Cardiogenic shock pathophysiology

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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

The most common insult for cardiogenic shock is left ventricular pump failure in the setting of acute myocardial infarction. It usually takes a considerable area of 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, other parts of the circulatory system may contribute, either alone or in combination, with inadequate compensation, or additional defects for this shock of cardiac origin, such as:[12]

Luckily many of these abnormalities are fully or partially reversible. This justifies the fact that most of the survivors have good chances of having a good outcome and living with considerable quality of life, assuming that they follow their physician's orders.[12]

The Pathophysiologic "Spiral" of Cardiogenic shock

The pathologic process begins with myocardial ischemia leading 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".[11] When ischemia reaches a point that the left ventricular myocardium fails to pump properly, parameters like stroke volume and cardiac output will therefore decrease. The pressure gradient produced between the pressure within the coronary arteries and the left ventricle, along with the duration of the diastole, dictate myocardial perfusion. This will be compromised by the hypotension and the tachycardia, worsening the myocardial ischemia and the perfusion of other vital organs. The fact that the heart is the only organ that benefits from a low blood pressure, as afterload decreases, makes these hemodynamical changes both beneficial and detrimental. The pump failure will then decrease the ability to push 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 raise, consequently propagating the ischemia.[11][12][13]

Other important reference to make in the setting of cardiac pump failure and hypoperfusion of the peripheral tissues is that this last one, leads to the release of catecholamines. Catecholamines such as norepinephrine, will increase the heart's contractility and peripheral blood flow, by causing constriction of arterioles, together with angiotensin II, to maintain perfusion, however, this will also increase the heart's oxygen demand and have proarrhythmic and myocardiotoxic consequences. The increased SVR coupled with the low cardiac output will lead to an even more pronounced reduction of tissue perfusion.[12]

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 of 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. These include:[14]

However, these compensatory mechanisms eventually become maladaptive seeing that:[12][15]

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.[16]

Right Ventricle Myocardial Infarction

Accounts for about 5% of the cases but represents as high mortality rate as left ventricular shock. The right ventricular regions more commonly affected by infarction are the inferior and inferior-posterior walls. The coronary arteries frequently occluded in this setting are the right coronary artery, or the left circumflex coronary artery, in a left dominant system.[17][18] Patients with right coronary artery occlusion, in a right dominant system, are at higher risk of developing papillary muscle rupture and therefore undergoing valvular heart disease, such as mitral regurgitation.[18][19][20]

Right ventricle failure may affect left ventricular performance by several means:[21][22]

Ventricular Septal and Free Wall Rupture

Ventricular septal rupture and free wall rupture, which constitute two entities of cardiac rupture, represent the second most common cause of death in patients with acute myocardial infarction, during hospital stay.[23][24][25]

In the case of ventricular septal rupture, in the SHOCK registry, it accounted for 4.6% of the cases of cardiogenic shock.[26] The most recent registries show that ventricular septal rupture generally develops within the first 16 to 24 hours post-MI and has the following characteristics:[27][28]

  • simple - "direct through-and-through any defect", generally an anterior defect;
  • complex - a serpigenous dissection tract radiating from the primary ventricular septal rupture site, generally an inferior defect.

The rupture of the ventricular septum leads to the formation of a "left-to-right shunt", which precipitates hemodynamic decompensation and congestive heart failure.[18]

In the case of free wall rupture, some studies show that half of the cases occur in the first 5 days after myocardial infarction, with about 90% happening within the first 2 weeks.[33][34] According to the SHOCK trial data, this type of rupture had 55% of mortality rate within the first 30 days.[34] Free wall rupture may also be classified as simple or complex. It may occur either on the anterior or the lateral and posterior left ventricular walls.[34][23] These last two are thought to rupture easier, however, because of the higher proportion of anterior MIs, they are seen less frequently.[18] The rupture may present with different types of courses:

Inflammation and Hemodynamics

Studies like the SHOCK trial show that not all patients follow this classic paradigm, since:[38][39][40]

These facts have introduced the concept that myocardial infarction may cause SIRS and that inflammation plays an important part in the development and persistence of cardiogenic shock, contributing to myocardial dysfunction and vasodilation. The possibility of developing SIRS raises with the increasing permanence in cardiogenic shock.[12][41][42]

At the time of the cardiac injury, the myocardium releases into circulation cytokines, particularly during the first 24 to 72 hours after the MI, these will induce the enzyme nitric oxide synthase, thereby increasing the level of nitric oxide, which will be responsible for vasodilation and worsening of hypotension, further jeopardizing left ventricle performance.[43][44][45][46][47][48] NO may also form a toxic radical, called peroxynitrite, when combined with superoxide, affecting myocardial contractility.[49] Among these released cytokines during cardiogenic shock, are interleukin-6 and tumor necrosis factor. In the case of IL-6, this specific cytokine is correlated with the degree of organ failure and therefore mortality.[50] These inflammatory mediators, among other actions, are responsible for the release of BNP, which makes the levels of BNP good markers, not only for the level of inflammation, but also to evaluate hemodynamic decompensation.[51] Other circulatory factors, such as procalcitonin, complement and CRP, have been reported in some studies to contribute to the development of SIRS in cardiogenic shock.[52][53] Besides the aforementioned macrocirculatory changes in cardiogenic shock, which may also be seen in septic shock, it is important to mention that microcirculatory abnormalities, caused in part by the inflammatory cascades, play an important part in the pathogenesis of organ failure as well.[54][55][56]

