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SASH : Shock by Dr Erin Mooney
Shock is a life-threatening condition caused by inadequate tissue perfusion and oxygen delivery. Early recognition and treatment is important to prevent progression. The main goals in treating shock are to restore oxygen delivery through fluid resuscitation and addressing the underlying cause. Fluid therapy aims to optimize cardiac output and tissue perfusion, but treating the cause of shock such as hemorrhage, sepsis, or heart failure is also critical for patient survival.
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SASH : Shock by Dr Erin Mooney
- 1. SHOCK ERIN MOONEY, BVSCDACVECC 7TH MAY, 2014
- 2. shock is common,but under-recognised • early recognition is important to prevent progression of the shock state • dramatic impact on survival
- 3. SHOCK • Inadequate cellularenergy production • oxygen or glucose • Usually due to inadequate oxygen delivery (DO2) • cardiovascular dysfunction
- 4. ENERGY PRODUCTION glycolysis tricarboxylic acid cycle oxidative phosphorylation anaerobicmetabolism yields 2 moles ATP aerobic metabolism yields 36 moles ATP
- 5. WHAT’S BAD ABOUT SHOCK? •Preferential shunting of blood away from splanchnic circulation, skin and muscle • GI translocation sepsis • Sluggish blood flow through capillary beds • renal • cerebral • myocardial • Further anaerobic metabolism • cellular energy deficit MOF
- 6. OXYGEN DELIVERY (DO2) DO2= CO x CaO2 HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2) EDV - ESV venous return and diastolic function systolic function and SVR blood volume and SVR
- 7. TYPES OF SHOCK •Hypovolaemic • Maldistributive • Cardiogenic • Obstructive • Metabolic • Hypoxic
- 8. HYPOVOLAEMIC SHOCK blood volumeis too low to maintain DO2
- 9. DO2 = COx CaO2 HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2) EDV - ESV venous return and diastolic function systolic function and SVR blood volume and SVR
- 10. CAUSES OF HYPOVOLAEMIC SHOCK •Haemorrhage • disruption of vessels • trauma • neoplasia • coagulopathy • Severe dehydration leading to hypovolaemia • prolonged v/d • massive polyuria • burns • third spacing • inadequate access to water
- 11. DEHYDRATION ≠ HYPOVOLAEMIA •Dehydration is a decrease in extracellular fluid volume, i.e- the interstitial and intravascular spaces • Because blood volume is spared at the expense of interstitial volume, “hydration” generally refers the interstitial fluid volume • Dehydrated patients may or may not be hypovolaemic • Hypovolaemic patients may or may not be dehydrated
- 12. HYDRATION • MM moistness •Skin turgor • Globe position VOLUME • Heart rate • MM colour, CRT • Pulse quality • Temperature
- 13. PCV/TS AND HAEMORRHAGE HypovolaemiaEuvolaemia Acute bleeding PCV: 50 TS: 60 PCV: 25 TS: 30 Improving hypovolaemia PCV: 40 TS: 45 Normal patient: PCV/TS 50/60
- 14. MALDISTRIBUTIVE SHOCK • Maldistributionis a loss of vascular tone (SVR) • Leads to sluggish blood flow and DO2, particularly in capillaries, and decreased venous return, with knock-on effects for cardiac output
- 15. DO2 = COx CaO2 HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2) EDV - ESV venous return and diastolic function systolic function and SVR blood volume and SVR
- 16. • Sepsis • abdominalsepsis • urosepsis – pyelonephritis/lower urinary tract infection • pneumonia • pyometra • pyothorax • deep pyoderma • hepatic/pancreatic abscess • SIRS • pancreatitis • polytrauma • burns • major surgery • Anaphylaxis • Addisonian Crisis
- 17. SEPSIS The pathogenesis ofmaldistributive shock in sepsis is multi- factorial: • increased production of nitric oxide • over-activation of K+/ATP channels • deficiency of vasopressin • critical illness-related corticosteroid insufficiency
- 18. CARDIOGENIC SHOCK Shock relatedto failure of the pump mechanism of the heart • failure to fill during diastole • failure to eject adequate stroke volume during systole CHF adds hypoxia to the mix
- 19. DO2 = COx CaO2 HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2) EDV - ESV venous return and diastolic function systolic function and SVR blood volume and SVR
- 20. CAUSES OF CARDIOGENIC SHOCK •Diastolic failure • HCM • severe mitral insufficiency • pericardial effusion • Systolic failure • DCM • sepsis-induced myocardial dysfunction • Tachyarrhythmias • Bradyarrhythmias both
- 21. OBSTRUCTIVE SHOCK • Physicalobstruction to arterial or venous blood flow • Examples: • GDV • PTE • heartworm disease • +/- pericardial effusion
- 22. METABOLIC SHOCK • Derangedintracellular metabolic activity • DO2 is normal • Examples: • hypoglycaemia • toxicities that cause uncoupling of ox phos: • cyanide • arsenic • 1080 • bromethalin • mitochondrial dysfunction in sepsis and SIRS
- 23. HYPOXIC SHOCK • Decreasein arterial blood oxygen content • i.e- not related to blood flow • Examples: • severe anaemia (PCV < 10%) • CO toxicity • methaemoglobinaemia • severe pulmonary disease
- 25. IDENTIFYING SHOCK Mixture ofhistory, physical exam and laboratory evidence Physical exam is your most important tool
- 26. IDENTIFYING SHOCK Perfusion parameters: •MM colour* • CRT • HR • pulse quality • temperature (particularly of extremities) • mentation • urine output • blood pressure * may be injected with maldistribution
- 27. LABORATORY EVIDENCE OF SHOCK Lessfancy: • metabolic acidosis • decreased SBE • decreased HCO3 • +/- acidaemia (depends on compensation) • hyperlactataemia • pre-renal azotaemia • oliguria/anuria • estimate volume status and CO via echocardiography
- 28. LACTATE • Produced frompyruvate, a waste product of glycolysis • During anaerobic metabolism, there is increased production of pyruvate increased lactate production • The most common cause of hyperlactataemia is anaerobic metabolism during shock (“Type A hyperlactataemia”) • Production also increases with SIRS/sepsis, administration of steroids and some types of neoplasia (“Type B hyperlactataemia”)
- 29. LABORATORY EVIDENCE OF SHOCK Fancy: •direct CO monitoring via PAC (gold standard) • mixed venous oxygen via PAC • combined CVP and direct BP • central venous oxygen via CVC
- 30.
