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.

1. SHOCK
ERIN MOONEY, BVSC DACVECC
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 cellular energy production
• oxygen or glucose
• Usually due to inadequate oxygen delivery (DO2)
• cardiovascular dysfunction

4. ENERGY PRODUCTION
glycolysis
tricarboxylic
acid cycle
oxidative
phosphorylation
anaerobic metabolism
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 volume is too low to maintain DO2

9. 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

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
Hypovolaemia Euvolaemia
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
• Maldistribution is 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 = 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

16. • Sepsis
• abdominal sepsis
• 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 of maldistributive 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 related to 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 = 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

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
• Physical obstruction to arterial or venous blood flow
• Examples:
• GDV
• PTE
• heartworm disease
• +/- pericardial effusion

22. METABOLIC SHOCK
• Deranged intracellular 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
• Decrease in 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 of history, 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
Less fancy:
• 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 from pyruvate, 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. CLASSIFYING SHOCK
compensated
shock
early,
decompensated
shock
late,
decompensated
shock

31. COMPENSATED SHOCK
• Catecholamine surge 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. Hypovolaemia
Sepsis

34. EARLY DECOMPENSATED
SHOCK
Compensatory mechanisms become 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
• During this 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 NOT SMALL 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 ¼ shock 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. http://www.impactednurse.com/pics5/notstatH.jpg

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 SHOCK FLUIDS …
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
• volume first
• 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
• hypovolaemia plays 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’t use them
…except in anaphylaxis and addisonian crisis

50. IN SUMMARY…
• Shock is common! Particularly after trauma
• Treating shock is relatively straight-forward
• Treating shock is a life-saving move!