Acute and Emergency Medicine

Question 1

Give an overview of acid/base abnormalities

Answer 1

Question 2

What is normal anion gap and what can cause it?

Answer 2

6-16 mmol/L

• Diarrhoea
• Renal tubular acidosis
• Addison disease (hyperkalaemia- acidosis)
• Acetazolamide

Question 3

What is raised anion gap and what can cause it?

Answer 3

> 16 mmol/L

• Lactic acidosis e.g. sepsis, metformin
• Diabetic ketoacidosis
• Alcohol (metabolic ketoacidosis with normal or low glucose- think alcohol)
• Uraemia

Question 4

What may cause a metabolic alkalosis:

Answer 4

Loss of H+ or gain of HCO3-

- Vomiting
- Diuretics
- Hyperaldosteronism & Cushing’s (hypokalaemia = alkalosis)

Loss of acid (H+) via the kidneys
Mineralocorticoid excess e.g. Conn’s syndrome
Cushing’s syndrome (as excess corticosteroids have some mineralocorticoid effects)
Loop and thiazide diuretics
Bartter’s and Gitelmann’s syndromes
Loss of acid (H+) via the gastrointestinal tract
Usually due to vomiting
Most marked if this is secondary to pyloric stenosis or obstruction as losses are primarily acidic gastric juices rather than a mixture of this and alkaline duodenal contents
NG suctioning of gastric juices may lead to a similar effect
Hypokalaemia (acts via multiple mechanisms including shifting hydrogen ions intracellularly)
Excessive bicarbonate
May be iatrogenic due to bicarbonate overdose
Milk-alkali syndrome (excessive antacid consumption)
Compensation for chronic respiratory acidosis

Question 5

What may cause a respiratory acidosis?

Answer 5

Hypoventilation

- Airway obstruction
- COPD
- Opioids/sedatives
- Weakening of resp muscles

Question 6

What may cause a respiratory alkalosis

Answer 6

Hyperventilation

• Anxiety/panic attack- hyperventilation leads to resp alk causing hypocalcaemia leading to tingling in lips and fingers
• PE
• Hypoxia e.g. due to high altitude
• Aspirin OD (in early stages)
  -Salicylate poisoning

Question 7

How do we evaluate arterial blood gases?

Answer 7

• 1. Evaluate Blood pH ⇒ <7.35 (acidosis) or >7.45 (alkalosis)
  2. Evaluate pCO2 ⇒ if pH and CO2 change in opposite direction = respiratory disorder. If pH and CO2 change in same direction = metabolic disorder.
  3. Evaluate HCO3- ⇒ high = metabolic alkalosis or compensated respiratory acidosis. Low = metabolic acidosis or compensated respiratory alkalosis.Base Excess ⇒ >+3 indicates metabolic alkalosis. <-3 indicates metabolic acidosis.
  4. Compensation
     
     • Metabolic Acidosis → hyperventilate (decrease CO2)
     • Metabolic Alkalosis → hypoventilate (increase CO2)
     • Respiratory Acidosis → HCO3- retention
     • Respiratory Alkalosis → HCO3- excretion

Question 8

What’s the anion gap equation?

Answer 8

Anion Gap = ([Na+] + [K+]) - ([Cl] + [HCO3])

Question 9

Treatment for Metabolic acidosis?

Answer 9

IV sodium bicarbonate

Question 10

Treatment for metabolic alkalosis?

Answer 10

Acetazolamide (carbonic anhydrase inhibiting diuretic)

Question 11

What is the aetiology of respiratory acidosis?

Answer 11

Increase in dead space: - Dead space is ventilated but not perfused and so there is no gas exchange - There is always some anatomical dead space e.g. the airways - There may also be dead space in unperfused alveoli - This alveolar dead space increases if capillaries are destroyed e.g. in emphysema or interstitial lung disease
Reduced minute ventilation - Minute ventilation is the total amount of air entering the lungs per minute - If it decreases, there is a decrease in alveolar ventilation - It is equal to respiratory rate x tidal volume - Conditions that reduce respiratory rate include respiratory depressants such as alcohol or opioid medications - Conditions that reduce tidal volume include neurological disorders such as motor neuron disease or chest wall deformities

Question 12

Treatment for respiratory acidosis?

