Materiały źródłowe

• #1 Cardiogenic Shock: Pathogenesis, Classification, and Management – PubMed

  https://pubmed.ncbi.nlm.nih.gov/37973356/

  Cardiogenic shock (CS) is a life-threatening circulatory failure syndrome which can progress rapidly to irreversible multiorgan failure through self-perpetuating pathophysiological processes. […] Recent developments in CS classification have highlighted its etiologic, mechanistic, and hemodynamic heterogeneity. […] Optimal CS management depends on early recognition, rapid reversal of the underlying cause, and prompt initiation of hemodynamic support.

• #2 Management of cardiogenic shock: a narrative review | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-024-01260-y

  Cardiogenic shock (CS) is characterized by low cardiac output and sustained tissue hypoperfusion that may result in end-organ dysfunction and death. […] CS is associated with high short-term mortality, and its management remains challenging despite recent advances in therapeutic options. […] Cardiogenic shock (CS) is a life-threatening syndrome defined by peripheral hypoperfusion and organ dysfunction due to primary cardiac dysfunction. […] It has several underlying aetiologies, the most common being acute myocardial infarction (AMI). […] CS involves several pathophysiologic mechanisms that may have consequences for clinical management. […] Thus, one has to differentiate de novo or acute cardiac conditions leading to CS and CS related to acute-on-chronic heart failure. […] Cardiogenic shock arises from an imbalance between input and demand, causing systemic hypoperfusion and organ dysfunction.

• #3 Cardiogenic Shock | RECAPEM

  https://recapem.com/cardiogenic-shock/

  Cardiogenic shock (CS) is the most severe form of acute heart failure. It is a potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. […] The following mechanisms may happen separately at different stages of CS, or each may occur simultaneously. The magnitude of the initial cardiac insult and/or early application of interventions may either mask or delay some of these stages. […] An initial cardiac insult that decreases cardiac output (CO) […] Left and/or right ventricular dysfunction causes a drop in LV cardiac output and stroke volume, resulting in: […] Elevated LV end-diastolic pressure. […] Central congestion (elevated LV and/or RV filling pressures) […] Vasoconstriction (including venoconstriction) will develop as a compensatory mechanism for hypotension. This will cause redistribution of blood volume into the circulating compartment, leading to elevated CVP and/or PCWP.

• #4 Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction – UpToDate

  https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-cardiogenic-shock-in-acute-myocardial-infarction

  Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to the inability of the heart to pump an adequate amount of blood. The reduction in tissue perfusion results in decreased oxygen and nutrient delivery to the tissues and, if prolonged, potentially end-organ damage and multi-system failure. […] Failure of the left or right ventricle (due to myocardial muscle dysfunction) to pump an adequate amount of blood is the primary cause of cardiogenic shock in acute MI. Hypotension, tissue hypoperfusion, and pulmonary congestion or systemic venous congestion result.

• #5 Cardiogenic shock

  https://www.openaccessjournals.com/articles/cardiogenic-shock-13122.html

  The cardiogenic shock is a state of endorgan dysfunction, secondary to insufficient cardiac output despite adequate preload, as a result of left ventricular, right ventricular or biventricular dysfunction. […] Cardiogenic shock is defined as systemic tissue hypoperfusion due to inadequate cardiac output despite adequate circulatory volume. […] The most common cause of cardiogenic shock is acute coronary syndrome, accounting for about 70% to 80% of cardiogenic shock cases. […] Cardiogenic shock can be caused by an acute cardiac condition or a systemic illness that triggers a chronic cardiac condition associated with minimal cardiac reserve. Unstable angina, postcardiotomy syndrome, valvular heart disease, myocardial disease (such as myocarditis), LV outflow obstruction in hypertrophic cardiomyopathy, stress-induced cardiomyopathy, pericardial tamponade, congenital lesions, and mechanical injury to the heart have all been implicated in the pathogenesis of cardiogenic shock.

