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Lumb & Jones, 6th Ed. > Chp. 5: Emergencies, Resuscitation, & Adverse Events > Flashcards

Chp. 5: Emergencies, Resuscitation, & Adverse Events Flashcards

1
Q

Adverse Event

A

An event that may result in patient harm and may be due to the effects of anesthetic drugs, the patient’s condition, the diagnostic or therapeutic procedure, or human error

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2
Q

Cardiopulmonary arrest

A

Acute cessation of cardiac mechanical function with concurrent apnea

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3
Q

Reported ROSC rates in dogs and cats

A

17-58% for dogs
21-57% for cats

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4
Q

Survival to discharge rates after ROSC for dogs, cats, and exotics

A

4-7% for dogs
3-19% in cats
1.2% in exotics

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5
Q

Rate of survival to discharge after CPA under anesthesia

A

25-50%

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6
Q

Why is survival to discharge after ROSC improved when CPA occurs under anesthesia?

A

Venous access established, are intubated and breathing enriched oxygen, and are being monitored continuously

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7
Q

What decreases likelihood of ROSC?

A

Increased time from CPA to initiating CPR and duration of CPR

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8
Q

BLS

A

Recognition of CPA, initiation of chest compressions, airway management, and assisted ventilation

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9
Q

Compression rate during CPR

A

At least 100 per minute

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10
Q

Cerebral Perfusion Pressure

A

CPP = MAP - ICP

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11
Q

Coronary Perfusion Pressure

A

CPP = ADP - RADP

ADP = aortic diastolic pressure
RADP = right atrial diastolic pressure

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12
Q

What interventions are beneficial to patients undergoing CPR?

A

Interventions that increase DAP or MAP or interventions that decrease RADP or ICP

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13
Q

True or False: During CPA, autoregulation of cerebral perfusion is maintained.

A

False. Autoregulation of cerebral perfusion is disrupted and cerebral blood flow becomes linearly related to perfusion pressure.

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14
Q

What should compression depth be? Why?

A

One-third to one-half of chest width. Greater depth of compression is associated with improved aortic pressures.

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15
Q

Thoracic Pump

A

Describes movement of blood out of the thoracic cavity due to changes in intrathoracic pressure.

Important in animals >15kg

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16
Q

Cardiac Pump

A

Describes movement of blood out of the heart due to direct, mechanical compression of the heart by the thoracic wall.

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17
Q

What is the consequence of the chest wall not recoiling fully during CPR?

A

Intrathoracic pressure remains positive, which decreases venous return and stroke volume.

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18
Q

What are the indications for open-chest CPR?

A

Cases of elevated IttP (pleural space disease, pericardial disease, severe abdominal dissension, or flail chest) or where closed-chest is ineffective.

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19
Q

ICS for open-chest CPR

A

Fourth or fifth ICS

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20
Q

Ventilation during CPR

A
  • Full breath delivered in approximately 1s with a 10mL/kg TV (prolonged inspiratory time increases length of high IttP, decreasing venous return, increasing RV afterload, and decreasing LV distensibility)
  • Manual ventilation with maximal FiO2
  • Ventilation rate of 10bpm
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21
Q

Order of preference for drug routes of administration during CPR

A

1) Central venous catheter
2) Peripheral catheter in thoracic limb
3) Any peripheral catheter
4) Intraosseous catheter
5) ETT

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22
Q

How are drug doses altered for ETT administration?

A

Omcmrease dose (10-fold for epinephrine) and deliver via long catheter advanced to level of carina

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23
Q

Is a high dose of epinpehrine (0.1mg/kg) recommended for CPR?

A

No.

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24
Q

True or False: Epinephrine’s beta-adrenergic effects are most beneficial during CPR

A

FALSE. May actually lead to detrimental increases in myocardial oxygen consumption once ROSC is achieved.

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25
Q

What are the potential benefits of corticosteroid administration during CPR?

A

Counteracting relative adrenal insufficiency in patients with longstanding critical disease, counteracting impairment of adrenal function as a result of CPA, exerting anti-inflammatory effects, improving CV function, or blunting a catecholamine surge.

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26
Q

Why is sodium bicarbonate administration during CPR not recommended?

A

May cause paradoxical cerebral acidosis, hyperosmolarity, and deceased catecholamine effectiveness.

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27
Q

True or False: Fluid administration during CPR to euvolemic patients improves outcome.

A

FALSE. Aggressive fluid therapy may be detrimental due to decreased tissue blood flow caused by compromised tissue perfusion pressures. However, it is essential if CPA is caused by hypovolemia.

28
Q

If VFib is identified during CPA, should defibrillation be performed before or after initiation of chest compressions?

A

After. A hypoxic myocardium is unlikely to be successfully defibrillated.

29
Q

What is the starting dose for electrical defibrillation?

A

2-5J/kg with 50% increase in energy on subsequent attempts

30
Q

True or False: Inhalational agents should be discontinued during CPR.

A

True, all cause myocardial depression.

31
Q

Monitoring during CPR

A
  • ECG to monitor for transition to treatable rhythm
  • ETCO2, a non-invasive surrogate for CPP (values >/= 18mmHg at 3-8 minutes after CPR are a sensitive predictor for ROSC)
32
Q

What are oxygenation goals during and after CPR?

A

Maintain PaO2 of 80-100mmHg or SpO2 of 94-98% (hyperoxemia of PaO2 > 100mmHg is undesirable due to free-radical formation).

33
Q

What is a common complication after ROSC?

A

Hypoventilation due to respiratory muscle weakness or poor responsiveness of the brainstem to CO2 levels. Target PaCO2 of 32-40mmHg.

34
Q

Postcardiac Arrest Syndrome

A

Damage to the brain, kidneys, and heart and derangements of coagulation. SIRS and ARDS can develop.

35
Q

Brain ischemia-reperfusion consequences after ROSC

A

Mitochondrial dysfunction, excitotoxicity, altered phospholipids, oxidative stress, increased lactate, endoplasmic reticulum stress, inflammation.

36
Q

Target MAP after ROSC

A

70-80mmHg

37
Q

Benefits of therapeutic hypothermia

A

Reduction in cerebral oxygen requirement, brain metabolic demand, excitatory neurotransmitters, inflammatory cytokines, and free radicals, along with inhibition of neuronal cell apoptosis

38
Q

MAP thresholds

A

> 60mmHg maintains visceral organ perfusion

> 70mmHg maintains muscle perfusion in large animals

DAP >40mmHg maintains myocardial perfusion

Consciousness requires SAP > 50mmHg

39
Q

Indications for treating hemorrhage

A

Absolute blood volume loss, increased BE or lactate, changes in CV paramters associated with hemorrhage (increases in HR, decreases in SBP)

40
Q

Absolute blood volume loss treatment

A

When estimated blood volume approaches 20% of total blood volume or 17mL/kg in the dog; when BE>6.6 or lactate >5mmol/L

41
Q

Shock Index

A

HR/SAP

> 1 may be a sensitive and specific indicator of 18% BV loss

42
Q

Effects of cardiac dysrhythmias

A

Decrease CO by affecting diastolic filling, contractility, and/or HR. Have potential to increase myocardial work.

43
Q

Anaphylaxis

A

Type I hypersensitivity reaction caused by IgE-mediated interactions. Results in release of substances from mast cells and basophils, primarily histamine.

44
Q

Anaphylaxis signs

A

Pruritus, urticaria, hypotension, tachycardia, bronchospasm, vomiting and diarrhea

45
Q

Direct effects of hypoventilation

A

Respiratory acidosis, tachycardia

46
Q

Indirect effects of hypoventilation

A

Hypoxemia, impaired uptake of inhalants, disrupted enzyme systems, decreased cardiac contractility, arrhythmias, hypertension, hypoxemia, narcosis, vasodilation, increased ICP

47
Q

MAC-sparing effect of hypercapnia

A

At 94mmHg, linearly decreasing MAC until 240mmHg

48
Q

NPPE

A

May occur as a results of upper airway obstruction. Treated with diuretics and oxygen supplementation.

