Term
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Definition
the state in which profound and widespread reduction of effective tissue perfusion leads to first *reversible and then *irreversible cellular injury.
Also: systemic derangement of perfusion (reduced cardiac output or effective circulating volume) leading to widespread organ dysfunction and cellular hypoxia |
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Term
| Normal circulation requires what...(4things) |
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Definition
- blood maintained in the fluid state
- apporpriate regulation of fluid balance and oncotic pressure
-normal patient blood vessels and appropriate vascular tone, which can be regulated at the tissue level
- a functional pump |
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Term
| What are the end results of shock (w/out treatment/intervention) |
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Definition
| hypotension, pooling of blood, impaired tissue perfusion, cellular hypoxia |
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Term
| Name & Describe the 4 classifications of shock |
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Definition
Hypovolemic- decreased total circ. vol.
Cardiogenic- pump failure
Obstructive- decreased blood flow
in/out of heart (decreased
preload or increased afterload)
Distributive- loss of peripheral
resistance (leaky vessels) |
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Term
| List some examples of hemorrhagic shock causes in horses |
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Definition
trauma: heel bulb laceration
clotting disorders
guttural pouch mycoses |
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Term
| List some clinical signs of cardiogenic shock |
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Definition
| respiratory distress, collapse, exercise intolerance, pulmonary edema, jugular distension, cyanotic mucous membranes, arrhythmias |
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Term
| List the pathogenesis and some causes of obstructive shock |
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Definition
Path: decreased preload or increased afterload
causes: pericardial effusion + cardiac tamponade, pulmonary thromboembolism (increased afterload), colon torsion, portal hypertension (decreased preload) |
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Term
| Describe the pathogenesis and causes of distributive shock |
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Definition
path: inappropriate vasodilation
causes: inflammatory mediators-> sepsis, *endotoxemia*, anaphylaxis; neurogenic loss of vascular tone and peripheral pooling with anesthesia or spinal cord injury |
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Term
| Describe the Compensatory stage of shock (what happens, clinical signs, prognosis, etc) |
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Definition
baroreceptor mediated release of catecholamines
- systemic vascular resistance
- increase HR and contractility
Renin angiotensin activation-> conserve water
Requires energy
clinical signs: tachypnea, tachycardia, injected mm, hyperemic mm, CRT<1, normal BP/pulses (due to compensation)
Px: good if caught in this stage and treated with fluids |
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Term
| Describe the early decompensatory stage of shock (pathogenesis, clinical signs, treatment,etc) |
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Definition
path: redistribution of blood to vital organs; tissue hypoxia; aerobic resp-> anaerobic glycolysis-> lactic acidosis; arteriolar dilation + pooling of blood-> further decreased CO; DIC; organ failure begins, decreased urine output
clinical signs: tachypnea, tachycardia, pale or toxic mm, prolonged CRT
Trx: aggressive fluid therapy |
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Term
| Describe the Decompensatory/Terminal phase of shock (pathogenesis, clinical signs, prognosis, etc) |
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Definition
Path: "autoregulatory escape" phenomenon; prolonged tissue hypoxia-> vasodilation in all organs; chronotropic and inotropic effects lost, brain non-responsive; circulatory collapse
clinical signs: low HR, low CO, severe hypotension, pale/cyanotic mm, absent CRT, weak/absent pulses, low body temp, no urine production, stupor/coma
Px: cardiopulmonary arrest imminent; unresponsive to trx |
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Term
| What is the most important category of shock in large animals? |
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Definition
Distributive shock
(esp. endotoxemic/septic shock) |
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Term
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Definition
| systemic inflammation triggered by gram-negative bacterial endotoxin |
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Term
| List some diseases often associated with endotoxemia in LA |
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Definition
| neonatal septicemia, colic, colitis, peritonitis, pleuropneumonia, metritis, cellulitis |
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Term
| What 2 species are most sensitive to endotoxin/LPS? |
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Definition