• #6 Cardiogenic shock – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/cardiogenic-shock/symptoms-causes/syc-20366739

  Cardiogenic shock is a life-threatening condition in which your heart suddenly can’t pump enough blood to meet your body’s needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock. […] In most cases, a lack of oxygen to your heart, usually from a heart attack, damages its main pumping chamber (left ventricle). Without oxygen-rich blood flowing to that area of your heart, the heart muscle can weaken and go into cardiogenic shock. […] Rarely, damage to your heart’s right ventricle, which sends blood to your lungs to get oxygen, leads to cardiogenic shock. […] Other possible causes of cardiogenic shock include: Inflammation of the heart muscle (myocarditis), Infection of the heart valves (endocarditis), Weakened heart from any cause, Drug overdoses or poisoning with substances that can affect your heart’s pumping ability.

• #7 SciELO Brazil – Cardiogenic shock Cardiogenic shock

  https://www.scielo.br/j/abc/a/ZN9XJ5QR56GbGCskm8WFDRC/?lang=en

  Cardiogenic shock remains a condition with a high mortality rate, varying from 30% to 90%, despite the great advances like thrombolytic therapy, development of several methods of partial or total artificial circulatory support, and of heart transplantation that have been made in the last two decades in the treatment of heart diseases. […] This complex clinical syndrome may have multiple causes, may be of acute occurrence or may be the final expression of the evolution of chronic ventricular dysfunction. […] Cardiogenic shock is a condition of systemic tissue hypoperfusion due to heart muscle incapacity to provide adequate output for organism needs. […] The shock is cardiogenic when the primary cause is heart dysfunction. […] Despite being found in several clinical situations, such as myocardial failure due to sepsis or pancreatitis, rupture of tendinous cords or valve secondary to endocarditis, myocarditis, rejection following heart transplantation, rupture or thrombosis of valve prosthesis, and ventricular or supraventricular arrhythmias producing low output, the main etiology of this condition is heart muscle loss by AMI.

• #8 SciELO Brazil – Cardiogenic shock Cardiogenic shock

  https://www.scielo.br/j/abc/a/ZN9XJ5QR56GbGCskm8WFDRC/?lang=en

  From a major coronary artery occlusion and loss of a significant amount of myocardial mass, a series of vicious cycles are triggered that, if perpetuated, culminate in shock, failure of multiple organs and systems, and death. […] Hypotension resulting from muscle mass loss may cause hypoperfusion of still viable myocardial areas, contributing to aggravation of the ventricular function. […] It is estimated that a minimum loss of 40% of the left ventricular mass is necessary for genesis of cardiogenic shock. […] The persistence of low cardiac output ends up accentuating hypoxia, with accumulation of metabolites, acidosis, and endothelial and cellular damage. […] Failure of multiple organs is the endpoint of this pathophysiological situation. […] From patients developing cardiogenic shock in the acute phase of AMI, 10-30% do it in the first 24 hrs, and the cardiogenic shock relates to the extensive loss of muscle mass.

• #9 Table: Mechanisms of Cardiogenic and Obstructive Shock-MSD Manual Professional Edition

  https://www.msdmanuals.com/professional/multimedia/table/mechanisms-of-cardiogenic-and-obstructive-shock

  Impaired myocardial contractility […] Myocardial ischemia or myocardial infarction, myocarditis, medications […] Abnormalities of cardiac rhythm […] Tachycardia, bradycardia […] Cardiac structural disorder […] Acute mitral or aortic regurgitation, ruptured interventricular septum, prosthetic valve malfunction

• #10 23. Cardiogenic Shock | Hospital Handbook

  https://hospitalhandbook.ucsf.edu/23-cardiogenic-shock/23-cardiogenic-shock

  Cardiac dysfunction leading to insufficient cardiac output and tissue hypoperfusion. […] The diagnosis of cardiogenic shock should be made with a low CI and high SVR. […] Myocardial infarction […] Acute decompensation of cardiomyopathy […] Severe valve disease (e.g. severe aortic stenosis, severe mitral stenosis, acute mitral insufficiency) […] Pericardial tamponade […] Arrhythmia […] Ventricular septal defect […] Myocarditis […] Pulmonary embolism […] RV failure […] Cardiotoxic medication […] Post-cardiotomy […] LVOT obstruction. […] The IABP-SHOCK II registry in 2012 did not demonstrate a benefit to IABP placement over placebo in patients with acute MI complicated by cardiogenic shock. […] Retrospective and registry based data have suggested a utility to mechanical circulatory support devices in specific scenarios.