49
Q

Causes of bronchospasm

A

Airway irritation or stimulation, anaphylactic reactions, underlying disease (asthma), or drugs (beta-blockers)

50
Q

Causes of tracheal tears

A

Overinflation of cuff, changing body position with ETT connected to circuit, forceful intubation

51
Q

Wooden Chest Syndrome

A

Intercostal muscles and diaphragm become rigid causes failure of chest wall expansion, higher than expected inspiratory airway pressures, and ventilatory failure. Associated with use of fentanyl and its analogues.

Tx with NMB; naloxone reversal does not resolve.

52
Q

APL Closure or Malfunction

A

May result in volutrauma or barotrauma and compromise venous return.

53
Q

What happens if you fill a sevo vaporizer with iso and vice versa?

A

A sevo vaporizer filled with iso will result in an overdose; an iso vaporizer filled with sevo will result in an underdose.

54
Q

Cushing Reflex

A

Acute increase in ABP and reflex bradycardia

55
Q

Hyperkalemia on ECG

A

Bradycardia (resistant to antimuscarinic treatment), absent P waves, tented T waves

56
Q

Risks for developing intraoperative hypothermia

A

ASA III or greater, body weight <6kg, receiving an alpha-2 agonist, receiving an opioid, anesthetic episode >1hr, orthopedic or neurologic surgery, undergoing MRI.

57
Q

Malignant hyperthermia

A

Rapid increase in body temperature caused by skeletal muscle contraction due to abnormal influx of calcium from the SR by defective RyR.

Other signs include increased HR, arrhythmias, and body temperature.

Tx with dantrolene (calcium channel blocker) at 2mg/kg IV

58
Q

How long should cessation of inhalant anesthesia to extubation take in SA patients?

A

30 minutes

59
Q

How long should cessation of inhalant anesthesia to extubation take in horses?

A

60 minutes

60
Q

DDx for prolonged recovery

A

Hypothermia, hypotension, hemorrhage, hepatic incompetance, renal dysfunction, hypoglycemia, neurologic disease, hypocalcemia, drug overdose

61
Q

Causes of post-anesthetic blindness

A

Decreases in cerebral perfusion

Maxillary artery occlusion (esp. in cats)

62
Q

Equine rhabdomyolysis causes, signs, diagnosis

A

Due to decreased perfusion of large muscles and subsequent reperfusion injury combined with increase muscle compartment pressure.

Results in lameness, poor recovery quality, fracture, death, euthanasia, renal failure due to myoglobinuria, and failure to recover from anesthesia.

Myoglobinuria and/or high CK will support diagnosis

63
Q

Risk factors for equine rhabdomyolysis

A

Prolonged duration of anesthesia, hypotension, lateral recumbency

64
Q

Interventions to reduce risk of equine rhabdomyolysis

A

Minimizing duration of anesthesia, MAP > 70 mmHg, providing IV fluids, adequate padding and positioning, avoiding excess muscle strain.

65
Q

Treatments for equine rhabdomyolysis

A

Aggressive IV fluid therapy, anti-inflammatory drugs, massage, water cooling

66
Q

Equine myelomalacia

A

Unable to stand, dog sitting position due to paraplegia, lack of anal tone and hind limb function.

Most often in horses in dorsal recumbency and draft breeds. 100% fatality rate.

67
Q

Equine neuropathy

A

Diagnosis of exclusion.

Treatment consists of anti-inflammatories and PT.

Ranges from neuropraxia (temporary loss of nerve conduction), to axonotmesis (significant axonal damange), to neurotmesis (nerve transection).

Lumb & Jones, 6th Ed. (17 decks)

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