Chapter 1: Shock Flashcards
What is shock?
Cascade of events when cells/tissues are oxygen deprived
Cascade that results from cellular oxygen deprivation
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.
What occurs when shock leads to liver and GI dysfunction?
shock cascade + increase absorption of endotoxins and bacteria= SIRS- MODS- Death
Activation of which cascades leads to further cellular injury and microvascular thrombosis?
1 inflammatory
2 coagulation
3 complement
What 3 major factors determine systemic blood flow and therefore tissue perfusion?
1 circulating volume
2 cardiac pump function
3 vasomotor tone OR peripheral vascular resistance
What does stroke volume regulate?
Cardiac output
CO= SV x HR
what 3 factors determine stroke volume?
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
Causes of decreased preload?
= 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)
Myocardial contractility
defintion
techniques to measure
causes of abnormal function
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
effect of hypertension on ventricular after load?
Hypertension increases vascular resist or tone- increase afterload- decrease CO2 + tissue perfusion
Effect of severe fall in vascular resistance
Formula for Cardiac Output?
pooling of blood in capacitance vessels- decrease BP- decrease preload- inadequate perfusion - shock
CO= BP/total peripheral vasculare resist
5 causes of shock
Hyperdynamic (vol deficit)
cardiogenic (pump failure)
distributive (loss of vascular tone)
hypoxia
obstructive (obstruct ventilation or CO)
3 causes of hypovolaemic shock
Profuse haemorrhage
Severe dehydration
3rd space sequestration (eg large colon volvulus)
What can worsen cariogenic shock?
TX for distributive shock
IVFT- worsens clinical signs as puts pressure on pump
IVFT- restores perfusion- incr preload- improves Co and perfusion
Causes of relative hypoxia (2)
Cause of obstructive shock and sequelae
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
How does body restore haemostasis in early shock?
Vasoconstriction of integument, viscera + kidney
ensures cerebral + cardiac blood flow maintained
Which receptors detect decreased vessel pressure in hyper dynamic stage of shock & where are they found?
What do the receptors do?
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
sequelae of incr symp tone, decreased vagal activity and decreased ANP?
which receptors detect local hypoxia- enhance vasoconstriction
Incr HR
Incr contractility
Incr SV + CO
vasoconstriction- incr total peripheral resistance
Incr BP
Peripheral chemoreceptors- enhance vasoconstriction
CX signs of hyper dynamic shock
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
What happens when renal perfusion dec?
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
What does Vasopressin do?
Where is ACTH produced?
What stimulates its release?
Produced in posterior pituitary - vasoconstriction in renal collecting ducts- inc H2O absorption
Hypothalamus
Inc serum osmolality “stress”
Where are ACTH receptors?
Effects when ACTH receptors stimulated (4)
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
What happens when dec BP is detected by baroreceptors?
1 detected by medulla oblongata
2 inc sympathetic stimulation
3 norepinephrine release
4 heart- inc rate + contractility- inc stroke volume- inc intravascular volume & CO
What % blood loss can compensatory mech’s become overwhelmed- uncompensated shock (ischaemia to brain + myocardium)
What are the clinical signs (10)
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
what happens when O2 delivery to cells is dec?
Which substrates do damaged cells release?
= 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
Which cascades are activated by endothelial cell damage?
mechanism?
- coagulation
- complement
- via exposure of sub epithelial tissue factor
what is the impact of coagulation cascade?
what leads to vascular smooth muscle failure and what is consequence?
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
organ level consequences of MODS:
GIT
Renal
cardiac
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
what happens when you restore blood flow in hypovolaemic shock?
products of cellular cascade go into circulation: ROS; lysosomal enzymes; lactic acid; micro thrombi
= SIRS, MODS, Death
Classifications of shock
(American college of surgeons advanced life support guidelines)
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
What is the aim of TX of shock
restore and maintain CO via:
Preload
Afterload
Myocardial contractility
HR
Equation for delivery of O2
delivery of O2 (DO2) = content of O2 in arterial blood CO x amt of blood perfusing the tissue (CaO2)
problems using crystalloids to restore circulating volume
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
Causes of microvasc permeability
lost endothelial glycocalyx
impaired endothelial cell function
sequelae of cellular swelling
affects protein kinase activity
inc intracellular Ca Conc
alter ion pump activity
membrane potential
cytoskeletal structure
activates phospholipase A2
Fluid therapy dose 500kg horse
crystalloid = 10-20mg/kg= 10L
hypertonic = 2-4 mg/kg = 1-2L
Hetastarch = 5-10mg/kg = 2.5- 5 L
In humans what is high volume resuscitation before haemorrhage controlled asc with?
