Table 2.

Diagnostic work-up and management in patients with CS-AKI, according to invasive and non-invasive monitoring strategies and laboratoristic and echocardiographic findings. Name of the parameters, normal values, frequency of measurements, and further comments are here reported. AKI, acute kidney injury; CS, cardiogenic shock; KDIGO, Kidney Disease: Improving Global Outcome; NGAL, neutrophil gelatinase–associated lipocalin and kidney injury molecule; SBP, systolic blood pressure

Parameter	Normal values	Frequency	Comments and management implications
Invasive and non-invasive monitoring
Arterial invasive blood pressure monitoring	SBP ≥ 90 mmHg	Continuous	Affords tissue perfusion and prevents peripheral vasoconstriction, thus reducing cardiac afterload. Pulse pressure and stroke volume as derived by arterial waveform predict AKI in CS after resuscitated cardiac arrest
Heart rate	60–100 bpm	Continuous	High values increase heart oxygen consumption
Central venous pressure	3–8 mmHg	Continuous	Reflects the venous return to the right heart from periphery, as well as the ability of the heart to pump into the arterial tree. Its increase is associated with a higher incidence of AKI and may guide right ventricular-focused assessment
Arterial oxygen saturation	≥ 94%	Continuous	Estimates the content of oxygen in arterial blood. Its information varies depending on the sampling point, whether in great vessels or in capillaries
Central venous oxygen saturation	≥ 70%	Continuous/every 4–6 h	Estimates the balance between oxygen delivery and consumption, thus reflecting tissue extraction of oxygen in relation to heart pump function
Respiratory rate	12–20 breaths per minute	Every 8 h	It is often controlled by the clinician because of the need for mechanical invasive support
Urine output	0.5 mL/kg/h	Hourly	A rough but effective marker of renal function. Urinary catheterization has to be performed in every patient. Whether a KDIGO-stated cut-off of 0.5 is generally accepted, a stricter one of 0.3 is more related to 90-day mortality in the setting of CS-AKI
Laboratory findings
Lactates	0.5–1.6 mmol/L	Every 4–6 h	Represents a marker of end-organ hypoperfusion, as it indicates a shift to anaerobic metabolism. Sample-to-sample differences in lactate values are more sensitive of the clinical outcome than single values
Serum creatinine	0.8–1.3 mg/dL (men) 0.6–1.1 mg/dL (women)	Every 12–24 h	A marker for the estimation of renal function. Completely filtered, partially secreted in the proximal tubule. Its elevation is significantly delayed with respect to the renal damage
Serum cystatin C	0.60–1.55 mg/L	First phases (if available)	A marker for the estimation of renal function. Completely filtered, no secreted or reabsorbed. Less dependent on age, gender, ethnicity, and muscle mass compared with creatinine. Its elevation is significantly delayed with respect to the renal damage
NGAL	28.7–167.0 ng/mL	First phases (if available)	A marker of renal damage. Its increase is way more precocious than markers of function, hence raising awareness of renal involvement
Echocardiographic findings
Stroke volume	50–80 mL	Daily	Evaluates left ventricular function, even if it is strictly dependent on preload and afterload. It affords a between-days comparison in pump function
Left ventricular ejection fraction	55–60%	Daily	Evaluates left ventricular function. Attention has to be paid to any pathological condition that falsely overestimates the ejection fraction, i.e., severe mitral regurgitation secondary to LV dilatation or papillary dysfunction or ischemic septal ventricular defect
E mitral wave deceleration time	> 150 ms	First phases	As part of the assessment of diastolic function, together with E/A (restrictive pattern if values ≥ 2). Values below the reference limit represent a strong predictor of outcome in the acute phase
Right ventricular fractional area change (RV-FAC)	≥ 35%	First contact and anytime right heart involvement is suspected	Evaluates right ventricular function. Attention has to be paid to a pseudo-normalization of this value under conditions of volume overload
Right ventricular free wall longitudinal strain	< − 13.1%	At admission and at 48 h	Evaluates right ventricular performance with higher sensitivity and reproducibility than RV-FAC. Useful in the prediction of right ventricular failure after left ventricular assisted device implantation
Hepatic veins flow	−	First contact and anytime right heart involvement is suspected	Evaluates right ventricular function. A bi- or tri-phasic waveform with D-wave greater than S-wave may suggest right heart failure, as well as tricuspid regurgitation. An irregular pattern of the waveform may suggest arrhythmias