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]
- 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 and 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 left ventricle free wall rupture
- Right ventricular failure - Pulmonary embolism and hypoxic pulmonary vasoconstriction
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 ventricle 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 in 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]
- Tachycardia and increased contractility through sympathetic stimulation
- Activation of the renin/angiotensin/aldosterone system, leading to fluid retention and consequently increased preload
However, these compensatory mechanisms eventually become maladaptive seeing that:[12][15]
- Tachycardia and increased contractility will increase 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 (SVR), increases myocardial afterload, leading to an impairment in myocardial performance and an increase in its oxygen demand, worsening ischemia;
- The activation of the neurohormonal cascade will promote retention of water and sodium, in order to compensate for the hypotension and improve perfusion, yet this will also exacerbate pulmonary edema.
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]
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.
- ↑ 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.
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.
- ↑ 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.
- ↑ 11.0 11.1 11.2 Hollenberg SM, Kavinsky CJ, Parrillo JE (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815.
- ↑ 12.0 12.1 12.2 12.3 12.4 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.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.
- ↑ Hasdai, David. (2002). Cardiogenic shock : diagnosis and treatmen. Totowa, N.J.: Humana Press. ISBN 1-58829-025-5.