Anesthesia III Master Question List

Created by smcguirl 

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Which drug classes may produce a decrease in aggression?

Drug classes that increase central serotonergic activity may produce a decrease in aggression
- decrease the tendency to engage in sudden outbursts
- increase the threshold of tolerance to potentially aggressive stimuli
(be careful using benzodiazepines)

What drugs are useful against compulsive disorders?

TCAs (Tricyclic antidepressants)
SSRIs (Selective serotonin re-uptake inhibitors)
opiod antagonists (naltrexone)

What drugs are useful against fear?

They generally benefit from anxiolytics (e.g. benzodiazepines - Diazepam and Alprazolam)

How many half lives before a drug reaches steady state level?

~5 half-lives before steady-state

Describe some general characteristics of psychotropic drugs

Many of the behavior drugs used in veterinary medicine are weak bases
- Good lipophilicity
- Poor water solubility
- Protein binding assumed low
- CNS penetration is generally good
- Ion-trapping
- BBB and blood-CSF barrier
- Short versus long t½
- Most behavior drugs are metabolized by liver
- Species variations in metabolism (CYP450's)
- Partly explains lack of immediate effects of some
psychotrophic drugs

How do anxiolytics operate (e.g. benzodiazapines)?

Through GABA-A receptors (modulation of 5-HT and NE neurons in the CNS)

What are some side effects of benzodiazapines?

Few - very safe
- Disinhibition possible; caution or avoid use in
cases of aggression
- Paradoxical excitement and amnesia possible
- Idiosyncratic hepatotoxicity in cats possible with
diazepam; not yet seen with other BZDs
- Sedation, muscle relaxation and hyperphagia

What is a GABA antagonist and a reversal for BZD?

Flumazenil (Romazicon®, generic)
D/C: 0.01 mg/kg IV; may need to be repeated

How do antidepressants work in general?

- different mechanisms of action with the general property of altering primarily NE and serotonin (5-HT) levels in the CNS

5-HT

serotonin (5-hydroxy-tryptamine)

How do Tricyclic antidepressants work?

The TCA's inhibit re-uptake of NE and 5-HT
increasing their concentration in the brain
- Demonstrate cholinergic and adrenergic (α-1) blocking effects
- Adverse cardiovascular, GI, and urinary tract effects
- Contraindicated in KCS and glaucoma
 Some agents block histamine receptors

Clomipramine mechanism of action
(& Amitriptyline)
What type of drug are they?

Primarily blocks 5-HT re-uptake
Major metabolite desmethyl-clomipramine blocks NE reuptake
(Amitriptyline same, but more selective for 5-HT)
They are Tricyclic antidepressants

What are the most common side effects of SSRIs (Selective serotonin re-uptake inhibitors)

Sedation and anorexia are most common complaints

Serotonin syndrome

high doses or combinations produce an exaggerated response= alerted cognition (losing it, confusion, delusions, disorientation), behavioral alterations (agitation, restlessness). autonomic (fever, chills, sweat, diarrhea), neuromuscular (ataxia, hyperreflexia), usually resolves in 24-48 hours.

"Serotonin syndrome"- reported in humans; possible when SSRI's combined with what drugs?

- 5-HT agonists eg. Buspirone
- MAOI's; decrease metabolism of SSRI's
- TCA's; also possess 5-HT re-uptake effect
- 5-HT can also slow metabolism of TCA's
- OTC herbal supplements; St. John's Wort

Fluoxetine

It is an SSRI and can be used for canine separation anxiety

What can SSRIs be used for?

- Anxiolytic; separation and generalized anxiety disorder
- Panic disorder, storm and noise phobias
- Anticompulsive; eg. lick dermatitis
- Anti-aggression
- Urine spraying and psychogenic alopecia

Monoamine oxidase inhibitors - give an example and the use

Selegiline is approved for use in the dog for
cognitive dysfunction (senility)

What are the two groups of afferent fibres to the brain?

