Cardiogenic shock overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
'''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 | '''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.<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> Despite the many possible causes for the [[heart failure|cardiac failure]], the most common is [[left ventricular failure]] in the setting of [[myocardial infarction]].<ref name="HochmanBuller2000">{{cite journal|last1=Hochman|first1=Judith S|last2=Buller|first2=Christopher E|last3=Sleeper|first3=Lynn A|last4=Boland|first4=Jean|last5=Dzavik|first5=Vladimir|last6=Sanborn|first6=Timothy A|last7=Godfrey|first7=Emilie|last8=White|first8=Harvey D|last9=Lim|first9=John|last10=LeJemtel|first10=Thierry|title=Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry|journal=Journal of the American College of Cardiology|volume=36|issue=3|year=2000|pages=1063–1070|issn=07351097|doi=10.1016/S0735-1097(00)00879-2}}</ref> | ||
In the presence of cardiogenic shock | In the presence of cardiogenic shock a pathological cycle develops in which [[ischemia]], the initial aggression, leads to [[myocardial]] dysfunction. This will affect parameters like the [[cardiac output]], [[stroke volume]] and [[myocardial]] [[perfusion]] thereby worsening the [[ischemia]]. The body will then initiate a series of compensatory mechanisms, such as [[sympathetic]] stimulation of the [[heart]] and activation of the [[RAAS|renin/angiotensin/aldosterone system]], trying to overcome the [[cardiac]] aggression, however, this will ultimately lead to a downward spiral worsening of the [[ischemia]]. [[Inflammatory]] mediators, originated in the [[MI|infarcted]] area, will also intervene at some point causing [[myocardial]] depression, decreasing [[contractility]] and worsening [[hypotension]]. [[Lactic acidosis]] will also develop, resulting from the poor [[tissue]] [[perfusion]], that is responsible for a shift in [[metabolism]] to [[glycolysis]], which will further depress the [[myocardium]], thereby worsening the clinical scenario.<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><ref name="pmid10391815">{{cite journal| author=Hollenberg SM, Kavinsky CJ, Parrillo JE| title=Cardiogenic shock. | journal=Ann Intern Med | year= 1999 | volume= 131 | issue= 1 | pages= 47-59 | pmid=10391815 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10391815 }} </ref> | ||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Revision as of 16:17, 16 May 2014
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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]
Overview
Cardiogenic shock is defined as a state of systemic hypoperfusion, originated in cadiac failure in the presence of adequate intravascular volume, typically followed by hypotension, which results in the insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues.[1] 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:[2][3][4]
- does not respond to isolated fluid administration;
- is secondary to cardiac failure;
- occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m², if on inotropic, vasopressor or circulatory device support, or < 1.8-2.2 L/min/m², if off support, and pulmonary artery wedge pressure > 18 mm Hg.[5][6][7][8]
Despite the importance of these values, the diagnosis of shock is primarily based on the clinical findings and only then, supported by the measurement of hemodynamic values, which may be obtained through pulmonary artery catheterization or doppler echocardiography. The level of hemodynamic derangement will directly dictate the short-term outcome of the patient.[9][10] Although there are several possible causes for cardiogenic shock, the most common remain the myocardial infarction and the left ventricular failure. Nevertheless, it is important to exclude possible mechanical complications, which in the presence of myocardial infarction might be responsible for the shock.[9] A subset of patients may be diagnosed with cardiogenic shock with systolic blood pressure > 90 mm Hg in the following circumstances:
- in the presence of medication or support devices;
- in the presence of systemic hypoperfusion with a low cardiac output and blood pressure maintained by important vasoconstriction;
- in cases of preexisting hypertension if mean systemic pressure is ≥ 30 mm Hg lower than baseline.
