Clinical/Surgical Aspects of Shock

Question 1

What is shock and why is it a syndrome?

Answer 1

Different causes and initial circ changes but will lead to a similar pathogenesis and clinical consequences
Its an incongruency btw the circ blood vol and the capacity of bv’s—
Leads to periph circ failure!!!

Question 2

How to classify shock?

Answer 2

Based on main cause:

1. haem.
2. neuro
3. anaphylactic
4. septic

Based on the circ changes:

1. hypovolaemic
2. Cardiogenic
3. Distributive
4. Hypoxic

Question 3

Hypovol shock

Answer 3

Decr Blood volume but normal bv capacity

Decr: CO, BP, CVP

Incr: Arterio-venous O2 diff and PVR (this is comp to conc the blood to the vital organs)

**decr CO will therefore decr SV and preload, afterload and contractility

**decr BP will affect the heart function after a while

Question 4

Causes of hypovol shock

Answer 4

1. HAEM= whole blood loss, ext or int if >40% then can be fatal!!
2. Plasma loss: chem or physical or by contusion- incr permeability of vessels. Or transudation (HF, peritonitis, pleuritis) or exudation
3. Water/electrolyte loss

Question 5

Cardiogenic shock= obstructive

Answer 5

Heart is the main issue!! Blood vol and capacity is ok

1. Decreased pump function
2. Circ obstrucition- usually around the heart (epi)

Decr: arterial BP and arterial O2 tension

Incr: ateriovenous O2 diff and CVP (background failure is venous congestion)

Self damaging because the heart supplies itself!

Question 6

Causes of Cardiogenic Shock

Answer 6

1. Cardiogenic- epi!

• Infarcts (LV)
• DCMP
• HCMP
• Valvular diseases
• Myocarditis
• Cardiac dyssrhytmias

2. Obstructive- pericard or pleura is compressing

• Tamponade- R sided HF
• Restrictive pericarditis (shrinking of the pericard)
• Haemo/pneumo thorax
• Thromboembolism in lungs
• IPPV- intermittent positive P vent- occurs if anaesth incr P and the frequency is too high

Question 7

Distributive shock

Answer 7

Healty heart, ok blood volume but vessel capacity too BIG

Decr: vasc resistance (vasoD), venous return (preload), BP, CVP, PaO2

Incr: venous capacitance, arteriovenous O2 difference

Question 8

Causes of distrib shock

Answer 8

VASC or NEURO

Trauma- severe acute pain

CNS vasomotor paralysis

Anaphylaxis- incr cap permeability- vasoD

Epidural anaesth

Rapid decr in abd P- vessels that were compressed are now able to dilate

Late decomp phase of hypovol shock

Question 9

Causes of distrib shock

Answer 9

SEPTIC/TOXIC

E. coli, klebsiella, pseudomonas, proteus

Gram (-) producing endotoxins!

Can originate from abscessed/tumours

SEPTIC/ENDOTOXIC SHOCK!!

Question 10

What can septic/ endotoxic shock lead to…?

Answer 10

SIRS!!

Can be infectious (sepsis) or non-infectious- pancreatitis, trauma, hypoxia, heatstroke

Question 11

Difference between sepsis and septic shock

Answer 11

Sepsis= infectious SIRS

Septic shock= infectious acute circ failure with arterial HyPOtension and hyPOperfusion

Question 12

Hypoxic shock

Answer 12

Inadequate arterial and cellular O2 utilisation is spite of adequate tissue perfusion–it is a circ phenomenon

Remains the same: venous return, BP, CVP

Decr: PaO2

Incr: arterio-venous O2 difference

Question 13

Causes of hypoxic shock

Answer 13

Anaemia: decr Hgb conc: anaemia hypoxia

Hypoxaemia: decr PaO2 and SaO2= hypoxaemic hypoxia

Toxicosis: Methaemoglobinaemia, CO toxicosis

Question 14

MEtabolic changes in the cell during hypoxia

Answer 14

Systemic Hypoperfusion

Anaerobic glycolysis

Cell destruction

Question 15

Anaerobic glycolysis

Answer 15

Incr lactate even >10mmol/l

Tissue acidosis: pH <6.8

Decr ATP

Question 16

Cell destruction

Answer 16

Catecholamines change membrane potential and perm

Incr IC Na, decr IC K

Incr ATP use therefore E loss

Lysosomal enzymes

Swelling, edema, necrosis

Question 17

What determines shocks impact on organs

Answer 17

Sensitivity to hypoxia

Severity/duration of ischaemia

Treatment

Question 18

Liver

Answer 18

Main shock organ in dogs, v sensitive because of the poorly oxygenated blood coming from the portal vein

MORPH changes can be seen 60-90 mins after onset: centrolobular necrosis and IC edema

Release of anaerobic bact— endotoxins!!

