A18. Shock syndrome. Clinical manifestations of shock and its management

Page created on October 21, 2021. Last updated on April 2, 2022 at 15:01

Definition and epidemiology

Shock is a hemodynamic disturbance which leads to inadequate oxygen supply to end-organs. The ensuing tissue hypoxia causes metabolic disorder in the tissues leading to temporary or permanent disturbance of function, and in severe cases to necrosis.

It’s a life-threatening condition which can develop as a complication of disease, procedure, or trauma. The most common form is septic shock, followed by cardiogenic and hypovolaemic.

Etiology and types

Cardiogenic Shock – cardiac dysfunction leads to inadequate tissue perfusion despite adequate intravascular volume.

  • Intrinsic (heart muscle insufficiency)
    • MI, low contractility
    • Severe tachy-or bradycardia, arrhythmias
    • Valve dysfunctions
  • Extrinsic
    • Tear in septum/ventricle wall
    • Extracardiac obstruction

Distributive Shock – vasodilatation of peripheral blood vessels, i.e. blood volume is normal but vascular volume is enlarged. CO increased but SVR decreased.

  • Septic shock
  • Systemic inflammatory response syndrome (SIRS)
    • Pancreatitis
    • Severe burns
  • Neurogenic shock
  • Anaphylactic shock
  • High output cardiac failure

Hypovolaemic shock

  • Non-haemorrhagic
    • Vomiting/diarrhoea
    • Pancreatitis
    • Burns
    • Adrenal insufficiency
  • Haemorrhagic
    • GI bleed
    • Trauma
    • AAA rupture
    • Ectopic pregnancy, postpartum bleeding

Obstructive shock – due to extracardiac obstruction

  • Cardiac tamponade
  • Massive pulmonary embolism
  • Tension PTX


See the corresponding pathophysiology 1 topics for rough details (although those details are not at all important for clinic).

Clinical features

Shock is characterised by features of decreased end-organ perfusion, including:

  • 5 P’s
    • Perfusion of skin – pale, cool skin
    • Pulse – weak peripheral pulse
    • Periphery – prolonged capillary refill time > 2 – 3 s
    • Pressure – systolic BP < 90 mmHg
    • Pee – oliguria (< 1 mL/kg/hour) or anuria (< 0,5 mL/kg/hour)
  • Hypotension
  • Tachycardia
  • Tachypnoea, dyspnoea
  • Altered mental status
  • Ileus

There may also be symptoms specific to the type and underlying cause of the shock. For example, hypovolaemic shock may cause decreased skin turgor and dry mucous membranes. Cardiogenic and obstructive shock may cause distended neck veins. Septic shock may present with flushed, warm skin in the early stages.

Diagnosis and evaluation

The diagnosis of shock is clinical and depends on the presence of typical clinical features. Metabolic acidosis, especially lactic acidosis, is often present. Can see features of end-organ dysfunction or the underlying cause.


Shock is an emergent state which requires emergency management. Treatment must be both supportive and, subsequently, targeted against the underlying cause. This involves:

  • Obtain large bore IV access
  • Give fluid challenge
    • If fluid responsive -> Fluid resuscitation with balanced crystalloid – 20 mL/kg
    • If not -> Vasopressor (norepinephrine) or inotrope (dobutamine)

A fluid challenge refers to giving a small amount of IV fluid and see whether the haemodynamic parameters improve, to assess whether the patient is fluid responsive (requires fluids) or not. A passive leg raise test can be used instead of a fluid challenge. In this test the patient’s legs are passively raised for one minute. This increases preload and will improve the haemodynamic parameters if the patient is fluid responsive.

Subsequent management depends on the type of shock and cause:

  • Hypovolaemic shock
    • Give balanced crystalloid, up to 3 L
    • If haemorrhagic -> give blood and colloid in 1:1
    • Treat underlying cause
  • Neurogenic shock
    • Cervical spine precaution
    • Fluid resuscitation
  • Anaphylactic shock
    • Intubation if airway is compromised (angioedema)
    • 0,5 mg epinephrine every 5 minutes
    • (Glucocorticoids, antihistamines)
  • Cardiogenic shock
    • Careful with fluids – may cause cardiogenic pulmonary oedema
    • Inotropes
    • Intra-aortic balloon pump
    • Ventricular assist device
    • ECMO
    • If AMI -> PCI
  • Obstructive shock
    • If tension PTX -> chest puncture at 3rd ICS mid-clavicular line or 5th ICS at mid-axillary line
    • If PE -> Alteplase or interventional catheterization


  • Acute renal failure
  • Delirium
  • Disseminated intravascular coagulation
  • Death

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