• #11 Cardiogenic shock: evolving definitions and future directions in management | Open Heart

  https://openheart.bmj.com/content/6/1/e000960

  Cardiogenic shock (CS) is a complex and highly morbid entity conceptualised as a vicious cycle of injury, cardiac and systemic decompensation, and further injury and decompensation. The pathophysiology of CS is incompletely understood but limited clinical trial experience suggests that early and robust support of the failing heart to allow for restoration of systemic homoeostasis appears critical for survival. […] The pathophysiology of CS is poorly understood owing to a paucity of high-quality clinical data. Even for the most common cause, ACS, significant heterogeneity (eg, STEMI vs type I and type II non-STEMI with more specific variables such as postcardiac arrest or renal failure) exists that likely informs management and influences outcomes. […] In general, CS is characterised by an initial insult resulting in impaired CO followed by progressive injury culminating in inadequate and ultimately maladaptive compensatory mechanisms and rapid deterioration to end-organ hypoperfusion and complete cardiovascular collapse.

• #12 Shock – Critical Care Medicine – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/critical-care-medicine/shock-and-fluid-resuscitation/shock

  Cardiogenic shock is a relative or absolute reduction in cardiac output due to a primary cardiac disorder. […] Impaired myocardial contractility is a mechanism of cardiogenic shock. […] Myocardial ischemia or myocardial infarction, myocarditis, medications, and abnormalities of cardiac rhythm are causes of cardiogenic shock. […] Structural disorders (eg, valvular dysfunction, septal rupture) are repaired surgically in cardiogenic shock. […] Coronary thrombosis is treated either by percutaneous interventions (angioplasty, stent placement), coronary artery bypass surgery, or thrombolysis. […] Shock after acute MI is treated with volume expansion if PAOP is low or normal; 15 to 18 mm Hg is considered optimal. […] Bedside cardiac ultrasound to assess contractility and vena caval respiratory variability can help determine the need for additional fluid or vasopressors; inotropic support is a better approach for patients with normal or above-normal filling. […] Intra-aortic balloon counterpulsation is valuable for temporarily reversing shock in patients with acute MI.

• #13 Cardiogenic Shock: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/152191-overview

  Cardiogenic shock is recognized as a low-cardiac-output state secondary to extensive left ventricular (LV) infarction, development of a mechanical defect (eg, ventricular septal defect or papillary muscle rupture), or right ventricular (RV) infarction. […] The pathophysiology of cardiogenic shock in the setting of coronary artery disease, is described below. […] Cardiogenic shock is characterized by systolic and diastolic dysfunction leading to end organ hypoperfusion. The interruption of blood flow in an epicardial coronary artery causes the zone of myocardium supplied by that vessel to lose the ability to shorten and perform contractile work. If a sufficient area of myocardium undergoes ischemic injury, LV pump function becomes depressed and systemic hypotension develops. […] Patients who develop cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis with infarct extension. Decreased coronary perfusion pressure and cardiac output as well as increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock and potentially death. […] Myocardial diastolic function is also impaired, because ischemia decreases myocardial compliance and impairs filling, thereby increasing LV filling pressure and leading to pulmonary edema and hypoxemia.

• #14 Cardiogenic Shock: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/152191-overview

  To compensate for the diminished stroke volume, the curvilinear diastolic pressure-volume curve also shifts to the right, with a decrease in diastolic compliance. This leads to increased diastolic filling and increased LV end-diastolic pressure. […] The attempt to enhance cardiac output by this mechanism comes at the cost of having a higher LV diastolic filling pressure, which ultimately increases myocardial oxygen demand and can lead to pulmonary edema. […] When a critical mass of LV myocardium becomes ischemic and fails to pump effectively, stroke volume and cardiac output are curtailed. The LV pump function becomes depressed; cardiac output, stroke volume, and blood pressure decline while end-systolic volume increases. […] Myocardial ischemia is further exacerbated by impaired myocardial perfusion due to hypotension and tachycardia.

• #15 Management of cardiogenic shock: a narrative review | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-024-01260-y

  This leads to microcirculatory changes, inflammatory activation, anaerobic metabolism, and oxidative stress, resulting in altered oxygen delivery and microvascular dysfunction that contribute to end-organ dysfunction. […] Distinguishing between acute CS and acute-on-chronic CS is essential because mortality is higher in acute CS. […] In acute CS, there is a sudden reduction in ventricular contractility, leading to decreases in stroke volume, CO and blood pressure and increases in pulmonary capillary wedge pressure and central venous pressure. […] Consequently to systemic hypoperfusion, organ compensatory mechanisms are triggered to restore CO and peripheral perfusion. […] Among the compensatory homeostatic responses to a drop in CO, the most well-recognized are activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, secondary to low mean blood pressure and decrease in renal blood flow, respectively.

