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CHAPTER 14
The Management of Cardiogenic Shock and Hemodynamic Support Devices and Techniques
Bimmer Claessen and José P.S. Henriques
Introduction
Even in the current era of primary percutaneous coronary intervention (PCI), cardiogenic shock complicating acute myocardial infarction (AMI) remains a dramatic and lethal condition. As of 2020, there is only one proven intervention that results in increased survival of cardiogenic shock complicating MI: prompt reperfusion as shown by the SHOCK (should we emergently revascularize occluded coronaries for cardiogenic shock) trial [1]. In this chapter evidence on medical and mechanical management of cardiogenic shock is discussed.
Definition of Shock
Shock is defined as a clinical condition where there is inadequate end‐organ perfusion due to failure of the heart to pump blood in adequate quantities. There is currently no uniform definition of cardiogenic shock in clinical practice or for research purposes. Several influential randomized clinical trials use definitions that are similar, but not identical.
SHOCK trial definition: In the SHOCK trial, cardiogenic shock was defined by a combination of clinical and hemodynamic criteria. [1, 2] Clinical criteria in SHOCK were hypotension (a systolic blood pressure of <90 mm Hg for at least 30 minutes or the need for supportive measures to maintain a systolic blood pressure of ≥90 mm Hg) and end‐organ hypoperfusion (cool extremities or a urine output of <30 ml per hour, and a heart rate of ≥60 beats per minute). The hemodynamic criteria were a cardiac index of no more than 2.2 liters per minute per square meter of body‐surface area and a pulmonary‐capillary wedge pressure of at least 15 mm Hg [1, 2].
IABP‐SHOCK and CULPRIT‐SHOCK definition: In the IABP‐SHOCK II (intra‐aortic balloon pump in cardiogenic shock) and CULPRIT‐SHOCK (Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock) trials, the following definition was used: (i) a systolic blood pressure of less than 90 mm Hg for more than 30 minutes or needing infusion of catecholamines to maintain a systolic pressure above 90 mm Hg, (ii) clinical signs of pulmonary congestion, and (iii) impaired end‐organ perfusion. The diagnosis of impaired end‐organ perfusion required at least one of the following: altered mental status; cold, clammy skin and extremities; oliguria with urine output of less than 30 ml per hour; or serum lactate level higher than 2.0 mmol per liter [3, 4].
The Society for Cardiovascular Angiography and Interventions (SCAI) has recently proposed a classification schema for CS which is now endorsed by the major North American cardiovascular societies [5]. This system describes five different stages of CS severity including stage A “at risk for CS”, stage B “beginning CS”, stage C “classic CS”, stage D “deteriorating CS” and stage E “CS in extremis”. A detailed overview of this definition is provided in Table 14.1.
Table 14.1 SCAI Classification of cardiogenic shock.
| Stage | Description | Physical exam/bedside findings | Biochemical markers | Hemodynamics |
|---|---|---|---|---|
| A“At risk” | Patient not currently experiencing signs or symptoms of CS but at risk for its development. E.G. those with large acute myocardial infarction or prior infarction and acute and/or acute on chronic heart failure symptoms | Normal JVPLung sounds clearWarm and well perfusedStrong distal pulsesNormal mentation | Normal labsNormal renal functionNormal lactic acid | Normotensive (SBP≥100 or normal for pt.) If hemodynamics done:cardiac index ≥2.5CVP <10PA sat ≥65% |
| B“Beginning CS” | A patient who has clinical evidenceof relative hypotension ortachycardia withouthypoperfusion. | Elevated JVPRales in lung fieldsWarm and well perfusedStrong distal pulsesNormal mentation | Normal lactateMinimal renal functionimpairmentElevated BNP | SBP <90 OR MAP <60 OR>30 mmHg drop frombaselinePulse ≥100If hemodynamics donecardiac index ≥2.2PA sat ≥65% |
| C“Classic CS” |
A patient that
|
