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Review
. 2021 May;26(3):487-496.
doi: 10.1007/s10741-020-10034-0. Epub 2020 Oct 2.

Cardiogenic shock and acute kidney injury: the rule rather than the exception

N Ghionzoli  1 , C Sciaccaluga  2 , G E Mandoli  2 , G Vergaro  3   4 , F Gentile  4 , F D'Ascenzi  2 , S Mondillo  2 , M Emdin  3   4 , S Valente  2 , M Cameli  2
Affiliations
Review

Cardiogenic shock and acute kidney injury: the rule rather than the exception

N Ghionzoli et al. Heart Fail Rev. 2021 May.

Abstract

Cardiogenic shock (CS) is a life-threatening condition of poor end-organ perfusion, caused by any cardiovascular disease resulting in a severe depression of cardiac output. Despite recent advances in replacement therapies, the outcome of CS is still poor, and its management depends more on empirical decisions rather than on evidence-based strategies. By its side, acute kidney injury (AKI) is a frequent complication of CS, resulting in the onset of a cardiorenal syndrome. The combination of CS with AKI depicts a worse clinical scenario and holds a worse prognosis. Many factors can lead to acute renal impairment in the setting of CS, either for natural disease progression or for iatrogenic causes. This review aims at collecting the current evidence-based acknowledgments in epidemiology, pathophysiology, clinical features, diagnosis, and management of CS with AKI. We also attempted to highlight the major gaps in evidence as well as to point out possible strategies to improve the outcome.

Keywords: Acute kidney injury; Cardiogenic shock; Heart failure; Outcome; Replacement therapy.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Fig. 1
Fig. 1
Hemodynamic and non-hemodynamic factors in CS, their interplay with the kidneys, and associated therapeutic strategies. Injuries to the heart can determine both a reduction in cardiac output and an increase in central venous pressure. Alongside, the activation of the sympathetic nervous system induces renal vasoconstriction and RAAS activation, thus reducing urine output. Replacement and pharmacological strategies are displayed for each organ. CO, cardiac output; CVP, central venous pressure; CVVH, continuous veno-venous hemofiltration; IABP, intra-aortic balloon pump; MCS, mechanical circulatory support; PEEP, positive end-expiration pressure; RAAS, renin-angiotensin-aldosterone system; RR, respiratory rate; RRT, renal replacement therapy; SNS, sympathetic nervous system; TV, tidal volume; UO, urinary output
Fig. 2
Fig. 2
Prerenal, renal, and post-renal main causes of acute kidney injury complicating cardiogenic shock. Causes are distinguished as part of the natural history of the disease and as iatrogenic factors during in-hospital management. AC, anticoagulation; CO, cardiac output; CVP, central venous pressure; obs., obstruction; RAAS, renin-angiotensin-aldosterone system; SNS, sympathetic nervous system
Fig. 3
Fig. 3
Clinical phenotypes of cardiogenic shock. Two additional types of cardiogenic shock have been described over the classic “wet and cold” phenotype. These are “dry and cold,” with cold extremities and no pulmonary congestion, and “wet and warm,” where a peripheral vasodilation is observed mainly as the consequence of a systemic inflammatory syndrome response. CS, cardiogenic shock; SIRS, systemic inflammatory response syndrome
See this image and copyright information in PMC

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