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Clinical Foundations Course > Anaesthesia > Flashcards

Anaesthesia Flashcards

1
Q

What is anaesthesia and describe types of anaesthesia.

A
  • Anaesthesia is a state in which there is lack of response to stimulus
  • Types of anaesthesia
    • General: A state of unconsciousness over the entire body
    • Localized: Insensibilty caused by distrupting the nerve conduction for any region of the body. Does not cause unconsciouness.
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2
Q

What are the aims of anesthesia in veterinary practice and how can they be achieved?

A
  • Aims of anaesthesia:
    • Unconsciousness
    • Immobility
    • Good operating conditions for patient and staff
  • The aims of anaesthesia can be achieved using the anaesthetic triad:
    • Narcosis
    • Analgesia
    • Muscle relaxation
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3
Q

What are the phases of anaethesia?

A
  • Pre-medication
  • Induction
  • Maintenance
  • Recovery
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4
Q

Which species are at relatively higher risk for anaesthesia?

A
  • Small mammals
  • Birds
  • Horses
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5
Q

How does age impact the risk of anaesthesia?

A
  • Younger animals are at higher risk of anaesthesia complications
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6
Q

How does animal morphology affect anaesthesia risk?

A
  • Animals with a lot of fat may have pressure on internal organs during anaesthesia
  • Animals with low body fat may become cold during anaesthesia. Low body fat may also be indicative of an underlying metabolic problem
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7
Q

What history questions must be asked in performing an anesthetic safety assessment?

A
  • Has the animal had previous anaesthetics? If so, were there any unusual responses/adverse events?
  • How old is the animal?
  • Is there any history of other diseases?
  • Any concurrent medication?
  • Is this aniamal exercise tolerant?
  • Is the animal vomiting or have diarrhoea?
  • Is the animal eating and drinking properly?
  • Does the animal have any coughing or respiratory abnormalities?
  • When did the animal last eat?
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8
Q

Describe the pre-anaesthetic exam.

A
  • Classify species, breed, animal morpholgy and age
  • Examine the following for abnormalities
    • Eyes
    • Mucous membranes
    • Skin tenting tone
    • Condition of the body in terms of swelling (oedema) or abnormalities
    • Lymph nodes/swellings retropharyngeal or neck areas
    • Jugular vein(s)
    • Heart rate, rhythm
    • Lung sounds
    • Pulse rate
    • Rectal temperature
    • Weight
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9
Q

What are the anaesthetic risks for brachycephalic dogs?

A

Brachycephalic dogs have airway problems

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10
Q

What are the anaesthetic risks for dogs with protuberant eyes?

A

Risk of globe proptosis

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11
Q

What are the anaesthetic risks associated with giant dog breeds?

A

Dilated cardiomyopathy and/or atrial fibrillation

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12
Q

Describe the American Society of Anesthesiologists (ASA) patient status classifcation system.

A
  • ASA I - Normal, healthy animal
  • ASA II - Mild systemic disease or impairment
  • ASA III - More severe systemic disease which is well-maintained by treatment
  • ASA IV - Severe systemic disease which is not maintained by treatment
  • ASA V - Moribund, unlikely to survive 24 hours
  • E - Emergency (added to any classification if the anaesthetic is an emergency)
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13
Q

What are the reasons for providing anaesthesia in veterinary practice?

A
  • Humane/moral reasons
  • Gives the ability to perform procedures safely and effectively
  • Legal requirments
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14
Q

In what ways can carbon dioxide be removed from an anaesthetic system? What are the advantages and disadvantages of the different methods?

A
  • Re-breathing
    • Carbon dioxide is removed by soda lyme crystrals in the system
    • Advantages
      • Good economy of fresh anaesthetic gas and anaesthetic agents
      • Warms and humidifies insipired air
      • Reduces contamination of atmophere by waste anaesthetic gases
    • Disadvantages
      • Is expensive to purchase
      • Denitrogenation required
      • Slow changes in anaesthetic concentration of insipired volatile agents in low flow systems
      • The concentrations of anaesthetic breathed by the patient will not be the same as that that is delivered by the vaporizer
      • Valves increase resistance to breathing
      • Soda lyme canister increases resistance, contributes to dead space and may be inhaled by the patient
      • Nitrous oxide may only be used when the fraction of inspired oxygen in a gas mixture can be monitored.
  • Non-rebreathing
    • Carbon dioxide is eliminated by high fresh gas flow
    • Advantages
      • Economical price purchase
      • Simple construction
      • Rapid changes in concentration of volatile agents is possilble
      • The concentration of anaesthetic breathed by the patient is the same that is delivered by the vaporizer
      • Low resistance to breathing
    • Disadvantages
      • High fresh gas flow required along with anaethetic agents
      • Increased potential for contamination of atmosphere by toxic gases
      • Dry, cold gases are delievered to the patient
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15
Q

Why is denitrogenation required for rebreathing systems?

