Pharmacology

Question 1

Provisional diagnosis and differentials for:
You are called to a rural home address for
an 83-year-old patient complaining of
severe nausea.
Bucket on floor; chesty cough.
C/o increasingly unwell for the last few days. Abnormal fatigue, difficulty breathing on exertion, cough, severe nausea, abdo pain, loss of appetite, and light-headedness.
Hx: Takes digoxin, spironolactone, captopril, pravastatin, isosorbide monotitrate, furosemide, bisoprolol and potassium. Also ventolin and spirits inhalers.
Was started on clarithromycin a few days ago.

Answer 1

Digoxin toxicity, due to recent clarithromycin commencement which interacts with renal clearance of digoxin (thus increasing serum levels). This causes N+V, anorexia, abdo pain, and weakness.

Differentials: ADR to clarithromycin, exacerbation of HF/COPD (but nil orthopnoea/oedema)

Question 2

Pathophysiology of N+V and likely mechanism caused by digoxin toxicity

Answer 2

1. Chemoreceptor Trigger Zone (CTZ): detects circulating toxins and drugs (e.g., digoxin) through dopamine (D2) and serotonin (5-HT3) receptors, as well as others.
2. Vomiting Centre (brainstem): integrates inputs from CTZ, vestibular system, GI tract, and higher CNS.
3. Vagal afferents from GI tract and vagal tone (enhanced by digoxin) contribute to nausea.

In this case:
- Stimulation of the CTZ as well as vagal afferents due to elevated digoxin levels.
- Digoxin acts centrally (CTZ) and peripherally (increased vagal tone → GI dysmotility), both of which contribute to nausea and vomiting.

Question 3

Treatment for nausea and vomiting

Answer 3

Primary survey
1. Ensure airway patent, check if at risk of airway compromise
2. Breathing and circulation adequate.
Then positioning for comfort/ease breathing.
Ondansetron first line.
Would consider oxygen if SpO2 declined and fluids if BP declined.
Cardiac monitoring for digoxin toxicity
Transport due to high risk and suspected toxicity

Question 4

Ondansetron:
- MOA
- Contraindications/ADRs/considerations
- Dose/route/repeat

Answer 4

MOA: antagonist of 5-HT3 receptors, which blocks the action of serotonin centrally (in CTZ) and peripherally (in GI tract), therefore preventing activation of vomiting reflex.

CI: <2y, concurrent apomorphine administration, allergy/hypersensitivity
ADRs: headache, movement disorders/seizures, visual disturbance
Considerations: use in the elderly and pregnancy, give slowly

Dose: 4mg IV or IM, no repeat
(2-<8y, 2mg)

Question 5

Metoclopramide:
- MOA
- Contraindications/ADRs/considerations
- Dose/route/repeat

Answer 5

• D2 receptor antagonist in the CTZ which blocks dopamine from activating the vomiting centre.
• Contraindications: <16y, Parkinson’s, suspected bowel obstruction, haematomesis/malaena, previous dystonic reaction, allergy/hypersensitivity to metoclopramide
• ADRs: restlessness/drowsiness/fatigue, extrapyramidal reactions, hypotension
• Considerations: undiagnosed abdominal pain

Dose: 10mg IM/IV nil repeat >=16

Question 6

What are these home medications used to treat and do they have any influence on the presentation/trx of N+V:

Digoxin, spironolactone, captopril,
pravastatin, isosorbide mononitrate,
furosemide, bisoprolol and potassium – all
packed into a dose administration aid
(webster pack). Ventolin and Spiriva inhalers

Answer 6

Digoxin: heart failure/AF, toxic at high levels and interacts with clarithromycin.

Spironolactone: K+ sparing antihypertensive/HF, risk of dehydration

Captopril: Angiotensin converting enzyme (ACE) inhibitor for HTN/HF

Pravastatin: for high hyperlipidaemia

Isosorbide monotitrate: angina prevention, HF

Furosemide: loop diuretic for fluid overload from HF

Bisoprolol: beta blocker for HTN

Potassium: for hypokalaemia

Ventolin: beta2 agonist for COPD

Spiriva: Long-acting muscarinic antagonist (LAMA); inhaled corticosteroid for COPD

Question 7

Asthma pathophysiology

Answer 7

Chronic inflammatory airway disease characterised by smooth muscle hypertrophy, increased mucus production and subepithelial fibrosis due to airway remodelling over time. In acute attacks, a trigger (antigen) initiates the release of IgE which activates mast cells to release histamine, leukotrienes and prostaglandins. This leads to bronchospasm, mucus production and airway oedema —> narrowed airways and increased resistance (wheeze, reduced BS, incr. HR/RR)

Question 8

Treatment of asthma

Answer 8

Primary survey: airway? O2?
Position sitting upright, loosen tight clothing, remove from trigger, reassurance about slowing breathing
Salbutamol and ipratropium bromide nebulised, if severe may require adrenaline and hydrocortisone.
Consider ICP/exctrication backup and transport urgently.

