Critical Care - Focus Questions Flashcards
What is the differential diagnosis of chest pain?
- What are the methods of risk stratification in chest pain of uncertain aetiology?
Describe the guideline for approach to acute coronary syndrome in the ED.
Describe the decision making pathway for the treatment of acute coronary syndrome.
MI Classification - 5 Types?
Describe the Definitive Management of ACS - STEMI?
- What procedure <90mins?
- 4 Options for Fibrinolysis?
“Time is muscle”: Revascularization should occur as soon as possible in patients with STEMI! All other interventions can wait!
List 10 Absolute & 10 Relative Contraindications for Fibrinolysis in STEMI.
Fibrinolytic therapy is not indicated in patients with unstable angina or NSTEMI.
Adjunct medical therapy for ACS?
Fibrinolytic therapy is not indicated in patients with unstable angina or NSTEMI.
Adjunct medical therapy in ACS?
NICE Guidelines for early management of STEMI?
NICE Guidelines for early management of NSTEMI/unstable angina?
NICE Guidelines for Cardiac rehabilitation and secondary prevention following ACS?
Describe 6 acute ECG patterns of transmural myocardial infarction.
- What are the diagnostic criteria?
The diagnostic criteria are a clinical history of typical chest discomfort or pain of 20 minutes duration
(which may have resolved by the time of presentation) and ECG criteria with persistent (>20 minutes) ST segment
elevation in 2 contiguous leads of:
- 2.5 mm ST elevation in leads V2-3 in men under 40 years, or
- 2.0 mm ST elevation in leads V2-3 in men over 40 years, or
- 1.5 mm ST elevation in V2-3 in women, or
- 1.0 mm in other leads
- or development of new onset left bundle-branch block (LBBB)
What are the clinical features of instability with a cardiac arrhythmia?
Instability with a cardiac arrhythmia refers to a state where the arrhythmia is causing hemodynamic compromise or significant symptoms that require urgent medical attention. Clinical features of instability with a cardiac arrhythmia can vary depending on the specific type of arrhythmia and its impact on cardiac function. Here are some general clinical features:
List 4 Examples of risk stratification systems in acute coronary syndrome?
- 8 Components of the GRACE? When would you use it?
- GRACE ACS Risk Calculator
- TIMI Risk Score for UA/NSTEMI2
- Decision making and timing considerations in reperfusion for STEMI.
- HEART Score
Outline the components of the TIMI Risk Score for UA/NSTEMI. (7)
TIMI score for NSTE-ACS -
Estimates the risk of mortality, new or recurrent myocardial infarction, or the need for urgent revascularization in patients with NSTE-ACS. Can help determine the therapeutic regimen and timing for revascularization.
Outline the components of the HEART Score. What is it used for? Who is it not used for?
HEART score
- The HEART score is an acronym of its components: history, ECG, age, risk factors, and troponin values.
- Risk assessment for major adverse cardiovascular events (MACE) in patients with chest pain presenting to the emergency department.
- Can be integrated into decision pathways for early discharge.
- Potentially reduces hospital admissions of low-risk patients
- Should not be used in patients with STEMI or those who are hemodynamically unstable
Recite the ACLS algorithm.
- What 6 things are you doing during CPR?
- Which 2 drugs are used for shockable vs. non-shockable rhythms and doses?
- 4Hs & 4Ts?
- 5 Post-resus care?
What is the Role of CPAP in treatment of acute pulmonary oedema (APO)? Pressures?
CPAP in cardiogenic pulmonary oedema
CPAP increases intrathoracic pressure, which reduces preload by decreasing venous return. CPAP lowers afterload by increasing the pressure gradient between the left ventricle and the extrathoracic arteries, which may contribute to the associated increase in stroke volume.
What are the CPAP settings for a patient with ACPE?
When possible, start with low pressures and titrate up to help with compliance.
CPAP from 8–12 cmH2O worked best for patients in most clinical studies.
Outline the 3 main components of the management of APO?
What is the Role of CPAP in treatment of acute pulmonary oedema (APO)?
What is the Role of Frusemide in APO?
