Anesthesia Depth Flashcards
An elevated ETCO2 value can indicate hypoventilation which normally indicates which…
a. Increased depth of anesthesia
b. Decreased depth = insufficient anesthesia
A
An organ considered “critical” by the anesthetist because it is part of the cardiovascular system and which receives almost a quarter of the heart output, and has the highest blood flow and oxygen consumption is the…
a. Kidney
b. Brain
c. Pancreas
d. Myocardium
e. Ilium
A
Which of the following signs would be an example of a noninvasive subjective monitoring technique?
a. Checking the patient’s pulse rate
b. Taking an Sp02
c. Watching the patient’s breathing pattern
d. Checking a patient’s jaw tone
e. Observing an End tidal capnography curve form from exhaled breath
D
All of these groups of patients are prone to moderate to severe hypothermia EXCEPT:
a. Kittens
b. Patients with low BCS
c. Brachycephalic patients
d. Cats
e. Alopecic patients
C
The ACVA recommends that all patients be monitored under sedation and anesthesia for ALL of the following EXCEPT
a. Circulation
b. Urine output
c. Oxygenation and ventilation
d. Thermoregulation
e. Anesthesia depth
B
Oxygen delivery is what we attempt to monitor and assure for our patients while they are under anesthesia. It is made up of (a product of) two things, namely
a. Systemic vascular resistance and blood pressure
b. Oxygen volume and hemoglobin concentration
c. Cardiac output and oxygen content
d. Oxygen content and carbon dioxide removal
e. Cardiac output and stroke volume
C
You have determined after viewing the patient’s jaw tone, eye position, and pupil size, and evaluating your monitors (blood pressure, pulse ox, ecg), that your patient is unfortunately light…at that time, he begins panting and even moves on the surgical table. The surgeon screams at you to “do something” to keep the patient asleep. You turn up your oxygen flow and vaporizer, but what else should you do?
a. Administer an intravenous opioid
b. Bag the patient until he’s down again
c. Ventilate the patient into submission
d. Lower your oxygen flow
A
- would want to increase oxygen flow and vaporizer
Low respiratory rates are almost always indicative of deep planes of anesthesia but tachypneas may be indicative of all of the following EXCEPT:
a. Hyperthermia
b. Anaphylaxis to a bolus of antibiotic
c. Light planes of anesthesia
d. Hypothermia
e. Incorrect ET tube placement (as in a tube placed too distal to the carina)
D
Which of the following is associated with very deep plane 3, Stage III anesthesia?
a. Palpebral reflex briskly present
b. MAC awake
c. Jaw tone active
d. Eyes rolled ventrally
e. Eyes straight forward
E
sweet spot = eyeballs rotated ventral with more sclera visible
Two user friendly alternatives to EEG analysis used in human anesthesia monitoring, but sadly not as reliable in veterinary anesthesia monitoring, are
a. ECG and ETC02
b. BIS and Sp02
c. EMB and EMG
d. SCI and ECG
e. BIS and CSI
E
Which of the following is a measure of the partial pressure of oxygen dissolved in arterial plasma?
a. PaO2
b. PvO2
c. SpO2
d. SaO2
e. PPO2
A
Contractility is one factor in determination of ______, and is often monitored via an _______under anesthesia.
a. Sp02, pulse ox
b. Hb dissociation, ECG
c. Stroke volume, ECG
d. Sp02, capnography
e. Oxygen content, ECG
C
True or false: While bradycardia often indicates adequate to excessive planes of sedation/anesthesia, tachycardia can indicate either too much inhalant (excessive sedation/anesthesia) or too little inhalant.
TRUE
What are the 6 critical organs that get a majority of the heart’s output?
- liver
- kidneys*
- brain
- heart
- muscles
- skin
How are cardiac output and oxygen content calculated?
HR x stroke volume = CO (stroke volume = preload x contractility x afterload) OR BP/systemic vascular resistance
(Hb x 1.34 x SaO2) + (PaO2 x 0.003)
What are the major goals of judging depth of anesthesia?