Answer 12

Management of a respiratory acidosis should focus on addressing the underlying cause, for example giving naloxone in cases of opioid overdose or inhalers in COPD

Severe respiratory acidosis may be treated with non-invasive ventilation (NIV) - This is often referred to as BIPAP (Bi-level Positive Airway Pressure) - This works by delivering higher pressures in inspiration and lower pressures in expiration to improve ventilation - Examples of when NIV may be used include COPD or neuromuscular disease with respiratory acidosis - Contraindications include confusion, vomiting (due to aspiration risk) or untreated pneumothorax Contraindications include confusion, vomiting

Intubation and ventilation is also an option for severely unwell patients not responding to other treatments - Consideration should be given to treatment escalation plans, involving the patient and their family as much as possible - For example, a patient with end-stage COPD may not have the physiological reserve to survive an ITU admission and so in the event that they were not responding to medical treatment +/- NIV, a decision may be made to palliate

Question 13

Management for respiratory alkalosis?

Answer 13

There is no specific treatment for respiratory alkalosis other than treating the underlying cause. This may involve:
Treating acute anxiety with education, breathing techniques and reassurance
Management of respiratory disease leading to hyperventilation (e.g. oxygen and antibiotics for pneumonia)
Salicylate poisoning may be treated with activated charcoal, urinary alkalinisation and electrolyte replacement
Patients undergoing therapeutic hyperventilation require close monitoring (including intracranial pressure monitoring) as there are several risks of treatment, the most important being cerebral hypoperfusion causing ischaemic brain injury

Question 14

Define anaphylaxis:

Answer 14

Anaphylaxis is a rapid onset syndrome of life-threatening airway, breathing or circulatory dysfunction. An immunological reaction occurs when patients are exposed to allergens such as medications, foods (such as peanuts or eggs) and bee or other insect stings. Many cases of anaphylaxis however are idiopathic with no known trigger, or may be mediated by other mechanisms other than the classical type 1 IgE-mediated pathway.

Question 15

Name some common causes of anaphylaxis:

Answer 15

Insect stings
Nuts
Other foods such as eggs or milk
Latex
Antibiotics (e.g. penicillins)
Intravenous contrast agents
Other medications (such as NSAIDs)

Question 16

To be classified as anaphylaxis what signs and symptoms does one need:

Answer 16

Airway (pharyngeal or laryngeal oedema)
Symptoms include difficulty swallowing and breathing, feeling that the throat is closing
Signs include stridor, hoarse voice and swelling of the tongue and lips

Breathing (bronchospasm)
Symptoms include difficulty breathing, wheeze and cough, stridor
Signs include increased work of breathing and respiratory distress, hypoxaemia may cause confusion and cyanosis
Patients may fatigue leading to respiratory arrest

Circulation (anaphylactic shock)
Symptoms include dizziness
Signs include pallor, clamminess, tachycardia and hypotension
Patients may develop arrhythmias and anaphylaxis can lead to cardiac arrest

Question 17

Name some other signs and symptoms of Anaphylaxis:

Answer 17

Disability (altered neurological state)
Symptoms include anxiety and a “sense of impending doom”
Signs include confusion, agitation and loss of consciousness
Exposure (skin and mucosal changes)
These range from mild erythematous patches to florid generalised rashes
Often occur prior to the onset of other symptoms
Urticaria (hives) are itchy and can occur anywhere on the skin
Angioedema involves swelling of the eyelids and lips (as well as the tongue and throat causing airway obstruction)
Gastrointestinal manifestations including abdominal pain, incontinence and vomiting are also commonly seen in cases of anaphylaxis.