- Furosemide is used for edema secondary to various clinical conditions, such as congestive heart failure exacerbation, liver failure, renal failure, and high blood pressure. It mainly works by inhibiting electrolyte reabsorption from the kidneys and enhancing the excretion of water from the body.
- It is a sulfonamide-derived loop diuretic that inhibits sodium and chloride resorption by competitively inhibiting the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle.
What is the Role of GTN in APO?
GTN, or glyceryl trinitrate, is a medication commonly used in the treatment of Acute Pulmonary Edema (APO), particularly when it is secondary to heart failure or ischemic heart disease. GTN belongs to a class of drugs called nitrates, and its role in the management of APO is primarily related to its vasodilatory properties and its effects on cardiac preload and afterload.
What are the recommended doses of furosemide for APO?
What are the recommended doses of nitrate for APO?
- 4 Clinical Circumstances where the Administration of Fibrinolytic Therapy (Assuming ‘Door-to-Needle’ Time <30 Minutes) Should be Considered the Default Reperfusion Strategy?
- 6 Contra-Indications to Administration of Fibrinolytic Therapy?
- 4 Clinical Circumstances where Primary PCI may be the Preferred Reperfusion Strategy due to Reduced Efficacy or Increased Bleeding Risk with Fibrinolytic Therapy?
What is the significance of acute coronary syndromes in Indigenous Australians?
List differentials for breathlessness.
Which conditions can cause Type 1 respiratory failure?
Type 1 respiratory failure occurs when there is impaired oxygenation of the blood (hypoxemia) without significant retention of carbon dioxide (hypercapnia).
Which conditions can cause Type 2 respiratory failure?
Type 2 respiratory failure occurs when there is both hypoxemia and hypercapnia (elevated carbon dioxide levels). Causes of Type 2 respiratory failure include conditions that impair ventilation, leading to inadequate removal of carbon dioxide.
How do you distinguish between of type I and type II respiratory failure? (5)
What are the clinical features of respiratory failure (8) and hypercarbia? (6)
What are the indications and contra-indications for non-invasive ventilation?
Can you describe the physiology of non-invasive ventilation? (7)
1) Improvement of Ventilation-Perfusion Matching: NIV helps improve ventilation-perfusion matching by increasing alveolar ventilation. Positive pressure delivered during NIV helps recruit collapsed alveoli and improve ventilation to areas of the lungs that may be underperfused, leading to better matching of ventilation and perfusion and improved gas exchange.
2) Reduction of Work of Breathing: NIV assists the work of breathing by providing positive pressure during inspiration, which helps overcome resistance in the airways and compliance of the respiratory system. This reduces the effort required by the respiratory muscles, making breathing easier and less fatiguing, especially in patients with conditions causing respiratory muscle weakness or fatigue.
3) Alveolar Recruitment: Positive pressure delivered during NIV helps recruit collapsed alveoli and maintain lung volume, particularly in conditions associated with atelectasis or alveolar collapse. This improves lung compliance and helps prevent further deterioration of respiratory function.
Discuss the severity and management of severe asthma.
What parameters can be used to monitor status during severe asthma? (7)
What ways do you know of administering oxygen to patients?
Give a description, flow rates, advantages & indications for the following oxygen delivery devices:
- 1. Nasal Cannula
- 2. Simple Face Mask
- 3. Venturi Mask
- 4. Partial Rebreather Mask
Give a description, flow rates, advantages & indications for the following oxygen delivery devices:
- 5. Non-Rebreather Mask
- 6. High-Flow Nasal Cannula (HFNC)
- 7. Oxygen Hood or Tent
What ways do you know of monitoring oxygen therapy? (6)
Which devices are able to deliver a known concentration of oxygen? (6)
What is Hyperkalaemia?
- 4 Mechanisms & examples?
Hyperkalaemia is a life-threatening condition, primarily due to its effect on the heart. It is defined as a serum potassium level higher than 5.5 mmol/L.
List 7 Examples of Drugs that cause impaired renal potassium excretion and their mechanism.
When is emergency treatment of hyperkalaemia indicated?
- 3 Treatment aims/steps?
TREATMENT AIMS IN HYPERKALAEMIA
1. Administer intravenous calcium for cardiac membrane stabilisation (only to be given if widened QRS or sine wave pattern).
