Respiratory & Cardiovascular problems

Question 1

the rate at which hypoxaemia develops is dependent on the:

Answer 1

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

Question 2

Describe an approach to intra-operative hypoxaemia

Answer 2

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

Question 3

Describe 4 important changes to capnograph tracing

Answer 3

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

Question 4

When is laryngospasm likely to occur

Answer 4

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.

Question 5

Differentiate partial from complete laryngospasm

Answer 5

Complete laryngospasm - silent with absent airflow into lungs

Incomplete laryngospasm - stridor with obstructed airflow into lungs

Question 6

What is the treatment of laryngospasm?

Answer 6

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

OR

2. 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.

Question 7

What are the causes of bronchospasm

Summarize treatment of bronchospasm

Answer 7

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)

Question 8

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

Answer 8

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

Question 9

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

Answer 9

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.

Question 10

What are the adverse effects of hypercarbia

Answer 10

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

Question 11

Classify the causes of hypercarbia

Answer 11

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

Question 12

How does ETCO2 differ from PaCO2

Answer 12

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

Question 13

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

Answer 13

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

Question 14

Why is a rise in ETCO2 observed during laparoscopy

Answer 14

Peritoneal absorption of insufflated CO2

Increased intra-abdominal pressure and reduced lung compliance.

Question 15

What is significant hypotension?

Answer 15

a drop of 20% below preoperative values

Question 16

List the common causes of intraoperative hypotension

Answer 16

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

Question 17

What is the immediate management of intraoperative hypotension

Answer 17

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

Question 18

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

Answer 18

Assess tissue perfusion

• CRT/Peripheral pulses
• Urine output
• ABG

Further fluid/vasopressor/inotropic management and post operative ICU

Question 19

List the causes of intraoperative hypertension

Answer 19

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

Question 20

When should intraoperative hypertension be treated during anaesthesia?

Answer 20

When all possible causes have been addressed and HPT remains

Question 21

What drugs are used to treat intraoperative hypertension

Answer 21

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

Question 22

List the causes of intraoperative bradycardia

Answer 22

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)

Question 23

How is intra-operative bradycardia managed

Answer 23

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

Question 24

Classify the causes of intra-operative tachycardia

Answer 24

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

Question 25

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

Answer 25

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)

Question 26

Classify and list common causes of AF

Answer 26

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

Question 27

When should anticoagulation be considered prior to cardioversion?

Answer 27

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

Question 28

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

Answer 28

Context and timing - High Paw - Cycling NIBP without display - Flushed face - Weak carotid pulse Shortly after induction !

Question 29

What is TRUE anaphylaxis

Answer 29

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

Question 30

What does the term anaphylactoid mean?

Answer 30

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

Question 31

How does acute management of anaphylaxis and anaphylactoid reactions differ?

Answer 31

Same treatment in the acute setting regardless of causative mechanism

Question 32

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

Answer 32

1. No pulse 2. Difficult ventilation 3. Angioedema

Question 33

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

Answer 33

62 % Muscle relaxant (Sux/Roc/Vec/Atrac) | 17% Latex: Catheters/gloves (30 - 60 minutes into the procedure)

Question 34

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

Answer 34

1. Stop suspected trigger 2. Get help and inform surgeon 3. Elevate legs 3. FIO2 100% with low [Volatile}] 4. 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) 5. Fluid (500 - 1000 ml or 20ml/kg in kids) 7. Start CPR if required

Question 35

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

Answer 35

α-receptor agonist - VC reverses peripheral VD and reduces oedema β-receptor activity - BD - Inotropy - Mast cell deactivation

Question 36

What is the second line therapy for anaphylaxis

Answer 36

1. Chlorphenamine (H1 - antagonist) (10/5/2.5/1.25) 2. Hydrocortisone (200/100/50/25) If bronchospasm is predominant - Salbutamol - Ipratroprium - Aminophylline

Question 37

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

Answer 37

Severity of reaction Stage of the procedure Consequences of abandoning surgery

Question 38

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

Answer 38

Tryptase levels

Question 39

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

Answer 39

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

Question 40

How should blood be sampled for tryptase analysis

Answer 40

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

Question 41

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

Answer 41

Refer to allergy clinic to: 1. Confirm the cause 2. Skin testing 4 - 6 weeks after the event 3. Education/Medicalert bracelet/Epipen

Question 42

How often do biphasic reactions occur in patients recovering from anaphylaxis

Answer 42

20%

Question 43

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

Answer 43

Trigger Agents % Muscle relaxants 62 Latex 17 Antibiotics 8 Hypnotics 5 Colloids 3 Opioids 3