Question 18

Name the investigations for Anaphylaxis:

Answer 18

The following investigations should be carried out in the emergency setting:
ECG - to look for myocardial ischaemia and arrhythmias which may be caused by anaphylaxis
Arterial blood gas should be considered in hypoxic patients, may show metabolic acidosis due to shock
Bloods for mast cell tryptase - the first sample should be taken as soon as possible after starting emergency treatment, with a second sample taken within 1 to 2 hours (no later than 4 hours from symptom onset) and a third sample taken after complete recovery (as a baseline)
An elevated serum tryptase from baseline is a useful confirmatory test for anaphylaxis especially where there is diagnostic uncertainty, although a normal level does not exclude anaphylaxis.

Question 19

What is the emergency management for anaphylaxis:

Answer 19

Early recognition is key - call for help (put out a medical emergency call if in hospital)
Remove any ongoing trigger e.g. stop causative medication, remove insect stinger
Lie patient flat and elevate legs if hypotensive, or help to a seated position to aid breathing
Give intramuscular adrenaline - 0.5ml of 1:1000 (500mcg) in adults, usually into the anterolateral thigh
Secure the airway
Administer high flow oxygen and ensure monitoring in place (oxygen saturations, blood pressure and ECG)
Consider inhaled bronchodilators (salbutamol or ipratropium) for wheeze
Give an IV fluid bolus in patients with hypotension or shock, or who do not respond to the initial adrenaline dose
IM adrenaline can be repeated after 5 minutes if no response
In the case of a cardiac arrest, start CPR and give further adrenaline via the IV or IO route (as intramuscular administration is unreliable in this scenario)

Question 20

Once stabilised after initial treatment what is the management for anaphylaxis:

Answer 20

Give an non-sedating oral antihistamine (e.g. 10-20mg cetirizine) - if not able to swallow can give IV or IM chlorphenamine
This helps to treat cutaneous symptoms of anaphylaxis but is not a first-line treatment as they do not treat life-threatening features
Steroids are no longer routinely advised but may be considered in patients with an asthma exacerbation/anaphylaxis overlap or in cases of ongoing shock
Observe patients for a biphasic reaction (when symptoms of anaphylaxis reoccur without further exposure to a trigger)
This occurs in around 5% of patients
Patients with severe initial presentations, those who require multiple adrenaline doses or who had a delay in treatment are at increased risk
Patients should be risk stratified - those at the lowest risk can be discharged after 2 hours of observation, those at intermediate risk should be observed for at least 6 hours and those at the highest risk for at least 12 hours
Prior to discharge, patients and families should be educated about anaphylaxis, what actions to take and the risk of a biphasic reaction
Give two adrenaline auto-injectors (e.g. an EpiPen) and demonstrate how to use these
Advise on trigger avoidance
Refer for follow up in a specialist allergy service

Question 21

Define an extradural haemorrhage:

Answer 21

An extradural haematoma occurs when a collection of blood forms between the dura mater, the outermost meningeal layer, and the inner surface of the skull. This commonly results from a traumatic arterial bleed, with the middle meningeal artery implicated in the majority of cases.

Question 22

What is the aetiology of extradural haemorrhages?

Answer 22

Extradural haematomas are almost always secondary to traumatic head injury, most commonly with a fracture of the temporal or parietal bone which damages underlying vessels.
The most common vessel damaged is the middle meningeal artery, however extradural haematomas can also result from a venous bleed.

Question 23

What is the clinical course of an extradural haemorrhage?

Answer 23

Brief loss of consciousness following the initial traumatic head injury
A period of regained consciousness and apparent recovery (the lucid interval)
There may be ongoing headache during this time
Subsequent deterioration with worsening symptoms and signs

Question 24

What are the symptoms and signs of extradural haemorrhages?

Answer 24

Symptoms may include:
Headache
Nausea and vomiting
Seizures
Limb weakness, numbness or other neurological symptoms
Confusion

Signs may include:
External injuries e.g. signs of skull fractures, haematomas or lacerations on the head
Reduced level of consciousness
Seizures
Cushings Triad: Bradycardia, hypertension and irregular breathing (sign of raised intracranial pressure)
6th nerve palsy (a false localising sign secondary to raised intracranial pressure
Cerebrospinal fluid otorrhea or rhinorhoea (sign of dural tearing)
Unequal pupils
Focal neurological signs e.g. visual field defects, ataxia

Question 25

What are the investigations for an extradural haemorrhage?