Question 9

Salbutamol:
1. MOA
2. CI, ADR, considerations
3. Route/dose/repeats

Answer 9

1. Short-acting beta2 adrenergic receptor agonist that acts on bronchiole smooth muscle to cause relaxation of smooth muscle and thus bronchodilation. Opens up airways to improve airflow and relieve bronchospasm
2. Nil CIs, ADR tachycardia, dysrhythmias, tremors/shakes. Considerations is 2 different preparations and can use spacer or nebuliser (Mod-sev)
3. 5mg nebulised repeat prn no max (>=5y). 2.5mg for <5.

Question 10

Ipratropium bromide
1. MOA
2. CI, ADR, considerations
3. Route/dose/repeats

Answer 10

1. Muscarinic antagonist which inhibits the M3 receptor on bronchial smooth muscle to reduce muscle contraction of smooth muscle stimulated by ACh, leading to bronchodilation and reduced mucus secretion
2. CI <6m, glaucoma, allergy/hypersensitivity. ADR: mild anticholinergic effects (urinary retention). Two different preparations.
3. > =6y 500mcg neb, one repeat.
   2-<6y 250mcg neb, 1 repeat
   6m-<2y 125mcg 1 repeat

Question 11

Home meds: what do they treat?

Seretide
Ventolin

Answer 11

Seretide is a combination inhaler made up of salmeterol (long-acting b2 agonist) and fluticasone (corticosteroid) to maintain asthma.

Ventolin is a short-acting b2 agonist used for acute exacerbations of asthma

Question 12

Adrenaline for the use of asthma:
1. MOA
2. CI/ADR
3. Route/dose/repeat

Answer 12

1. Non-selective adrenergic receptor agonist which stimulates beta 2 receptors in lungs to cause bronchodilation (reverse bronchoconstriction), alpha 1 receptors (peripheral vasoconstriction increasing BP and decreases vascular permeability (reduces swelling)), beta 1 receptors (increased HR and contractility to support CO)
2. CI: Nil, ADRs: tachycardia, HTN, dysrhythmias, anxiety, N+V. Different preparations
3. > =16y IM 500mcg (1:1000) q5min no max or IV 50mcg (1:10,000) q1min no max
   <16 IM 10mcg/kg (max 500mcg), q5min, no max OR IV 2mcg/kg (max 50mcg, q2min, no max)

Question 13

Hydrocortisone in asthma:
1. MOA
2. CI/ADR
3. Route/dose/repeat

Answer 13

1. binds to glucocorticoid receptors to reduce airway inflammation by inhibiting pro-inflammatory cytokines, suppressing immune cells, and decreasing capillary permeability. It also upregulates β2 receptors, enhancing the effect of bronchodilators during asthma exacerbations.
2. CI: active peptic ulcer disease, allergy to corticosteroids, sodium succinate, or sodium phosphate. ADR may elevate BGL, caution in diabetics.
3. Adult IM/IV 100mg no repeat. Paediatric (only for severe if <6y) IM/IV 4mg/kg max 100mg (no repeats)

Question 14

Anaphylaxis: Pathophysiology

Answer 14

Allergen binds to IgE antibodies attached to mast cells and basophils, which causes the release of mediators including histamines, leukotrienes, cytokines and prostaglandins leading to smooth muscle contraction (bronchospasm, V+D), vasodilation and incr. vascular permeability (reduced BP, swelling), and urticaria.