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Term
| List the clinical signs of endotoxemia |
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Definition
| tachycardia, tachypnea, hyperthermia (early) or hypothermia (late), hyperemic mm/"toxic line", depression, edema, prolonged CRT, poor peripheral pulses, hypotension, weak, trembling, cool extremities |
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Term
| List the clinical signs of endotoxemia |
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Definition
| tachycardia, tachypnea, hyperthermia (early) or hypothermia (late), hyperemic mm/"toxic line", depression, edema, prolonged CRT, poor peripheral pulses, hypotension, weak, trembling, cool extremities |
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Term
| What are some typical lab findings assoc. w/ endotoxemia? |
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Definition
CBC: hemoconcentration (high RBC count), systemic inflammation(high FB, high WBC, low mature PMN, high bands, low PLT
Chem: organ dysfunction (high creatinine, high BUN, high GGT, high AST); poor perfusion (low pH, high anion gap, high lactate, low pO2v
UA: high SG, hematuria, proteinuria |
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Term
*Endotoxic shock patients should be treated aggressively!*
How would you treat endotoxemia? |
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Definition
1. stop absorption/ treat source
- hasten GI mucosal healing
- drain abscesses/ treat infxs
- Di-tri-octohedral smectite (Bio
sponge); dietamacaous earth
(directly absorbs endotoxin)
- activated charcoal
2. antagonize LPS
- J5 polyclonal anti-LPS antibody
(J5 hyperimmune plasma)
- polymyxin B
- Banamine, NSAIDs
3. *Increase perfusion*
- increase BP; improve blood
distribution; reduce vascular
leak syndrome; GIVE fluids!
4. control coagulation/platelet activation
5. +/- antibiotics
(if circulating bacteria present;
if seticemia is suspected, if a
source of infxn is found/
documented) |
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Term
| What crystalloids should you give for SHOCK? |
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Definition
*Hypertonic (5%)saline = increases CO, increases perfusion during endotoxic shock
*Pressors- dopamine, dobutamine, norepinephrine
(isotonic fluids -effective if the animal is dehydrated but not effective for trx shock because they redistribute quickly) |
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Term
| How does polmyxin B work to antagonize LPS? |
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Definition
binds LPS with high affinity; blocks LPS binding to LPS binding protein
*Caution: this drug may be nephrotoxic in some species |
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Term
1. List some disadvantages with using NSAIDs to trx endotoxic shock
2. What drugs should you use instead? |
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Definition
1. nephrotoxicity
GI mucosal ulceration
inhibited repair of injured mucosa
2. COX-2 inhibitors
- **Equioxx (Firocoxib)
- Meloxicam |
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Term
Pentoxifylline may also be used in anti-endotoxic therapy.
How does it work? |
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Definition
inhibits neutrophil and macrophage activation by LPS
reduces RBC stiffness |
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Term
| List some goals of fluid therapy |
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Definition
maintain hydration
correct electrolyte abnormalities
correct acid-base abnormalities
correct hypovolemia
diuresis |
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Term
What % of your body weight is blood volume?
How much of this can you lose before it becomes a big problem? |
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Definition
8% BW = blood volume
can lose up to 40% |
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Term
| What is the approximate mainenance fluid dose for adults and neonates? |
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Definition
adults: 50 mL/kg/day
neonates: 75-100 mL/kg/day |
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Term
| What things do you need to consider when choosing a fluid type? |
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Definition
electrolyte abnormalities
acid-base derangements
blood glucose status
plasma oncotic pressure
need for oxygen carrying capacity* |
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Term
List some conditions that would effect Na levels.
What fluids would you give to correct sodium abnormalities. |
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Definition
Hyponatremia:
cerebral edema, cerebral disease
*give LRS or Normosol*
Hypernatremia:
cerebral dehydration (blindness, depression, ataxia, seizures)
*Give NaCl followed by 5% dextrose*
[Note: correct Na slowly!!!] |
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Term
| When would you want to add potassium to the fluids? |
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Definition
[Note: potassium is affected by acid-base status]
Give when:
K+<3.0mEq/L
anorexia for several days
if K+ is low or low normal
correcting acidosis
(Acidosis: H+ into cell, K+ out) |
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Term
What conditions may cause hyperkalemia?
