SHOCK

1. SHOCK CVS Monitoring and Shock

2. Case 1 A 40 year old man comes to the ED having fallen on the path and hurt his left lower ribs. His observations are: pulse 110 bpm blood pressure 140/90 mmHg You notice how clammy he feels to touch. Q 1. Could this man have a life‑threatening haemorrhage? Q 2. Do you think this patient is in some kind of shock?

3. Definitions of shock: “An acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised cellular hypoxia and global hypoperfusion.” “A situation when the intravascular space is larger than the existing intravascular volume – volume deficit ” “A complex clinical syndrome that isthe body’sresponse to cellular metabolic insufficiency”

4. Global hypoperfusion Clinical assessment: Peripheries: • Evaluate skin colour and temperature • Sweating • Pulse volume • Capillary refill • Skin turgor Level of consciousness: • as indicator of the cerebral perfusion

5. Global hypoperfusion Measurement: Vital signs: • Heart rate • Blood pressure* • Respiratory rate • Pulse oximetry • Urine output (a measure of renal perfusion) *NB: some patients will maintain a normal blood pressure, despite hypovolaemia as a result of massive catecholamine release

6. Global hypoperfusion Laboratory: compromised tissue perfusion leads to cellular hypoxia, anaerobic glycolysis and production of lactic acid, resulting in: • Metabolic acidosis (Base deficit) • Low pH • Raised blood lactate level (above 2.0 mmol/l) • Reduced mixed venous oxygen saturation (SvO2 <65%) or central venous oxygen saturation (SCVO2 <70%)

7. Host responses • Microcirculatory changes • Early: • blood / fluid returns to circulation due to increased sympathetic tone and autoregulation (sympatho-adrenalresponse) • mobilization of interstitial fluid • Late: • tissue damage promotes release of inflammatory mediators • complement, cytokines, platelet activating factor, productsof arachidonic acid metabolism, lysosomal enzymes • inappropriate vasodilatation • capillary permeability increases (capillary leak syndrome) causing: • hypotension • Increased viscosity • intravascular coagulation • .

8. Effects of Sympatho-adrenal response • Immediate: • Increased contractility and heart rateto support cardiac output in patient with moderate hypovolaemia • Venoconstriction increases cardiac filling • Arteriolar constriction maintains blood pressure • Blood flow re-distributed (centralisation) to vital organsbrain, heart, kidneys, liver, respiratory muscles

9. Effects of Sympatho-adrenal response Delayed: • Kidney reduced filtration and increased re-absorption restores circulating volume via Renin-Angiotensin-Aldosterone System • Capillary reduced hydrostatic pressure leads to fluid moving from ECF to intravascular space, causing haemodilution and volume expansion

10. Effects of Sympatho-adrenal response

11. Could be irreversible! In the 1940s, Carl Wiggers simulated haemorrhagic shock in dogs and developed an animal model of 'irreversibleshock' in which all animals would die despite aggressive resuscitation. If abnormalities of tissue perfusion are allowed to persist, the function of vital organs will be impaired (from compensated to uncompensated and finally irreversible phases). “Shock is a syndrome resulting from a depression of many functions but in which reduction of effective circulating volume and pressure are of basic importance and in which impairment of the circulation steadily progresses until it eventuates in a state of irreversible circulatory failure.”

12. Types of shock Shock with low CVP: Hypovolaemic shock - lack of circulating blood volume Distributive shock - abnormal peripheral microcirculation Shock with raised CVP: Cardiogenic shock - “pump failure” Obstructive shock - mechanical impediment to forward flow

13. Hypovolaemic Shock • Exogenous losses • haemorrhage • diarrhoea and vomiting • burns • Endogenous losses • into the surrounding tissues or into the body cavities • intestinal obstruction • occult haemorrhage • ascites

