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Anesthesiology Flashcards

1
Q

Receptor theory of anesthesia

A
  • GABA: major inhibitory neurotransmitter
  • Membrane structure and function; future of anesthesiology
  • Glutamate: major excitatory neurotransmitter
  • Endorphins: analgesia
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2
Q

What needs to be monitored/controlled during closed loop anesthesia?

A
  1. Ventilation control
  2. Hypnosis control
  3. Nociception control
  4. Metabolic control
  5. Temperature control
  6. Hemodynamic control
  7. Neuromuscular control
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3
Q

ASA physical status scale

A
  1. Normal healthy patient
  2. 2: Mild systemic disease (no limitation)
  3. Moderate to severe systemic disease with limitation of function
  4. Severe systemic disease (threat to life)
  5. Moribund (in a dying state) patient
  6. Brain dead patient (organ donation)
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4
Q

Pre- anesthetic plan

A
  • Patient baseline condition and medical history
  • Planned procedure
  • Drug sensitivities
  • Physiological makeup
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5
Q

The main anesthetic plan

A
  • ASA physical status scale
  • General vs regional anesthesia
  • Airway
  • Induction anesthesia to choose
  • What to monitor
  • Intraoperative management
  • Postoperative management
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6
Q

Examples of ventilation management?

A
  • Breathing systems
  • Open drop anesthesia
  • Mapleson circuits (pediatric anesthesia circuits)
  • Anesthesia machines
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7
Q

Functions of the anesthesia machine?

A
  1. Recieve medical gases from gas supply
  2. Permits other gases (anesthetics) only if there is enough oxygen in the mixture
  3. Vaporizers are agent-specific
  4. Deliver and control tidal volume
  5. Wastegas scavenger system
  6. Regular inspections

Failure of the machine is a significant percentage of the mishaps in anesthesia practice

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8
Q

Ways of airway management and complications:

A
  1. Supraglottic device
  2. Endotracheal intubation: most common and safe protection of airways during anesthesia

Complications:

  • Difficulty in managing the airway
  • Difficult/traumatic intubation
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9
Q

Types of special airway techniques

A
  1. Fiberoptic Retrograde wire intubation
  2. Transtracheal jet ventilation
  3. Lighted stylets
  4. Laryngeal masks
  5. Combitube
  6. Surgical airway
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10
Q

Types of patient monitors

A

Common:

  1. Arterial BP (obligatory)
  2. ECG (obligatory)
  3. Pulsoxymetry (obligatory)
  4. Capnometry
  5. CVP (Central Venous Pressure) & PAC (Pulmonary Artery Catheter)

Less Common: EEG with BIS (bi-spectral index), Temperature, Nerve stimulation

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11
Q

Why monitor Arterial BP?

A
  • Obligatory!
  • Direct BP measured using arterial canule
  • Helps monitor effectiveness of chest compressions during CPR
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12
Q

Why monitor ECG?

A
  • Obligatory!
  • 12 lead ECG is preferred (but not necessary)
  • Helps monitor heart rate as well
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13
Q

Why monitor CVP (Central Venous Pressure)?

A
  • Important for monitoring circulatory system
  • Obligatory in cardiac procedures
  • Monitored by inserting Central Venous Catheter into right atrium
  • Normal central venous pressure is between 2-5 mmHg
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14
Q

Functions of a PAC (Pulmonary Artery Catheter)?

A

Also called Swan-Ganz catheter

  • Measures pressure in right ventricle (20-25mmHg) -
  • Measures pressure in pulmonary artery (10-25 mmHg) -
  • Measures cardiac output - Monitor function of left ventricle
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15
Q

What complicates monitoring LV function using PVC?

A

When there is a high pulmonary resistance, the function of LV is harder to assess

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16
Q

How do we measure cardiac output using PVC?

A

By injecting cold saline into the catheter and measure how long it takes before the temperature changes at the end of the catheter

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17
Q
  • CVP -1 to 1
  • HR 80
  • Systolic BP 100 mmHg

What do you suspect?

A

Hypovolemic shock

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18
Q

Capnomatry: What is it used for, normal/abnormal values?

A
  • Measures exhaled CO2 from the body
  • Most important parameter to be monitored during anesthesia because it reflects the effect of BOTH the respiratory and the circulatory system (used during CPR)
  • Normal value: 30-35 mmHg
  • May fall to 15 mmHg in resucitation, if as low as 10 or below = poor prognosis
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19
Q

What is BIS (bi-spectral index)?

A

An algorithm used to inturpret conciousness based on EEG results:

  • 100%: conscious patient
  • 80% = premedicated
  • 60% = Anesthesia

If it remains around 60, the patient is in deep anesthesia

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20
Q

Indications for temperature monitoring in surgery:

A
  • Surface temperature is important in long surgeries
  • Esophageal temperature in thorax and abdominal operations
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21
Q

Indication of nerve simulation in surgery:

A

Gives you an idea of how much neuromuscular relaxants the patients need.

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22
Q

Definition of General Anasthesia

A

A reversible state of CNS depression, resulting in loss of response to and perception of external stimuli

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23
Q

Why do we use preanestethic medications?

A

They lower the dose of anesthetic required to maintain desired level of surgical anesthesia

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24
Q

Preanesthetic medications which can be used:

A
  1. H2-blockers: Famotidine/Ranitidine Reduce gastric acidity
  2. Benzodiazepines: Alprazolam/Midazolam Relieve anxiety and facilitate amnesia
  3. Opioids: Fentanyl Reduce postoperative pain
  4. Antihistamines: Diphenhydramine Avoid allergic reactions
  5. Antiemetics: Odansetron Prevents nausea and aspiration of stomach contents
  6. Anticholinergics: Glycopyrolate Prevent bradycardia and secretion of fluids into the respiratory tract
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25
Q

Stages and depth of anesthesia

A
  1. Loss of pain sensation
  2. Combative behaviour
  3. Surgical anesthesia
  4. Medullary paralysis and death
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26
Q

Modern Inhaled Anesthetics:

What are they?

What are they used for?

A
  • They are volatile, halogenated hydrocarbons (exception: N2O)
  • They are used primarily for the maintenance of anesthesia after administration of an i.v agent.
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27
Q

Advantage of inhaled anesthetics

A

The depth of anesthesia can be rapidly altered.

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28
Q

Disadvantage of inhaled anesthetics

A

They have a very narrow therapeutic index (from 2-4)

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29
Q

4 factors that influence inhalation anesthetic uptake:

A
  1. Solubility in blood
  2. Lipid solubility
  3. Alveolar blood flow
  4. Difference in partial pressure between alveolar gas and venous blood
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30
Q

What is Minimum Alveolar Concentration (MAC)?

A

The concentration of inhaled anesthetics in the alveoli which prevents movement in 50% of patients in response to a standardized stimulus. Potent anesthetic = small MAC Weak anesthetic = large MAC

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31
Q

Factors that DECREASE MAC:

A
  1. Increased age
  2. Hypothermia
  3. Pregnancy
  4. Sepsis
  5. Acute ethanol poisoning
  6. Concurrent administration of i.v anesthetics
  7. a2-adrenergic agonists (e.g clonidine).
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32
Q

Factors that INCREASE MAC:

A
  1. Hyperthermia (>42C degrees)
  2. Drugs that increase CNS catecholamines
  3. Chronic ethanol abuse.
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33
Q

Contraindications of volatile inhaled anesthetics:

A
  1. Severe hypovolemia
  2. Malignant hyperthermia
  3. Intracranial hypertension
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34
Q

5 inhalational drugs used:

A
  1. Nitrous Oxide (MAC: 105%)
  2. Desflurane (MAC: 6%)
  3. Sevoflurane (MAC: 2%)
  4. Isoflurane (MAC: 1.2%)
  5. Halothane (MAC: 0.75%)
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35
Q

Nitrous Oxide, mechanism of action?

A

It’s an NMDA receptor antagonist

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36
Q

Nitrous Oxide, function:

A
  1. Used for anesthesia in dentistry
  2. Depresses myocardial contractility but stimulates sympathetic nervous system
  3. Dilates coronary arteries
  4. Does NOT relax muscles, unlike the other inhalation anesthetics
  5. Decreases renal blood flow –> decreased urinary output
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37
Q

Nitrous Oxide, other effects:

A
  1. Analgesia
  2. Depersonalisation
  3. Derealistation
  4. Dizziness
  5. Euphoria
  6. Sound distortion
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38
Q

Side effects of Nitrous Oxide:

A

Mainly due to long-term exposure

  • Reproductive side effects i pregnant females
  • Bone-marrow depression (megaloblastic anemia)
  • Peripheral neuropathies
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39
Q

Halothane, function:

A
  1. Used for inhalation induction
  2. Direct myocardial depression: lowers blood pressure and cardiact output
  3. Lowers cerebral vascular resistance, increases cerebral blood flow
  4. Reduces renal blood flow –> decreased urinary output
  5. Causes rapid, shallow breathing
  6. Potent bronchodilator
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40
Q

Side effects with Halothane:

A
  • Sensitizes the heart to arrythmogenic effects of sympathomimetic agents (e.g epinephrine dosage, etc…)
  • Depresses clearance of respiratory tract mucus = promotes postop hypoxia and atelectasis
  • Postoperative hepatitis –> centrilobular necrosis
  • Intracranial hypertension in patients with intracranial mass (increased cerebral blood flow)
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41
Q

Isoflurane is often used for

A

potentiation of nondepolarizing Neuro-Muscular Blockers

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42
Q

Isoflurane, effects:

A
  1. Decreases systemic vascular resistance –> increased skeletal muscle flow & low BP
  2. Partial preservation of carotid baroreflex –> increased HR –> increased cardiac output
  3. Decreased renal blood flow –> decreased urinary output
  4. Dilates coronary arteries (not as much as N2O) (Tachypnea, but less prominent than other anesthetics = less prominent fall in minute ventilation)
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43
Q

Desflurane, characteristics:

A
  1. Los solubility in the blood –> quick induction and emergence
  2. Ultrashort duration of action
  3. Moderate potency
  4. Dosage often adjusted based on peripheral nerve stimulation (increased stimuli –> decrease the dosage)
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44
Q

Desflurane, other effects:

A
  1. Increased dose –> fall in SVR –> fall in blood pressure
  2. Decreases tidal volume and increases respiratory rate
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45
Q

Sevoflurane, functions:

A
  1. Useful in pediatric patients as induction (quick induction, 1 min)
  2. SVR and BP decreases slightly less than with isoflurane or desflurane
  3. May prolong QT-interval
  4. Depresses respiration and reverses bronchospasm smilar to isoflurane
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46
Q

How is Sevoflurane given (mixture)?