more severe blood loss
poorer O2 delivery
Higher mortality
what does the electrolyte conc of lactated ringers sol’n mimic?
extracellular fluid TF is a replacement fluid not a maintenance fluid
Effects of large vol’s of crystalloids alone in mod to sev blood loss
dilution anemia
Hypoproteinaemia
Unchanged or improved O2 carrying capacity
Effects of crystalloid only therapy in severe blood loss
Dilution coagulopathy via:
-Thrombocytopenia
-Dilution of clotting Factors
If you give whole blood or plasma - effects:
- improved coagulation
- oncotic pressure
- O2 content of blood
What is the tonicity of. hypertonic 7.2% saline cf plasma
X 8
How much do hypertonic crystalloids expand the intra-vascular space?
And how?
X 2
Pulls volume from the intravascular space due to Na+ co-effecient
Effects of hypertonic on endothelial cells + Neut
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
What is normal plasma colloid oncotic pressure?
20 mmHg
What is the COP of hydroxyethyl starch & consequence?
Why are colloids retained in intravascular space?
30mmHg
-Draws water into the intravascular space
Size and charge
Advantages (4)
Disadvantages (2)
of natural colloids eg plasma whole blood bovine albumin
+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
3 groups colloids recommended for?
1 hypo-oncotic patients with capillary leak syndrome
2 cardiac - excess fluid detrimental
3 Oedema- prevent further fluid overload
How long will 10L/kg colloid inc Cop for?
At what dose of colloid does spontaneous inc in bleed time occur + why?
120 hrs
20-40 ml/kg due to decreased in von Willebrand factor antigen
Whole bloods:
+ves
-ves
+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
Formula for shock dose of fluids
shock dose fluids= %blood vol (L/kg BWT X 100) X BWT
signs that intravasc vol is improving:
recommended MAP if continued bleeding during resuscitation
what is adult horse blood vol?
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)
Indications for use of vasopressors?
which horses are vasopressors not normally used in?
which drugs are vasopressors?
progression of shock - vasomotor tone + cardiac ischemia = fall in perfusion
standing awake horses
Dobutamine, norepinephrine, vasopressin
what is dobutamine
- action
-dosage
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
what is norepinephrine?
Action:
Uses:
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
What is vasopressin?
released from pituitary gland during hypotension - vasoconstrictor
also acts in renal collecting ducts incr water absorption
What does CVP indicate?
Normal?
How do you test?
What does low vs high indicate?
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
what is normal urine output
Adults
foals
significant depletion
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
what does arterial BP reflect?
At what blood loss % does BP decreased?
Target MAP for tx?
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
sites for BP measurement
How much ATP is produced from one molecule of glucose?
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
Types of hyperlactaemia?
How can monitoring lactate indicate response to tx for hypovolaemia?
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
formula for O2 extraction
normal course of incr O2 extraction
ways of measure
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
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?
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%)
What is DYSOXIA?
incr PvO2 in presence of perfusion or supply deficit= impaired O2 consumption by mitochondria or cellular dysfunction. Occurs on septic shock after cardiopulmonary ressuss
formula for cardiac output
= stroke vol X HR
OR
= blood pressure/ total peripheral vascular resistence
how do you measure cardiac output?
1 pulmonary thermodilution (gold standard)
2 lithium dilution
3 transcut 2 D echocardiography
benefits of controlled fluid resuscitation (MBP 40-60 mmHg)
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
predicting survival after tx
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
what may replace blood transfusion in future?
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
How does pain lead to incr cortisol prod in stress response?
What are effects of cortisol secretion?
pian- cortex- cortisol via HPA axis- incr sympathetic output
NA+ H2O retention (oedema)
insulin resistance
gluconeogenesis
protein catabolism
- suppressed immune response
function of endogenous opiods
released from pituitary + adrenal glands
-modulate pain
-catecholamine release
insulin secretion
L + N function
Counter cortisol effects on immune system