- assure lack of patient awareness, recall, pain, and movement
- avoid excessive levels of cardiocerebrorespiratory depression, resulting in hypotension, hypothermia, and hypoventilation
- maintain physiologic functions of the patient
- use tools, but do not rely on them
What is required of the anesthetized state? Why is measuring depth hard?
unconsciousness and the lack of processing of perceptions, thoughts, and function
unconsciousness cannot be measured directly
How do non-invasive and invasive techniques of monitoring anesthesia depth compare?
NON-INVASIVE = little risk of complications, not as challenging, not as accurate
INVASIVE = higher risk of complications, technically challenging, more accurate, completely objective (direct BP catheterization)
How do subjective and objective non-invasive techniques of monitoring anesthesia depth compare?
SUBJECTIVE = no equipment needed; palpebral reaction
OBJECTIVE = equipment required; oscillometer BP
What information obtained from monitors are most useful?
trends —> one data piece is not completely indicative of the whole picture
What are common pitfalls in monitoring anesthetic depth?
- depending only on one machine monitor or only machines
- reacting to one reading
- monitor without decision making (log data without reacting to data)
- ignore common sense regarding patient care
What is the classical subjective test of anesthesia depth?
cranial nerves
- like Goldilocks, helps decide if depth is adequate, too little, or too much and determine if our “cocktails” are adequate
Anesthesia stages:
What is indicative of a too light anesthesia depth? What 4 manual signs are observed? 3 vital parameters?
overt movement to surgical manipulation
- jaw tone tight or clamped
- eyes rolled straight forward
- pupils reactive
- palpebral response present
tachypnea, tachycardia and increased blood pressure
What 4 manual signs are observed in too deep anesthesia depth? 3 vital parameters?
- jaw tone lax
- eyes rolled straight forward
- pupils widely dilated or pinpoint
- no palpebral response
bradypnea/apnea, bradycardia, and low blood pressure
What are some anesthesia depth determinants?
- amount of anesthesia in CNS
- magnitude or surgical or external stimuli
- preexisting discomfort, stress, and pain
- underlying conditions that have CNS depressant effects: anesthesia (hypotension, hypothermia), comorbidities (Cushing’s, osteoarthritis), medications (enalapril, amlodipine, prednisone)
What signs of anesthesia depth commonly change first?
subjective/classic signs
- monitoring variables change after and can indicate many things outside of depth, like ungrounded cautery, blood loss, and used sodasorb
What is the “sweet spot” of sedation depth? What are the 4 classic subjective signs?
Stage III, plane 2
- some jaw tone, “spring” present
- eyeballs rotated ventral, with more sclera visible
- palpebral not present or very weak
- pupils are mid-size and may be reactive
What are the ideal PR, RR, and BP found in Phase III, plane 2 of sedation?
- PR = 50-120 (species and breed specific)
- RR = under 20
- BP = systolic 80-120
What 6 things are modified to alter depth and stage/plane of anesthesia?
- level of inhalant general anesthetic on vaporizer settings
- rates of intraoperative CRIs
- continued boluses of induction agents (propofol, alfaxalone)
- full or partial reversal of potent conscious sedation agents (dex, opioids)
- cardiovascular and respiratory control
- administration of other drugs
What are the 4 stages to electroencephalographic monitoring?
- awake
- low amplitude, high frequency waves
- plane II = high amplitude, low frequency; plane III = burst suppression
- electrical silence
What are 2 alternatives to EEG analysis?
- bispectral index (BIS) - quantified degree of anesthetic-induced cortical depression, ensuring patients are pain free and unaware
- cerebral state index (CSI) - collects EEG and EMG and calculates a numerical value for level of sedation
What is the major problem with BIS monitoring? CSI? What is the major reason these are not used in veterinary anesthesia?
not all anesthetics affect BIS in the same way
CSI decreases with propofol, but doesn’t correlate with classic signs of depth in dogs; lacked discrimination for lighter planes
- studies are equivocal on reliability based on breeds, species, and individuals
- EEG parameters examine hypnotic changes, but not analgesia
- $$$
What cardiovascular variable have little to do with anesthesia depth and safety?
mucus membrane color and CRT —> circulation
What are 6 possible causes of bradycardia under sedation or anesthesia?
- excessive inhalant anesthesia depth
- hypothermia
- anesthetic drugs
- increased vagal tone
- hypoglycemia
- mechanical ventilation
What are 6 possible causes of tachycardia under sedation or anesthesia?