A

Room air is composed of 79% nitrogen and at the start of the anaesthetic period patients expire this gas. If the nitrogen is not removed from the rebreathing system it will recirculate within the system and dilute the oxygen, anaesthetic gases and vapours.

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16
Q

Describe the oxygen flow requirments for different anaesthetic systems.

A
  • Non-rebreathing system
    • Anaesthetic provided to match the animal’s minute volume
    • Oxygen provided as Respiratory minute volume * [Number depending on efficiency of system used]
      • ~200 mls/kg/min * 1
  • Re-breathing system
    • Anaesthetic provided to match the animal’s metabolic requirment
    • Oxygen supplied for
      • 20 kg small animal at ~10 mls/kg/min = 200 mls/minute
      • 500 kg large animal at 5 mls/kg/min = 2.5 litres/minute
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17
Q

Describe Diazepam.

A
  • Benzodiazepine
    • Benzodiazepines are positive allosteric modulators of the GABA type A receptors (GABAA). The GABAA receptors are ligand-gated chloride-selective ion channels that are activated by GABA, the major inhibitory neurotransmitter in the brain. Binding of benzodiazepines to this receptor complex promotes binding of GABA, which in turn increases the total conduction of chloride ions across the neuronal cell membrane. This increased chloride ion influx hyperpolarizes the neuron’s membrane potential. As a result, the difference between resting potential and threshold potential is increased and firing is less likely
  • Causes tranquilization and sedation
  • Minimal cardiovascular restrictive effects or respiratory effects
  • Induces muscle relaxation
  • Can cause panic-like state in horses
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18
Q

Describe alpha-2 agonists as well as the advantages/disadvantages of their use.

A
  • Act on pre- and post-synaptic alpha-2 adrenoreceptors
  • Alpha-2 receptors are found in the CNS and peripherally
  • Produces central and peripheral cardiovascular effects
  • Dose-dependent sedation
  • Has analgesic properties
  • Advantages
    • Rapid reversal sedation
    • Analgesia
    • Dramatic reduction in requirments of other drugs
    • Conveniant
    • Licenced products available
  • Disadvantages
    • Marked bradycardia (atrioventricula block common and may increase risk of other arrhythmias)
    • Uterine contractions (with xylazine)
    • Reduced gut motility
    • Slowed respiratory rate
    • Peripheral vasoconstriction
    • High glucose, high glucose urea and increased amount of urine produced
    • Mydriasis
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19
Q

Describe acepromazine.

A
  • Phenothiazine
  • Blocks alpha-1 (dopamine agonist), causing vasodilation and lower blood pressure
  • Good anxiolysis
  • May cause priapism in horses causing penile damage
  • Very well absorbed by sub-cutaneous and intra-muscular doses
  • Can be administered orally but is not very well absorbed
  • Can keep animals calm during recovery
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20
Q

What are the popular alpha-2 agonists for horses in order of weakest-acting to most potent-acting?

A
  • Romifidine
  • Detomidine
  • Xylazine
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21
Q

Describe the reversal of alpha-2 agonist sedation?

A
  • Atipamazole is given (usually IM) as an antagonist used to counteract the effects of alpha-2 agonist drugs. It should be given when there is only alpha-2 agonist drug on-board the animal
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22
Q

Describe the path of an injected anaesthetic drug in a patient.

A
  • Be absorbed in a vein
  • Travel in the blood to, and through the right side of the heart
  • Traverse the lungs
  • Travel through the left side of the heart
  • Travel in arterial blood to the effect site
  • Cross the blood-brain barrier
  • is metabolised and excreted
    • Metabolism occurs mainly in the liver where a more water-soluble molecule is created which can be more easily excreted by the kidneys
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23
Q

What factors determine the rate of uptake for an inhaled anaesthetic drug?

