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At least 19 recordsLinked to original sources
PubMed1997

Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia.

OBJECTIVES: To determine and compare the respective concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, soluble TNF receptors, nitrite/nitrate (NO2-/NO3-), and procalcitonin in the plasma of patients with septic shock, cardiogenic shock, and bacterial pneumonia without shock; and to assess the predictive value of these mediators in defining patients with septic shock. DESIGN: Cohort study, comparing normal volunteers (controls) and patients with septic shock, cardiogenic shock, and bacterial pneumonia. SETTING: A collaborative study among an intensive care unit, an emergency room, and three research laboratories. PATIENTS: Mediators were measured at various times in 15 patients with septic shock (during the shock phase and during the recovery phase), in seven patients with cardiogenic shock during the shock phase, and in seven patients with severe bacterial pneumonia on day 1 of admission. INTERVENTIONS: Blood samples were collected at various times during the course of the disease. MEASUREMENTS AND MAIN RESULTS: TNF-alpha values were highest in the acute phase of septic shock (53 to 131 pg/mL during septic shock), while patients with bacterial pneumonia had intermediate concentrations (32 pg/mL). TNF-alpha concentrations were normal in patients with cardiogenic shock. IL-6 concentrations were highest in patients with acute septic shock (85 to 385 pg/mL). However, in contrast to TNF-alpha concentrations, IL-6 concentrations were normal in patients with bacterial pneumonia and increased in patients with cardiogenic shock (78 pg/mL). Soluble TNF receptors were increased in all three groups vs. controls, with the highest increase in patients with septic shock. NO2-/NO3- concentrations were highest (72 to 140 mM) in patients with septic shock, and were < 40 mM in the other groups of patients. Procalcitonin concentrations were only markedly increased in patients with septic shock (72 to 135 ng/mL, compared with approximately 1 ng/mL in the three other groups). The best predictive value for septic shock was found to be the measurements of NO2-/NO3- and procalcitonin concentrations. CONCLUSIONS: These observations showed that increase of proinflammatory cytokines was a consequence of inflammation, not of shock. In this study comparing various shock and infectious states, measurements of NO2-/NO3- concentration and procalcitonin concentration represented the most suitable tests for defining patients with septic shock.

Adult↗
PubMed2001

CD14 expression on monocytes and TNF alpha production in patients with septic shock, cardiogenic shock or bacterial pneumonia.

OBJECTIVES: In patients with septic shock, circulating monocytes become refractory to stimulation with microbial products. Whether this hyporesponsive state is induced by infection or is related to shock is unknown. To address this question, we measured TNF alpha production by monocytes or by whole blood obtained from healthy volunteers (controls), from patients with septic shock, from patients with severe infection (bacterial pneumonia) without shock, and from patients with cardiogenic shock without infection. MEASUREMENTS: The numbers of circulating monocytes, of CD14+ monocytes, and the expression of monocyte CD14 and the LPS receptor, were assessed by flow cytometry. Monocytes or whole blood were stimulated with lipopolysaccharide endotoxin (LPS), heat-killed Escherichia coli or Staphylococcus aureus, and TNF alpha production was measured by bioassay. RESULTS: The number of circulating monocytes, of CD14+ monocytes, and the monocyte CD14 expression were significantly lower in patients with septic shock than in controls, in patients with bacterial pneumonia or in those with cardiogenic shock (p < 0.001). Monocytes or whole blood of patients with septic shock exhibited a profound deficiency of TNF alpha production in response to all stimuli (p < 0.05 compared to controls). Whole blood of patients with cardiogenic shock also exhibited this defect (p < 0.05 compared to controls), although to a lesser extent, despite normal monocyte counts and normal CD14 expression. CONCLUSIONS: Unlike patients with bacterial pneumonia, patients with septic or cardiogenic shock display profoundly defective TNF alpha production in response to a broad range of infectious stimuli. Thus, down-regulation of cytokine production appears to occur in patients with systemic, but not localised, albeit severe, infections and also in patients with non-infectious circulatory failure. Whilst depletion of monocytes and reduced monocyte CD14 expression are likely to be critical components of the hyporesponsiveness observed in patients with septic shock, other as yet unidentified factors are at work in this group and in patients with cardiogenic shock.

