Cardiogenic shock pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
The most common cause for ''cardiogenic shock'' is [[left ventricular failure]] in the setting of acute [[myocardial infarction]]. It usually takes a considerable area of [[MI|infarcted myocardium]] (around 40%) to lead to cardiogenic shock nevertheless, a smaller [[infarct]] may also originate this condition in a patient with a previously compromised [[ventricle]] function. However, there may also be other [[etiologies]], either alone or in combination, for the [[shock]] of [[cardiac]] origin, such as:
*'''Systolic Left Ventricular Dysfunction''' - acute [[myocardial infarction]], [[CHF]], [[Cardiomyopathy]], [[Coronary artery bypass grafting]], [[Myocarditis]], [[Myocardial contusion]] and [[Hypophosphatemia]]
*'''Diastolic Left Ventricular Dysfunction''' - [[Ischemia]]
*'''Obstruction of Left Ventricular Outflow, with Increased Afterload''' - [[Aortic stenosis]], [[Hypertrophic Cardiomyopathy]], [[Coarctation of the Aorta]] and [[Malignant Hypertension]]
*'''Reversal of flow into the left ventricle''' - Acute [[aortic insufficiency]] and [[Endocarditis]]
*'''Inadequate left ventricular filling due to mechanical causes''' - [[Tamponade]], [[Pulmonary Embolism]]
*'''Inadequate left ventricular filling due to inadequate filling time''' - [[Tachycardia]] and [[Tachycardia]]-mediated [[Cardiomyopathy]]
*'''Conduction abnormalities''' - [[Atrioventricular block]] and [[Sinus Bradycardia]]
*'''Mechanical defect''' - [[VSD]] and [[Free wall rupture|Left ventricle free wall rupture]]
*'''Right ventricular failure''' - [[Pulmonary embolism]] and [[Hypoxic pulmonary vasoconstriction]]
===The Pathophysiologic "Spiral" of Cardiogenic shock===
The pathologic process begins with [[myocardial]] [[ischemia]] that leads to an abnormal function of the [[cardiac muscle]]. This abnormality worsens the initial [[ischemia]], which then deteriorates even further the [[ventricular function]], creating the so called ''downward spiral''.<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> When [[ischemia]] reaches a point that the [[left ventricle]] [[myocardium]] fails to pump, parameters like [[stroke volume]] and [[cardiac output]] will therefore decrease. The pressure gradient produced between the pressure within the [[coronary arteries]] and within the [[left ventricle]], along with the duration of the [[diastole]], will dictate [[myocardial]] [[perfusion]]. This will then be compromised by the [[hypotension]] and the [[tachycardia]], worsening the [[myocardial]] [[ischemia]]. The pump failure will decrease the ability to pump the blood out of the ventricle, thereby increasing the ventricular diastolic pressures. This will not only reduce the [[coronary]] [[perfusion pressure]], as it will also increase the [[ventricle]] wall stress, so that the [[myocardial]] [[oxygen]] requirements will also increase, which will consequently propagate the [[ischemia]].<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>
The [[ischemia]] generated by all these processes increases the [[diastolic]] stiffness of the [[ventricle]] wall and this, along with the [[left ventricular dysfunction]], will increase the [[left atrial]] pressure. The increased [[left atrial]] pressure will propagate through the [[pulmonary veins]], generating [[pulmonary congestion]], which by decreasing [[oxygen]] exchanges, leads to [[hypoxia]]. The [[hypoxia]] will further worsen the [[ischemia]] in the [[myocardium]] and the [[pulmonary congestion]] will propagate its effect through the [[pulmonary arteries]] to the [[right ventricle]], hence jeopardizing its performance. Once myocardial function is affected, the body will put in motion compensatory mechanisms to try to increase the cardiac output, which include:<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>
*[[Tachycardia]] and increased [[contractility]] through [[sympathetic]] stimulation
*Activation of the [[RAAS|renin/angiotensin/aldosterone system]], leading to fluid retention and consequently increased [[preload]]
However, these compensatory mechanisms eventually become maladaptive seeing that:<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>
*[[Tachycardia]] and increased [[contractility]] will increase [[myocardium|cardiac muscle]] [[oxygen]] demand, thereby exacerbating the initial [[ischemia]]
*[[Vasoconstriction]], as a response to impaired [[cardiac output]], in order to try to maintain [[coronary artery]] [[perfusion]] and systemic [[blood pressure]], increases [[myocardial]] [[afterload]], leading to an impairment in [[myocardial]] performance and an increase in its [[oxygen]] demand, worsening [[ischemia]].
The prolonged systemic [[hypoperfusion]] and [[hypoxia]] will cause a shift in [[cellular metabolism]], prioritizing [[glycolysis]], leading to a state of [[lactic acidosis]], which jeopardizes [[contractility]] and [[systolic]] performance, thereby affecting the previously described system.
All these factors affecting [[oxygen]] demand and [[cardiac]] performance create a vicious cycle that if not interrupted, may eventually lead to death. The [[therapeutic]] approach to cardiogenic shock focuses in disrupting this cycle.<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>


==References==
==References==

Revision as of 20:07, 11 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 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 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 do 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.[2][3][4][5][6][7][8] Despite the many possible causes for this cadiac failure, the most common is left ventricular failure in the setting of myocardial infarction.[9] In the presence of cardiogenic shock develops a pathological cycle in which the 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 heart sympathetic stimulation 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 muscle depression decreasing contractility and worsening hypotension. Lactic acidosis will also develop, resulting from the poor tissue perfusion, that causes a shift in the metabolism to glycolysis, which will also depress the myocardium, thereby worsening the clinical scenario.[10][11]

Pathophysiology

References

  1. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  2. ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 1405179260.
  3. ↑ 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. ↑ 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.
  5. ↑ 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. ↑ 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. ↑ 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. ↑ 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. ↑ 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.
  10. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  11. ↑ Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.


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