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Diploma in Anaesthesia > Respiratory & Cardiovascular problems > Flashcards

Respiratory & Cardiovascular problems Flashcards

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1
Q

the rate at which hypoxaemia develops is dependent on the:

A
  1. Adequacy of ventilation
  2. Effectiveness of gas exchange
  3. Metabolism (O2 consumption and CO2 production)
  4. O2 reserve (FRC volume and composition)
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2
Q

Describe an approach to intra-operative hypoxaemia

A

CHECK PATIENT

  1. Airway
  2. Breathing
  3. Circulation
  4. Disability - depth of anaesthesia

CHECK MACHINE AND EQUIPMENT

  1. FGF and FiO2
  2. Manual ventilation
  3. Monitors: FiO2, ETCO2, SpO2, ETCO2 morphology
  4. IPPV mode and settings check
  5. Check airway pressure and flow monitoring
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3
Q

Describe 4 important changes to capnograph tracing

A
  1. Absent trace - complete failure of ventilation
  2. Notched trace - Patient respiratory effort during IPPV
  3. Slow rising initial phase - Upper airway obstruction
  4. Slow rising ‘plateau’ phase - Bronchospasm
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4
Q

When is laryngospasm likely to occur

A

Laryngospasm may be provoked by stimulation of the airway during light planes of anaesthesia by airway instrumentation, blood, secretions or volatile anaesthetic agents.

Strong surgical stimuli away from the larynx, such as anal dilatation, may also produce laryngospasm if the depth of anaesthesia is inadequate.

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5
Q

Differentiate partial from complete laryngospasm

A

Complete laryngospasm - silent with absent airflow into lungs

Incomplete laryngospasm - stridor with obstructed airflow into lungs

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6
Q

What is the treatment of laryngospasm?

A
  1. Increasing the depth of anaesthesia, (e.g. boluses of IV propofol)

OR

  1. Muscle relaxation (give suxamethonium if dangerous hypoxaemia is present or impending).

Application of gentle CPAP with 100 % oxygen may improve oxygenation until the above takes effect.

Be aware that stomach inflation may occur as a result of attempted positive pressure ventilation against a closed glottis.

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7
Q

What are the causes of bronchospasm

Summarize treatment of bronchospasm

A
  1. Exclude anaphylaxis
  2. Drugs
    - Beta blockers
    - NSAIDS
    - Atracurium
  3. Irritable airways in GA
    - Asthma/COPD
    - Smokers
    - Recent LRTI
Rx: 
Remove secretions (suction) Inhaled/IV bronchodilators
IV salbutamol: 0.5 mg IV slowly (5 - 10 mins) followed by maintenance 0.5 mg over 1 hour (watch for hypokalaemia)
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8
Q

What are risk factors for a pneumothorax in the anaesthetic context?

A 
chest trauma, 
bullous lung disease, 
subclavian CVC placement
brachial plexus block 
laparoscopic and thoracic surgery.
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9
Q

Hypoxaemia may occur in the face of apparently normal ventilation. What may cause this?

A

Ventilation/perfusion mismatch causing shunt. V/Q mismatch results when ventilation of areas of the lung is inadequate to fully oxygenate blood flow. Shunting occurs when blood passes though areas of the lungs that have no ventilation. Causes include, alveolar collapse and bronchial intubation.

Shunt will not be corrected by increasing the FiO2.

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10
Q

What are the adverse effects of hypercarbia

A 
Increased SNS (dysrhythmia) 
Direct myocardial depression
Acidosis
Increased ICP and intraocular pressure
Narcosis
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11
Q

Classify the causes of hypercarbia

A

Inadequate ventilation

Rebreathing

  • Excessive dead space
  • Exhausted soda lime
  • Inadequate FGF

Increased CO2 load

  • Carboperitoneum (laparoscopy)
  • MH
  • Following tissue revascularization (aortic cross clamp release

Severe lung disease

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12
Q

How does ETCO2 differ from PaCO2

A

In health PaCO2 is about 0.5 kPa higher (must be a concentration gradient for diffusion)

In severe lung disease the PaCO2 - ETCO2 gradient may be larger

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13
Q

What adjustment to ventilation settings is the most effective for the elimination of CO2 and why?