Question 15

Anaphylaxis trx plan

Answer 15

ABCs: adjunct, high flow O2 via BVM, IV ventilation
Adrenaline (IM up to x4 then needs infusion), compound sodium lactate if signs of hypovolaemia, glucagon in pts taking b-blockers if signs of hypovolaemia persist after initial bonus, salbutamol, hydrocortisone if wheeze persists, nebulised adrenaline if continuing signs of upper airway obstruction after IM adrenaline.
Non-pharm: positioning supine for venous return, or sitting with legs straight if trouble breathing, reassurance, stop from standing or walking.
Consider ICP backup if long transport time, early notification to hospital prn
Urgent transport, continually re-assess

Question 16

Adrenaline in anaphylaxis
1. MOA
2. CI/ADR/considerations
3. Route/dose/repeat

Answer 16

1. Non-selective adrenergic agonist. Acts on alpha 1 receptors to vasoconstrict vessels and reduce permeability; beta 2 to reduce bronchoconstriction; beta 1 to improve contractility and incr. HR
2. Nil. ADRs: tachycardia, dysrhythmias, HTN, N+V. Precaution: 2 different preparations
3. IM 500mcg q5min no max for >=16y. IM 10mcg/kg (max 500mcg) q5min no max. If unresponsive after 4 doses then can nebulise or infusion if >=16y

Question 17

Home meds:
Perindopril
Pantoprazole
Atorvastatin

Answer 17

ACE inhibitor for HTN
Proton pump inhibitor for GORD, contraindicated with hydrocortisone
Used for dyslipidemia

Question 18

Fexofenadine
1. MOA
2. CI/ADR
3. Route/dose/repeat

Answer 18

1. Selective H1 receptor antagonist which block the effects of histamine released during allergic reactions
2. CI <12, previous admin within 24hrs. ADR drowsiness, dry mouth, nausea, headache
3. 180mg PO no repeat (>12)

Question 19

Patho of pain

Answer 19

Nociceptors activated by stimuli (mechanical deformation, inflammation, tissue damage) and covert it into an electrical impulse (transduction). The electrical impulse is conducted along afferent nerve fibres from the injury site to the spinal cord (conduction). Pain signals enter the dorsal horn and are relayed to second-order neurons, which ascend the spinothalamic tract to the thalamus then the cortex (Transmission). Pain is then perceived in the cerebral cortex (and heightened by emotional and cognitive factors) (perception).

Question 20

Treatment plan for pain (e.g. femur fracture)

Answer 20

ABCs and rapport/reassurance/positioning, consider c-spine.
Stop bleeding, splint fracture
Methoxyflurane, fentanyl, IV fluids if signs of hypovolaemia, antiemetic prn
Consider ICP backup if unable to control emotions

Question 21

Fentanyl
1. MOA
2. CI/ADRs/Considerations
3. Dose/route/repeat

Answer 21

1. Opioid agonist at mu (kappa and delta) receptors at the neurons pre- and post-synaptically. Agonism of mu receptors pre-synaptically inhibits Ca2+ ions from entering the cell in response to incoming AP, preventing release of neurotransmitters such as glutamate into the synapse and thus preventing signal transmission. Post-synaptically it increases the amount of K+ leaving the cell, hyperpolerising it and thus making it harder to reach threshold and potentiate action potentials.
2. CI: pregnant >=20w, IN is epistaxis and occluded nasal passages. ADRs: N+V, constipation, rash, bradycardia
3. ADULT: IN 50-100mcg initial, q5min, no max. IV 25-50mcg, max 5mcg/kg
   CHILD: IN 1.5mcg/kg (max 50) q10min undiluted max 5mcg/kg. IV 0.5-1mcg/kg diluted (max 25) q5min max 5mcg/kg

Question 22

Morphine
1. MOA
2. CI/ADR
3. Route/dose/repeat

Answer 22

1. Opioid receptor agonist in the CNS; Ca2+ influx presynaptic and K+ postsynaptically to prevent electrical impulse transmission
2. CI: neonates <40w, pregnant >20w, kidney disease. ADRs: N+V, drowsiness, constipation, dry mouth, miosis, urinary retention. Consider resp depression, and shock pts, and elderly
3. ADULT: IV 2.5-5mg diluted, q5min, total 0.5mg/kg. IM 5-10mg q15m, total 2 doses
   PAED (>1y) IV 100mcg/kg diluted max 5mg, q5min, total 0.5mg/kg. IM 100mcg/kg, q15min, max 2 doses.

