Recommendations

Key Recommendations

Treatment aims are to restore regional perfusion and improve oxygen delivery, to reverse hypotension, and to prevent organ damage from hypoperfusion. Volume resuscitation is generally accepted as the first-line intervention for shock, except for anaphylaxis (which requires immediate administration of intramuscular epinephrine [adrenaline]).[63][64][65] Further interventions are guided by the response to intravenous fluids and the likely etiology as investigations proceed. Evidence-based guidelines have been published for various subtypes of shock, including septic shock and acute heart failure, but not for the immediate management of undifferentiated shock.[2][3][66][67]  Early involvement of the critical care team is important for optimal management of the shock patient.

Airway, breathing, and circulation

As with any critically ill patient, airway patency is the first priority, and frequent reassessment is advised. After assurance that the airway is patent, high-flow oxygen is provided as required by mask or nasal cannula, commonly aiming for arterial oxygen saturations of 94% to 98%.[34] Routine supplementation of oxygen to achieve higher oxygen saturations has been linked to coronary and pulmonary arterial vasoconstriction in acute myocardial infarction.[68][69] The goal is adequate oxygenation but not routine excessive oxygenation. The use of positive pressure ventilation or noninvasive ventilation (NIV) (continuous positive airway pressure and bilevel positive airway pressure) in shock resuscitation is controversial due to NIV-induced increase in intrathoracic pressure, which may decrease cardiac preload from the pulmonary circulation. NIV is well supported for hypoxemic respiratory failure.[70] However, the use of NIV in the setting of shock is not well supported in the literature, and has been clinically associated with worsening hypotension and perfusion. If NIV is used in patients with shock, rigorous monitoring of blood pressure and perfusion of vital organs must be maintained. For patients with sepsis-induced hypoxemic respiratory failure, high-flow nasal oxygen is recommended over NIV.[2]

Intravenous fluids aim to improve perfusion by increasing intravascular volume and preload. The benefit outweighs the risk in the majority of cases except frank pulmonary edema. If a ruptured aortic aneurysm is thought likely, systolic blood pressure should be maintained at no more than 100 mmHg systolic. Commonly, systolic blood pressure of 90 mmHg or a mean arterial pressure of 65 mmHg is targeted during volume resuscitation; infusion is stopped if concerns of volume overload develop (pulmonary rales or suspected pulmonary edema). If there is no evidence for, or suspicion of, pulmonary edema secondary to cardiac failure, early fluid delivery is more important than the type of fluid (crystalloid or colloid).[71][72][73] [ Cochrane Clinical Answers logo ] [Evidence B]​​​​​​ There is some evidence that balanced crystalloids may be preferable to normal saline in critically ill patients in intensive care and are recommended in patients with sepsis or septic shock.[2][76]​​​ Fluids should be given via a large-bore peripheral intravascular catheter. If there is acute inferior (right coronary artery) occlusion, or right ventricular infarct, hypotension is initially (before thrombectomy) corrected with careful fluid administration to improve right ventricular filling and overall cardiac output.[77] Blood products should be administered in patients with acute blood loss (hemorrhage) or profound anemia from chronic red blood cell loss.[78] Caution is needed in patients with suspected cardiogenic shock; intravenous fluids may be administered cautiously in the absence of signs of fluid overload (clinically determined by auscultation of the lungs to assess for rales, or by chest radiography).

Monitoring

Continuous monitoring is imperative to monitor response to therapy and to guide treatment. This includes clinical observation, repeated blood pressure readings, respiratory rate, oxygen saturations, pulse, level of consciousness, monitoring of urine output in relation to fluid resuscitation or use of vasoactive agents, and monitoring of cardiac rhythm. Direct blood pressure measurement via automatic cuff devices or an arterial line is preferred over routine sphygmomanometry, because direct blood pressure measurement is more precise and allows for continuous monitoring. If an arterial line is used, it also provides access for arterial blood sampling.[79] Lactate levels can be monitored to assess response to treatment. In the critical care setting, continuous capnography can aid the assessment of shock.[36] Side stream or direct capnography (when endotracheal airway is in place) can be helpful in assessing pulmonary perfusion matched to ventilation.[36] The lactate level will usually decrease if the patient is clinically improving.[2] Treatment is dependent on continuous monitoring of these variables and guided by their response. Patients requiring vasoactive drugs (vasopressor/inotrope) need continuous monitoring in a critical care setting.

