FINAL OSCE REVISON

Cardiovascular Conditions

• Acute Coronary Syndrome (ACS)

  • Definition: ACS represents a spectrum of conditions caused by acute myocardial ischemia due to a sudden reduction or complete interruption of coronary blood flow, most commonly resulting from plaque rupture or thrombus formation.
  • Pathophysiology Flowchart:
  • Presence of cardiovascular risk factors.
  • Long-term accumulation of low-density lipoprotein (LDL) lining the arterial wall due to poor diet, smoking, and other systemic factors.
  • Development of an atherosclerotic plaque.
  • Initial plaque rupture or endothelial injury.
  • Recruitment of macrophages to engulf LDL particles, transforming them into foam cells.
  • Over time, foam cells accumulate and form a hard, fibrous cap, causing arterial stiffening and narrowing (stenosis).
  • Progressive stenosis combined with hypertension (HTN) and turbulent blood flow increases wall stress, damaging and eventually rupturing the fibrous cap.
  • Fibrous cap rupture exposes subendothelial collagen, triggering an inflammatory response and platelet activation.
  • Platelets aggregate at the injury site.
  • Formation of a coronary thrombus (blood clot).
  • Partial or complete occlusion of the coronary artery.
  • Decrease in coronary blood flow downstream from the obstruction.
  • Decreased oxygen delivery to the myocardium.
  • Development of myocardial ischemia and cellular injury.
  • Clinical manifestation of chest pain combined with impaired cardiac contractility and reduced function.
  • Prolonged ischemia leads to cell death and myocardial infarction (classified as NSTEMI for partial occlusion or STEMI for complete occlusion).
  • Risk Factors and Associated Conditions:
  • Smoking history
  • Alcohol consumption
  • Previous cardiac conditions
  • Elevated body mass index (BMI)
  • Past history of ACS
  • Differential Diagnoses:
  • Anxiety
  • Musculoskeletal chest pain
  • Pleuritic chest pain
  • Respiratory infection
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Place the patient in a position of comfort.
  • Administer Aspirin $300\,\text{mg}$ tablet orally (once only).
  • Administer Glyceryl Trinitrate (GTN) $300\,\text{mcg}$ sublingually, repeated every $5\,\text{minutes}$ until contraindications arise or symptoms resolve, plus apply a $50\,\text{mg}$ transdermal GTN patch.
  • Provide appropriate pain management.
  • Initiate symptomatic management.
  • Transport to an appropriate healthcare facility.

• Bundle Branch Blocks

  • Definition: A bundle branch block is a delay or complete blockage in electrical conduction through one of the main bundle branches (left or right), causing the ventricles to depolarize asynchronously.
  • Pathophysiology Flowchart:
  • Presence of underlying structural heart disease.
  • Conduction system damage, interruption, or delay within the bundle branch network.
  • Inability of the right or left bundle branch to conduct electrical impulses normally.
  • The electrical impulse travels unimpeded down the unaffected bundle branch.
  • The ventricle supplied by the intact bundle depolarizes first.
  • The electrical wave then spreads slowly, cell-to-cell, through the ventricular myocardium to reach the affected side.
  • Delayed depolarisation of the affected ventricle.
  • Ventricular depolarisation becomes asynchronous, producing a widened $QRS$ complex on the electrocardiogram ($QRS > 120\,\text{ms}$).
  • Asynchronous contraction reduces overall stroke volume and cardiac output.
  • Risk Factors and Associated Conditions:
  • Acute Coronary Syndrome (ACS)
  • Hypertension
  • Previous Myocardial Infarction (MI)
  • Advanced age
  • Past history of ACS and established cardiovascular risk factors
  • Differential Diagnoses:
  • Acute Myocardial Infarction (AMI)
  • Pulmonary Embolism
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Place in a position of comfort.
  • Deliver management as per the ACS protocol.
  • Provide symptomatic treatment.

• Pericarditis

  • Definition: Pericarditis is the acute or chronic inflammation of the pericardial sac surrounding the heart, most commonly caused by a viral infection.
  • Pathophysiology Flowchart:
  • Trigger event (e.g., viral infection, bacterial infection, autoimmune disorder, myocardial infarction, myocardial injury, uraemia, trauma, or malignancy; can be idiopathic).
  • Inflammation of the visceral and parietal layers of the pericardium.
  • Pericardial layers become irritated and inflamed.
  • Inflamed pericardial layers rub against one another during cardiac movement.
  • Increased capillary and vascular permeability within the pericardium.
  • Accumulation of inflammatory exudate, fluid, and fibrin in the pericardial cavity.
  • Ongoing pericardial irritation resulting in sharp, pleuritic chest pain that characteristically worsens on inspiration or when lying flat, and improves when sitting forward.
  • Inflammatory process stimulates excess fluid production in the pericardial space.
  • Rapid accumulation of pericardial fluid causes cardiac tamponade, restricting ventricular filling and severely compromising cardiac output.
  • Risk Factors and Associated Conditions:
  • Recent viral or bacterial infection
  • Myocarditis
  • Acute Coronary Syndrome (ACS)
  • Differential Diagnoses:
  • Musculoskeletal chest pain
  • Red Flags:
  • Pain exacerbated by deep inspiration or lying flat
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Place in a position of comfort (typically sitting upright and leaning forward).
  • Provide symptomatic management.

• ST-Elevation Myocardial Infarction (STEMI)

  • Definition: Complete coronary artery occlusion resulting in transmural (full-thickness) myocardial necrosis.
  • Pathophysiology Flowchart:
  • Presence of cardiovascular risk factors.
  • Endothelial accumulation of LDL over time (promoted by poor diet, smoking, etc.).
  • Formation of an atherosclerotic plaque.
  • Plaque erosion or rupture.
  • Macrophages infiltrate and phagocytose LDL, transforming into foam cells.
  • Progression into a fibrous-capped plaque that stiffens and narrows the coronary lumen (stenosis).
  • Elevated systemic pressure (HTN) and turbulent blood flow rupture the fibrous cap.
  • Exposure of subendothelial matrix recruits platelets, triggering aggregation.
  • Platelet aggregation causes rapid thrombus formation.
  • Complete occlusion of the lumen of the affected coronary artery.
  • Total cessation of downstream blood flow beyond the site of blockage.
  • Complete absence of oxygen delivery to the dependent myocardium.
  • Severe myocardial ischemia leading to cell death and necrosis.
  • Impaired ventricular wall movement and reduced cardiac contractility.
  • Characteristic ST-segment elevation visible on a 12-lead ECG.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Position of comfort.
  • Transmit 12-lead ECG.
  • Request Mobile Intensive Care Ambulance (MICA) support.
  • Apply defibrillation/monitoring pads.
  • Administer Aspirin $300\,\text{mg}$ tablet.
  • Administer GTN $300\text{--}600\,\text{mcg}$ sublingually.
  • Provide active pain management.
  • Prepare for clinical deterioration or arrhythmia development.
  • Provide symptomatic management.

• Non-ST-Elevation Myocardial Infarction (NSTEMI)

  • Definition: Partial coronary artery occlusion resulting in subendocardial (partial-thickness) myocardial ischemia and necrosis.
  • Pathophysiology Flowchart:
  • Presence of cardiovascular risk factors.
  • Subendothelial infiltration and buildup of LDL particles.
  • Development of an atherosclerotic lesion.
  • Plaque destabilization.
  • Infiltration of macrophages and formation of foam cells.
  • Development of a hard, fibrous cap causing luminal stenosis.
  • Stenosis causes high shear stress and turbulent flow, leading to cap rupture.
  • Inflammatory response and activation of blood platelets.
  • Platelet aggregation at the site of rupture.
  • Thrombus formation.
  • Subtotal or partial coronary artery occlusion.
  • Sustained reduction in downstream coronary blood flow.
  • Inadequate myocardial oxygen supply relative to metabolic demand.
  • Ischemic cell injury and partial-thickness necrosis.
  • Electrocardiographic manifestations including ST-segment depression and/or T-wave inversion (without persistent ST elevation).
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Position of comfort.
  • Administer Aspirin $300\,\text{mg}$ tablet.
  • Administer GTN $300\text{--}600\,\text{mcg}$ sublingually.
  • Manage pain effectively.
  • Provide symptomatic management.

• Supraventricular Tachycardia (SVT)

  • Definition: An abnormal electrical conduction circuit originating above the ventricles, causing a rapid, regular heart rate that decreases ventricular filling time and compromises cardiac output.
  • Pathophysiology Flowchart:
  • Initiating trigger occurs (e.g., premature atrial or ventricular contraction, elevated sympathetic tone, emotional stress, anxiety, stimulants, caffeine, or underlying structural heart disease).
  • Propagation of a premature electrical impulse.
  • Establishment of a micro- or macro-re-entry circuit within or adjacent to the Atrioventricular (AV) node.
  • High-frequency generation of electrical impulses circulating through specialized cardiac conduction tissue.
  • Rapid and repetitive electrical depolarisation of the tissue.
  • Tachycardic activation of both atria and ventricles.
  • Markedly shortened diastolic filling time for the ventricles.
  • Reduced end-diastolic volume, leading to decreased stroke volume.
  • Fall in overall cardiac output.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Place in a position of comfort.
  • Request MICA dispatch.
  • Perform a Valsalva manoeuvre.
  • Repeat the Valsalva manoeuvre every $2\,\text{minutes}$ for a maximum of 3 total attempts.

• Aortic Dissection

  • Definition: A structural tear in the tunica intima and inner media of the aortic wall, allowing high-pressure blood flow to dissect the layers of the aorta and create a false lumen.
  • Pathophysiology:
  • Initiation of a split or tear in the medial layer of the aortic wall, occurring most frequently in the aortic arch due to elevated hydraulic forces ejected from the left ventricle.
  • High-pressure blood enters the tear and dissects between the layers of the media.
  • Formation of a false lumen running parallel to the true arterial lumen.
  • The expanding false lumen compresses the true lumen, severely impeding downstream tissue perfusion and branch vessel blood flow.
  • Clinical Features and Red Flags:
  • Sudden onset of severe chest pain characterized as "ripping" or "tearing" in quality.
  • Radiation of pain through to the interscapular back region.
  • Significant inter-arm systolic blood pressure differential exceeding $20\,\text{mmHg}$.