14. Hypovolaemic Shock Clinical signs reflecting intravascular volume deficit include: • Capillary refill, pulse volume and heart rate • Jugular (central) venous pressure (JVP/CVP) • Oliguria - urine output less than 0.5ml/kg/hr for 2 consecutive hours / less than 400ml per 24 hours • Urine output should be interpreted in the light of all other clinical signs • Trend in arterial pulse waves (increased Stroke Volume Variability - SVV)

15. Distributive Shock • associated with severely decreased SVR leading to intravascular volume deficit • sepsis • anaphylaxis • spinal cord injury • vasodilatory drugs

16. Cardiogenic Shock • Reduced contractility • acute LVF • myocardial infarction • arrhythmias • cardiomyopathy

17. Obstructive Shock • Impediment to forward flow: • tension pneumothorax • pulmonary embolus • cardiac tamponade

18. Management of shock • A-B-C: • OXYGEN THERAPY • VENTILATORY SUPPORT • HAEMODYNAMIC SUPPORT • MONITOR AND CLOSE OBSERVATION: • - BP, HR, SpO2, resp. rate every ½-1 hr depending on situation, • - Fluid balance - input/output hourly, • - Consider invasive monitoring early in A&E. • - Temperature, • - GCS when indicated • TIME-SENSITIVE CARE: • Correct the underlying cause • e.g. - surgical intervention to stop haemorrhage, treat ileus or diarrhoea, identify fluid losses, treat infection and sepsis

19. Areas of circulatory support Circulatory support involves manipulation of the main determinants of Cardiac Output: • Preloadvia volume replacement • Myocardial contractilityvia inotropicagents • Afterloadvia vasoactive agents

20. 1:Preload and volume replacement

21. General principles • The appropriate rate of fluid administration should be guided by clinical reassessment and sensible limits • Choose the type of fluid which will best treat the deficit or maintain euvolaemia • Where a fluid deficit is identified (e.g. haemorrhage, diarrhoea, vomiting, insensible or renal losses), the nature (content) of this deficit should be identified • “Goal Directed Therapy” - implementation of the proposed clinical endpoints and monitoring of fluid status

22. Initial fluid resuscitation strategy Dehydration vs. Shock • Dehydration does not cause death, but shock does. • Dehydration includes significant depletion of all fluid compartments in the body and may eventually lead to shock • The treatment of dehydration requires gradual replacement of fluids, with electrolyte content similar to the specific losses • The treatment of shock requires rapid restoration of intravascular volume by giving fluid that approximates plasma electrolyte content (bolus 20 ml/kg over 30 min)

23. Fluid requirements in illness Crystalloids: Pro: cheap, convenient to use, free of side effects Con: volume expansion transient (half-life 20-30 min) fluid accumulates in interstitial space pulmonary oedema may result (initial resuscitation: 20 ml/kg bolus over 30 min) Colloids:(starch - Volulyte, gelatin - Isoplex) Pro: greater increase in plasma volume more sustained (half-life 3-6 hrs) Con: cost allergic reactions clotting abnormalities (initial resuscitation: 0.2-0.3g/kg bolus over 30 min)

24. Fluid requirements in illness Blood and blood products: Pro: clearly indicated in haemorrhagic shock maintain Hb concentration at an acceptable level* Con: cost risk (small, but significant consequences) (keep Hb>7g/dl unless patient has ischaemic heart disease, then 10g/dl) Albumin Pro: similar to colloid in terms of long half-life possibly some benefit from transport function of albumin Con: cost (should be used only in special circumstances - for example: burns, cirrhotic liver disease and children with septic shock)

25. Fluid requirements in illness Table: Contents of common crystalloids in mmol/L Na K Ca Cl HCO3 Osmolality pH Plasma 140 4.3 2.3 100 26 285-300 7.4 Na Cl 0.9% 154 0 0 154 0 3085.0 Dextrose 5% 0 0 0 0 0 278 4.0 Dextrose Saline (4%/0.18%) 30 0 0 00 283 4.0 Hartmann’s solution 131 5.0 2.0 111 0 275 6.5 Lactate 29 Lactated Ringer’s sol’n 130 4.0 2.2 109 0 273 6.9 Lactate 28 Na Bicarbonate 1.2% 150 0 0 0 150 300 8.0 Na Bicarbonate 8.4% 1000 0 0 0 1000 2000 8.0