Answer 25

Bedside investigations:
ECG in bradycardic patients to rule out other causes e.g. heart block
Capillary blood glucose to rule out hypoglycaemia as a cause of decreased consciousness

Blood tests:
Full blood count looking for anaemia from blood loss (especially if other injuries)
U&Es and LFTs as a baseline in case a general anaesthetic is needed for surgical management
Coagulation screen looking for a bleeding diathesis
Group and save in preparation for possible surgery

Imaging:
Non-contrast CT Head is the diagnostic investigation, looking for a lentiform or biconvex hyperdense extra-axial collection
Complications resulting from raised intracranial pressure such as midline shift or subfalcine/uncal herniation may necessitate urgent neurosurgical intervention

Question 26

What is the conservative management for extradural haemorrhages?

Answer 26

Patients with small extradural haematomas may be admitted for neurological observations and monitoring with serial imaging
This may also be the treatment of choice in patients who are unfit for neurosurgery due to frailty or comorbidities
Patients undergoing medical or surgical management also require conservative management with neurorehabilitation, optimisation of nutrition and multidisciplinary team involvement

Question 27

What is the medical management for extradural haemorrhages?

Answer 27

Initial A to E assessment and resuscitation (e.g. patients with a GCS < 8 may require airway support)
Ensure other life-threatening injuries are addressed
Reverse any anticoagulant medication or coagulopathy (may require haematology input)
Anticonvulsants may be required for seizure prophylaxis
Prophylactic antibiotics may be started e.g. in cases of open skull fracture
Consider place of care - patients with raised intracranial pressure are often admitted to intensive care for intubation and ventilation
Intracranial pressure (ICP) can be monitored and neuroprotective measures put in place to help normalise this: - Ensure sedation and paralysis are adequate - Maintain oxygen and carbon dioxide levels in the normal range - Maintain a normal temperature - Consider raising head to 30 degrees (if appropriate in context of other injuries) - Hypertonic saline or mannitol may be used to reduce ICP

Question 28

What is the surgical management for extradural haemorrhages?

Answer 28

Burr hole craniotomy may be used to evacuate the haematoma
Trauma craniotomy is another emergency procedure that can relieve raised intracranial pressure and evacuate the haematoma
Vessels with ongoing bleeding should be ligated or cauterised

Question 29

Define respiratory arrest:

Answer 29

Respiratory arrest is the complete cessation of respiratory effort. It typically is the result of progressive respiratory distress and can result in cardiac arrest.

Question 30

Name some causes of respiratory arrest:

Answer 30

Respiratory distress and ultimately arrest can be the result of:
Infections: Croup, Epiglottitis, Bronchiolitis, Pneumonia
Inflammation and bronchoconstriction: Asthma, viral-induced wheeze
Foreign body aspiration
Neuromuscular: respiratory muscle paralysis
Cardiovascular conditions: myocarditis, dilated cardiomyopathy, pericarditis

Question 31

Name some signs and symptoms of respiratory arrest:

Answer 31

Tachypnoea
Sternal, subcostal and intercostal recession
Accessory muscle use
Nasal flaring
Additional respiratory sounds (i.e. stridor, wheeze, grunt)
Cyanosis
Reduced air entry and poor chest expansion

Question 32

What are the investigations for respiratory arrest?

Answer 32

Airway:
Inspection and listening for signs of airway obstruction
Breathing:
Pulse oximetry for oxygen saturation
ABG
Chest x-ray to detect pneumonia, pulmonary oedema, pneumothorax and foreign body aspiration
Circulation:
Blood pressure and assessment of pulse for determination of shock or asystole
Bloods: may include VBG, cultures, FBC and CRP
ECG to consider arrhythmia and cardiac cause
Further investigations to complete the A to E assessment and determine the underlying cause of respiratory arrest may include:
Disability
Exposure

Question 33

What is the management for respiratory arrest?