Vasoactive drugs

Patients with a systolic BP <90 mmHg with critical reduction in cardiac output and end-organ hypoperfusion are defined as being in cardiogenic shock.[4]

Short-term intravenous infusion of a vasoactive agent (vasopressor and/or inotrope) should be considered in patients with hypotension (systolic BP <90mmHg) and/or signs or symptoms of hypoperfusion, despite adequate filling status.[3][4] Vasoactive agents may cause tachycardia, and induce arrhythmias and myocardial ischemia.[3][4]

Intravenous inotropic support can increase cardiac output and improve hemodynamics in patients presenting with cardiogenic shock.[4] There is a lack of robust evidence to suggest the clear benefit of one inotropic agent over another in cardiogenic shock.[80] In general, the choice of a specific inotropic agent is guided by blood pressure, concurrent arrhythmias, and availability of drug.[4] Inotropes should be used with caution because there is evidence that they result in increased mortality.[3][4][81] Inotropes should be discontinued if there are sustained arrhythmias or symptomatic coronary ischemia. Continuous monitoring of cardiac rhythm is recommended during infusion of inotropes.

Vasopressors are commonly recommended in hypotension refractory to volume resuscitation. Vasopressors are recommended only after adequate volume resuscitation.[2][3] Therapeutic vasoconstriction aims at reversing the mismatch between vessel tone and intravascular volume. Dose is commonly titrated to achieve a mean arterial blood pressure of ≥65 mmHg, or a systolic blood pressure of ≥90 mmHg.[2][79][82] Vasopressors increase the risk of tissue ischemia and necrosis in a dose-dependent manner.

Consult a specialist for guidance on suitable vasopressor/inotrope regimens. Selection of appropriate vasoactive agents should only take place under critical care supervision, and may vary according to the type of shock, clinician preference, and local practice guidelines.

Temporary mechanical circulatory support

Temporary mechanical circulatory support (MCS) devices (e.g., extracorporeal membrane oxygenation or intra-aortic balloon pump) should be considered in patients with persistent cardiogenic shock despite inotropic therapy.[3][4]​​[83]

Temporary MCS in appropriately selected candidates should be initiated as soon as possible with sufficient support to fully reverse the potential hemometabolic consequences of shock. If there is a delay to sufficient early support with temporary MCS, worsening end-organ perfusion and metabolic derangements can make future attempts difficult.[83] The hemodynamic benefits of the specific devices vary, and few head-to-head randomized comparisons exist. Vascular, bleeding, and neurologic complications are common to MCS devices, and the risk of such complications should generally be considered in the calculation to proceed with such support.[4] MCS requires specialist multidisciplinary expertise for implantation and management.[3][83]

The escalation of either pharmacologic and mechanical therapies should be considered in the context of multidisciplinary teams of heart failure and critical care specialists, interventional cardiologists, and cardiac surgeons.[4][83]

Treatment of underlying cause

Volume resuscitation and vasoactive agents only buy time in most patients with shock. Successful reversal of shock requires treatment specifically aimed at the main cause of shock (e.g., cardiogenic shock, cardiac tamponade, pulmonary embolism, anaphylaxis, sepsis, hemorrhagic shock due to trauma, tension pneumothorax). The choice of specific treatment is guided by the individual results of continued and repeated patient evaluation.

Identification of cardiogenic shock is important because aggressive fluid administration may worsen the shock state and lead to the onset (or worsening) of acute pulmonary edema. Early involvement of specialist multidisciplinary teams (e.g., heart failure and critical care specialists, interventional cardiologists, and cardiac surgeons) is recommended when cardiogenic shock is suspected. Cardiogenic shock (secondary to a large myocardial infarction) needs urgent revascularization of the coronary arteries by percutaneous coronary intervention, direct coronary infusion of thrombolytics, or cardiovascular surgery.[50][84]​ Mechanical support with an intra-aortic balloon pump (IABP) may also be indicated.[50] However, multiple IABP studies have not shown an improvement in mortality.[50][85][86][87]​​​ [ Cochrane Clinical Answers logo ]

Severe rhythm disturbances should be corrected urgently in patients with acute heart failure and unstable conditions, using medical therapy, electrical cardioversion, or temporary pacing.[3] Cardiac tamponade needs urgent drainage by pericardiocentesis under ECG monitoring.[88] This can have an effect by draining as little as 30 mL, but may be unsuccessful if the blood is clotted. A pericardial drain or surgical pericardial window may be required, with evaluation and treatment of the underlying cause of bleeding.