A

Inhalation induction with 4-8% Sevoflurane in a mixture of 50% N2O and O2

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47
Q

Classes of intravenous anesthetics:

A
  1. Barbiturates
  2. Benzodiazepines
  3. Ketamine
  4. Etomidate
  5. Propofol
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48
Q

Barbiturates, function and mechanism:

A
  • Depress the reticular activating system (RAS) in the brainstem, which controls multiple functions, including consciousness
  • They bind to GABA type A receptor, and potentiate the action of GABA in increasing the duration of openings of a chloride-specific channel
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49
Q

Benzodiazepines, mechanism:

A

Binds to allosteric site of the GABA-receptors; increases frequency of openings of the associated chloride ion channel

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50
Q

Antidote of benzodiazepines?

A

Flumazenil

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51
Q

Ketamine, mechanism of action

A

NMDA-receptor antagonist + norepinephrine reuptake inhibitor

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52
Q

Ketamine, functions:

A
  1. Dissociates the thalamus from the limbic cortex (patient is consious, but don’t response to sensory input)
  2. Has a sympathetic stimulation (useful for hypovolemya or trauma)
  3. Combined with other agents for deep CONCIOUS sedation (usefull for endoscopy)
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53
Q

Ketamine other effects:

A
  1. Hallucinogenic effects (avoid by giving midazolam)
  2. Increases HR, BP and CO (due to it being NE-reuptake inhibitor)
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54
Q

Etomidate, function

A

Depresses RAS, mimicks inhibitory effects of GABA

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55
Q

Etomatide, main side effect:

A

30-60% incidence of myoclonus at induction (cause it partly inhibits extrapyramidal system)

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56
Q

Propofol, functions:

A
  1. Induction, produces unconsciousness within 30-40 sec
  2. Decreases SVR –> decreased BP
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57
Q

Main problem with Propofol formulation:

A

It’s water-insaluable = need to be emulsified = may support bacterial growth (need to use sterile technique)

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58
Q

Function of Opioids:

A

Principally used to produce analgesia, although they can give sedation in large doses

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59
Q

Opioids, mechanism of action:

A

Stimulates opioid-receptors distributed throughout the CNS, especially substantia gelatinosa of spinal cord and periacqueductal grey matter of the midbrain

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60
Q

Opioids, effects:

A
  1. CNS: Analgesia, sedation, euphoria, nausea/vomiting, miosis, depressed ventilation (rate more than depth, reduced response to CO2), depression of vasomotor centre
  2. Respiratory: Antitussive, bronchospasm in some
  3. Cardiovascular: Peripheral venodilatation, bradycardia (due to vagal stimulation)
  4. Urinary: Increased sphincter tone, urinary retention
  5. GIT: Reduced peristalsis –> constipation and delayed gastric emptying, sphincter constriction
  6. Endocrine: Release of ADH and catecholamines
  7. Skin: Itching
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61
Q

Transient use of N2O during labour might cause…

A

…the child to have aplastic anemia.

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62
Q

Why shouldn’t benzodiazepines be used routinely during labour?

A

Newborns often have temporary hypotonia and thermal irregularaties, benzodiazepines might be too strong for their bodies to handle!

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63
Q

What kind of struggles do we face in anesthesia of geriatric patients?

A

Physiological changes during aging

  1. The metabolism/clearance of the drugs get slower
  2. The effect on the organs get stronger
  3. Worse self-repair –> high drug-related damage –> more side-effects
  4. Most geriatric patients present with co-morbidities they have developed over the years –> more side effects
  5. Most geriatric patients take additional medications for co-morbidities = cross-reaction
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64
Q

Most common complications in preoperative evaluation:

A
  1. Difficult airway
  2. Asthma
  3. Insulin dependent diabetes
  4. Drug abuse
  5. Heart disease
  6. Pacemakers and defibrillators
  7. Peripheral motor neuropathy
  8. Pregnancy
  9. Pulmonary TB
  10. Renal insufficiency
  11. Liver insufficiency
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65
Q

Types of examinations for assesing the airways:

A
  1. Mallampati criteria
  2. Thyromental distance
  3. Calder test
  4. Wilson score
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66
Q

What is Mallampati criteria?

A

A test to assess the airway, and predict which patients may be difficult to intubate. The patient should be sitting upright, open their moiuth and protrude their tongue maximally. The view of pharyngeal structures is noted and graded I-IV.

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67
Q

How to measure Thyromental distance

A

With the head fully extended on the neck, distance between the bony point of the chin and the prominence of the thyroid cartilage is measured. Distance <7 cm suggests intubation will be difficult.

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68
Q

How to do a Calder test

A

Patient is asked to protrude their mandible as far as possible. The lower incisors will either lie anterior to, aligned with, or posterior to the upper incisors. The latter two suggests reduced view at laryngoscopy.

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69
Q

What is the Wilson Score used for and what are the parameters?

A

Increasing weight, reduction in head and neck movement, reduced mouth opening, and the presence of a receding mandible or buck-teeth all predispose to difficulty with intubation.

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70
Q

What is PACU?

A

PACU = Post-Anesthesia Care Unit

A unit dedicated to care for patients with respiratory or cardiovascular complications after undergoing anesthesia. Close to the ICU, but is not a part of the ICU.

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71
Q

Most common post-anesthesia respiratory & cardiovascular complications:

A

Respiratory:

  1. Airway obstruction
  2. Laryngospasm
  3. Hypoventilation
  4. Hypoxemia

Cardiovascular:

  1. Hypertension
  2. Hypotension
  3. Arrythmias
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72
Q

Other potential complications post-anesthesia:

A
  1. Airway obstruction
  2. Shivering
  3. Agitation
  4. Delirium
  5. Pain
  6. Nausea and vomiting
  7. Hypothermia
  8. Autonomic liability
  9. Arterial pressure fluctuations.
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73
Q

What is delayed emergence?

A

Patient fails to regain consciousness within 60-90 min following general anesthesia

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74
Q

What medicine to give for delayed emergence?

A
  1. Naloxone (0,2 mg)
  2. Flumazenil (0,5 mg)
  3. Physostigmine (1-2 mg)
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75
Q

Causes of delayed emergence:

A

Most common cause is residual anesthetic in the system that causes a delayed sedative/analgesic effect:

Other causes (6H rule):

  1. Hypothermia (core temp < 33)
  2. Hypoxemia and hypercapnia
  3. Hypercalcemia
  4. Hypermagnesemia
  5. Hyponatremia
  6. Hypo/hyperglycemia
  7. Perioperative stroke.
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76
Q

Discharge criteria of PACU (to be sent to normal ward):

A
  1. Normal color
  2. Respiration (maintains own airway)
  3. Circulation,
  4. Consciousness (easy arousability)
  5. Stable vital signs
  6. No post-op complications
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77
Q

Definiton of shock

A

Lack of delivery of oxygen into the tissues

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78
Q

What’s the connection between shock and lactate level?

A

Lactate level increases with higher anaerobic metabolism and can help predict the outcome after a shock.

2-4 mmol/L in over 2-3 hours = drastic increase in mortality

(BUT REMEMBER: lactate can also increase in aerobic metabolism when high amount of pyruvate is metabolised)

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79
Q

Signs of circulatory insufficiency:

A
  1. Changes in filling pressure
  2. Systolic and or diastolic dysfunction
  3. Emptying disturbances
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80
Q

Compensation of circulatory insufficiency:

A
  1. Increased vascular volume
  2. Increased filling pressures
  3. Tachycardia
  4. Hypertrophy
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81
Q

Possible outcomes after altered myocardial state (e.g ischemia):

A
  1. Myocardial Infarction: Irreversible decrease in contractility due to high tissue damage
  2. Stunning: a reversible myocardial state where contraction is reduced due to mild tissue damage (may recover immediatly or last for weeks)
  3. Decreased contractility in some segments due to low flow. Not ischemia. Treatment = CABG
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82
Q

Classification of shock:

A
  1. Hypovolemic
  2. Obstructive
  3. Cardiogenic
  4. Distibutice
  5. Endocrine
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83
Q

What is preload and afterload?

A

Preload: The initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.

Afterload: The force or load against which the heart has to contract to eject the blood.

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84
Q

Drugs for circulatory failure:

A
  • Vasodilators:
  1. Noradrenaline. Can increase TPR, and stabilize pressure. (dangerous: can decrease the flow)
  2. ACE inhibitors: captopril, enlapril
  3. Nitrovasilators: NTG, NPS, hydralazine
  4. Calcium channel blockers
  5. Potassium channel activators: diazoxide, minoxidil, pinacidi
  • Phosphodiesterase inhibitors: Amrinone
  • Calcium sensitizers: used for saving energy (contraindicated in diastolic dysfunction)
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85
Q

What does these abbreviations stand for?

  1. CBF
  2. CPP
  3. CVR
  4. DP-LVEDP
A
  1. CBF: Coronary Blood Flow
  2. CPP: Coronary Perfusion Pressure
  3. CVR: Coronary Vascular Resistance
  4. aortic Diastolic Pressure minus Left Ventricular End-Diastolic Pressure
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86
Q

Formula for Coronary Blood Flow:

A

CBF = CPP/CVR = DP-LVEDP/CVR

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87
Q

Definition of hypotension in the operating room?

A

A drop in systolic BP > 40-50 mmHg from baseline (systolic value <95 or MAP <65 may be considered as criteria for hypotension)

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88
Q

How to monitor circulation in the operating room?

A
  1. Intermittent with brachial cuff
  2. Arterial line
  3. CVP
  4. ScvO2
  5. SaO2
  6. ABG analysis
  7. Echocardiography
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89
Q

Approach to hypotension:

A

COVER: Circulation, Oxygen, Ventilation, Endotracheal tube, Review monitor

  1. Improve posture!
  2. IV fluids: crystalloid bolus
  3. IV vasopressors: if severe use adrenaline
  4. Increase levels of monitoring (e.g TEE)

PS: HR of 40-60 in adults is normal during anesthesia

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90
Q

What is the function of a Cardiopulmonary bypass machine?