Answer 33

Clear the Airway with suction or removal of any clearly visible obstructing foreign body
If there is a foreign body aspirated, 5 back blows followed by 5 chest thrusts (if the child is under 1 year old) or 5 abdominal thrusts (for children over the age of 1 year)
Maintain the airway using head tilt, chin lift or jaw thrust
For infants, a neutral head position should be maintained. A folded towel can be placed below the neck and shoulders.
In children over the age of 1, the “sniffing” position, with more extension of the neck to enable the airways to be opened.
Airway adjuncts may be used (i.e. oropharyngeal or nasopharyngeal airway)
In cases of epiglottitis or severe airway compromise, early intubation should be considered.
Oxygen should be provided to maintain saturations >94%
Bag valve mask ventilation will likely be required for respiratory arrest
Tidal volume is normally started at 6-8 ml/kg in children
Ventilatory rate should be 8-10 breaths/minute
Further establishing a secure airway with good ventilation, the rest of the A to E assessment should be completed and may include:
Breathing
Circulation - IV access should be established, if difficult to attain, the intraosseous route may be used - IV fluid resuscitation is given as required (10 ml/kg bolus of balanced isotonic fluids)
If the respiratory distress and arrest result in cardiac arrest, CPR should be commenced following the ALS algorithm.

Question 34

What are the complications of respiratory arrest?

Answer 34

Hypoxic brain damage
Cardiac arrest
Death

Question 35

Define unstable angina:

Answer 35

Unstable angina, a clinical syndrome part of acute coronary syndrome, is characterised by chest discomfort typically occurring at rest or with minimal exertion. It’s due to transient myocardial ischaemia, often resulting from atherosclerotic plaque rupture and subsequent thrombus formation in the coronary arteries. This condition differs from stable angina as it can occur unpredictably and isn’t necessarily triggered by physical exertion or emotional stress.

Question 36

What is the aetiology for unstable angina?

Answer 36

Unstable angina (UA), a clinical syndrome part of acute coronary syndromes (ACS), is primarily caused by an imbalance between myocardial oxygen demand and supply. The underlying cause is often the disruption of an atherosclerotic plaque in a coronary artery, leading to partial or transient vessel occlusion due to thrombus formation.

Question 37

What are the risk factors for unstable angina?

Answer 37

Age: The risk of developing unstable angina increases with age, particularly in men over 45 years and women over 55 years.
Tobacco use: Smoking and long-term exposure to secondhand smoke damage the interior walls of arteries, allowing deposits of cholesterol and other substances to collect and form plaques.
Dyslipidaemia: High levels of low-density lipoprotein (LDL) cholesterol or low levels of high-density lipoprotein (HDL) cholesterol can lead to the build-up of plaques in the arteries.
Hypertension: Elevated blood pressure can accelerate the process of atherogenesis by damaging arterial walls, making them more susceptible to plaque accumulation.
Diabetes mellitus: This condition significantly increases the risk for coronary artery disease and unstable angina, especially if blood sugar levels are poorly controlled. Diabetes also accelerates atherosclerosis and increases platelet aggregation.
Obesity: Excess weight typically worsens other risk factors such as dyslipidaemia, hypertension, and diabetes.
Sedentary lifestyle: Lack of regular physical activity contributes to obesity, high blood pressure, elevated cholesterol levels, and diabetes which are all risk factors for unstable angina.
Family history: A family history of heart disease, particularly if a first-degree relative has had coronary artery disease or unstable angina at an early age, increases the risk.

Question 38

What are the underlying causes for unstable angina?

Answer 38

Atherosclerotic plaque disruption: Most cases of unstable angina are caused by rupture or erosion of an atherosclerotic plaque. The subsequent platelet aggregation and thrombus formation lead to partial or transient occlusion of the coronary artery.

Vasospasm: Coronary vasospasm can lead to episodes of unstable angina, even in the absence of significant atherosclerosis. This is often seen in Prinzmetal’s (variant) angina.

Cocaine use: Cocaine can induce coronary vasospasm leading to unstable angina. It also accelerates atherosclerosis and increases platelet aggregation.

Question 39

What is the pathophysiology of unstable angina?