- pain, stress, inflammation (insufficient inhalant anesthesia)
- excessive inhalant anesthesia
- hemorrhage
- hypovolemia
- anesthetic drugs
- endocrine tumors
When should bradycardia be corrected? What initial conservative steps can be taken?
when blood pressure is affected
- check plane of anesthesia, adjust inhalant, oxygen flow, and CRI
- warm patient
- check for causes of increased vagal tone
- check for hyperkalemia
- change mechanical ventilation settings
What class of drugs are used to help bradycardic patients under anesthesia? In what 4 situations are they used?
anticholinergic
- conservative fixes fail
- blood pressure fails
- vagal tone is excessive, common in ocular/CNS diseases and breeds
- pediatrics and neonates
When are reversal agents used in bradycardic patients under anesthesia?
- emergent care
- anticholinergic fails
(be ready with rescue agents, the animal will hurt and be stressed)
What is the difference between compensatory and primary tachycardia?
COMPENSATORY - adequate premed, proper dose of inhalant anesthesia, hemorrhage, drugs
PRIMARY = accompanied with arrythmia
How does the dosage of inhalant anesthesia contribute to tachycardia?
TOO HIGH = vasodilation and compensatory tachycardia
TOO LOW = pain awareness and epinephrine release causes tachycardia
What are the 3 major fixes to sinus tachycardia in a sedated patient?
- opioids: hydromorphone, methadone, oxymorphone, morphine, fentanyl (requires follow-up), pre-med opioid IV
- ketamine
- microdose of dexmedetomidine
What is contractility? How is it monitored?
force and rhythm by which the heart expulses its preload against the body’s afterload (myosin, actin interaction)
ECG
What is an arrhythmia? How are they monitored?
disturbance in rate, rhythm or site of cardiac impulse generation
ECG - surface recording of electrical activity of the myocardium using various electrodes
What are the 3 initial steps to take when an arrhythmia is first noticed under anesthesia?
- palpate pulse and obtain a pulse rate
- establish plane of anesthesia (increased/reduce inhalant, administer opioids, sedatives, or anti-inflammatories)
- determine BP - fluid boluses, anticholinergics
What are some causes of pulseless electrical activity (PEA)?
- hypobolemia
- hypoxia
- hypothermia
- hyperkalemia
- pneumothorax
- PE
- tamponade
- overdoses of anesthetics, antiarrhythmics, beta/alpha blockade, toxins
- acidosis
- acute myocardial infarction
What are the expected normal and sedated pulse rates of kittens, cats, toy breeds/puppies, average-sized dogs, and giant breeds?
What 4 drugs are used to treat sinus tachycardia in patients under anesthesia?
- ketamine
- morphine
- lidocaine
- propofol
What is the sweet spot for intra-anesthetic BP in smaller and larger patients? When is hypotension and hypertension defined?
SMALL = 100-160; LARGE = 80-120
SMALL = < 80; LARGE = < 60
SMALL = > 150; LARGE = > 120
How can anesthetics cause hypotension?
excessive anesthetic inhalant or CRI
Why is central venous pressure not commonly utilized under anesthesia? What does it signify?
not a great predictor of cardiac output or depth
relationship between blood volume and blood volume capacity
What is the normal central venous pressure of small animals?
in awake patients = 3-10 cm H20
What patients are most prone to moderate-severe hypothermia?
- smaller breeds
- cats
- alopecic
- pediatric/neonatal
- geriatric
- low BCS
- heavily premedicated
What are the 3 ranges of hypothermia?
- 96-99F expected drop - immune function impaired, recovery not or mildly prolonged
- 90-96F moderate-severe drop - reduced anesthetic requirements, recovery prolonged
- 90-92F severe hypothermia - CO and cerebral metabolism reduced, myocardial automaticity increased, increased blood viscosity
What is the most common cause of hypothermia under anesthesia and sedation? What are some other causes?
excessive inhalant or CRI depth
- hypotension
- high oxygen flow
- open body cavities
- cold fluids and flush
What are the 2 most common causes of hyperthermia in anesthesia and sedation? What are some other causes?
