Abstract:Purpose of reviewCardiogenic shock continues to carry a high mortality, and recent randomized trials have not identified novel therapies that improve survival. Early optimization of patients with confirmed or suspected cardiogenic shock is crucial, as patients can quickly transition from a hemodynamic shock state to a treatment-resistant hemometabolic shock state, where accumulated metabolic derangements trigger a selfperpetuating cycle of worsening shock.
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“…These metabolic derangements contribute to a worsening shock state termed hemometabolic shock . 8 , 17 , 18 , 19 Breaking this shock‐acidosis‐shock vicious cycle using alkali therapy (such as sodium bicarbonate) to reverse systemic acidemia seems logical, but this approach remains controversial and has not been clearly demonstrated to improve outcomes in critically ill patients. 29 , 31 Greater benefits of alkali may be observed in patients with acute kidney injury, and we anticipate that patients with CS with lower blood pH might more likely to benefit.…”
Section: Discussionmentioning
confidence: 99%
“…A therapeutic trial of alkali therapy can be considered for patients with CS with severe systemic acidemia from metabolic acidosis if they are not responding appropriately to standard doses of vasopressors, but future studies are need to determine the benefit of this approach. 18 , 30 …”
Section: Discussionmentioning
confidence: 99%
“… 5 , 6 , 8 During CS, tissue hypoperfusion and organ failure lead to metabolic deficiencies and a treatment‐resistant hemometabolic CS phenotype. 5 , 8 , 17 , 18 , 19 Simple blood biomarkers can capture this, as lactic acidosis (defined as an elevated blood lactate level) is a well‐established predictor of mortality in patients with CS. 8 , 20 , 21 , 22 , 23 , 24 , 25 Likewise, systemic acidemia (defined as a low blood pH) predicts mortality in patients with CS and may quantify the severity of the hemometabolic disturbance.…”
Background
Lactic acidosis is associated with mortality in patients with cardiogenic shock (CS). Elevated lactate levels and systemic acidemia (low blood pH) have both been proposed as drivers of death. We, therefore, analyzed the association of both high lactate concentrations and low blood pH with 30‐day mortality in patients with CS.
Methods and Results
This was a 2‐center historical cohort study of unselected patients with CS with available data for admission lactate level or blood pH. CS severity was graded using the Society for Cardiovascular Angiography and Intervention (SCAI) shock classification. All‐cause survival at 30 days was analyzed using Kaplan‐Meier curves and Cox proportional‐hazards analysis. There were 1814 patients with CS (mean age, 67.3 years; 68.5% men); 51.8% had myocardial infarction and 53.0% had cardiac arrest. The distribution of SCAI shock stages was B, 10.8%; C, 30.7%; D, 38.1%; and E, 18.7%. In both cohorts, higher lactate or lower pH predicted a higher risk of adjusted 30‐day mortality. Patients with a lactate ≥5 mmol/L or pH <7.2 were at increased risk of adjusted 30‐day mortality; patients with both lactate ≥5 mmol/L and pH <7.2 had the highest risk of adjusted 30‐day mortality. Patients in SCAI shock stages C, D, and E had higher 30‐day mortality in each SCAI shock stage if they had lactate ≥5 mmol/L or pH <7.2, particularly if they met both criteria.
Conclusions
Higher lactate and lower pH predict mortality in patients with cardiogenic shock beyond standard measures of shock severity. Severe lactic acidosis may serve as a risk modifier for the SCAI shock classification. Definitions of refractory or hemometabolic shock should include high lactate levels and low blood pH.
“…These metabolic derangements contribute to a worsening shock state termed hemometabolic shock . 8 , 17 , 18 , 19 Breaking this shock‐acidosis‐shock vicious cycle using alkali therapy (such as sodium bicarbonate) to reverse systemic acidemia seems logical, but this approach remains controversial and has not been clearly demonstrated to improve outcomes in critically ill patients. 29 , 31 Greater benefits of alkali may be observed in patients with acute kidney injury, and we anticipate that patients with CS with lower blood pH might more likely to benefit.…”
Section: Discussionmentioning
confidence: 99%
“…A therapeutic trial of alkali therapy can be considered for patients with CS with severe systemic acidemia from metabolic acidosis if they are not responding appropriately to standard doses of vasopressors, but future studies are need to determine the benefit of this approach. 18 , 30 …”
Section: Discussionmentioning
confidence: 99%
“… 5 , 6 , 8 During CS, tissue hypoperfusion and organ failure lead to metabolic deficiencies and a treatment‐resistant hemometabolic CS phenotype. 5 , 8 , 17 , 18 , 19 Simple blood biomarkers can capture this, as lactic acidosis (defined as an elevated blood lactate level) is a well‐established predictor of mortality in patients with CS. 8 , 20 , 21 , 22 , 23 , 24 , 25 Likewise, systemic acidemia (defined as a low blood pH) predicts mortality in patients with CS and may quantify the severity of the hemometabolic disturbance.…”
Background
Lactic acidosis is associated with mortality in patients with cardiogenic shock (CS). Elevated lactate levels and systemic acidemia (low blood pH) have both been proposed as drivers of death. We, therefore, analyzed the association of both high lactate concentrations and low blood pH with 30‐day mortality in patients with CS.