• #16 Cardiogenic shock: evolving definitions and future directions in management | Open Heart

  https://openheart.bmj.com/content/6/1/e000960

  This is conceptualised as a vicious cycle of cardiac injury, systemic deterioration and further cardiac impairment. […] Interrupting this shock spiral and restoring cardiovascular homoeostasis is central to the overarching treatment paradigm of CS. […] Maladaptive compensatory mechanisms accelerate the self-perpetuation of injury. […] The ability to interrupt these processes and prevent or reverse the extension of myocardial injury before unsalvageable damage is central to the hypothesis that CS is treatable. […] The central paradigm in the treatment of CS is interrupting the self-perpetuating feedback loop of myocardial insult, worsening cardiac power, and further coronary and systemic perfusion mismatch in the context of increasingly maladaptive compensatory mechanisms. […] Current understanding of the pathophysiological process of CS suggests that interrupting the shock spiral and restoration of cardiovascular homoeostasis early before end-organ hypoperfusion occurs may be ultimately critical to survival.

• #17 Cardiogenic Shock – CVRTI

  https://cvrti.utah.edu/cardiogenic-shock/

  Cardiogenic shock (CS) is a medical disorder in which the heart suddenly stops pumping enough oxygen and blood to the rest of the body. […] Cardiogenic shock has a complex pathophysiology involving a vicious cycle. Ischemia causes myocardial dysfunction to both diastolic and systolic left ventricular function. As a result, contractility of the heart is depressed, leading to a reduced cardiac output, which further impairs contractility and coronary ischemia, leading to worse cardiogenic shock and potentially multiorgan dysfunction. […] The most common cause of cardiogenic shock is a severe heart attack. […] When a patient presents with cardiogenic shock symptoms, doctors will run multiple tests to provide an accurate diagnosis. Once a diagnosis is confirmed, the medical team will decide the best course of treatment based on the individual as well as the stage of shock the patient is in.

• #18 Current evidence in the diagnosis and management of cardiogenic shock complicating acute coronary syndrome

  https://www.imrpress.com/journal/RCM/22/3/10.31083/j.rcm2203078/htm

  Cardiogenic shock (CS) is a hemodynamically complex and highly morbid syndrome characterized by circulatory collapse and inadequate end-organ perfusion due to impaired cardiac output. […] CS has been conceptualised as a vicious cycle of injury and decompensation, both cardiac and systemic. […] The main mechanism of CS is acute MI, including its mechanical complications, that causes left ventricular (LV) pumping failure. […] Severe ischemia leads to elevated ventricular filling pressures, reduced CO, hypotension, and systemic tissue hypoperfusion, that eventually affect all body organs. […] This uninterrupted maladaptive vicious cycle is eventually deadly. […] The acute cardiac event can also provoke a systemic inflammation that leads to pathological vasodilation, due to the release of inflammatory mediators and nitric oxide (NO).

• #19 Cardiogenic Shock: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/152191-overview

  Tissue hypoperfusion, with consequent cellular hypoxia, causes anaerobic glycolysis, the accumulation of lactic acid, and intracellular acidosis. Also, myocyte membrane transport pumps fail, which decreases transmembrane potential and causes intracellular accumulation of sodium and calcium, resulting in myocyte swelling. […] If ischemia is severe and prolonged, myocardial cellular injury becomes irreversible and leads to myonecrosis, which includes mitochondrial swelling, the accumulation of denatured proteins and chromatin, and lysosomal breakdown. […] Activation of inflammatory cascades, oxidative stress, and stretching of the myocytes produces mediators that overpower inhibitors of apoptosis, thus activating the apoptosis. […] Cardiogenic shock is the most severe clinical expression of LV failure. The primary mechanical defect in cardiogenic shock is a shift to the right for the LV end-systolic pressure-volume curve, because of a marked reduction in contractility. As a result, at a similar or even lower systolic pressure, the ventricle is able to eject less blood volume per beat. Therefore, the end-systolic volume is usually greatly increased in persons with cardiogenic shock.