A

Collects venous blood –> adds oxygen –> returns blood to a large artery

(may cause activation of stress hormones or give air embolism)

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91
Q

What is Systemic hypothermia?

A
  • Decreasing core temperature to under 35C (can go as low as close to 20)
  • Usefull for organ injuries, especially brain injuries (O2 demand halved with each 10C decrease)
  • Decreases circulatory function
  • Rewarming achieved by Cardiopulmonary bypass machine
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92
Q

Side effect of Systemic Hypothermia?

A

Platelet dysfunction –> reversible coagulopathy

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93
Q

What is Profound Hypothermia?

A

Decreasing core temperature to <20C (around 15-20C)

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94
Q

What is Cardioplegia?

A

Intentional and temporary cessation of cardiac activity (primarily for cardiac surgery)

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95
Q

How is Cardioplegia achieved?

A

Patient is attached to cardiopulmonary machine while set into systemic hypothermia and given a mix of Ka, Mg and Ca in the coronary vessels during diastole.

  • We make sure to maintain a Ka of 10-40mEq/L (normal is 3.5 -5)
  • We make sure to maintan a Na of <140mEq/L (normal is 135-145)
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96
Q

Which medications is important to administer during Cardioplegia to avoid side effects?

A

To avoid coagulation within vessels:

  • Heparin 3mg/kg by central line (keep anticogulation going for 400-450sec then reverse by giving Protamine)

Bleeding prophylaxis for the anticoagulation:

  • Tranexamic Acid 10mg/kg
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97
Q

Best placements for Central Venous Lines (CVS):

A
  1. Subclavian Vein
  2. Jugularis Interna (2nd choice due to many nerves around it)
  3. Femoral Vein (easy, but non-sterile area = use for short time)
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98
Q

Explain insertion of Jugularis Interna CVS

A
  • Lies between two heads of SCM
  • .Patient lies with head down due to risk of air embolism
  • 2nd choice due to lots of nerves passing by it
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99
Q

Explain peripheral venous line insertion

A
  • Use cubital veins
  • 2 sets: 45 and 75 cm (45 used most)

(Measure distance between cubital vein and subclavian vein to know how far to push the wire)

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100
Q

Explain insertion of Subclavian CVS

A
  • Can be reached from over and under the clavicle
  • The vein lies just over the 2nd rib and crosses under the clavicle
  • Movement is flat, directly under the clavicle, do not go deep
  • The catheter should stay in vena cava sup (or the subclavian itself).
  • The catheter is only 20 cm.
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101
Q

What is a venous port?

A
  • A small medical appliance that is installed beneath the skin and attached to a CVS
  • Allows for easy IV injections for home and hospital use
  • Can stay in the skin for 3-6 months
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102
Q

Indications for CVK?

A
  1. Long-term infusions of hypertonic, ptassium-containing and other irritating solutions
  2. Need for long term (>10days)
  3. Venous hemodialysis
  4. No accessible peripheral superficial veins
  5. As an access for pulmonary artery catheterization
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103
Q

What to do after CVK insertion?

A

Always take an X-ray to see if the tip of the catheter is placed correctly.

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104
Q

What is Central Venous Pressure and what does it reflect?

A

The CVP reflects the amount of blood returning to the heart and the ability of the heart to pump blood back in the arterial system’

Normal CVP: 3-8 mmHg

60yr old or smoker CVP: around 15 mmHg

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105
Q

Examples of causes for change in CVP:

A
  1. Patient on a ventilator –> high thoracic pressure; CVP rarely below 18-20 mmHg
  2. Patient is recieving fluids –> 1-2 mmHg increase/hour (sing of improvments)
  3. Patient recieving fluids –> decrease or no change in CVP = Patient is bleeding somewhere!!!
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106
Q

Other factors affecting CVP?

A
    • The zero reference point
    • Posture
    • Fluid status
    • Raised intrathoracic pressure;
  5. mechanical ventilation, coughing,
  6. straining
    • Pulmonary embolism
    • Pulmonary hypertension
    • Tricuspid valve disease
    • Pericardial effusion, tamponade
    • Superior vena cava obstruction
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107
Q

Risk factors of CVK procedure:

A
  1. Punctre artery by mistake (HT, coagulopathy, long & large needle etc…)
  2. Puncture lymph nodes by mistake (portal HT, i.v drug abuse etc…)
  3. Puncture lung apex by mistake (apical blebs, emaciation, lung disease, etc…)
  4. Pnumothorax: the most common complication of CVK procedure
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108
Q

How can air embolism occur in patients with CVK?

A
  1. Hypovolemia and low venous blood pressure (high risk for air embolism)
  2. Labored inspiratory effects and tachypnea
  3. Inappropriate position of the patient during procedure (head elevated during subclavian or int.jugular puncture or cannulation)
  4. Accidental disconnection of the catheter from the i.v tubind (patient in upright position)
  5. When subclavian or int. jugular catheter is just removed and skin not covered by sterile bandage.
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109
Q

Risk factors of infection in CVK patients?

A
  1. Contaminated technique of insertion and or maintenance
  2. Immunocompromised state
  3. Terminal cancer state
  4. Long term i.v catheter therapy
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110
Q

What can cause clot formation in CVK patients?

A
  1. Catheter malposition
  2. Hypercoagulability states
  3. Catheter infection
  4. Chemically and physically irritative catherter and infusion fluids
  5. Long term indwelling catheter
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111
Q

Contraindications for CVK?

A
  1. Severe bleeding tendency and coagulopathy states (e.g patients on warfarin)
  2. Persistent shock
  3. Obstruction of sup. and inf. vena cavae, innominate, subclavian and int. jugular
  4. Local infection/necrosis at site of insertion
  5. Recently failed attempts at cannulation
  6. Resp. distress, tachypnea and labored inspirations
  7. Traumatic injury to sup. vena cava, innnominate, int. jugular or subclavian
  8. Patients refusal or retraction of previously given consent (important!

ABSOLUTE contraindications: Bleeding disorders and patient refusal!

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112
Q

What is a Cut-Down?

A

If you don’t have a peripheral vein and you don’t know how to do a CVK, you can do a «cutdown» in the cubital or popliteal vein. Open the skin, dissect around the vein and cut it with a scissor to introduce the catheter. Before cutting you should put two sticthes on the distal end of the vein to stop hemorrhage.

(This is an old method used before catheters were invented)

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113
Q

Where are arterial catheters placed?

A
  1. Radialis (most used artery)
  2. Dorsalis pedis
  3. Brachialis (not used for long-term)
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114
Q

Advantages of arterial catheters:

A
  1. Blood samples can be taken from it
  2. Can be used to measure blood pressure

(remember to flush it with heparin to keep it open)

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115
Q

What is the average daily water loss and what is the recommended treatment dosage of hypovolemia-risk patients?

A
  1. 2500ml is the average daily water loss
  2. 30ml/kg is recommended dosage (patient on operating table, add extra 15-20ml/kg)
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116
Q

How do we monitor and assess hydration lvl of patient at risk of hypovolemia?

A
  1. Urine output, normal 1ml/kg/h (best evaluation)
  2. General: HR, BP, pH, CVP, direct aBP + tilt test
  3. Lab: hemoconcentration, azotemia and high serum kreatinine, low urinary sodium, metabolic acidosis late sign of hypovolemia
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117
Q

Examples of Crystalloid IV fluids:

A
  1. Normal saline (0,9%NaCl)
  2. Ringer’s solution
  3. Hartmann Glucose (Plasmalyte)
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118
Q

Crystalloids, advantage & disadvantage:

A

Advantage:

  1. Less expense
  2. Greater urinary flow
  3. Replaces interstitial fluid (4 Liters must be given to equal 1 L of colloid!)

Disadvantage:

  1. Short-lived hemodynamic improvement
  2. More peripheral edema
  3. Pulmonary edema
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119
Q

Examples of Colloid IV fluids:

A
  1. Hydroxyethyl starch
  2. Gelofusine
  3. Albumin solution
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120
Q

Colloids, advantage & disadvantage:

A

Advantage:

  1. Smaller infused volume
  2. Prolonged increase in plasma volume
  3. Less peripheral edema
  4. Lower intracranial pressure

Disadvantage:

  1. Greater expense
  2. Coagulopathy/dextrane HES)
  3. Pulmonary edema /capillary leak
  4. Decreased Ca2+
  5. Decreased GFR
  6. Osmotic diuresis
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121
Q

What is hypertonic fluid resuscitation?

A

IV solution of 4-10% dextrose to replenish fluid loss in burn victims and treat hyponatremia

(very irritating to vessels, consider other solutions first)

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122
Q

What is defined as hypokalemia?

A

Serum K+ of < 3.5 mEq/l

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123
Q

Possible causes of Hypokalemia?

A
  1. Insufficient diet
  2. Fluid therapy
  3. Intravellular movement of K+ (alkalosis, insulin therapy, Beta-adrenergic agonists, hypothermia, transfsion of frozen RBCs)
  4. Losses (almost always renal or GIT)
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124
Q

Symptoms of hypokalemia?

A
  1. Weakness
  2. Cramping
  3. Tetany
  4. Myalgia
  5. Constipation
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125
Q

Treatment procedure for hypokalemia?

A
  • Replace slowly, and only to big veins!
  • No more than 8 mEq/h IV in peripheral vein or 10-20 mEq/h to CVK
  • Up to 240 mEq/day potassium chloride
  • Mild hypokalemia (3 - 3.5mEq/L) can be treated by oral potassium chloride
  • Generally safe rate of IV infusion = 10mEq/hour.
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126
Q

Main symptom of abnormal Na lvls?

A

Neurologic symptoms (both hyper-and hyponatremia)

E.g hypernatremia –> rupture of cerebral vessels

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127
Q

Which substances do we see in higher concentration after few days of starvation?

A

Ketones and Glycerol

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128
Q

Hormone changes when body undergoes catabolism?

A
  1. Higher glucagon lvl
  2. Cathecolamine-induced gluconeogenesis

In diabetic patents catabolism is very harder to stop (improper insulin –> improper glucose intake by cells)

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129
Q

How does protein half life play into account in starvation?

A

Different proteins = different half lifes

Shortest: (prealbumin, enzymatic proteins, prothrombin, clotting factors)

Longest: Albumin

(this is why people bleed out of their orifices during starvation)

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130
Q

Indications for parenteral nutrition?

