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Large Animal Surgery > Chapter 1: Shock > Flashcards

Chapter 1: Shock Flashcards

1
Q

What is shock?

A

Cascade of events when cells/tissues are oxygen deprived

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2
Q

Cascade that results from cellular oxygen deprivation

A

O2 deprivation- 1 inadequate tissue perfusion- 2 lack of energy supply- 3 build up of waste products- 3b failure of energy dependent functions- release of cellular enzymes- accumulation of Ca+ ROS- cell injury- cell death.

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3
Q

What occurs when shock leads to liver and GI dysfunction?

A

shock cascade + increase absorption of endotoxins and bacteria= SIRS- MODS- Death

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4
Q

Activation of which cascades leads to further cellular injury and microvascular thrombosis?

A

1 inflammatory
2 coagulation
3 complement

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5
Q

What 3 major factors determine systemic blood flow and therefore tissue perfusion?

A

1 circulating volume
2 cardiac pump function
3 vasomotor tone OR peripheral vascular resistance

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6
Q

What does stroke volume regulate?

A

Cardiac output

CO= SV x HR

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7
Q

what 3 factors determine stroke volume?

A

1 ventricular preload = amt of blood returning from body entering heart
2 myocardial contractility = muscle function (systolic cardiac)
3 after load = arterial BP heart must overcome to push through pulmonic and aortic valves into peripheral or pulmonary vasculature

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8
Q

Causes of decreased preload?

A

= affected by circulating volume or amt of blood returning to heart
1 hypovolaemia (Haemorrhage or dehydration)
2 decreased ventricular filling time (tachycardia or impaired ventricular relaxation)
3 decreased vasomotor tone + vasodilation (pooling of blood in capacitance vessels and decreased return to heart- total volume doesn’t change but effective volume decreases)

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9
Q

Myocardial contractility
defintion
techniques to measure
causes of abnormal function

A

1 rate of cross bridge cycling between actin + myosin filaments with cardiomyocytes
2 measurement= echocardiogram - measure global systolic function eg L vent ejection fraction, fractional shortening NB highly influenced by preload and after load
3 shock, sepsis, endotoxins, ischeamic/reperfusion injury

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10
Q

effect of hypertension on ventricular after load?

A

Hypertension increases vascular resist or tone- increase afterload- decrease CO2 + tissue perfusion

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11
Q

Effect of severe fall in vascular resistance

Formula for Cardiac Output?

A

pooling of blood in capacitance vessels- decrease BP- decrease preload- inadequate perfusion - shock

CO= BP/total peripheral vasculare resist

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12
Q

5 causes of shock

A

Hyperdynamic (vol deficit)
cardiogenic (pump failure)
distributive (loss of vascular tone)
hypoxia
obstructive (obstruct ventilation or CO)

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13
Q

3 causes of hypovolaemic shock

A

Profuse haemorrhage
Severe dehydration
3rd space sequestration (eg large colon volvulus)

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14
Q

What can worsen cariogenic shock?

TX for distributive shock

A

IVFT- worsens clinical signs as puts pressure on pump

IVFT- restores perfusion- incr preload- improves Co and perfusion

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15
Q

Causes of relative hypoxia (2)

Cause of obstructive shock and sequelae

A

1 incr metabolic demand- perfusion deficit
2 mitochondrial failure impairs O2 uptake

1 tension pneumothorax: decreased vascular return
2 pericardiac tamponade: inadequate ventricular filling & stroke volume

= decreased aortic BP, decreased coronary artery blood flow- myocardial ischemia- myocardial failure

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16
Q

How does body restore haemostasis in early shock?

A

Vasoconstriction of integument, viscera + kidney
ensures cerebral + cardiac blood flow maintained

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17
Q

Which receptors detect decreased vessel pressure in hyper dynamic stage of shock & where are they found?

What do the receptors do?

A

1 Baroreceptors
2 stretch receptors in :
carotid sinus
right atrium
aortic arch

They incr sympathetic tone inhibit vagal activity, stop cardiac myocytes releasing atrial natricelia peptide

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18
Q

sequelae of incr symp tone, decreased vagal activity and decreased ANP?

which receptors detect local hypoxia- enhance vasoconstriction

A

Incr HR
Incr contractility
Incr SV + CO
vasoconstriction- incr total peripheral resistance
Incr BP

Peripheral chemoreceptors- enhance vasoconstriction

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19
Q

CX signs of hyper dynamic shock

A

incr HR
incr pulse pressure
Short CRT

inc pre capillary sphincter tone- dec capillary hydrostatic pressure- fluid movement from interstitial to cap bed- inc circulating fluid vol

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20
Q

What happens when renal perfusion dec?