• Pericardial Tamponade

  • Definition: Pathological accumulation of fluid or blood within the pericardial sac, exceeding its anatomical compliance limit and exerting severe pressure on the heart.
  • Pathophysiology:
  • Fluid accumulates rapidly or extensively in the pericardial space.
  • Intra-pericardial pressure rises, exceeding normal cardiac filling pressures.
  • Ventricular diastolic stretch is mechanically restricted.
  • Severe reduction in ventricular diastolic filling, stroke volume, and cardiac output.
  • Clinical Features and Red Flags:
  • Chest pain that may be partially alleviated by the "lean and lay" test (leaning forward).
  • Potential history of blunt or penetrating chest trauma, or systemic infection with fever.
  • Presence of Beck's Triad:
    • Systemic hypotension
    • Jugular venous distension (JVD)
    • Muffled or distant heart sounds

Respiratory Conditions

• Acute Pulmonary Oedema (APO)

  • Definition: An acute accumulation of fluid within the pulmonary interstitium and alveoli, impairing alveolar-capillary gas exchange and leading to severe hypoxaemia and respiratory distress.
  • Pathophysiology Flowchart:
  • Left ventricular failure secondary to impaired contractility, despite sustained or elevated systemic vascular resistance (SVR).
  • Reduction in left ventricular ejection fraction, stroke volume, and cardiac output.
  • Increase in left ventricular end-diastolic pressure (LVEDP).
  • Blood volume returning to the left atrium exceeds the volume ejected by the left ventricle.
  • Retrograde transmission of pressure causes elevated left atrial pressure, pulmonary venous pressure, and pulmonary capillary hydrostatic pressure.
  • Hydrostatic pressure inside the pulmonary capillaries exceeds the plasma colloid oncotic pressure.
  • Net movement of fluid out of the capillary bed into the interstitial space surrounding the alveoli, decreasing lung compliance and slowing oxygen diffusion.
  • Compensatory increase in lymphatic drainage is eventually overwhelmed.
  • Fluid spills directly into alveolar spaces, diluting and washing away surfactant.
  • Alveolar instability, widespread micro-atelectasis, and marked reduction in surface area available for gas exchange.
  • Markedly increased work of breathing, acute respiratory distress, severe ventilation-perfusion ($V/Q$) mismatch, and systemic hypoxaemia.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Place in an upright position of comfort.
  • Initiate oxygen therapy as clinically indicated.
  • Administer GTN $300\text{--}600\,\text{mcg}$ sublingually plus apply a $50\,\text{mg}$ transdermal GTN patch, titrated to clinical response (if the etiology is cardiogenic).
  • Request MICA dispatch.
  • Apply Continuous Positive Airway Pressure (CPAP) at $10\,\text{cm H}_2\text{O}$ if full-field pulmonary crackles are present on auscultation.

• Chronic Obstructive Pulmonary Disease (COPD)

  • Definition: Progressive airflow limitation caused by chronic airway inflammation and structural parenchymal destruction, leading to mucosal hypersecretion, loss of elastic recoil, air trapping, impaired gas exchange, hypoxaemia, and hypercapnia.
  • Pathophysiology Flowchart:
  • Long-term inhaled exposure to environmental irritants (e.g., cigarette smoke) triggers chronic pulmonary inflammation.
  • Inflammatory processes induce chronic bronchitis (airway narrowing) and emphysema (destruction of lung parenchyma).
  • Chronic bronchitis leads to submucosal gland hypertrophy and goblet cell hyperplasia, causing hypersecretion of mucus and mechanical lumen narrowing.
  • Emphysema causes destruction of inter-alveolar septa, loss of pulmonary elastic recoil, and small airway collapse during expiration.
  • Destruction of alveolar-capillary membrane area, combined with dynamic hyperinflation and mucus plugging, causes severe air trapping and dynamic obstruction.
  • Reduced expiratory airflow rate, increased end-expiratory lung volume, and severe impairment of carbon dioxide elimination and oxygen absorption.
  • Impairment of innate mucociliary clearance mechanisms significantly increases susceptibility to secondary lower respiratory tract infections.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent.
  • Position of comfort.
  • Administer Salbutamol via pressurized Metered Dose Inhaler (pMDI), $4\text{--}12\,\text{puffs}$.
  • Administer nebulised Salbutamol $5\,\text{mg}$ combined with Ipratropium Bromide $500\,\text{mcg}$ if unable to effectively operate a pMDI; repeat Salbutamol hourly as required.
  • Initiate controlled oxygen therapy titrated strictly to maintain oxygen saturation at $88\text{--}92\%$.
  • Administer Dexamethasone $8\,\text{mg}$ in $2\,\text{ml}$ via IV, IM, or oral routes.
  • If severe respiratory distress persists, request MICA support and initiate CPAP at $7.5\,\text{cm H}_2\text{O}$.

• Asthma

  • Definition: A chronic inflammatory disorder of the airways characterized by hyper-responsiveness, reversible bronchoconstriction, mucosal oedema, and mucus hypersecretion leading to widespread airflow obstruction.
  • Pathophysiology Flowchart:
  • Exposure to an initiating trigger (e.g., allergen, physical exercise, respiratory virus, environmental smoke, cold air exposure).
  • Exaggerated airway hyper-responsiveness.
  • Rapid release of pro-inflammatory mediators (including histamine and leukotrienes) from mast cells and basophils.
  • Induction of smooth muscle contraction around the bronchial tree (bronchoconstriction), causing sudden narrowing of the conducting airways.
  • Concurrent inflammation of the airway mucosa leading to endothelial leakage, mucosal oedema, and excessive high-viscosity mucus production.
  • Progressive reduction in internal airway lumen diameter and marked increase in airway resistance.
  • Impairment of expiratory airflow causing distal gas trapping and progressive thoracic hyperinflation.
  • Dramatic increase in the work of breathing, leading to severe alterations in $V/Q$ matching and systemic hypoxaemia.
  • Respiratory muscle exhaustion, hypercapnia, respiratory fatigue, and impending respiratory failure.
  • Management Protocol:
  • Mild to Moderate Exacerbation:
    • Rest and reassurance.
    • Consent and position of comfort.
    • Salbutamol pMDI $4\text{--}12\,\text{doses}$.
    • Dexamethasone $8\,\text{mg}$ in $2\,\text{ml}$ orally.
  • Severe Exacerbation:
    • Request MICA dispatch.
    • Salbutamol $5\,\text{mg}$ nebulised, repeated every $20\,\text{minutes}$ as required.
    • Ipratropium Bromide $500\,\text{mcg}$ nebulised.
    • Dexamethasone $8\,\text{mg}$ in $2\,\text{ml}$ IV, IM, or oral.
    • Prepare for clinical deterioration.
  • Life-Threatening Asthma:
    • Request MICA dispatch.
    • Continuous nebulised Salbutamol $5\,\text{mg}$.
    • Ipratropium Bromide $500\,\text{mcg}$ nebulised.
    • Adrenaline $500\,\text{mcg}$ IM, repeated every $5\,\text{minutes}$ titrated to clinical response.
    • Dexamethasone $8\,\text{mg}$ in $2\,\text{ml}$ IV, IM, or oral.
    • Administer IV Adrenaline via clinical consultation if unresponsive to IM administration and MICA is not present on scene.
    • Prepare for immediate loss of airway and respiratory arrest.

• Pulmonary Embolism

  • Definition: Occlusion of one or more pulmonary arteries by a thromboembolus originating elsewhere in the systemic venous system, disrupting pulmonary blood flow and straining the right ventricle.
  • Pathophysiology Flowchart:
  • Presence of predisposing risk factors (e.g., prolonged immobilization, recent major surgery, tissue trauma, systemic hypercoagulable states, or established Deep Vein Thrombosis [DVT]).
  • Formation of a venous thrombus, typically in the deep veins of the lower extremities.
  • Thrombus detaches from the vessel wall, becoming a circulating embolus.
  • Embolus travels superiorly through the vena cava into the right atrium.
  • Moves through the right ventricle and is ejected into the pulmonary arterial trunk.
  • Vascular occlusion occurs as the embolus lodges in a main, lobar, or segmental pulmonary artery.
  • Abrupt cessation of perfusion to downstream pulmonary parenchymal tissue.
  • Development of severe ventilation-perfusion mismatch ($V/Q$ mismatch), where ventilated alveoli receive zero capillary blood flow.
  • Marked increase in physiological dead space.
  • Impairment of alveolar gas exchange, leading to arterial hypoxaemia.
  • Acute elevation of pulmonary vascular resistance (PVR).
  • Development of acute right ventricular pressure overload and right ventricular strain.
  • Reduced left ventricular filling (preload), leading to a rapid fall in stroke volume and cardiac output.
  • Potential progression to acute right-sided heart failure, obstructive shock, or cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Initiate oxygen therapy tailored to measured arterial oxygen saturations.
  • Administer appropriate analgesia.
  • Provide symptomatic supportive treatment.
  • Transport to a definitive care facility.

• Croup (Laryngotracheobronchitis)

  • Definition: A viral respiratory infection causing mucosal inflammation and oedema of the subglottic region, leading to upper airway obstruction, inspiratory stridor, and respiratory distress.
  • Pathophysiology Flowchart:
  • Infiltration of a viral pathogen into the upper respiratory tract.
  • Localized inflammatory response within the epithelial lining of the larynx, trachea, and bronchi.
  • Rapid accumulation of subglottic airway oedema.
  • Anatomical narrowing of the rigid subglottic lumen.
  • Sharp increase in upper airway resistance to airflow.
  • Airflow becomes highly turbulent during inspiration, producing characteristic inspiratory stridor.
  • Dynamic increase in the work of breathing.
  • Progressive airway obstruction leading to alveolar hypoventilation, hypoxaemia, and potential respiratory failure.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain consent and maintain a position of comfort (minimizing agitation).
  • Mild Croup: Dexamethasone $150\,\text{mcg/kg}$ orally.
  • Moderate Croup: Dexamethasone $600\,\text{mcg/kg}$ orally.
  • Severe Croup:
    • Dexamethasone $600\,\text{mcg/kg}$ orally.
    • Administer nebulised Adrenaline $5\,\text{mg}$, repeating every $5\,\text{minutes}$ as clinically required.

• Tension Pneumothorax

  • Definition: Continuous accumulation of trapped air within the pleural space due to a one-way valve effect, creating intra-pleural pressures that collapse the ipsilateral lung and shift mediastinal structures.
  • Pathophysiology:
  • Disruption of the visceral or parietal pleura allows air to enter the pleural space during inspiration without escaping during expiration.
  • Intra-pleural pressure progressively increases, exceeding atmospheric pressure.
  • Complete mechanical collapse of the ipsilateral lung parenchyma.
  • Progressive tension shifts the mediastinum toward the contralateral hemithorax.
  • Mechanical compression of the contralateral lung and severe kinking of the superior and inferior vena cava.
  • Immediacy of severe preload reduction leading to obstructive shock and cardiac arrest.
  • Clinical Features and Red Flags:
  • Localized chest pain exacerbated by inspiration.
  • Diminished or absent breath sounds over the affected hemithorax.
  • History of thoracic trauma.
  • Distended neck veins (JVD).
  • Tracheal deviation away from the affected side.
  • Systemic hypotension and respiratory failure.

• Pneumonia

  • Definition: Infectious consolidation of the pulmonary parenchyma causing inflammatory exudate accumulation within the alveoli.
  • Clinical Features:
  • Chest pain localized to the site of infection, typically pleuritic in character.
  • Productive cough with purulent sputum, systemic fever, and dyspnoea.
  • Auscultation reveals localized coarse crackles or bronchial breath sounds.

• Pleurisy

  • Definition: Acute inflammation of the parietal and visceral pleural membranes surrounding the lungs.
  • Pathophysiology:
  • Inflammatory friction between the rubbing pleural layers during movement of the thoracic cage.
  • Clinical Features:
  • Acute onset of sharp, localized, unilateral chest pain.
  • Exacerbated by deep inspiration, coughing, or trunk movement.
  • Pleural friction rub audible on auscultation.

