ECP 3 Flashcards

1
Q

Define shock and the steps of shock

A
  • Severe haemodynamic and metabolic derangements that lead to an imbalance of oxygen delivery and oxygen consumption, leading to decreased cellular energy production
    Progressive cellular dysfunction
    -> Progressive organ dysfunction (SIRS and MODS)
    -> Failure of compensatory mechanisms
    -> Irreversible organ damage
    -> Death
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2
Q

What are the 4 types of circulatory shock and the 2 types of non-circulatory shock

A

Circulatory shock
1. Cardiogenic -> heart isn’t working
2. Hypovolaemia -> not enough volume - MOST COMMON
3. Distributive -> vessels are overly constricted or dilated
4. Obstructive -> something preventing movement
Non-circulatory shock
1. Hypoxic - low haematocrit
2. Metabolic - hypoglycaemia etc.

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3
Q

Hypovolaemic shock what is it, 2 main causes and the 4 main areas that the body responds to this shock

A
Decreased circulating blood volume 
Causes 
- Blood and fluid loss 
- Decreased intake 
1) Sympathetic nervous system 
2) renal blood flow 
3) Angiotensin II
4) Pituitary gland
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4
Q

Clinical assessment of shock what are the clinical signs for milk, moderate and severe and which shock doesn’t go through this pathway

A

Mild -> increase pulse and heart rate due to sympathetic drive body responding
Moderate -> heart rate increased, starting to get pale, femoral pulse reduced, metatarsal bearable
Severe -> grey/white, dull, severely decreased pulses
- All go through this pathway except for distributive

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5
Q

Distributive shock what is the definition and list some causes

A
- DEFINTION: maldistribution of blood flow, inappropriate vasomotor tone (altered SVR)
○ Vasodilation - usually 
○ (Vasoconstriction)
Causes
- Septic shock, SIRS** (systemic inflammatory response syndrome)
- Anaphylaxis
- Severe acidosis
- Adverse drug reaction or drug overdose
- Electrolyte derangements
- (Pharmacologic vasoconstriction)
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6
Q

Distributive shock what are the main clinical signs in dogs and cats

A
  • Hyperdynamic (early)
    ○ Hyperaemic mucous membranes
    ○ Fast CRT
    ○ Tachycardia, tachypnea (bounding pulses)
    ○ Normotension or hypertension
    ○ Tall narrow pulses
    Cats are different! - always pale, smaller increases in heart rate
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7
Q

Obstructive shock define and causes

A
- DEFINITION: obstruction to blood flow 
CAUSES
- GDV
- Cardiac tamponade - pericardial effusion 
- Pulmonary thromboembolism
- Aortic thromboembolism
- Pulmonary hypertension
- Pneumothorax
- Neoplasia
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8
Q

Obstructive shock clinical signs

A

depend on underlying cause

  • Distended abdomen (GDV)
  • Muffled heart sounds (pericardial eff)
  • Dull lung sounds (pneumothorax)
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9
Q

Cardiogenic shock define and what can it be associated with, do you use fluids

A
  • DEFINTITION: decreased FORWARD flow (pump failure)
    ○ Decrease contractility - systolic or diastolic failure
    ○ Inappropriate heart rate, arthmia
  • Can be associated with backward failure (congestive heart failure) -> hypoxia
    ○ Mitral valve disease may not have forward failure but can have backward failure -> NO CARDIOGENIC
  • Fluids are generally contraindicated
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10
Q

Cardiogenic shock what are the 3 main causes and causes within

A
- Systolic failure
○ DCM, Myocardial dysfunction in sepsis, Drug overdose
- Diastolic failure
○ Hypertrophic cardiomyopathy
- Arrhythmias
○ Tachy-or bradyarrhythmias
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11
Q

Cardiogenic shock what are the 3 main clinical signs groups and signs within

A
  • Similar to hypovolaemicshock AND…
  • Signs of cardiac disease and R/L forward failure
    ○ Murmur / gallop
    ○ Pulse deficits
    ○ Poor pulses
    ○ Tachy-or bradyarrhythmia
    ○ Distended jugulars
    ○ Ascites
  • +/-Respiratory distress - if backward failure is also present
    ○ Tachypnea
    ○ Dyspnea
    ○ Pulmonary crackles
    ○ Decreased lung sounds
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12
Q

Metabolic shock define and clinical signs

A
  • DEFINITION: deranged cellular metabolic machinery
    CLINICAL SIGNS
  • Dependent upon underlying disease
  • Mental depression universal
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13
Q