A
  1. GI disturbances
  2. GI surgery
  3. Malabsorption syndrome
  4. Unconsciousness, comatose
  5. Cranio-cerebral trauma
  6. Tetanus
  7. Anorexia
  8. Malignant disease
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131
Q

What is hyperalimentation?

A

Providing parenteral nutrition to a patient that requires it.

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132
Q

What is the protocol for hyperalimentation of a patient in a catabolic state?

A

Patient in catabolic state is recommended to start with only basic requirements, then later (after ~8 days) increase amount when they reach anabolic state

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133
Q

In hyperalimentation, when does the caloric requirement increase?

A
  1. If patent has a fever of 39C –> 20% increase
  2. Fever above 40C or major surgery –> 30%
  3. Sever burns –> 150% increase
  4. Brain concussion –> 300% increase (5400kcal daily)
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134
Q

Which parameters do you check in a patient receving nutrition?

A

Glucose and Osmolarity every few hours!

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135
Q

What is parenteral nutrition?

A

“Feeding” the patient by giving a nutritious IV solution

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136
Q

What do you need to do right after parenteral nutrition is discontinued?

A

Give 10% IV glucose for 24 hours, to avoid hypoglycemia or hypokalemia due the still active insulin

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137
Q

Recommended glucose % in parenteral nutrition?

A

Given by PVK : up to 15%

Given by CVK: above 15%

138
Q

What are the 3 types of liquid enteral diets?

A

Elemental diet: Proteins are completely broken down into individual amino acids. All of the energy from the food can be taken up as it has already been partly digested. (patients with GI-related problems)

Semi-elemental diet: Short chains of amino acids

Polymeric diet: Complete whole proteins (anabolic state patients)

139
Q

Side effects of elemental diet?

A
  1. Gastric retention
  2. Altered bowel habits
  3. Fluid balance problemds
  4. Abnormal lvls of proteins, fats, sugars or electrolytes

Some disorders may cause further side effects (eg. patients with azoetmia, hepatotox, necrotizing enterocolitis etc.)

140
Q

What is Midazolam?

A
  • A benzodiazepine
  • Short elimination half-life & high dosage variability
  • Water soluble
  • Lack of adverse hemodynamic side-effects
  • Withdrawal effects after long term therapy: tachycardia, restlessness, hypermetabolism
141
Q

What kind of cardiovascular anitarrythmatic agents are commonly used in the ICU?

A
  1. General - Amiodarone (or sometimes lidocaine)
  2. Calcium channel blockers - control of supraventricular arrythmias (blocks SA and AV node up to several hours)
  3. Betablockers - Useful if Amiodarone is not working properly (need to hydrate the patient before giving betablockers due to hypotension)
142
Q

Which cathecolamines are naturally occurring and which are synthetic?

A

Natural:

  • Dopamine
  • Epinephrine
  • Norepinephrine

Synthetic:

  1. Isoproterenol
  2. Dobutamine
  3. Phenylephrine
143
Q

The most important feature of cathecolamines?

A

They are vasopressors and have inotropic effect

144
Q

Best cathecholamine for keeping normal BP even though blood fluid is low?

145
Q

Cathecholamine of choice in septic shock?

A

Norepinephrine

146
Q

What is a common side effect of spinal anesthesia and how do we counteract it?

A

BP goes down due to pooling of blood in lower extremities.

Phenylephrine is the drug of choice to keep BP within normal range in this case.

147
Q

Narcotic analgesics with sedative effects, name them!

A
  1. Morphine sulphate
  2. Meperidine
  3. Fentanyl - 100 times more potent than morphine
  4. Sufentanil - the epidural anesthesia in labour
  5. Alfentanil - very short acting. Used for short procedure. -
  6. Remifentanil = new drug for total i.v anesthesia. More potent than fentanyl.
148
Q

Non-narcotic analgesics, name them!

A
  1. Diclofenac
  2. Ketorelac

(both are types of NSAIDs)

149
Q

Which vasodilating antihypertensive medicines are commonly used in the ICU?

A
  1. Nitroglycerine (mostly used)
  2. Nitroprusside
  3. Hydrolasine

(decrease MAP and perfusion pressure, and increase intracranial pressure)

150
Q

What kind of toxicity is nitroprusside associated with?

A

Cyanide toxicity (nitroprusside gets metabolised to cyanide, dangerous in high levels, contraindicated for labour)

151
Q

What are neuromuscular-blocking agents used for in the ICU?

A
  1. To facilitate respiratory management, only used in the start when they are being intubated, not for long-term
  2. Reduce muscle activity and O2 consumption during tetanus, status epilepticus and severe shivering
  3. Decrease potental for injury in patients with uncontrolled agitation and hyperactivity

Depolarizing agents are used ONLY for intubation in ICU (non-depolarizing for prolonged skeletal muscle blockade)

152
Q

Name the Neuromuscular blocking agents

A
  1. Suxamethonium (only for intubation…depolarizing)
  2. Atracurium
  3. Pancuronium
  4. Vecuronium
  5. Esmeron
153
Q

What are the complications in long-term neuromuscular blockade therapy?

A
  1. Muscle weakness
  2. Pooling of blood
  3. Lack of calf pump
  4. Decubitus ulcers
  5. Infections
  6. Patients can become profoundly agitated and require concurrent sedative and anxiolytic therapy
154
Q

Which non-benzo sedatives are there?

A
  1. Propofol - has vasodilating proterties
  2. Thiopental - patient feels pain but doesn’t remember it later
  3. Etomidate
  4. Haloperidol - mainly for sedation of elderly
155
Q

Theophylline, what is it used for and what are the side effects?

A
  1. Treatment of respiratory disorders (FEV & FVC improve 2% for each mg/ml increase in serum)
  2. Side effects: seizures, arrythmias
156
Q

Which emergency medication is commonly used for stroke victims?

A

Alteplase 10mg IV over 1-2min followed by slow infusion of 90mg

157
Q

What is a common disadvantage of Amphotericin B and which drug is often used instead?

A

Amphotericin B is a very toxic and expensive antifungal, use Fluconazole if possible

158
Q

Which drug is commonly used for malignant hyperthermia?

A

Dantrolene - a skeletal-muscle relaxant

159
Q

Which drug do we use to reverse effects of benzodiazepines?

A

Flumenazil

160
Q

Explain the 3 stages of labor

A

1st stage: onset of regular labor pains (contraction 5-15 mins apart), thinning + shortening of cervix, progressive cervical dilation

End of 1st: the cervix is fully dilated (8-12 hours); usually within this time the amniotic sac ruptures.

2nd stage: begins as baby’s head enters birth canal, ends when baby is fully delivered. Should not last more than 2 hours.

3rd stage: delivery of placenta (should not last more than 1 hour)

161
Q

What is dilutional anemia?

A

Occurs when blood volume increases during pregnancy –> decreased RBC/ml

162
Q

What is Aortocaval compression?

A

At >16 weeks of pregnancy, uterus may push against IVC when lying down –> decreased preload. some may also compress the aorta = low stroke volume.

163
Q

Which respiratory system changes may occur during pregnancy?

A
  1. Expiratory reserve decreases
  2. Tidal volume is increases
  3. RR increases
  4. FVC is decreases (even more if patient is obese), leading to functional hyperventilation
164
Q

What anatomical effects may ocurr during pregnancy?

A
  1. Airway edema
  2. Widened mediastinum
  3. Widened subcostal angle
  4. Elevated diaphragm
  5. Enlarging uterus
165
Q

What causes pain during labor?

A
  1. Maternal anxiety
  2. Delayed gastric emptying
  3. Increased symp. activity (noradrenaline and catecholamine release –> constriction of uterine vessels –> fetal hypoxia, and dysfunctional labor)
166
Q

What can we block for pain relief during labor?

A
  1. Paravertebral block T10-L1
  2. Segmental epidural T10-L1
  3. Lumbar sympathetic block
  4. Sacral nerve root block S2-S4
  5. Pudendal block
167
Q

When do we usually give epidural?

A

Epidural is usually given at 2-3 cm dilatation, before the active phase of the 1st stage of labor

168
Q

Explain the physiology of pain in 1st stage of labor

A
  • Mostly visceral pain
  • Dilation of cervix, distention of lower uterine segment
  • Dull, aching, poorly localized
  • Visceral C-fibers.
169
Q

Explain the physiology of pain in 2nd stage of labor

A
  • More somatic, sharp, severe, well localized
  • Distention of pelvic floor, vagina and perineum
  • Rapidly conducting alpha-delta fibers.
170
Q

Pain relief for 1st stage labor?

A

T10-L1 block

171
Q

Pain relief for 2nd stage labor?

A

S1-S4 (+T10-L1) block

172
Q

Alternatives to nerve block for labor pains?

A
  1. Abdominal decompression
  2. TENS (transcutaneous electrical nerve stimulation)
  3. Opioid analgesics
  4. Paracervical block in first stage
  5. Inhalational anesthesia or spina/pudendal block in second stage
173
Q

Explain procedure of epidural injection during labor.

A

Tuohy needle is used, pointed cervically between the vertebrae, feel for loss of resistance in ligamentum flavum during injection

(ligamentum flavum also loses resistance due to high lvls of relaxin hormone produced by pregnant women)

174
Q

Explain complications of epidural injection

A
  • High incidence of dural rupture –> more CSF eflux –> higher incidence of Post-Puncture Headache & PDHD (Pyruvate Dehydrogenease Deficiency)
  • Chance of penetrating vessels and injecting the bupivacaine (cardiotoxic) into them –> cardiac arrest
  • Uptake into epidural fat –> less pain block
175
Q

Contraindications of lumbar epidural anesthesia (LEA)

A

Absolute contraindication:

  1. Patient refuse or doesn’t cooperate
  2. Increased ICP
  3. Coagulopathy
  4. Sever hypovolemia

Relative contraindication:

  1. Systemic maternal infection
  2. Spine abnormalities
  3. Slight coagulopathy
  4. Positioning problems
176
Q

Why should you consider combining spinal and epidural anesthesia?

A

By combining them, the disadvantages of both methods are eliminated and their advantages are enhanced.

(can be done with one injection, a bigger needle into the epidural space and a smaller needle goes through it further into subarachnoid space)

177
Q

Which agents are most commonly used for epidural anesthesia?