Level of spinal cord withdrawal and flexion
reflexes
2) Ascending pathways to higher brain centres

What is the basis for euthanasia?

To render the animal unconscious before the termination of cardiac or respiratory.
Respiratory or cardiac arrest should never occur before
unconsciousness in any species.
function and the final loss of brain function

What must be functional for pain to be experienced?

the cerebral cortex and sub cortical structures must be functional
(if they are not, there shouldn't be a corneal response & no coordinated movement)

Nerve impulse activity generated by nociceptors is conducted via nociceptor primary afferent fibres to the spinal cord or brainstem where it is transmitted to which general sets of neural networks?

1) nociceptive reflexes such as withdrawal and flexion that are mediated at the spinal level and the 2) ascending pain pathways to the brain for sensory processing (see pain physiology notes). This is an important distinction when evaluating euthanasia methods.

What are 4 major euthanasia methods

1. Hypoxia (CO, N2. Argon, and chloral hydrate)
2. Cardiac Arrest (KCl)
3. CNS depression (anesthetic gases, barbiturates)
4. Direct brain concussion or damage (gunshot, captive-bolt)

AVMA Acceptable Methods of Euthanasia in Dogs and Cats (2 acceptable, 5 conditionally acceptable)

Acceptable: Barbiturates, KCl in conjunction with general anesthesia
• Conditionally acceptable: inhalant anesthetics, CO, CO2, N2, Argon

Acceptable Methods of Euthanasia in Horses & Ruminants

• Acceptable: Barbiturates, KCl in conjunction with general anesthesia, penetrating captive bolt
• Conditionally acceptable: chloral hydrate (IV after sedation), gunshot, electrocution

Acceptable Methods of Euthanasia in Rodents and other small mammals

• Acceptable: Barbiturates, inhalant anesthetics, CO2, CO, KCl in conjunction with general anesthesia, microwave irradiation
• Conditionally acceptable: methoxyflurane, ether, N2, Argon, cervical dislocation (rats<200g), decapitation

What is T-61?

It is a non-barbiturate injectible euthanasia mixture containing a hypnotic (embutramid), a
neuromuscular junction blocker (mebezonium iodide, and a local anesthetic (tetracaine hydrochloride.

What can you do if you want have a hypotensive patient and you want to increase blood pressure?

- epinephrine if this is an extreme condition
- specific B2 such as Salbutamol which is a broncho-dilators.
- antihistamine
- NSAIDs for the fever

How fast should you give blood?

•Use 1mL/kg/hr ideally
or ¼ mL/kg in 15 minutes, and then proceed with necessary rates after this (10-30 ml/kg/hr). You can go up to shock rates if needed (10 mL/kg*hr is best)
If serious blood loss? Rate depends on hypotension. Should replace at 1:1 between 10 and 60 mL/kg*hr

At what amount of blood loss will an animal show signs of shock?

From 10-30% the animal can show signs of shock.

How much is 1 unit of blood?

1 unit of blood is around 450 mL

What is the likely acid base state for an animal in shock?

Shock = poor perfusion = anaerobic metabolism = lactic acid = metabolic acidosis

Neurogenic shock

Hypotensive and relatively hypovolemic situation resulting from the loss of sympathetic activity of vital functions from the brain. Happens with animals with an injury to the brain or spinal cord or due to stressneurogenic shock

What's good to keep in mind with older dogs?

They may be hypovolemic to begin with.
Need to be careful how fast or how slow you give fluids.
Too slow? Longer to stabalize
Too fast? Severe change to the system, need to balance the distribution between compartments (pulmonary edema, hemodilution- low PCV, TP).

What is the highest level of dehydration which is still subclinical?

Subclinical dehydration, usually <5%.

How fast should you give replacement fluids?

For a shock patient, 10-20 mL/kg given in 10-15 min to improve pressures
(this really means you are doing shock rate, since 10-20 mL/kg in 10-15 min is the same as saying 60-90 mL/kg/h)

If a patient has lost blood, how might you adjust the depth of anesthesia?

You would want to slightly increase the depth temporarily until you corrected for the blood loss. They will have fewer RBC, and so there is less O2 being carried and therefore less anesthetic is being passed into the blood. (check on this answer!!)

How does diarrhea affect acid/base balance?

With diarrhea, you will lose bicarbonate, so you will be in metabolic acidosis

What are the acute effects of metabolic acidosis?

pH is decreased
PCO2 is increased
HCO3- is decreased
Base excess is decreased

How does low cardiac output affect anesthesia depth?

Low cardiac output = higher lung concentrations of the inhalant = greater CNS depression being passed into the blood.

Strong Ion Difference

= Na + K - Cl
Metabolic acidosis: < 44
Metabolic alkalosis: > 44
(hint, low chloride (Cl-) is seen with cases of metabolic alkalosis)

Normosol-R

replacement crystalloid - contains gluconate and acetate as bicarbonate precursor (liver not needed for conversion); contains Mg but no Ca; useful in metabolic acidosis

If bicarbonate is high

Alkalotic
Not a lot of hydrogen atoms around, they are in high demand
Negative environment allows chloride to be lost, further push to bicarbonate to achieve electro neutrality

What does clear vomit usually mean for the acid/base balance?

Clear vomit = loss of gastric content = loss of chloride (Vomit with bile may indicate presence of bicarbonate but they still loose significant amounts of Cl)

What is a good replacement fluid if metabolically acidotic?

Since the chloride needs to be corrected, then NaCl 0.9% is ideal since it has 154 mEq/L of Cl- higher than other replacement solutions.
May need to add KCl to the fluids to avoid hypokalemia if the animal isn't eating

What fluid volume is needed for maintenance?

volume that is necessary for maintenance (2-4 mL/kg/h)
(will change if diarrhea etc)

What replacement fluids are good for metabolic acidosis?

N-R, PLA, LRS are all ideal for the acidosis.

What are some ways to treat hyperkalemia?

- Control acidosis: bicarbonate
- Help bring the K into the cell: dextrose ± insulin
- Crystalloids without K: NaCl 0.9%
- Maintain membrane potential by administering Calcium

What is shock?

- Inadequate oxygen delivery to the tissues
- A condition of severe hemodynamic and metabolic dysfunction characterized by reduced tissue perfusion, impaired oxygen delivery and inadequate cellular energy production.

10 clinical Signs of Shock

(5 to do with specifics, 5 to do with circulation)
1. Reduced level of mentation (head)
2. Increased respiratory rate and effort (lungs)
3. Tachycardia (or bradycardia in cats) (heart) + ionotropy
4. Decreased GI blood flow/ GI ulceration (gut)
5. Decreased urine production (kidneys)
6. Decreased blood pressure (circ)
7. Pale mucous membranes (circ)
8. Prolonged capillary refill time (circ)
9. Hypothermia / Cool extremities (circ)
10. Poor peripheral pulses (circ)

Where are epinephrine (adrenaline) & norepinephrine is released from?

adrenal glands & vasomotor endplates

Epinephrine and norepinephrine stimulate an increase in:

- Heart rate
- Cardiac contractility (ionotropy)
- Vasoconstriction (except distributive shock)
- Endocrine response to conserve water - not making much pee!!!

3 major endocrine responses to shock

1. Epinephrine and norepinephrine released from the adrenal glands & vasomotor endplates
- Immediate response
2. Antidiuretic hormone released from the pituitary
- To conserve water
- Response within minutes
3. Renin-Angiotensin-Aldosterone (RAS) system
- Stimulated to conserve water
- Response within hours

Shock is associated with what two general things?

Increased sympathetic output
Increased endocrine response

Angiotensin

A normal blood protein produced by the liver, angiotensin is converted to angiotensin I by renin (secreted by kidney when blood pressure falls). Angiotensin I is further converted to angiotensin II by ACE (angiotensin converting enzyme). Angiotensin II is a powerful systemic vasoconstrictor and stimulator of aldosterone release, both of which result in an increase in blood pressure.

Ace inhibitor

Drug that causes dilation of blood vessels and lowers blood pressure, prevents heart attacks, strokes, and congestive heart failure. ACE stands for angiotensin-converting enzyme, which normally constricts blood vessels. (e.g. benazepril)

What are the 3 stages of shock?

1. Early Compensatory Shock
2. Early Decompensatory Shock
3. Late Decompensatory Shock

Describe Early Compensatory Shock

• Appropriate cardiovascular compensation; physiologic responses successfully maintain normal (or exaggerated) blood pressure
•Clinical signs:
- Tachycardia, normal or elevated BP, normal or increased pulses, hyperemic mm, CRT< 1 sec
• Easily missed, animal essentially normal
• Result of baroreceptor mediated release of catecholamines
- successful increase in cardiac output (CO) & systemic vascular resistance (SVR)
• Heart rate is KEY
• Good response noted to volume replacement, good outcome

baroreceptor reflex

reflex that maintains appropriate blood pressure; responds to changes in pressure in the aorta and carotid arteries

Describe Early Decompensatory Shock

•The compensatory mechanisms have difficulty keeping up
•Associated with clinical signs of shock:
-Tachycardia, tachypnea, poor peripheral pulses, hypotension, prolonged CRT, pale mm, hypothermia, depressed mentation
•Redistribution of blood flow:
-Decreased blood flow to the kidneys, gut, skin & muscles.
•Prognosis - fair to good with immediate intervention

Describe Terminal Shock; irreversible

• Intrinsic compensatory mechanisms no longer provide oxygen delivery
• Clinical signs:
- Slowed heart rate (relative), pale cyanotic mm, absent CRT, weak / absent pulses, severe hypotension, hypothermia, mentally unresponsive / coma, no urine production.
• Generally irreversible
-Mitochondrial oxygen depletion
->40% blood loss results in irreversible shock and death if not treated effectively in under 2 hours

What are the 4 broad categories of shock? (Based on pathophysiologic mechanisms)

• Cardiogenic
• Hypovolemic
• Obstrucitve
• Distributive = vasodilatory = hyperdynamic
A patient can suffer from more than one category

Cardiogenic Shock

• Inadequate ventricular pump function
• May be due to:
-Arrhythmias
-Myocardial failure (ie. Cardiomyopathy)
-Valvular dysfunction (ie. Severe mitral valve disease)

Describe Hypovolemic Shock

•Profound decrease in intravascular (blood) volume
-Loss of 30-40% of circulating blood volume
OR
-10-15% dehydration
•Inadequate blood volume to deliver to vital organs
•Hypoperfusion

Etiology
-Blood loss / hemorrhage
•Internal
•External
-Dehydration
•Polyuria
•GI loss
•Burns
•3rd space losses (eg. ascites

How much blood loss will result in clinical signs of shock?

Expect at least 30% blood loss for clinical signs of shock to be present

Describe Non-Cardiogenic, Obstructive Shock

-Diminished cardiac output secondary to compression on the vascular system or obstruction to blood flow
-Blood can't get to the heart, therefore blood can't be ejected from the heart!
-Examples
•Gastric dilation volvolus
•Tension pneumothorax
•Pericardial tamponade
•Pulmonary embolism

Describe Distributive (Vasodilatory) Shock

-A fundamental maldistribution of blood flow; and an inability of tissues to extract oxygen
-Failure of the vascular smooth muscle to constrict
•Vasodilatory shock
•Normally 70% of blood volume is in the venous system
•Massive vasodilation leads to
-Massive pooling of blood.... decreased effective circulating blood volume .... decreased arterial BP
-Decreased systemic vascular resistance
-Initially increased cardiac output (little afterload for the heart to work against)
•Despite no lack of blood
-Fluids are necessary to fill the pool

How do the clinical Signs of Shock change when the shock is distributive?