Metabolic shock causes

A
- Mitochondrial dysfunction
○ Severe pH derangements
○ Sepsis - in addition to distributive shock and hypovolaemia 
○ Cyanide toxicity
○ Bromethalinpoisoning
- Hypoadrenocorticism
- Hypoglycaemia
- Hyperkalaemia
- Hypocalcaemia
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14
Q

Hypoxic shock define and causes

A
  • DEFINITION: decreased blood oxygen content
  • Mostly related to Haemoglobin levels - haematocrit
    ○ Haemoglobin concentration times 3 = PCV (haematocrit)
    CAUSES
  • Anemia
  • Severe pulmonary parenchymal disease
  • Hypoventilation
  • Dyshaemoglobinaemias
  • Carbon monoxide
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15
Q

Hypoxic shock clinical signs

A
CLINICAL SIGNS
- Dyspnea
- Crackles
- Increased BV sounds
- Mucous membranes
○ Pale, cyanotic, brown
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16
Q

What are the 6 questions in terms of treating shock

A

Approach to treating shock

  1. Is it shock?
  2. If so, what type?
  3. Is it a type that requires fluid therapy?
  4. Is there any reason to be especially cautious?
  5. Is fluid therapy contraindicated?
  6. Either way, what other therapies will you administer?
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17
Q

How to answer the question is it shock?

A
Clinical signs
- “Flat” might mean shock
- Circulatory forms of shock can all look similar
- Distributive (septic) looks different
- Cats look different
- Non-circulatory… depends on underlying cause
Other ‘objective’ information
- Haemodynamic
- Heart rate
- MAP < 80 mmHg
Tissue perfusion parameters
- Lactate > 2.5 mmol/L
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18
Q

How to answer the questions if so what type of shock

A
  1. Hypovolaemic –imaging, history, UOP, CVP
  2. Distributive –CBC, cultures, imaging
  3. Cardiogenic –ECG, echo
  4. Obstructive –AXR, CXR imaging, echo
  5. Metabolic –glucose, calcium, etc
  6. Hypoxic –SpO2, arterial blood gas (ABG), CXR
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19
Q

How to answer the question is it a type that rewquires fluid therapy

A
Circulatory
- Hypovolaemic–yes!
- Distributive –yes!
- Obstructive –yes!
- Cardiogenic –no!
Non-circulatory
- Metabolic (often) -> may need to give to rebalance the electrolytes (sodium derangements) 
- Hypoxic (sometimes)
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20
Q

How to answer the question if shock is there any reason to be cautious

A
  • Heart disease - MAIN - more likely to get fluid overload

Pulmonary disease - MAIN - may make respiratory distress worse

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21
Q

How to answer the questions if shock what other therapies will you administer

A
- Hypovolaemic
○ Special fluids, blood products
- Cardiogenic
○ Inotropes, anti-arrhythmics, diuretics
- Distributive
○ Vasopressors, antibiotics
- Metabolic
○ Glucocorticoids, dextrose, calcium
- Hypoxic
○ Oxygen, ventilation
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22
Q

Acute resuscitative fluid therapy what is important in terms of administration and the types of catheters

A
  • QUICK EXPANSION OF VASCULAR VOLUME
  • No subcutaneous administration - NOT FAST ENOUGH
    1. Peripheral venous catheter
    2. Central venous catheter
    3. Intraosseous catheter
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23
Q

Acute resuscitative fluid therapy peripheral venous catheter characteristics

A
  • Most commonly used
  • Cephalic or lateral saphenous
  • Short and large: less resistance
  • Percutaneous vs cut-down
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24
Q

Acute resuscitative fluid therapy central venous catheter characteristics

A
  • External jugular vein
  • May be more time consuming
  • Long term placement or
  • Severely compromised patients
  • Cardiopulmonary arrest
  • Regular over-the-needle catheter
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25
Q

Acute resuscitative fluid therapy intraoesseous catheter when used

A
  • Routinely in very small patients (kittens and puppies)
  • In adult patients where IV access fails
  • Cardiopulmonary arrest
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26
Q

List the 4 main resuscitation fluids

A
  1. Isotonic crystalloid fluids
  2. Synthetic colloids
  3. Hypertonic saline
  4. Blood products:
    ○ Whole blood
    ○ Packed red blood cells
    ○ Fresh frozen plasma
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27
Q

Hypertonic saline tonicity, 3 indications and what to combine with

A
  • Tonicity&raquo_space; ECF -> fluid from interstitial space to intravascular space
  • Indications:
    ○ Rapid volume expansions
    ○ Large dogs - GDV
    ○ Head trauma (may decrease ICP)
  • Combination with colloids -> water clings to colloid so contain water within vascular - provides prolonged affect
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28
Q