Question 23

Naloxone
1. MOA
2. CI/ADR
3. Dose/route/repeat

Answer 23

1. Mu receptor antagonist which prevents the inhibition of Ca2+ channels and prevents the stimulation of K+ channels to promote AP conduction/transmission
2. CI neonates born to opioid addicted mothers due to risk of inducing opioid withdrawal. ADRs: opioid withdrawal, PO in pts with pre-exisiting cardiac disease, dysrhythmias
3. > 16 IV 100mcg diluted bonus, q2min, max 2mg. IM 400mcg undiluted bonus q2min, max 2mg.
   <16 IM/IV 5mcg/kg diluted max 100mcg. Q2min, max 2mg

Question 24

Home meds:
Fluticasone
Salbutamol
Topical corticosteroid

Answer 24

Fluticasone: inhaled corticosteroid for asthma maintenance
Salbutamol: SABA for asthma exacerbations
Topical corticosteroid for asthma

Question 25

Patho of seizure

Answer 25

Abnormal, excessive neuronal discharge in the brain, especially the cerebral cortex. Imbalance of GABA (too little) and glutamate (too much). People with epilepsy have a reduced threshold which can be worsened by lack of seep, ETOH, hypoglycaemia, medication non-adherence. Widespread neuronal involvement = tonic-clonic activity; postical phase is due to temporary neuronal exhaustion, reduced SpO2 due to hypoventilation.

Question 26

Trx of seizure

Answer 26

Protect from injury, ABCs - consider adjunct, oxygen. Midazolam IN or IV +/- glucose 10% if hypoglycaemic Consider ICP backup, transport

Question 27

Midazolam 1. MOA 2. CI/ADR 3. Dose/route/repeat

Answer 27

1. Allosteric binding to GABAa receptors to increase the action of GABA (inhibitory neurotransmitter) which increases chloride in the cell leading to hyperpolarisation, making it harder for the neuron to depolarise and preventing the AP from continuing 2. CI: allergy to benzodiazepines. ADR: hypotension, hiccups, cough. Precautions: consider lower dose in those with LBW, resp disease, ETOH intox, etc. To prevent resp depression prolongation 3. ADULT IV 2.5mg diluted slow bolts q5min, max 15mg IM 5mg bolus, q5min, max 15mg PAED IN 0.3mg/kg (max 5mg), no repeat IM 0.15mg/kg (max 5mg) q5min max 0.45mg/kg IV 0.15mg/kg diluted (max 2.5mg) q5min, max 045mg/kg

Question 28

Pathophysiology of delirium

Answer 28

Neurochemical imbalance leading to fluctuating disturbance in attention and cognition. Key mechanisms are through decreased acetylcholine (attention/memory), increased dopamine (agitation/aggression), change in serotonin/GABA/glutamate levels

Question 29

Trx for behavioural disturbance

Answer 29

De-escalate, keep safe distance, ABCs Build rapport, speak to them Olanzapine, droperidol, then if still not improving/SAT 2+, then ICP for ketamine or midazolam to sedate Transport

Question 30

Olanzapine 1. MOA 2. CI/ADRs 3. Route/dose/repeat

Answer 30

1. Antagonist at dopamine and serotonin receptors, which blocks dopamine receptors to counteract excessive dopamine (subsequently reducing agitation/aggression) 2. CI: Known hypersensitivity. ADR: sedation, dizziness, orthostatic HoTN. Precautions: may cause resp depression, use with caution in those with hx seizures, elderly have higher risk of adverse effects 3. >14y 10mg PO, 1 repeat q15m Elderly: 5mg PO, 1 repeat q15m 6-<14y but >40kg 10mg PO no repeat 6-<15y but <40kg 5mg PO no repeat

Question 31

Droperidol 1. MOA 2. CI, ADR, precautions 3. Route/dose/repeat

Answer 31

1. Antagonist at dopamine D2 receptors to reduce effects of excessive dopamine in the CNS 2. CI <6y, Parkinson’s disease, allergy 3. >14y IM/IV 10mg 1 repeat q15min Elderly IM/IV 5mg, 1 repeat q15min 6-<14y IM/IV 0.15mg/kg (max 10), repeat once q15min

Question 32

Ketamine in behavioural disturbance 1. MOA 2. CI/ADRs 3. Dose/route/repeat

Answer 32

1. Antagonist at NMDA receptors (blocking glutamate binding). Therefore, prevents membrane depolarisation through preventing influx of Ca2+ ions and decreases neuronal excitability in the brain, contributing to sedation 2. <6y, suspected ACS/acute HF, allergy. ADRs: incr. BP and HR, incr. mm tone, N+V, hypersalivation. Precautions: emergence reactions, resp compromise 3. IM undiluted 2mg/kg no repeat (6+) IV diluted 0.25mg/kg (max 30mg), repeat 3-5min max 200mg.

