Lecture 12 Intra-operative Fluid therapy & Peri-Anesthetic Complications Part 2 Flashcards

1
Q

What is the 2nd most frequent anesthetic complication?

A

Hypotension

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2
Q
  1. What MAP is hypotension?
  2. SAP?
A
  1. MAP < 60 mmHg
  2. —SAP < 90 mmHg
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3
Q

What is the driving force for blood flow through capillaries?

A

MAP

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4
Q

How do you calculate MAP?

A
  • —MAP = CO x SVR
    • CO = cardiac output
    • SVR = systemic vascular resistance
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5
Q

What are Hypotension Causes because of decreased HR during anesthesia

A
  1. —Drugs:
    • opioids
    • alpha-2 agonists**(not dexmedetomidine)
  2. —Hypothermia
  3. —Physiologic condition
    • —Cardiac/neurologic disease
    • brachycephalic
    • pediatric patients
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6
Q

How do you treat hypotension

A
  • —Anti-cholinergic
    • —Atropine, glycopyrrolate
  • —Underlying cause
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7
Q

What are Hypotension Causes because of decreased Stroke volume (SV) during anesthesia

A
  • —SV depends on preload, contractility, afterload (SVR)
  • —↓preload
    • —↓ blood volume
    • —Vasodilation
    • —IPPV
  • —↓contractility
    • —Anesthetic drugs
    • —Cardiac disease
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8
Q
  1. Decreased preload will do what to blood volume?
  2. How to treat?
A
  1. —↓ blood volume
  2. —Hypovolemia
    • —Goal directed intra-op IV fluid therapy
      • —Crystalloid fluid bolus => 5 – 10ml/kg
      • —Colloid => 2 – 5 ml/kg
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9
Q

Which anesthetic drugs vasodilate leading to decreased preload?

A
  1. —Acepromazine
  2. —Propofol induction
    • —Related to dose & rate of administration
    • —Usually short lived in healthy patients
  3. —Inhalants
    • use ‘inhalant sparing’ techniques
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10
Q

What are 3 ways to do ‘Inhalant sparing’ or ‘Balanced’ anesthesia

A
  1. —Use drugs with mild CV effects
  2. —Nitrous oxide
  3. —Local Anesthesia/Analgesia
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11
Q

What are —drugs with mild CV effects to try and prevent hypotension

A
  • —Mu-agonist Opioids + Benzodiazepines
    • —Hydromorphone, Morphine, Oxymorphone, Methadone, Fentanyl
    • —↓ MAC of inhalant in dose-dependent manner
    • —Minimal CV effects, do not cause vasodilation
      • —May cause bradycardia => treatable
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12
Q

Why use nitrous oxide

A
  • —↓ MAC Sevoflurane by 20-30%
  • —**must scavenge waste gas
  • —50% O2, 50% nitrous
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13
Q

What can —↓contractility

A
  1. —Anesthetic drugs
  2. —Cardiac disease
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14
Q

How do you manage —↓contractility

A
  1. —Drugs with mild CV effects (opioids, benzodiazepines)
  2. —‘Inhalant Sparing’ techniques
  3. —Goal directed IV fluid therapy* Caution with cardiac
  4. —Positive inotropes
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15
Q

What will cause hypotension due to decreased MAP?

A
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16
Q

What can —↓ SVR (vasodilation)

A
  • —↓Vascular tone
    • —Anesthetic drugs
      • —Inhalants, Acepromazin, Propofol
    • —Shock, sepsis
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17
Q

Hypotension Treatment (in order)

A
  1. —Assess/Reduce Anesthetic depth
  2. —Treat bradycardia if associated with hypotension
  3. —IV Fluids
  4. —+inotropes or vasopressors
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18
Q

How do you —Assess/Reduce Anesthetic depth to treat hypotension

A
  • Want to use least amount of inhalent
    • Inhalants cause DOSE DEPENDENT CV depression
      • •↓ contractility, vasodilation
      • •‘Inhalant Sparing’, ‘balanced anesthesia’ techniques
      • •opioids, benzodiazepines, nitrous oxide, local blocks
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19
Q

How do you Treat bradycardia if associated with hypotension

A
  • Anti-cholinergics
    • Make sure to check for underlying cause
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20
Q

Hypotension Treatment with fluids

A
  1. —Crystalloids
  2. —Colliods
    • —Hetastarch
  3. —Hypertonic Saline
  4. —Blood products
    • —Blood loss > 20-30%
    • —Packed RBC
    • —Whole blood
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21
Q

What are the 3 drugs you can use to treat hypotension with positive inotropes and vasopressors

A
  1. Ephedrine
  2. —Dopamine
  3. Dobutamine
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22
Q

How does —Ephedrine work

A
  • —Direct & indirect sympathomimetic
  • —β1>β2 => positive inotropy, ↑contractility
  • —α vasoconstriction
  • —Also causes release of norepinephrine
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23
Q

