Cardiogenic Shock

doi:10.1378/chest.83.6.893

Chest

Volume 83, Issue 6, June 1983, Pages 893-898

https://doi.org/10.1378/chest.83.6.893 Get rights and content

The definition, pathophysiology, and diagnosis of cardiogenic shock are presented. Its management is detailed, including specific forms of therapy for the various subgroups of patients in whom cardiogenic shock is an integral part. The choice of patients for and results of circulatory support using the intra-aortic balloon pump followed by early cardiac surgery are presented. The importance of treating hypovolemia, when present, and recognizing cardiogenic shock, a result of right ventricular infarction, is stressed. Early and late prognoses are given. Although the prognosis still remains grave, early aggressive therapy along the lines outlined often succeeds in reducing a mortality rate that otherwise is unacceptably high.

Section snippets

Pathology

Pathology studies that we have conducted³ and have been confirmed by others,⁶ demonstrate that cardiogenic shock occurs when at least 45 percent of the left ventricular myocardium has been damaged by the acute infarct and associated ischemia. A very common cause of such an extensive area of necrotic and ischemic myocardium occurs when there is an occlusion of the proximal portion of the left anterior descending artery, a very common finding in patients presenting with cardiogenic shock. In

Management

Drug therapy alone has not significantly altered the mortality of cardiogenic shock. Nevertheless, great benefit may well occur if vasodilation therapy is started before cardiogenic shock is truly established in order to treat left ventricular failure and pulmonary edema.¹⁰ Recognizing that traditional treatment of cardiogenic shock with sympathomimetic amines resulted in an unacceptably high mortality rate of 90 percent or more, a great deal of effort has gone into developing other approaches

Prognosis

The immediate prognosis in the presence of cardiogenic shock remains grave, but early support of the ventricle by mechanical means and drugs, followed by surgery if possible, have significantly reduced a mortality rate that previously had been close to 100 percent. In very favorable circumstances, those with mechanical lesions of the ventricle will have a 30-day survival rate of 40–60 percent; aortocoronary bypass graft surgery performed alone without any further surgery to the ventricle

Prevention of Cardiogenic Shock

Every effort should be made to reduce the extent of necrosis and continuing acute ischemia following myocardial infarction. The sooner the patient is brought under appropriate medical treatment the lesser the incidence of cardiogenic shock. An incidence of 10 percent cardiogenic shock following myocardial infarction often occurs, but in Belfast where a mobile coronary unit has ensured treating patients early, an incidence of 4 percent has been reported when patients were brought under medical

Conclusion

An appropriate method for managing cardiogenic shock can be summarized as follows: the patient should be cared for in an intensive care unit. An initial hemodynamic study should be performed to determine filling pressure of the ventricles, cardiac output, ventricular stroke/work index, peripheral and pulmonary vascular resistances, and to exclude hypovolemia. An intra-aortic balloon catheter should be inserted, preferably by percutaneous techniques, and intraaortic balloon pumping should be

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Cited by (16)