A

Increasing Vt is more effective than increasing respiratory rate as an increase in Vt increases alveolar ventilation relative to the dead space.

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14
Q

Why is a rise in ETCO2 observed during laparoscopy

A

Peritoneal absorption of insufflated CO2

Increased intra-abdominal pressure and reduced lung compliance.

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15
Q

What is significant hypotension?

A

a drop of 20% below preoperative values

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16
Q

List the common causes of intraoperative hypotension

A
  1. Hypovolaemia (haemorrhage or other fluid loss)
  2. Impaired venous return (Compressed IVC or Tension Pneumothorax)
  3. Vasodilatation (Excessive anaesthetic depth, neuraxial block esp. when combined with GA)
  4. Obstructive shock: PE, Air embolus
  5. Ventricular impairment
  6. Dysrhythmia
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17
Q

What is the immediate management of intraoperative hypotension

A

FLUID
Assess fluid status and administer fluid bolus (250 - 500 mL) - caution in cardiac impairment

VASOPRESSOR INCREMENTS
High heart rate: Phenylephrine 50 - 100 mcg/dose
N/low heart rate: Ephidrine 3mg

INOTROPIC SUPPORT (If there is evidence of ventricular impairment)
Adrenalin
Dobutamine

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18
Q

What actions should be taken if intraoperative hypotension persists despite initial management

A

Assess tissue perfusion

  • CRT/Peripheral pulses
  • Urine output
  • ABG

Further fluid/vasopressor/inotropic management and post operative ICU

19
Q

List the causes of intraoperative hypertension

A
  1. SNS response to laryngoscopy or surgery
  2. Surgical (Aortic cross clamping)
  3. Pharmacological (Error or absorption of adrenalin from LA solutions)
  4. Pathological (Pre-ecclampsia, RICP - Cushings response, Phaeochromocytoma)
  5. Hypoxia and Hypercarbia
20
Q

When should intraoperative hypertension be treated during anaesthesia?

A

When all possible causes have been addressed and HPT remains

21
Q

What drugs are used to treat intraoperative hypertension

A
  1. Increase volatile anaesthetic (be aware of myocardial depression)
  2. Hydralazine 5mg IV increments
  3. Phentolamine 1 - 2 mg IV increments
  4. Labetalol 5 - 10 mg IV increments
  5. Glyceryl trinitrate 1mg/ml - start at 3ml/hr
22
Q

List the causes of intraoperative bradycardia

A

SURGICAL STIMULATION (VAGAL REFLEX)

  • Peritoneal traction/distension
  • Extraocular muscle traction
  • Carotid sinus manipulation

DRUGS

  • Neostigmine
  • Succinylcholine (second dose)
  • Opioids
  • Phenylephrine/metaraminol

HIGH NEURAXIAL BLOCK
HYPOXIA (Brady is a late sign)
CARDIAC PATHOLOGY (Ischaemia, SSS, heart block)

23
Q

How is intra-operative bradycardia managed

A

Most will resolve once the vagal surgical stimulus is stopped.

Find and treat cause

If persistent
Atropine 0.5 mg
OR
Glycopyrrolate 0.5 mg

If ineffective:
Adrenalin 50 ug increments –> 0.5 mL of a 1: 10 000

If ineffective:
Pacing

24
Q

Classify the causes of intra-operative tachycardia

A 
SNS (Laryngoscopy/response to surgery)
Hypotension
Drugs: (e.g. cyclizine)
Pathological causes (Sepsis)
Hypercarbia
25
Q

Name 3 beta blockers used intra-operatively. What receptors do these agents act at and what is the dose administered of each

A

Metoprolol 1 -2 mg IV increments (beta blocker)

Esmolol 0.5 mg/kg then 0.05 - 0.2 mg/kg/min infusion

Labetalol 5 - 10 mg IV increments (some alpha blocking action present)

26
Q

Classify and list common causes of AF

A

Metabolic

  • HypoK
  • HypoMg
  • Acidosis
  • Sepsis
  • Hypercarbia
  • Hyperthyroidism

Myocardial ischaemia

  • Tachycardia
  • Hypotension
  • Hypoxaemia
  • Coronary artery disease

Direct stimulation

  • Thoracic/upper GI surgery
  • Central line/PAFC

Patient factors

  • Valvular disease
  • Hypertension
27
Q

When should anticoagulation be considered prior to cardioversion?