2. Drive potassium into cells via a glucose and insulin infusion.
3. Eliminate potassium from the body via administration of sodium polystyrene sulfonate.
STEP 1: Antagonism of the cardiac effects of hyperkalaemia
STEP 2: Rapid reduction in serum potassium by redistribution into cells STEP 3: Removal of potassium from the body
Outline the emergency treatment for hyperkalaemia.
Overview
Emergency treatment for life-threatening hyperkalaemia of any cause (except acute digoxin toxicity or chronic digoxin accumulation) is to:
1. give intravenous calcium gluconate (which has an immediate cardiac stabilising effect)
2. correct any volume depletion.
- In kidney failure, intravenous glucose and insulin are effective.
- If metabolic acidosis is present, intravenous bicarbonate is effective but may not lower potassium immediately.
- Emergency treatment for primary adrenal insufficiency should include intravenous hydrocortisone but not insulin.
- Less urgent treatment (generally for patients in kidney failure) is to use a sodium or calcium exchange resin.
- 4 ECG changes in hyperkalaemia?
- 4 Signs & Symptoms?
- Causes?
Clinical features of hyperkalaemia are demonstrated through ECG changes including:
1. Peaking of the T waves
2. Prolongation of the PR interval and flattening P wave
3. Widening of the QRS complex
4. Ventricular fibrillation/asystole
Signs and symptoms of hyperkalaemia:
1. Muscle weakness
2. Flaccid paralysis
3. Bradycardia
4. Hypotension
Treatment of Hyperkalaemia - 1) Stabilising the cardiac membrane?
Treatment of Hyperkalaemia - 2) Enhance renal potassium elimination?
Treatment of Hyperkalaemia - 3) Reduce serum potassium concentration?
Insulin lowers serum potassium by stimulation of the Na+/K+-ATPase. This effect is reliable, reproducible, dose-dependent and effective.
Treatment of Hyperkalaemia - 4) Remove potassium from the body?
Hyponatraemia
- Definitions?
- Severity?
- Causes?
Clinical Features of Hyponatraemia
- Severely symptomatic?
- Mild and moderately symptomatic?
Severely symptomatic hyponatremia - Symptoms usually develop acutely (onset < 48 hours). The severity tends to correlate with the extent of cerebral edema.
3. Confusion, stupor, coma
4. Seizures
5. Ataxia
6. Respiratory failure
7. Other: malaise, lethargy, headache, nausea, vomiting
Mild and moderately symptomatic hyponatremia
Symptoms usually develop slowly (onset > 48 hours) and are typically nonspecific (patients can also be asymptomatic).
1. Forgetfulness
2. Gait disturbances
3. Muscle weakness
4. Malaise
5. Headache
6. Dizziness
7. Fatigue
8. Lethargy
9. Nausea, vomiting
Diagnostic approach to hyponatremia?
Serum osmolality measurement is the first step in the evaluation of verified hyponatremia!
Outline the complications of hyponatraeamia.
Osmotic Demyelination Syndrome
- Definition?
- 3 Causes?
- Clinical features?
- Diagnostics?
- Treatment?
- Prognosis?
- Prevention?
.Definition: damage to the myelin sheath of the white matter in the CNS caused by a sudden rise in serum osmolality
- Central pontine myelinolysis = Most common type. Affects the central region of the pons
- Extrapontine myelinolysis: can affect the cerebellum, lateral geniculate body, thalamus, putamen, cortical, and/or subcortical white matter.
Causes
1. Iatrogenic: rapid correction of chronic hyponatremia. High-risk factors for ODS: alcohol use disorder, malnutrition, liver disease, hypokalemia, initial sodium concentration ≤ 105 mEq/L.
3. Rapid changes in other osmotically active solutes (e.g., glucose)
4. Acute severe hypernatremia
Outline the SCGH ED guidelines for managing hyponatraemia.
- Making 3% saline: add 26mL of 23.4% NaCl to 250mL normal saline (total volume 276mL, total Na is 142.5 mmol).
- Dextrose solutions DO NOT contain Na and should be avoided in patients with hyponatraemia.
- