Approach

All patients who are clinically in a state of shock should be managed in a resuscitation, high-dependency, or intensive care setting.

Transfer out of the resuscitation room should only be considered when the patient's vital signs are stabilized. In any evaluation of shock, hemodynamic measurements have to be interpreted in the clinical context of some basic principles. The following questions are useful:

  • Is the patient in shock? (Is oxygen delivery or cellular metabolic demand not being met?)

  • Does the patient respond to fluids? (Do they have a decreased preload?)

  • If the patient is fluid responsive, is the arterial tone (afterload) increased or decreased?

  • Is pump function (cardiac contractility) increased or decreased?

The answer to these questions will help to determine the type of shock.

[Figure caption and citation for the preceding image starts]: Parameters to differentiate between types of shock and examplesAdapted with permission from "Rady MY. Bench-to-bedside review: Resuscitation in the emergency department. Crit Care. 2005;9:170-176". [Citation ends].com.bmj.content.model.assessment.Caption@470e38f4

Indicators of regional perfusion, such as arterial or venous serum lactate and base deficit, are important because early hemodynamic assessment based on vital signs and central venous pressure (CVP) does not detect early or persistent global hypoxia.[44]

Parameters to evaluate shock

Clinical criteria, including vital signs, level of consciousness and assessments of peripheral perfusion (core-periphery temperature gradient, capillary return time) are mandatory.

Hemodynamic monitoring

  • Mean arterial pressure (MAP), systolic BP, and diastolic BP can be done continuously with an arterial line and confirmed with hourly noninvasive BP monitoring.

  • MAP may be estimated by adding the diastolic pressure to one third of the difference between the systolic and diastolic pressures.

Ultrasonography[45]​​

  • Decreased inferior vena cava filling and diameter are suggestive of hypovolemic shock.

  • Point of care abdominal-thoracic ultrasound (e.g, FAST [focused assessment with sonography for trauma]) may reveal pneumothorax (that may be complicated by tension pneumothorax), or free fluid in the abdominal cavity.[46]​​

  • Echocardiography to determine ventricular volumes and cardiac output is helpful in assessing cardiogenic shock.[47]​​ Cardiac sonography may reveal valvular disorders, or pericardial effusion that may be associated with cardiac tamponade.

Shock Index[48]

  • Defined by the ratio of heart rate to systolic BP.

  • A ratio of <1 is associated with decreased response to volume loading, but if >1, it usually indicates a variable response to fluid administration.[49]

  • Use of the shock index is mostly confined to hypovolemic shock. It may be unreliable in septic and cardiogenic shock (when heart rate may increase in response to other factors), and in the setting of older age, hypertension, or beta-blocker or calcium-channel blocker therapy.[48][50]

Monitoring organ system effects

  • Urine output of <0.5 mL/kg/hour, and change in mental status and tachypnea, indicate decreased organ perfusion.

  • Urine output is usually recorded each hour.

Serum markers of tissue metabolism

  • A normal serum lactate level in a stressed patient is considered to be below 18 mg/dL (2 mmol/L).

  • Lactate levels >36 mg/dL (>4 mmol/L) have been associated with greater mortality in shock. Early lactate clearance is associated with better prognosis.[51]

  • Lactate can be measured from an arterial or venous gas sample 2 or 3 times a day, or more often if required, to monitor response to treatment.

  • Base deficit, negative base excess, also correlates with outcome in shock. Initial base deficit does not correlate well with initial blood lactate because there are numerous causes of an elevated lactate (e.g., metformin, beta-2 agonists) other than hypoperfusion. The base excess is defined as the amount of hydrogen ions that would be required to return the pH of the blood to 7.35 if the PaCO₂ levels were adjusted to normal.[52]

Scoring systems

Several risk stratification approaches have been proposed. All rely on a structured clinical assessment and recording of the patient’s vital signs.[35][37][38]​[40]​​ It is important to check local guidance for information on which approach your institution recommends. The timeline of ensuing investigations and treatment should be guided by this early assessment.[40]

Sepsis screening tools are designed to promote the early identification of sepsis, and consist of manual methods or the automated use of the electronic health record (EHR). These include the Sequential (or Sepsis-related) Organ Failure Assessment (SOFA) score, the quick SOFA (qSOFA) criteria, National Early Warning Score (NEWS), and Modified Early Warning Score (MEWS). The accuracy of each tool varies, but they are an important component of identifying sepsis early for timely intervention.[36]

Of these scoring systems, the SOFA scoring system has been subject to greatest study and has been adopted for use in emergency and critical care management of potential shock victims, including screening for shock and ongoing assessment.[53][54][55] A SOFA score of 7 or more on initial evaluation has been associated with significant shock, with a score of 13 or greater associated with significant risk for mortality in the intensive care setting.

