Detection of relevant CT signs must be accurate, reproducible, and feasible over time, for which a state-of-the-art CECT technique is needed. Nowadays, CT technology consists of a multidetector-spiral CT between 8- and 640-slice CT. Acquisition times and number of contrast-enhanced phases are not standardized for all CT scanners.

CECT should be performed in critical patients with a volumetric technique, with craniocaudal acquisition, in a supine position, and, when possible, preferably in a “feet first” position [34]. Breath-hold acquisition can ensure the avoidance of motion artifacts if clinical condition permits [35]. The CECT multiphasic protocol should include an abdomen/pelvis pre-contrast scan followed by chest/abdomen/pelvis dynamic images acquired in the arterial and portal venous phases without oral contrast medium (CM). CM volume should be calculated according to patient size based on total body weight (BW), injecting about 0.625 gI per kilogram of total BW. High concentrations (370–400 mg I/mL) of IV CM (80–120 mL of iodinated CM, depending on the patient’s weight) should be administered through an 18–20-gauge needle into the antecubital vein at a rate of 3.5–4 mL/s. This should be followed by a bolus of 30–40 mL of saline at the same flow rate. The acquisition of the arterial phase is timed using bolus tracking, placing the region of interest (ROI) on the aortic arch and starting at an attenuation threshold of 100 Hounsfield Units (HU) [34,35,36,37]. The portal venous phase is acquired with a delay of 60–70 s. The suggested acquisition includes scanning the abdomen and pelvis in the arterial phase, and the chest, abdomen, and pelvis in the portal venous phase. Additionally, a late scan of the abdomen and pelvis at 3–5 min may be acquired to address various causes of shock. Oral or rectal CM is not recommended. Each institution should regularly assess image quality, review protocols regarding dose, and consider the possibility of reducing the quantity of CM [34]. The development of new technologies aims to reduce radiation exposure while maintaining good image quality through iterative reconstruction or automatic tube current modulation [35]. Another option to reduce the radiation dose is the adoption of dual-energy CT, allowing the possibility of virtual noncontrast (VNC) image acquisition [38]. An unenhanced CT brain should be considered for patients presenting with altered mental status, to exclude the presence of acute ischemic stroke or intracranial hemorrhage. Head CT can also be conducted during the late phase of a total body study to rule out the presence of intracranial abscess formation or malignancy [35]. To ensure proper analysis and post-processing, it is recommended to use an effective slice thickness of 2.5 mm with reconstruction at 0.625 mm, allowing for maximum intensity projection (MIP) and multiplanar reformation (MPR) techniques.

CECT images may be used to assess three possible hemodynamic instabilities in acutely sick patients:

(a)

In cases of hemodynamic stability, IV CM into an upper limb vein is delivered to the right atrium via the superior vena cava (SVC), and is then pumped via the right ventricle to the pulmonary arteries. Contrast subsequently returns via the pulmonary veins to the left-side cardiac chambers before reaching systemic circulation [39]. As it undergoes first pass circulation and re-circulation, the contrast bolus gradually mixes with the blood pool, leading to dilution while moving downstream from the injection site. Due to its small molecular size, iodinated CM exhibits high diffusibility, readily redistributing from the intravascular space to organic interstitial spaces [39,40]. This may be called the “physiological” pattern and can correspond to an early compensatory stage of shock. Particularly in these patients without advanced shock symptoms, an image-based morphological indicator promises information about the identification of patients “at high risk”.

(b)

In a state of advanced hemodynamic instability, many homeostatic mechanisms try to maintain arterial pressure and adequate tissue perfusion to critical organs, such as the brain and heart, by reflex stimulation of the sympathetic nervous system, elevated levels of angiotensin II, adrenaline, and noradrenaline, and vasoconstriction (compensated shock). Carotid baroreceptors respond to decreased blood pressure by triggering increased sympathetic signaling and maintaining cardiac output (sympathetic “fight or flight” response). In cases of decompensated shock, when compensatory mechanisms falter and prior to the onset of death, the pumping action of the heart ceases, leading to a substantial decline in systemic arterial and venous pressures. Consequently, the arteriovenous pressure gradient diminishes [6,41,42]. This altered hemodynamic state results in stasis of CM in the venous system in the presence of the left chamber and arterial opacification, and of other infrequent and often unappreciated ominous MDCT vascular signs that represent a true hypovolemic state and must be recognized early by the radiological staff to improve survival [24,43,44,45,46,47,48]. This may be called the “venous CM pooling and layering” pattern, indicating that compensatory mechanisms are becoming insufficient and the patient must receive immediate treatment.

(c)

In irreversible end-organ dysfunction, injected IV CM circulation is supported only by the pressure applied by the automated power injector and the density of contrast material. Circulatory arrest leads to dense contrast pooling and layering in the SVC, IVC (inferior vena cava), and right heart chambers with non-opacified left heart chambers or arterial vessels (Figure 1) [43,45,49,50,51,52]. This may be called the “non-beating heart” pattern. Cardio-pulmonary aggressive resuscitation must immediately be initiated within the framework of a predetermined emergency plan.

Figure 1. Non-beating heart in a 72-year-old man with sudden-onset severe dyspnea/shock and asystole during thoraco-abdominal CT. (A) CECT axial image shows dense contrast in the round superior vena cava, and reflux in the azygous arch; (B) contrast pooling and layering in the right atrium and IVC with retrograde opacification of coronary sinus (arrow). (C) CM fills the round inferior vena cava with hypostatic reflux into the hepatic veins, hemiazygos vein, partially splenic vein, and (D) right renal vein. Note no mixing of blood with CM and no opacification of the pulmonary arteries, aorta, and left cardiac chambers, suggestive of a non-beating heart. Prompt initiation of cardio-pulmonary resuscitation to restore circulation was useless. Autopsy: ruptured myocardial infarction.

CECT shock-associated findings partially overlap with those referred to previously in the literature as CT “hypoperfusion or hypovolemic shock complex” (HSC) [15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32]. This refers to a constellation of findings that reflect hypovolemia and is often described in traumatic hemorrhagic shock [15,16,18,21,24,25,26,27,29]. HSC findings can be grouped into vascular (morphological and functional) and, based on their various anatomic locations, visceral/solid organ findings. It is now clear that vascular signs represent the true hypovolemic state and visceral findings represent hypoperfusion [30].

5. CECT Findings/Biomarkers as Prognostic Indicators