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
