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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)
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
- 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
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
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
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
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
What can SSRIs be used for?
- Anxiolytic; separation and generalized anxiety disorder
- Panic disorder, storm and noise phobias
- Anticompulsive; eg. lick dermatitis
- 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
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.
- 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.
What is the likely acid base state for an animal in shock?
Shock = poor perfusion = anaerobic metabolism = lactic acid = metabolic acidosis
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)
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
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
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.
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
- 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
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)
• Distributive = vasodilatory = hyperdynamic
A patient can suffer from more than one category
• Inadequate ventricular pump function
• May be due to:
-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
•Inadequate blood volume to deliver to vital organs
-Blood loss / hemorrhage
•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!
•Gastric dilation volvolus
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
•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)
bounding peripheral pulses
injected mucous membranes (brick red)
Rapid capillary refill time (< 1 sec)
- Normal to increased CO
What are some common causes for distributive (vasodilatory) shock?
-> 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)
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
• Pale mm
• Prolonged CRT > 2-3 seconds
At what point do you have severe hypotension? (without anesthesia)
- Systolic < 90 mmHg
- MAP <60 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
- recommend an EKG
MM Colour and CRT
Urine output (urine = good)
PCV & total solids (Baseline; 15minutes; 30-60 minutes)
Lactate production (< 2)
Blood gas analysis
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
- Mild jaw tone
- Brisk palpebral reflex
- Fast respiratory rate (tendency)
- 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 ventilation? (5 things)
Thoracic wall movement
Reservoir bag movement
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)
Reflexes (palpebral, corneal, nystagmus, pedal)
Relaxation (jaw tone)
Normal pulse rates for
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 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)
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 are 2 indirect methods and one direct method of measuring blood pressure
1. Doppler (systolic)
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)
What are some methods used in veterinary medicine to measure cardiac output?
- lithium (LiDCO)
- thermodilution (TDCO)
- partial rebreathing of CO2 (NICO)
Normal respiration for
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
Pulse Oximetry (O2)
What is the best way of assessing the efficiency of ventilation?
Through the measurement of PaCO2 or end-tidal
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?
3. Bright red
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
What is the normal saturation of hemoglobin with room air?
Under anesthesia we might bring that up to 100
Values under 90% saturation are going to have a big slope.
Name 8 things which affect oximetry (blood saturation of O2)
1. Heart rate
6. Dry mucous membranes
7. Compression at the site
8. Anemia and dysfunctional hemoglobin
Recurrent, spontaneous impairment of brain function manifested as episodic:
- loss of consciousness,
- abnormal motor phenomena,
- psychic or sensory disturbances
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 clonus and tonus
Clonus means alternating, rapid contraction and relaxation (e.g. paddling), whereas tonus means continual contraction.
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.
Generalized tonic-clonic seizures
- sudden unconsciousness & generalized convulsions
- loss of bladder and bowel control
Two anticonvulsant drugs that are commonly used in veterinary medicine to prevent
potassium bromide (KBr).
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 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
- 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
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
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)
What is the normal pulse rates for
Normal respiration for
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 are the optimal & acceptable blood pressures in adult animals? (& neonates)
Optimal: 140/80 M:100 (Neonates 100/60 M:75) -> note, some say 120/80 M:100
Acceptable: 90/40 M:60 (Neonates 75/40 M:50)
What are the requirements for
•Cerebral perfusion requires MAP > 40 mmHg
•Renal perfusion requires MAP > 60 mmHg
•Muscle perfusion requires MAP > 70 mmHG
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