A
  • Concentration of anaesthetic adminstered
  • Alveolar ventilation rate
  • Cardiac output
  • Uptake of anaesthetic from tissues
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24
Q

How can an inhaled anaesthetic be monitored in terms of the concentration reaching the nervous tissue?

A

The brain concentration of an inhaled anaesthetic is approximately the same as alveolar concentration.

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25
Q

Describe Propofol and its clinical use.

A
  • General anaesthetic
  • Acts through potentiation of GABAA receptor activity, thereby slowing the channel-closing time, and also acting as a sodium channel blocker.
  • Licensed in cats and dogs
  • Given intravenously as single bolus injection with 30-60 seconds to effect
  • Highly lipid soluble and causes rapid induction
  • Pre-medication with sedatives recommended
  • Highly protein bound
  • Causes hyporeflexia and muscle relaxation (allow endotracheal intubation)
  • Recovery complete in 20-30 minutes
  • Causes dose-dependent respiratory depression
  • Causes dose-dependent cardiovascular depression
  • Causes bronchodilation
  • Crosses placenta
  • Metabolized to gluconurides derivatives and quinol sulfate
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26
Q

Which animal species is at risk when using propofol and why?

A

Propofol metabolism and clearance occurs in the liver and extra-hepatically forming quiol sulfate and glucoronide conjugates. Cats lack enzymes to conjugate glucoronides and have problems metabolizing triglycerides (struggle to metabolise lipid carrier). Cats administered propofol are at risk of accumulation causing possible oxidative injury to red blood cells (Heinz bodies).

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27
Q

Describe Aflaxalone and its clinical use.

A
  • General anaesthetic
  • Neuroactive steroid molecule causing muscle relaxation
  • Licensed in dogs and cats
  • Given as single bolus injection given over 30-60 seconds to effect
  • Highly lipid soluble allowing rapid induction (pre-medication with sedatives are recommended)
  • Excellent pharmacokinetic properties for rapid metabolism and clearance in the liver
  • Can give repeat doses or infusion in dogs and cats
  • Causes dose-dependent respiratory depression and post-induction apoea
  • Causes dose-dependent cardiovascular depression (Systemic vascular resistance, reduced stroke volume and reduced cardiac output)
  • Decreases intracranial pressure
  • Crosses placenta
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28
Q

Describe the ketamine and its clinical use.

A
  • General anaesthetic
  • Non-competitive NMDA antagonist
  • Lipid and water soluble
  • Analgesic and antihyperalgesic effects (dose-dependent)
  • Direct negative inotropic effects
  • To be used in combination with sedatives
  • Maintains cranial nerve and laryngeal reflexes
  • Metabolized in liver
  • Increases intraocular pressure
  • Increases sympathetic tone
  • Increases myocardial oxygen demand, cerebral metabolic oxygen requirment and causes bronchodilation
29
Q

Describe thiopental and its clinical use.

A
  • Barbiturate
  • Not licensed for veterianry use in the UK
  • Short-acting anasthetic
  • Causes dose-dependent respiratory depression
  • Causes cardiovascular depression
  • Decreases intracranial pressure and is therefore useful for cases with head trauma and seizure
  • Crosses placenta
  • Provides inadequate depth of anaesthesia in large animals
30
Q

Describe pentobarbital and its clincal use.

A
  • Barbiturate
  • Long-acting
  • Licensed for euthanasia use
  • Not prepared in sterile formulas
31
Q

What is the minimum alveolar concentration (MAC)?

A

The amount of inhalation anaesthetic required required to prevent movement in response to a painful stimulus in 50% of the subjects tested

32
Q

Give examples of the effects of volatile anaesthetic agents?

A
  • Unconsciousness
  • Immobility
  • Cardiovacular despression
  • Respiratory depression
  • Reduction of hepatic and renal flow
  • Reduction of insulin secretion
  • Increased cerebral perfusion
  • Decreased cerebral metabolism
33
Q

Describe isoflurane and its clinical use.

A
  • Volatile anaesthetic agent
  • Allows for fast recovery
  • Irritates mucus membranes
  • Causes decreased blood pressure and vascular resistance
  • Allows for rapid recovery
34
Q

Describe sevoflurane and its clinical use.