Antigens, CD↗
PubMed1999

[Reperfusion therapy and mechanical circulatory support in patients in cardiogenic shock].

Cardiogenic shock is a state of inadequate tissue perfusion due to cardiac dysfunction, which is most commonly caused by acute myocardial infarction. The pathophysiology of cardiogenic shock is characterized by a downward spiral: ischemia causes myocardial dysfunction, which, in turn, augments the ischemic damage and the energetical imbalance. With conservative therapy, mortality rates for patients with cardiogenic shock are frustratingly high reaching more than 80%. Additional thrombolytic therapy has not been shown to significantly improve survival in such patients. Emergency cardiac catheterization and coronary angioplasty, however, seem to improve the outcome in shock-patients, which most probably is due to rapid and complete revascularization generally reached by angioplasty. In addition to interventional therapy with rapid coronary revascularization, the use of mechanical circulatory support may interrupt the vicious cycle in cardiogenic shock by stabilizing hemodynamics and the metabolic situation. Different cardiac assist devices are available for cardiologists and cardiac surgeons: 1. intraaortic balloon counterpulsation (IABP), 2. implantable turbine-pump (Hemopump), 3. percutaneous cardiopulmonary bypass support (CPS), 4. right heart, left heart, or biventricular assist devices placed by thoracotomy, and 5. intra- and extrathoracic total artificial hearts. Since percutaneous application is possible with IABP, Hemopump and CPS, these devices are currently used in interventional cardiology. The basic goals of the less invasive intraaortic balloon counterpulsation (IABP; Figure 1) are to stabilize circulatory collapse, to increase coronary perfusion and myocardial oxygen supply, and to decrease left ventricular workload and myocardial oxygen demand (Figure 2). Since the advent of percutaneous placement, IABP has been used by an increasing number of institutions (Figure 3). In addition to cardiogenic shock, the system may be of use in a variety of other indications in the catheterization laboratory and intensive care unit, including weaning from percutaneous cardiopulmonary bypass, in ischaemic left ventricular failure, in unstable angina, in high risk PTCA, and in prophylactic support in patients with myocardial infarction and successful revascularization. Animal experimental data showed that IABP may improve success of thrombolysis and recent clinical data suggest that survival is enhanced and transfer for revascularization is facilitated when patients with myocardial infarction and cardiogenic shock undergo thrombolysis and IABP rather than thrombolysis alone. A lot of studies had demonstrated before, that combined use of counterpulsation and revascularization therapy (i.e. coronary bypass surgery or angioplasty) may improve prognosis in patients with myocardial infarction complicated by cardiogenic shock (Table 1). In such patients, early treatment with IABP is most important: Multivariate analysis identified early IABP-support with a duration of shock to IABP-treatment of > or = 4 hours as an independent predictor of a positive short-term outcome. In shock-patients with postinfarction ventricular septal defect, IABP provides a marked hemodynamic improvement, and a significant decrease in shunt-flow (Figure 5). However, despite initial stabilization with IABP, such patients need immediate surgical repair of the septal defect to avoid hemodynamic deterioration. The rate of complications related to percutaneous IABP was significantly attenuated by employing catheters of reduced size. Using 9.5-F catheters, a long duration of counterpulsation emerged as the most significant factor associated with complications. In our hospital, those patients with 9.5-F catheters in whom counterpulsation did not exceed 48 hours had a low complication rate of 3.9%. The Hemopump is a catheter-mounted transvalvular left ventricular assist device intended for surgical placement via the femoral artery (Figures 6 and 7). (ABSTRACT TRUNCATED)

Cardiopulmonary Bypass↗
PubMed1981

Cardiogenic shock.