• #20 Cardiogenic Shock

  https://www.csh.org.tw/dr.tcj/educartion/f/web/Cardiogenic%20Shock/index.htm

  The pump failure increases ventricular diastolic pressures concomitantly, causing additional wall stress, hence elevating myocardial oxygen requirements. […] Increased myocardial oxygen demand with simultaneous inadequate myocardial perfusion worsens myocardial ischemia, initiating a vicious cycle that ultimately ends in death if uninterrupted. […] Usually, both systolic and diastolic myocardial dysfunction are present in patients with cardiogenic shock. […] The key to achieving a good outcome is rapid diagnosis, prompt supportive therapy, and expeditious coronary artery revascularization in patients with myocardial ischemia and infarction.

• #21 Cardiogenic Shock | Diseases and Disorders

  https://nursing.unboundmedicine.com/nursingcentral/view/Diseases-and-Disorders/73546/all/Cardiogenic_Shock

  Cardiogenic shock occurs when cardiac output is insufficient to meet the metabolic demands of the body, resulting in inadequate tissue perfusion. It is a medical and nursing emergency. There are four stages of cardiogenic shock: initial, compensatory, progressive, and refractory. […] In the compensatory stage, the baroreceptors respond to the decreased cardiac output by stimulating the sympathetic nervous system to release catecholamines to improve myocardial contractility and vasoconstriction, leading to increased venous return and arterial blood pressure. […] Compensatory mechanisms, aimed at improving cardiac output and tissue perfusion, place an increased demand on an already compromised myocardium. […] As tissue perfusion remains inadequate, the cells begin anaerobic metabolism, leading to metabolic acidosis and fluid leakage out of the capillaries and into the interstitial spaces.

• #22 Management of cardiogenic shock: a narrative review | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/s13613-024-01260-y

  These mechanisms lead to fluid reabsorption and systemic vasoconstriction, increasing volume overload and ventricular afterload and worsening myocardial contractility. […] Chronic heart failure progresses to CS when impaired ventricular contractility is severe enough to cause a critical reduction in cardiac output (CO). […] This reduction of CO may be due to an increase in demand because of a triggering factor or to the natural progression of the disease with a progressive reduction in cardiac output. […] End organ hypoperfusion results in acute-on-chronic hepatic and renal insults, lactic acidemia, decreased coronary perfusion pressure, and further activation of mechanoreceptors and chemoreceptors, all of which cause a vicious circle of worsening cardiac function.

• #23 The Role of Inflammation in the Pathogenesis of Cardiogenic Shock Secondary to Acute Myocardial Infarction: A Narrative Review

  https://www.mdpi.com/2227-9059/12/9/2073

  The Role of Inflammation in the Pathogenesis of Cardiogenic Shock Secondary to Acute Myocardial Infarction: A Narrative Review […] Cardiogenic shock (CS) is one of the most serious complications of myocardial infarction (MI) with a high mortality rate. […] This review considers the role of the systemic inflammatory response in the pathogenesis of MI CS. The primary processes involved in its initiation are described, including the progression from the onset of MI to the generalization of the inflammatory response and the development of multiple organ dysfunction. […] One of such pathogenic mechanisms of development and progression of MI CS is activation of the systemic inflammatory response. […] The inflammatory response is typically more pronounced in MI CS patients, although it does not reach the level observed during septic shock. […] The pivotal role of inflammation in the pathogenesis of CS is further supported by encouraging, but not yet comprehensive, outcomes of hemoadsorption and anti-inflammatory therapy in patients with and at high risk of CS. […] The development of systemic inflammation in patients with MI CS commences at the myocardial injury stage. […] The aim of the present narrative review was to update and summarize the existing data on the inflammatory component of MI and MI CS pathogenesis, its fundamental and translational aspects, and to provide information on the completed or ongoing clinical trials aiming to control inflammation during MI CS. […] Ultimately, the imbalance between inflammation and its resolution, which may be based on genetic, epigenetic, infectious and metabolic mechanisms, tends to generalize the inflammatory process, which can cause significant damage to the myocardium and impairment of myocardial function. […] MI CS develops typically 6 h after the onset of MI. […] Other mechanisms of MI CS development in MI patients include mechanical complications such as ventricular septal defects, acute mitral regurgitation due to papillary muscle rupture, pseudo-aneurysm development, and left ventricular free-wall rupture. […] The identification of the predominant stage at which dysfunction of the inflammatory response develops in a patient with MI CS may facilitate the implementation of anti-inflammatory therapy in MI CS patients in a more targeted and personalized manner, enhancing its efficacy.