A
  1. Chloroprocaine
  2. Lidocaine
  3. Mepivacaine
  4. Bupivacaine
  5. Ropivacaine
178
Q

What is an epidural blood patch?

A

An epidural blood patch is where you inject 15-20 mL of autologous blood into the epidural space. It stops further leakage of CSF by either mass effect or coagulation. 90% of patients will respond to a single blood patch.

179
Q

What does the term “Neuraxial Anesthesia” mean?

A

Local anesthesia placed around the nerves of the CNS (such as a spinal or epidural anesthesia)

180
Q

What is the effect of Neuraxial opioids?

A

Cuase analgesia without motor block

  1. For early labor, may be used alone
  2. For advanced labor, may be combined with local anesthesia
  3. May be used postop after cesarean delivery
181
Q

What are C-fibers?

A
  • C-fibers are the smallest and slowest nerves
  • Are the first ones to respond to local anesthesia
182
Q

Risk factors of maternal mortality?

A
  • Individual: obesity, extremes of maternal age, increasing parity
  • Obstetric factors: operative delivery, IVF, massive blood loss, HT, sepsis, lenghtened 2nd stage of delivery
  • Social: ethnic, non-attendance at antenatal appointments, violence at home
183
Q

What is the difference between direct and indirect maternal death?

A
  • Direct maternal death = complications of pregnancy or medical interventions
  • Indirect maternal death = results from preexisting disease or illness developed during pregnancy (not directly related to pregnancy but aggravated by it)
184
Q

Low arterial pO2 without any other sign of patient being compromised is a sign of?

A

Faulty procedure, you are propably in a vein

185
Q

How do we calculate amount of dead space and what is the average?

A

Calculate: 2ml * body weight (kg) = dead space ml

Average: 150ml

186
Q

What are the causes of tissue hypoxia?

A
  1. Hypoxemia
  2. Impaired blood flow
  3. Impaired arterial O2 carrying capacity
  4. Increased O2 demand by tissues
  5. Impaired O2 utilization
187
Q

What is the Fick principle?

A

We can measure the uptake of a substance (e.g O2) by a tissue, by attaching a marker to it and comparing the amount of it in the arteries going to the tissue with the veins going from the tissue.

188
Q

The most basic definition of a shunt?

A

When the desaturated blood returns to the left heart without being resaturated with O2

189
Q

What are absolute shunts?

A

Perfusion without ventilation, V/Q is ZERO. Hypoxemia created by an absolute shunt can NOT be corrected by increasing the inspired O2 concentration.

190
Q

What is a relative shunt?

A

Perfusion with decreased ventilation (decreased V/ Q). Clinically, hypoxemia from a relative shunt can usually be partially corrected by increasing the inspired O2 concentration.

191
Q

What is physiological shunting?

A

The alveoli are well-vascularized, but not well-ventilated

192
Q

What is Nunn’s iso-shunt diagram?

A

A diagram that we use to estimate if there is a shunt based on measuring Fraction of inspired oxygen (FiO2) and Arterial oxygen (PaO2)

193
Q

What is Henry’s law?

A

The amount of oxygen dissolved is proportional to its partial pressure , for each mmHg of PO2 there is 0.003 ml O2/dL (thos acounts for the very small amount of dissolved O2, not the one carried by heme.

194
Q

Effects of pH on the Oxygen Dissociation Curve?

A
  • High pH: less PaO2 needed, shift to left
  • Low pH: more PaO2 needed, shift to right
195
Q

How do you calculate minute consumption of O2 in an average 70 kg patient with a normal RR?

A

Values:

Standard O2 content in blood is 19,5 ml/dl blood

Body consumes about 25% of the O2 content in blood / min

19.5 ml/dl * 0.25/min = 4.87 ml/dl/min

196
Q

What is the theoretical amount of O2 stores in an adult?

A

1500ml (1000ml in Hb, 480ml in lungs (FRC), the rest is bound to Mb and dissolved in body fluids)

197
Q

Tissue O2 requirements at rest are?

198
Q

What types of oxygen therapy is there?

A
  1. Nasal cannula
  2. Face masks
  3. Intubation
  4. Hyperbaric Chamber
200
Q

The function of nasal canula?

A
  • Goes up the nostrils
  • Max 40-50% O2 is used
  • Adds 4% saturation for every additional Liter (up to 6L)
  • >6L/min flow rate is poorly tolerated (causes dry nose)
201
Q

What type of face masks may be used for oxygen therapy?

A
  1. Venturi mask
  2. Open mask
  3. Non-rebreather masks
  4. Partial-rebreather masks
202
Q

How does venturi masks work?

A
  • Deliver spesific O2 concentration by entraping room air and mixing it with the O2 supply
  • Come in several % types (e.g 24%, 31%, 40%…)
203
Q

How does an open mask work?

A
  • It’s a face mask with large holes to let in room air
  • Can deliver 50-60% O2
  • Requires >6L/min
204
Q

How do non-rebreather masks work?

A
  1. 100% O2 supply mixed with a little room air that may leak into the mask (Provides FiO2 of 80% at flow rates of 10-15L/min)
  2. An attached reservoir bag provides volume to meet patient’s PIFR
  3. One way valves on the sides of the mask prevent entrapment of room air in the mask, while letting exhaled air out through this valve
205
Q

How do partial-rebreather masks work?

A
  • Up to 80% O2 is given
  • Like non-rebreather, but with a two-way valve
206
Q

What may hyperbaric chambers be used for?

A
  1. Decompression sickness
  2. Gas gangrene
  3. Gas embolism
  4. CO poisoning
207
Q

What are the hazards of oxygen therapy?

A
  1. Hypoventilation; in patients with COPD (insufficient)
  2. Absorption atelectasis; the high amount of O2 replaces the N2 found in the alveoli (because N2 stimulate alvoli to keep open, the decreased amount –> closure of alveoli)
  3. Pulmonary toxicity; prolonged O2 therapy –> ROS –> O2-mediated injury of alveolar-capillary membrane = ARDS
  4. Retrolental fibroplasia; a retinopathy in neonates <44th week of gestational age
  5. Hyperbaric O2 toxicity; the high O2 pressure may cause dyspnea (=2 atm) and neuropathy (>2 atm)
  6. Fire hazards; O2 is very flammable
208
Q

Name the 2 types of respiratory failure.

A

Type 1: Hypoxemic (PaO2 <60 mmHg)

Type 2: Hypercapnic (PaO2 <60 mmHg & PaO2 >50 mmHg)

209
Q

How much ATP is made from one glucose molecule (aerobic vs anaerobic)?

A
  • Aerobic: 38 ATP
  • Anaerobic: 2 ATP
210
Q

What is Total Cycle Time?

A

Total cycle time is the time it takes to complete one cycle of breathing. Can be set on ventilators, inspiratory time within the TCT can also be changed

(If RR is 12, this will be 60 sec/12 = 5. I.e, TCT is 5 seconds.)

211
Q

What is PPV?

A

Positive Pressure Ventilation

Lung inflation is achieved by periodically applying positive pressure to the upper airway through an endotraccheal or tracheostomy tube

212
Q

Major disadvantages of PPV?

A
  1. Altered ventilation/perfusion ratios
  2. Adverse circulatory effects; it decreases venous return = decreased CO
  3. Risk of pulmonary barotrauma
213
Q

What are the 4 phases of all ventilators?

A
  1. Inspiration
  2. Change from inspiration to expiration
  3. Expiration
  4. Change from expiration to inspiration
214
Q

Ventilators are most commonly classified according to?

A
  1. Their inspiratory phase characteristics
  • Constant flow
  • Nonconstant flow
  • Constant pressure
  1. Their method of cycling (changeover, inspiration to expiration)
  • Time-cycled
  • Volume-cycled
  • Pressure-cycled
  1. Their limit (what determines size of breath)
  2. Their trigger (what tells ventilator to start)
215
Q

What are the 3 most common types of ventilators used in the ICU?

A
  1. Control breath
  2. Assisted breath
  3. Spontaneous/pressure support
216
Q

How does Assist-control ventilation (ACV) mode work?

A
  • We control the volume by setting the tidal volume. Choose a respiratory rate. Also FiO2, PEEP, flow etc.
  • The ventilator is in full control of the breathing.
  • The trigger variable in this ventilation is TIME = time triggered breath (time since last expiration is measured)
  • If the patient is not paralyzed and needs to breathe themselves , they will start to breathe and this will trigger the ventilator to deliver a set tidal volume = patient triggered breath (assisted breath).
217
Q

How does Synchronous intermittent mandatory ventilation (SIMV) mode work?

A
  • The ventilator attempts to synchronize the patient’s respiratory effort with the mandatory machine breaths.
  • The patient can breathe himself between controlled breaths (may be pressure supported)
  • If patient is not breathing, SIMV can work like ACV
218
Q

How does pressure-controlled ventilation (PCV) mode work?

A
  • In PCV, pressure is the controlled parameter and time is the signal that ends inspiration, with the delivered tidal volume determined by these parameters.
  • The highest flow is provided at the beginning of inspiration, charging the upper airways early in the inspiratory cycle and allowing more time for pressures to equilibrate.
  • Flow decelerates exponentially as a function of the rising pressure, and the preset inspiratory pressure is maintained for the duration of the operator-set inspiratory time.
219
Q

What are time-cycled ventilators?

A
  • Ventilators that cycle to the expiratory phase once a predetermined interval elapses from the start of inspiration (interval time is based on TV which is determined by inspiratory time and flow rate)
  • Often seen in positive-pressure machines
  • Often used in neonates
220
Q

How does BIPAP work?

A
  • Positive pressure at the end of inspiration AND expiration. The ventilators pushes a pressure when the patient spontaneously breathes to keep airways open and to achieve the desired volume, and thereafter also keeps a pressure when patient breathes out to keep alveoli open.
  • This is beneficial in atelectasis, COPD etc.
221
Q

What is Inverse I:E ratio ventilation (IRV)?

A
  • Inverse-ratio ventilation (IRV) is positive-pressure ventilation with an inspiratory-expiratory (I : E) ratio of greater than 1
  • Positive end-expiratory pressure (PEEP) is produced beacues each new breath begins prior to the complete exhalation of the chest
  • Does not allow for spontanous breathing
  • Can cause barotrauma
222
Q

Complications of Inverse I:E ratio ventilation?

223
Q

Complications of mechanical ventilation?

