PEARLS

  • Shock is a life-threatening globally insufficient delivery and/or utilisation of oxygen at the cellular level
  • Four main broad categories: Cardiogenic, Hypovolaemic, Obstructive, Distributive
  • Early recognition and treatment are key to preventing irreversible organ dysfunction

DEFINITION

Shock is a life-threatening state where there is globally insufficient delivery and/or utilisation of oxygen at the cellular level(1). It is characteristically (but not always) associated with low blood pressure and impaired tissue perfusion. The consequence of shock is cellular and tissue hypoxia and ultimately cellular death and organ dysfunction.

Early effects of shock can be reversible, however, a delay in diagnosis or without appropriate and timely treatment can lead to irreversible damage including multiorgan dysfunction syndrome (MODS) and death.

PATHOPHYSIOLOGY

  • Oxygen delivery (DO2) is the product of cardiac output (CO) and the oxcygen content of arterial blood, where:
    • DO2 (mL/min) = CO x ([1.39 x Hb x SaO2] + [PaO2 x 0.003])
      • Hb (g/L), SaO2 %, PaO2 O2 pressure in mmHg, 1.39 is the theoretical O2 carrying capacity of Hb (also 1.34mL directly measured), 0.003mL = capacity of O2 in plasma
  • If there is adequate arterial O2 concentration, the CO is the main determinant of (DO2) where:
    • CO = HR x Stroke volume (SV)
      • Stroke volume determinants include: Preload, afterload, contractility
  • Normal VO2 (Oxygen uptake) is about 250mL/min at rest, compared with normal global DO2 which is about 1000mL/min
  • When DO2 becomes critical, inadequate supply results in a transition to anaerobic cellular metabolism and results in impaired end-organ function with the characteristic clinical signs of drowsiness, reduced capillary refill, oliguria and hyperlactataemia
  • In septic shock, there is a massive proinflammatory response involving: cytokines, the complement cascade, activation of coagulation and platelet aggregation, increased arachidonic acid metabolites, reactive oxygen species and nitric oxide.
    • The result is: Vasodilation, increased CO (despite impaired contractility) and reduced intravascular volume secondary to increased permeability
  • DO2 in septic shock is increased, however, VO2 is also increased due to increased metabolic activity.
    • Abnormalities in the microcirculation (e.g. shunting, microvascular thrombosis), as well as induced mitochondrial dysfunction drive the altered cellular metabolism and the resulting damage

CLASSIFICATION

CHOD (Classic four main types, further elaborated below)

  • Cardiogenic
  • Hypovolaemic
  • Obstructive
  • Distributive

PROVED?

  • cardiogenic (Pump)
  • Rhythm abnormalities (some purists exclude dysrhythmia as a cause of cardiogenic shock)
  • Obstructive
  • hypovolemia (Volume)
  • Endocrine causes (often mixed classification, but a useful subheading to make sure endocrine causes aren’t missed!)
  • Distributive (due to vasodilation)
  • ? = is it real? (check the BP measurement, is the arterial line in an artery, is the transducer at the correct height?)

Remember that drugs and toxic exposures can contribute to cardiogenic, rhythm, or distributive causes of shock.

CARDIOGENIC SHOCK

Impaired contractility

  • Myocardial ischemia and compliations
    • Infarction — anterior MI, reinfarction, right ventricular infarction, myocardial stunning
    • Acute mitral regurgitation due to papillary muscle rupture
    • Ventricular septal rupture
    • Left ventricular free wall rupture and tamponade
  • Myocarditis
  • Myocardial contusion
  • Takotsubo Cardiomyopathy
  • Septic shock
  • Poisoning or toxic exposure including calcium channel blockers, beta-blockers and digoxin
  • End stage cardiomyopathy

Dysrhythmia

  • Tachycardias
  • Bradycardias

Valvular dysfunction

  • Severe aortic regurgitation
  • Severe aortic or mitral stenosis

Left ventricular outflow tract obstruction

  • Hypertrophic cardiomyopathy
  • Left atrial myxoma

OBSTRUCTIVE SHOCK

Within the circulatory system

  • Massive pulmonary embolus
  • atrial thrombus or myxoma
  • occulsive valvular lesion
  • other emboli (e.g. air, amniotic fluid)

External to the circulatory system

  • Cardiac tamponade
  • abdominal compartment syndrome
  • Tension pneumothorax
  • Dynamic hyperinflation (e.g. severe asthma)
  • Tension pneumomedistinum
  • caval compression (e.g. supine hypotension syndrome in the pregnant female)

HYPOVOLAEMIC SHOCK

Hemorrhage

  • Traumatic
    • Major vessel injury
    • Pelvic vessel disruption
    • Massive hemothorax
    • Intra-abdominal hemorrhage
    • Retroperitoneal hemorrhage
    • Long bone fracture
    • External blood loss
  • Non-traumatic
    • Gastrointestinal bleeding
    • Epistaxis
    • Hemorrhagic pancreatitis
    • Aneurysm rupture
    • Ectopic pregnancy
    • Postpartum
    • Coagulopathy

Fluid loss

  • GI losses (vomiting, diarrhoea, short gut, etc)
  • Excessive diuresis (diabetes insipidus, diuretics)
  • Excessive diaphoresis (heat-related illness)
  • Diabetic ketoacidosis
  • Burns
  • “Third spacing” (pancreatitis, severe sepsis, anaphylaxis)
  • Iatrogenic (post-dialysis)

DISTRIBUTIVE SHOCK

  • neurogenic shock
  • liver failure
  • adrenal insufficiency
  • anaphylaxis
  • septic shock
  • post-bypass vasoplegia
  • drugs and toxic exposures, e.g. calcium channel blockers, epidural anaesthesia

ENDOCRINE AND METABOLIC CAUSES OF SHOCK

  • Adrenal insufficiency
  • Hypothyroidism
  • Hyperthyroidism
  • Diabetic ketoacidosis
  • Severe acidosis/ alkalosis and electrolyte disturbances (e.g. hypocalcemia)

? (ERRORS AND ARTEFACTS)

  • non-invasive blood pressure measurement error
  • arterial line inadvertently sited in a vein
  • arterial line transducer position higher than the right atrium

HAEMODYNAMIC VALUES IN DIFFERENT TYPES OF SHOCK

CIPCWPCVPSVRDO2
Septic shockN or N or
Cardiogenic shockN or
Hypovolaemic shock
Obstructive shockN or
CI = Cardiac Index, PCWP = Pulmonary Capillary Wedge Pressure, CVP = Central Venous Pressure, SVR = Systemic Vascular Resistance, DO2 = Oxygen Delivery

LITFL

Books and Journal Articles

  • (1) Haseer Koya H, Paul M. Shock. [Updated 2021 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK531492/
  • Marshall, S., Cadogan, M., Celenza, A., Ruedy, J. and Brown, A., 2011. Marshall & Ruedy’s On Call: Principles & Protocols: Australian Version. Elsevier Australia.
  • Bersten, A. and Soni, N., 2014. Oh’s Intensive Care Manual. 7th ed. Elsevier.
Cite this article as: Chris Nickson and James Pearlman, "Shock," In: LITFL - Life in the FastLane, Accessed on September 29, 2022, https://litfl.com/shock/.

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

ICU Advanced Trainee BMedSci [UoN], BMed [UoN], MMed(CritCare) [USyd] from a broadacre farm who found himself in a quaternary metropolitan ICU. Always trying to make medical education more interesting and appropriately targeted; pre-hospital and retrieval curious; passionate about equitable access to healthcare; looking forward to a future life in regional Australia. Student of LITFL.

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