• #24 Cardiogenic shock elicits acute inflammation, delayed eosinophilia, and depletion of immune cells in most severe cases | Scientific Reports

  https://www.nature.com/articles/s41598-020-64702-0

  We confirm here that CS is associated with such acute inflammation, evidenced by high plasma CRP, increased WBC counts with neutrophilia, and elevated levels of IL-6, IL-10 and MCP-1. […] The increased concentrations of these cytokines correlated with the severity of circulatory failure, as indicated by their negative correlation with blood pressure, and positive correlation with norepinephrine treatment and NT-proBNP during the first 2 days, which is in full agreement with the above-cited reports showing a direct link between the degree of acute inflammation and the severity of hemodynamic deterioration in CS. […] An important novelty of our study was the progressive increase of blood eosinophils in patients with CS. […] Therefore, the delayed increase in blood eosinophils could represent an adaptation to the severe inflammation and tissue injury at the acute phase of CS.

• #25 Cardiogenic Shock | RECAPEM

  https://recapem.com/cardiogenic-shock/

  Microcirculatory dysfunction […] It is present early in CS, and may precede central hemodynamic congestion. […] Activation of systemic inflammatory response syndrome (SIRS) […] Clinically overt inflammation is seen in ~30% of CS patients by day 2 post-CS onset and may result in an initially reduced SVR. […] Multi-organ dysfunction (MOD) […] It can result from altered macrocirculation and microcirculation. MOD carries a poor prognosis. […] The gut appears to be among the first organs involved in shock. […] Progressive reduction in coronary perfusion pressure (CPP) will happen due to the above mechanisms. This causes a double-hit impact on myocardial performance, resulting in worsening myocardial function and progressive end-organ dysfunction. […] The left ventricle is perfused mainly in diastole. […] The right ventricle is perfused in both systole and diastole. […] These equations underscore the significance of raising CPP in hypotensive CS to prevent further myocardial damage.

• #26 Cardiogenic shock as a health issue. Physiology, classification, and detection | Medicina Intensiva

  https://www.medintensiva.org/en-cardiogenic-shock-as-health-issue–articulo-S2173572724000225

  When cardiac output decreases sufficiently, both systemic and coronary perfusion are lowered. […] The decrease in myocardial perfusion in turn induces or worsens ischemia, generating a vicious circle of increased cardiac dysfunction and lowered cardiac output. […] When these mechanisms are exceeded and cardiac output is unable to meet the metabolic and oxygen demands of the tissues, the latter enter anaerobic metabolism, generating lactic acidosis and depletion of the adenosine triphosphate (ATP) reserves. […] The pro-inflammatory state produces endothelial dysfunction, resulting in capillary leakage that contributes to multiorgan dysfunction. […] As hypoperfusion becomes generalized and anaerobic metabolism sets in, several initially reversible organ dysfunctions develop. […] The initial cardiac dysfunction, tissue hypoperfusion and multiorgan dysfunction generate increasingly greater hypotension that worsens the ischemia, perpetuating a vicious circle that becomes irreversible.

• #27 Organ dysfunction, injury, and failure in cardiogenic shock | Journal of Intensive Care | Full Text

  https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-023-00676-1

  Cardiogenic shock (CS) is caused by primary cardiac dysfunction and induced by various and heterogeneous diseases (e.g., acute impairment of cardiac performance, or acute or chronic impairment of cardiac performance). […] Organ dysfunction has traditionally been attributed to the hypoperfusion of the organ due to either progressive impairment of the cardiac output or intravascular volume depletion secondary to CS. However, research attention has recently shifted from this cardiac output (forward failure) to venous congestion (backward failure) as the most important hemodynamic determinant. Both hypoperfusion and/or venous congestion by CS could lead to injury, impairment, and failure of target organs (i.e., heart, lungs, kidney, liver, intestines, brain); these effects are associated with an increased mortality rate.