Question 33

Home meds: Serotonin Temazepam Candesartan

Answer 33

Serotonin is an SSRI for anxiety/depression Temazepam is for insomnia; can incr. risk of delirium/sedation/falls in elderly Candesartan: ARB for HTN, may contribute to low BP during sedation

Question 34

Pathophysiology of bradycardia

Answer 34

Decreased firing of the SA node or impaired conduction through the AV node, leading to slower transmission of electrical impulses through the heart. This results in less frequent myocardial contractions, reducing heart rate and potentially lowering cardiac output.

Question 35

Trx of bradycardia

Answer 35

supportive ABCs Atropine, and if required adrenaline infusion and transcutaneous pacing Positioning supine for perfusion Backup for extrication/deterioration Transport

Question 36

Atropine 1. MOA 2. CI/ADR/consid 3. Route/dose/repeat

Answer 36

1. muscarinic acetylcholine receptor antagonist that blocks parasympathetic (vagal) stimulation at the SA node, reducing vagal tone. This allows the sympathetic system to dominate, increasing SA node firing, heart rate, and cardiac output. 2. CI: Nil. ADRs: tachycardia, dysrhythmias, N+V, dry mouth. 2 different preparations 3. 16+ IV 600mcg undiluted, repeat 1min, max 3mg IM 600mcg undiluted, repeat 3min, max 3mg <16y IV 20mcg/kg diluted, nil repeat IM 20mcg/kg undiluted, nil repeat

Question 37

Adrenaline in bradycardia 1. MOA 2. CI/ADR 3. Route/dose/repeat

Answer 37

1. β1-adrenergic receptor agonist that acts on the SA node, AV node, and myocardium, increasing SA node automaticity, AV node conduction, and myocardial contractility, leading to an increase in heart rate and cardiac output. 2. Nil. ADRs: tachycardia, dysrhythmias, anxiety, N+V, HTN 3. 16+ IV infusion 50mcg q1min until PR >40 and/or adequate perfusion, no max <16y 2mcg/kg (max 50mcg) q2min no max

Question 38

Home meds: Lisonopril Metformin

Answer 38

Lisonopril ACE inhibitor for HTN Metformin for T2DM

Question 39

Pathophysiology of STEMI

Answer 39

A plaque rupture in a coronary artery exposes the underlying collagen and lipid core, triggering platelet activation, aggregation, and the coagulation cascade. Platelets undergo a shape change and degranulate, releasing ADP, thromboxane A2 (TXA2), and Ca²⁺, which amplify platelet recruitment and activation. ADP binds to P2Y receptors to further promote aggregation, and thrombin is generated, converting fibrinogen to fibrin to stabilise the clot. Complete occlusion of the coronary artery results in myocardial ischaemia and infarction (STEMI).

Question 40

Trx of STEMI

Answer 40

ABCs, ECG, cardiac monitoring and vitals Transmit ECG if suspicious of STEMI. Thrombolysis checklist Load and go, ICP backup if extended transport to hospital, pre-notify Clopidogrel, tenecteplase, enoxaparin Reassurance

Question 41

Clopidogrel 1. MOA 2. CI/ADR/Consideration 3. Route/dose/repeat

Answer 41

1. An antiplatelet agent that irreversibly antagonises the P2Y₁₂ receptor on platelets. This leads to increased cAMP, decreased intracellular Ca²⁺, and thus inhibits platelet activation, shape change, and aggregation. 2. CI: bleeding tendency, exclusion via Prehospital Thrombolysis Checklist, <18y, pregnant/BF. ADRs: gastric irritation, bleeding 3. 18-<75y is 300mg PO no repeat >75 is 75mg PO no repeat

Question 42

Tenecteplase 1. MOA 2. CI/ADR/Consideration 3. Route/dose/repeat

Answer 42

1. Fibrinolytic that activates plasminogen to plasmin, which breaks down fibrin in the existing thrombus to dissolve the clot. 2. CI: <18, any exclusion as per prehospital thrombolysis checklist. ADRs: ICH, repercussion arrhythmias, aggravation of bleeding tendencies 3. Dose is weight-based to a max of 50mg, no repeat (18-<75). Or up to max of 25mg for 75+

Question 43

Enoxaparin 1. MOA 2. CI/ADR/Consideration 3. Route/dose/repeat

Answer 43

1. Anticoagulant which binds to antithrombin III to inhibit factor Xa and inactivate it. This interrupts the intrinsic and extrinsic clotting pathways by preventing thrombin generation and subsequent fibrin formation 2. CIs: any exclusion as per PTC, allergy. ADR: bleeding may take longer to stop. Precautions: 2 preparations 3. 18-<75: 30mg IV with 30mL flush of NaCl, 15min after tenecteplase. Then second dose SC 1mg/kg (max 100mg) 15mins after 1st dose. >75y: No IV dose, 15mins after tenecteplase give SC 0.75mg/kg (max 75mg).