A

renin is secreted from juxtaglomerular cells in afferent arteriole- Angiotensin 1- angiotensin 2- inc symp tone peripheral vasc- aldosterone released from adrenal cortex- inc renal Na + H2O absorption - inc circulating vol and inc thirst

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21
Q

What does Vasopressin do?

Where is ACTH produced?

What stimulates its release?

A

Produced in posterior pituitary - vasoconstriction in renal collecting ducts- inc H2O absorption

Hypothalamus

Inc serum osmolality “stress”

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22
Q

Where are ACTH receptors?

Effects when ACTH receptors stimulated (4)

A

Adrenal medulla

1 Aldosterone release- kidneys inc Na + H2O retention
2 cortisol release- kidneys inc Na + H2O retention Liver gluconeogenesis + protein synthesis: inc nutrients in dec blood volume
3 epinephrine release- vessels - inc constrict & after load- heart
4 norepinephrine release- heart inc HR + contractility: inc SV

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23
Q

What happens when dec BP is detected by baroreceptors?

A

1 detected by medulla oblongata
2 inc sympathetic stimulation
3 norepinephrine release
4 heart- inc rate + contractility- inc stroke volume- inc intravascular volume & CO

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24
Q

What % blood loss can compensatory mech’s become overwhelmed- uncompensated shock (ischaemia to brain + myocardium)

What are the clinical signs (10)

A

15%

1 normal BP, may dec
2 Inc HR
3 Inc RR
4 Prolonged CRT
5 cool extremities
6 agitated to lethargic
7 Sweating from inc symp activity
8 dec urine output
9 low CVP
10 inc O2 extraction ratio
11 dec venous pressure O2
12 arterial pH normal to acidotic

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25
Q

what happens when O2 delivery to cells is dec?

Which substrates do damaged cells release?

A

= loss of energy dependent functions
1 enzyme activity
2 membrane pumps
3 mitochondrial activity
- cellular swelling
- intracellular Ca release

1 cytotoxic lipids
2 enzymes
3 ROS

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26
Q

Which cascades are activated by endothelial cell damage?

mechanism?

A
  • coagulation
  • complement
  • via exposure of sub epithelial tissue factor
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27
Q

what is the impact of coagulation cascade?

what leads to vascular smooth muscle failure and what is consequence?

A

lead to micro thrombus formation and coagulopathy - dec blood flow to local tissues

1 lack of energy
2 toxic metabolites
3 micro thrombi formation
4 inflammatory injury

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28
Q

organ level consequences of MODS:
GIT

Renal

cardiac

A

loss of mucosal barrier integrity- endotoxin absorption; bacterial translocation

renal tubular necrosis, inability to absorb solute sand H2O, can’t excrete waste

1 dec BP + venous return- dec coronary blood flow
2 cardiac muscle ischeamia- dec contractility + cardiac output- further dec coronary artery blood flow
3 metabolic acidosis + ischeamia- further dec cardiac muscle function- worsens hypotension & tissue perfusion

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29
Q

what happens when you restore blood flow in hypovolaemic shock?

A

products of cellular cascade go into circulation: ROS; lysosomal enzymes; lactic acid; micro thrombi
= SIRS, MODS, Death

30
Q

Classifications of shock
(American college of surgeons advanced life support guidelines)

A

Class 1: mild compensated <15% blood loss= min CX
Class 2: moderate hypotension, 15-30% blood loss = CX
Class 3-4: severe hypotension, > 30% blood loss, Bradycardia; Obtundation; Anuria; Profound hypertension; Circulatory collapse

31
Q

What is the aim of TX of shock

A

restore and maintain CO via:
Preload
Afterload
Myocardial contractility
HR

32
Q

Equation for delivery of O2

A

delivery of O2 (DO2) = content of O2 in arterial blood CO x amt of blood perfusing the tissue (CaO2)

33
Q

problems using crystalloids to restore circulating volume

A

80% volume diffuse out of vascular space to interstitial and intracellular space
4-5 x vol lost req-asc problems
-excess total body water
extreme excess Na + Cl
if patient has microvasc permeability inc this is worsened
if fluid electrolytes don’t = intracellular space- cellular swelling
abdo compart synd
acute respiratory distress
cong heart failure
GI motility disturbance
dilution coagulopathy

34
Q

Causes of microvasc permeability

A

lost endothelial glycocalyx
impaired endothelial cell function

35
Q

sequelae of cellular swelling

A

affects protein kinase activity
inc intracellular Ca Conc
alter ion pump activity
membrane potential
cytoskeletal structure
activates phospholipase A2

36
Q

Fluid therapy dose 500kg horse

A

crystalloid = 10-20mg/kg= 10L
hypertonic = 2-4 mg/kg = 1-2L
Hetastarch = 5-10mg/kg = 2.5- 5 L

37
Q

In humans what is high volume resuscitation before haemorrhage controlled asc with?