A
  • Volatile anaesthetic agent
  • Allows rapid induction of anaesthesia, recovery from anaesthesia, and changes in anaesthetic depth due to low solubility in blood
35
Q

Describe desflurane and its clinical use.

A
  • Inhalational anaesthetic
  • Requires headed vaporizer
  • Boiling point is close to room temperature
36
Q

Describe the relationship between inhalational anaesthetic solubility and rapidity of induction.

A
  • Speed of anaesthetic induction and recovery is slower for more soluble agents as a greater amount of the inhalational agent has to dissolve into the blood before it saturates the blood and can then exert a pressure in the brain
37
Q

Describe nitrous oxide and its clinical use.

A
  • Non-irritant
  • Lowers the minumum alveolar concentration (MAC) of other volatile inhalational anaesthetics
38
Q

How is the second gas effect used to facilitate anaesthesia?

A
  • Based on the fact that the uptake of nitrous oxide is rapid because it is insoluble in blood and leads to relative increases in alveolar concentration of remaining inhaled gases. The initial rapid absorption or removal of N2O from the alveoli results in a relative increase in concentration of the gases (volatile agent and oxygen) which are left behind in the alveoli. This enhances the rate of rise of alveolar, and then brain, anaesthetic agent concentration to hasten anaesthetic induction
39
Q

What quality of nitrous oxide must be compensated for when the anaesthetic machine is turned off? How is this done? What other precautions must be taken when using nitrous oxide for this reason?

A
  • Nitrous oxide will leave tissues quickly causing dilution of alveolar oxygen concentration and can cause hypercapnea
  • Supplementation of oxygen for 5-10 minutes recommended after turning off anaesthetic machine
  • Nitrous oxide enters air filled spaces more rapidly than nitrogen leaves. Care must be taken to avoid dangerous accumulation of nitrous oxide gas in gas-filled spaces in the body. It is recommended that use of nitrous oxide be avoided in situations such as closed pneumothorax or air embolus (where gas pressure may build up with no communication to atmosphere).
40
Q

List the advantages and disadvantages of inhalational anaethetic agents.

A

Advantages:

  • Increased fraction of oxygen is provided
  • Airway protection by endotracheal tube
  • Rapid induction and recovery from general anaesthesia and rapid change of anaesthetic depth

Disadvantages:

  • Additional equipment required for administration (Anaesthetic machine, vaporiser, scavenging)
  • Control of waste gases is required to avoid personnel exposure
  • Toxic or harmful components may be produced by contact with soda lime or by liver metabolism
41
Q

Describe the nociceptive pathway.

A
  • Pain impusle travels via Unmyelinated slow (C-fibres) and myelinated fast (Ad-fibres) and terminate in superficial dorsal horn of spinal cord. Nociceptive cell bodies are located in Dorsal Root Ganglia.
  • Pain fibres syapse with the spinothalamic tract on the contralateral side of the pain stimulus.
  • The impulse traveling via the spinothalamic tract sypases with the thalamus
  • The thalamus syapses with the cerebral cortex
42
Q

By what mechanisms do analgesics affect the percetion of pain?

A
  • Act at the site of injury
  • Alter nerve conduction
  • Modify transmission in the dorsal horn
  • Affect the central component and the emotional aspects of pain
43
Q

Describe the action of opioids at the cellular level.

A
  • Opioids act as ligands to opioid receptors on pre-synaptic neurons in the central nervous system
    • Opioid receptors are coupled with inhibitory G-proteins and their activation has a number of actions including: closing of voltage sensitive calcium channels; stimulation of potassium efflux leading to hyperpolarization and reduced cyclic adenosine monophosphate production. Overall, the effect is a reduction in neuronal cell excitability that in turn results in membrane hyperpolarization and decreased transmission of nervous impulses
  • Inhibit neurotransmitter substance P which is related to the transmission of nociceptive signals
44
Q

What is sedation?

A

Reduction of agitation or irritability

45
Q

Describe Fentanyl and its clinical use.