Question 44

Home meds: Irbesartan Bisoprolol Metformin

Answer 44

Irbesartan: ARB for HTN Bisoprolol: beta blocker for HTN Metformin: Oral antihyperglycaemic for T2DM

Question 45

MOA aspirin

Answer 45

Antiplatelet agent which irreversibly inhibits COX-1 enzyme in platelets to prevent the synthesis of thromboxane A2 and prostacyclin. This inhibits platelet activation and aggregation

Question 46

Pathophysiology of APO

Answer 46

Left ventricular failure leads to increased pressure in the left atrium and pulmonary circulation. This raises pulmonary capillary hydrostatic pressure above oncotic pressure, causing fluid to shift from the capillaries into the interstitial space and alveoli. The resulting alveolar fluid impairs gas exchange, leading to hypoxia, shortness of breath, and auscultated crackles.

Question 47

Trx of APO

Answer 47

ABCs, positioning upright, reassurance to take deep breaths. GTN, oxygen prn, furosemide CPAP if indicated Transport, backup for extrication?

Question 48

GTN in APO: 1. MOA 2. CI/ADR/considerations 3. Route/dose/repeats

Answer 48

1. metabolised to nitric oxide (NO) in vascular smooth muscle, which increases cyclic GMP (cGMP), leading to smooth muscle relaxation and vasodilation. This primarily reduces preload (venous return), lowering pressure in the pulmonary circulation, relieving pulmonary congestion, and reducing myocardial oxygen demand. 2. CI: erectile dysfunction medications, SBP <90, HR <50 or >150, <16y. ADRs flushing, HoTN, headache. Considerations: monitor BP 3. SL 600mcg q5min max 1.8mg (16+)

Question 49

Furosemide in APO: 1. MOA 2. CI/ADR/considerations 3. Route/dose/repeats

Answer 49

1. loop diuretic that inhibits the Na⁺/K⁺/2Cl⁻ co-transporter in the thick ascending limb of the loop of Henle, reducing reabsorption of sodium, potassium, chloride, and water. This increases urinary output, reduces intravascular volume, and lowers preload, helping relieve pulmonary congestion. By reducing preload, it also shifts the heart's function back toward the optimal part of the Frank-Starling curve, improving cardiac efficiency. 2. BP <100, <16y. ADRs excessive diuresis. Precautions: risk of hypovolaemic shock, K+ loss can precipitate dysrhythmias 3. If taking diuretics 80mg IV/IM 1 repeat after 10mg If not taking diuretics 40mg IV/IM 1 repeat after 10mins

Question 50

Oxygen 1. MOA 2. CI/ADR/considerations 3. Route/dose/repeats

Answer 50

1. Directly increases the alveolar oxygen concentration to increase diffusion of O2 into the blood to enhance tissue oxygenation 2. CI: paraquat poisoning if SpO2 90%, concurrent use of methoxyflurane except when administered via nasal prongs. ADRs: increase fire and explosion risk 3. In CPO 100% via IPPV

Question 51

Compound sodium lactate 1. MOA 2. CI/ADR 3. Route/dose/repeats

Answer 51

1. Increases intravascular volume to increase preload, which increases pressure and wall stress in the heart to increase SV and CO via Frank-Starling’s law mechanism. The increased BP is recognised by baroreceptors and this signal is sent to the CNS to restore blood flow to ischaemic tissues. 2. Nil CIs. ADRs: PO, hypothermia, can contribute to coagulopathy when given in excess 3. In medical hypoperfusion/hypovolaemia: IV 20mL/kg bolus whilst indicated, nil max.

Question 52

MOA of methoxyflurane

Answer 52

modulates GABA-A receptors and potassium channels, causing neuronal hyperpolarisation and reduced excitability in the CNS. This leads to central analgesia and sedation, reducing the perception of pain.