(all circulatory signs of shock are opposite)
warm extremities
bounding peripheral pulses
injected mucous membranes (brick red)
Rapid capillary refill time (< 1 sec)
But:
- Normal to increased CO

What are some common causes for distributive (vasodilatory) shock?

-Sepsis (Endotoxemia)
-Anaphylaxis
-Drug reactions
-Massive trauma
-> But...final common pathway for decompensatory shock of any cause

How does sepsis cause vasodilatory shock?

There is a proinflammatory and procoagulant response to invading pathogens (bacteria) causing vasodilation

What are some proposed mechanisms for vascular failure?

-Vascular cell death due to prolonged hypotension
-Inadequate oxygen extraction by the tissues
-Increased prostaglandin vasodilatory activity
-Activation of Nitric Oxide
-Deficiency in ADH (vasopressin)

Nitric Oxide

A biologic effector molecule with a broad range of activities that, in macrophages, function as a potent microbicidal agent that kills ingested organisms. It is also a vasodilator, and is released by many small neurons; alters blood flow as well as neuronal activity.

Decompensation in distributive shock

• Decreased cardiac contractility
• Decreased CO
• Poor peripheral pulses
• Hypotension
• Pale mm
• Prolonged CRT > 2-3 seconds

At what point do you have severe hypotension? (without anesthesia)

- Systolic < 90 mmHg
- MAP <60 mmHg

Femoral pulses are absent once systolic BP gets how low?

< 40 mmHg

Peripheral pulses are absent once systolic BP gets how low?

Peripheral pulses (dorsal pedal, radial) are absent when systolic BP < 60 - 70 mmHg

What are good things to monitor when an animal is showing signs of shock?

Heart Rate & Rhythm
- pulse quality
- auscultate
- recommend an EKG
MM Colour and CRT
Blood pressure
Urine output (urine = good)
PCV & total solids (Baseline; 15minutes; 30-60 minutes)
Lactate production (< 2)
Blood gas analysis
Blood glucose/BUN
Central venous pressure

Describe Central venous pressure

• Normal CVP is 0-5 cmH2O
• The measurement is determined by venous return and right ventricular compliance
• CVP should be regarded as a trend. It is conventional to volume load an under-resuscitated patient to a target CVP of 8 - 10 cmH2O

What are 7 possible consequences of shock?

- GI hemorrhage / ulceration
- Acute renal failure
- Bacterial translocation
- Endotoxemia / sepsis
- Disseminated intravascular coagulation
(DIC) (Blood clotting abnormalities)
- Respiratory failure (ARDS)
- Multiple organ failure

8 basic signs associated with light anesthesia

- Eye rotates centrally, starts to rotate craniomedially
- Nystagmus
- Movement
- Mild jaw tone
- Brisk palpebral reflex
- Fast respiratory rate (tendency)
- Normotension
- May respond to surgical stimulation

8 basic signs associated with an adequate plan of anesthesia

- Eye rotates centrally (after being craniomedial) or lateral
- Slight or absent palpebral reflexes
- No movement
- Normo to hypotensive (due to drugs)
- Normo to hypercapnia

8 basic signs associated with deep anesthesia

- Eye rotates centrally (after being craniomedial)
- Corneal reflex is still present (should always be)
- No jaw tone
- Absent palpebral reflexes
- Slow respiratory rate (tendency)
- No movement
- No pain response
- Normo to hypotensive
- Normo to hypercapnia

How do you monitor circulation? (5 things)

Pulse
EKG
Cardiac Output
Auscultation
Blood pressure

How do you monitor ventilation? (5 things)

Thoracic wall movement
Reservoir bag movement
Auscultation
Capnography
Blood gasses

Capnography

a recording or display of the measurement of exhaled carbon dioxide concentrations.