Hypertonic saline what are the effects and contraindications

A
- Other effects:
○ Decrease intracranial pressure 
○ Reduce endothelial swelling 
○ Decrease leucocyte adhesion
○ Increase cardiac contractility 
○ Milkd peripheral vasodilation 
- Contraindications
○ Dehydration
○ Normovolaemia/hypercolaemia
○ Hypernatraemia -> adding to the imbalance of sodium 
○ Inability to handle sodium load (renal disease)
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29
Q

Synthetic colloids what is the maximum can give for cat and dog, what volume want to give and adverse effects

A
  • Dog: Up to 20ml/kg total/day
  • Cat: Up to 10ml/kg total/day
  • Small volume resuscitation -> if give large volumes and increase vascular permeability movement of colloid into interstitium and moves water into interstitium resulting in loss of water instead of gain in intravascular system
  • Adverse effects
    ○ Coagulation impairment -> covers platelets so platelet activation is impaired
    ○ Renal failure in people, in dogs?
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30
Q

Packed red blood cells/whole blood what does it do, when used and how to increase

A
  • Increase PCV and O2 transport capacity
  • For acute haemorrhage
    ○ Replace what is lost (estimate)
    ○ Target PCV > 20%
  • To increase PCV by 1%
    ○ Packed red blood cells: 1ml/kg
    ○ Whole blood: 2ml/kg
  • Cats: always blood type
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31
Q

Rates and volumes of resuscitation fluids what are the 5 things it depends on

A
  1. Species
  2. Severity of hypoperfusion
  3. Presence of risk factors
  4. Type of fluid used
  5. Response of patient
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32
Q

What is the blood volume of dogs and cats

A
  • Dogs: -90ml/kg

- Cats: -50-60ml/kg

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33
Q

Assessment of shock how occurs

A
  • Resuscitation endpoints -> what is your endpoint, what is your heart rate target, mentation etc. (measured)
  • You may also stop if you hit a safety endpoints (measured) -> crackles in lungs etc
    Assessment of sock -> fluid aliquot -> assessment of shock -> fluid aliquot (adjust if needed) -> assessment of shock etc until NO SHOCK
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34
Q

What occurs with body weight and fluid therapy equations

A
  • Higher body weight more variance in fluid therapy totals depending on formula -> need to be careful with horses
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35
Q

How is Poiseuilles law important with needles and flow

A
  • According to Poiseuille’s law an increase in the radius by 2times will increase the flow rate by 16 times
    ○ In larger animals need to use a larger radius for more flow
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36
Q

What is a balacned fluid therapy, what are the 2 main types of fluids and are they balanced

A
  • Balanced fluid therapy: isotonic to plasma and electrolytes similar
    ○ Lactated ringers solution - balanced
    ○ Normal saline - not-balanced
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37
Q

What is the maximum osmolality of fluids safety administered into peripheral vessels and why

A

600mOsm/L
○ Due to damage to vessels leading to phlebitis
○ If need to give more administer via central veins

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38
Q

What is the difference between PCV and Haematocrit

A

PCV = manual measurement

Haematocrit HCT = RBC count x RBC volume

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39
Q

RBC indices define MCV, MCH, MCHC, RDW and NRBC

A

MCV - mean corpuscular volume = average size
MCH - mean corpuscular haemoglobin = total Hb per cell
- less accurate
MCHC - mean corpuscular haemoglobin concentration = concentration of Hb in each cell
- more accurate
RDW - red cell distribution width (measure of anisocytosis/size variation)
- If large size variation and low MCV generally due to lower average size RBCs etc.
○ Best way to check is via the smear
NRBC - nucleated red blood cells

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40
Q

What are the 3 main questions in assessing anaemia and differentiation

A
  1. Regenerative or non-regenerative anaemia
    ○ Loss (haemorrhage, haemolysis) - regenerative -> reticulocytes or polychromatophils present
    ○ Decreased production - non-regenerative
  2. Is the protein level low, normal or high
    ○ If haemorrhaging red cells and plasma lost -> losing protein so low protein
    ○ Haemolysis -> only destroying RBCS -> normal protein
    ○ Internal haemorrhage -> protein level can be close to normal as reabsorbed
  3. Are there clues on the blood film
    ○ Oxidative damage, sheer injury -> haemolysis
    ○ Haemangiosarcoma
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41
Q