Iatrogenic Cardiogenic Shock

An important number of patients in cardiogenic shock complicating myocardial infarction (around 3/4), develop it after hospital admission.[57][58] In some of these patients, it is reported that the development of shock, particularly in high risk patients, is related to the use of certain classes of medications, used to treat the MI. These include:[59][60][61][62]

Pathology

Myocardium

The myocardial infarction, more than an isolated event, is a process that develops over several hours. Initially there is a central area of infarction surrounded by a border of ischemic myocardium. As time goes by, and in the absence of reperfusion measures, this area of ischemia will enlarge outwards from the central area.[63] As this area of infarcted myocardium grows, so does the chances of developing cardiogenic shock, leading to the conclusion that pump failure follows severe loss of myocardial mass. This loss usually develops over several hours, to days.[64] This conclusion is supported by the fact that most patients develop cardiogenic shock in hospital, several hours after being admitted for acute MI.[26][65]

These patients who develop shock after admission usually suffer of what is known as infarct extension, which may result from:[66][67][68]

These myocytes around the initial area of infarction are more prone to additional ischemic episodes, being at higher risk of becoming necrotic. This extension of necrosis is sometimes called "piecemeal necrosis".[69][70][71]

Other important concept is infarct expansion. It differs from the first in the way that it refers to the expansion and trim of the infarcted area, during the first hours/days, due of the movement of myocytes, slipping past each other, constituting an early form of remodeling. This can change both the regional and global ventricular configuration, leading to an increased wall stress and also contributing to left ventricular enlargement. [72][71] It is more often seen in myocardial infarction of the anterior wall.[67][71]

Despite the distinction between these two concepts, it is thought that infarct enlargement is the result of a combination of the infarct extension and expansion.[73]

Besides the local myocardial impact caused by the infarct, other mechanisms are involved in the deterioration of cardiac performance and hence the development of cardiogenic shock:

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. ↑ 11.0 11.1 11.2 Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 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.
  13. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  14. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  15. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  16. ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
  17. ↑ Isner JM, Roberts WC (1978). "Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction". Am J Cardiol. 42 (6): 885–94. PMID 153103.
  18. ↑ 18.0 18.1 18.2 18.3 18.4 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.
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  25. ↑ Becker RC, Hochman JS, Cannon CP, Spencer FA, Ball SP, Rizzo MJ; et al. (1999). "Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study". J Am Coll Cardiol. 33 (2): 479–87. PMID 9973029.
  26. ↑ 26.0 26.1 Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA; et al. (2000). "Cardiogenic shock complicating acute myocardial infarction--etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?". J Am Coll Cardiol. 36 (3 Suppl A): 1063–70. PMID 10985706.
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  52. ↑ Granger CB, Mahaffey KW, Weaver WD, Theroux P, Hochman JS, Filloon TG; et al. (2003). "Pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to primary percutaneous coronary intervention in acute myocardial infarction: the COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA) trial". Circulation. 108 (10): 1184–90. doi:10.1161/01.CIR.0000087447.12918.85. PMID 12925454.
  53. ↑ APEX AMI Investigators. Armstrong PW, Granger CB, Adams PX, Hamm C, Holmes D; et al. (2007). "Pexelizumab for acute ST-elevation myocardial infarction in patients undergoing primary percutaneous coronary intervention: a randomized controlled trial". JAMA. 297 (1): 43–51. doi:10.1001/jama.297.1.43. PMID 17200474.
  54. ↑ De Backer D, Creteur J, Dubois MJ, Sakr Y, Vincent JL (2004). "Microvascular alterations in patients with acute severe heart failure and cardiogenic shock". Am Heart J. 147 (1): 91–9. PMID 14691425.
  55. ↑ De Backer D, Creteur J, Preiser JC, Dubois MJ, Vincent JL (2002). "Microvascular blood flow is altered in patients with sepsis". Am J Respir Crit Care Med. 166 (1): 98–104. PMID 12091178.
  56. ↑ Trzeciak S, Dellinger RP, Parrillo JE, Guglielmi M, Bajaj J, Abate NL; et al. (2007). "Early microcirculatory perfusion derangements in patients with severe sepsis and septic shock: relationship to hemodynamics, oxygen transport, and survival". Ann Emerg Med. 49 (1): 88–98, 98.e1–2. doi:10.1016/j.annemergmed.2006.08.021. PMID 17095120.
  57. ↑ Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS; et al. (2005). "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock". JAMA. 294 (4): 448–54. doi:10.1001/jama.294.4.448. PMID 16046651.
  58. ↑ Jeger, R. V. (2006). "Emergency revascularization in patients with cardiogenic shock on admission: a report from the SHOCK trial and registry". European Heart Journal. 27 (6): 664–670. doi:10.1093/eurheartj/ehi729. ISSN 0195-668X.
  59. ↑ Meine TJ, Roe MT, Chen AY, Patel MR, Washam JB, Ohman EM; et al. (2005). "Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative". Am Heart J. 149 (6): 1043–9. doi:10.1016/j.ahj.2005.02.010. PMID 15976786.
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