Is —Ephedrine a long or short term treatment of hypotension

A

—Short-term treatment

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24
Q

what are the different Dopamine dosages and what are the effects (mostly remember effects)

A
  1. —<2.5 ug/kg/min
    • —DA1 & DA2
    • —Vasodilation esp. kidney
  2. —2.5-5 ug/kg/min
    • —β1 agonist, + inotropy
  3. —>5-10 ug/kg/min
    • —α1 & α2
    • —Vasoconstriction, ↑afterload
    • —BP ↑ but ↑ myocaridal work
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25
Q

How does dobutamine work to treat hypotension

A
  • —β1 agonist, ↑contractility, no effect on SVR
  • —Some β2 & α
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26
Q

What lead is used for —dysrhythmia detection

A

Lead II

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27
Q

What is the —Simple systematic approach to detect cardiac dysrhythmias

A
  1. —Identify P, QRS, T waves
  2. —Is there a P for every QRS?
  3. —Is there a QRST for every P?
  4. —Is the R-R interval constant or vary?
    • —Is there a pattern to variation?
  5. —Do complexes come earlier than expected?
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28
Q
  1. What will sinus bradycardia lead to
  2. What are the normal HR for dogs and cats
A
  1. —Low HR, ↓ CO => ↓MAP
  2. —Normal range
    • —Dogs 60-120 bpm
    • —Cats 90-160 bpm
29
Q

Sinus Bradycardia Causes

A
  1. —↑ vagal tone => Opioids
  2. —Hypothermia
  3. —Profound hypoxemia
  4. —Systemic disease
    • —Hypothyroid, hypoglycemia, hyperkalemia, cardiac disease
  5. —α-2 agonists
30
Q

Sinus Bradycardia treatment

A
  • —Treatment*if affecting BP:
    • —Underlying cause
    • —Anti-cholinergic
      • —Atropine, glycopyrrolate
    • —Reversal => α2-agonist
      • —dexmedetomidine
31
Q
  1. When do —Alpha-2 agonists (—Dexmedetomine) cause bradycardia
  2. Do you treat with anti-cholinergics?
A
  1. —Reflex bradycardia due to vasoconstriction and high - normal BP
  2. —*Do NOT treat with anti-cholinergics
32
Q

What are the consequences of Sinus Tachycardia

A
  1. —↓SV => ↓CO, ↓MAP
  2. —↑myocardial work/O2 consumption, ↓cardiac perfusion
33
Q

Sinus Tachycardia Causes

A
  1. —Drugs:
    • —Ketamine - usually short-lived after induction
    • Anti-cholinergics - esp. if given IV, caution in heart disease, geriatric patients
  2. —Pain
  3. —Hypovolemia/Anemia
  4. —Hypoxia/hypercarbia
  5. —Hyperthyroid
34
Q

Sinus Tachycardia Treatment

A
  1. —Underlying cause:
    • —Drugs:
      • —Ketamine - usually short-lived after induction
      • —Anti-cholinergics – wait, usually self-limiting
    • —Pain =>
      • opioids, adjunct analgesics, local blocks
    • —Hypovolemia/Anemia =>
      • fluids, colloids, blood products
    • —Hypoxia/hypercarbia =>
      • intubation, ventilation, IPPV (manual or mechanical)
  2. —Beta-blocker =>
    • Hyperthyroid + Ketamine => sustained tachycardia
35
Q

What is 2 Degree A-V Block (check notes

A

PR interval is the same, dropped QRS

36
Q
  1. 2 Degree A-V Block causes
  2. Treatment
A
  1. —Causes:
    • —↑ vagal tone
      • —Opioids, brachycephalic breeds
    • —Other causes of bradycardia
  2. —Treatment:
    • —Anti-cholinergics
37
Q

What is a Ventricular Premature Contractions

A
  • —No P wave with QRS
  • —R-R interval varies
  • —R wave wide and bizarre
  • —Compensatory pause after QRS
  • —Complex comes BEFORE expected**
38
Q

Ventricular Premature Contractions Causes

A
  1. —Pain
  2. —Shock
  3. —Traumatic myocarditis – 3 – 5 days post trauma
  4. —Hypoxemia, ischemia => myocardial, global
  5. —Electrolyte, acid/base abnormalities
  6. —GDV, pancreatitis, osteosarcoma, splenic hemangiosarcoma
  7. —Cardiac disease
  8. —Drugs
    • —Thiopental, digitalis
39
Q

Ventricular Premature Contractions indications to treat

A
  1. —> 20-30/min
  2. —Rate > 150-180bpm
  3. —Hypotension
  4. —‘runs’
  5. —Multi-focal
  6. —R on T
  7. —Bigeminy, trigeminy
  8. —Ventricular tachycardia
  9. (> 3 in a row)
  10. —Likelihood of progressing to Ventricular fibrillation
40
Q