What are the 3 types of anaemia

A
  1. Regenerative = elevated reticulocyte count
    ○ Increased RBC loss - haemorrhage or haemolysis
  2. Non-regenerative = normal or low reticulocyte count
    ○ Reduced rbc production - chronic disease/inflammation, marrow disease, iron deficiency
  3. Pre-regenerative = too soon since RBC loss for an apparent marrow response to be evident in the blood
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42
Q

leukogram what are the 3 main types and characteristics

A
  1. Is there evidence of an inflammatory response?
    ○ Neutrophilia and/or monocytosis
    ○ Left shift (bands) or toxic change -> ALWAYS INFLAMMATORY
  2. Is there evidence of stress response?
    ○ Lymphopenia (most consistent finding)
    ○ +/- mature neutrophilia
    ○ +/- monocytosis (dogs)
  3. Is there a physiologic leucocytosis?
    ○ Mature neutrophilia and lymphocytosis in young animal
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43
Q

What are the 4 ways to loss chemical levels and 3 ways to increase

A
Loss via
1. Consumption
2. Destruction
3. Sequestration
4. Haemo-dilution
Increase via
1. Production 
2. Absorption
3. Haemo-concentrations
44
Q

What makes an azotaemia

A
  • Increase in either or both = azotaemia -> pre-renal, renal, post-renal
45
Q

pre-renal azotaemia what does it lead to, 2 main causes and what increases

A

○ Decrease renal blood flow -> Decrease Glomerular filtration rate
○ Causes
§ Dehydration -> concentrated urine
□ Greater increase in urea than creatinine
□ Clinical evidence -> skin tenting, capillary refill time
§ GIT protein absorption or bleeding
Increased urea only unless co-current dehydration

46
Q

Renal azotaemia what does it lead to, main cinical presentation and 2 main causes with clinical signs

A

○ Decrease functional nephrons -> Decrease glomerular filtration rate
○ Poorly concentrated urine despite dehydration (in context of how dehydrated they are)
○ Causes
1) Acute renal insufficiency
□ Acute history
□ Hyperkalaemia
□ Oliguria or anuria (present like post-renal azotaemia)
2) Chronic renal insufficiency
□ Chronic history - weight loss
□ Often anaemic
□ Polyuria -> hypokalaemia as losing potassium and stops eating as much

47
Q

Post-renal azotaemia what does it lead to, main clinical signs and 4 causes

A

○ Decrease in urine output
○ Generally diagnosed based on clinical findings - stranguria, haemuria
○ Causes
§ Urinary obstruction
§ Uroabdomen
§ Hyperkalaemia - good clue
§ Variable USG depending on hydration status

48
Q

What is some conditions that look like kidney disease on biochemistry

A

metabolic disease resulting in decreased kidney response
- Medullary hypotonicity or impaired ADH can mimic renal failure
○ Hypochloridemia
○ Hypoadrenocorticism
○ Hyperadrenocorticisim
○ Diabetes insipidus -> can’t respond to ADH
○ Pyometron - E.coli toxin stops ADH

49
Q

Dehydration clinical signs, CBC or biochem

A
  • Clinical signs - decreased skin turgor, tacky membranes
  • CBC or biochemistry
    ○ Increase Hct/RBC/Hb (masked by blood loss)
    ○ Increase albumin (masked by protein loss)
    ○ Increase Na and Cl (masked by electrolyte loss)
    ○ Urea with normal creatinine
50
Q

What are some functions of the liver

A
  • Urea synthesise
  • Cholesterol synthesise -> cholesterol can go high with cholestasis (so can be normal if liver disease makes decrease and cholestasis makes increase)
  • Albumin synthesise
  • Glucose synthesise
  • Bilirubin conjugation
  • Bile acids uptake and excretion
  • Ammonia uptake and metabolism
51
Q

List some enzymes that reflect liver damage and those that reflect cholestasis

A
Enzymes that reflect liver damage (leakage)
- ALT (muscle)
- GLDH
- AST (muscle, rbc)
- LDH (muscle, rbc)
- SDH
Enzyme that reflects cholestasis or induction 
- ALP
- Corticosteroid ALP in dogs 
- GGT
52
Q

What are the 3 main questions when assessing liver damage

A
  1. Is there evidence of cell damage?
    ○ Increased ALT, AST, GLDH, SDH
  2. Is there evidence of cholestasis?
    ○ Increased bilirubin, ALP, GGT
  3. Is there evidence of hepatic insufficiency?
    ○ Decreased urea, cholesterol, albumin, glucose
    ○ Increased unconjugated bilirubin
53
Q

Pancreatic disease what are the 2 main enzymes involved, how sensitive, and other findings

A

1) Amylase
2) lipase
Not as sensitive
- 70% of dogs with not have an increase in amylase and lipase with pancreatitis
Remember: amylase and lipase undergo renal excretion -> so can be high with renal disease and decreased glomerular filtration rate
Other findings with pancreatitis
- Inflammatory leukogram
- Lipaemia
- Hyperglycaemia