Cardiogenic shock is a complication of acute myocardial infarction characterized by reduction in systemic blood pressure and clinical evidence of impaired blood flow to the skin, central nervous system, and kidneys. Circulatory changes of cardiogenic shock result from excessive loss of contracting myocardium and impaired mechanical performance of the left ventricle. Hemodynamic measurements of left ventricular filling pressure (recorded as the pulmonary artery end-diastolic pressure) and the cardiac index can identify four different subgroups with hospital mortality ranging from 13 to 100 percent when managed with available pharmacologic agents. Patients in cardiogenic shock with a normal or near normal left ventricular filling pressure may respond to volume expansion by restoration of blood pressure and organ flow. The pharmacologic management of cardiogenic shock can be effectively enhanced by measuring the changes in cardiac index and left ventricular filling pressure before and after various vasopressor, inotropic, and volume expansion agents. A clinical scheme for the management of cardiogenic shock based on hemodynamic measurements delineates optimal medical management as well as recognition of rupture of the ventricular septum or the papillary muscle. Despite the combined medical and surgical advances in cardiogenic shock, hospital mortality remains high due to the extensive loss of contracting myocardium of the left ventricle.

Cardiotonic Agents↗
PubMed2004

Cardiogenic shock.

Cardiogenic shock is a pathophysiologic cascade that often leads to death. Although there has been a dramatic decrease in the cases of cardiogenic shock since the 1970s, the mortality rate of those patients who are diagnosed with cardiogenic shock remains as high as 50% to 80%. As stated throughout the article, cardiogenic shock in its later stages cannot be reversed, but clinical signs and symptoms of the syndrome may be identified early enough to prevent a patient from developing irreversible end-stage cardiogenic shock. As a prehospital care provider, you must be able to ensure the pre-shock patient has adequate oxygenation of the myocardium and can be effectively treated before it is too late.

Emergency Medical Services↗
PubMed1983

Pharmacologic support in cardiogenic shock.

Cardiogenic shock is a relatively specific clinical syndrome characterized by decreased cardiac output, elevated left ventricular filling pressure, and arterial hypotension with vital organ hypoperfusion. It most commonly occurs as the consequence of extensive left ventricular damage due to myocardial infarction. The prognosis of patients with cardiogenic shock is very poor, because by definition there are no readily correctable metabolic, hemodynamic, humoral, or infectious problems whose treatment may lead to improved circulatory function. Pharmacologic support of the patient with cardiogenic shock plays a major role in clinical management. Diuretics, inotropic agents, and vasodilator drugs all have a place in the management of selected patients with low output states and cardiogenic shock following myocardial infarction. Diuretics such as furosemide may be used to relieve symptoms of pulmonary congestion, but are not effective in reversing hypotension or vital organ hypoperfusion; in advanced shock states with acute renal failure, they may be totally ineffective. The most commonly employed and effective inotropic agents are the sympathomimetic amines dopamine and dobutamine, which have complex effects on important variables in cardiogenic shock, including the heart's inotropic and chronotropic states, myocardial oxygen requirements, left ventricular filling pressure, and peripheral vascular tone. All inotropic agents have the capacity to intensify myocardial ischemia because they may increase myocardial oxygen requirements in the face of limited arterial blood flow; isoproterenol, epinephrine, and norepinephrine appear to be particularly troublesome in this regard. Vasodilator agents (phentolamine, nitroprusside, and nitroglycerin) have also been used to alter left ventricular loading conditions in patients otherwise supported by inotropic drugs, and may be particularly useful in the management of "mechanical" complications of infarction such as mitral regurgitation and interventricular septal rupture. The use of these drugs, just as that of inotropic agents, must be tailored to specific hemodynamic abnormalities documented in individual patients.

Animals↗
PubMed2006

Obesity is associated with higher mortality in patients with cardiogenic shock.