Endocrine and Metabolic Conditions

• Hypoglycaemia

  • Definition: Pathologically low concentration of blood glucose ($< 4\,\text{mmol/L}$), depriving the brain of essential metabolic substrate and causing progressive neuroglycopenia and autonomic excitation.
  • Pathophysiology Flowchart:
  • Precipitating factor occurs (e.g., exogenous insulin overdose, missed meal, unaccustomed physical exertion, acute alcohol ingestion, or excess oral hypoglycaemic agents).
  • Systemic blood glucose concentration drops below $4\,\text{mmol/L}$.
  • Reduced extracellular glucose available for passive cellular transport.
  • Hypothalamic detection of systemic energy deficit.
  • Neurons are unable to synthesize sufficient adenosine triphosphate (ATP) to sustain membrane potentials.
  • Activation of an acute counter-regulatory stress response (surge in systemic adrenaline, glucagon, cortisol, and growth hormone release).
  • Neuroglycopenic manifestations emerge as neuronal depolarization fails (e.g., confusion, altered conscious state, focal neurological deficits, seizures).
  • Simultaneous activation of the sympathoadrenal system produces adrenergic warning signs (e.g., profuse diaphoresis, fine tremor, palpitations, anxiety, tachycardia).
  • Severe untreated neuroglycopenia leads to generalized tonic-clonic seizures, deep coma, and irreversible brain death or cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent and position safely.
  • Patient Suitable for Oral Intake:
    • Administer $15\,\text{g}$ of oral glucose.
    • Active management of nausea or vomiting.
    • If oral route becomes unfeasible or untolerated, convert immediately to parenteral therapy.
  • Patient Unsuitable for Oral Intake:
    • Administer Dextrose $10\%$ ($15\,\text{g}$ in $150\,\text{ml}$ IV).
    • Repeat after $10\,\text{minutes}$ using Dextrose $10\%$ ($10\,\text{g}$ in $100\,\text{ml}$ IV) if BGL remains low.
    • If IV access cannot be established, administer Glucagon $1\,\text{IU}$ IM.
    • Provide ongoing supportive symptomatic treatment.

• Hyperglycaemia

  • Definition: Severe elevation of blood glucose levels caused by relative or absolute insulin insufficiency, resulting in cellular starvation, hyperosmolarity, and profound osmotic diuresis.
  • Pathophysiology Flowchart:
  • Absolute deficiency or peripheral resistance to circulating insulin.
  • Unopposed action of counter-regulatory hormones (glucagon, cortisol, adrenaline).
  • Failure of glucose uptake by insulin-dependent muscle and adipose tissues.
  • Marked elevation of systemic blood glucose concentrations.
  • Cellular energy deprivation despite extreme extracellular nutrient abundance.
  • Systemic blood glucose exceeds the renal reabsorption threshold ($\approx 10\,\text{mmol/L}$).
  • Filtered glucose spills into the renal tubules (glucosuria).
  • Unabsorbed luminal glucose exerts an osmotic gradient, preventing water reabsorption (osmotic diuresis).
  • Massive loss of free water and essential electrolytes through the urine.
  • Severe intravascular hypovolaemia and intracellular dehydration.
  • Systemic hypoperfusion, altered sensorium, and metabolic failure.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain informed consent and position of comfort.
  • Request MICA dispatch.
  • Initiate continuous cardiac monitoring and obtain a 12-lead ECG.
  • Administer Normal Saline $1000\text{--}2000\,\text{ml}$ IV, titrated to clinical perfusion status.
  • Provide symptomatic management and transport.

• Diabetic Ketoacidosis (DKA)

  • Definition: A life-threatening metabolic complication of absolute insulin deficiency characterized by severe hyperglycaemia, hyperketonaemia, metabolic acidosis, and profound dehydration.
  • Pathophysiology Flowchart:
  • Severe absolute deficiency of insulin accompanied by a surge in stress hormones.
  • Extreme elevation of hepatic glucose production combined with suppressed peripheral uptake.
  • Severe intracellular starvation forces the body to switch to fat metabolism.
  • Uncontrolled lipolysis in adipose tissue releases large amounts of free fatty acids (FFAs) into the circulation.
  • Hepatic beta-oxidation converts FFAs into acidic ketone bodies (acetoacetate and beta-hydroxybutyrate).
  • Rapid accumulation of circulating ketones exceeds the blood buffering capacity.
  • Development of a high-anion-gap metabolic acidosis, resulting in a fall in arterial pH.
  • Compensatory respiratory alkalosis via hyperventilation (Kussmaul respirations) to blow off carbon dioxide.
  • Excessive filtered glucose exceeds renal threshold, driving massive osmotic diuresis.
  • Severe electrolyte wasting (sodium, potassium) and intravascular volume depletion.
  • Profound dehydration, progressive hypotension, hypovolaemic/metabolic shock, and multi-organ breakdown.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Request MICA support.
  • Continuous cardiac monitoring and 12-lead ECG.
  • Administer Normal Saline $1000\text{--}2000\,\text{ml}$ IV, titrated to fluid status.
  • Symptomatic supportive care and emergency transport.

• Hyperosmolar Hyperglycaemic State (HHS)

  • Definition: A metabolic emergency secondary to relative insulin deficiency, characterized by extreme hyperglycaemia, hyperosmolarity, and severe dehydration without significant ketoacidosis.
  • Pathophysiology Flowchart:
  • Triggering event (e.g., acute infection, major systemic illness, missed medication, or new diabetic agent).
  • Relative deficiency of insulin (enough to inhibit lipolysis, preventing ketogenesis, but insufficient to facilitate peripheral glucose uptake).
  • Unopposed hepatic gluconeogenesis and glycogenolysis driven by stress hormones.
  • Severe, profound hyperglycaemia (often exceeding $30\text{--}50\,\text{mmol/L}$).
  • Massive filtration of glucose through the nephrons, vastly exceeding the renal reabsorption capacity.
  • Extreme, sustained osmotic diuresis.
  • Loss of massive volumes of hypotonic fluid and electrolytes.
  • Intravascular volume depletion and profound hyperosmolar plasma state.
  • Severe intracellular dehydration, especially within the central nervous system.
  • Altered mental status, focal neurological signs, coma, profound hypovolaemic shock, and high mortality.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Request MICA dispatch.
  • Cardiac monitoring and 12-lead ECG.
  • Administer Normal Saline $1000\text{--}2000\,\text{ml}$ IV, titrated to perfusion.
  • Symptomatic management and rapid transport.

• Adrenal Insufficiency (Adrenal Crisis)

  • Definition: Inadequate production of steroid hormones (primarily cortisol and aldosterone) by the adrenal cortex, impairing vascular tone, carbohydrate metabolism, and fluid homeostasis.
  • Pathophysiology Flowchart:
  • Etiology: Addison's disease, direct adrenal damage (primary), or secondary failure of ACTH secretion by the pituitary gland.
  • Marked deficiency in circulating cortisol levels.
  • Loss of vascular smooth muscle responsiveness to circulating catecholamines.
  • Widespread systemic vasodilation and drop in SVR.
  • Severe, refractory hypotension.
  • Concurrent deficiency of aldosterone reduces renal sodium and water reabsorption while impairing potassium excretion.
  • Hyponatremia, fluid loss, hypovolaemia, and hyperkalaemia.
  • Fall in venous return, cardiac preload, and stroke volume.
  • Impaired gluconeogenesis leading to acute hypoglycaemia.
  • Severe tissue hypoperfusion, progression to acute adrenal crisis, shock, and organ collapse.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain consent and place in a position of comfort.
  • Administer Hydrocortisone $100\,\text{mg}$ IM or IV.
  • Fluid resuscitation: Normal Saline $1000\,\text{ml}$ IV, titrated to clinical response.
  • Symptomatic management and rapid transport.

• Hyperthyroidism (Thyroid Storm)

  • Definition: Pathological hypersecretion of thyroid hormones ($T_3$ and $T_4$), causing excessive basal metabolic rate, hyperadrenergic states, and cardiovascular distress.
  • Pathophysiology Flowchart:
  • Etiology: Graves' disease or toxic multinodular goitre causing unregulated thyroid hormone production.
  • Elevated circulating $T_3$ and $T_4$ concentrations.
  • Widespread elevation of the body's basal metabolic rate (BMR).
  • Upregulation of beta-adrenergic receptors, inducing hypersensitivity to circulating adrenaline and noradrenaline.
  • Increased cellular oxygen consumption, heat production, and metabolic energy expenditure.
  • Manifestation of heat intolerance, profuse diaphoresis, and rapid weight loss.
  • Direct chronotropic and inotropic cardiac stimulation, dramatically increasing heart rate, stroke volume, cardiac output, and myocardial oxygen demand.
  • Severe cardiovascular strain, tachyarrhythmias, and potential progression to life-threatening thyroid storm.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain consent and position of comfort.
  • Provide supportive symptomatic care.

• Hypothyroidism (Myxoedema Coma)

  • Definition: Severe deficiency of thyroid hormones causing systemic slowing of metabolic processes, bradycardia, hypothermia, and potential respiratory depression.
  • Pathophysiology Flowchart:
  • Underlying autoimmune destruction (e.g., Hashimoto's thyroiditis) or surgical excision of the thyroid gland.
  • Depressed circulating thyroid hormone levels.
  • Universal reduction in cellular basal metabolic rate.
  • Decreased cellular ATP production and metabolic output.
  • Generalized depression of physiological functions.
  • Cardiovascular changes: decreased chronotropy (bradycardia), impaired contractility, and reduced cardiac output.
  • Metabolic changes: reduced heat generation leading to cold intolerance, profound fatigue, dry skin, constipation, and weight gain.
  • Extreme end-stage progression: Myxoedema coma, characterized by severe hypothermia, refractory hypotension, hypoventilation, and respiratory arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain consent and position of comfort.
  • Symptomatic supportive treatment.

• Cushing's Syndrome

  • Definition: A hormonal disorder caused by prolonged tissue exposure to high levels of systemic corticosteroids (cortisol).
  • Pathophysiology Flowchart:
  • Etiology: Chronic exogenous administration of glucocorticoids, or endogenous hypersecretion secondary to a pituitary adenoma (Cushing's disease) or adrenal tumor.
  • Excess production and sustained elevation of circulating cortisol levels.
  • Prolonged hypercortisolaemia.
  • Metabolic alterations: enhanced gluconeogenesis leading to persistent hyperglycaemia, enhanced muscle protein catabolism causing muscle atrophy/weakness, centripetal fat redistribution, and mineralocorticoid-like sodium/water retention.
  • Cardiovascular consequences: sustained volume expansion and increased vascular tone resulting in systemic hypertension.
  • Systemic consequences: profound suppression of cell-mediated immunity, bone resorption, and skin fragility.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Supportive symptomatic treatment.

• Hyperkalaemia

  • Definition: Pathological elevation of serum potassium levels leading to dangerous alterations in cardiac membrane resting potentials and fatal cardiac dysrhythmias.
  • Pathophysiology Flowchart:
  • Causes: Acute or chronic renal failure, severe tissue injury/crush syndrome, potassium-sparing medications, or systemic metabolic acidosis.
  • Impaired renal excretion or transcellular shift of potassium out of cells into the blood.
  • Elevation of extracellular serum potassium concentration.
  • Alteration of the resting membrane potential of cardiac myocytes (bringing it closer to threshold).
  • Depressed cardiac conduction velocity and abnormal membrane repolarization.
  • ECG changes: Tall peaked T waves, widening of the $QRS$ complex, loss of P waves, and development of sine-wave patterns.
  • Progressive cardiac conduction failure, severe bradycardia, ventricular fibrillation, or asystole.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Request MICA support.
  • Treat and manage underlying precipitating conditions (e.g., shock, hyperglycaemia, adrenal crisis).

