All Other Anesthesia Flashcards

1
Q

What are the 3 components of nociception?

A

Transduction (conversion of noxious stimulas into electrical energy by peripheral nociceptor)

Transmission (propagation from site of injury through trigeminal afferent nerves) – A fibers for inital fast, c fibers for throbbing pain.

Modulation - neurons synapse with nociceptive specific neurons in nucleas caudalis in the medula.

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2
Q

What is peripheral sensitization?

A

Enhanced nociceptor response to additional stimulus after injury. Due to ATP, potassium, hydrogen, prostaglandins, bradykinin, and nerve growth factors released by damaged tissue. Inflammatory cells attracted and release cytokines such as histamine.

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3
Q

What is central sensitization?

A

Occurs when peripheral sensitization is untreated, Chemicals increase sensitivity of neurons and intensity of the pain signal in the brain. Glutamate partially responsible by binding to NMDA receptor. One of primary chemicals involved in central hypersensitization.

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4
Q

In “ Early Analgesic Efficacy of Morphine,
Butorphanol, Lidocaine, Bupivacaine
or Carprofen After Periodontal
Treatment in Dogs” by Rauser in JVD 2020 what were the main takeaways?

A
  • Compared effecacy of morphine, butorphanol, lidocaine, bupivacaine, and carprofen post-operatively after perio treatment. 84 dogs. Had control group, and one group for each drug. Gave the drugs 30 minutes before the pre-med with dex. Lidocaine and Bupivacaine after induction as bilateral maxillary and inferior alveolar blocks.
  • Evaluated glucose, and cortisol before and 2 hours after treatment.
  • 1 patient in morphine and 1 in carprofen group needed rescue.
  • Pain scores in Bupivacaine group sign. lower than Lidocaine group
  • Carprofen provided improved analgesia to morphine but not statistically significant
  • No rescue needed in the control group?
  • Overall carprofen and bupivacaine gro0ups best.
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5
Q

What are the overall anesthetic death rates?

A

0.1-0.3% in small animals overall.

Healthy 0.05-0.3% and sick 1-4%

Referral institutions - 0.3-0.6%

From Lumb and Jones – summarizing all recent research.

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6
Q

Atropine would be contraindicated with what underlying cardiac condition?

A

HCM or restrictive cardiomyopathy

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7
Q

What is the pKa of a drug?

A

The pH at which the two forms of the drug (Non-ionized - lipid soluble, and ionized - water soluble).

For all clinically used drugs the pKa is >7.4

Only the iuonized charged form can interact with the sodium channel, but the main access of anesthetics is by penetration of lipophilic neutral form through the lipid membrane.

Higher pKa means greater degree of ionization and slower onset of action.

Lidocaine = LOWER pKa - more non-ionized lipid soluble form and more rapid onset of action.

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8
Q

What is the main determinant of intrinsic local anesthetic potency?

A

Lipid solubility!

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9
Q

Which is more likely to have more systemic absorption, a highly lipid soluble drug or a less lipid soluble drug??

A

The less lipid soluble drug because there is less going directly into the cell.

A drug with greater lipid solubility and protein binding will result in lower systemic absorption.

Lidocaine has less systemic absorption than bupivacaine or ropivacaine.

Bupivacaine is HIGHLY liupid soluble, and has a higher pkA, and is about 4 times as potent as lidocaine.

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10
Q

What doses of commonly used local blocks would cause convulsions in dogs?

A

5mg/kg for bupivacaine, 22mg/kg for lidocaine

In cats - 12mg/kg lidoacine, and 5mg/kg bupivacaine.

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11
Q

Early Analgesic Efficacy of Morphine, Butorphanol, Lidocaine, Bupivacaine or Carprofen After Periodontal Treatment in Dogs

JVD 2020 Rauser, Fichtel

KEY POINTS

A

Evaluation of 84 client owned dogs. Groups were either control, morphine, butorphanol, lidocaine, bupivacaine, or carprofen (did not eval pain meds with the local blocks). Administered systemic pain meds 30 minutes before sedation. Administered local blocks right after injection. ONLY evaluated scaling and simple extractions–excluded any surgical extractions!

  • VAS Scoring:
    • Significantly lower VAS scores in butorphanol and bupivicaine groups compared to control. VAS also significnatly lower in bupivicaine compared to lidocaine.
  • UMPS scoring:
    • Significantly lower in bupivicaine compared to control, butorphanol, and lidocaine groups.
    • Significantly lower in carprofen compared to control and lidocaine groups.
  • SOO:
    • VAS - bupivicaine and butorphanol lower, and for UMPS bupivicaine and carprofen groups lower.
  • Cortisol
    • Increased in morphine and lidocaine
    • Decreased in bupivicaine group.
      • However, the results of this study indicate that analgesia induced by bupivacaine nerve blocks or systemic carprofen are superior to butorphanol, morphine or lidocaine.
      • Nevertheless, the use of combined analgesics could be more beneficial as the multimodal approach provides considerable benefits. Based on our study, carprofen (or a COX-2 selective/preferential NSAIDs to avoid bleeding) combined with bupivacaine nerve blocks is recommended.
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12
Q

How do you calculate heart rate on an ecg strip?