Answer 39

The initial step in the pathogenesis involves the disruption of an atherosclerotic plaque within a coronary artery. This disruption can be triggered by various stimuli such as physical exertion, emotional stress, or spontaneous rupture:
Plaque Disruption: The disrupted plaque exposes its core contents to circulating blood, which contains thrombotic substances such as collagen and tissue factor.

Following plaque disruption, platelet adhesion and activation occur. These processes are mediated through several key steps:
Platelet Adhesion: Platelets adhere to the exposed sub-endothelial collagen via glycoprotein (GP) Ib receptors on their surface.
Platelet Activation: Adherent platelets undergo activation, leading to a conformational change in GP IIb/IIIa receptors that enables them to bind fibrinogen and von Willebrand factor (vWF).

The binding of fibrinogen and vWF leads to platelet aggregation and clot formation:
Platelet Aggregation: The binding of fibrinogen bridges adjacent activated platelets together, causing aggregation.
Fibrin Clot Formation: Concurrently with platelet aggregation, coagulation factors are activated. Thrombin converts soluble fibrinogen into insoluble fibrin strands forming a meshwork that stabilises the aggregated platelets into a clot.

The newly formed thrombus partially or completely occludes the coronary artery, reducing blood flow to the myocardium:
Coronary Artery Occlusion: The clot obstructs the lumen of the coronary artery either partially (resulting in UA) or completely (resulting in myocardial infarction). This leads to a decrease in oxygen supply to the downstream myocardium.

Finally, the imbalance between myocardial oxygen supply and demand results in transient ischaemia manifesting as angina. The severity and duration of ischaemia determine whether it will progress to unstable angina or evolve into a full-blown myocardial infarction:
Myocardial Ischaemia: The reduced blood flow cannot meet the metabolic demands of the myocardium under stress, leading to ischaemia. Ischaemic cells switch from aerobic to anaerobic metabolism, producing lactic acid and causing chest pain characteristic of angina.

Question 40

The classification of unstable angina is based on the severity, frequency and duration of symptoms, as well as response to therapy. It is broadly classified into what three categories:

Answer 40

New-onset severe angina: This refers to angina pectoris that has developed within the last month. Patients with new-onset severe angina require immediate evaluation and treatment due to the high risk of myocardial infarction.

Increasing or crescendo angina: Crescendo angina is characterised by a progressive increase in severity, frequency or duration of anginal episodes over time. It often indicates worsening coronary artery disease and impending acute coronary syndrome.

Rest or nocturnal angina: Anginal pain at rest or during sleep usually suggests significant coronary artery obstruction. Rest angina often occurs without any physical exertion and may be a sign of critical myocardial ischemia.

Question 41

Unstable angina can also be categorised based on the Braunwald Classification, which further stratifies patients according to what three clinical circumstances:

Answer 41

Braunwald Class I: Unstable angina secondary to increased oxygen demand such as fever, tachycardia, thyrotoxicosis or anaemia.

Braunwald Class II: Unstable angina secondary to decreased oxygen supply such as hypoxia, anaemia or hypotension.

Braunwald Class III: Unstable angina at rest; subdivided into A (not previously treated), B (treated but recurrent) and C (post-infarction).

Question 42

What are the clinical features of unstable angina:

Answer 42

Anginal Pain: The hallmark symptom of unstable angina is anginal pain which occurs at rest, with minimal exertion or with an increasing frequency. It is often described as a sensation of pressure, heaviness or squeezing located centrally in the chest behind the sternum.

Radiation: The pain can radiate to other parts of the body including the neck, jaw, epigastrium, and down both arms but more commonly to the left arm. This radiation pattern is due to referred pain from common nerve pathways.

Dyspnoea: Shortness of breath may occur due to reduced cardiac output resulting from impaired ventricular function. Additionally, pulmonary congestion secondary to left ventricular dysfunction can also lead to dyspnoea.

Syncope: Transient loss of consciousness (syncope) might occur due to significant reduction in cardiac output during episodes of severe angina.