Cardiogenic shock is the leading cause of death in patients with acute myocardial infarction. Studies that have focused on identifying mortality predictors in patients with cardiogenic shock have not evaluated outcomes in obese patients. A study of sixty-one patients with cardiogenic shock demonstrated that obese patients with cardiogenic shock have a higher mortality risk compared to non-obese patients.

Body Mass Index↗
PubMed1992

Efficacy of percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction complicated by cardiogenic shock.

Cardiogenic shock still remains a highly lethal complication of acute myocardial infarction (AMI). This study reviews our hospital experience in treating AMI complicated by cardiogenic shock to evaluate whether coronary angioplasty improves survival or not. We have treated 523 AMI patients from 1985 to 1990, and among these, 26 patients with AMI complicated by cardiogenic shock who underwent percutaneous transluminal coronary angioplasty (PTCA) compose the study group. In 16 patients, PTCA was successful (Groups S) and in 10 patients, unsuccessful (Group F). There were no statistical differences between the Groups with respect to clinical background, intraaortic balloon counterpulsation (IABP) or emergency coronary bypass graft surgery. Before PTCA, hemodynamic variables including cardiac index, pulmonary capillary wedge pressure and systolic blood pressure were similar in the 2 groups. After PTCA, cardiac index in Group S patients was better than in Group F patients (2.18 +/- 0.61 versus 1.62 +/- 0.65, p less than 0.05). Thirty day and 1 year survivals were also better in Group S than in Group F (30 day survival: Group S 56.2%, Group F 10%, 1 year survival: Group S 31.2%, Group F 0%, p less than 0.05). Multivariate analysis showed that age under 75 years old, systolic blood pressure over 90 mmHg after PTCA and successful PTCA were independent predictors of 30 day survival (p less than 0.05). It was suggested that PTCA was an effective procedure to reduce mortality in patients with cardiogenic shock.

Adult↗
PubMed1994

[Therapy of cardiogenic shock].

Cardiogenic shock is a syndrome of different etiologies resulting in the inability of the heart to provide adequate O2 delivery to peripheral organs and tissues with or without signs of severe pulmonary congestion or pulmonary edema. Clarification of the underlying etiologies is essential for prognosis and therapy. Depending on the various etiologies, the therapeutic procedure may be totally different. Furthermore, it is decisive to differentiate between an acute shock (e.g., acute myocardial infarction) and the development of a cardiogenic shock state on the basis of preexisting chronic congestive heart failure (e.g., congestive cardiomyopathy). Whenever possible the underlying disease should be treated causally (e.g., PTCA or thrombolytic therapy in AM, lysis in acute pulmonary embolism) in addition to symptomatic pharmacologic treatment with vasodilators and/or inodilators. In myogenic cardiogenic shock, the treatment with inotropic drugs (with and without vasodilatory potency) and, if necessary, in combination with additional vasodilators may be life-saving. At present, there is no alternative to catecholamines in the acute state with apparent hemodynamic instability. Catecholamines still represent the initial first line treatment. A Swan-Ganz catheter is mandatory in such situations. In view of the rapid beta 1-receptor down-regulation induced by endogenous catecholamines, long-term administration of exogenous catecholamines (adrenalin, dopamine, dobutamine), seems essentially problematic, since these compounds intensify and accelerate this process.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed2005

Modified release verapamil induced cardiogenic shock.

Cardiogenic shock due to acute myocardial infarction is commonly seen in the accident and emergency department. Refractory cardiogenic shock has been reported after a therapeutic dose of modified release verapamil with concomitant use of beta blocker, metoprolol, but not after a single therapeutic oral dose of modified release verapamil alone. We report what we believe to be the first case of potentially life threatening cardiogenic shock resulting from the myocardial depressant effect of a single therapeutic oral dose of modified release verapamil. The patient made a dramatic recovery minutes after an injection of intravenous calcium chloride. The case is a reminder of the negative inotropic effect of verapamil and how it should be treated.