54
Q

Muscle damag what are the 2 main enzymes and how specific, what can detect within urine

A

1) CK
2) AST - also haemolysis and liver damage
Urine -> Myoglobin -> looks like haemoglobinuria on dipstick as cross-react

55
Q

What is total protein made up of and what are 4 main things the levels depend on

A

Total protein = albumin + globulins
Level depends on:
- Colostrum absorption in neonates
- Synthesise (liver function, inflammation, immunocompetence)
- Hydration status
- Loss (renal, GIT, third space, exudation)

56
Q

What are the 6 main aims of premedication

A
  • to calm the patient - removing stress from animal and people -> decrease negative experiences
  • to provide peri-operative analgesia
  • to reduce the total amount of anaesthetic - decrease drug concentrations needed to maintain anaesthesia
  • to reduce nausea and vomiting -> important with opioids
  • to smoothen recovery -> relying on the drugs given during premedication still being in the system
  • To reduce autonomic side-effects
57
Q

What are the 5 main considerations when choosing the right premedication

A
  1. animal temperament
    - alpha2-adrenoceptor agonist + opioid - more aggressive animals
    ○ phenothiazine + opioid - more relaxed
  2. duration of procedure
    ○ antagonism may be desirable -> if short procedure with longer lasting drugs
  3. health status of patient
    ○ cardiovascular disease / hypovolaemia
  4. availability of drugs
  5. personal preference
58
Q

What is the main combination for premedication and why

A

Most commonly - Tranquilizer/sedative agent + opioid
Why
- synergistic effects
- produces reliable “safe” sedation
- reduces dose of induction and maintenance agent -> reduce the side-effects
- pre-emptive analgesia

59
Q

What are the 3 main classes of drugs used for sedative in premedication and examples within

A
What can we use for sedation?
1. Phenothiazine
○ Acepromazine - preferred
2. Alpha2-adrenoceptor agonist
○ Xylazine, (dex)medetomidine, romifidine, detomidine
3. Benzodiazepine
○ Diazepam, midazolam
60
Q

Acepromazine what used for and main effects

A

Sedation in premedication
Main effects:
- Tranquillization -> good for horses!!!!
- anti-arrhythmic -> decrease sensitivity of myocardium to catecholamines
- anti-emetic
- spasmolytic
- Antihistamine -> effect the skin test for allergic reactions - don’t use when doing this
- Alpha1 receptor blockade (antagonist)

61
Q

Acepromazine what used for and 4 main side effects

A

Sedative in premedication

  • hypotension - care with hypovolaemic patients! -> vasodilation - pink mucous membranes, fast capillary refill time (MAIN DIFFERENCE WITH ALPHA-2 AGONISTS)
  • collapse in some families of Boxers -> UK breed for high vagal tone, blood pressure decrease (vasodilation) and heart rate cannot increase
  • decrease seizure threshold - don’t use in patient with history of seizures
  • Hypothermia - due to vasodilation
62
Q

Can you give Acepromazine on its own, why, why not

A

There is probably no good reason for ever giving a patient acepromazine on its own! - not high enough sedation without seeing side effects

63
Q

Alpha2-adrenoceptor agonists what used for where act in the body

A
Sedative during premedication
- Widespread distribution throughout the body
○ sympathetic nervous system - most important 
○ vascular endothelium - most important 
○ CNS (spinal and supra-spinal)
○ platelets
○ uterus
○ Gut
64
Q

What are the 6 main effects of alpha2-agonists

A

1) dose-dependent sedation (way stronger than ACE) / hypnosis
2) Analgesia (very good)
3) Muscle relaxation (very good)
4) respiratory depression (mild)
5) initial period of hypertension, followed by a more prolonged normotensive (?) phase
○ Reflex bradycardia
6) cardiac arrhythmias (where A-V blocks 1 and 2) -> no ventricular complex

65
Q

Alpha2-ahonists how does the bi-phasic blood pressure response work

A

Phase one:
- Initial increase (hypertension) in blood pressure (peripheric origin) with reflex bradycardia
Phase two:
- Decrease in blood pressure (back to normal or below) due to centrally mediated decreased sympathetic tone.
- Bradycardia is maintained (main problem)

66
Q

Should anticholinergics be administered with α2-adrenoceptor agonists to offset the bradycardia, produced by these drugs?