A

Count number of beats in 15 large boxes.

If paper is at 50mm/sec multiply by 40

If paper is at 25 mm/sec multiply by 20

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13
Q

What are the 3 hallmarks of Afib?

A

No identifiable P waves

Supraventricular QRS

Irregularly irregular rhythm

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14
Q

Name this arrhythmia

A

Paroxysmal VT

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15
Q

Name this arrhythmia

A

Unifocal VT

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16
Q

Name this arrhythmia

A

Sinus Tachycardia

  • The underlying mechanism of sinus tachycardia is enhanced normal automaticity of the sinoatrial (SA) node. In general, there are P waves for every QRS complex and the PR interval is consistent. However, at faster rates the P waves may become superimposed on the preceding T wave and the rate may be fast enough to cause intermittent atrioventricular (AV) block. The heart rate may gradually slow during a vagal maneuver, ultimately allowing identification of P waves.
    • The most common cause of sinus tachycardia is high sympathetic tone, usually associated with excitement or stress during examination. Other causes include fever, pain, hyperthyroidism, anemia, shock, heart failure, and treatment with sympathomimetic agents such as bronchodilators or catecholamines.
17
Q

Name this arrhythmia, treatment?

A

SVT

Associated with significant heart disease and atrial enlargement

18
Q

Name this arrhythmia

A

Atrial Standstill

Atrial standstill (Figure 5) is an uncommon arrhythmia caused by idiopathic destruction of atrial myocardium or severe hyperkalemia. The atrial myocardium becomes unresponsive to sinus impulses and does not depolarize. A junctional or ventricular escape rhythm takes over control of the ventricles. The prognosis in dogs with idiopathic disease is guarded, as many experience progressive myocardial disease and eventual heart failure. However, some dogs will live several years with pacemaker implantation and prevention of congestive heart failure.

19
Q

Name this arrhythmia

A

Sinus arrest

If a P wave is not present for every QRS complex, sinus arrest (Figure 6) may be present. Some patients with sinus arrest may have sick sinus syndrome, which may be complicated with periods of AV block and/or SVT. Sinus arrest occurs when the SA node fails to depolarize because of deceased normal automaticity, resulting in a pause in the heart rhythm that can last from <1 second to many seconds. Longer periods of sinus arrest may be accompanied by signs of weakness or syncope.

  • Historically, the criteria for sinus arrest involved a pause that lasted >2 R-R intervals; however, dogs with pronounced sinus arrhythmia can also display pauses of this duration, resulting in some overlap between the diagnoses. Possible causes of sinus arrest include excessive vagal tone, sick sinus syndrome, and hyperkalemia. In general, treatment is not required in asymptomatic patients.
20
Q

Name this arrhythmia

A

SInus bradycardia

Sinus bradycardia (Figure 7) occurs when criteria for sinus rhythm are met but the heart rate is slower than normal. The exact rate at which sinus bradycardia is considered pathologic is subjective: 40 bpm in a sleeping dog is considered normal, but the same would be considered abnormal during examination. A common cause of sinus bradycardia is elevated vagal tone caused by athletic conditioning, increased intracranial pressure, severe GI or respiratory disease, or administration of parasympathomimetic or sympatholytic drugs. Other causes include sedative or anesthetic agents, hypothermia, hyperkalemia, sick sinus syndrome, and severe hypothyroidism.

21
Q

Name this arrhythmia

A

2nd degree AV block

  • Second-degree AV block occurs when a proportion of atrial impulses are prevented from reaching the ventricles. High-grade second-degree AV block is often secondary to idiopathic conduction system disease and may cause transient weakness, syncope, or sudden death. Other causes include high vagal tone, treatment with digoxin, calcium-channel blockers, β-blockers, or underlying heart disease or electrolyte abnormalities (uncommon).
22
Q

Name this arrhythmia

A

3rd degree AV block

  • Third-degree or complete AV block is present when none of the atrial impulses reach the ventricles, indicating complete AV dissociation. Instead, ventricular depolarization relies on subsidiary pacemaker cells that depolarize more slowly than the sinus node or AV node. Canine patients with third-degree AV block usually present with weakness, exercise intolerance, syncope, congestive heart failure, and/or dyspnea; some have experienced sudden death. Dogs reportedly may also be asymptomatic and the arrhythmia will be detected during routine or preoperative examination. AV block is often idiopathic, although other causes include degenerative, infiltrative, inflammatory, infectious, and/or immune-mediated heart disease; hyperkalemia or severe digoxin toxicity can also be a cause.
    • Cats with third-degree AV block rarely display clinical signs as a result of an adequate ectopic pacemaker rate to maintain cardiac output. Some cats with transient AV block will present with syncope. Atropine or oral sympathomimetics can be administered but are often ineffective.
23
Q

Risk of anesthesia-related complications in brachycephalic dogs

JAVMA 2018 Gruenheid

What was the post-anesthetic complication rate for brachycephalic vs non-brachycephlic dogs?