A

If AF has been present > 48 hours but NOT if patient is haemodynamically unstable

28
Q

What is important with regard to the diagnosis of intra-operative anaphylaxis

A

Context and timing

  • High Paw
  • Cycling NIBP without display
  • Flushed face
  • Weak carotid pulse

Shortly after induction !

29
Q

What is TRUE anaphylaxis

A

Type 1 immediate hypersensitivity reaction which involves prior sensitization to an allergen with the presence of IgE

Allergen binds to IgE on Mast cells –> cell membrane breakdown and release of inflammatory mediators

  • Histamine
  • Proteases
  • Cytokines
30
Q

What does the term anaphylactoid mean?

A

PRIOR EXPOSURE TO CAUSATIVE AGENT NOT NEEDED
Same presentation as anaphylaxis but different causative mechanism (NO IgE)
- possible mechanisms include IgG-linked direct mast cell activation or complement-mediated mechanisms

31
Q

How does acute management of anaphylaxis and anaphylactoid reactions differ?

A

Same treatment in the acute setting regardless of causative mechanism

32
Q

List the 5 presenting symptoms of anaphylaxis during anaesthesia in descending order of likelihood

A
  1. No pulse
  2. Difficult ventilation
  3. Angioedema
33
Q

List the 3 most common causative agents for anaphylaxis in an anaesthetic context

A

62 % Muscle relaxant (Sux/Roc/Vec/Atrac)

17% Latex: Catheters/gloves (30 - 60 minutes into the procedure)

34
Q

What immediate action should be taken if a patient is difficult to ventilate, hypotensive, CVS collapse ± angioedema shortly after induction?

A
  1. Stop suspected trigger
  2. Get help and inform surgeon
  3. Elevate legs
  4. FIO2 100% with low [Volatile}]
  5. Adrenalin 1ml of 1:10 000 IV increments titrated
    (IM adrenalin 0.5 - 1mg works within 1 - 2 mins and has a more sustained duration of action)
  6. Fluid (500 - 1000 ml or 20ml/kg in kids)
  7. Start CPR if required
35
Q

What is the mechanism of action of adrenalin specific to the treatment of anaphylaxis

A

α-receptor agonist
- VC reverses peripheral VD and reduces oedema

β-receptor activity

  • BD
  • Inotropy
  • Mast cell deactivation
36
Q

What is the second line therapy for anaphylaxis

A
  1. Chlorphenamine (H1 - antagonist) (10/5/2.5/1.25)
  2. Hydrocortisone (200/100/50/25)

If bronchospasm is predominant

  • Salbutamol
  • Ipratroprium
  • Aminophylline
37
Q

In the context of intra-operative anaphylaxis what governs the decision regarding proceeding with surgery

A

Severity of reaction
Stage of the procedure
Consequences of abandoning surgery

38
Q

What blood test can be ordered with regard to the CONFIRMATION of the diagnosis of anaphylaxis

A

Tryptase levels

39
Q

What is tryptase
When do tryptase levels peak
When are tryptase levels normal subsequent to anaphylaxis

A

Major protein component in mast cell granules
Peak: 1 -2 hours
Normalize: 6 - 8 hours

40
Q

How should blood be sampled for tryptase analysis

A

Sample 1 - ASAP
Sample 2 - at 1 - 2 hours after
Sample 3 - > 24 hours (excludes elevated baseline levels

41
Q

What action should be taken with regard to the long term management of patient’s who recover from anaphylaxis

A

Refer to allergy clinic to:

  1. Confirm the cause
  2. Skin testing 4 - 6 weeks after the event
  3. Education/Medicalert bracelet/Epipen
42
Q

How often do biphasic reactions occur in patients recovering from anaphylaxis

A

20%

43
Q

In the anaesthetic context list in descending order the most likely causative agents for anaphylaxis

A

Trigger Agents
%

Muscle relaxants
62

Latex
17

Antibiotics
8

Hypnotics
5

Colloids
3

Opioids
3

Diploma in Anaesthesia (73 decks)

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