A
  1. Laryngomalacia (risk after 2 hours of endotrachial intubation)
  2. Subglottic stenosis (when the ET tube is present >2 weeks)
  3. Subglottic hemangioma
224
Q

What are the typical ventilator settings?

A
  1. For full ventilatory support: RR 14-30 and TV 6-7 ml/kg.
  2. For partial ventilatory suppert: low SIMV settings (<8bpm)
225
Q

Which monitoring /maintenancemay be used during mechanical ventliation?

A
  1. Airway pressure
  2. Exhaled TV
  3. Fractional concentration of O2
  4. Continuous ECG
  5. Pulse oximetry
  6. Direct intraarterial pressure
  7. ABG (4 per day)
  8. Suctioning of airway secretions (mandatory every 2 hours
226
Q

What are the criteria for removing mechanical ventilation?

A
  1. Inspiratory pressure 5ml/kg
  2. Vital capacity >10ml/kg
  3. Minute ventilation <10L
  4. Saturation >90% on 40%O2 with PEEP <5 cmH2O
  5. Lab and radiological findings
  6. Intact airway reflexes
  7. Cooperative patient
227
Q

Criteria for hemorrhage in obstetrics?

A
  1. Blood loss: >500 ml in vaginal delivery / >1000 ml in cesarean
  2. Decrease in Hb >4 gram/dl
228
Q

Reasons for bleeding during delivery (4 T’s):

A
  1. Tone (abnormalities in uterine muscle tone)
  2. Tissue (placental complications)
  3. Trauma (injury either now or previous, or rupture)
  4. Thrombin (coagulopathy)
229
Q

Which uterine tone abnormalities can cause hemorrhage during delivery?

A
  1. Uterine atony
  2. Overdistention
  3. Muscle fatigue
  4. Also inflammation due to infection (e.g chorioamnionitis), affects muscle tone
230
Q

Which placental complications can cause hemorrhage during delivery?

A
  1. Accreta
  2. Increta
  3. Percreta
  4. Praevia
  5. Placental abruption
231
Q

Which complications related to trauma may cause hemorrhage during delivery?

A
  1. Laceration of cervix, perineum, vagina)
  2. Uterine rupture
  3. Previous: C-section, multiparity, or vertical uterine incision
232
Q

Which coagulopathy-related complications can cause hemorrhage during delivery?

A
  1. Hemophilia
  2. vWD
  3. DIC
  4. Hyperfibrinolysis
  5. Hypofinrinogenemia
  6. Pharmacologic anticogulation
233
Q

Protocol in case of hypovolemia due to hemorrhage during delivery?

A
  1. Give crystalloids
  2. Ensure normothermia (promotes clotting)
  3. Blood transfusion (be sure to give Ca2+, it decreases during transfusion)
  4. Correct pH if patient experiences acidosis
  5. Consider giving uteroconstrictors
234
Q

Which uteroconstrictors can we give for hemorrhage during delivery?

A
  1. Oxytocin: 5 IU/ml IV slow injection (s.e BP & HR disturbance)
  2. Methergine: 200 ug IM (s.e hypertension!)
  3. Carbetocine (Pabal): 100 ug IV (oxytocin analog, stronger)
  4. PGF2, PGE1 (not commonly used)
235
Q

What is a B-lynch suture?

A
  • A form of suture of the uterus
  • Used for hemorrhage during delivery
  • Balloon is inflated in the uterus to decompress it, then it is stured in a special way to keep its shape when the balloon is removed
236
Q

Which blood tests are usefull to assess risk of bleeding during delivery?

A
  1. Fibrinogen (the most accurate)
  2. Hb & platelets
  3. D-dimer (not as usefull as the previous ones)

(APTT if heparin is used, INR if warfarin is used)

237
Q

What should Fibrinogen levels be during delivery, and what are they otherwise?

A
  • In normal people normal level is 2g/L
  • During delivery it should be >6g/L (lvl >4g/L is also acceptable, but 2 or lower is a risk of bleeding)

(high fibrinogen lvl during delivery is not a clot risk)

238
Q

How do we give fibrinogen if lvl is low during labour? Risks?

A
  1. Fibrinogen concentrate
  2. Crypresipitate (has more than FFP)
  3. Fresh Frozen Plasma

Risks:

  • TRALI (Transfusion-related acute lung injury)
  • TACO (transfusion associated cardiovascular overload)
  • Infections: hepatitis, HIV etc
  • Coagulopathy due to fluid overload
239
Q

What coagulopathy is especially of concern and may cause bleeding either during or hours after delivery? Treatment?

A

Hyperfibrinolysis

  • Peak in 3h after delivery
  • Increased risk in presence of other vascular pathologies (e.g shock or amniotic fluid embolism)

Treatment:

  • TXA (Tranexamic Acid)
  • First give 4g IV over 1h, then 1g IV over 6h
  • Safe for both mother and child
241
Q

What is a Cell Saver (Intraoperative blood salvage)?

A

A method using a special machine during surgery to cellect lost blood, filter it and tranfuse it back to the patient.

Commonly used for C-sections

242
Q

Last resort treatment when deling with bleeding during delivery?

A

Give Factor VII (last resort!)

  • Increased risk of thromboembolic events
  • Hb should be at least 7-8 g/dl
243
Q

What to check during a neurological exam?

A
  1. Mental status
  2. GCS
  3. Cranial nerves
  4. Motor and sensory exam
  5. Reflexes
  6. Cerebellar (ataxia etc..)
  7. Posture (decorticate or decerebrate)
  8. Respiratory pattern (e.g Cheyne -Stokes etc…)
  9. Breath smell (ketones, alcohol, fetid)
244
Q

How does decorticate and decerbrate posturing look like and what are they each signs of?

245
Q

Explain the Glasgow Coma Scale.

246
Q

Conditions that may cause changes in mental status?

A
  1. Stroke
  2. Trauma
  3. Mass effect
  4. Infection
  5. Meningitis
  6. Encephalitis
  7. Sepsis
  8. Psychiatric disorder
  9. Seizure
  10. Shock
  11. Uremia
  12. Temperature (42C can cause coma)
  13. Endocrine (Thyroidism
  14. Electrolyte (Hyper/hyporglcemia, Natremia)
  15. Hepatic encephalopathy
  16. Toxins / drugs (Heroin, psychiatric medications)
247
Q

Risk factors for stroke?

A
  1. Prior TIA (30% will have stroke in 5 years)
  2. Hypertension
  3. Atherosclerosis
  4. DM
  5. Hyperlipidemia
  6. Smoking
248
Q

What types of stroke are there?

A
  1. Ischemic Stroke (2/3 most common)
  2. Hemorrhagic Stroke
  3. Thrombotic syndromes
  4. Embolic syndomes
249
Q

What can cause an ischemic stroke?

A
  1. Cerebral thrombi (2/3): Atherosclerosis, Infective arteritis, Vasculitis, Hypercoagulable states…
  2. Cerebral emboli (1/3): Arotic plaques, Endocarditis, Air or Fat embolism due to trauma
250
Q

What can cause a Hemorrhagic stroke?

A
  1. Spontaneous rupture of berry aneurysm or AV malformation (subarachnoid hemorrhage)
  2. Rupture of arteriolar aneurysms due to: HT, congenital anomalies, blood dyscrasias or anticoagluant usage, infection, neoplasm
  3. Trauma (epidural or subdural hematoma)
  4. Hemorrhagic transformation of embolic stroke
251
Q

What can you tell about Subarachnoid Hemorrhage?

A
  • Highest incidence in 35-65 year old
  • Usually from rupture of berry aneurysm
  • Clincally: «worst headache of my life», nuchal rigidity, photophobia, vomiting, retinal hemorrhages
  • Diagnosis: CT (92% sensitive within 24 hours after event, looses sensitivity >24 hours from headache onset, >72 hours can not rule out without lumbar puncture)
  • Management: Nimodipine 60 mg to reduce vasospasm
252
Q

Causes of Intracerebral hemorrhage?

A
  • Hypertension
  • Trauma: contusion, coup/contracoup
  • Rupture of small blood vessels inside brain parenchyma
253
Q

Treatment protocol for mild strokes?

A
  1. Aspirin 81-325 mg (mild ischemic stroke)
  2. Keep SBP >90 mmHG
  3. Keep CPP >60 mmHG (CPP = MAP - ICP)
  4. Treat fever; mild hypothermia is beneficial;
  5. Oxygenate (SAT >95)
  6. Elevate head of bed 30 degrees (clear c-spine first!)
  7. Frequent neurological checks, CT, reassess GCS.
  8. Patients with systolic BP >220, diastolic >120 need BP control with nitroprusside or labetalol
254
Q

When are thromolytics used for stroke?

A
  • Mainly used for ischemic infarcts with large deficits
  • < 3hours since onset of symptoms
255
Q

Relative contraindications to thrombolytics?

A

Though there is no ABSOLUTE contraindication, there are relative contraindications to thrombolytics:

  1. Evidence of hemorrhage on CT
  2. Active internal bleeding within last 21 days
  3. Known bleeding
  4. Within 3 months of IC injury, prior surgery or prior ischemic stroke
  5. Within 2 weeks of serious trauma or major surgery
  6. History of previous ICH, tumor or aneurysm
  7. Systolic BP >185 mmHg or diastolic BP >110 mmHg
256
Q

Approach for 1st seizure?

A
  1. ABC’s first
  2. Monitor: blood CBC, O2, anticonvulsant levels, prolactin, lactate
  3. CXR / UA / Head CT
  4. Is patient actively seizing? Consider treatment options
  5. Complete history and physical exam, including neurological evaluation with repeat after some time!
257
Q

What is Status Epilepticus?

A

Seizure lasting >5 minutes OR two seizures between which there is incomplete recovery of consciousness

258
Q

Indications for head CT of postictal patients?

A
  1. Status epilepticus
  2. Abnormal neurological findings
  3. No return to GCS 15
  4. History of malignnacy
  5. Closed head injury
  6. HIV infection or at risk for HIV
  7. Anticoagulant use
  8. Age >40
259
Q

What is the Monro-Kellie Doctrine?

A

A description of the relationship between the contents of the cranium and intracranial pressure.

260
Q

Possible findings in patients with Closed head injury (CHI)?