Anti-Arrhythmia Agents↗
PubMed2004

Recognition and treatment of cardiogenic shock.

Cardiogenic shock has long been a difficult problem for clinicians. The most common cause is left ventricular pump failure after myocardial infarction, but other important causes include mechanical complications of infarction, right ventricular dysfunction, prolonged cardiopulmonary bypass, valvular disease, and cardiomyopathy. Cardiogenic shock is the leading cause of in-hospital death after myocardial infarction. Despite advances in management of heart failure and acute myocardial infarction, clinical outcomes had remained frustratingly poor, with reported mortality rates ranging from 50 to 80%. Recently, however, survival rates have been improving. Improved understanding of the pathophysiology of cardiogenic shock has led to renewed emphasis on the notion that stunned or hibernating myocardium may recover function with hemodynamic support and restoration of flow. This concept has underscored the importance of expeditious initiation of supportive measures to maintain blood pressure and cardiac output, including both medications and intraaortic balloon counterpulsation. Finally, the theory that coronary revascularization would be beneficial by reversing the vicious cycle in which ischemia causes myocardial dysfunction, which in turn worsens ischemia, which had been supported by an extensive body of observational and registry studies, has now been strongly buttressed by the results of two randomized, controlled trials, both of which show improved mortality with early revascularization for cardiogenic shock in the setting of acute infarction.

Journal Article↗
PubMed1993

Mechanisms and management of cardiogenic shock.

Cardiogenic shock remains the most dreaded complication of acute myocardial infarction. Mortality rates remain high despite modern interventional therapy. Patients with a variety of other cardiovascular entities may also develop cardiogenic shock. Management consists of rapid stabilization of systemic arterial blood pressure, expeditious diagnostic evaluation, and definitive therapy when possible. New therapeutic modalities will be needed if patients with cardiogenic shock are to survive.

Critical Care↗
PubMed2001

Dynamic left ventricular outflow tract obstruction: an unusual mechanism mimicking anterior myocardial infarction with cardiogenic shock.

Cardiogenic shock is a frequent and threatening complication in the course of acute myocardial infarction. Besides the well known causes (left ventricular failure, acquired interventricular defect, papillary muscle rupture, free wall rupture) other less frequent mechanisms recognize a functional substrate. The recognition of such mechanisms makes us to revert to the treatments with completely different prognostic implications. In our Coronary Care Unit we encountered, in a period of 12 months, 4 patients who presented clinical, electrocardiographic and/or echographic signs and symptoms of acute myocardial infarction, with different degrees of heart failure up to cardiogenic shock. Only 1 patient showed a severe stenosis of the left anterior descending coronary artery and a significant creatine kinase reduction. Left ventriculography, performed at admission, was unable to disclose the true mechanism of clinical presentation. Only a thorough echographic examination disclosed the presence of a dynamic left ventricular outflow tract obstruction as the cause of heart failure culminating in cardiogenic shock. Once recognized, pathophysiological treatment (administration of beta-blockers and withdrawal of vasodilators, inotropic drugs and intra-aortic balloon pump) led to a dramatic improvement, with an almost complete left ventricular function recovery. Left ventricular outflow tract obstruction is a mechanism that can lead to severe heart failure as a complication of an acute myocardial infarction. Conversely such a mechanism can be precipitated by other causes (hypotension, hypovolemia, especially in hypertensive patients) and can mimic an acute myocardial infarction. Its incidence is not negligible: in our Coronary Care Unit it accounted for about 15% of all cases of myocardial infarction requiring inotropic support. An accurate echocardiographic examination is mandatory even after coronary angiography, and always permits the physician to select the appropriate therapy.

Adrenergic beta-Antagonists↗
PubMed1995

[Therapeutic options in cardiogenic shock].