How do you monitor oxygenation? (3 things)

Mucous membrane colour
Pulse oximetry
Blood gasses

Pulse oximetry

noninvasive method of estimating the percentage of oxygen saturation in the blood using an oximeter with a specialized probe attached to the skin at a site of arterial pulsation; used to monitor hypoxemia

What is the mortality for people/small animals/large animals under anesthesia?

People- 1 death for every 10,000 cases
Small animals- 1 / 250 to 1 / 1000
Large animals- 1 / 50 (emergency) to 1 / 100 (elective)

What is basic anesthetic monitoring you can using only your own senses? (7)

Pulse
Respiration
Mucous membranes
Reflexes (palpebral, corneal, nystagmus, pedal)
Relaxation (jaw tone)
Eye position
Temperature

Normal pulse rates for
Dog
Cat
Horse
Foal
Ruminants

Dog 60-140
Cat 100-160
Horse 28-40
Foal 60-90
Ruminants 50-80

What is abnormal in this anesthetized 24 kg dog?
Heart rate 109
BP 54/39, 44
C/O 2.8 L/min

HR - normal (60 - 140)
BP - hypotensive (anesthetized = 90/40, 60)
Cardiac Output - 116 mL/kg/min x

What do you look for in a pulse?

Quality (based on blood pressure & BP delta)
Rate
Rhythm

CO = ?

CO = SV x HR
Stroke volume x Heart rate
CO = BP/VR
Blood Pressure / Vascular resistance

BP = ?

BP = CO x VR or BP = (HR x SV) x VR
Cardiac output x Vascular resistance

What can you give a dog that has a low heart rate under anesthesia?

atropine or glycopyrolate, or reduce the plane of anesthesia if possible.

If you want to increase more stroke volume and enhance contractility (heart rate is normal to high), what might you give a patient?

Inotropes -> (dobutamine, dopamine, norepinephrine)

Inotrope

An agent that changes the force or contractility of the heart. A positive inotrope will increase contractility.

What is the important to note on an EKG?

- For every P wave there should be a QRS after it
- P may be negative, that is ok, but it should be present

What could you use as an antiarrythmetic?

Inject lidocaine

What are 2 indirect methods and one direct method of measuring blood pressure

Indirect:
1. Doppler (systolic)
2. Oscillometric
Direct: catheterization of an artery

What is good to note about doppler usage in cats and small dogs?

Pressure obtained underestimates the SBP (systolic) - > Add 15 mmHg to the value obtained, or Interpret the value as MBP (mean)

What are the optimal & acceptable blood pressures in adult animals? (& neonates)

140(or 120?)/80 M:100 (Neonates 100/60 M:75)
90/40 M:60 (Neonates 75/40 M:50)

How do vasoconstrictors effect BP and CO?

increase BP
can decrease CO

How do vasodilators Vasodilators effect BP and CO?

- can decrease BP
- can increase CO

What are some methods used in veterinary medicine to measure cardiac output?

- lithium (LiDCO)
- thermodilution (TDCO)
- partial rebreathing of CO2 (NICO)

VE = ?
Mean ventilation

VE = VT x RR
Mean ventilation = Tidal volume x Rate

Normal CO2 levels in blood

around 40 mmHg

Normal respiration for
Dog
Cat
Horse
Foal
Ruminants

Dog 6 - 40
Cat 10 - 40
Horse 4 - 12 (8-16 in Clin Med)
Foal 6 - 20
Ruminants 6-40 (10 - 30 in Clin Med)

What should you monitor during anesthethesia w.r.t. ventilation/respiration? (4)

Rate and rhythm
Arterial blood gases
Capnography (CO2)
Pulse Oximetry (O2)

What is the best way of assessing the efficiency of ventilation?