A
  1. Concussion: Loss of concioussness, retrograde amnesia
  2. Coup: injury beneath side of trauma
  3. Contrecoup: injury to opposite side of traumatized area
  4. Diffuse axonal injury: Tearing of nerve fibers at the time of impact. Causes prolonged coma, normal initial CT but poor outcome.
  5. Cerebral contusion: bruise of the brain tissue
261
Q

What can you tell about Subdural Hematoma?

A
  1. Trauma causing tearing of the bridging veins that extend from subarachnoid space to dural sinuses
  2. Blood dissects over the cerebral cortex and collects in the dura
  3. Appears as sickle shape
  4. Patients at risk: alcoholics, elderly, anticoagulant users
262
Q

What can you tell about Epidural hematoma?

A
  • Commonly seen in blunt trauma to the head (especially over parietal/temporal area)
  • Presents as: LOC –> lucid interval –> progressive deterioration –> coma –> death
  • Associated with linear skull fracture (mainly due to tear of artery, especially middle meningeal)
  • Other symptoms: ipsilateral pupil dilatation with contralateral hemiparesis
  • CT: bioconvex shape, can extend across midline.
263
Q

Management protocol of Closed Head Injuries (CHI)?

A
  1. ABC (c-spine precautions!)
  2. Monitoring
  3. Stabilize and resuscitate if needed
  4. SaO2 >95%
  5. SBP >110
  6. CPP between 60-70 mmHg
  7. Treat fever (if patient has fever)
  8. Head of bed 30 degrees elevated (once c-spine is cleared)
  9. Head CT with neurosurgical evaluation for surgical lesions
264
Q

What is the most important factor in the neurologic assessment of the head injured patients?

A

Level of consciousness

265
Q

Most common intracranial bleed in CHI?

A

Subarachnoid hemorrhage

266
Q

Signs of herniation or increased ICP?

A
  1. Headache, nausea, vomiting
  2. Decreasing consciousness
  3. Sixth nerve palsies (one or both eyes adducted)
  4. Decreased respiratory rate
  5. Cushing reflex (hypertension/bradycardia/bradypnea)
  6. Papilledema
  7. Fixed and dilated pupil
  8. Contralateral hemiparesis
267
Q

Which factors has to be in place to suspect something other than hypovolemia to be the cause of hypotension in CHI patients?

A

To suspect something other than hypovolemia to be the cause of hypotension in CHI patients, their must be this following combination of symptoms:

  1. Hypotension
  2. Bradycardia
  3. Warm extremities

This combination is a sign of spinal cord injury

268
Q

What is Uncal herniation, and what are the symptoms?

A

Unilateral mass presses the uncus (temporal lobe) through tentorial incisa

Symptoms:

  1. Ipsilateral pupil dilatation
  2. Contralateral hemiparesis
  3. Deepening coma
  4. Decorticate posturing
  5. Apnea
269
Q

What is Cerebellar herniation, and what are the symptoms?

A

Downward displacement of cerebellar tonsils through the foramen magnum.

Symptoms:

  1. Pinpoint pupils
  2. Flaccid quadriplegia
  3. Apnea
  4. Circulatory collapse
270
Q

What is “brain death” defined as?

A

An abscence of cerebral function, brainstem function and apnea

271
Q

The most common causes brain death?

A
  1. Cerebral anoxia
  2. Cerebral hemorrhage
  3. Subarachnoid hemorrhage
  4. Trauma
  5. Meningitis
272
Q

Clinical factors for diagnosing brain death?

A
  1. Known irreversible cause
  2. Exclusion of potentially reversible conditions
  3. Core body temperature >32 degrees
  4. Coma
  5. No response to noxious stimuli (no pain response)
  6. No brain stem reflexes (pupillary, gag, cough etc…)
  7. Apnea (no spontanous breathing)
  8. Brain perfusion test (cerebral angiography)
273
Q

Which infections most commonly cause infectious neurological emergencies?

A
  1. Meningitis
  2. Encephalitis
274
Q

Types of headache?

A
  1. Migraine
  2. Cluster headache
  3. One sided, beyond eye
  4. Subarachnoid hemorrhage
  5. Temporal arteritis
  6. Trigeminal neuralgia
275
Q

How are the airways of the typical pediatric patient structured?

A
  • Large head
  • Relatively narrow nasal passages
  • Large tongue
  • Position of larynx (C3-4)
  • Lower respiratory tract immature at birth (we are born with 20 mill alveoli at birth, which increase to 300 mill by age 6)
276
Q

What kinds of disadvantages do neonates have in lower resp-tract and chest wall when compared to adults?

A
  1. Soft, non-calcified ribs
  2. The lower, non-cartilagenous airways show increased closing capacity (risk of shunting)
  3. Poorly developed intercostal muscles (minor contribution to ventilation)
  4. Diaphragm is easily fatigueable, and has lower mechanical efficiency
277
Q

Factors preventing closure of the ductus arteriosus?

A
  1. Hypoxemia
  2. Acidosis
  3. Fluid overload
  4. Hypothermia
278
Q

Differences in the heart of a neonate when compared to one of an adult?

A
  1. Right and left ventricles are similarin size at birth
  2. low muscle content in the ventricular wall –> low compliance of the ventricles
  3. Cardiac output in the neonate heart is HR - dependent!
  4. Autonomic innervation of the heart at birth is predominantly parasympathetic
279
Q

Differences in the CNS of a neonate when compared to one of an adult?

A
  1. Soft cranium wit non-fused sutures and two open fontanelles
  2. Brain is incompletely myelinated
  3. The cortex is poorly developed
  4. Fragile supendymal blood vessels (pre-term)
  5. Newborn brain metabolism is 30-50% of the total metabolism (in an adult is 20%)
280
Q

How is fluid homeostasis different in a newborn?

A

Renal function is immature!

  1. Neonate is unable to concentrate urine (800 mOsm/l
  2. Neonate is unable to excrete a larger water load (low glomerular filtration rate)
  3. Limited tubular secretion and resorption of water, glucose, Na+ and bicarb
281
Q

How is thermal homeostasis different in a newborn?

A
  • Infant have larger surface area in relation to body mass, and start developing hypothermia at an ambient temperature of 23 degrees celcius
  • Decreased temperature in the neonate increases oxygen and glucose demands –> acidosis
  • The only mechanism available to the neonate to maintain thermal neutrality is non-shivering thermogenesis (metabolism of brown fat)
282
Q

What are some distinct factors to take into account when considering general anesthesia in children?

A
  1. History of difficult airway?
  2. Opening of the mouth, and resp-tract
  3. Craniofacial dysmorphias
  4. Presence or absence of nasal flaring
  5. Presence or absence of mouth breathing
  6. Presence or absence of retractions
  7. Is the childe above 8? (cannot use cuffed tubes for <8)
283
Q

How does giving inhalation agents to pediatric patient differ than adults?

A
  • Sevoflurane is the main choice!
  • Uptake and distribution in children is more rapid than in adults
  • The ratio of alveolar ventilation to FRC is 5:1 compared to 1,5:1 in adults
  • In neonates, the low protein and lipid contents of both blood and tissues reduces the solubility of volatile anesthetics compared with adult
284
Q

What are some of the intravenous anesthetic used in pediatric patients?

A
  1. Sodium thiopental: the most used for IV induction
  2. Ketamine: for neonates with hypotension
  3. Propofol: induction and maintenance (not for <2 months age)
  4. Fentanyl: much lower dose than adults
  5. Remifentanil: good for short procedures
  6. Morphine: last choice (s.e respiratory depression)
285
Q

Which muscle-relaxants are used for pediatric patients?

A

Depolarizing:

  • Succinylcholine

Non-depolarizing:

  1. Atracurium
  2. Cisatracurium
  3. Rocuronium
  4. Wecuronium
286
Q

Side effects of Succinylcholine in pediatric pateints?

A
  1. Jaw stiffness
  2. Arrythmias
  3. Hyperkalemia
  4. Myoglobinemia
  5. Fasciculations
287
Q

Reversal agent used against muscle relaxants in pediatric patients?

288
Q

Limitations of Bridion?

A
  1. Slow in reversing neuromuscular blockade
  2. Limited ability to reverse deep blockade
  3. Efficacy influenced by maintenance anesthetics
  4. Require concomittant administration of anticholinergics (due to Bridion’s pro-cholinergic side-effects)
289
Q

Side effects of Bridion?

A

Pro-cholinergic side effects

  1. Bradycardia
  2. Hypersalivation
  3. Bronchospasm
  4. Increased bronchial secretions
290
Q

Safety issues of regional anesthesia in pediatric patients?

A
  1. Need for children to be anesthezied for placement of the regional block
  2. Risks of infection
  3. The regional anesthesia might mask an underlying compartment syndrome
291
Q

Why does Amide-anesthetics have high risk of toxicity in infants?

A

Amide anesthetics are in the plasma. Infants <6 months have decreased levels of plasma proteins –> larger free fraction of local anesthetic –> greater risk of toxicity

292
Q

Local anesthetics used in children?

A
  1. Lidocaine
  2. Lidocaine with epinephrine
  3. Bupivacaine
  4. Levobupivacaine
  5. Ropivacaine

(all of these are Amide-anesthetics)

293
Q

What factors must be in place before removing breathing tube in postop pediatric patient?

A
  1. Normothermic
  2. Normocapnic
  3. Normal serum Hb and electrolytesl
  4. Any residual neuromuscular blockade should be reversed
294
Q

Chemical compounds that can inhibit the excitation-conduction process in the peripheral nerve?

A
  1. Biotoxins (saxitoxin, tetrodotoxin)
  2. Phenothiazines (phenergan)
  3. Betablockers (propanolol)
  4. Opioids (fentanyl, pethidine)
  5. Tricyclic antidepressants
  6. Alpha-adrenergic agonists (clonidine)
  7. Local anesthetics; aminoesters and aminoamides
295
Q

Difference between aminoester- and aminoamide anesthetics?

A

Aminoesters:

  • Relatively unstable linkage, and are broken down in plasma by cholinesterase
  • They can produce allergic reactions

​​Aminoamides:

  • Not damaged by high temperatures
  • Their linkage is much more stable than an ester
  • Are metabolized in the liver
296
Q

Which pharmacologic factors affect the anesthetic action?

A
  1. pKa - affect the onset of the drug
  2. Lipid solubility - affect the potency of the drug
  3. Protein binding - affect the drug’s duration of action
297
Q

Why does pKA affect the onset of drug action?