A

NO - leads to severe hypertension

- If worried give an antagonist however generally doesn’t work too well

67
Q

What are 4 other effects of alpha2 agonists

A
  • Hyperglycaemia - very common
  • diuresis (problem in horses?) -> if recovering in the box, increase in urination leads to slipping hazard, make sure pee before the box
  • decreased intestinal motility
  • Vomiting (mainly xylazine in SA)
68
Q

Xylazine what is it, when use and side effects

A

Alpha2-agonist used for premedication
- extreme care when used as premed high side effects
sensitize myocardium to catecholamine
emesis (higher than others)

69
Q

Medetomidine what is it, when use

A

Alpha2-agonist used for premedication
more specific less unwanted side effects
- use higher dose in cats prior to ketamine

70
Q

Levomedetomidine what is it

A
Alpha2-agonist used for premedication 
- Possibly α2 antagonistic properties
- Drug interaction
- High α1 affinity
○ Anti-sedative effect
○ Myometrial activity
○ Arrhythmias
71
Q

What is the example of alpha2-antagonists and what do they reverse

A
  • Only one licensed is atipamezole (“Antisedan”)
  • will reverse xylazine, medetomidine and dexmedetomidine (tho’ only licensed for last 2 and only in dogs for dexmedetomidine)
  • will not fully reverse CV depression but worth a try
72
Q

Benzodiazepines what used for, 2 main examples and 7 main effects

A
Premedication (sedative
Two agents in this class:
1. diazepam (“Valium”; “Diazemul”)
2. midazolam (“Hypnovel”)
NOT LICENSED IN ANIMALS!
Main effects of benzodiazepines
1. muscle relaxation - good 
2. anxiolytic
3. appetite stimulation - used for this 
4. minimal cardiovascular and respiratory effects
5. anti-convulsant
6. potential for complete reversal (flumazenil)
7. anti-arrhythmic
73
Q

What are 5 main clinical uses of benzodiapines

A
  1. to increase muscle relaxation during anaesthesia
  2. to offset muscle hypertonicity caused by ketamine (ketamine creates muscle spasm so decrease this)
  3. to stimulate appetite in anorexic patients
  4. treatment of seizures
  5. to decrease dose of induction agent
74
Q

What patients are benzodiasepines good and bad for and why

A

The benzodiazepines are excellent agents for sedation in the “poor risk” patient, either alone or in combination with opioid drugs.
- Cardiovascular or respiratory compromise -> SICK GOOD DRUG
The benzodiazepines are unreliable agents for sedation in the “healthy adult” patient
- Due to anxiolytic properties -> brain unreliable, may have sedation and may not

75
Q

Diazepam what is it, what are main effects

A

Benzodiazepines - premedication

  • thrombophlebitis may be seen with “Valium” - inflammatory action
  • high oral bioavailability
76
Q

Opioids where do they act

A
  • Act on specific opioid receptors in CNS
    ○ μ (mu) (OP3 - used in some literature)
    ○ κ (kappa) (OP2)
    ○ δ (delta) (OP1)
  • Brain, spine and periphery
77
Q

What are the 3 classifications of opioid efficacy and examples of drugs within

A

1) Full (pure μ) agonists - BEST
○ morphine, methadone, meperidine, hydromorphone, fentanyl, alfentanil, remifentanil
2) Partial μ agonists - UNRELIABLE - need to give 2 doses, one before and one afterwards
○ buprenorphine
3) κ agonist – μ antagonists - excellent for sedation but poor analgesia (EXCEPT IN REPTILES)
○ butorphanol, nalbuphine

78
Q

What are full agonists best for and limitations

A

○ are reliable analgesics, and can be titrated to effect
○ best choice for severe pain
○ can be topped up - but the more you give the more side affects you may see

79
Q

Opiod CNS, CVS, respiratory effects and 6 others

A
  1. CNS - Depression vs excitation (horses, cats? - need to use less)
  2. CVS- Minimal effects
    ○ Possible sinus bradycardia (vagal centre) - usually the blood pressure is maintained
  3. Respiratory system
    ○ Depression
    ○ Drug and dose-dependent
    Others…
  4. Histamine release (pethidine - DON’T GIVE IV, morphine)
  5. GIT depression
  6. Release of ADH (urine retention)
  7. Hypothermia (but sometimes hyperthermia in cats, horses, swine…..CNS excitation? )
  8. Emesis (chemoreceptor trigger zone)
  9. Pupillary diameter (miosis in dog; midriasis in cat) - dog has O - miosis etc. -> if working in eye don’t give - IMPORTANT
80
Q

What are the 4 main full pure opioid agonists, gold standard and how others compare to that

A

1) morphine - gold standard, may cause vomiting, - duration of 4 hrs (dog) & 6-8 hrs (cat)
2) Methadone hydrochloride - like morphine but no vomiting
3) hydromorphone - 8x stronger than morphine, emesis less likely, no histamine release
4) Fentanyl and Alfentanil - 100 (fent) or 50 (alfen) x morphone, short acting, severe pain good but bradycardia and respiratory depression common