Through the measurement of PaCO2 or end-tidal
CO2 monitoring

How does the end-tidal CO2 usually compare to the PaCO2?

Usually the end-tidal CO2 is 5-10 mm Hg lower than the PaCO2 (10 in large, 5 in small animals)

How does a build up in systemic CO2 change the respiration rate?

As we build up CO2 in our system, it makes us breath faster and deeper
(Under anesthesia this effect is decreased)

What do the following mucous membrane colours mean?
1. White
2. Blue
3. Bright red
4. Yellow

1. Pale or white membranes due to anemia, vasoconstriction, hypotension
2. Cyanosis due to hypoxemia from lung disease, low inspired oxygen, endobronchial intubation, depressed cardiovascular function
Cyanosis only manifests if the reduced hemoglobin concentration is higher than 5-8 g/dL.
Therefore, cyanosis could go unnoticed in anemic patients
3. Bright red due to hypercapnia, septic shock
4. Icteric due to hepatic disease

Oximetry

process of measuring the oxygen saturation of blood

What is the normal saturation of hemoglobin with room air?

97-98%
Under anesthesia we might bring that up to 100
Values under 90% saturation are going to have a big slope.

What is the normal PaO2 range at sea level?

Normal PaO2 at sea level is 90-100mmHg

Name 8 things which affect oximetry (blood saturation of O2)

1. Heart rate
2. Hypotension
3. Pigment
4. Hypothermia
5. Vasoconstriction/dilation
6. Dry mucous membranes
7. Compression at the site
8. Anemia and dysfunctional hemoglobin

Oximetry tends to _____ the arterial saturation of hemoglobin

underestimate

What is Isoflurane's
1 .MAC
2. Solubility Blood:Gas

MAC = 1.28-1.63
Solubility Blood:Gas = 1.4

hypercapnia

the presence of an abnormally high level of carbon dioxide in the circulating blood

Which drugs used during anesthesia can dilate the pupil?

Atropine
Ketamine

hypercapnia

the presence of an abnormally high level of carbon dioxide in the circulating blood

Define epilepsy

Recurrent, spontaneous impairment of brain function manifested as episodic:
- loss of consciousness,
- abnormal motor phenomena,
- psychic or sensory disturbances

Define seizure

a sudden, intense electrical discharge in the cerebrum. It can be thought of as a transient "de-cerebration" in that goal-directed behaviours are not possible during a seizure. The clinical presentation varies from twitching to "status epilepticus"

Define convulsion

a generalized tonic-clonic motor seizure.

Define clonus and tonus

Clonus means alternating, rapid contraction and relaxation (e.g. paddling), whereas tonus means continual contraction.

Status epilepticus

series of seizures occurring in rapid succession, without intervening periods of consciousness, that lasts 30 minutes or more. Status epilepticus can cause brain damage and may be fatal.

Absence seizures (or petit mal)

Mild
- sudden momentary loss of consciousness
- limited twitching

Generalized tonic-clonic seizures

Severe
- sudden unconsciousness & generalized convulsions
- loss of bladder and bowel control

Two anticonvulsant drugs that are commonly used in veterinary medicine to prevent

phenobarbital
potassium bromide (KBr).

Anticonvulsant that is used in most cases to stop seizures that are in progress

Diazepam

If phenobarbital and potassium bromide aren't effective for treatment of cases, what human drug may be used?

Levetiracetam (Keppra®) is one of the preferred add-on drugs for refractory cases

Pros of using phenobarbital for controlling seizures

- effective
- inexpensive
- effective for long-term therapy in cats (and dogs)

How does phenobarbital work?

- stimulates GABA receptors in the brain, inhibiting action potential generation
(It differs from other barbiturates in that it can inhibit seizures at concentrations lower than those that produce anesthesia.)

