Clinical/Surgical Aspects of Shock Flashcards
What is shock and why is it a syndrome?
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!!!
How to classify shock?
Based on main cause:
- haem.
- neuro
- anaphylactic
- septic
Based on the circ changes:
- hypovolaemic
- Cardiogenic
- Distributive
- Hypoxic
Hypovol shock
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
Causes of hypovol shock
- HAEM= whole blood loss, ext or int if >40% then can be fatal!!
- Plasma loss: chem or physical or by contusion- incr permeability of vessels. Or transudation (HF, peritonitis, pleuritis) or exudation
- Water/electrolyte loss
Cardiogenic shock= obstructive
Heart is the main issue!! Blood vol and capacity is ok
- Decreased pump function
- 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!
Causes of Cardiogenic Shock
- Cardiogenic- epi!
- Infarcts (LV)
- DCMP
- HCMP
- Valvular diseases
- Myocarditis
- Cardiac dyssrhytmias
- 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
Distributive shock
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
Causes of distrib shock
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
Causes of distrib shock
SEPTIC/TOXIC
E. coli, klebsiella, pseudomonas, proteus
Gram (-) producing endotoxins!
Can originate from abscessed/tumours
SEPTIC/ENDOTOXIC SHOCK!!
What can septic/ endotoxic shock lead to…?
SIRS!!
Can be infectious (sepsis) or non-infectious- pancreatitis, trauma, hypoxia, heatstroke
Difference between sepsis and septic shock
Sepsis= infectious SIRS
Septic shock= infectious acute circ failure with arterial HyPOtension and hyPOperfusion
Hypoxic shock
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
Causes of hypoxic shock
Anaemia: decr Hgb conc: anaemia hypoxia
Hypoxaemia: decr PaO2 and SaO2= hypoxaemic hypoxia
Toxicosis: Methaemoglobinaemia, CO toxicosis
MEtabolic changes in the cell during hypoxia
Systemic Hypoperfusion
Anaerobic glycolysis
Cell destruction
Anaerobic glycolysis
Incr lactate even >10mmol/l
Tissue acidosis: pH <6.8
Decr ATP
Cell destruction
Catecholamines change membrane potential and perm
Incr IC Na, decr IC K
Incr ATP use therefore E loss
Lysosomal enzymes
Swelling, edema, necrosis
What determines shocks impact on organs
Sensitivity to hypoxia
Severity/duration of ischaemia
Treatment
Liver
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
GIT
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!!
Pancreas
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!!
Heart
Adequate coronary flow:60-70 mmHg
Catechol– tachy– exhaustion
Hypoxaemia, acidosis: arrhythmia, bradycard, asystole
MDF pancreas- neggy ino
Lungs
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)
Kidney
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
CNS
Can adapt to changes in BP up to 40-50mmHg above this: ischaemia and impaired glucose supply!
>1hr- irreversible hypoxic changes
Endocrine System
Increased CAAP:
- Cortisol
- Aldosterone
- ACTH
- ADH
- Prolactin
Benefits of these:
- Incr ATP synth
- Inhibits EPI glycolysis and lipolysis
- Stabilzed cap membranes
- BLocks MDF
DIC: 2 main pathomechanisms
Uncontrolled haemostasis followed by increased bleeding tendency
Hypercoagulability becomes hypocoag…
DIC: uncontrolled haemostasis
- Hugh tissue destruction: trauma, sepsis, tumour
- Endothel tissue factor– triggers haemostasis
- Sytemic vasoC
- Incr clotting factors
- Incr blood viscosity
- Microthrombi
- Infarcts
- Destruction of thrombocytes
DIC: Increased bleeding tendency
Depletion of clotting factors
Anaemia, hypoglobinaemia
Thrombocytopenia (because of the destruction)
Decr Fibrinogen
Incr:
- Bleeding time
- APTT/ PTT
- Fibrin (the already clotted fibrin is present)
- FDP/ D-dimer
Therapy for DIC
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
Compensation of shock: main goal is maintain HOMEOSTASIS: 4 priorities
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
- autoreg: prioritise renal, coronary and cerebral
Diagnosis of shock: clinical signs (5 organ systems)
- Circ
- Resp
3 Neuro
- Uro
- GIT
Circ compensatory stage
15-30% blood loss
- Pink/red mm
- Normal or incr CRT
- Bounding tall and wide pulse
- Normal/ incr BP, TPP, PCV
- normal acid base parameters
Circ early decomp stage
30-40% blood loss
- Pale/dark red mm (vessels contracting as not a priority organ)
- Lower, weak pulse
- Incr CRT
- Hypotherm- cold extremities
- Tachycard/ arrhythmias
- HypoT
- Faint heart sounds
- Incr PCV and TPP
- Metab acidosis
Circ: late decomp stage
>40% blood loss
- White mm
- no palpable pulse
- Cant detect CRT
- Severe hypotherm <34
- Cold extremities
- Tachycard turns to bradycard because of exhaustion
- Severe hypoT
- Incr PCV, TPP
- Severe metab acidosis
What is essential when there are circ changes
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
Resp
Tachypnoea/ hypervent
Supf breathing
Abnormal resp murmurs due to pum edema
Neuro
Compens may be hyperactive but then becomes depressed/ no reaction to stimuli in the decompens stage
Uro
Oliguria/ anuria…. in order to decrease output
GIT
Late decomp stage: ulcers, bloody mucous Dx
Cholecystitis
Cholestasis
Icterus
Treatment of shock
- Restore blood vol, treat the cause, reverse the ischaemia, ideally try to get above the threshold values!!
- Control severe blood loss, catheter, fluid resuscitation
- Rewarming
- Diuretics
- Corticosteroids
- Cardiac and vasoactive drugs- only in certain cases
- Alkalising
- Analgesics and Anaesthetics
- Antibiotics
Fluid Resuscitation: CRYSTALLOIDS
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
Colloids
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
Plasma/ whole blood trasnfusion
Indications: PCV decrease: dogs <0.15
cats <0.12
When O2 transport of blood decr
Use fresh citarted over stored
Type and crossmatch prior
Diuretic therapy
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
Corticosteroid therapy
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
Cardiac and vasoactive drugs
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
Alkalising agents
Used for the metab acidosis but may not be needed because the diuretics have buffer capacities
Sodium bicarbonate
Lactate, acetate and gluconate solutions
Antibiotic therapy
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