Neurological and Behavioural Conditions

• Seizures and Status Epilepticus

  • Definition: Paroxysmal, abnormal, excessive, and synchronous electrical discharges within cerebral neurons resulting in transient neurological impairment, involuntary motor activity, or altered awareness.
  • Pathophysiology Flowchart:
  • Initiating precipitant or structural focus (e.g., idiopathic epilepsy, traumatic brain injury, acute ischaemic/haemorrhagic stroke, CNS infection, severe hypoglycaemia, cerebral hypoxia, or toxic ingestions).
  • Sudden disruption in the balance of inhibitory (GABA) and excitatory (glutamate) neurotransmission within the cerebral cortex.
  • Synchronous, high-frequency discharge of cortical neurons.
  • Normal brain electrical activity is suspended.
  • Clinical motor activity (tonic-clonic movements) and immediate alteration or loss of consciousness.
  • Widespread firing across both hemispheres produces a generalized tonic-clonic seizure; localized localized recruitment produces a focal seizure.
  • Persistence of seizure activity (Status Epilepticus) exponentially increases cerebral metabolic, glucose, and oxygen demand.
  • Post-ictal recovery phase: neuronal exhaustion, gradual restoration of ionic gradients, and transient cerebral dysfunction (manifesting as drowsiness, acute confusion, headache, and fatigue).
  • Management Protocol:
  • Treatment Thresholds: Non-convulsive status epilepticus lasting $> 10\,\text{minutes}$ or multiple seizures without return to baseline; Convulsive status epilepticus lasting $> 5\,\text{minutes}$ or repeated seizures without full recovery between events.
  • Rest and reassurance.
  • Consent and safety position (if conscious).
  • Request MICA dispatch.
  • Maintain airway patency via manual manoeuvres.
  • Supplemental oxygen administration.
  • Measure blood glucose level (BGL).
  • Administer Midazolam $10\,\text{mg}$ IM (in $2\,\text{ml}$), repeating once after $10\,\text{minutes}$ if required; OR administer Midazolam $5\,\text{mg}$ IV, repeating once after $5\,\text{minutes}$.
  • Prepare equipment for advanced ventilatory support.

• Stroke and Transient Ischaemic Attack (TIA)

  • Definition: Acute focal neurological deficit resulting from disrupted cerebral blood flow due to dynamic vascular occlusion (Ischaemic) or vascular rupture (Haemorrhagic).
  • Pathophysiology Flowchart:
  • Interruption of arterial blood supply to a specific territory of brain tissue.
  • Immediate deprivation of essential oxygen and glucose delivery to dependent neurons.
  • Failure of mitochondrial oxidative phosphorylation and rapid fall in cellular ATP production.
  • Inability of energy-dependent sodium-potassium ion pumps ($\text{Na}^+/\text{K}^+\text{-ATPase}$) to maintain cellular membrane potential.
  • Influx of sodium and water into neurons, driving acute cytotoxic oedema.
  • Rapid loss of neuronal function, structural cell death, and permanent neurological deficits.
  • Ischaemic Subtype:
    • Cerebral artery occlusion via a localized thrombus or embolic fragment.
    • Cessation of tissue perfusion, cellular pump failure, cerebral oedema, and tissue necrosis.
  • Haemorrhagic Subtype:
    • Rupture of a cerebral blood vessel (e.g., berry aneurysm or arteriovenous malformation).
    • Extravasation of arterial blood directly into the brain parenchyma or subarachnoid space.
    • Rapid rise in intracranial pressure (ICP) causing localized tissue compression, secondary hypoperfusion, ischemia, and mass-effect brain herniation.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Accurately establish and document time of symptom onset or time last seen well.
  • Systematically rule out stroke mimics (e.g., hypoglycaemia, seizure, migraine).
  • Perform Melbourne Ambulance Stroke Screen (MASS) assessment.
  • Perform ACT FAST assessment.
  • Establish an $18\,\text{G}$ IV catheter in the antecubital fossa (ACF).
  • Rapid transport to the nearest thrombolysis-capable facility or direct rendezvous with a Mobile Stroke Unit (MSU).

• Autonomic Dysreflexia

  • Definition: An unmodulated, massive sympathetic nervous system response triggered by a noxious stimulus below the level of a spinal cord lesion (typically at or above $T_6$).
  • Pathophysiology Flowchart:
  • Established spinal cord lesion located at or above the $T_6$ vertebral level.
  • Disruption of descending inhibitory conduction from the brain stem to the splanchnic sympathetic bed.
  • A noxious stimulus occurs below the level of the injury (e.g., distended urinary bladder, fecal impaction/bowel distension, pressure injury, ingrown toenail, or kinked urinary catheter).
  • Afferent sensory nerve signals enter the lower spinal cord.
  • Inability of sensory signals to ascend past the spinal lesion to reach the brain.
  • Intersegmental excitation triggers a massive, uncontrolled sympathetic discharge below the lesion.
  • Severe splanchnic and peripheral vasoconstriction.
  • Acute, massive elevation in SVR resulting in severe hypertension.
  • Baroreceptors in the carotid sinus and aortic arch detect extreme hypertension and stimulate the vagal parasympathetic system.
  • Descending parasympathetic inhibitory signals cannot pass down through the spinal cord lesion.
  • Parasympathetic activation above the injury level produces compensatory bradycardia, arterial vasodilation, cutaneous flushing, and profuse diaphoresis.
  • Sympathetic vasoconstriction below the lesion remains completely uninhibited, sustaining severe hypertension and risk of intracranial haemorrhage.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Identify and immediately remove the offending noxious stimulus.
  • If Systolic Blood Pressure (SBP) remains $> 160\,\text{mmHg}$, administer GTN $300\text{--}600\,\text{mcg}$ sublingually, repeating every $10\,\text{minutes}$ until symptom resolution, onset of side effects, or SBP drops below $160\,\text{mmHg}$.
  • Rapid transport.

• Acute Alcohol Intoxication

  • Definition: Systemic toxicity secondary to high blood ethanol levels, causing generalized central nervous system depression and deterioration of neurological, respiratory, and protective airway functions.
  • Pathophysiology Flowchart:
  • Ingestion of significant quantities of ethanol.
  • Rapid absorption through the gastrointestinal mucosa into the systemic bloodstream.
  • Progressive rise in Blood Alcohol Concentration (BAC).
  • Ethanol readily crosses the blood-brain barrier.
  • Allosteric modulation of GABA-A receptors and inhibition of NMDA receptors, driving central nervous system depression.
  • Disruption of normal neurotransmission.
  • Progressive decline in conscious level, motor coordination, and protective airway reflexes (gag/swallow).
  • Severe intoxication depresses the medullary respiratory center.
  • Suppression of central respiratory drive.
  • Loss of upper airway tone and aspiration of gastric contents.
  • Alveolar hypoventilation leading to hypoxaemia, hypercapnia, and respiratory arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Maintain upper airway integrity and provide ventilatory support as required.
  • Active management of nausea, pain, hypoglycaemia, and shock state.

• Alcohol Withdrawal Syndrome

  • Definition: Hyperexcitability of the central nervous system following abrupt cessation or reduction of alcohol intake in a chronically alcohol-dependent individual.
  • Pathophysiology Flowchart:
  • Sustained long-term alcohol ingestion.
  • Chronic CNS depression forces neuroadaptation (downregulation of inhibitory GABA receptors and upregulation of excitatory NMDA glutamate receptors).
  • Sudden reduction or complete cessation of alcohol ingestion.
  • Unopposed removal of the central depressant effect.
  • Rebound CNS hyper-excitation.
  • Massive increase in systemic sympathetic nervous system activity.
  • Clinical state: tachycardia, marked hypertension, diaphoresis, coarse tremor, and severe agitation/anxiety.
  • Severe progression: withdrawal seizures and Delirium Tremens (DTs), marked by autonomic instability, severe hyperthermia, confusion, and life-threatening cardiac dysrhythmias.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Administer antiemetics and analgesia as required.
  • Administer Midazolam as per the Acute Behavioural Disturbance protocol.

• Drug-Induced Hyperthermia

  • Definition: Severe elevation of core body temperature caused by pharmacologic or toxic agents that increase metabolic heat production or impair heat dissipation.
  • Pathophysiology Flowchart:
  • Ingestion or exposure to toxic substances or drugs (e.g., sympathomimetics, serotonergic agents, anticholinergics).
  • Pharmacological stimulation causes uncontrolled metabolic heat generation while simultaneously blunting peripheral heat dissipation mechanisms.
  • Rapid elevation of core body temperature.
  • Normal physiological thermoregulatory mechanisms are completely overwhelmed.
  • Critical core hyperthermia develops ($> 40^\circ\text{C}$).
  • Heat-induced cellular and enzymatic denaturation.
  • Neurotoxicity, muscle tissue breakdown (rhabdomyolysis), and metabolic crisis.
  • Development of profound metabolic acidosis, severe hyperkalaemia, acute kidney injury (AKI), disseminated intravascular coagulation (DIC), dysrhythmias, multi-organ failure, and cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Request MICA dispatch.
  • Administer Midazolam to control muscular agitation.
  • Initiate aggressive physical external cooling.
  • Administer Normal Saline $1000\text{--}2000\,\text{ml}$ IV for fluid resuscitation.

• Opioid Toxicity

  • Definition: Excessive exogenous binding to opioid receptors, inducing severe central nervous system and respiratory depression.
  • Pathophysiology Flowchart:
  • Ingestion, inhalation, or injection of exogenous opioid compounds.
  • Binding to mu-opioid receptors within the central nervous system and brainstem.
  • Severe central nervous system depression.
  • Marked suppression of the medullary respiratory center response to carbon dioxide.
  • Decreased respiratory rate and tidal volume (hypoventilation).
  • Accumulation of arterial carbon dioxide (hypercapnia) and reduction in oxygenation (hypoxaemia).
  • Development of respiratory acidosis.
  • Severe cerebral and systemic hypoxia.
  • Secondary bradycardia, systemic hypotension, cardiorespiratory collapse, and cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Uncomplicated IV Opioid Toxicity:
    • Airway positioning and ventilatory support.
    • Administer Naloxone $800\,\text{mcg}$ IM, repeated once after $10\,\text{minutes}$.
  • Complex Adult Opioid Toxicity:
    • Airway positioning and ventilatory support.
    • Administer Naloxone $100\,\text{mcg}$ IV, repeating every $2\,\text{minutes}$ up to a maximum dose of $2000\,\text{mcg}$.
    • If IV access cannot be obtained, administer a single dose of Naloxone $400\,\text{mcg}$ IM.

• Anxiety and Panic Response

  • Definition: A psychological and physiological stress reaction causing somatic symptoms that mimic severe cardiovascular or respiratory pathology.
  • Clinical Features:
  • Acute onset of chest pain, frequently pleuritic or atypical in nature.
  • Feeling of severe dyspnoea and hyperventilation.
  • Altered distal sensation (perioral and acral paresthesias).
  • Profound emotional distress, motor restlessness, and apprehension.

Immunological, Infectious, and Systemic Conditions

• Anaphylaxis

  • Definition: A severe, life-threatening, systemic IgE-mediated hypersensitivity reaction characterized by rapidly progressive airway compromise, bronchospasm, and distributive shock.
  • Pathophysiology Flowchart:
  • Initial exposure to a specific foreign allergen.
  • Immune processing induces allergen-specific Immunoglobulin E (IgE) antibody production; IgE binds to high-affinity receptors on tissue mast cells and circulating basophils (sensitization phase without clinical symptoms).
  • Re-exposure to the specific allergen occurs.
  • Allergen cross-links surface-bound IgE molecules on mast cells and basophils.
  • Sudden cell degranulation, releasing potent inflammatory mediators (histamines, leukotrienes, prostaglandins, and cytokines).
  • Systemic biological effects:
    • Upper/Lower Airway: Intense bronchial smooth muscle constriction (bronchospasm) combined with mucosal hypersecretion and severe upper airway oedema (laryngeal/orolingual stridor).
    • Vascular Bed: Widespread systemic arteriolar vasodilation combined with severe endothelial capillary leak.
    • Integument: Urticarial rash, erythema, and angioedema.
  • Massive fluid extravasation into the interstitial tissue spaces.
  • Precipitous fall in SVR and circulating intravascular volume.
  • Severe hypotension, profound hypoperfusion, anaphylactic shock, and rapid cardiac arrest if untreated.
  • Management Protocol:
  • Rest and reassurance.
  • Obtain consent and place in a position of comfort (do not allow sudden standing).
  • Request MICA dispatch.
  • Immediately remove the offending allergen if applicable.
  • Administer Adrenaline $500\,\text{mcg}$ IM, repeated every $5\,\text{minutes}$ as clinically required.
  • Establish IV access.
  • Supplemental oxygen therapy as per critical illness guidelines.
  • If upper airway stridor is present: Administer nebulised Adrenaline $5\,\text{mg}$.
  • If bronchospasm is present: Administer nebulised Salbutamol $5\,\text{mg}$ and Ipratropium Bromide $500\,\text{mcg}$.
  • Administer Dexamethasone $8\,\text{mg}$ in $2\,\text{ml}$ IV, IM, or oral.
  • Fluid resuscitation: Administer Normal Saline $20\text{--}40\,\text{ml/kg}$ IV, titrated to clinical response.
  • Refractory Anaphylaxis: Administer Glucagon $1\,\text{IU}$ IV or IM if hypotension persists following 2 doses of IM Adrenaline in patients with a history of heart failure or taking beta-blockers.

• Allergic Reaction

  • Definition: An immune-mediated response to an allergen that remains localized to cutaneous or mucosal tissues without systemic vascular or respiratory collapse.
  • Pathophysiology Flowchart:
  • Exposure to a foreign allergen.
  • Recognition of the antigen by the immune system as harmful.
  • Localized immune activation.
  • Degranulation of mast cells and basophils releasing histamine and prostaglandins.
  • Localized inflammatory response.
  • Localized tissue manifestations (urticaria, pruritus, localized erythema, and mild localized swelling).
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Carefully monitor and prepare for potential evolution into systemic anaphylaxis.

• Shock

  • Definition: A state of acute, widespread circulatory failure resulting in inadequate cellular tissue perfusion and oxygen delivery to meet metabolic demands.
  • Pathophysiology Flowchart:
  • Underlying initiating etiology categorized into 4 main physiological classes:
    • Hypovolaemic Shock: Absolute deficit in circulating blood volume (haemorrhagic or non-haemorrhagic) decreasing cardiac preload, stroke volume, and cardiac output.
    • Cardiogenic Shock: Inability of the heart pump to generate sufficient cardiac output, increasing ventricular filling pressures, myocardial oxygen demand, and compensatory afterload.
    • Obstructive Shock: Mechanical impairment to blood flow through the central circulatory circuit (e.g., tension pneumothorax, pulmonary embolism, pericardial tamponade).
    • Distributive Shock: Severe loss of vascular tone resulting in pathological vasodilation and maldistribution of blood flow (septic, neurogenic, anaphylactic).
  • Systemic drop in cardiac output and/or effective circulating blood volume.
  • Failure of adequate tissue and organ microvascular perfusion.
  • Inadequate oxygen and nutrient delivery to peripheral cells.
  • Cellular hypoxia.
  • Transition from aerobic metabolism to anaerobic metabolic pathways.
  • Rapid accumulation of lactic acid and hydrogen ions.
  • Progressive metabolic acidosis.
  • Widespread loss of cellular function and ionic integrity.
  • Endothelial disruption, organ injury, multi-organ dysfunction syndrome (MODS), and cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Supplemental oxygen titrated to arterial saturations.
  • Fluid resuscitation: Administer Normal Saline $1000\text{--}2000\,\text{ml}$ IV, titrated to clinical response.
  • Symptomatic supportive treatment.

• Sepsis and Systemic Infection

  • Definition: A dysregulated host immune response to infection causing life-threatening organ dysfunction, extreme vasodilation, microvascular permeability, and tissue hypoperfusion.
  • Pathophysiology Flowchart:
  • Pathogenic microorganism penetrates host immune barriers.
  • Rapid proliferation of the pathogen within body tissues.
  • Systemic activation of host immune cells.
  • Excessive, dysregulated release of pro-inflammatory cytokines, prostaglandins, and endothelial mediators.
  • Severe systemic vascular inflammation, pan-vascular vasodilation, and widespread capillary leakage.
  • Marked drop in SVR combined with loss of plasma volume into interstitial spaces.
  • Precipitous fall in blood pressure and circulating blood volume.
  • Severe tissue hypoperfusion and impaired cellular oxygen utilization.
  • Cellular shift to anaerobic pathways, resulting in elevated blood lactate levels.
  • Progressive cellular dysfunction leading to acute organ failure, septic shock, and multi-organ collapse.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Symptomatic management.
  • Calculate National Early Warning Score 2 (NEWS2).
  • Sepsis Criteria (NEWS2 score $> 7$):
    • Supplemental oxygen therapy.
    • Administer Normal Saline $500\text{--}1000\,\text{ml}$ IV.
    • Initiate Priority 1 (Signal 1) transport with pre-hospital facility notification.

• Meningococcal Septicaemia

  • Definition: Severe fulminant systemic infection caused by Neisseria meningitidis, driving rapid vascular collapse, purpuric rash, and septic shock.
  • Pathophysiology Flowchart:
  • Proliferation of meningococcal bacteria in the nasopharynx followed by invasion into the bloodstream.
  • Shedding of bacterial endotoxins into the blood.
  • Activation of an overwhelming systemic immune and inflammatory cascade.
  • Uncontrolled release of vasoactive inflammatory mediators.
  • Rapid, extreme systemic vasodilation.
  • Disruption of vascular endothelial integrity, causing extreme capillary permeability.
  • Fluid shifts rapidly from the intravascular space into the tissues.
  • Severe decrease in effective circulating volume and total peripheral resistance.
  • Profound, refractory hypotension.
  • Systemic tissue hypoperfusion and severe cellular hypoxia.
  • Anaerobic metabolism and exponential rise in serum lactate.
  • Rapid onset of multi-organ failure, disseminated intravascular coagulation (DIC), septic shock, and cardiac arrest.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Symptomatic supportive care.
  • Calculate NEWS2 score (Score $> 7$: administer oxygen, Normal Saline $500\text{--}1000\,\text{ml}$ IV, Signal 1 transport with pre-notification).
  • Administer Ceftriaxone $2\,\text{g}$ IM or IV if transport time to a definitive hospital exceeds $60\,\text{minutes}$.

Gastrointestinal and Renal Conditions

• Nephrolithiasis (Renal Calculi)

  • Definition: Formation of crystalline mineral deposits within the urinary tract causing mechanical tract obstruction, ureteric spasm, severe flank pain, and potential acute kidney injury.
  • Pathophysiology Flowchart:
  • Presence of risk factors (e.g., chronic dehydration, high urinary mineral concentration, specific dietary factors, or metabolic disorders).
  • Supersaturation of solute particles within the renal tubular urine.
  • Minerals precipitate out of solution and crystallize.
  • Microscopic crystals aggregate and grow into kidney stones.
  • The stone dislodges and migrates distally into the narrow ureter.
  • Physical obstruction of urine flow within the ureteral lumen.
  • Increased intra-luminal hydrostatic pressure proximal to the site of obstruction.
  • Violent hyper-peristaltic smooth muscle contractions (spasms) of the ureter attempting to clear the stone.
  • Activation of visceral nociceptors causing severe renal colic (flank pain).
  • Secondary complications: Haematuria, nausea, vomiting, localized infection, and acute kidney injury (AKI).
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Symptomatic management and analgesia.

• Urinary Tract Infection (UTI)

  • Definition: Bacterial colonization and multiplication within the urinary tract causing local mucosal inflammation, which may ascend to the kidneys or disseminate into the bloodstream.
  • Pathophysiology Flowchart:
  • Pathogenic bacteria enter the urethral meatus and multiply within the lower urinary tract.
  • Acute mucosal inflammation of the bladder and urethra.
  • Development of localized UTI manifestations (dysuria, urinary frequency, urgency, suprapubic pain).
  • Infection ascends superiorly through the ureters.
  • Involvement of the renal parenchyma (pyelonephritis).
  • Bacteria translocate into the renal capillary network and enter the systemic circulation.
  • Triggering of a systemic inflammatory response syndrome (SIRS).
  • Progression to sepsis, acute organ dysfunction, and septic shock.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Supportive symptomatic treatment.
  • Calculate NEWS2 score.
  • NEWS2 score $> 7$: Supplemental oxygen, Normal Saline $500\text{--}1000\,\text{ml}$ IV, Signal 1 transport with notification.

• Cholecystitis

  • Definition: Acute inflammation of the gallbladder wall, most commonly resulting from cystic duct obstruction by a gallstone.
  • Pathophysiology Flowchart:
  • Risk factors present (e.g., gallstones, obesity, female sex, age, rapid weight loss).
  • A gallstone becomes mechanically impacted within the cystic duct.
  • Stasis of bile behind the point of obstruction.
  • Continuous accumulation of bile increases intra-gallbladder pressure.
  • Chemical irritation and mechanical distension of the gallbladder wall.
  • Progressive distension compromises venous and lymphatic drainage of the gallbladder wall.
  • Ischaemic injury releases inflammatory mediators.
  • Oedema and thickening of the gallbladder wall, establishing acute cholecystitis.
  • Management Protocol:
  • Rest and reassurance.
  • Consent and position of comfort.
  • Supportive symptomatic care.

• Mediastinitis

  • Definition: Severe, life-threatening infection and inflammation of the tissues of the mediastinum, frequently resulting from oesophageal rupture.
  • Pathophysiology:
  • Transmural tear of the oesophagus secondary to violent, persistent vomiting (Boerhaave syndrome) or recent thoracic instrumentation/surgery.
  • Contamination of the sterile mediastinal space with gastric contents and oral flora.
  • Rapid development of overwhelming mediastinal bacterial infection and necrosis.
  • Clinical Features:
  • Systemic signs of severe sepsis and high fever.
  • History of severe, forceful vomiting or recent chest surgery.

• Gastrooesophageal Reflux Disease (Reflux)

  • Definition: Retrograde flow of acidic gastric contents past the lower oesophageal sphincter into the oesophagus.
  • Clinical Features:
  • Chest pain described as a burning sensation located in the epigastric or retrosternal regions.
  • Radiation of burning pain superiorly into the neck.
  • Nausea, regurgitation, and frequent eructation (burping).
  • Pain relief upon administration of antacids.

• Pancreatitis

  • Definition: Inflammatory auto-digestion of pancreatic tissue caused by premature intracellular activation of proteolytic enzymes.
  • Pathophysiology:
  • Triggering factors (such as chronic heavy alcohol consumption or gallstone migration).
  • Intracinar activation of zymogens leading to enzymatic destruction of pancreatic parenchyma and surrounding tissues.
  • Clinical Features:
  • Severe, constant epigastric pain that characteristically radiates straight through to the chest and back.
  • Pain exacerbated by abdominal palpation.
  • Associated nausea, persistent vomiting, and systemic fever.

• Oesophageal Spasm

  • Definition: Uncoordinated, high-amplitude contractions of the oesophageal smooth muscle caused by neurogenic dysmotility.
  • Clinical Features:
  • Sudden onset of severe retrosternal chest pain.
  • Sensation of a foreign object or food bolus stuck in the chest.
  • Dysphagia (difficulty swallowing).
  • Symptoms occurring during or immediately following food intake.