Risk factors for noninvasive ventilation failure in patients with acute cardiogenic pulmonary edema: A prospective, observational cohort study
2017, Journal of Critical Care
Citation Excerpt :
This conversion factor provides an approximation of percent oxygen delivered, is influenced by minute ventilation and breathing patterns, and may be inaccurate when air leakage occurs around the mask or through the mouth [24,29]. Diagnoses of AMI [30], respiratory tract infection [31,32], cardiac arrest [33], cardiogenic shock [34,35], pulmonary embolism [36], nosocomial pneumonia [37], sepsis and septic shock [38], and MOF [39] were made on the basis of published criteria. Continuous variables are presented as mean ± SD with normal distribution or as median (25th–75th percentiles) with nonnormal distribution unless otherwise specified.
We identified risk factors for noninvasive ventilation (NIV) failure in patients with acute cardiogenic pulmonary edema (ACPE).
We conducted an observational cohort study over a 3-year period in a 28-bed emergency intensive care unit (EICU) and prospectively included all consecutive patients in whom NIV was attempted as initial ventilatory support for ACPE. The primary outcome variables were NIV failure rate and risk factors for NIV failure.
Among the 118 patients in the study, NIV failed for 44 (37.3%) patients. Risk factors for NIV failure were Killip class IV (odds ratio [OR], 28.56; 95% confidence interval [CI], 2.17–375.73; p = 0.011), left ventricular ejection fraction (LVEF) < 30% (OR, 9.54; 95% CI, 1.01–90.55; p = 0.050) and B-type natriuretic peptide (BNP) ≥ 3350 pg/mL (OR, 39.63; 95% CI, 3.92–400.79; p = 0.002) at baseline, and fluid balance ≥ 400 mL within 24 h after ACPE (OR, 13.19; 95% CI, 1.18–147.70; p = 0.036).
NIV failure occurred in 37.3% of ACPE patients in a real-world EICU. When patients had Killip class IV, a lower LVEF, a higher BNP, and a more positive fluid balance within 24 h after ACPE, the risk of failure was higher.
NCT02653365.
Cardiogenic shock: Current understandings and future research directions
1994, The American Journal of Cardiology
Prognosis in cardiogenic shock after acute myocardial infarction in the intervencional era
1992, Journal of the American College of Cardiology
Objectives. The purpose of this study is to describe the outcome in cardiogenic shock treated with aggressive reperfusion therapy and to identify factors predictive of in-hospital and long-term mortality.
Background. Cardiogenic shock is the most common cause of death in patients admitted to the coronary care unit. Although studies have reported lower mortality rates in shock treated with angioplasty, few studies have described a cohort of patients with shock who were not selected because they were most likely to benefit from reperfusion therapy.
Methods. A consecutive series of 200 patients admitted with acute myocardial infarction complicated by cardiogenic shock were studied.
Results. The in-hospital mortality rate was 53%. Variables with significant univariable association with in-hospital death included patency of the intarct-related artery, patient age, lowest cardiac index, highest arteriovenous oxygen difference and left main coronary artery disease. The most important independent predictors of in-hospital death were patency of the Infarct-related artery, cardiac Index and peak creatine kinase, MB fraction. The mortality rate in patients with patent infarct-related arteries was 33% versus 75% in those with closed arteries and 84% in those in whom arterial patency was unknown. Patients who survived to hospital discharge were followed up for a median of 2 years, with a mortality rate of 18% after 1 year. The best descriptors of the relation between these variables and postdischarge mortality included age, peak creatine kinase, ejection fraction and patency of the infarct-related artery.
Conclusions. In a large consecutive series of patients with cardiogenic shock with complete follow-up, patency of the infarclrelated artery was most strongly associated with in-hospital and long-term mortality. This finding supports an aggressive Interventional strategy in patients with cardiogenic shock.
Administration of enoximone in cardiogenic shock
1988, The American Journal of Cardiology
Thirteen patients in severe cardiogenic shock, persisting despite the use of adrenergic agents, were treated with enoximone, a recently available phosphodiesterase inhibitor. Cardiogenic shock was characterized by low cardiac output (< 2.5 liter · min⁻¹ · m⁻²), elevated pulmonary artery balloon-occluded pressure (≥ 15 mm Hg), decreased urine output (< 20 ml · hour⁻¹) and increased blood lactate (> 2.0 mEq · liter⁻¹). Ten patients were mechanically ventilated. A short-term intravenous infusion of 0.5 mg · kg⁻¹ in 20 minutes of enoximone resulted in significant increases in cardiac index (from 1.8 ± 0.3 to 2.9 ± 0.3 liter · min⁻¹ · m⁻², p < 0.001) and stroke index (from 17.8 ± 3.3 to 21.9 ± 5.1 ml · m⁻², p < 0.001) and significant decrease in pulmonary artery balloon-occluded pressure (from 21.7 ± 5.8 to 19.8 ± 6.0 mm Hg, p < 0.01) without a consistent change in mean arterial pressure (from 79 ± 8 to 76 ± 9 mm Hg, difference not significant). Enoximone administration decreased arterial oxygen tension (from 108 ± 42 to 94 ± 36 mm Hg, p < 0.01) and increased venous admixture (from 12.8 ± 6.5 to 16.0 ± 8.0%, p < 0.01). In 8 patients, a second infusion of 0.5 mg · kg⁻¹ immediately thereafter amplified these changes. All patients but one survived the episode of cardiogenic shock and 5 patients left the hospital alive. These results indicate that the addition of enoximone to adrenergic agents in the treatment of cardiogenic shock can markedly increase cardiac output and stroke volume without substantial effects on arterial pressure.
The prevention and treatment of shock in acute myocardial infarction
1988, Chest
Left ventricular geometry during intermittent positive pressure ventilation in dogs
1987, Journal of Critical Care
We have analyzed how regional left ventricular (LV) performance may contribute to global LV performance during a single intermittent positive pressure ventilation (IPPV) respiratory cycle using chronically instrumented dogs with endocardial piezoelectric crystals in the three orthogonal axes, anterior-posterior (AP), septal-lateral freewall (SL), and long axis (LA) dimensions (D). Right ventricular (RV) SLD and aortic flow were also measured. Changes in LV geometry were evaluated during IPPV at two respiratory rates (10 and 20 breaths/min) and during inferior vena caval (IVC) occlusion since a change in systemic venous return is a major component of an IPPV inspiration. During an IPPV inspiration the RV SL end-diastolic D decreased, while the LV AP end-diastolic D increased (P < .01) and LV SL end diastolic D decreased (P < .001). LV end-diastolic and end-systolic volumes tended to increase during early inspiration and then diminished to an early expiratory minimum (P < .05) associated with early expiratory minimum stroke volumes and measured aortic flows (P < .02). In contrast, during IVC occlusion, the LV SL end-diastolic D initially increased while the AP end-diastolic D was falling. Thus, entirely different changes in LV end diastolic geometry result from IVC occlusion and lung inflation. These studies suggest a common factor of cardiac compression by the lung during inspiration altering diastolic intraventricular distribution of the LV preload and raise the question of whether respiratory-induced changes in LV geometry may independently modulate LV systolic pump function.

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Chest

Accp Council on Critical CareCardiogenic Shock

Section snippets

Pathology

Management

Prognosis

Prevention of Cardiogenic Shock

Conclusion

Circulatory assistance for the failing heart

Br Heart J

Hemodynamic findings in 123 patients with acute myocardial infarction on admission

Circulation

Circulatory effects of acute myocardial infarction as a rational basis for therapy

Ann Clin Res