Massive congestion, ascites. icterus

Question 19

GIT

Answer 19

Main shock organ in horses and dogs– because of splanchnic vasoC

If perfusion <30mmHG for 30 mins– mucosal erosion/ulceration– haem enteritis (bloody Dx could be pathognomic)

Loose: water, protein, electrolytes

LSA: gram neggy rods and endotoxins can be abs to circ- sepsis!!

Question 20

Pancreas

Answer 20

Alters the severity of shock- becomes life threat!!

Sensitive to hypoxia and acidosis

Autolysis of serosa by the digestive enzymes

activates MDF– (-) ino, splanchnic vasoC, incr perm of vessels, inhibs phagocytosis!!

Question 21

Heart

Answer 21

Adequate coronary flow:60-70 mmHg

Catechol– tachy– exhaustion

Hypoxaemia, acidosis: arrhythmia, bradycard, asystole

MDF pancreas- neggy ino

Question 22

Lungs

Answer 22

Main shock organ on horses and cats

Failure within 2-6 hrs

Direct trauma: PTX, haemothorax and pulm haem (incr perm of vessels- edema and vasoD)

Microthrombi and endotoxins- edema, cor pulmonale (on R side and caused by congestion in the lungs)

Question 23

Kidney

Answer 23

Autoreulation of shock!

Failure within 12-24 hrs

Ischaemia- acute tubular necrosis- oliguria and glycosuria

**has only 1 vessel system for both nutritional and functional supply

**give diuretics immediately because cannot fix broken kidney

Question 24

CNS

Answer 24

Can adapt to changes in BP up to 40-50mmHg above this: ischaemia and impaired glucose supply!

>1hr- irreversible hypoxic changes

Question 25

Endocrine System

Answer 25

Increased CAAP: * Cortisol * Aldosterone * ACTH * ADH * Prolactin Benefits of these: 1. Incr ATP synth 2. Inhibits EPI glycolysis and lipolysis 3. Stabilzed cap membranes 4. BLocks MDF

Question 26

DIC: 2 main pathomechanisms

Answer 26

Uncontrolled haemostasis followed by increased bleeding tendency Hypercoagulability becomes hypocoag...

Question 27

DIC: uncontrolled haemostasis

Answer 27

1. Hugh tissue destruction: trauma, sepsis, tumour 2. Endothel tissue factor-- triggers haemostasis 3. Sytemic vasoC 4. Incr clotting factors 5. Incr blood viscosity 6. Microthrombi 7. Infarcts 8. Destruction of thrombocytes

Question 28

DIC: Increased bleeding tendency

Answer 28

Depletion of clotting factors Anaemia, hypoglobinaemia Thrombocytopenia (because of the destruction) Decr Fibrinogen Incr: 1. Bleeding time 2. APTT/ PTT 3. Fibrin (the already clotted fibrin is present) 4. FDP/ D-dimer

Question 29

Therapy for DIC

Answer 29

Is v difficult, must determine which stage it is in: eng if hypercoag give heparin (to reduce clotting tendency) but if hypocoag ansolutely no heparin Shcok therapy Restore factors with PRP or blood transfusion Treat the primary cause e.g sepsis, peritonitis etc

Question 30

Compensation of shock: main goal is maintain HOMEOSTASIS: 4 priorities

Answer 30

1.Maintain MAP: symp and adrenal glands, incr HR and contraction, vasoC, no circ in GIT and skin 2 Conserve and expand the plasma vol: Na and water reabs: ADH and aldosterone, vasoC by RAAS 3 activate stress hormones for E: glucogon, GH, ACTH and cortisol 4. autoreg: prioritise renal, coronary and cerebral

Question 31

Diagnosis of shock: clinical signs (5 organ systems)

Answer 31

1. Circ 2. Resp 3 Neuro 4. Uro 5. GIT

Question 32

Circ compensatory stage

Answer 32

15-30% blood loss 1. Pink/red mm 2. Normal or incr CRT 3. Bounding tall and wide pulse 4. Normal/ incr BP, TPP, PCV 5. normal acid base parameters

Question 33

Circ early decomp stage

Answer 33

30-40% blood loss 1. Pale/dark red mm (vessels contracting as not a priority organ) 2. Lower, weak pulse 3. Incr CRT 4. Hypotherm- cold extremities 5. Tachycard/ arrhythmias 6. HypoT 7. Faint heart sounds 8. Incr PCV and TPP 9. Metab acidosis

