PARA2007 Exam Prep

Resp: ACPO

Think: ABC, posture, O2, hx. taking, resp assessment, GTN, ?clinical support for CPAP, minimise movement/ semi-recumbent (reduce myocardial workload/ WOB), optimise gas exchange

Fine crackles, peripheral pitting oedema, paroxysmal nocturnal dyspnoea, drowning sensation

Patho:

L) HF → blood backs up into pulmonary valve → hydrostatic pressure exceeds oncotic pressure → moves into interstitial space → alveoli (produces crackles - fluid on lungs)

Tx.:

GTN: Reduce preload → reduce backup

Contras:

• PDE-5 inhibitors (erectile dysfunction, pulmonary hypertension)

  • 24hrs – Sildenafil, vardenafil, avanafil

  • 48hrs – Tadalafil

• SBP <100mmHg

• Inadequate rate/ rhythm

• R) HF (preload dependent)

Dose: 300mcg SL every 5mins PRN

MOA: Nitrate vasodilator that releases nitric oxide (NO), activating guanylate cyclase and increasing cyclic GMP (cGMP) in vascular smooth muscle → smooth muscle relaxation and vasodilation → reduces myocardial O2 demand

CPAP: Stent open alveoli, provides positive pressure during inspiration/ exhalation

1. Reduce WOB

2. Maximise gas exchange

3. Reduce alveolar recruitment

Resp: Asthma

Think: ABC, posture, O2, hx. taking, resp assessment, asthma severity, MDI/NEB salbutamol/ ipratropium, prednisolone, minimise exertion

Patho:

Allergen binds to IgE antibodies on pre-sensitised mast cell/ basophil → mass degranulation → release of inflammatory mediators (cytokines, leukotrienes, prostaglandins) → bronchodilation/ increased mucous production

Tx.:

Salbutamol:

Dose: MDI 1200mcg (12 puffs)/ NEB 5mg/2.5ml/ NEB 15mg/7.5ml

MOA: Salbutamol agonises B2 receptors on bronchial smooth muscle → activates adenylyl cyclase to convert ATP to cAMP → modulates Ca+ → decreased Ca+ → decreased actin-myosin filament contraction → bronchodilation

Ipratropium: Non-selective muscarinic receptor antagonist, anticholinergic

Dose: MDI 168mcg (8 puffs)/ NEB 500mcg

MOA: Non-selectively binds to muscarinic receptors in bronchial smooth muscle, inhibiting ACh release from vagal nerve (normally increases cGMP = increased Ca+), therefore reducing bronchoconstriction

Prednisolone:

Dose: PO 50mg if not had in past 24hrs

MOA: Binds to intracellular glucocorticoid receptors to suppress airway inflammation, reduce mucosal swelling, and decrease hyper-reactivity

Resp: COPD exacerbation

Think: ABC, posture, O2, hx. taking, resp assessment, asthma severity, MDI/NEB salbutamol/ ipratropium, prednisolone, minimise exertion

Patho:

Emphysema: Destruction of alveoli walls

Chronic bronchitis: Chronic inflammation of bronchi

*Exacerbated by infection (i.e. pneumonia)

Tx.:

Salbutamol:

Dose: MDI 1200mcg (12 puffs)/ NEB 5mg/2.5ml/ NEB 15mg/7.5ml

MOA: Salbutamol agonises B2 receptors on bronchial smooth muscle → activates adenylyl cyclase to convert ATP to cAMP → modulates Ca+ → decreased Ca+ → decreased actin-myosin filament contraction → bronchodilation

Ipratropium: Non-selective muscarinic receptor antagonist, anticholinergic

Dose: MDI 168mcg (8 puffs)/ NEB 500mcg

MOA: Non-selectively binds to muscarinic receptors in bronchial smooth muscle, inhibiting ACh release from vagal nerve (normally increases cGMP = increased Ca+), therefore reducing bronchoconstriction

Prednisolone:

Dose: PO 50mg if not had in past 24hrs

MOA: Binds to intracellular glucocorticoid receptors to suppress airway inflammation, reduce mucosal swelling, and decrease hyper-reactivity

Resp/ chest pain: Tension pneumothorax

Indications:

1. Decreased/ absent breath sounds on affected side

2. Complete bagging resistance

3. Ipsilateral hyperinflation

4. Unequal breath sounds

5. Increased JVD

Resp: PE

Think: ABC, posture, O2, hx. taking, resp assessment, minimise exertion

Sharp, stabbing pain, aching pain in legs

Virchow’s Triad: Endothelial wall damage, stasis, hypercoagulability

Patho:

Clot forms in peripheries (i.e. legs), mostly from deep vein thrombosis → embolus breaks off → lodged in smallest capillary network (lungs)