- inadequate or light depth of anesthesia
- poor premedication
- heavy har coat breeds
- overzealous use of heat sources
- low oxygen flows
- inappropriate ET tubes
- hypoventilation
- inadequate CO2 waste removal
- endocrine or neoplastic release
How is hyperthermia under anesthesia treated?
- increase oxygen flow
- assure appropriate ET tube placement
- reduce ET tube dead space
- stop external heating devices
- check capnography
What are the normal respiratory rates of awake and anesthetized patients? When is bradypnea and tachypnea defined?
AWAKE = 10-30 bpm
ANESTHETIZED = 3-15 bpm, or 1/3 resting rate
- bradypnea = 0-3 bmp
- tachypnea = > 15 bmp
What are the most common causes of bradypnea and tachypnea in anesthetized patients?
BRADYPNEA = excessive inhalant or CRI depth of anesthesia*, hypothermia, diaphragm or intercostal impairment, CNS or ocular pressure, gastric reflux or increased vagal tone
TACHYPNEA = pain, stress, anxiety, or inadequate depth of anesthesia
What seems to be the most sensitive indicator of depth of anesthesia?
respiratory rate changes
What are 4 reasons Doxapram is not given in cases of bradypnea in patients under anesthesia?
- use potentiates hypocapnia (CO2 is stimulus to breathing)
- hyperventilation is transient and often followed by apnea
- increases cerebral oxygen demand
- central stimulant
What should be done in patients that are undergoing intraoperative wakening due to tachypnea?
- give additional partial dose induction (“leftover” propofol, ketamine, valium, alfaxalone)
- treat pain, stress, and inflammation with rescue medication
- increase oxygen flow
- increased vaporizer settings by 30-50%
How does pulse oximetry and arterial blood gas analysis compare?
PULSE OX = SpO2; non-invasive, continuous, establishes pulse and oxygenation, safe, many variables can lead to poor readings
ART BLOOD GAS = SaO2, PaO2; invasive, intermittent, establishes respiration (oxygenation and ventilation), reliable for respiration, but says littler directly about cardiac output
What are the ideal SpO2 levels in intubated and non-intubated patients?
INTUBATED = on 100% oxygen, >95-97% (>93% accepted due to technical error
NON-INTUBATED = on room air >90% is ideal; on oxygen supplementation >93% is expected
What should be done if there is a low pulse ox reading?
- INTUBATED = technical vs. non-respiratory
- NOT INTUBATED = true hypoxia
~ TACHYCARDIC or TACHYPNEIC = true hypoxia
~ NOT = technical vs. non-respiratory
What are the most common technical and non-respiratory causes of inconsistently low SpO2 readings?
TECHNICAL = insufficient inhalant or CRI depth, prob slipping, ambient lighting, probe compressing vessel
NON-RESPIRATORY = excessive inhalant or CRI depth, cold, wet, vasoconstricted
What does PaO2 and SaO2 measure?
partial pressure of arterial oxygen dissolved in plasma —> ability of lungs to move oxygen from atmosphere to blood
hemoglobin saturation —> calculated value from blood gas results (commonly reduced in cats and horses)
Why are SpO2, PaO2, and SaO2 not commonly as valuable for determining depth of anesthesia?
- influenced by a lot of underlying components
- 100% O2 is the carrier gas, so these levels are normally excellent in intubated patients
What are the main 2 things end tidal concentrations are used to evaluate?
- circulation and perfusion
- respiratory and ventilation issues
What are the 5 most common causes of decreasing ETCO2 readings and waveform height?
- hyperventilation
- dead space ventilation
- hypothermia
- hypovolemia
- vasoconstriction
What is the most common cause of increasing ETCO2 readings and waveform height?
- hypoventilation —> decreased CO2 removal
- increased CO2 production —> hypermetabolism, malignant hyperthemia
If other issues have been ruled out and there is a truly deep patient, what should be done?
- flush the circuit
- decrease vaporizer to 30-50%
- keep oxygen flow the same or reduced by 30%
- reduce or cease CRI
- warm patient
f other issues have been ruled out and there is a truly light patient, what should be done?
- increase oxgyen flow (0.5-1 L/min) and vaporizer
- use leftover induction agent IV bolus
- check for leaks
- give fluid bolus
- rule out technical and nonsurgical discomfort
- IV analgesia, sedative, and anti-inflammatory