What would you keep in mind when prescribing phenobarbital? (5 things)

- long and variable half-life
- induces cytochrome P450 enzyme activity, causing drug tolerance & decreasing half life
- Over the course of the animal's life you will likely have to give a hepatotoxic dose in order to achieve the necessary effects
- blood levels must be monitored
- NEVER STOP ANTICONVULSANT THERAPY SUDDENLY -> seizures! Instead, reduce the blood levels by about 10% every 3 weeks (takes months).

At the onset of therapy phenobarbital causes what?

- sedation, which varies widely from animal to animal
- polydipsia/polyuria, polyphagia, vomiting
(Note: these effects usually subside after about two or three weeks)

What are 3 rare but possible side-effects of phenobarbital?

1. hepatocutaneous syndrome (superficial necrolytic dermatitis in some dogs on high dose therapy)
2. idiosyncratic anemia
3. potentially fatal pancreatic adverse events (possible with either phenobarbital or KBr or combination therapy)

What is the mechanism of potassium bromide?

Br- ions enter cells through chloride channels, setting up a new equilibrium potential that hyperpolarizes the plasma membranes of neurons

What are the pros of potassium bromide

- cheap
- good anti-epileptic effects
- doesn't lose its effectiveness
- not metabolized by the liver

What are the cons of potassium bromide?

- very long half-life taking months to stabilize dose
- narrow therapeutic index
- possible CNS depression & pancreatic adverse effects
- vomiting can last for many months
- cats get something resembling allergic airway disease

What would you keep in mind when prescribing potassium bromide? (5 things)

Chloride levels will probably appear higher than they are
Eating lots of salt (Na+) may cause a loss of Br- (and Cl-) so this may lead to an increase in seizure activity
You not only have to be careful of the dose (small therapeutic index) but also have to spend months finding the right dose

Why isn't diazepam used for the life-long control of seizures?

1) its short half-life in dogs would require that it be administered 3-4 times per day
2) tolerance often develops rapidly (over 1-2 months), making it ineffective for seizure control as well as in emergencies to stop seizures.

How would give diazepam to a seizing dog?

1. per rectum via syringe & teat cannula
2. ideally give at prodromal phase (or first sign)
3. repeat at 20 and 40 minutes even if no seizure has occurred

prodromal phase

Initial phase where symptoms develop instantaneously, the longer the worse

What do you do if diazepam fails to stop a seizure?

You should then consult an emergency medicine textbook; possible approaches include IV phenobarbital or propofol if IV access is possible, or masking the animal down with an inhalant.

Give some examples of drugs that can lower the seizure threshold

beta lactam
fluoroquinolone antimicrobials

Name some other anti-convulscents (other than phenobarbital and KBr)

LEVETIRACETAM (Keppra®): requires TID administration; expensive (>$200/month); a common alternative or add-on drug in dogs that do not respond to phenobarbital or KBr alone or in combination; no significant adverse effects yet documented; mechanism of action uncertain.
PRIMIDONE: no more effective than phenobarbital, but more hepatotoxic; an option in some dogs that do not respond to phenobarbital
PHENYTOIN: half-life in dogs too short to be useful (3-4 hr) - would require TID administration
(for life!); adverse effects common; not recommended for dogs or cats
CLONAZEPAM: effectiveness wears off after 1-2 months
FELBAMATE: requires TID administration; expensive (~$200/month)
GABAPENTIN: requires TID administration; oral formulation contains xylitol which is toxic to
dogs; used in combination with other drugs in some refractory dogs and cats
ZONISAMIDE: sulphonamide-related drug, BID administration in dogs; expensive (>$200/month)
but sometimes used in combination therapy in refractory dogs
TOPIRAMATE: BID; expensive (>$200/month)

pH
Carnivores/Herbivores

Carnivores: 7.26-7.38
Herbivores: 7.4-7.43

PaCO2
Carnivores/Herbivores

Carnivores: 40
Herbivores: 40

See More

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