27. Fluid requirements in illness Goals of fluid therapy may be: • Resuscitation restoration of intravascular volume • Replacement of deficit and ongoing losses • Maintenance alone Maintenance- Normal requirements could be estimated from table: WEIGHTRATE For the first 10 kg 100 ml/kg/24hrsor 4 ml/kg/hr For the next 10-20 kg Add 50 ml/kg/24hrsor +2 ml/kg/hr For each kg above 20kg Add 20 ml/kg/24hrsor +1 ml/kg/hr So, the maintenance fluid requirement for a 25kgchild is: 1000 + 500 + 100 = 1600 (ml/24hrs) or 40 + 20 + 5 = 65 (ml/hr)

28. Replacement Overt losses Loss of fluid to the exterior bleeding, vomiting, excessive diuresis or diarrhoea Occult losses Fluid sequestration in body cavities or tissues obstructed bowel,ascites, intramuscular haematoma

29. Replacement Predictable fluid losses Increased insensible losses hyperventilation, fever and sweating (extra 500ml/day is required for every degree Celsius above 37°C) “Capillary leak syndrome” characterized by prolonged and severe increase in capillary permeability as a result of hypoalbuminaemia, septicemia and toxins Evaporative losses due to large wounds or burns; directly proportional to the surface area exposed and/or the duration of the surgical procedure “Third spacing“ internal redistribution of fluids within soft tissues; massive fluid shifts (tissue swelling in peritonitis, pancreatitis, other infection sites)

30. Some examples of predictable losses Redistributive and evaporative perioperative surgical losses Degree of Tissue Trauma Additional Fluid requirement Minimal (eg herniorrhapy) 0-2 ml/kg/hr (25ml/kg/day) Moderate (eg cholecystectomy) 2-4 ml/kg/hr (>50ml/kg/day) Severe (eg bowel resection) 4-8 ml/kg/hr (>100ml/kg/day) PARKLANDS FORMULA for patient with severe burns: 4ml x body weight (kg) x % burns = ml/day Regime: -1st 8 hours: ½ the calculated volume - Next 16 hours: remaining ½ calculated volume Fluid to use: -Use predominantly crystalloid in the first 12-24 hrs -Add colloids after 24 hrs

31. GIFTASUP 2008

32. GIFTASUP recommendations

33. 2:Contractility and Inotropicagents

34. General principles • If signs of shock persist despite volume replacement, inotropic or other vasoactive agents may be given to improve blood pressure and cardiac output. • The effects of a particular drug in an individual patient are unpredictable and the response must be closely monitored. • An invasive monitoring (CVP line, arterial line) is mandatory for most of the cases • All drugs have very short biological half lives (1-2 min). Steady state concentration achieved in 5-10 min from the beginning of IV infusion • Effects are associated with an increased myocardial oxygen consumption and could be damaging to the myocardium.

35. Choice of Drugs Inotropes • Predominant Beta effect (Direct or Indirect) Vasopressors • Predominant Alpha Agonists • Vasopressin Vasodilators • Nitrates • Some Beta-2 Agonists • Phosphodiesterase Inhibitors (Inodilators)

36. 2. Contractility and Inotropic agents Inotropes: Direct predominant action on β receptors: • Adrenaline (via CVP line only) • Dobutamine (might reduce SVR) • Dopamine (cardiac versus renal doses) Pure Beta agonists: • Dopexamine (β1 » β2) • Isoprenaline (β1 > β2) Indirect acting: • Ephedrine