Ventricular Premature Contractions treatments

A
  • —Lidocaine 2mg/kg, repeat then CRI—
  • Underlying cause
41
Q

What are the 4 Cardiac Arrest Rhythms

A
  1. —Asystole
  2. —Pulseless Electrical Activity
  3. —Pulseless Ventricular tachycardia, HR>180 - 200
  4. —Ventricular fibrillation
42
Q
A

Asystole

43
Q
A

—Pulseless Electrical Activity

44
Q
A

—Pulseless Ventricular tachycardia, HR>180 - 200

45
Q
A

—Ventricular fibrillation

46
Q

What is the equation for minute ventilation

A
  • MV = TV x f
    • TV = tidal volume
    • f = frequency
47
Q
  1. As minute ventilation decreases what happens to PaCO2 & EtCO2
  2. What is the normal PaCO2
  3. At what point is there hypoventilation
A
  1. —PaCO2 & EtCO2 ↑
  2. —Normal PaCO2 35-40 mmHg
  3. —> 45 = hypoventilation
    4.
48
Q

Causes of Hypoventilation & Hypoxemia

A
  1. —Anesthetic drugs
  2. —Patient factors
    • —Obesity, Cushings, CNS disease
49
Q
  1. —Normal PaO2
  2. At 100% O2?
A
  1. —95-100 mmHg room air
  2. —Up to 500 on 100% O2
50
Q

Causes of decreased PaO2

A
  1. —Hypoventilation**
  2. —low inspired O2
  3. —V/Q mismatch
  4. —shunt
  5. —diffusion abnormality
51
Q
  1. Hypoventilation & Hypoxemia is common with all induction agents?
  2. Duration/ severity related to what?
A
  1. —Common with all agents
  2. —Duration/severity related to dose/rate of administration
52
Q

How do you prevent Hypoventilation & Hypoxemia during Induction

A
  1. —Pre-oxygenation delays onset of hypoxemia
    • —O2 @ 100ml/kg/min delays onset of hypoxemia to ~5min vs 1 min on room air
  2. —Low frequency manual IPPV (hand-bagging)
53
Q

Why do Inhalants cause hypoventilation

A
  • —Dose dependent respiratory depression
  • —↓ chemoreceptor response to CO2
  • —↓ respiratory rate & tidal volume
  • —↑ PaCO2 => ↑ EtCO2
54
Q

How do you manage hypoventilation during anesthesia

A
  1. —Monitor EtCO2
  2. —“permissive” hypercarbia
    • —EtCO2 up to ~60mmHg
  3. —Titrate level of anesthetic
  4. —IPPV
55
Q

Hypoventilation & Hypoxemia during recovery causes

A
  1. —Too deep => turn down gas as nearing end of procedure
    • —Hypoventilation will cause hypoxemia as patient transitions from 100% O2 to room air
  2. —Ventilation/perfusion mismatch, atelectasis
  3. —Upper airway obstruction
56
Q

Hypoventilation & Hypoxemia during recovery management

A
  1. —5-10 minutes supplemental O2
  2. —Monitor SpO2 @ transition to room air**
    • —100% to 21% O2
  3. —SpO2 < 93%
    • —Supplement O2
      • —Flow by
      • —Nasal O2
    • —Partial reversal
  4. Brachycephalic breeds try and keep endotracheal tube for as long as possible
57
Q

Should you monitor Monitor SpO2 @ transition from 100% O2 to room air?

A

YES!

58
Q

How can you do a reversal if prolonged oxygen dependence

A

—Partial reversal if prolonged O2 dependence

  • —.1ml (1mg) Butorphanol + .9ml NaCl
    • —Give in .2ml (.2mg) increments
59
Q

Do flashcards for consequences of hypothermia

A
60
Q
  1. What temp is Hypothermia
  2. What temp do you see clinical consequences of Hypothermia
A
  1. —Defined as < 100°F
  2. —Clinical consequences @ < 95°F
61
Q

Hypothermia – Clinical Consequences

A
  1. —Central Nervous System depression
    • — ↓ MAC
    • —Confusion ~95⁰F, unconscious ~86⁰F
  2. —↓ immune function
    • —↑post-op infections, metastasis
  3. —↓ Metabolic rate
    • —Prolonged recovery
  4. —↑ blood viscosity, hypercoagulability
  5. —Conduction velocity slows
62
Q
  1. Because —Conduction velocity slows during hypothermia, can you treat with anticholinergics?
  2. What are consequences?
A
  1. —Bradycardia non-responsive to anti-cholinergics
  2. Consequences:
    • —Myocardium irritable = ventricular arrhythmias
    • —hypotension
    • —Fibrillation ~ 68°F
63
Q
A
64
Q
A
65
Q

Hyperthermia treatment

A
  1. —Remove external heat
  2. —Supplement O2
  3. —IV fluids
  4. —Tranquilizers
  5. —Active cooling
    • —Alcohol, ice, steel table
66
Q
A
67
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68
Q
A