Despite the improvements made in the earlier diagnosis, prompt and adequate treatment and resources for patients presenting with myocardial infarction, cardiogenic shock remains as the most common cause of death in patients following MI.[11] However, evidence shows that patients in cardiogenic shock may benefit greatly from an invasive early approach, increasing their chances of short and long-term survival and quality of life.[9]
Pathophysiology
Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in 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.[12] 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 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.[13][3][4][14][6][7][8] Despite the many possible causes for the cardiac failure, the most common is left ventricular failure in the setting of myocardial infarction.[15] In the presence of cardiogenic shock a pathological cycle develops in which ischemia, the initial aggression, leads to myocardial dysfunction. This will affect parameters like the cardiac output, stroke volume and myocardial perfusion thereby worsening the ischemia. The body will then initiate a series of compensatory mechanisms, such as sympathetic stimulation of the heart and activation of the renin/angiotensin/aldosterone system, trying to overcome the cardiac aggression, however, this will ultimately lead to a downward spiral worsening of the ischemia. Inflammatory mediators, originated in the infarcted area, will also intervene at some point causing myocardial depression, decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that is responsible for a shift in metabolism to glycolysis, which will further depress the myocardium, thereby worsening the clinical scenario.[16][17]
Epidemiology and Demographics
In defiance of the historic numbers of mortality from cardiogenic shock of 80% to 90%, in the modern era, this type of shock comprises a mortality risk of around 50%, in the face of the diagnostic and treatment techniques, which have greatly been developed in recent years. Depending on the demographic and clinical factors, this risk can range from 10% to 80%. The incidence of cardiogenic shock among patients with acute MI is approximately 5% to 10%.[18][19] Because atherosclerosis and myocardial infarction are both more frequent among males, cardiogenic shock is more common in this gender. However, because women tend to present with acute myocardial infarction at a later age, along with the fact that they have a greater chance of having multivessel coronary artery disease when they first develop symptoms, a greater proportion of women with acute MI develop cardiogenic shock.[20]
Risk Factors
The identification of high-risk groups for developing cardiogenic shock and its promoting factors is mandatory for the improvement of the survival rate of these patients. This will facilitate the providing of adequate therapeutic measures and the avoidance of others which would otherwise lead to iatrogenic shock.[21] Considering that the most common cause of cardiogenic shock is acute coronary syndrome, either with or without persistent ST-segment elevation, these patients are at higher risk and will benefit highly from these measures.[22]
Diagnosis
Electrocardiogram
An electrocardiogram may be useful in distinguishing cardiogenic shock from septic shock or neurogenic shock. A diagnosis of cardiogenic shock is suggested by the presence of ST segment changes, new left bundle branch block or signs of a cardiomyopathy. Cardiac arrhythmias may also be present.
Chest X-ray
The chest x ray will show pulmonary edema, pulmonary vascular redistribution, enlarged hila, kerley's B lines, and bilateral pleural effusions in patients with left ventricular failure. In contrast, a pneumonia may be present in the patient with septic shock.
Echocardiography
Echocardiography is important imaging modality in the evaluation of the patient with cardiogenic shock. It allows the clinician to distinguish cardiogenic shock from septic shock and neurogenic shock. In cardiogenic shock due to acute MI, poor wall motion will be present. In septic shock, a hypercontractile ventricle may be present. Mechanical complications such as papillary muscle rupture, pseudoaneurysm, and a ventricular septal defect may also be visualized. Valvular heart disease such as aortic stenosis, aortic insufficiency and mitral stenosis can also be assessed. Dynamic outflow obstruction such as HOCM can also be identified and quantified. The magnitude of left ventricular dysfunction in patients with cardiomyopathy can be evaluated.
References
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 1405179260.
- ↑ 3.0 3.1 Goldberg, Robert J.; Gore, Joel M.; Alpert, Joseph S.; Osganian, Voula; de Groot, Jacques; Bade, Jurgen; Chen, Zuoyao; Frid, David; Dalen, James E. (1991). "Cardiogenic Shock after Acute Myocardial Infarction". New England Journal of Medicine. 325 (16): 1117–1122. doi:10.1056/NEJM199110173251601. ISSN 0028-4793.