81
Q

Give the example of a opioid partial agonist and agonist-antagonist and uses

A
  1. Buprenorphine - partial
    - Duration 4-6 hours in dogs and 6-8 in cats
    - Onset of action 30 to 60 min after IM injection
  2. Butorphanol - agonist-antagonist
    - good sedative but ? analgesic efficacy
    ○ Good anaesthesia for reptiles and birds
    - probably relatively short-duration (1hr)
82
Q

List 3 contraindications for opioids and why

A
  1. Pre-existing respiratory depression
  2. Head trauma - increase CO2 due to respiratory depression which increases intracranial pressure
  3. Pancreatitis - unsure
83
Q

What are the 3 main pathways for induction and maintenance of general anaesthesia

A

Most common - induce with intravenous, maintain with inhalant
Total intravenous anaesthesia - induce with intravenous, maintain with intravenous
Other less common - induce with Inhalant, maintain with inhalant

84
Q

Inhalant induction the 2 types and when used

A
NOT COMMON 
1) Chamber induction 
○ Don't have much control 
○ Box full of gas when remove patient will be exposed to the gas 
2) Mask induction 
Mainly for neonates and puppies
85
Q

Intravenous induction what are the important pharmacokinetic effects

A

the plasma concentration decreases rapidly as a result of both distribution (most important) out of the vascular space and elimination.
- Recovery depends upon distribution and elimination half-lives

86
Q

What are the 7 main factors that determine the rate and speed of onset of intravenous induction

A
  1. Anesthetic used
    ○ Lipid solubility - increase anaesthesia
    ○ Molecular size - decrease increase anaesthesia
    ○ Protein Binding - only unbound into the brain
    ○ Ionization - ionised will not cross BBB
  2. Dose -> higher faster an aesthesia but more side effects - TITRATE TO EFFECT
  3. Rate of administration -> same as above
  4. Route of administration -> IV faster than IM (Propofol IM doesn’t work)
  5. Animals level of consciousness
  6. Acid-base, electrolyte and serum protein status
  7. Animals cardiac output - higher CO quicker induced - OPPOSITE TO INHALANT
87
Q

What are the 5 main intravenous agents for anaesthesia induction

A

Intravenous agents

  1. Barbiturates (thiopental,…)
  2. Dissociative agents (ketamine,…)
  3. Imidazole derivative (etomidate)
  4. Steroids (alfaxolone)
  5. Phenol derivatives (propofol)
88
Q

Barbiturates what are the 3 main examples and onset of GA after injections

A

1) Phenobarital - 12 mins
2) Pentobarbital - 30-60 seconds
3) Thiopental - 15-30 seconds

89
Q

What are the CNS and respiratory effects of barbiturates

A

CNS effects
- Depression
- GABA receptors
- NO analgesia (anti-analgesic at sub-hypnotic doses)
Respiratory effects
- post-induction apnoea common, especially following opioid premedication.
- decreased ventilatory rate and tidal volume, offset to some extent by surgical stimulation

90
Q

What are the main CV effects of barbiturates

A

CV effects
- Usually increase in heart rate
- Decrease in arterial blood pressure
○ more marked in hypovolaemic patients, or following excessive doses
○ decrease peripheral resistance, decrease stroke volume and myocardial contractility
- Increased sensitivity of myocardium to circulating catecholamine (arrhythmias common at induction especially in highly stressed animals)

91
Q

Thiopental what is it, mainly used for, how administer and what does causes elinimation

A

Barbiturate
- Induction agent (after premedication)
0 have to give a bolus cannot titrate -> as moves into stage 2 anaesthesia (excitation)
- Induction and arousal from anesthesia depends largely on redistribution not from metabolism
- Hepatic metabolism 5% total dose is metabolised per hour - recover via redistribution

92
Q

What are the 6 main precautions when using thiopental

A

1) IV only!!!!
○ Skin slough - treatment saline and lidocaine
2) Thin dogs - main way to wake up is redistribution into fat, less fat -> less redistribution -> longer recovery
3) Hypovolaemia
4) Liver dysfunction - due to liver metabolism
5) Age - again metabolism is an issue
6)Obesity - calculate the dose without the fat content as redistribution will occur, overdose is common

93
Q

Dissociative agents what are the main effects and 2 drugs

A
Cataleptic state
• CNS excitation - high brain activity 
• Analgesia
• Immobility
- Dissociation from one’s environment
• Amnesia
Drugs
• Ketamine
Tiletamine (Telazol) - mixed drug
94
Q