- 31. COMPENSATED SHOCK • Catecholaminesurge to maintain perfusion/DO2 causes tachycardia and vasoconstriction • Can be hard to identify; tachycardia in a patient that’s not boisterous or stressed
- 32. • HR 130- 160 • tall, narrow pulses • pink/pale pink MM (+/- “injected” in sepsis/SIRS) • CRT 0.5 – 1.5 sec • normal body temperature (+/- elevated in sepsis/SIRS) • extremities may be cool • quiet mentation • normal BP • normal UOP • normal mild hyperlactataemia
- 33.
- 34. EARLY DECOMPENSATED SHOCK Compensatory mechanismsbecome overwhelmed and DO2 starts to fall
- 35. • HR 160– 200 • reduced femoral pulse quality, absent metatarsal pulses • pale pink MM (+/- injected in SIRS/sepsis) • CRT (1.5 – 2 sec) • mild hypothermia with cool extremities • quiet mentation • mild moderate hypotension • decreased UOP • mild moderate hyperlactataemia
- 36. LATE DECOMPENSATED SHOCK • Duringthis phase, DO2 is inadequate to maintain organ function. • Death is imminent
- 37. • HR >200 •** bradycardia may develop shortly before death. • weak to absent femoral pulses • grey/patchy MM • CRT > 2 sec or undetectable • hypothermia and cold extremities • obtundation • severe hypotension • decreased absent urine output • severe hyperlactataemia
- 38. CATS ARE NOTSMALL DOGS • Cats tend to become bradycardic and hypothermic earlier in shock, particularly in sepsis • A sick bradycardic cat is a very sick cat indeed
- 39. TREATING SHOCK DO2 =CO x CaO2 HR x SV (Hgb x 1.36 x SaO2) + (0.0031 x PaO2) EDV - ESV venous return and diastolic function systolic function and SVR blood volume and SVR
- 40. FLUID THERAPY IN SHOCK •Fluid “resusc” is usually performed with isotonic crystalloids • Shock dose: • 90ml/kg in dogs • 60ml/kg cats • How do we give it? • Fast! respective blood volumes
- 41. • Administer ¼shock dose over 10 – 15 min then re-assess your patient. • If your goals of resusc have not been met, keep going • Goals of resusc: • HR 80 – 120 • pink MM, CRT 1 – 2 s • normal pulse quality • warm extremities, normothermia • normal mentation • SBP 100 – 140 • normal UOP FAST?
- 43.
- 44. OTHER FLUID TYPES •Hypertonic saline (7%) • hypertonic crystalloid • dose: 3 – 5ml/kg once • Artificial colloids • use in shock is controversial • renal failure, coagulopathies • NEVER bolus hypotonic fluids • 0.45% saline • 0.45% saline + 2.5% glucose • 5% glucose in water • plasmalyte-56 • normosol-M
- 45. I’VE GIVEN SHOCKFLUIDS … NOW WHAT? • In cases of uncomplicated hypovolaemia, your work is done • In most cases, shock will continue unless you address the the underlying cause, because only 25% of your crystalloids will still be in IV space 30 min after infusion • Must diagnose and address the underlying cause ASAP
- 46. • Sepsis • volumefirst • vasopressors if needed, once resusc • treat the septic focus • Active haemorrhage • need to stop the haemorrhage • large amounts of fluids can exacerbate bleeding • patients may benefit from a low-volume resusc strategy until haemostasis can be achieved • blood products early
- 47. • GDV • hypovolaemiaplays a role • need to also relieve the obstruction • Concurrent shock and head trauma • treat the CV system first! • essential for adequate cerebral DO2 • once perfusion is restored, administer hyperosmolar agents
- 48. OTHER TYPES OF SHOCK •Cardiogenic shock • NO FLUIDS • pulmonary oedema • oxygen, furosemide • nitroprusside • pleural effusion • thoracocentesis • dobutamine/pimobendan for systolic failure • anti-arrhythmics for tachycardias • pacemaker for bradycardias • pericardial effusion • pericardiocentesis STAT! • Severe anaemia • red cells! • usually pRBC
- 49. STEROIDS IN SHOCK Don’tuse them …except in anaphylaxis and addisonian crisis
- 50. IN SUMMARY… • Shockis common! Particularly after trauma • Treating shock is relatively straight-forward • Treating shock is a life-saving move!