A pulmonary embolus may require thrombolysis, anticoagulation, and occasionally surgery if very large.

Anaphylactic shock requires administration of intramuscular epinephrine and supportive therapy.

Early recognition and treatment of septic shock is key to improving outcomes. The Surviving Sepsis Campaign (SSC) treatment guidelines remain the most widely accepted standards.[2] Current best practice is based on evidence for care bundles in sepsis.[2][89][90][91] The SSC guidelines recommend: 

  • Obtaining blood cultures prior to administration of antibiotics

  • Administering antimicrobials immediately, ideally within 1 hour of recognition (in adults with possible septic shock or a high likelihood for sepsis)

  • Administering empiric antimicrobials with MRSA coverage in patients with sepsis or septic shock at high risk of MRSA

  • Administering 30 mL/kg crystalloid for hypotension within the first 3 hours of resuscitation

  • Obtaining serial measurement of blood lactate

  • Aiming for a mean arterial pressure (MAP) of ≥65 mmHg in patients with septic shock on vasopressors.

For adults with an initial diagnosis of sepsis or septic shock, and adequate source control where optimal duration of therapy is unclear, a combination of procalcitonin and clinical evaluation is recommended to decide when to discontinue antimicrobials.[2]

Resuscitation should be guided by dynamic measures rather than physical exam or static measures alone. Dynamic parameters include the response to a passive leg raise or a fluid bolus, using stroke volume, stroke volume variation, pulse pressure variation, or echocardiography, where available. In patients with septic shock and an ongoing requirement for vasopressor therapy, the SSC treatment guidelines suggest intravenous corticosteroids.[2]

Hemorrhagic shock due to trauma requires a team approach with attention to identification of cause for, and control of, hemorrhage as soon as possible. Massive hemorrhage due to trauma is often associated with fibrinolysis, which further exacerbates hemorrhage by inhibiting clot formation. Antifibrinolytic agents may have a beneficial effect in addition to fluid and blood transfusion in stabilizing a trauma patient with shock.[92] Overly aggressive fluid infusion may increase the bleeding rate in hemorrhagic shock: in particular, when MAPs are >40 mmHg.[79] 

Tension pneumothorax requires urgent decompression through needle thoracocentesis.

Special considerations for suspected cardiogenic shock

Aggressive fluid administration in the setting of cardiogenic shock may worsen the shock state and lead to the onset (or worsening) of acute pulmonary edema. Intravenous fluids may be administered cautiously in the absence of signs of fluid overload (clinically determined by auscultation of the lungs to assess for rales, or by chest radiography) with small initial boluses [250mL] of crystalloid such as normal saline or Ringer lactate.[93]​ Ongoing management is guided by the continuous monitoring of organ perfusion and hemodynamics. Specialized treatments for afterload reduction with nitroglycerin and the inotrope dobutamine may be of benefit in the management of these patients.[94] Cardiogenic shock is classically considered a state of decreased cardiac index, increased systemic vascular resistance, and increased pulmonary artery pressure (often termed “wet cardiogenic shock” or with vascular volume overload); euvolemic cardiogenic shock presents with decreased cardiac index, increased systemic vascular resistance, and normal-range pulmonary artery pressure (“dry cardiogenic shock”). Afterload reduction is an important initial step in the management of both forms of cardiogenic shock.[50]


Needle decompression of tension pneumothorax: animated demonstration
Needle decompression of tension pneumothorax: animated demonstration

How to decompress a tension pneumothorax. Demonstrates insertion of a large-bore intravenous catheter into the fourth intercostal space in an adult.



Central venous catheter insertion: animated demonstration
Central venous catheter insertion: animated demonstration

Ultrasound-guided insertion of a non-tunnelled central venous catheter (CVC) into the right internal jugular vein using the Seldinger insertion technique.



Peripheral intravascular catheter: animated demonstration
Peripheral intravascular catheter: animated demonstration

How to insert a peripheral intravascular catheter into the dorsum of the hand.



Female urethral catheterization: animated demonstration
Female urethral catheterization: animated demonstration

How to insert a urethral catheter in a female patient using sterile technique.



Male urethral catheterization: animated demonstration
Male urethral catheterization: animated demonstration

How to insert a urethral catheter in a male patient using sterile technique.


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Pocket mask ventilation animated demonstration
Pocket mask ventilation animated demonstration

How to use a pocket mask to deliver ventilation breaths to an adult patient.


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