Ketamine characteristics what does it produce and which animal popular in

A
  • acidic pH (3.5) -> usually used in combination with other drugs as PAINFUL if give first
  • produces a state of “dissociative anaesthesia”.
  • Popular in horses
95
Q

Ketamine CNS effects

A

CNS stimulation

  • Increase ICP (intracranial pressure) - if use muscle relaxation may decrease
  • Might cause seizure in dogs and cats - history of seizures DON’T USE
  • Analgesia somatic > visceral
  • NMDA antagonist (chronic pain)
  • Hallucinations/delirium in recovery
96
Q

CV effects of ketamine

A

Boost cardiovascular system
- increased sympathetic tone in vivo.
- increased heart rate and contractility.
- increased cardiac output and arterial blood pressure.
- increased myocardial oxygen demands.
Adrenergic system must be intact - if in overdrive then will not lead to boost but depression - NOT USED IN VERY SICK AND DEPRESSED PATIENTS CARDIOVASCULARLY

97
Q

Ketamine respiratory effects

A
  • transient apnoea possible with IV administration.
  • ventilation usually well maintained.
  • laryngeal and pharyngeal reflexes maintained
  • Bronchodilation -> good for asthma patients
  • Apneustic breathing - breathe in, pause, breathe out pause etc. instead of no pause between in and out
98
Q

Pharmacokinetics of ketamine, metabolism, excretion and recovery

A
  • extensive hepatic metabolism in dogs and horses.
  • mainly excreted unchanged via the kidney, in cats - DO NOT GIVE TO A CAT WITH KIDNEY PROBLEMS
  • rapid recovery in most species is due to redistribution from CNS to body tissues.
99
Q

What are the 7 main adverse effects of ketamine

A
  1. CNS stimulation.
  2. pain on injection (not with IV route).
  3. emergence delirium.
  4. hypertension and tachycardia.
  5. prolonged recovery.
  6. salivation.
  7. increased muscle tone
100
Q

What are 7 important summary facts about ketamine

A
  • Not for epileptic patients or brain disorder
  • Increases sympathetic tone
  • Not in cat with kidney dysfunction
  • Provides analgesia
  • Must be used with muscle relaxant
  • Patient will keep oculo-palpebral, laryngeal, swallowing reflexes and the eyes will be in place with slight nystagmus
  • Not in glaucoma or “brain” patient
101
Q

Imidzaole derivative what used for, CVS and respiratory effects

A

etomidate) - EMERGENCY DRUG - not in Aus
- induction agent NOT maintenance
- No CVS effect
- Mild resp depression

102
Q

What is the main steriod used in intravenous induction the main characteristics and side effects

A

Alfaxalone
- lack of cumulation in the body (ideal for CRI (constant rate infusion))
- rapid, complete recovery of consciousness
- lack of irritant effects and activity when given peri-venously (IM/SC routes)
- No preservative (keep in the fridge - no longer than 1 week)
- twitching / paddling in recovery is possible in cats -> noise induced generally
Side effects
- respiratory depression and decrease in arterial BP - same as propofol

103
Q

Phenol derivative what is the main example, what is important about storage and the 3 adverse effects

A
Propofol 
- Emulsion lipid based (the white stuff)
- Support bacterial growth and must be discarded 6 hours after opening (glass ampoules as well as multi-dose bottle)
- Do not keep in the fridge!!!!!!!!!!!!
Adverse effects
- cardiovascular depression.
- respiratory depression.
- pain on injection (colorless > white) - can get burning affect in humans
104
Q

Propofol what is it and the main advantages

A

Intravenous induction agent - phenol derivative
The major benefit of propofol in veterinary anaesthesia is the “to effect” induction and the smooth, rapid recovery
- Lack of excitement at induction
- Lack of hangover at recovery
- Non-cumulative nature - can give as infusion
- Ability to use as CRI (constant rate of infusion)
- Hepatic disease and kidney disease - can give in these patients

105
Q

Recovery of induction with propofol how occurs

A
  • hepatic metabolism and redistribution
  • extra-hepatic metabolism
    ○ lung?
    ○ kidney?
    ○ blood?
  • slower in cats than in dogs - 2 hour infusion for cats okay just not repeated
    ○ Phenol compound!!!
106
Q

Give 3 examples of some induction drugs that are in a combined product

A
  • Propofol/Thiopental 50:50 mixture - NOT USED NOW AS PROPOFOL CHEAP
  • Triple Drip (GGE (Muscle relaxant guaifenesin), alpha2, ketamine or thio)
  • Ketamine/Valium (dizepam - can be used as induction agent) (mixed)