A

14% brachycephalic

3.6% non-brachycephalic

24
Q

Risk of anesthesia-related complications in brachycephalic dogs

JAVMA 2018 Gruenheid

what was the most common post-anesthetic complication?

A

Aspiration pneumonia – in 4% of brachycephlic and 0% of non-brachycephalic

Regurgitation second most common at 3% for brachycephalic

Dysphoria, prolonged recovery, stertorous breathing, and death (0.9% brachycephlic) also common compliations

had 446 dogs overall in study

25
Q

Risk of anesthesia-related complications in brachycephalic dogs

JAVMA 2018 Gruenheid

What were risk factors associated with outcome?

A

No associations with any evaluated outcome were identified for sedatives, opioids, hypothermia, or anesthetic maintenance agents used or dog age.

Brachycephalic status, body weight, duration of anesthesia, reproductive status, and attending hospital service all significantly associated!

26
Q

Risk of anesthesia-related complications in brachycephalic dogs

JAVMA 2018

How much more likely were brachycephalic dogs to have intra-anesthetic or perianesthetic complication? 2 diff numbers.

A
  • 1.6x as likely to have intra-anesthetic complication
    • 2x as likely to have to have perianesthetic complicatin (including intra and post)
      • Note - intacdt females also at increased risk
27
Q

Influence of halothane, isoflurane, and sevoflurane on gastroesophageal reflux during anesthesia in dogs

JAVMA 2006

A
  • No significant difference in GER (measured by esophageal pH probe) or regurgitation between the agents.
  • Propsective study with 90 dogs
  • Dogs that developed GER soon after induction of anesthesia were more likely to regurgitate.
28
Q

Comparison of recovery from anesthesia with isoflurane, sevoflurane, or desflurane in healthy dogs

Lopez AJVR 2009

A
  • No difference in recovery quality
    • Recovery order – desflurane fastest (11min), then sevo (18 min), then iso (26 min)
29
Q

Effects of carprofen on renal function during medetomidine-propofol-isoflurane anesthesia in dogs

Fren 2006 AJVR

A

Carprofen administered IV before anesthesia did not cause detectable, significant adverse effects on renal function during medetomidine-propofol-isoflurane anesthesia in healthy Beagles.

Measured GFR via scintigraphy

30
Q

Effect of prewarming on the body temperature of small dogs undergoing inhalation anesthesia

Rigotti, JAVMA 2015

A

Prewarming in an incubator prior to IOA failed to improve or maintain body temperature of dogs weighing < 10 kg during inhalation anesthesia.

31
Q

Randomized, blinded, controlled clinical trial to assess gastroesophageal reflux and regurgitation in dogs undergoing general anesthesia after hydromorphone premedication with or without acepromazine or dexmedetomidine

AJVR 2021

A
  • The incidence of GER was lower for dogs premedicated with dexmedetomidine and hydromorphone (group DH), compared with dogs premedicated with acepromazine and hydromorphone (group AH) or hydromor-phone alone (group H [control group]).
  • In the present study, there was an 89% lower incidence of GER when dexmedetomidine was added to the hydromorphone premedication, compared with premedicating with hydromorphone alone.
  • In the present study, 13 dogs vomited and only 3 of these 13 developed GER. Also, none of the dogs that vomited went on to regurgitate later. These findings suggested that vomiting induced by premedication could be beneficial because it results in a reduction in gastric contents, potentially decreasing the risk of GER and regurgitation.5,13 However, previous studies5,15,18,19 show no association between preanesthetic vomiting and development of GER in dogs. Further studies investigating the association between vomiting, regurgitation, and GER are required.
32
Q

Small animal oxygen flow rates (circle system)

A

* Induction 100-200 ml/kg/min
* Maintenance: 40-60 ml/kg/min
* Minimum = 0.5 L/min

33
Q

Evaluation of analgesic effect and absorption of buprenorphine after buccal administration in cats with oral disease

Statholopoulu J. Fel. Med Surg. 2017

A

6 cats with stomatitis, treated with saline or OTM buprenorphine

Measured plasma levels

Peak at 30minutes, lasted 360 minutes

Significant difference in eating and pain at 60 and 90 minutes

Predictable absorption

PH of saliva 8.1-9 in this study. Favors unionized form, good for absorption.

34
Q
A

Know this!

35
Q

With sPo2 at 99-100% what is the paO2?

A

300-400mmHg

At 97-98% - the paO2 is 85-95 (this is healthy patient on room air)

at 90% SpO2, the paO2 is critical at 60-70mmHg

36
Q

Name which each of these are related to.

A
  1. Hypoventilation
  2. Airway/ and/or ET tube obstruction, increase in expiratory plateau, can happen with stiffened airways
  3. EtCo2 not returning to baseline–check sodasorb and system
  4. Abnormal down stroke– could be et tube leak
  5. no values, apnea, cardiac arrest, esophageal intubation etc.
37
Q

What is a curare cleft?

A

Appearance on an et waveform usually due to patient takin ga small breath against a ventilated breath. Shows as a small downward stroke in the expiratory plateau.