A

more severe blood loss
poorer O2 delivery
Higher mortality

38
Q

what does the electrolyte conc of lactated ringers sol’n mimic?

A

extracellular fluid TF is a replacement fluid not a maintenance fluid

39
Q

Effects of large vol’s of crystalloids alone in mod to sev blood loss

A

dilution anemia
Hypoproteinaemia
Unchanged or improved O2 carrying capacity

40
Q

Effects of crystalloid only therapy in severe blood loss

A

Dilution coagulopathy via:
-Thrombocytopenia
-Dilution of clotting Factors

41
Q

If you give whole blood or plasma - effects:

A
  • improved coagulation
  • oncotic pressure
  • O2 content of blood
42
Q

What is the tonicity of. hypertonic 7.2% saline cf plasma

A

X 8

43
Q

How much do hypertonic crystalloids expand the intra-vascular space?
And how?

A

X 2
Pulls volume from the intravascular space due to Na+ co-effecient

44
Q

Effects of hypertonic on endothelial cells + Neut

A

as fluid pulled from intracellular space- decreased end cell volume- inc Capp diameter- improved perfusion
Hypertonic blunts N activation & may alter balance between inflammatory and anti-inflam cytokine responses to haemorrhage + ischemia
Quickly inc CO + perfusion pre-op. Then further blood vol req after sx

45
Q

What is normal plasma colloid oncotic pressure?

A

20 mmHg

46
Q

What is the COP of hydroxyethyl starch & consequence?

Why are colloids retained in intravascular space?

A

30mmHg
-Draws water into the intravascular space

Size and charge

47
Q

Advantages (4)
Disadvantages (2)
of natural colloids eg plasma whole blood bovine albumin

A

+ves also provide
1 protein eg Albumin
2 antibodies
3 Critical clotting factors
4 Antithrombin 3

-ves
1 must be defrosted
10% have hypersensitivity reaction

48
Q

3 groups colloids recommended for?

A

1 hypo-oncotic patients with capillary leak syndrome
2 cardiac - excess fluid detrimental
3 Oedema- prevent further fluid overload

49
Q

How long will 10L/kg colloid inc Cop for?

At what dose of colloid does spontaneous inc in bleed time occur + why?

A

120 hrs

20-40 ml/kg due to decreased in von Willebrand factor antigen

50
Q

Whole bloods:
+ves
-ves

A

+ves:
Ideal if hypovol due to blood loss
Provides clotting factors
prevents dilutional coagulopathy
prevents dilutional hypoproteinaemia
prevents aenemia
provides O2, COP, platelets, coag factors (Good for severe bleeding)

-ves:
unusual to store TF must collect every time
high viscosity TF cannot give high vol in emergency

51
Q

Formula for shock dose of fluids

A

shock dose fluids= %blood vol (L/kg BWT X 100) X BWT

52
Q

signs that intravasc vol is improving:

recommended MAP if continued bleeding during resuscitation

what is adult horse blood vol?

A

Decr. HR
improved CRT
skin warmer
incr mentation
urine SG- assess perfusion (if high likely still fluid deficit)

> 65mmHG instead of > 90mmHg as incr BP promotes Incr bleeding

8% BWT (40L in 500kg horse)

53
Q

Indications for use of vasopressors?

which horses are vasopressors not normally used in?

which drugs are vasopressors?

A

progression of shock - vasomotor tone + cardiac ischemia = fall in perfusion

standing awake horses

Dobutamine, norepinephrine, vasopressin

54
Q

what is dobutamine

  • action

-dosage

A

strong B1- adrenoreceptor agonist
weaker B2 + adrenoreceptor

positive inotrope- improves O2 delivery to tissues
improves splenic perfusion

dose= 1-5 ug/kg
dose too high = hypertension, tachycardia, arrythmias

55
Q

what is norepinephrine?

Action:

Uses:

A

Strong B1 + alpha - adrenergic affinity
-vasocon incr cardiac contractility

used with dobutamine in hypotensive foals to inc arterial pressure + urine output

adults : counteracts vasodilatory + hypotensive effects of ACP

56
Q

What is vasopressin?

A

released from pituitary gland during hypotension - vasoconstrictor
also acts in renal collecting ducts incr water absorption

57
Q

What does CVP indicate?

Normal?

How do you test?

What does low vs high indicate?