Musculoskeletal and Atypical Chest Pain Differentials

• Costochondritis

  • Definition: Inflammatory condition affecting the costochondral or costosternal cartilaginous junctions connecting the ribs to the sternum.
  • Clinical Features:
  • Highly localized chest wall pain.
  • Sharp and pleuritic in nature.
  • Exacerbated by direct focal palpation of the affected costochondral joints and changes in body position.

• Muscular Chest Pain

  • Definition: Irritation, strain, or spasm of the skeletal muscles of the thoracic wall (e.g., intercostal muscles or pectoralis major).
  • Clinical Features:
  • Precise, highly localized (pinpoint) pain.
  • Sharp character.
  • Directly reproducible by movement of the upper torso, chest wall exertion, or physical palpation.

Emergency Pharmacology and Medication Protocols

• Adrenaline (1 mg in 1 ml)

  • Mechanism of Action:
  • Beta-1 Agonism: Increases heart rate by accelerating the firing rate of the SA node; increases conduction velocity through the AV node; increases myocardial contractility; increases ventricular irritability.
  • Beta-2 Agonism: Relaxes bronchial smooth muscle, causing bronchodilation, lowering airway resistance, opening conducting airways, and reducing dynamic air trapping.
  • Alpha-1 Agonism: Induces intense peripheral arterial and venous vasoconstriction, decreasing capillary permeability ("less leaky") and raising systemic blood pressure.
  • Indications:
  • Anaphylaxis
  • Severe asthma
  • Bradycardia with poor perfusion
  • Cardiac arrest
  • Severe croup
  • Shock state
  • Orolingual oedema secondary to tissue plasminogen activator (TPA) infusion
  • Contraindications:
  • Nil in life-threatening emergency settings.
  • Side Effects:
  • Dysrhythmias
  • Palpitations
  • Systemic hypertension
  • Angina pectoris
  • Headache
  • Anxiety and motor tremors
  • Hyperglycaemia
  • Precautions:
  • Hypovolaemic shock without adequate fluid resuscitation
  • Elderly or frail patients
  • Mechanism of injury / concurrent toxicity involving Tricyclic Antidepressants (TCAs), Beta-blockers, or Quetiapine
  • Dosages and Administration:
  • Adult Anaphylaxis (IM): $500\,\text{mcg}$ IM ($1:1000$); repeat every $5\,\text{minutes}$ as required. No maximum dose.
  • Adult Anaphylaxis (Nebulised): $5\,\text{mg}$ nebulised; repeat via medical consultation.
  • Adult Asthma (IV): $20\,\text{mcg}$ IV; repeat every $2\,\text{minutes}$. No maximum dose.
  • Adult Asthma (IM): $500\,\text{mcg}$ IM; repeat every $5\,\text{minutes}$. No maximum dose.
  • Cardiac Arrest: $1\,\text{mg}$ IV/IO; repeat every $4\,\text{minutes}$. No maximum dose.
  • Paediatric Dose: $10\,\text{mcg/kg}$ IM (up to a single maximum dose of $500\,\text{mcg}$).

• Amiodarone (150 mg in 3 ml)

  • Mechanism of Action:
  • Class III anti-arrhythmic agent. Prolongs the cardiac action potential duration and effective refractory period; blocks inactivated sodium channels, non-competitively blocks beta-receptors, and blocks calcium channels.
  • Indications:
  • Ventricular Fibrillation (VF)
  • Pulseless Ventricular Tachycardia (VT)
  • Sustained monomorphic VT
  • Contraindications:
  • Tricyclic antidepressant toxicity
  • Baseline $QTc > 500\,\text{ms}$
  • Ventricular tachycardia secondary to Ondansetron administration
  • Pregnancy (unless in cardiac arrest)
  • Side Effects:
  • Rebound bradycardia
  • Systemic hypotension
  • Local venous phlebitis at injection site
  • Nausea and vomiting
  • Metallic taste disturbance
  • Precautions:
  • Older or frail patients
  • Dosages and Administration:
  • Initial Adult Dose: $300\,\text{mg}$ IV/IO.
  • Repeat Dose: $150\,\text{mg}$ IV/IO after $4\,\text{minutes}$ for sustained VF/VT.
  • Maximum Cumulative Dose: $450\,\text{mg}$.
  • Paediatric Dose: Not applicable in standard basic protocol.

• Aspirin (300 mg Chewable Tablet)

  • Mechanism of Action:
  • Irreversible cyclooxygenase-1 (COX-1) inhibitor. Inhibits the synthesis of thromboxane $A_2$, providing anti-platelet aggregation, anti-inflammatory, analgesic, and antipyretic actions. Slows the progression of platelet aggregation and arterial thrombus formation.
  • Indications:
  • Acute Coronary Syndrome (ACS)
  • Contraindications:
  • Known hypersensitivity to salicylates or NSAIDs
  • Actively bleeding peptic ulcer disease
  • Established bleeding disorders
  • Suspected dissecting Abdominal Aortic Aneurysm (AAA)
  • Chest pain associated with psychostimulant overdose in the presence of $SBP > 160\,\text{mmHg}$
  • Side Effects:
  • Heartburn and epigastric discomfort
  • Nausea
  • Gastrointestinal mucosal bleeding
  • Prolonged bleeding time
  • Hypersensitivity responses
  • Precautions:
  • History of peptic ulcer disease
  • Asthma
  • Patients currently taking systemic anticoagulants
  • Dosages and Administration:
  • Adult Dose: $300\,\text{mg}$ chewable tablet (single dose).
  • Repeat Dose: Not for repeat administration.
  • Maximum Dose: $300\,\text{mg}$.
  • Paediatric Dose: Not applicable.

• Ceftriaxone (1 g Vial)

  • Mechanism of Action:
  • Third-generation cephalosporin antibiotic. Inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs), causing cell wall lysis and rapid bacterial cell death.
  • Indications:
  • Suspected Meningococcal Septicaemia
  • Severe Sepsis (where transport time to definitive hospital care exceeds $60\,\text{minutes}$)
  • Contraindications:
  • Anaphylaxis or severe allergy to cephalosporins
  • Preterm neonates ($< 14\,\text{weeks}$ corrected gestational age)
  • Side Effects:
  • Diarrhoea
  • Nausea and vomiting
  • Local pain and irritation at injection site
  • Urticarial or maculopapular rash
  • Precautions:
  • History of penicillin allergy
  • Reconstitution and Dosages:
  • IM Reconstitution: $3.5\,\text{ml}$ of 1% Lidocaine per vial.
  • IV Reconstitution: $9.5\,\text{ml}$ of Water for Injection per vial.
  • Adult Dose: $2\,\text{g}$ IM or IV (single dose).
  • Repeat Dose: Not for repeat administration.
  • Maximum Dose: $2\,\text{g}$.
  • Paediatric Dose: $50\,\text{mg/kg}$ IM/IV up to a maximum dose of $2000\,\text{mg}$.

• Dexamethasone (8 mg in 2 ml)

  • Mechanism of Action:
  • Long-acting synthetic glucocorticoid corticosteroid. Suppresses the migration of polymorphonuclear neutrophils, inhibits lymphocyte proliferation, and decreases the synthesis of pro-inflammatory cytokines, reducing mucosal oedema and inflammation within bronchial epithelial structures.
  • Indications:
  • Anaphylaxis with associated bronchospasm
  • Asthma
  • COPD exacerbation
  • Severe COVID-19 infection
  • Croup
  • Non-foreign body airway obstruction causing stridor
  • Contraindications:
  • Nil in emergency indications.
  • Side Effects:
  • Nil of significance following acute single-dose emergency administration.
  • Precautions:
  • Nil for single acute emergency administration.
  • Dosages and Administration:
  • Adult Dose: $8\,\text{mg}$ in $2\,\text{ml}$ IV, IM, or Oral.
  • Repeat Dose: Not for repeat administration.
  • Maximum Dose: $8\,\text{mg}$.
  • Paediatric Croup Dose: $600\,\text{mcg/kg}$ oral (up to a single maximum dose of $12\,\text{mg}$).

• Dextrose 10% (25 g in 250 ml)

  • Mechanism of Action:
  • Hypertonic simple sugar solution that raises blood glucose levels directly upon intravascular administration, restoring cellular substrate and reducing hepatic glycogen depletion.
  • Indications:
  • Hypoglycaemia ($BGL < 4\,\text{mmol/L}$) accompanied by altered conscious state or unresponsiveness to oral glucose agents.
  • Contraindications:
  • None in confirmed symptomatic hypoglycaemia.
  • Side Effects:
  • Local tissue irritation and venous phlebitis at the insertion site.
  • Precautions:
  • Ensure IV line patency prior to administration to avoid extravasation.
  • Dosages and Administration:
  • Initial Adult Dose: $15\,\text{g}$ in $150\,\text{ml}$ IV.
  • Repeat Dose: $10\,\text{g}$ in $100\,\text{ml}$ IV after $10\,\text{minutes}$ if BGL remains $< 4\,\text{mmol/L}$.
  • Maximum Dose: $25\,\text{g}$ in $250\,\text{ml}$.
  • Paediatric Dose: Not applicable in this formulation.

• Droperidol (10 mg in 2 ml)

  • Mechanism of Action:
  • Neuroleptic dopamine antagonist ($D_2$ receptor blocker) providing central sedative, anti-agitation, and tranquilizing effects.
  • Indications:
  • Moderate agitation
  • Acute behavioural disturbance
  • Contraindications:
  • Nil when indicated for severe acute agitation.
  • Side Effects:
  • Over-sedation
  • Dizziness
  • Hypotension
  • Reflex tachycardia
  • Prolongation of the $QTc$ interval
  • Extrapyramidal side effects (dystonia)
  • Precautions:
  • Elderly or frail status
  • Established Parkinson's disease
  • Lewy body dementia
  • Dosages and Administration:
  • Standard Adult Dose: $5\text{--}10\,\text{mg}$ ($1\text{--}2\,\text{ml}$) IM/IV.
  • Frail / Elderly Adult Dose: $5\,\text{mg}$ ($1\,\text{ml}$) IM/IV.
  • Repeat Dose: Repeat original dose after $15\,\text{minutes}$ if agitation persists.
  • Maximum Cumulative Dose: $20\,\text{mg}$ ($10\,\text{mg}$ in elderly/frail).
  • Paediatric Dose: $0.1\text{--}0.2\,\text{mg/kg}$ via clinical consultation.

• Fentanyl (100 mcg in 2 ml)

  • Mechanism of Action:
  • Potent synthetic opioid agonist that selectively binds to central mu-opioid receptors, inhibiting ascending pain pathways and altering perception/response to pain.
  • Indications:
  • Moderate to severe pain
  • Sedation to facilitate endotracheal intubation, transthoracic pacing, or synchronized cardioversion
  • Contraindications:
  • Serotonin syndrome
  • Monoamine Oxidase Inhibitor (MAOI) therapy within the preceding 14 days
  • Late second stage of labor
  • Side Effects:
  • Bradycardia
  • Respiratory depression
  • Chest wall (diaphragmatic) rigidity
  • Nausea and vomiting
  • Cutaneous rash and localized erythema
  • Precautions:
  • Elderly or frail status
  • Impaired hepatic function
  • Pre-existing respiratory depression or active severe asthma
  • Facial trauma (for intranasal route)
  • Dosages and Administration:
  • Adult Analgesia (IM): $100\,\text{mcg}$ IM; repeat $50\,\text{mcg}$ every $15\,\text{minutes}$ (Max: $150\,\text{mcg}$).
  • Adult Analgesia (IV): $25\text{--}50\,\text{mcg}$ IV; repeat $25\text{--}50\,\text{mcg}$ every $5\,\text{minutes}$ (Max: $200\,\text{mcg}$).
  • Adult Analgesia (IN): $100\,\text{mcg}$ IN; repeat $50\,\text{mcg}$ every $5\,\text{minutes}$ (Max: $400\,\text{mcg}$).
  • Frail Adult Dose (IN): $50\,\text{mcg}$ IN; repeat $50\,\text{mcg}$ every $5\,\text{minutes}$ (Max: $200\,\text{mcg}$).
  • Paediatric IN Dosing:
    • Weight $10\text{--}17\,\text{kg}$: $25\,\text{mcg}$ IN.
    • Weight $18\text{--}39\,\text{kg}$: $25\text{--}50\,\text{mcg}$ IN.
    • Weight $> 40\,\text{kg}$: $50\text{--}75\,\text{mcg}$ IN.