Question 34

Circ: late decomp stage

Answer 34

\>40% blood loss 1. White mm 2. no palpable pulse 3. Cant detect CRT 4. Severe hypotherm \<34 5. Cold extremities 6. Tachycard turns to bradycard because of exhaustion 7. Severe hypoT 8. Incr PCV, TPP 9. Severe metab acidosis

Question 35

What is essential when there are circ changes

Answer 35

Haemodynamic monitoring of MAP and CVP MAP: Direct (catheter) indirect (doppler or oscillometry) Severe hypoperfusion when MAP\< 60 mmHg CVP: Central venous catheter or electronic tras=nsducer in the cran v. cava or RA, should be 0.5cm of H2O Decr CVP: severe hypoperfusion Incr CVP: cardiogenic shock or acute bleeding

Question 36

Resp

Answer 36

Tachypnoea/ hypervent Supf breathing Abnormal resp murmurs due to pum edema

Question 37

Neuro

Answer 37

Compens may be hyperactive but then becomes depressed/ no reaction to stimuli in the decompens stage

Question 38

Uro

Answer 38

Oliguria/ anuria.... in order to decrease output

Question 39

GIT

Answer 39

Late decomp stage: ulcers, bloody mucous Dx Cholecystitis Cholestasis Icterus

Question 40

Treatment of shock

Answer 40

1. Restore blood vol, treat the cause, reverse the ischaemia, ideally try to get above the threshold values!! 2. Control severe blood loss, catheter, fluid resuscitation 3. Rewarming 4. Diuretics 5. Corticosteroids 6. Cardiac and vasoactive drugs- only in certain cases 7. Alkalising 8. Analgesics and Anaesthetics 9. Antibiotics

Question 41

Fluid Resuscitation: CRYSTALLOIDS

Answer 41

Saline, ringers, Lactated or acetated ringers, dectrose 2.5 or 5% Expands IV volume.. incr bf and incr O2 delivery In 1 hr will fill up the interstitium therefore can dilute the endotoxins in the interstitium Decr blood viscosity- prevents DIC In acute bleeding use hypotensive resusc!! keep MAP at around 60 because you don't want to dislodge the thrombus and cause bleeding again Remember there is an incr permeability of the vessels- dont want them to escape to the interstium and cause pulm edema (is this why you use colloids in combo- to keep the crystalloids in the vessels?) 3-12% BW as infusion Dogs: 60-90ml in bolus and the 10-40ml for maint Cats: 40-60ml in bolus

Question 42

Colloids

Answer 42

to expand the PLASMA vol and prevent fluid getting out of the vessels Hetastarch (25)--- HAES (15)-- dextran 70 (6) 10-20ml bolus Danger: vW and brain edema

Question 43

Plasma/ whole blood trasnfusion

Answer 43

Indications: PCV decrease: dogs \<0.15 cats \<0.12 When O2 transport of blood decr Use fresh citarted over stored Type and crossmatch prior

Question 44

Diuretic therapy

Answer 44

Is obligatory- to maintain the autoreg of the kidney Qhen MAP \<80mmHg but must be above 60mmHg Combo with fluid therapy Check if working by checking the urine- 0.5-1ml of urine/bwkg/hour Mannitol- increases the osmolarity of glomerular filtrate, removal of toxins via the urine, not if there is pum edema

Question 45

Corticosteroid therapy

Answer 45

Incr ATP synth and glyconeogenesis Decr lactic acidosis Stabilize cap membranes Block MDF \*\*always given too late and can cause septic complication! maybe give if endosteroids are low or for irresponsive hypotension- low dose hydrocortisone

Question 46

Cardiac and vasoactive drugs

Answer 46

adrenergic agonists: dop, dobutamine, Adr Only when severe hypoT VasoC by alpha receptor Incr HR and contractility by beta receptor Adr- resuscitation Anticholinergic: atropine and glycopyrrolate: in the late decomp stage when there is bradyarrhyth to incr HR Antiarrhyth when there is tachyarrhyth or ventricular extrasystoles

Question 47

Alkalising agents

Answer 47

Used for the metab acidosis but may not be needed because the diuretics have buffer capacities Sodium bicarbonate Lactate, acetate and gluconate solutions

Question 48

Antibiotic therapy

Answer 48

Because the immune system is compromised therefore secondary infections are more likely Start with broad spec and then do culture for further treatment Corticosteroid in combo with AB's - decreases risk of AB induced endotoxic shock! \*might contribute to sepsis because they kill the good bact in the GIT