[Figure caption and citation for the preceding image starts]: Sequential (or Sepsis-related) Organ Failure Assessment (SOFA) criteriaCreated by BMJ, adapted from Vincent JL, Moreno R, Takala J, et al. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. On behalf of the Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. Intensive Care Med. 1996;22:707-710. [Citation ends].com.bmj.content.model.assessment.Caption@4f1a48d8

SOFA criteria

The Third International Consensus Group (Sepsis-3) recommends using the SOFA score (primarily validated in patients in intensive care) to assess for sepsis, with a score ≥2 in a patient with a suspected infection being suggestive of sepsis.[34]

For patients with suspected sepsis outside the intensive care setting, a modified SOFA score, qSOFA, has been found to have better predictability of in-hospital mortality.[56] However, there is evidence that qSOFA may have poor sensitivity compared with other bedside early warning scores.[57] Therefore, the Surviving Sepsis Campaign advises against using qSOFA, compared with NEWS or MEWS, as a single screening tool for sepsis or septic shock.[36]

Early recognition of sepsis is essential because early treatment improves outcomes.[35]

See urgent considerations section for more details on immediate management.

Measuring the preload

Preload is measured by dynamic response of the CVP to a fluid challenge (e.g., 250 to 500 mL of balanced crystalloid solution). Mini-fluid challenges (e.g., 100 mL) may be used to predict the effects of larger fluid challenges in critically ill patients.[58]​​

Echocardiography or pulse-induced continuous cardio-output monitoring are also used to determine cardiac output. In selected situations, pulmonary artery catheters may be helpful in initial and ongoing monitoring of preload.

Measuring preload responsiveness

Measures of preload responsiveness can guide fluid administration. Methods include stroke volume variation, systolic pressure variation, pulse pressure variation, plethysmographic variation, and passive leg raising.[59]​​​​​[60]​​[61][62]​​​​​​​​[63]​​​​​​​​[64]​​​

Typically an increase in cardiac output of 10% to 12% after a fluid bolus of 300 to 500 mL of crystalloids is considered to be a positive response.

Evaluation of hemodynamic status is difficult in some situations, including in mechanically ventilated patients. Inappropriate fluid administration can be harmful, and measures of preload (e.g., CVP) are unhelpful because, as end-diastolic pressure exceeds a given value, giving further fluids does not increase stroke volume (Starling principle).[60]

Measuring contractility and afterload

Cardiac output is the output of the left ventricle/right ventricle per minute. There are various methods of calculating cardiac output, but an ideal standard has not been established.

The most commonly used method is bedside echocardiography.[47]​ Alternative noninvasive methods include Doppler ultrasound and measurements of pulse pressure, although the latter is a function of both cardiac output and arterial function. As cardiac output is affected by the phase of respiration, it needs to be measured at the same point in the respiratory cycle each time to enable comparison. 

Other methods include dilution and thermodilution using a pulmonary artery catheter. These use the Fick principle, and the rate at which an indicator substance is diluted or temperature falls is proportional to the cardiac output.

The ratio of the cardiac output (stroke volume x heart rate) to the body surface area in meters squared is the cardiac index. Normal values of the cardiac index range from 2.2 to 2.5 L/minute/m². In cardiogenic shock the cardiac index is typically <1.8 without inotropes and <2.0 to 2.2 with inotropes.[65]

Systemic vascular resistance: a measure of afterload derived from the cardiac output, MAP, and CVP.

Measures of tissue perfusion

Oxygen delivery (DO₂): the amount of oxygen delivered to the tissue is calculated as the product of cardiac output, oxygen saturation, and hemoglobin level in the blood. A DO₂ of >600 ml/min/m² has been associated with better outcomes.[66]

  • DO₂ = cardiac output x oxygen saturation x hemoglobin level g/L (1.36) x 100.

Mixed venous oxygen saturations: the saturation of oxygen in the pulmonary artery, and the standard for defining global adequacy of tissue perfusion.[67][68] Normal venous saturations are between 65% and 75%. Superior vena cava oxygen saturation is usually higher by about 8% compared with inferior vena cava oxygen saturation, but they parallel each other in shock.[69][70] A sustained elevation of >80% in the presence of low oxygen delivery carries a poor prognosis, as it indicates tissue inability to utilize oxygen, and is usually seen after cardiac arrest resuscitation.[71] During initial stabilization, even after attaining global indices such as BP and urine output, tissue hypoxia can still persist. If uncorrected, it can lead to oxygen debt.[44] Oxygen debt is due to an imbalance between supply and demand, which is associated with increased organ dysfunction.[72] Early correction of venous saturations to >70% is associated with better outcomes.[15] Venous saturations of <70% are an independent predictor of mortality.[73]

Lactate: levels >36 mg/dL (>4 mmol/L) are associated with greater mortality in shock. Base excess levels are used during bedside resuscitation in determining fluid volume replacement for acute trauma victims.

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