A

pKa the pH at which the ionized and neutral forms of local anesthetic are present in equal amounts. The closer the the drug pKa is to the normal body pH, the shorter onset of action.

298
Q

Which non-pharmacologic factors can affect local anesthetic action?

A
  1. Dosage of LA administered
  2. Addition of vasoconstriction
  3. Site of administration (nerve amount vs vascular absorption)
299
Q

How does vasoconstriction affect local anesthetic potency?

A
  • Vasodilation enhances vascular uptake of LA, therefore vasoconstriction slows it down
  • Result: prolonging duration of action, greater nerve block
  • Epinephrine 5mg/ml most commonly used
300
Q

Most commonly used local anesthetics (adults):

A
  1. Lidocaine
  2. Prilocaine
  3. Mepivacaine
  4. Bupivacaine
  5. Articaine
  6. EMLA (mix of lidocaine and prilocaine)
301
Q

What is Lidocaine?

A
  1. Most versatile and commonly used LA
  2. Rapid onset, moderate duration
  3. Duration prolonged with epinephrine
  4. Available for infiltration, peripheral and epidural analgesia
  5. Topical anesthetic activity (1-7,5%)
  6. Total dose 5mg/kg, with epinephrine 7,5mg/kg (REMEMBER!)
  7. Used as i.v agent for treatment of ventricular arrythmias and neuropathic pain
302
Q

Which injection sites can mixing epinephrine with lidocaine cause risk of necrosis?

A
  1. Digits
  2. Nose
  3. Ears
  4. Penis
303
Q

What is Prilocaine?

A
  • Similar to lidocaine in terms of anesthetic profile
  • Used for infiltration and peripheral nerve blockes and epidural analgesia
  • Can be used without epinephrine, with same duration as lidocaine/epinephrine
  • Significantly less toxic than lidocaine
  • Doses >600 mg may cause methemoglobinemia (especially in pediatric patients)
304
Q

What is Mepivicaine?

A
  1. Similar to lidocaine
  2. Rapid onset with deeper anesthesia
  3. Used mostly in dental practice
  4. Used for infiltration, peripheral nerve blocks and epidural analgesia
  5. Duration prolonged with epinephrine
  6. Total dose same as lidocaine
  7. Not effective for topical anesthesia
305
Q

What is Bupivicaine?

A
  1. LA with a long duration of action (3-10 hours), slow onset
  2. Causes long sensory bock and short motor block
  3. Used in concentration 0.1-0.5%
  4. Can be given with epinephrine
  5. Total dose 2-3 mg/kg
  6. Cardiotoxic in obstetric patients.
306
Q

What is Articaine?

A
  1. Best choice of local anesthetic in dentistry
  2. Metabolized in serum
  3. Can be used with adrenaline
  4. Better safety than other aminoamides
307
Q

What is EMLA?

A
  • Lidocaine 25mg/ml + prilocaine 25 mg/ml, available in oily cream
308
Q

What is the most common side-effect of Local Anesthesia?

A

Psychogenic side-effects:

  • Syncope
  • Hyperventilation
  • Nausea and vomiting
  • Abnormal HR and BP
309
Q

Signs of local anesthetic-induced cardiovascular toxicity?

A

FIRST sign is numbness of the tongue and metallic taste!

Stage:

  1. CNS excitation, Hypertension, tachycardia
  2. Myocardial depression, decreased CO, mild-moderate hypotension
  3. Peripheral vasodilation, profound hypotension, sinus bradycardia, conduction defects, ventricular arrythmias, circulatory collapse
310
Q

Most common symptoms of intoxication of local anesthetics?

311
Q

Explain the main factors of topical application of local anesthetics.

A
  • Site of action: sensory nerve endings of skin or mucosa
  • Agent: Lidocaine 1-10%
  • Formulations: Spray, ointments, powders
312
Q

Explain the main factors of infilitrative application of local anesthetics.

A
  1. Site of action: Sensory nerve and nerve endings in subcutis
  2. Agent: Lidocaine, prilocaine, mepivacaine, bupivacaine
  3. Formulations: Solutions with or without vasoconstrictor
  4. Popular in surgery before surgical incision
  5. Recommended in acute post-traumatic pain
313
Q

What is the monitoring protocol during nerve blocks?

314
Q

Advantages of regional anesthesia?

A
  1. Patient is conscious during surgery, can maintain own airway
  2. Smooth recovery
  3. Postoperative analgesia
  4. Reduction in surgical stress
  5. Earlier discharge for day-patients
  6. Less expensive
315
Q

Disadvantages of regional anesthesia?

A
  1. Patient may prefer to be asleep
  2. Practice and skill is required
  3. Some blocks require up to 30 minutes for effect
  4. Analgesia may not always be totally effective
  5. Generalized toxicity may occur
  6. Some operations are unsuitable for local anesthetics -
  7. Widespread symphathetic blockade can occur with spinal or epidural blockade
  8. There is some incidence of prolonged nerve damage
316
Q

Treatment for acute LA toxicity?

A
  1. Airway: establish clear airway, suction if required
  2. Breathing: oxygen with face mask, respirator if needed
  3. Circulation: Elevate legs, increase i.v fluid if hypotension, cardioversion if ventricular arrythmias
  4. Drugs:
  • Diazepam 5-10 mg
  • Thiopental 50-100 mg
  • Suxamethonium 50-100 mg
317
Q

What does pain mediators do?

A
  • Assist in transduction of signals for perception of pain (endocrine signaling and some are neurotransmitters)
  • Bring pain treshold down
318
Q

Example of pain mediators?

A
  1. Prostanoids
  2. Bradykinin
  3. Histamine
  4. Kalium ions
  5. Cytokines: TNF, IL-1, IL-6
319
Q

Symptoms of the typical chronic pain patient?

A
  1. Sleep disturbances
  2. Appetite changes
  3. Irritability
  4. Decreased libido and sexual activity
  5. Low confidence in ability
  6. Decreased pain threshold
  7. Fatigue
  8. Mental retardation
320
Q

Most common body location for chronic pain?

A
  1. Lower back
  2. Head
  3. Leg
  4. Knee
  5. Joints
  6. Abdomen
321
Q

Most common causes for chronic pain?

A
  1. Arthritis/osteoarthritis
  2. Tension headache
  3. Herniated/deteriorating disc
  4. Traumatic injury
  5. Rheumatoid arthritis
  6. Migraine headaches
  7. Nerve damage
  8. Surgery
322
Q

Symptoms of osteoarthritis?

A
  1. Pain (acute and chronic)
  2. Morning stiffness
  3. Restriction in range of movement
  4. Joint laxity
  5. Joint deformity
  • The KNEE is the principal large joint to be affected
  • The HIP is the next most prevalent site for large joint OA
323
Q

Treatment of osteoarthritis?

A
  1. Weight loss 5-10% of bodyweight –> pain relief
  2. Analgesics, topical agents, NSAIDS, opioids
  3. Dietary supplements: Glucosamine sulphate
  4. Surgery
324
Q

How are NSAIDS classified?

A

Group 1: Non-selective, Group 2: Preferential, Group 3: Selective

325
Q

Contraindications and risk factors for NSAID use?

A
  1. Bleeding disorders
  2. Peptic ulcer
  3. History of hypersensitivity to NSAIDs
  4. Cardiovascular abnormalities
  5. Severe renal impairment
  6. Severe hepatic disease
  7. Elderly
326
Q

Acute low back pain causes?

A
  1. Disc and zygapophyseal joint trauma or degeneration - 90%
  2. Tumors - 0.7%
  3. Infections - 0.01%
327
Q

Chronic low back pain causes?

A
  1. Internal disc disruption - 40%
  2. Sacroiliac joint pain - 20%
  3. Zygapophyseal joint pain - 10-15%
328
Q

RED FLAGS in low back pain?

A
  1. Possible fracture
  2. Possible tumor or infection
  3. Possible cauda equina syndrome
329
Q

Treatment of low back pain?

A
  1. Analgesics
  2. Topical NSAIDS (if not enough, systemic)
  3. Muscle relaxants in some patients
  4. Walking around and spinal manipulation
330
Q

What is Neuropathic pain?

A
  • Non-nociceptive pain
  • It is pain arising as direct consequence of a lesion or disease affecting the somatosensory system
  • Often experienced in parts of body that otherwise appear normal
  • Often chronic and severe
  • Resistant to analgesics
331
Q

Causes of Neuropathic pain?

A

MOST common causes:

  • Postherpetic neuralgia
  • Diabetic neuropathy

Other causes:

  1. Post-amputation pain
  2. MS
  3. Myelopathy
  4. Spinal cord injury pain
  5. Trigeminal neuralgia
332
Q

Pain in Postherpetic neuralgia?

A
  • Pain persisting or recurring at the site of shingles, at least THREE MONTHS after onset of acute rash
  • Can persist even after treatment of the herpetic infection
333
Q

Treatment of neuropathic pain in postherpetic neuralgia?

A
  1. Antiviral medication: Acyclovir, Valacyclovir etc…
  2. Nerve blocks
  3. Tricyclic Antidepressants
  4. Antaconvulsants: Gabapentin etc…
334
Q

Treatment protocol for neuropathic pain?

A

Initiate therapy of the disease causing neuropathic pain and give one or a combination of following:

  1. Secondrary amine TCA
  2. SNRI (duloxetine, venlafaxine)
  3. Topical lidocaine for localized pain
  4. Opioid analgesics or tramadol
335
Q

What is Cancer pain?

A
  • Pain indicates recurrence of cancer
  • >80% can be controlled using low-cost, low-tech, simple methods
  • Character can be nociceptive, neuropathic, or both.
336
Q

What are the causes of pain in cancer?

A
  1. Cancer itself - 85%
  2. Treatment - 17%
  3. Concurrent disorder - 9%
337
Q

What is Breakthrough pain?

A
  • Specific short pain seen in cancer patients
  • Treatment: Fentanyl (intranasal or intrabuccal)
338
Q

Pain-managment protocol in cancer patients?

339
Q

The drug of choice for severe cancer-related pain in the elderly?

A

Buprenorphine: a mixed partial agonist opioid receptor modulator.

340
Q

Side effects of opioids?

A
  1. Nausea & vomiting (tolerance develop after few days)
  2. Respiratory depression (0.2%)
  3. Sedation
  4. Constipation (prescribe laxatives with it, no tolerance development)

5 MD (7 decks)

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