• #28 Organ dysfunction, injury, and failure in cardiogenic shock | Journal of Intensive Care | Full Text

  https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-023-00676-1

  Vital organ dysfunction is thought to be directly linked to poor prognosis in patients with CS. […] Both macrohemodynamic alterations and microcirculatory dysfunction have been associated with multi-organ dysfunction; however, the pathophysiology of organs in CS remains unclear. […] AKI has been traditionally attributed to the hypoperfusion of the kidneys through progressive impairment of the cardiac output or intravascular volume depletion secondary to CS. However, attention has shifted from cardiac output (forward failure) to venous congestion (backward failure) as the most important hemodynamic determinant. The development of congestive kidney failure induced by the increased renal venous pressure arising from venous congestion (increased renal after-load) and increased renal interstitial pressure (intrinsic renal compromise) might play an important role in the development of AKI in patients with CS.

• #29 Organ dysfunction, injury, and failure in cardiogenic shock | Journal of Intensive Care | Full Text

  https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-023-00676-1

  The components of AKI were recently introduced in the field of intensive care. […] The hemodynamic approach is a primary concern for the treatment of AKI in CS. […] In the absence of specific therapies for liver injury in CS, particular attention must be paid to the improvement of the hemodynamic profile, including reduction in pulmonary vascular resistance and right atrial pressure. […] Acute hypoperfusion in CS can compromise the barrier and absorptive functions of the intestines; this clinical situation is termed cardiointestinal syndrome. […] It has been reported that approximately 20% of patients with CS develop a systemic inflammatory response (SIRS) after the initial phase. […] Brain dysfunction and injury (e.g., cerebral infarction, bleeding, and anoxic brain damage) are frequently observed in the initial phase. Cerebral dysfunction is associated with an independent increase in mortality in patients with CS.

• #30 Cardiogenic shock as a health issue. Physiology, classification, and detection | Medicina Intensiva

  https://www.medintensiva.org/en-cardiogenic-shock-as-health-issue–articulo-S2173572724000225

  The classification of CS may improve the outcomes by guiding the intensity and timing of patient management. […] The SCAI could have a favorable impact when used as a triage tool, offering a window of opportunity for early detection, treatment adjustment or even patient transfer to a reference center in order to avoid CS progression and improve the prognosis.

• #31 Cardiogenic Shock | Diseases and Disorders

  https://nursing.unboundmedicine.com/nursingcentral/view/Diseases-and-Disorders/73546/all/Cardiogenic_Shock

  Lactic acidosis causes depression of the myocardium and a decrease in the vascular responsiveness to catecholamines, further reducing cardiac output. […] If there is no effective intervention at this point, the shock will progress to the refractory stage, when the chance of survival is extremely limited. […] Most experts acknowledge that cardiogenic shock is often unresponsive to treatment and has a mortality rate ranging from 20% to 50% if prompt medical intervention occurs. […] The most common cause of cardiogenic shock is acute myocardial infarction (MI) resulting in a loss of more than 40% of the functional myocardium. […] Cardiogenic shock occurs with 5% to 10% of all hospital admissions for acute MI. […] Cardiogenic shock is an emergency because of an unstable cardiovascular system that requires immediate intervention to reverse shock before vital organs are damaged.

• #32

  https://link.springer.com/article/10.1007/s12928-024-01031-3

  Takotsubo syndrome (TTS) can mimic acute coronary syndrome despite being a distinct disease. […] While typically benign, TTS can lead to serious complications like cardiogenic shock. Cardiogenic shock occurs in 120% of TTS cases. Various mechanisms can cause shock, including pump failure, right ventricular involvement, left ventricular outflow tract obstruction, and acute mitral regurgitation. […] Because treatment depends on the mechanism, early identification of the mechanism developing cardiogenic shock is essential for optimal treatment and improved outcomes in TTS patients with cardiogenic shock. This review summarizes current knowledge on causes and treatment of cardiogenic shock in patients with TTS. […] Given the typical spontaneous recovery of ventricular systolic dysfunction, in-hospital management for TTS is primarily supportive. Because different mechanisms can be related to cardiogenic shock in patients with TTS, early identification of patients at high risk of cardiogenic shock and careful assessment for the etiology of cardiogenic shock are crucial.

