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SAM 2 > Clinical/Surgical Aspects of Shock > Flashcards

Clinical/Surgical Aspects of Shock Flashcards

1
Q

What is shock and why is it a syndrome?

A

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!!!

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2
Q

How to classify shock?

A

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
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3
Q

Hypovol shock

A

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

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4
Q

Causes of hypovol shock

A
  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
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5
Q

Cardiogenic shock= obstructive

A

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!

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6
Q

Causes of Cardiogenic Shock

A
  1. Cardiogenic- epi!
  • Infarcts (LV)
  • DCMP
  • HCMP
  • Valvular diseases
  • Myocarditis
  • Cardiac dyssrhytmias
  1. 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
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7
Q

Distributive shock

A

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

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8
Q

Causes of distrib shock

A

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

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9
Q

Causes of distrib shock

A

SEPTIC/TOXIC

E. coli, klebsiella, pseudomonas, proteus

Gram (-) producing endotoxins!

Can originate from abscessed/tumours

SEPTIC/ENDOTOXIC SHOCK!!

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10
Q

What can septic/ endotoxic shock lead to…?

A

SIRS!!

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

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11
Q

Difference between sepsis and septic shock

A

Sepsis= infectious SIRS

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

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12
Q

Hypoxic shock

A

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

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13
Q

Causes of hypoxic shock

A

Anaemia: decr Hgb conc: anaemia hypoxia

Hypoxaemia: decr PaO2 and SaO2= hypoxaemic hypoxia

Toxicosis: Methaemoglobinaemia, CO toxicosis

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14
Q

MEtabolic changes in the cell during hypoxia

A

Systemic Hypoperfusion

Anaerobic glycolysis

Cell destruction

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15
Q

Anaerobic glycolysis

A

Incr lactate even >10mmol/l

Tissue acidosis: pH <6.8

Decr ATP

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16
Q

Cell destruction

A

Catecholamines change membrane potential and perm

Incr IC Na, decr IC K

Incr ATP use therefore E loss

Lysosomal enzymes

Swelling, edema, necrosis

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17
Q

What determines shocks impact on organs

A

Sensitivity to hypoxia

Severity/duration of ischaemia

Treatment

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18
Q

Liver

A

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

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19
Q

GIT

A

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!!

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20
Q

Pancreas

A

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!!

21
Q

Heart

A

Adequate coronary flow:60-70 mmHg

Catechol– tachy– exhaustion

Hypoxaemia, acidosis: arrhythmia, bradycard, asystole

MDF pancreas- neggy ino

22
Q

Lungs

A

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)

23
Q

Kidney

A

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

24
Q

CNS

A

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

>1hr- irreversible hypoxic changes

25
Q

Endocrine System

A

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
26
Q

DIC: 2 main pathomechanisms

A

Uncontrolled haemostasis followed by increased bleeding tendency

Hypercoagulability becomes hypocoag…

27
Q

DIC: uncontrolled haemostasis

A
  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
28
Q

DIC: Increased bleeding tendency

A

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
29
Q

Therapy for DIC

A

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

30
Q

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

A

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

  1. autoreg: prioritise renal, coronary and cerebral
31
Q

Diagnosis of shock: clinical signs (5 organ systems)

A
  1. Circ
  2. Resp

3 Neuro

  1. Uro
  2. GIT
32
Q

Circ compensatory stage

A

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
33
Q

Circ early decomp stage

A

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
34
Q

Circ: late decomp stage

A

>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
35
Q

What is essential when there are circ changes

A

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

36
Q

Resp

A

Tachypnoea/ hypervent

Supf breathing

Abnormal resp murmurs due to pum edema

37
Q

Neuro

A

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

38
Q

Uro

A

Oliguria/ anuria…. in order to decrease output

39
Q

GIT

A

Late decomp stage: ulcers, bloody mucous Dx

Cholecystitis

Cholestasis

Icterus

40
Q

Treatment of shock

A
  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
41
Q

Fluid Resuscitation: CRYSTALLOIDS

A

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

42
Q

Colloids

A

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

43
Q

Plasma/ whole blood trasnfusion

A

Indications: PCV decrease: dogs <0.15

cats <0.12

When O2 transport of blood decr

Use fresh citarted over stored

Type and crossmatch prior

44
Q

Diuretic therapy

A

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

45
Q

Corticosteroid therapy

A

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

46
Q

Cardiac and vasoactive drugs

A

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

47
Q

Alkalising agents

A

Used for the metab acidosis but may not be needed because the diuretics have buffer capacities

Sodium bicarbonate

Lactate, acetate and gluconate solutions

48
Q

Antibiotic therapy

A

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

49
Q
A

SAM 2 (12 decks)

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