Cardiogenic shock continues to be a clinical situation which is related with high mortality. Although its etiology is varied, the most frequent cause is an acute myocardial infarction. The poor prognosis of cardiogenic shock can be favourably modified with the diagnosis of the underlying cause followed by the stabilization of the patient and early revascularization. Early treatment with inotropic or vasopressor drugs improves the condition of most patients and the use of circulatory assistance, such as the intraaortic balloon, lead to an acceptable hemodynamic situation in 80% of cases. However, they do not significantly modify the mortality rates. In addition, thrombolytic therapy does not appear to be effective for this kind of patients. Only revascularization methods have proved to be effective; surgery is the only option where ventricular septal, free wall, or papillary muscle rupture occurs, resulting in survival rates of between 50 and 60% with coronary artery by-pass surgery. Angioplasty is frequently successful in reperfusion of the infarct-related artery; the survival rate in these cases is approximately 70%, according to the different series published. As the mortality rate is exceedingly high (70-90%) when conventional therapy is used; when appropriate diagnostic and therapeutic means are available and when the patient's condition is recoverable, the attitude should be aggressive and coronary angiography and angioplasty applied as soon as possible. In centers where these means are not available, once measures have been taken to achieve the stabilization of the patient, the most suitable procedure is to transfer him or her to a hospital in which qualified staff and such treatment methods are available.

Amrinone↗
PubMed1989

Mechanical assistance in cardiogenic shock.

Cardiogenic shock following myocardial infarction or surgical interventions with extracorporeal circulation, not responding to conventional treatment, is an "intractable" condition, unless mechanical assistance is applied. In today's practice mechanical assistance consists in counterpulsating an intraaortic balloon or, if this does not improve the condition, in using a left ventricle bypassing pump. In spite of the complexity of the procedures and the complications, a number of patients can recover with or without a subsequent corrective intervention or heart transplantation. The need for developing systems for chronic assistance to non-correctable hearts and the difficulties of the endeavour are pointed out.

Aged↗
PubMedDate not supplied

[Clinical stratification of cardiogenic shock].

Cardiogenic shock (CHC) associated to acute myocardial infarct has high mortality and their manifestations are heterogenous. In our institution historical mortality, was 98%, but with different methods of reperfusion, its reduced to 53%. In other hand, with opportune clinical stratification is useful to improve the treatment strategy. This stratification on basis in clinical signs: age, infarction location, cardiac frequency and systemic arterial pressure, and hemodynamical valuation with the use of right catheterism with quantification miocardial work parameters like "Cardiac power" that is the product of flow and arterial pressure and that is of utility to know the "Miocardial reserve". In our experience after reperfusion procedure patients with CHC and cardiac power less than 1.0 had highly mortality.

Cardiac Output↗
PubMedDate not supplied

[Acute myocardial infarct with cardiogenic shock].

Cardiogenic shock is the most severe complication of acute myocardial infarction (AMI). The Acute Myocardial Infarction (AMI) complicated with shock has the highest mortality. Between january 1980 and june 1983, 903 patients with AMI were admitted to the CCU of the Instituto Nacional de Cardiolog ía; in 38 of them (4.2%) shock ensued. Of the patients with shock, 52.6% died soon after arrival and 25% died soon after shock developed. Only 10 patients could be controlled with a Swan-Ganz catheter and could be treated according to the hemodynamic features. Nine of them were males, the majority older than 60. Three of the 10, had a previous myocardial infarction, 4 had angina 1 arterial hypertension, and 1 diabetes. The AMI was anterior in five patients, diaphragmatic and lateral in one, diaphragmatic with right ventricular extension in two, lateral in one and antero septal in the last one. The clinical manifestations of angina persisted in 6. The shock state appeared in most of the cases during the first 6 hours. The PWP was higher than 18 mm Hg in all the patients. The cardiac index was less than 2, the systemic blood pressure under 90 mmHg and the peripheral resistance was elevated in all the cases. They were treated with digitalis, Dopamine and Sodium Nitroprusiate . Nine of the 10 patients died; five had post mortem examination. The coronary arteries were occluded with a recent thrombi and the necrosis involved more than 40.0% of the ventricular mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