Chapter 1: Shock

Question 1

What is shock?

Answer 1

Cascade of events when cells/tissues are oxygen deprived

Question 2

Cascade that results from cellular oxygen deprivation

Answer 2

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.

Question 3

What occurs when shock leads to liver and GI dysfunction?

Answer 3

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

Question 4

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

Answer 4

1 inflammatory
2 coagulation
3 complement

Question 5

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

Answer 5

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

Question 6

What does stroke volume regulate?

Answer 6

Cardiac output

CO= SV x HR

Question 7

what 3 factors determine stroke volume?

Answer 7

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

Question 8

Causes of decreased preload?

Answer 8

= 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)

Question 9

Myocardial contractility
defintion
techniques to measure
causes of abnormal function

Answer 9

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

Question 10

effect of hypertension on ventricular after load?

Answer 10

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

Question 11

Effect of severe fall in vascular resistance

Formula for Cardiac Output?

Answer 11

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

CO= BP/total peripheral vasculare resist

Question 12

5 causes of shock

Answer 12

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

Question 13

3 causes of hypovolaemic shock

Answer 13

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

Question 14

What can worsen cariogenic shock?

TX for distributive shock

Answer 14

IVFT- worsens clinical signs as puts pressure on pump

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

Question 15

Causes of relative hypoxia (2)

Cause of obstructive shock and sequelae

Answer 15

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

Question 16

How does body restore haemostasis in early shock?

Answer 16

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

Question 17

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

What do the receptors do?

Answer 17

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

Question 18

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

which receptors detect local hypoxia- enhance vasoconstriction

Answer 18

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

Peripheral chemoreceptors- enhance vasoconstriction

Question 19

CX signs of hyper dynamic shock

Answer 19

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

Question 20

What happens when renal perfusion dec?

Answer 20

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

Question 21

What does Vasopressin do?

Where is ACTH produced?

What stimulates its release?

Answer 21

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

Hypothalamus

Inc serum osmolality “stress”

Question 22

Where are ACTH receptors?

Effects when ACTH receptors stimulated (4)

Answer 22

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

Question 23

What happens when dec BP is detected by baroreceptors?

Answer 23

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

Question 24

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

What are the clinical signs (10)

Answer 24

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

Question 25

what happens when O2 delivery to cells is dec? Which substrates do damaged cells release?

Answer 25

= 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

Question 26

Which cascades are activated by endothelial cell damage? mechanism?

Answer 26

- coagulation - complement - via exposure of sub epithelial tissue factor

Question 27

what is the impact of coagulation cascade? what leads to vascular smooth muscle failure and what is consequence?

Answer 27

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

Question 28

organ level consequences of MODS: GIT Renal cardiac

Answer 28

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

Question 29

what happens when you restore blood flow in hypovolaemic shock?

Answer 29

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

Question 30

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

Answer 30

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

Question 31

What is the aim of TX of shock

Answer 31

restore and maintain CO via: Preload Afterload Myocardial contractility HR

Question 32

Equation for delivery of O2

Answer 32

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

Question 33

problems using crystalloids to restore circulating volume

Answer 33

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

Question 34

Causes of microvasc permeability

Answer 34

lost endothelial glycocalyx impaired endothelial cell function

Question 35

sequelae of cellular swelling

Answer 35

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

Question 36

Fluid therapy dose 500kg horse

Answer 36

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

Question 37

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

Answer 37

more severe blood loss poorer O2 delivery Higher mortality

Question 38

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

Answer 38

extracellular fluid TF is a replacement fluid not a maintenance fluid

Question 39

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

Answer 39

dilution anemia Hypoproteinaemia Unchanged or improved O2 carrying capacity

Question 40

Effects of crystalloid only therapy in severe blood loss

Answer 40

Dilution coagulopathy via: -Thrombocytopenia -Dilution of clotting Factors

Question 41

If you give whole blood or plasma - effects:

Answer 41

- improved coagulation - oncotic pressure - O2 content of blood

Question 42

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

Answer 42

X 8

Question 43

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

Answer 43

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

Question 44

Effects of hypertonic on endothelial cells + Neut

Answer 44

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

Question 45

What is normal plasma colloid oncotic pressure?

Answer 45

20 mmHg

Question 46

What is the COP of hydroxyethyl starch & consequence? Why are colloids retained in intravascular space?

Answer 46

30mmHg -Draws water into the intravascular space Size and charge

Question 47

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

Answer 47

+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

Question 48

3 groups colloids recommended for?

Answer 48

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

Question 49

How long will 10L/kg colloid inc Cop for? At what dose of colloid does spontaneous inc in bleed time occur + why?

Answer 49

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

Question 50

Whole bloods: +ves -ves

Answer 50

+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

Question 51

Formula for shock dose of fluids

Answer 51

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

Question 52

signs that intravasc vol is improving: recommended MAP if continued bleeding during resuscitation what is adult horse blood vol?

Answer 52

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)

Question 53

Indications for use of vasopressors? which horses are vasopressors not normally used in? which drugs are vasopressors?

Answer 53

progression of shock - vasomotor tone + cardiac ischemia = fall in perfusion standing awake horses Dobutamine, norepinephrine, vasopressin

Question 54

what is dobutamine - action -dosage

Answer 54

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

Question 55

what is norepinephrine? Action: Uses:

Answer 55

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

Question 56

What is vasopressin?

Answer 56

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

Question 57

What does CVP indicate? Normal? How do you test? What does low vs high indicate?

Answer 57

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

Question 58

what is normal urine output Adults foals significant depletion

Answer 58

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

Question 59

what does arterial BP reflect? At what blood loss % does BP decreased? Target MAP for tx?

Answer 59

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

Question 60

sites for BP measurement How much ATP is produced from one molecule of glucose?

Answer 60

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

Question 61

Types of hyperlactaemia? How can monitoring lactate indicate response to tx for hypovolaemia?

Answer 61

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

Question 62

formula for O2 extraction normal course of incr O2 extraction ways of measure

Answer 62

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

Question 63

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?

Answer 63

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%)

Question 64

What is DYSOXIA?

Answer 64

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

Question 65

formula for cardiac output

Answer 65

= stroke vol X HR OR = blood pressure/ total peripheral vascular resistence

Question 66

how do you measure cardiac output?

Answer 66

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

Question 67

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

Answer 67

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

Question 68

predicting survival after tx

Answer 68

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

Question 69

what may replace blood transfusion in future?

Answer 69

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

Question 70

How does pain lead to incr cortisol prod in stress response? What are effects of cortisol secretion?

Answer 70

pian- cortex- cortisol via HPA axis- incr sympathetic output NA+ H2O retention (oedema) insulin resistance gluconeogenesis protein catabolism - suppressed immune response

Question 71

function of endogenous opiods

Answer 71

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