Resp: Resp infection

Resp: Croup

Respiratory assessment

1. Speech

2. Sounds

3. Depth/ WOB

4. Patten

5. Accessory muscle use

+ Inspect, auscultate, palpate (deep breath → feel ribs)

Think: Worse on inhalation, supine, onset, hx. of asthma, COPD, anaphylaxis, trauma, infection, illness, communicable disease, recent events, DOLORS, SAMPLE

Altered states of consciousness

A - Alcohol

E - Epilepsy, electrolytes, endocrine, environment

I - Insulin

O - OD, oxygen

U - Uraemia, UD

T - Trauma, toxins, tension pneumo, tamponade, toxins

I - Infection

P - Psych, pharmacological

S - Stroke, syncope, shock

ASoC: CVA

Think: ABC, O2, posture, minimal movement, ROSIER, ACT, ?clinical support, code stroke GRN, ?Cushing’s triad

ROSIER:

- 1 - LOC, seizure activity

+1 - Facial droop, speech, visual field, arm weakness, leg weakness

*BGL >3.5

*Pre-morbid independence

ACT: R) chat, L) tap

Cushing’s triad: Widening PP, irregular resps, bradycardia

Monroe-Kellie Doctrine: Blood, brain, CSF

Patho:

1. Ischaemic: Embolus/ emboli (formed elsewhere), thrombus (locally formed)

2. Haemorrhagic: Intracerebral, subarachnoid (aneurysm rupture, trauma)

3. Posterior: 5 Ds - Dizziness, diplopia, dysarthria, dysphagia, dystaxia (+ headache, N&V, blurry vision, unilateral limb weakness)

ASoC: Seizure

Think: ABC, posture, O2, ETCO2, duration, tonic clonic = midaz, ?cause (febrile, infection, meningococcal septicaemia, hypo/hyper, OD, ETCOH), secondary (headstrike, witnessed, LOC, head → toe), seizure hx., onset, event recall, ?clinical support if 2nd dose ineffective

• Neuro assessment: BGL, pupils, temp, GCS

• Resp assessment: RR, speech, sounds, WOB/depth, pattern, accessory muscles, inspect, ausc, palpate

• Cardio assessment: HR, CR, BP, colour, warmth, turgor

Patho:

Excessive hypersynchronous neuronal firing from the outer layer of the cerebral cortex.

Tx.:

Midaz:

Dose: 0.15mg/kg > 10mg/10ml (5ml max per IM site)

RPT: Twice PRN

2nd line: leviteracitam (ICP)

MOA: Short-acting benzodiazepine that enhances the effect of GABA (the brain's primary inhibitory neurotransmitter) at GABA-A receptors → increases chloride ion channel opening frequency → neuronal hyperpolarisation → reduced CNS activity

ASoC: Diabetes

Types:

T1: IDDM

T2: NIDDM

Hypo:

Tx:

Glucose:

PO: 15g gel

IV: Glucose dextrose 10% 250mL aliquots until stable (BGL 4.0)/ increased GCS to admin PO gel/ complex carbs

Glucagon: Glucagon acts on liver → tells glycogen to release glucose

Hyper:

• DKA

• HHS

ASoC: OD

Think: ABC, adjunct, O2, posture, ?naloxone, clinical support, GRN

Track marks, CNS depression, resp depression, miosis

Types:

• Stimulants: Cocaine, MNDA, meth

• Depressants: Heroin, cannabis, GHB, benzos, fentanyl

• Psychogenics: Ketamine, PCP, LSD, mescaline, psilocybin, DMT

Patho:

Opioids bind to Mu, Kappa, Delta opioid receptors → CNS depression, resp depression, miosis

Tx:

Naloxone:

IV: 50mcg/0.5ml - 100mcg/1ml (400mcg/1ml + 3ml saline)

IM: 400mcg/1ml

IN: 120mcg/0.3ml + 0.1ml to prime MAD (1st dose) (if doses >1mg req., IN impractical due to nasal SA saturation)

RPT every 2-3mins PRN

MOA: Competitively antagonises opioid receptors, displacing opioids

Gen med: Sepsis

Think: PPE, HAT, O2, posture, clinical support, fluid, GRN, ?ceftriaxone

Hypotension

Altered mental status

Tachypnoea

+ Evidence of infection

Patho: Life-threatening extreme immune response to infection, causing organ dysfunction

Infection triggers immune response → immune system recognises pathogen-associated molecular patterns → release inflammatory mediators → stimulate NO production → vasodilation, insert aquaporins (increased capillary permeability)