A
  • Opioid
  • Schedule 2 controlled drug licensed for veterinary use
  • full µ receptor agonist (targeting supraspinal and spinal areas)
  • injection provides rapid onset of analgesia with effect duration of 15-20 minutes after administration
    • Good for use for a quick, painful procedure
  • Transdermal administration forms a subcutaneous depot and provides 4 days’ worth of analgesia
    • Requires online training before use
46
Q

Describe buprenorphine and its clinical use.

A
  • Opioid
  • Schedule 3 controlled drug licenced for veterinary use
  • Partial µ agonist with high affinity for µ receptor
    • Can be used for partial reversal of full µ agonist
  • Has a slow onset and long duration
47
Q

Describe Naloxon and its clinical use.

A
  • Opioid
  • Antagonist of endogenous opioids
  • Short duration of action
  • For use in emergencies and caesarean operations
48
Q

Describe butorphenol and its clinical use.

A
  • Prescription-only medication licensed for veterinary use
  • Synthetic partial opioid k-agonist and µ-antagonist
  • Onset takes 15 minutes and effect lasts 2-4 hours
  • Effective anti-tussive
49
Q

What is the mechanism of action of local anaesthetic agents?

A

Binds to cellular sodium channels to prevent depolarization and propagation of nociceptive action potential

50
Q

Describe the chemical structure of local anaesthetic agents.

A
  • Benzene ring
    • Allows molecule to cross nerve cell membrane
  • Hyrophilic unit
    • Allows water solubility, interaction with sodium channels, and ionization
  • Hydrocarbon chain- either ester-linked or amide-linked
    • Ester group provides poor tissue penetration and is rapidly metabolized
    • Amide group provides good tissue penetration
51
Q

What impact does lipid solubility have on an anaesthetic drug?

A
  • Determines the potency of drug and amount of drug needed to induce effect
  • Higher lipid solubility allows for higher potentcy
    • Will be attracted to nervous material in the body rather than the blood
  • Higher lipid solubility causes a slower on-set
  • Higher lipid solubility allows for sequestration of drug into lipid-soluble compartment which allows for longer duration of effect
52
Q

What impact does protein-binding have on local anaesthetic drugs?

A
  • Agents will bind to albumin and α-acid glycoprotein (acute phase protein)
  • Only unbound drug will have clinical effect
  • Highly bound proteins will have a slower elimination
  • More lipid-soluble agents show higher degrees of protein-binding
53
Q

What impact does tissue pH have on local anaesthetic agents?

A

Local anaesthetic agents are weak bases that are able to best infiltrate tissue when unioninzed (under less acidic conditions). A lower pH tissue, such as during an inflammatory process, will cause the drug molecule to become ionized and inhibit its absorption into tissue.

54
Q

Describe N-Methyl-D-aspartate (NMDA) agonist and its clinical use. Give an example of this drug

A
  • NMDA agonists block the NMDA receptors
    • NMDA receptors are found in the CNS and are ligand receptors for excitatory animo acids (EAA), namely glutamate and aspartate.
  • Ketamine
  • Clinical use
    • For starting and maintaining anesthesia
    • Cranial nerve reflexes maintained
    • Laryngeal reflexes maintained
    • Increased intracranial pressure, cerebral metabolic oxygen requirement and intraocular pressure
    • Myadriasis
    • Increased sympathetic tone
    • Direct negative inotropic effect
    • Minimal respiratory depression
    • Laryngeal and pharyngeal reflexes maintained
    • Can be used in subanaesthetic doses for analgesia
    • Can be administered to conscious animals without any effects on mentation
55
Q

What are some effects of increased respiratory resistance?

A
  • Hypoventilation
    • Causing hypercapnia
  • Increased work of breathing
    • Causing increased VO2
  • Inspiratory reserve promotes atelectasis (partial collapse or incomplete inflation of the lung)
  • Causing hypoxia
  • Expiratory resistance creates Positive end-expiratory pressure (PEEP; pressure in the lungs (alveolar pressure) above atmospheric pressure (the pressure outside of the body) that exists at the end of expiration)
    • Decreases QT (ventilation perfusion)
56
Q

What is Harmann’s solution? What are its indications?

A
  • Also known as lactated Ringer’s solution
  • Isotonic replacement solution
  • Electrolyte composition similar to plasma which contains Na, Cl, K, Ca, and lactate
  • Indicated in electrolyte losses (especially with acidosis)
    • Intestinal losses (diarrhoea)
    • Diabetic ketoacidosis
    • Renal failure
57
Q

What is a Colloid Solution Infusion? What are its indications?

