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Shock

Shock. Sarah Leyland Practice Educator – General ICU. Learning Outcomes. Review shock at a cellular level Discuss categories of shock Describe clinical features of the different types of shock Identify management strategies for shock. Shock. Shock is “circulatory insufficiency”

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Shock

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  1. Shock Sarah Leyland Practice Educator – General ICU

  2. Learning Outcomes • Review shock at a cellular level • Discuss categories of shock • Describe clinical features of the different types of shock • Identify management strategies for shock

  3. Shock • Shock is “circulatory insufficiency” • Often goes unrecognised in its early stages • Shock is never the primary diagnosis • Reflects the bodies attempts to preserve vital functions

  4. Shock definition “Failure to deliver and / or utilise adequate amounts of oxygen leading to tissue dysoxia” Antonelli et al (2007) Intensive care medicine 33, 575-590 • n.b definition does not include hypotension (but this is usually present). • If hypotension absent markers include ScvO2, SvO2, base deficit, lactate, perfusion related low pH

  5. Shock at a cellular level • Hypoxaemia or perfusion failure result in anaerobic metabolism =2 ATP molecules, (aerobic=36 ATP molecule) • Na-K pumps fail, ( K, Na and water enter cell) (Darovic 2002)

  6. ESCIM (2014)

  7. Capillary function • Swollen cells reduce capillary lumen diameter, reducing blood flow • Clumping of blood cells plugs capillaries • Cell junctions between cells widen allowing leaking • Unstable cellular environment > lysosomes release (Darovic 2002)

  8. Organ systems • Depending on number of cells lost organ damage may occur • Persons response to shock depends on pre- existing disease, drug use, age, magnitude if illness and time period of development of shock (Darovic 2002)

  9. Stage 1 –Compensated (Initial) • A fall in BP is detected this causes the release of adrenaline and noradrenaline that increase heart rate, contractility and vasoconstrict blood vessels. • BP may be normal, but heart rate is increased, urine output decreased, patient may be cool to touch and restless

  10. Stage 2 – Decompensated (Progessive) • BP falls, cerebral and myocardial hypoperfusion result in deteriorating mental status, myocardial ischaemia and absent peripheral pulses • Stress response causes vasoconstriction - waxy, pale, cold, clammy skin. Pale mucous membranes and nail beds, low UO

  11. Stage 3 – Irreversible (Refractory) • All major organ systems are affected • Systemic hypoperfusion will ultimately become incompatible with life (Darovic 2002)

  12. “Double Edged Sword” of compensation in shock • Darovic (1995p. 448) • Systemic vasoconstriction maintains blood flow to vital organs • Inflammatory mediator release facilitates phagocytosis and resolution of injury • But: • Less essential circulations sacrifices:massive tissue ischaemia and lactic acidosis • Prolonged or overwhelming mediator release leads to SIRS and multiple organ failure.

  13. What is blood pressure made of? • CO (= HR x SV) • SVR • Contractility

  14. Categories: • Cardiogenic shock • Hypovolaemic shock • Distributive shock : - Septic shock - Neurogenic shock - Anaphylactic shock. More than one type of shock can exist in an individual.

  15. Cardiogenic Shock • The most common cause is MI • What is the spiral of events that follows a drop in blood pressure?

  16. Hypovolaemic shock • This is a reduction in the circulating volume leading to decreased venous return and cardiac output

  17. Sepsis: • Pathophysiology related to mediator and neuro endocrine repsonse: • Maldistribution of circulating blood volume • Imbalance of oxygen supply and demand • Alterations of metabolism

  18. Definitions – Changed in 2016 Seymour et al (2016) Singer et al (2016) Sepsis – “life threatening organ dysfunction caused by disregulated host response to infection” (Singer et al 2016) Organ dysfunction = change in SOFA score (Seymour et al 2016) Septic Shock = subset of sepsis in which profound circulatory, cellular and metabolic abnormalities are assoc. with a greater risk of mortality than sepsis alone (Singer et al 2016)

  19. Anaphylactic shock • An exaggerated systemic allergic reaction to an antigen • The antigen-antibody or substances such as contrast media cause release of mediator substances. This causes ‘leaky capillaries’ and generalised swelling and acute pulmonary oedema. • Arteries dilate causing hypotension • Smooth muscle contraction can cause bronchospasm

  20. Neurogenic Shock • May be produced by spinal cord damage or pharmacological blockade at T6 or above • Brain stem messages to the peripheral nerves to maintain vasoconstriction and cardioaccelerator reflexes are interrupted. • This may cause hypotension and bradycardia