• Glucagon (1 mg / 1 IU)

  • Mechanism of Action:
  • Pancreatic hormone that binds to specific glucagon receptors on hepatocytes, stimulating hepatic glycogenolysis and gluconeogenesis, elevating blood glucose levels.
  • Indications:
  • Hypoglycaemia ($BGL < 4\,\text{mmol/L}$) with altered conscious state where IV access is unachievable.
  • Refractory anaphylactic shock with persistent hypotension unresponsive to 2 doses of IM Adrenaline in patients with a history of heart failure or concurrent beta-blocker therapy.
  • Contraindications:
  • Known pancreatic tumors (e.g., insulinoma)
  • Known adrenal gland tumors (e.g., phaeochromocytoma)
  • Side Effects:
  • Nausea and vomiting
  • Precautions:
  • Reduced efficacy in patients with depleted hepatic glycogen reserves (e.g., adrenal insufficiency, prolonged fasting, chronic liver disease, recent prior glucagon administration, or acute alcohol intoxication).
  • Position patient in the lateral recovery position to protect airway against emesis.
  • Dosages and Administration:
  • Adult Hypoglycaemia: $1\,\text{IU}$ IM (single dose, no repeat).
  • Refractory Anaphylaxis: $1\,\text{IU}$ IV/IM; repeat $1\,\text{IU}$ once after $5\,\text{minutes}$ (Max: $2\,\text{IU}$).
  • Paediatric Dose:
    • Weight $< 25\,\text{kg}$: $0.5\,\text{IU}$ IM.
    • Weight $> 25\,\text{kg}$: $1\,\text{IU}$ IM.

• Glyceryl Trinitrate - GTN (300 mcg Sublingual Tablet / 50 mg Transdermal Patch)

  • Mechanism of Action:
  • Organic nitrate that donates nitric oxide, stimulating cyclic guanosine monophosphate (cGMP) production to induce venous and arterial vasodilation. Decreases myocardial preload and afterload, reduces myocardial oxygen demand, and dilates collateral coronary arteries.
  • Indications:
  • Ischaemic chest pain secondary to ACS
  • Systemic hypertension associated with ACS
  • Cardiogenic Acute Pulmonary Oedema (APO)
  • Autonomic Dysreflexia
  • Preterm labor
  • Contraindications:
  • $SBP < 100\,\text{mmHg}$ ($< 160\,\text{mmHg}$ in Autonomic Dysreflexia)
  • Heart rate $< 50\,\text{bpm}$ (except in Autonomic Dysreflexia)
  • Heart rate $> 150\,\text{bpm}$ or active VT
  • Concurrent use of Phosphodiesterase-5 (PDE-5) inhibitors (e.g., sildenafil, tadalafil)
  • Active bleeding in pregnancy
  • Concurrent use of Riociguat
  • Side Effects:
  • Hypotension
  • Reflex tachycardia or paradox bradycardia
  • Pulsatile headache
  • Dizziness and syncope
  • Facial flushing
  • Precautions:
  • Elderly or frail status
  • Confirmed right ventricular infarction or inferior STEMI with $SBP < 160\,\text{mmHg}$
  • Dosages and Administration:
  • Autonomic Dysreflexia: $300\text{--}600\,\text{mcg}$ S/L every $5\,\text{minutes}$ until resolution, onset of side effects, or $SBP < 160\,\text{mmHg}$.
  • Cardiogenic APO: $300\text{--}600\,\text{mcg}$ S/L every $5\,\text{minutes}$ if $SBP > 100\,\text{mmHg}$ + $50\,\text{mg}$ transdermal patch. Stop S/L if $SBP < 100\,\text{mmHg}$; remove patch if $SBP < 90\,\text{mmHg}$.
  • ACS Chest Pain: $300\text{--}600\,\text{mcg}$ S/L every $5\,\text{minutes}$ + $50\,\text{mg}$ patch. Stop S/L if $SBP < 100\,\text{mmHg}$; remove patch if $SBP < 90\,\text{mmHg}$.
  • Preterm Labor: $50\,\text{mg}$ transdermal patch; apply a second patch if uterine contractions persist after $1\,\text{hour}$ (Max: 2 patches).
  • Paediatric Dose: Not applicable.

• Hydrocortisone (100 mg Powder for Injection)

  • Mechanism of Action:
  • Short-acting corticosteroid possessing equal glucocorticoid (anti-inflammatory, immunosuppressive, gluconeogenic) and mineralocorticoid (renal sodium/water retention and potassium excretion) properties.
  • Indications:
  • Acute adrenal insufficiency (Adrenal Crisis)
  • Contraindications:
  • Nil in acute emergency management.
  • Side Effects:
  • Nil of significance following single emergency administration.
  • Precautions:
  • Reconstitute powder using $2\,\text{ml}$ of Normal Saline prior to IV or IM administration.
  • Dosages and Administration:
  • Adult Dose: $100\,\text{mg}$ IM or IV (single dose).
  • Maximum Dose: $100\,\text{mg}$.
  • Paediatric Dosing:
    • Age $< 2\,\text{years}$: $25\,\text{mg}$ IM.
    • Age $3\text{--}11\,\text{years}$: $50\,\text{mg}$ IM.
    • Age $12\text{--}15\,\text{years}$: $100\,\text{mg}$ IM.

• Ipratropium Bromide (250 mcg in 1 ml)

  • Mechanism of Action:
  • Anticholinergic (parasympatholytic) agent. Non-selectively blocks muscarinic acetylcholine receptors ($M_3$) in bronchial smooth muscle, inhibiting vagally-mediated bronchoconstriction and decreasing mucosal secretions.
  • Indications:
  • Severe asthma or anaphylactic bronchospasm
  • Acute exacerbation of COPD
  • Contraindications:
  • Nil in emergency therapy.
  • Side Effects:
  • Palpitations and mild tachycardia
  • Nausea
  • Dizziness and headache
  • Dry mouth
  • Precautions:
  • Avoid contact with eyes (risk of acute angle-closure glaucoma or pupillary dilation)
  • Underlying cardiovascular disorders
  • Dosages and Administration:
  • Adult Asthma / Anaphylaxis: $500\,\text{mcg}$ nebulised (single dose, no repeat).
  • Adult COPD Exacerbation: $500\,\text{mcg}$ nebulised; repeat once after $1\,\text{hour}$ (Max: $1000\,\text{mcg}$).
  • Paediatric Dose:
    • Age $1\text{--}4\,\text{years}$: $250\,\text{mcg}$ nebulised.
    • Age $5\text{--}15\,\text{years}$: $500\,\text{mcg}$ nebulised.

• Ketamine (200 mg in 2 ml)

  • Mechanism of Action:
  • Dissociative anaesthetic agent. Non-competitive antagonist at central NMDA receptors; induces profound analgesia, amnesia, and sedation while preserving airway reflexes and blood pressure.
  • Indications:
  • Facilitation of endotracheal intubation
  • Sedation for pacing/cardioversion
  • Patient movement interfering with CPR quality
  • Severe acute pain
  • Severe acute behavioural disturbance
  • Contraindications:
  • Nil when indicated.
  • Side Effects:
  • Systemic hypertension and tachycardia
  • Emergence reactions and vivid hallucinations
  • Increased skeletal muscle tone
  • Transient respiratory depression or apnoea
  • Nausea, vomiting, and local injection site pain
  • Excessive lacrimation, hypersalivation, and nystagmus
  • Precautions:
  • May exacerbate severe pre-existing cardiovascular conditions
  • Dosages and Administration:
  • Interfering with CPR (IM): $200\,\text{mg}$ IM single dose.
  • Interfering with CPR (IV): $50\text{--}100\,\text{mg}$ IV; repeat every $1\text{--}2\,\text{minutes}$ as required.
  • Moderate / Severe Pain (IN): $75\,\text{mg}$ IN; repeat $50\,\text{mg}$ every $20\,\text{minutes}$ as needed.
  • Frail Pain (IN): $50\,\text{mg}$ IN; repeat $25\,\text{mg}$ every $20\,\text{minutes}$.
  • Severe Agitation (IM): $300\,\text{mg}$ IM single dose.
  • Severe Agitation (IV): $50\text{--}100\,\text{mg}$ IV single dose (Max: $100\,\text{mg}$).
  • Paediatric Dose: Not specified in standard basic protocol.

• Lidocaine (50 mg in 5 ml)

  • Mechanism of Action:
  • Class IB anti-arrhythmic and local anaesthetic. Blocks fast voltage-gated sodium channels, suppressing cardiac automaticity, slowing conduction velocity, and interrupting neuronal impulse propagation.
  • Indications:
  • Local anaesthetic prior to Ceftriaxone IM administration
  • Refractory VF / Pulseless VT
  • Contraindications:
  • Known hypersensitivity to amide local anaesthetics
  • Side Effects:
  • Systemic allergic reactions
  • Localized tissue irritation
  • Manifestations of systemic toxicity (visual disturbances, motor agitation, muscle twitching, convulsions, severe hypotension, bradycardia)
  • Precautions:
  • High potential for systemic toxicity if administered rapidly IV
  • Dosages and Administration:
  • Adult VF / VT: $100\,\text{mg}$ IV; repeat $50\,\text{mg}$ once after $4\,\text{minutes}$ for sustained VF/VT.
  • Maximum Cumulative Dose: $150\,\text{mg}$.
  • Local Anaesthesia for Ceftriaxone: Mixed directly into Ceftriaxone vial ($3.5\,\text{ml}$ of 1% lidocaine per vial).
  • Paediatric Dose: Not applicable.

• Methoxyflurane (3 ml Volatile Liquid)

  • Mechanism of Action:
  • Inhaled fluorinated hydrocarbon halogenated ether providing potent analgesia at low vapor concentrations.
  • Indications:
  • Moderate to severe pain relief
  • Contraindications:
  • Pre-existing renal disease or impairment
  • Personal or family history of malignant hyperthermia
  • Side Effects:
  • Dizziness and lightheadedness
  • Drowsiness and sedation
  • Systemic hypotension
  • Nausea and vomiting
  • Precautions:
  • Maximum total dose of $6\,\text{ml}$ within a single $24\text{-hour}$ period
  • Do not administer or discharge within enclosed, non-ventilated operational spaces
  • Dosages and Administration:
  • Initial Adult Dose: $3\,\text{ml}$ inhaled via Penthrox inhaler.
  • Repeat Dose: Administer a second $3\,\text{ml}$ bottle after $25\,\text{minutes}$ if pain persists.
  • Maximum Dose: $6\,\text{ml}$ per 24 hours.
  • Paediatric Dose: $3\text{--}6\,\text{ml}$ (maximum $6\,\text{ml}$ per 24 hours).

