Ch 1 Shock Flashcards
Expected change in SAA with healthy horse undergoing surgery
After minor surgical procedures UGA, without PO infection, SAA concentrations from 100-400 mg/L with a peak at approximately 3d PO can be expected.
Procedures which have been studied include TCJ ASY and OC fragment removal, laryngoplasty and ventriculectomy (peaked 50–150 mg/L at day 2; return to normal concentration by day 7), carotid exteriorisation and flexor tendon division (peaked 100–400 mg/L at day 2; return to normal concentration by 7–14 days) and a variety of elective procedures including minor airway and orthopaedic surgeries (peaked 16.4 mg/L at 24 h)
Definition of shock
Cascade beginning with cell/tissue oxygen deprivation dt inadequate tissue perfusion, rx in failure of energy-dependent functions and build-up of waste products
Enzyme release and accumulation of ROS & Ca rx in cell death
Equation for cardiac output (CO)
CO = HR x SV
3 components of SV
- Preload (ventricular filling) - decr by hypovolaemia, extreme tachycardia
- Myocardial contractility - rate of cross bridge cycling between actin and myosin filaments in cardiomyocytes
- Afterload (systemic vascular resistance SVR) - . Hypertension = ↑SVR = ↑afterload and ∴ decreased CO
Main categories of shock (3 mainly, 4th as addition)
- Hypovolaemic - actual volume defecit (bloodloss, 3rd spacing..)
- Cardiogenic - pump failure (volume resuscitation contraindicated - only type this is the case
- Maldistributive - inappropriate vasodilation/loss of vasomotor tone; eventually preload dramatically reduced
- Obstructive - physical obstruction eg tension pheumothorax, cardiac tamponade, severe abdominal distension etc
Define compensated shock
Early or mild dz; compensatory responses are able to maintain homeostasis. Mediated by baroreceptors in great vessels which ↑sympathetic tone in response to ↓pressure, as well as ↓ ANP release from cardiac myocytes (released in hypervolaemic states)
↑sympathetic tone + ↓ANP = VASOCONSTRICTION, ∴ ↑TPR & ∴↑MAP
MAP equation
MAP = CO x SVR(or TPR)
CSs & consequences of compensated shock
↑HR, ↑SV, ↓CRT = hyperdynamic shock. MAP typically maintained
Briefly describe the RAAS
- Renin release from juxtaglomerular cells dt 3 factors; ↓renal bloodflow, 𝜷1 stimulation & ↓Na delivery to macula densa of DCT
- Renin cleaves angiotensinogen to angiotensin I, converted to angiotensin II by ACE in the lungs
- Angiotensin II rx in ↑ sympathetic tone, vasoconstriction, AVP release from PP, ↑Na+ absorbtion and aldoserone secretion
- Aldosterone release from ZG of adrenal cortex & acts on the principal cells in the collecting ducts to ↑Na absorption and ↑K+ excretion
Define decompensated shock
Ischaemia of vital organs (brain/heart) begins
Tachycardia, thready pulse, cold extremities
Lack of energy/oxygen and accumulation of lactate & toxic metabolites ultimately rx in vascular smooth mm failure, vasodilation & pooling of blood in peripheral tissue beds, additional decreases in BP, venous return, CO, and perfusion, ultimately resulting in organ failure
Describe CSs of shock by class
Class 1 - <15% blood loss. May be little/no △in CE except ↓urine output. MAP/BP maintained
Class 2 - 15-30% loss. CSs apparent at losses >15%. This class is the onset of hyperdynamic shock. See tachycardia/tachypnoea, bounding pulse
Class 3 - hypodydamic/decompensatory. Mechanisms become insufficient to restore circulating volume. See profound tachycardia/tachypnoea, oligo/anuria, prolonged jugular fill and CRT, weak thready pulse, cold extremities. MAP ↓ & lactic acidosis present.
Class 4: severe uncompensated shock - if uncontrolled, progresses to bradycardia, obtundation, anuria, profound hypotension, collapse and death
Distribution of TBW
2/3 Intracellular
1/3 Extracellular - of which 1/4 IV and 3/4 interstitial
Equation for oxygen delivery (DO2)
DO2 = CO x CaO2
CaO2 is oxygen content of arterial blood, dependent on amount of Hb and its saturation (SaO2)
Fluid therapy general recommendations for shock
‘Balanced approach’
Start w BES @ 20ml/kg (10L/500kg) w regular assessment, additional boluses if req and alternate fluid (colloid, plasma etc) if no improvement in 3hr. Avoids -ve effects of aggressive IVFT (eg old ‘shock dose’ of 60-90ml/kg)
Aim of tx should be ‘permissive hypotension’ - MAP ≈65mmHg; idea being that incr too much can exacerbate bleeding/dislodge clot etc
Dose and benefits of hypertonic saline (HSS- 7.2% NaCl)
Approx 8X tonicity of plasma so each 1L expands plasma volume by approx 2L by drawing fluid from intracellular (primarily) space
Short lived effect - 45mins
Dose is 4ml/kg - 2L/500kg
Need to follow with crystalloid for replacement of intracellular losses
Mainly used colloids, dose and duration of effect
- Plasma and hydroxyethyl starch (HES)
- HES - debate in human med - ideally use lower molwt to avoid complications?; 6% HES, 130 kDa/0.4: tetrastarch has replaced the previous higher molecular weight and molar substitution HES (6% HES, 600 kDa/0.75)
- HES @ 10ml/kg, ↑COP for >120hrs
- Plasma calculation:
- Plasma volume (L) = (desired - actual TP) X 0.05BW
- donor TP
Normal volume urine production
Approx 1ml/kg/hr
<0.5ml/kg/hr suggestive of volume depletion
Monitoring of shock/response to tx
- CRT
- CVP - jugular fill is a crude measure; should fill in 5sec of raising in normal horse w head elevation, delayed in hypovolaemia. Normal CVP @ R atrium = 7-12mmHg, higher in jugular measurements. Will incr w resuscitation, fluid overloa, cardiogenic shock
- MAP - doesnt fall until >30% bloodloss. Aim to maintian >65mmHg to maintain brain perfusion. Normal awake indirect MAP is 105-135mmHg
- Lactate - may temporarily incr. post tx as flushed out of tissues and exceeds clearance capacity. Prolonged elevated poor px
- O2ER - usually 20-30%. May get to 50-60% in shock
- CO
- Regional perfusion
What is the oxygen extraction ratio and how is it calculated
Measure of difference between arterial and venous oxygen SATURATION. Normally, DO2 far exceeds consumption and O2ER ranges from 20-30% (1 of the 4 O2 molecules from each Hb is removed).
↓perfusion may rx ↑in O2ER to 50-60% (can’t get higher than this)
O2ER = (SaO2 - SvO2) ÷ SaO2
HIGH O2ER >50% is indication for blood transfusion (see ch4)