- ↑ 4.0 4.1 Goldberg, Robert J.; Samad, Navid A.; Yarzebski, Jorge; Gurwitz, Jerry; Bigelow, Carol; Gore, Joel M. (1999). "Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction". New England Journal of Medicine. 340 (15): 1162–1168. doi:10.1056/NEJM199904153401504. ISSN 0028-4793.
- ↑ Menon, V.; Slater, JN.; White, HD.; Sleeper, LA.; Cocke, T.; Hochman, JS. (2000). "Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry". Am J Med. 108 (5): 374–80. PMID 10759093. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 Hasdai, D.; Holmes, DR.; Califf, RM.; Thompson, TD.; Hochman, JS.; Pfisterer, M.; Topol, EJ. (1999). "Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries". Am Heart J. 138 (1 Pt 1): 21–31. PMID 10385759. Unknown parameter
|month=ignored (help) - ↑ 7.0 7.1 Fincke, R.; Hochman, JS.; Lowe, AM.; Menon, V.; Slater, JN.; Webb, JG.; LeJemtel, TH.; Cotter, G. (2004). "Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry". J Am Coll Cardiol. 44 (2): 340–8. doi:10.1016/j.jacc.2004.03.060. PMID 15261929. Unknown parameter
|month=ignored (help) - ↑ 8.0 8.1 Dzavik, V.; Cotter, G.; Reynolds, H. R.; Alexander, J. H.; Ramanathan, K.; Stebbins, A. L.; Hathaway, D.; Farkouh, M. E.; Ohman, E. M.; Baran, D. A.; Prondzinsky, R.; Panza, J. A.; Cantor, W. J.; Vered, Z.; Buller, C. E.; Kleiman, N. S.; Webb, J. G.; Holmes, D. R.; Parrillo, J. E.; Hazen, S. L.; Gross, S. S.; Harrington, R. A.; Hochman, J. S. (2007). "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". European Heart Journal. 28 (9): 1109–1116. doi:10.1093/eurheartj/ehm075. ISSN 0195-668X.
- ↑ 9.0 9.1 9.2 Reynolds, H. R.; Hochman, J. S. (2008). "Cardiogenic Shock: Current Concepts and Improving Outcomes". Circulation. 117 (5): 686–697. doi:10.1161/CIRCULATIONAHA.106.613596. ISSN 0009-7322.
- ↑ Giannuzzi P, Imparato A, Temporelli PL, de Vito F, Silva PL, Scapellato F; et al. (1994). "Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction". J Am Coll Cardiol. 23 (7): 1630–7. PMID 8195524.
- ↑ Ng, R.; Yeghiazarians, Y. (2011). "Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies". Journal of Intensive Care Medicine. 28 (3): 151–165. doi:10.1177/0885066611411407. ISSN 0885-0666.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 1405179260.
- ↑ Menon, V.; Slater, JN.; White, HD.; Sleeper, LA.; Cocke, T.; Hochman, JS. (2000). "Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry". Am J Med. 108 (5): 374–80. PMID 10759093. Unknown parameter
|month=ignored (help) - ↑ Hochman, Judith S; Buller, Christopher E; Sleeper, Lynn A; Boland, Jean; Dzavik, Vladimir; Sanborn, Timothy A; Godfrey, Emilie; White, Harvey D; Lim, John; LeJemtel, Thierry (2000). "Cardiogenic shock complicating acute myocardial infarction—etiologies, management and outcome: a report from the SHOCK Trial Registry". Journal of the American College of Cardiology. 36 (3): 1063–1070. doi:10.1016/S0735-1097(00)00879-2. ISSN 0735-1097.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.
- ↑ Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8.
- ↑ Hasdai D, Holmes DR, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock during acute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III. Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J. Jan 1999;20(2):128-35.
- ↑ Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai D, Harrington RA, Hochman JS, Califf RM, Battler A, Box JW; et al. (2000). "Platelet glycoprotein IIb/IIIa blockade and outcome of cardiogenic shock complicating acute coronary syndromes without persistent ST-segment elevation". J Am Coll Cardiol. 36 (3): 685–92. PMID 10987585.