Nausea and Vomiting: These symptoms are thought to be mediated by vagal stimulation and may accompany severe episodes of angina.

Sweating: Diaphoresis may be present due to increased sympathetic activity during an episode of unstable angina.

Question 43

What are the physical findings in unstable angina?

Answer 43

The physical examination findings in patients with unstable angina are often normal. However, during an episode of angina, signs of myocardial ischaemia such as a fourth heart sound (S4), hypotension, or transient mitral regurgitation due to papillary muscle dysfunction may be present.

Patients may also exhibit signs of congestive heart failure including elevated jugular venous pressure, pulmonary rales and peripheral oedema if left ventricular function has been significantly impaired.
Pallor and cool extremities can be seen in severe cases due to reduced cardiac output.

Question 44

Name some atypical presentations of unstable angina:

Answer 44

It is important to note that atypical presentations are common especially in elderly patients, women and those with diabetes. These patients may experience dyspnoea or fatigue as their primary symptom rather than chest pain. Other atypical symptoms include epigastric discomfort, indigestion-like symptoms and isolated diaphoresis. Asymptomatic presentation can also occur but is less common.

Question 45

What are the initial investigations for unstable angina?

Answer 45

Initial Investigations
Troponin Test: Troponin I or T levels should be measured at presentation and 3 hours after symptom onset. A rise in troponin levels indicates myocardial damage but does not distinguish between unstable angina and myocardial infarction.

Electrocardiogram (ECG): An ECG should be performed immediately. It may show ST-segment changes, T wave inversion, or new bundle branch block which are suggestive of ischemia. However, a normal ECG does not exclude unstable angina.

Further Investigations
Echocardiogram: This can provide information about left ventricular function, wall motion abnormalities indicative of ischemia, and other structural heart diseases that could present with chest pain.
Chest X-ray: This can exclude other causes of chest pain such as pneumonia or pneumothorax.

Question 46

What risk stratification do we do in unstable angina?

Answer 46

Risk Stratification

Risk stratification using scoring systems like the GRACE score or TIMI risk score for Unstable Angina/Non-ST elevation MI can help guide further management. These scores take into account age, vital signs, kidney function, cardiac markers among others.

Invasive Investigations
Coronary Angiography: This is recommended in high-risk patients as identified by risk stratification scores or ongoing symptoms despite medical therapy. It allows visualisation of coronary artery stenosis which may be amenable to revascularisation.

Question 47

What is the management for unstable angina?

Answer 47

The management approach includes risk stratification, pharmacological treatment, and invasive strategies such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). Patient education about lifestyle modification is also important.
Risk Stratification:
Use tools like the GRACE score to assess the severity of UA and predict future cardiovascular events.
Perform non-invasive testing such as ECG and cardiac biomarkers for diagnosis confirmation.
Pharmacological Management:
Administer dual antiplatelet therapy (DAPT), typically aspirin and a P2Y12 inhibitor.
Nitroglycerin for immediate relief from chest pain.
Beta-blockers and/or calcium channel blockers to reduce myocardial oxygen demand.
Statins for lipid-lowering effect and stabilisation of atherosclerotic plaques.
Invasive Strategies:
Percutaneous coronary intervention (PCI) is recommended in high-risk patients or those with refractory symptoms despite optimal medical therapy.
Coronary artery bypass grafting (CABG) may be considered in patients with multivessel disease or left main coronary artery disease, especially if diabetes is present.
Patient Education:
Educate patients on lifestyle modifications including smoking cessation, dietary changes, increasing physical activity, weight management, and stress reduction techniques.
Ensure patients understand the importance of medication adherence and regular follow-up.

Question 48

What are the complications of unstable angina:

Answer 48

Acute Myocardial Infarction (AMI)
As the most serious complication, AMI results from prolonged ischaemia leading to irreversible myocardial cell death. This can occur due to the progression of unstable angina where there’s complete occlusion of a coronary artery.

Arrhythmias
These are common in unstable angina due to ischaemia-induced electrical instability in the myocardium. Arrhythmias such as ventricular tachycardia or fibrillation can lead to sudden cardiac death if not treated immediately.