• Midazolam (5 mg in 1 ml)

  • Mechanism of Action:
  • Short-acting benzodiazepine central nervous system depressant. Potentiates inhibitory effects of GABA on GABA-A receptors, increasing neuronal membrane permeability to chloride ions, inducing sedation, anxiolysis, muscle relaxation, anterograde amnesia, and anticonvulsant activity.
  • Indications:
  • Status Epilepticus
  • Acute Behavioural Disturbance
  • Drug-Induced Hyperthermia
  • Alcohol Withdrawal Syndrome
  • Contraindications:
  • Known hypersensitivity to benzodiazepines
  • Severe unmanaged respiratory depression or respiratory arrest
  • Side Effects:
  • Laryngospasm and airway obstruction
  • Paradoxical excitement or agitation
  • Muscle weakness
  • Hypoventilation
  • Precautions:
  • Myasthenia gravis
  • Known untreated glaucoma
  • Hypovolaemic shock
  • Acute concurrent alcohol or central depressant intoxication
  • Significant pre-existing end-organ functional impairment
  • Dosages and Administration:
  • Acute Agitation / Hyperthermia (IM): $5\text{--}10\,\text{mg}$ IM; repeat $5\text{--}10\,\text{mg}$ after $10\,\text{minutes}$ (Max: $20\,\text{mg}$).
  • Acute Agitation / Hyperthermia (IV): $2.5\text{--}5\,\text{mg}$ IV; repeat $2.5\text{--}5\,\text{mg}$ after $5\,\text{minutes}$ (Max: $20\,\text{mg}$).
  • Frail Agitation (IM): $2.5\text{--}5\,\text{mg}$ IM; repeat after $10\,\text{minutes}$ (Max: $10\,\text{mg}$).
  • Frail Agitation (IV): $1\text{--}2\,\text{mg}$ IV; repeat after $5\,\text{minutes}$ (Max: $20\,\text{mg}$).
  • Seizure Management (IM): $10\,\text{mg}$ IM; repeat $10\,\text{mg}$ after $10\,\text{minutes}$ (Max: $20\,\text{mg}$).
  • Seizure Management (IV): $5\,\text{mg}$ IV; repeat $5\,\text{mg}$ after $5\,\text{minutes}$ (Max: $10\,\text{mg}$).
  • Frail Seizure Management: $5\,\text{mg}$ IM or $2\,\text{mg}$ IV; repeat same dose after $5\text{--}10\,\text{minutes}$ (Max IM: $10\,\text{mg}$, Max IV: $4\,\text{mg}$).
  • Paediatric Seizure Dosing:
    • Newborn: $0.5\,\text{mg}$.
    • Infant ($< 12\,\text{months}$): $1\,\text{mg}$.
    • Small Child ($1\text{--}4\,\text{years}$): $2.5\,\text{mg}$.
    • Medium Child ($5\text{--}11\,\text{years}$): $2.5\text{--}5\,\text{mg}$.
    • Adolescent ($12\text{--}15\,\text{years}$): $5\,\text{mg}$.
  • Paediatric Agitation: $0.1\text{--}0.2\,\text{mg/kg}$ (Consultation only).

• Morphine (100 mg in 1 ml)

  • Mechanism of Action:
  • Opioid analgesic agonist. Binds to central mu-opioid receptors, depressing nociceptive neurotransmission, producing profound analgesia, sedation, and central respiratory depression.
  • Indications:
  • Moderate to severe pain
  • Sedation to maintain or facilitate intubation
  • Contraindications:
  • History of severe hypersensitivity
  • Severe renal impairment
  • Late second stage of labor
  • Side Effects:
  • Drowsiness and sedation
  • Respiratory depression
  • Euphoria
  • Nausea and vomiting
  • Potential for addiction
  • Pinpoint pupils (miosis)
  • Systemic hypotension and bradycardia
  • Precautions:
  • Elderly or frail status
  • Pre-existing hypoventilation or active asthma
  • Severe respiratory tract burns
  • Known opioid dependence
  • Acute alcoholism
  • Concurrent MAOI therapy
  • Dosages and Administration:
  • Standard Adult Analgesia (IM): $10\,\text{mg}$ IM; repeat $5\,\text{mg}$ after $15\,\text{minutes}$ (Max: $15\,\text{mg}$).
  • Frail Adult Analgesia (IM): $0.1\,\text{mg/kg}$ IM single dose.
  • Standard Adult Analgesia (IV): $2.5\text{--}5\,\text{mg}$ IV; repeat $2.5\text{--}5\,\text{mg}$ every $5\,\text{minutes}$ (Max: $20\,\text{mg}$).
  • Paediatric Dose: $0.05\text{--}0.1\,\text{mg/kg}$ (Maximum cumulative dose without consult: $0.2\,\text{mg/kg}$).

• Naloxone (400 mcg in 1 ml)

  • Mechanism of Action:
  • Pure competitive opioid antagonist. High affinity for central mu, kappa, and delta opioid receptors, rapidly displacing exogenous opioids and reversing respiratory and CNS depression.
  • Indications:
  • Altered conscious state and respiratory depression secondary to opioid administration or suspected overdose.
  • Contraindications:
  • Nil in severe respiratory depression.
  • Side Effects:
  • Profuse diaphoresis
  • Piloerection ("goose bumps")
  • Coarse tremor
  • Nausea and vomiting
  • Acute agitation and violent behavior
  • Mydriasis (pupillary dilation)
  • Lacrimation
  • Acute withdrawal seizures
  • Precautions:
  • Known chronic opioid addiction (may precipitate acute withdrawal syndrome)
  • Neonatal resuscitation setting
  • Dosages and Administration:
  • Uncomplicated IV Opioid Toxicity (IM): $800\,\text{mcg}$ IM; repeat once after $10\,\text{minutes}$ (Max: $1600\,\text{mcg}$).
  • Complex Adult Opioid Toxicity (IV): $100\,\text{mcg}$ IV; repeat every $2\,\text{minutes}$ (Max: $2000\,\text{mcg}$).
  • Complex Adult Opioid Toxicity (IM): $400\,\text{mcg}$ IM (single dose if no IV access).
  • Paediatric Dosing:
    • Opioid Naïve: $10\,\text{mcg/kg}$ IM (Max: $800\,\text{mcg}$).
    • Opioid Dependent: $1\text{--}2\,\text{mcg/kg}$ IM (Max: $100\,\text{mcg}$).

• Olanzapine (5 mg Oral Tablet)

  • Mechanism of Action:
  • Second-generation (atypical) antipsychotic. Antagonizes multiple neuronal receptors, including serotonin ($5\text{-HT}_{2A/2C}$), dopamine ($D_{1-4}$), histamine ($H_1$), and alpha-1 adrenergic receptors, providing tranquilization without severe extrapyramidal effects.
  • Indications:
  • Mild to moderate agitation
  • Acute behavioural disturbance
  • Contraindications:
  • Nil when indicated.
  • Side Effects:
  • Sedation
  • Dizziness
  • Mild extrapyramidal symptoms
  • $QTc$ interval prolongation
  • Precautions:
  • Reduced clinical efficacy in patients with severe acute alcohol or stimulant intoxication
  • Elderly or frail status
  • Dosages and Administration:
  • Standard Adult Dose: $10\,\text{mg}$ oral tablet; repeat once after $20\,\text{minutes}$ if required (Max: $20\,\text{mg}$).
  • Frail Adult Dose: $5\,\text{mg}$ oral tablet; repeat once after $20\,\text{minutes}$ (Max: $10\,\text{mg}$).
  • Paediatric Dosing (Consultation Only):
    • Weight $< 60\,\text{kg}$: $5\,\text{mg}$ oral.
    • Weight $> 60\,\text{kg}$: $10\,\text{mg}$ oral.

• Ondansetron (4 mg Tablet / 8 mg in 4 ml Vial)

  • Mechanism of Action:
  • Selective serotonin $5\text{-HT}_3$ receptor antagonist. Blocks central $5\text{-HT}_3$ receptors in the chemoreceptor trigger zone (CTZ) and peripheral $5\text{-HT}_3$ receptors on vagal nerve terminals in the gastrointestinal tract, suppressing emesis.
  • Indications:
  • Undifferentiated nausea and vomiting
  • Prophylaxis against motion/procedural emesis
  • Contraindications:
  • Concurrent use of Apomorphine
  • Side Effects:
  • Headache
  • Dizziness
  • $QTc$ interval prolongation
  • Constipation
  • Transient visual disturbances
  • Precautions:
  • First trimester of pregnancy
  • Congenital Long $QT$ Syndrome
  • Severe hepatic impairment
  • Dosages and Administration:
  • Adult Oral Dose: $4\,\text{mg}$ tablet; repeat after $5\text{--}10\,\text{minutes}$ if needed (Max: $8\,\text{mg}$).
  • Adult IV Dose: $8\,\text{mg}$ IV slowly (single dose, no repeat; Max: $8\,\text{mg}$).
  • Paediatric Dosing:
    • Small Child: $2\,\text{mg}$.
    • Medium Child / Adolescent: $4\,\text{mg}$.

• Oxytocin (10 IU in 1 ml)

  • Mechanism of Action:
  • Synthetic peptide hormone matching endogenous posterior pituitary oxytocin. Stimulates smooth muscle contractions within the uterine myometrium, compressing uterine blood vessels to control postpartum bleeding.
  • Indications:
  • Primary Postpartum Haemorrhage (PPH)
  • Contraindications:
  • Nil following the delivery of all fetuses.
  • Side Effects:
  • Nausea and vomiting
  • Precautions:
  • Ensure full expulsion/delivery of all fetuses prior to administration.
  • Dosages and Administration:
  • Adult Dose: $10\,\text{IU}$ IM; repeat once after $5\,\text{minutes}$ if severe bleeding continues.
  • Maximum Cumulative Dose: $20\,\text{IU}$.
  • Paediatric Dose: Not applicable.

• Paracetamol (500 mg Tablet / 120 mg in 5 ml Solution)

  • Mechanism of Action:
  • Centrally acting non-opioid analgesic and antipyretic. Inhibits central prostaglandin synthesis in the CNS and modulates central serotonergic inhibitory pathways.
  • Indications:
  • Mild to moderate pain
  • Acute headache
  • Contraindications:
  • Infants under $1\,\text{month}$ of age
  • Known hypersensitivity
  • Side Effects:
  • Severe hypersensitivity cutaneous reactions (rare)
  • Haematological alterations
  • Severe hepatotoxicity in overdose
  • Precautions:
  • Hepatic impairment or chronic malnutrition
  • Frail adult status
  • Dosages and Administration:
  • Standard Adult Dose: $1000\,\text{mg}$ oral (single dose, no repeat; Max: $1000\,\text{mg}$).
  • Frail / Hepatic Sensitive Adult Dose: $500\,\text{mg}$ oral.
  • Paediatric Dose: $15\,\text{mg/kg}$ oral ($120\,\text{mg}$ in $5\,\text{ml}$ formulation).

• Prochlorperazine (12.5 mg in 1 ml)

  • Mechanism of Action:
  • Phenothiazine dopamine antagonist ($D_2$ blocker) acting on the chemoreceptor trigger zone; provides central antiemetic and antivertigo effects.
  • Indications:
  • Severe nausea and vomiting in patients aged $> 21\,\text{years}$ presenting with vestibular nausea or contraindications to Ondansetron.
  • Contraindications:
  • Pre-existing central nervous system depression
  • Patients aged $< 21\,\text{years}$
  • Side Effects:
  • Sedation
  • Blurred