  21. ESCIM (2014) • Three ‘windows’ through which to view signs of hypoperfusion: • Peripheral – skin that is cold, clammy and blue ,pale or discoloured • Renal - urine output < 0.5 ml/kg/hour • Neurologic – obtundation, confusion • Low BP may not be present

  22. Patient Assessment • Consciousness level / Mentation reports of pain • Blood pressure • Heart rate / Pulses • Respiratory system • Cutaneous • Urine output • Invasive haemodynamic monitoring – needs to be PAC if severe, need dynamic assessment of fluid status

  23. General Principles of Treatment • Correct the primary cause. • Ensure adequate airway, ventilation, and arterial oxygenation • Fluid resuscitation ? (Probably crystalloids) • Followed by vasoactive drugs • ESCIM (2014) – targets for BP initially Map> 65mmHg……. But alterations if haemorrhage and also for sepsis in known hypertensive patient

  24. ESCIM (2014)

  25. Starling Curve

  26. Most important inotrope? • Fluid! • Fluid challenge should be given over 5-10 mins • Assessment before and after to see where you are on Starling curve • If SV rises 10% or more you are on the up slope and more fluid can be given to good effect • If you give inotropes or vasopressors to an under-filled patient, side effects and mortality worsen

  27. Inotropes and Vasopressors • Correct terminology seldom used • Vasopressor – causing vasoconstriction • Inotrope – increasing contractility • Chronotrope – increasing heart rate • Inodilator – inotrope and vasodilator

  28. Commonly seen in ICU • Noradrenaline – vasopressor • Vasopressin – vasopressor (consultant direction only G ICU) • Dobutamine – inodilator • Milrinone – inodilator • Dopamine – inotrope (& vasopressor) • Dopexamine – mild inotrope and selective (gut & mesentery) dilator • Adrenaline – inotrope, vasopressor and chronotrope

  29. Hypovolaemia - management • Hypovolaemia – aim is to stop fluid loss and restore blood volume - fluid challenges. • Note massive haemorrhage protocol (new Nov 2015) • Ensure adequate ventilation and oxygenation. • N.B care required with opiates (inhibit arteriolar constriction)

  30. Cardiogenic shock • Cardiogenic shock – systolic BP< 90mmHg for at least 30 mins, CI <2.2l/min/m2, PAOP >15mmHg • Investigations – ECG, Bloods (inc. novel trial device) • Interventions include: Thrombolysis, angiography, PCI, CABG may be required for re perfusion • Analgesia – Morphine < sympathetic response and < diaphoresis • Control rhythm disturbances • Pharmocological adjustment to SVR

  31. Neurogenic shock - management • Continuous ECG monitoring • Atropine may be required if Heart rate <50 and systolic BP<80. • This type of shock MUST be distinguished from hypovolaemia • Aggressive fluid therapy may precipitate pulmonary oedema in neurogenic shock. • Vasopressors may also be required. • Careful monitoring is needed – signs of abdominal trauma may be missed due to flaccid abdominal wall in tetraplegic patients. (Adam and Osborne 2005)

  32. Singer et al (2016) 33

  33. Singer et al (2016) 34

  34. Surviving sepsis campaign (2016) www.survivingsepsis.org

  35. ‘Survive Sepsis’ • UK initiative – education programme • The Sepsis Six • High flow oxygen • Take blood cultures • Give IV antibiotics • Start IV fluid resuscitation • Check lactate • Monitor hourly urine output • All to be completed within 1 hour of suspected sepsis diagnosis

  36. What next? • Revision of sepsis bundles 2016 • References: • Adam S & Osborne S (2005) Critical Care Nursing; science and practice (2nd Ed). Oxford: Oxford Medical Publications. • Cecconi et al (2014) Consensus on circulatory shock and haemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Int Care Med. 40 1795-1815 • Darovic G (2002) Haemodynamic Monitoring:invasive and noninvasive clinical application. Saunders. Philadelphia • Dellinger et al (2012) International guidelines • for the management of severe sepsis and septic shock Int Care Med. • www.resus.org.uk anaphylaxis algorithm • Seymour et al (2016)Assessment of clinical criteria for sepsis For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis -3). JAMA 315 (8) p. 762-774 • Singer et al (2016) The third International Consensus Definitions for sepsis and Septic Shock (Sepsis -3) JAMA 315(8) p. 801-810

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