A
  • Natural or synthetic fluid composed of large macromolecules which increase oncotic pressure
  • Uses
    • Inceases volume
    • Oncotic support
58
Q

Give examples of neuromuscular blocking agents.

A
  • Suxamethonium (Succynyl Choline)
    • Facilitates endotracheal intubation
  • Atracurium
  • Vecuronium
59
Q

List some possible reasons for bradycardia. How can this condition be treated?

A
  • Reasons for bradycardia
    • Drug Overdose
    • Terminal hypoxia
      • From failing to change the soda lyme, for example
    • Terminal hypercapnea
    • Hyperkalaemia
    • Vagal stimulation
    • Hypothermia
    • Hypoglycaemia
  • Possible methods to treat bradicardia
    • Decrease potassium infusion
    • Atropine use
    • Warming of patient
    • 50% dextrose
60
Q

List some possible reasons for tachycardia. How can this condition be treated?

A
  • Possible reasons for tachycardia
    • inadequate anaesthesia or analgesia;
    • hypoxia;
    • hypercapnia;
    • hypotension;
    • drugs: parasympatholytic drugs e.g. atropine, β 1 agonist drugs, e.g. epinephrine, and dobutamine, β 2 agonist drugs, e.g. clenbuterol (horses);
    • hypothermia;
    • hyperthermia;
  • Can be treated by
    • Opioids
    • Alpha1-agonists
    • Cool lavage
    • Rectify underlying cause
    • Administer fluids
    • Ensure adequate oxygenation
    • Decrease oxygen rate given to animal if cause is not apparent
61
Q

What can cause cardiopulmonary arrest? What are signs of this condition in the anaesthetised patient?

A
  • Causes of cardiopulmonary arrest
    • Hypoxia.
    • Hypovolaemia.
    • Hypercapnia.
    • Hypotension.
    • Hypothermia.
    • Acid – base abnormalities.
    • Electrolyte imbalances (hyperkalaemia, hypokalaemia, hypocalcaemia etc.).
    • Dysrhythmias.
    • Pre - existing heart disease.
    • Vagal stimulation.
    • Toxaemia (relative or absolute anaesthetic overdose; toxins and drugs).
    • Tamponade (tension pneumothorax or cardiac tamponade)
  • Signs of cardiopulmonary arrest
    • No heart sounds on auscultation.
    • Absence of palpable pulse.
    • Fixed and dilated pupils (30 – 45 sec) and central eye position (Figure 11.1 ).
    • Apnoea or ‘ agonal ’ gasps.
    • Grey or cyanotic mucous membranes (can be unreliable as may remain normal for several minutes after arrest).
    • Dry cornea with loss of refl exes.
    • Arrhythmia.
    • Bleeding at surgical site stops or slows; blood becomes dark in colour.
    • Loss of muscle tone and loss of cranial nerve refl exes.
62
Q

How can hyperkalaemia be detected using an echocardiogram?

A

P wave will be absent

63
Q

How can hypokalaemia be detected using an echocardiogram?

A

T wave will be absent

64
Q

What is the function of inotropic agents?

A

Positively inotropic agents increase the strength of muscular contraction. These can be used to treat hypotension.

65
Q

How can accidental extra-vascular injection be avoided?

A
  • Use non-irritant alternatives
  • Adequate physical restraint
  • Adequate chemical restraint
  • Venous catheterization
  • Dilute solutions
66
Q

What are the “follow up” steps that should be taken after recovery from cardiac arrest?

A
  • Administer fluids
  • Ensure renal perfusion (adequate urine production)
  • Provide warmth
  • Provide analgesics for chest pain
  • Provide other drugs required to support
67
Q

What is the required frequency of external cardiac compressions?

A

100 compressions per minute

68
Q

What are signs of effective cardiopulmonary resuscitation?

A
  • Palpable pulse during cardiac compression
  • Retinal blood flow (as detected by using a doppler probe on the cornea)
  • Carbon dioxide detectable on capnography
  • Improvement in colour of mucous membranes
  • ECG changes
  • Lacrimation
  • Pupillary constriction
  • Return of cranial nerve reflexes
  • Return of other neurological function
  • Return of spontaneous ventilation

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