A

CVP indicates:
1 cardiac function
2 blood volume
3 vascular resistance or tone (use to prevent fluid overload esp in patients at risk of deem)
Test:
1 hold jugular vein for 5 s- should visibly fill. Delay = decreased CVP
2LArge bore jugular catheter and H2o manometer placed at level of heart/point of shoulder - falsely high
3 catheter in cr vena cava/right atrium

CVP < 0 if loose 15-26 % blood vol
loose 4-6 %BWT
low CVP: hypovol decreased circulation volume

high CVP: cardiogenic shock
fluid overload
pericardial effusion- forward failure of pump- backup blood in venous side of system

normal CVP but deteriorate clin signs: hypovol alone not cause

58
Q

what is normal urine output

Adults

foals

significant depletion

A

adult: 1ml/kg/h

Neonates: 6ml/kg/h

vol depletion: 0.5mL/kg/h

urine SG not adequate measure of hydration once bolus IVFT starts

59
Q

what does arterial BP reflect?

At what blood loss % does BP decreased?

Target MAP for tx?

A

Cardiac output
total vascular resistance

30%
incr peripheral vascular resist
maints BP
Normal BP doesn’t rule out shock

65 mmHG to ensure adequate perfusion to brain

60
Q

sites for BP measurement

How much ATP is produced from one molecule of glucose?

A

Direct art catheter
trans facial artery adults
mat tarsal
radial
auricular

Indirect
coccygeal art - adults
metatarsal art - foals

aerobic resp= 36 moles
anaerobic resp = 2 moles

61
Q

Types of hyperlactaemia?

How can monitoring lactate indicate response to tx for hypovolaemia?

A

Type a: inadequate O2 delivery to tissues inc blood lactate conc
type b: develops in spite of appropriate tissue O2- hepatic dysfunction pyruvate dehydrogenase inhibition catecholamine surges, sepsis SIRS

decr lactate = improved perfusion
if severe decreased perfusion lactate may incr @ start of therapy as flushed out of tissues before improving. delayed clearance = poor px

62
Q

formula for O2 extraction

normal course of incr O2 extraction

ways of measure

A

oxygen extraction= (O2 sat art blood- O2 sat venous blood)/o2 sat art blood

decr in perfusion or Co2 leads to inc O2 extra ratio

measure central venous saturation & arterial oxygen sat or jugular venous saturation + pulse to measure arterial

63
Q

normal O2 ER

Max o2 ER during decr perfusion

How do you measure mixed venous partial pressure O2?

What is normal jugular venous pressure of O2?

A

20-30%

50-60%

ideal= pulmonary artery; easier = jugular vein or cr venue cava but only assess blood return from head
40-50 mmHg (65-75%)

64
Q

What is DYSOXIA?

A

incr PvO2 in presence of perfusion or supply deficit= impaired O2 consumption by mitochondria or cellular dysfunction. Occurs on septic shock after cardiopulmonary ressuss

65
Q

formula for cardiac output

A

= stroke vol X HR

OR

= blood pressure/ total peripheral vascular resistence

66
Q

how do you measure cardiac output?

A

1 pulmonary thermodilution (gold standard)
2 lithium dilution
3 transcut 2 D echocardiography

67
Q

benefits of controlled fluid resuscitation (MBP 40-60 mmHg)

A

1 decr blood loss
2 better splenic perfusion
3 less acidemia
4 decr haemodilution
5 decr thrombocytopenia
6 decr coagulopathy
7 decr apoptosis of cells + tissue inj
8 incr survival

good for pregnant mares with uterine artery bleed

68
Q

predicting survival after tx

A

non- survivors:
decr CO + PO2 intra-and post op

survivors
lower O2 ER
Higher HT
Higher VO2
Higher blood vol
normal bl gas
rapid haemorrhage control
rapid restoration of perfusion
normalisation of blood gas
prevented dilution coat
faster lactate clearence

69
Q

what may replace blood transfusion in future?

A

liposome encapsulated haemoglobin vesicles

1 ebb phase- 1st few hours
hypovolaemia
low flow to injured site

2 flow phase- starts when perfusion restored, continues easy to weeks

catabolic period= mediators + signs of shock
anabolic period= return to hemostasis

70
Q

How does pain lead to incr cortisol prod in stress response?

What are effects of cortisol secretion?

A

pian- cortex- cortisol via HPA axis- incr sympathetic output

NA+ H2O retention (oedema)
insulin resistance
gluconeogenesis
protein catabolism
- suppressed immune response

71
Q

function of endogenous opiods

A

released from pituitary + adrenal glands
-modulate pain
-catecholamine release
insulin secretion
L + N function
Counter cortisol effects on immune system

Large Animal Surgery (1 decks)

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