Methods and Results
This was a 2‐center historical cohort study of unselected patients with CS with available data for admission lactate level or blood pH. CS severity was graded using the Society for Cardiovascular Angiography and Intervention (SCAI) shock classification. All‐cause survival at 30 days was analyzed using Kaplan‐Meier curves and Cox proportional‐hazards analysis. There were 1814 patients with CS (mean age, 67.3 years; 68.5% men); 51.8% had myocardial infarction and 53.0% had cardiac arrest. The distribution of SCAI shock stages was B, 10.8%; C, 30.7%; D, 38.1%; and E, 18.7%. In both cohorts, higher lactate or lower pH predicted a higher risk of adjusted 30‐day mortality. Patients with a lactate ≥5 mmol/L or pH <7.2 were at increased risk of adjusted 30‐day mortality; patients with both lactate ≥5 mmol/L and pH <7.2 had the highest risk of adjusted 30‐day mortality. Patients in SCAI shock stages C, D, and E had higher 30‐day mortality in each SCAI shock stage if they had lactate ≥5 mmol/L or pH <7.2, particularly if they met both criteria.
Conclusions
Higher lactate and lower pH predict mortality in patients with cardiogenic shock beyond standard measures of shock severity. Severe lactic acidosis may serve as a risk modifier for the SCAI shock classification. Definitions of refractory or hemometabolic shock should include high lactate levels and low blood pH.
“…Early recognition with identification and treatment of the underlying cause is a central goal in the initial management of patients with CS ( Supplemental Table 1 , http://links.lww.com/CCM/H343) (1, 2, 6, 38, 39). An electrocardiogram and point-of-care cardiac ultrasound are useful to screen for myocardial ischemia, left ventricle (LV)/RV dysfunction, and structural heart disease (38, 39).…”
Section: Contemporary Standard Care For Csmentioning
confidence: 99%
“…Noninvasive ventilation with continuous positive airway pressure can reduce work of breathing and improve pulmonary edema; high-flow nasal cannula may be useful, particularly when positive airway pressure is not desirable (44). When invasive mechanical ventilation is needed, lung-protective ventilation limiting the tidal volume and driving pressure may be considered in the absence of supporting evidence (1, 38, 44). While positive pressure ventilation may improve LV loading conditions and ameliorate pulmonary edema, it is essential to recognize the potential for positive pressure ventilation to potentially worsen hemodynamics depending on volume status and RV function (44).…”
Section: Contemporary Standard Care For Csmentioning
OBJECTIVES:
To review a contemporary approach to the management of patients with cardiogenic shock (CS).
DATA SOURCES:
We reviewed salient medical literature regarding CS.
STUDY SELECTION:
We included professional society scientific statements and clinical studies examining outcomes in patients with CS, with a focus on randomized clinical trials.
DATA EXTRACTION:
We extracted salient study results and scientific statement recommendations regarding the management of CS.
DATA SYNTHESIS:
Professional society recommendations were integrated with evaluated studies.
CONCLUSIONS:
CS results in short-term mortality exceeding 30% despite standard therapy. While acute myocardial infarction (AMI) has been the focus of most CS research, heart failure-related CS now predominates at many centers. CS can present with a wide spectrum of shock severity, including patients who are normotensive despite ongoing hypoperfusion. The Society for Cardiovascular Angiography and Intervention Shock Classification categorizes patients with or at risk of CS according to shock severity, which predicts mortality. The CS population includes a heterogeneous mix of phenotypes defined by ventricular function, hemodynamic profile, biomarkers, and other clinical variables. Integrating the shock severity and CS phenotype with nonmodifiable risk factors for mortality can guide clinical decision-making and prognostication. Identifying and treating the cause of CS is crucial for success, including early culprit vessel revascularization for AMI. Vasopressors and inotropes titrated to restore arterial pressure and perfusion are the cornerstone of initial medical therapy for CS. Temporary mechanical circulatory support (MCS) is indicated for appropriately selected patients as a bridge to recovery, decision, durable MCS, or heart transplant. Randomized controlled trials have not demonstrated better survival with the routine use of temporary MCS in patients with CS. Accordingly, a multidisciplinary team-based approach should be used to tailor the type of hemodynamic support to each individual CS patient’s needs based on shock severity, phenotype, and exit strategy.
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