1. Hypotension

2. Reduced cerebral perfusion → altered mental status

3. Absence of O2, pyruvate formed during glycolysis cannot enter the Kreb’s cycle → converts to lactic acid → lactate → releases H+ → lowers pH → carotid/ aortic bodies detect low pH (acidosis) → increases ventilation to remove CO2

Tx:

O2:

High flow O2 (titrate to SpO2 94-98%)

Sodium chloride 0.9%:

If MAP <65/ SBP <100

250ml aliquots > 20mL/kg to MAP >65/ SBP >100

*Consult for >30mL/kg

Ceftriaxone:

Fluid refractory + >60mins from hospital

MOA: Antibiotic binds to penicillin-binding proteins → inhibits bacterial wall synthesis → weakens cell wall → cell death

Gen med: Meningococcal septicaemia

Think: PPE, HAT, O2, posture, clinical support, fluid, GRN, ceftriaxone

Non-blanching rash, headache, seizures, altered consciousness, tachycardia, tachypnoea, fever, malaise, N&V

Patho:

Tx:

O2:

High flow O2 (titrate to SpO2 94-98%)

Sodium chloride 0.9%:

If MAP <65/ SBP <100

250ml aliquots > 20mL/kg to MAP >65/ SBP >100

*Consult for >30mL/kg

Ceftriaxone:

Dose: 50mg/kg > single max 2g

IV/IO: 1g vial + 9.5ml saline = 1g/10ml (admin total dose slow over 4mins)

IM: 1g vial + 3.5ml saline = 1g/4ml (max 1g/4ml per IM site)

MOA: Antibiotic binds to penicillin-binding proteins → inhibits bacterial wall synthesis → weakens cell wall → cell death

Gen med: Anaphylaxis

Think: ABC, O2, posture, adrenaline, fluid, ?clinical support, GRN

2+ body systems, upper airway angioedema, bronchospasm, persistent wheeze, hypotension, persistent itch

Patho:

1st exposure: Allergen binds to

2nd exposure: Allergen binds to IgE mediators on pre-sensitised mast cell/ basophil → mass degranulation → inflammatory mediator release (histamines, prostaglandins, leukotrienes) → vasodilation, increased capillary permeability, bronchospasm, upper airway angioedema

Tx:

Adrenaline:

IM: 10mcg/kg > 500 mcg/0.5ml (RPT every 5mins PRN)

MOA: A1: Vasoconstriction, B1: Ino (contract), dromo (conduct), chrono (rate)

Sodium chloride 0.9%:

10mL/kg > 20mL/kg (max 250mL aliquots) to SBP 100

Consult if fluid refractory at 20mL/kg

Upper airway angioedema:

Adrenaline: NEB 5mg/5ml

Bronchospasm:

Salbutamol: 12 puffs, NEB 5mg/2.5ml, NEB 15mg/7.5ml

Ipratropium: 8 puffs/ NEB 500mcg/1ml

Persistent wheeze:

Prednisolone: PO 50mg

Presistent itch:

Fexofenadine: 180mg

Trauma/ TBI

Think: DRC (cat haem) A (c-spine) BCDE, call for help (?vasopressors), trauma triad, analgesia, Cushing’s Triad, fluid resus 250mL aliquots (max 20mL/kg) to MAP 90mmHg/ SBP 110mmHg, 30 degree head ramping in TBI to optimise cerebral venous drainage

Cushing’s triad:

1. Widening PP

2. Bradycardia

3. Hypotension

Trauma triad:

1. Hypothermia

2. Coagulabiity

3. Acidosis

Tx.:

TXA:

Indications: Sev/ suspected haemorrhage, HR >120 OR SBP <90mmHg

MOA: Antifibrinolytic agent by competitively and reversibly blocking the lysine-binding sites on plasminogen.

Dose: 1mg/10ml, slow push over 2-3mins

Analgesia:

• Methoxyflurane

• IV paracetamol (1g/100ml, flush with 100ml saline, 3-4 drops/sec)

• IN fentanyl 120mcg (0.3mL + 0.1mL to prime MAD)

• IV fentanyl 100/2ml + 8ml saline (25-50mcg) RPT every 5mins to max dose 300mcg in first hr, 100mcg/hr subsequent hr

Environmental: Hypothermia

Think: ABCDE, remove wet clothing, passive warming, ?limit fluids

<28: Sev

28-32: Mod

32-35: Mild

Osborn J wave

Environmental: Hyperthermia

Think: ABCDE, remove wet clothing, apply cold pack to axilla, groin

Cardiac: Brady

Atropine

Transcutaneous pacing

Cardiac: SVT

Patho:

Tx.:

Modified Valsalva manoeuvre

Adenosine

Cardioversion

Organophosphate poisoning

Think:

Envenomation

Think: ABC, photo, pressure immobilisation, mark, splint, peripheral limb assessment, ?clinical support, analgesia, minimise movement, GRN, IV access, snake type, cardio obs (peaked T wave in ECGS)

S&Ss:

PIB:

VICC: Venom-induced consumption coagulopathy - Procoagulant venom enzymes activate clotting factors (prothrombin, Factor V/VIII) → mass fibrin generation and consumption of clotting factors/fibrinogen → complete defibrinogenation → severe coagulopathy and high risk of life-threatening bleeding (e.g. intracranial haemorrhage)

Cardiac: STEMI

Think: Cardiac cause, ECG within 10mins + every, cardiovascular assessment (cardiac obs), hx. taking, secondary survey (head → toe, inspection, palpation, auscultation), aspirin, GTN, minimal movement, ICP, 2nd crew, code STEMI GRN, pads

S&Ss: L) chest pain, radiating to scapula, shoulder, L) arm, heavy

Patho:

Tx.:

GTN:

Contras:

• PDE-5 inhibitors (erectile dysfunction, pulmonary hypertension)

  • 24hrs – Sildenafil, vardenafil, avanafil

  • 48hrs – Tadalafil

• SBP <100mmHg

• Inadequate rate/ rhythm

• R) HF (preload dependent)

Dose: 300mcg every 5mins PRN

MOA: Nitrate vasodilator - Releases NO → activates guanylate cyclase → increases cyclic GMP in vascular smooth muscle → relaxation and vasodilation → reduces myocardial O2 demand

Aspirin:

Dose: 300mg PO, can give if taken in past 24hrs

MOA: Irreversibly inhibits COX-1 in platelets → reduces thromboxane A₂ (TXA₂) production → decreases platelet aggregation and thrombus formation

Cardiogenic shock: Cardiac chest pain, ECG changes, SBP <90mmHg

• Urgent clinical support

• IV access

• Posture

Salbutamol

MOA: Salbutamol (SABA) binds to B2 receptors, activates Ac, increase cAMP, modulates intracellular Ca+, reduced Ca+ = reduced actin-myosin filament contraction, causing bronchodilation

Ipratropium

MOA: Ipratropium non-selectively binds to muscarinic receptors in bronchial smooth muscle, inhibiting ACh release from vagal nerve (normally increases cGMP = increased Ca+), therefore reducing bronchoconstriction

GTN

Contras:

• PDE-5 inhibitors (erectile dysfunction, pulmonary hypertension)

  • 24hrs – Sildenafil, vardenafil, avanafil

  • 48hrs – Tadalafil

• SBP <100mmHg

• Inadequate rate/ rhythm

• R) HF (preload dependent)

MOA: Nitrate vasodilator that releases nitric oxide (NO), activating guanylate cyclase and increasing cyclic GMP (cGMP) in vascular smooth muscle → smooth muscle relaxation and vasodilation → reduces myocardial O2 demand

Trauma triad

1. Coagulopathy: Severe blood loss, consumption of clotting factors, dilution from fluid replacement and tissue injury

2. Acidosis: Significant blood loss → reduced circulating volume → reduced tissue perfusion and oxygen delivery → increased anaerobic glycolysis (pyruvate cannot enter Krebs cycle) → increased conversion of pyruvate to lactate → increased lactate and associated acid accumulation → metabolic acidosis (reduced pH) → aortic/ carotid bodies chemoreceptors detect increased H⁺ → increased RR

3. Hypothermia: Reduced body temperature impairs platelet function, slows coagulation enzyme activity, reduces the effectiveness of clot formation, and increases the risk of continued bleeding

Cushing’s triad

1. Widening PP (brain triggers SNS response to maintain cerebral perfusion → increases ICP)

2. Irregular resps

3. Bradycardia

*Increased ICP → Monroe Kellie’s Doctrine (CSF, blood, brain through foramen magnum) → compresses cardioresp centres

Monroe-Kellie Doctrine

‘The brain is a fixed vault’

CSF, blood, brain - compresses down through foramen magnum (compressing brainstem centres - cardio, resp)

CPP = … - …

CPP = MAP - ICP

CO = … x …

CO = HR x SV

MAP = … + (1/3) … - …

MAP = DBP + (1/3) SBP - DBP

BP = … x …

BP = CO x SVR

Fluid resus limitations

1. Haemodilutes → reduced O2 carrying capacity

2. Doesn’t contain clotting factors

3. Knocks off clots

4. Metabolic acidosis (high levels of chloride compared to plasma → lowers pH)

Aspirin

MOA: Irreversibly inhibits COX-1 in platelets → reduces thromboxane A₂ (TXA₂) production → decreases platelet aggregation and thrombus formation