37. 3: Afterload and Vasoactive drugs

38. 3. Afterload:Vasopressors Alpha agonist with some beta effects: • Noradrenalinethe most potent (via CVP line only) Synthetic Alpha agonists: • Metaraminol • Phenylephrinecan all be given peripherally • Methoxamine Others • Ephedrine indirect Alpha and Beta effect • Vasopressin if patient not responding to Noradrenaline

39. 3. Afterload:Vasodilators • Nitrates: GTN (GlycerylTrinitrate) donate nitrosyl group - Sodium nitroprussideaka nitric oxide • Beta Agonists: Dopexamineincreased cardiac output Isoprenalinecauses reflex vasodilation • Phosphodiesterase inhibitors: Milrinonedecrease SVR plus Enoximonepositive inotropic effect

40. Properties of commonly usedinotropic and vasopressoragents

41. Summary of circulatory support • First priority is to secure the Airway and, if necessary, provide mechanical ventilation (B) • Adequate volume replacement is essential in all cases (C) • In patients with continued evidence of impaired tissue oxygenation moderate doses of inotropes may be given to further increase oxygen delivery. • Tissue perfusion must be restored by maintaining an adequate cardiac output and systemic blood pressure with reference to premorbid values

42. Case 1 A 40 year old man comes to the ED having fallen on the path and hurt his left lower ribs. His observations are: pulse 110 bpm blood pressure 140/90 mmHg You notice how clammy he feels to touch. Q 1. Could this man have a life‑threatening haemorrhage? Q 2. Do you think this patient is in some kind of shock?

43. Case 1 Yes. It is highly possible that this man has ruptured his spleen. He could have lost 20‑30% of his circulating blood volume already and needs urgent fluid resuscitation, imaging and surgery. Immediate management: A-B-C. A -Airway is okay. B - Check breathing (for pneumothorax) and insert two large bore cannulae for fluid. C - Circulation is assessed by looking at the vital signs and for signs of hypoperfusion (for example, skin temperature, capillary refill). This patient has cold peripheries and is tachycardic but not hypotensive. A 40‑year‑old man with a severe bleed may compensate by vasoconstriction.

44. Case 1 • Treatment of CVS failure: • IV fluid boluses 1l Hartmann’s over 30 min. • Blood given to maintain Hb above 7.5 • Regular reassessment of all parameters • Repeated fluid boluses including blood products colloids and crystalloids with Cryst:Colloid ratio 3:1 • Definitive treatment – surgical with or without imaging • If becomes hypotensive despite fluid resuscitation consider invasive monitoring and vasopressors or inotropic drugs via central line catheter.

45. Cardiogenic shock

46. Cardiogenic shock Reduced contractility (usually) due to ischaemia and infarction of myocardium • Features of shock: • High LVEDP • Low CO • Pulmonary congestion Shock with high CVP

47. Management Diagnosis • Hx IHD, chest pain, ECG, • troponin, enzymes Treatment • Supportive measures Oxygenation, filling, cardiac support • Thrombolysis • Angiography - PTCA and stenting

48. Case 2 • A 55‑year‑old man is on the coronary care unit when he develops a low urine output (<0.5 ml/kg per hour for the last 2 hours). He has cool hands and feet. His vital signs: • pulse 90bpm, • blood pressure 110/50 mmHg, • respiratory rate 22 per minute, • core temperature 37°C. He had an inferolateral myocardial infarction 24 hours ago. The nurse is concerned about his urine output. How do you assess his volume status?

49. Case 2 Patients admitted to hospital following a myocardial infarction can be dehydrated due to vomiting, sweating, and reduced oral intake. In this case, you would want to know if there are any crackles audible in the lungs. Arterial blood gases may reveal a base deficit. A fluid challenge can be given safely if there are signs of hypovolaemia or if there is any uncertainty about this patient's volume status. The definition of cardiogenic shock includes a low cardiac output state, which is unresponsive to fluid and this implies that fluid is still used in the assessment of this condition.

50. Obstructive shock • Tension pneumothorax • Cardiac tamponade • Pulmonary embolism