What clinical signs/PE findings might you see due to hyperkalemia? |
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Definition
HYPP
Renal failure, uroperitoneum
severe acidosis
laboratory error
signs: bradycardia, ECG abnormalities, cardiac arrest |
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Term
| How would you trx severe hyperkalemia? |
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Definition
Saline vs LRS
*saline is acidic-> more acidosis
*LRS has potassium-> but has
alkalinizing effects and will
effectively restore fluid volume
IV 5% dextrose
NaCHO3-> alkalinizing
Calcium gluconate
Insulin
carrying glucose into cell will pull
K+ w/ it...so give insulin or 5%
dextrose |
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Term
List some conditions that would effect Cl- levels.
What fluids should you give to correct? |
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Definition
[Cl- usu. proportionally changes w/Na+]
[Cl- varies inversely w/ HCO3-]
Hypochloridemia:
hypochloremic metabolic acidosis, excess reflux (DA in cattle)
*Give LRS or saline*
Hyperchloridemia:
hypernatremia/dehydration, renal tubular acidosis
*correct H2O or HCO3- loss |
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Term
List some conditions in which Calcium is increased or decreased.
How would you correct is decreased? |
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Definition
Hypocalcemia:
hypoalbuminemia, Thumps, Cantharadin, GI disturbance
*Give 23% calcium gluconate 1ml/kg/day*
can give 2-4x maintenance in 24hrs
do NOT give in HCO3- fluids
(makes chalk)
Hypercalcemia:
acidosis, renal failure, neoplasia |
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Term
What are some causes of hypomagnesemia?
clinical signs?
correction? |
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Definition
colic surgery, decreased intake, GI and renal loss, endotoxemia, excess sweating
signs: ventricular arrhythmias, muscle tremors, ataxia, seizures
Trx: magnesium sulfate (16mL of 250mg/mL solution per 5L bag of crystalloids)
also helps in horses with
arrhythmias |
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Term
What are some causes of hypermagnesemia?
clinical signs?
trx? |
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Definition
iatrogenic in colic patients (impacted with epsom salts)
signs: weakness, recumbency
trx: calcium gluconate |
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Term
| contrast metabolic vs resipiratory acid-base problems |
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Definition
Metabolic: kidneys and endogenous buffers
build up H+-> increase CO2
Respiratory: compensation
NEVER over corrects the problem
build up of CO2-> increase H+ |
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Term
How to assess acid base status, ie when do you have:
metabolic acidosis vs. alkalosis
respiratory acidosis vs alkalosis |
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Definition
Normal bicarb ~26
bicarb<26 = metabolic acidosis
bicarb>26 = metabolic alkalosis
Normal PaCO2 ~40
PaCO2>45-50 = respiratory acidosis
PaCO2<35 = respiratory alkalosis |
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Term
| Describe trx for metabolic acidosis |
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Definition
Alkalinizing fluids
LRS
Sodium bicarb (NaHCO3)
if base deficit >10 |
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Term
| Describe trx of metabolic alkalosis |
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Definition
| 0.9%NaCl = acididifying solution |
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Term
When might you see hypoglycemia? How would you correct?
What happens in relation to the kidneys with hyperglycemia? |
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Definition
Hypoglycemia: neonates, hyperlipidemia, severe sepsis
signs: seizures, lethargic
*correct with IV dextrose*
[avoid osmotic diuresis]
Hyperglycemia-> will potentiate diuresis |
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Term
What is an important clinical sign indicating hypoalbuminemia?
How would you correct this? |
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Definition
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Term
List some routes of fluid admin
What factors influence the route you select |
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Definition
IV, Oral, SQ, intraosseous, intraperitoneal
influenced by: volume, type, cost, availability
IV: large volumes, rapid, costly,
IV catheter ideal
Oral: inexpensive, must be able to
tolerate, limited volume in
horses, excellent route in
ruminants, may not be
adequate |
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Term
| Describe how you would give a shock fluid dose (rate, monitoring, etc) |
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Definition
total of 50-100ml/kg/hr
*Give 10mL/kg every 10-20 min
-reevaluate after each dose
(look for improved pulse quality,
warming of extremities, urine
production, return of GI sounds,
improved mental status)
Give balanced crystalloid solution or hypertonic saline (esp if head trauma)
rapid vascular volume expansion,
pulls fluid from interstitial
space
MUST follow w/isotonic fluids |
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