• #33

  https://link.springer.com/article/10.1007/s12928-024-01031-3

  Cardiogenic shock is a major contributor to acute mortality in TTS, with reported incidence ranging from 1% to 20%. […] In the acute phase of TTS, various mechanisms can contribute to cardiogenic shock, including pump failure (e.g., extensive left ventricular wall motion abnormality), right ventricular (RV) involvement, left ventricular outflow tract obstruction (LVOTO), and acute mitral regurgitation (MR), often occurring in combination. Identifying the predominant mechanism underlying cardiogenic shock is crucial for selecting the most effective treatment strategy. […] Extensive LV wall motion abnormalities can lead to cardiogenic shock in TTS due to pump failure. […] If RV involvement is the primary cause or an exacerbating factor of cardiogenic shock in TTS, fluid administration is the first-line treatment.

• #34 Levosimendan in Cardiogenic Shock | ECR Journal

  https://www.ecrjournal.com/articles/levosimendan-promising-pharmacotherapy-cardiogenic-shock-comprehensive-review?language_content_entity=en

  Levosimendan is a calcium sensitiser and adenosine triphosphate-dependent potassium (KATP) channel opener that improves myocardial contractility without significantly increasing intracellular calcium levels and oxygen demand. […] Levosimendan enhances myocardial contractility through calcium sensitisation of cTnC without increasing intracellular calcium concentration, avoiding excessive oxygen consumption. […] By increasing the calcium sensitivity of the heart muscle, levosimendan effectively increases the force of cardiac muscle contraction under conditions where calcium concentration would not normally be sufficient to produce such a strong response. This is particularly beneficial in heart failure, where the hearts ability to contract effectively is compromised. […] Levosimendan has been shown to have cardioprotective effects by activating mitochondrial KATP channels, contributing to its efficacy in treating heart failure and cardiogenic shock. This protection mechanism involves several cellular and molecular pathways that collectively help to preserve mitochondrial function, reduce oxidative stress, and enhance cell survival under ischaemic conditions.

• #35 Review of Advancements in Managing Cardiogenic Shock: From Emergency Care Protocols to Long-Term Therapeutic Strategies

  https://www.mdpi.com/2077-0383/13/16/4841

  Cardiogenic shock (CS) is a complex multifactorial clinical syndrome of end-organ hypoperfusion that could be associated with multisystem organ failure, presenting a diverse range of causes and symptoms. […] Recent research has focused on improving early detection and understanding of CS through standardized team approaches, detailed hemodynamic assessment, and selective use of temporary mechanical circulatory support devices, leading to better patient outcomes. […] This review examines CS pathophysiology, emerging classifications, current drug and device therapies, standardized team management strategies, and regionalized care systems aimed at optimizing shock outcomes. […] Cardiogenic shock (CS) is characterized by sustained hypotension (SBP < 90 mmHg or vasopressor requirement) and tissue hypoperfusion secondary to reduced cardiac output (CI < 2.2 L/min/m²) and congestion (PCWP > 15 mmHg, or pulmonary congestion on imaging, or CVP > 12 mmHg).

• #36 Review of Advancements in Managing Cardiogenic Shock: From Emergency Care Protocols to Long-Term Therapeutic Strategies

  https://www.mdpi.com/2077-0383/13/16/4841

  Despite phenotypic variability, a low cardiac index is universally observed in CS. […] Progressive hemodynamic deterioration leading to CS results from a critical reduction in contractile mass due to ischemic or necrotic myocardium. […] The resulting decrease in cardiac output lowers arterial blood pressure, reduces coronary perfusion pressure, and increases left ventricular end-diastolic pressure. […] This vicious cycle exacerbates myocardial ischemia, further impairing left ventricular function and cardiac output. […] To compensate for the reduced cardiac output, a series of neurohumoral responses is activated. […] However, these compensatory mechanisms eventually lead to decompensation. […] Loss of vascular endothelial integrity and microvascular thrombosis contribute to multiorgan failure.

• #37 Review of Advancements in Managing Cardiogenic Shock: From Emergency Care Protocols to Long-Term Therapeutic Strategies

  https://www.mdpi.com/2077-0383/13/16/4841

  Ultimately, this downward spiral results in decreased tissue perfusion, lactic acidosis, and death. […] CS may develop acutely or subacutely, and it can be precipitated by many etiologies, such as AMI, heart failure (HF) cases complicated by CS, acute myocarditis, valvular dysfunction, right ventricle shock, or postcardiotomy shock.

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