a phase II dose-ranging study|journal=European Heart Journal|volume=28|issue=9|year=2007|pages=1109–1116|issn=0195-668X|doi=10.1093/eurheartj/ehm075}}</ref>
The Society for Cardiovascular Angiography and Intervention (SCAI) developed an expert consensus statement, endorsed by multiple relevant societies, proposing a novel CS
classification scheme, which categorizes patients with or at risk of CS into worsening stages of hemodynamic compromise for the purposes of facilitating patient care and research. The SCAI CS classification consensus statement describes 5 stages of CS, each of which may have an “A” modifier signifying the occurrence of cardiac arrest (CA). This classification schema was developed based on expert consensus opinion and its ability to discriminate among levels of mortality risk in critically ill patients remains to be established. The goal of this study was to examine the construct validity of the SCAI CS staging schema by demonstrating the ability of a simple functional classification of SCAI shock stages at the time of cardiac intensive care unit (CICU) admission to predict mortality in CICU patients.The purpose of the classification schema is to assist in clear communication among clinicians and researchers regarding the patient’s current clinical status, recognizing that CS encompasses a spectrum, including those at high risk of developing shock from myocardial dysfunction to those who develop hemodynamic collapse and cardiac arrest. The CS classification schema includes five stages of shock labeled A through E. The authors categorized patients in three domains, including laboratory findings, physical exams findings, and hemodynamics. When cardiac arrest has occurred the modifier (A) is added to stage classification (i.e. stage CA).


==Classification==
==Classification==

Revision as of 15:20, 31 December 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

The Society for Cardiovascular Angiography and Intervention (SCAI) developed an expert consensus statement, endorsed by multiple relevant societies, proposing a novel CS classification scheme, which categorizes patients with or at risk of CS into worsening stages of hemodynamic compromise for the purposes of facilitating patient care and research. The SCAI CS classification consensus statement describes 5 stages of CS, each of which may have an “A” modifier signifying the occurrence of cardiac arrest (CA). This classification schema was developed based on expert consensus opinion and its ability to discriminate among levels of mortality risk in critically ill patients remains to be established. The goal of this study was to examine the construct validity of the SCAI CS staging schema by demonstrating the ability of a simple functional classification of SCAI shock stages at the time of cardiac intensive care unit (CICU) admission to predict mortality in CICU patients.The purpose of the classification schema is to assist in clear communication among clinicians and researchers regarding the patient’s current clinical status, recognizing that CS encompasses a spectrum, including those at high risk of developing shock from myocardial dysfunction to those who develop hemodynamic collapse and cardiac arrest. The CS classification schema includes five stages of shock labeled A through E. The authors categorized patients in three domains, including laboratory findings, physical exams findings, and hemodynamics. When cardiac arrest has occurred the modifier (A) is added to stage classification (i.e. stage CA).

Classification

In cardiogenic shock, the root abnormality is the inability of the heart to pump out enough blood to maintain normal organ perfusion and blood pressure. However, this failure may be due to different factors, which allow us to classify cardiogenic shock into two categories:[1][2][3]

  • Intrinsic - this includes the conditions affecting the heart or the structures that allow it to function properly. In this category, the affected structures may be: the myocardial muscle, responsible to pump out the blood; the heart valves allowing the blood in and out of the heart chambers; the conduction system, responsible for the transmission of the electrical signals that allow the myocardium to contract in a coordinated fashion or, a combination of the previous. Examples of such factors are: myocardial infarction, mitral regurgitation and electrolyte imbalances.
  • Compressive - this includes the conditions in which an otherwise "healthy heart" is prevented from working properly and pumping the blood through the vascular system, by a mechanism not related to it. The degree of impact that an extrinsic factor must have on the heart will depend on the overall "health status" of this last one. An "healthy heart" might take a more aggressive outside influence without compromising its function, while a heart already weakened by another disease, such as atherosclerosis, might fail more promptly. An example of such factor is cardiac tamponade.

Often times both factors are affecting the heart's ability to perform its function, at which times it might be hard to identify clearly the underlying mechanism of the cardiogenic shock.[4]

References

  1. Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
  2. Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.
  3. Kheng CP, Rahman NH (July 2012). "The use of end-tidal carbon dioxide monitoring in patients with hypotension in the emergency department". Int J Emerg Med. 5 (1): 31. doi:10.1186/1865-1380-5-31. PMC 3585511. PMID 22828152.
  4. Myers, Jeffrey (2002). Principles of pathophysiology and emergency medical care. Albany: Delmar/Thomson Learning. ISBN 978-0766825482.


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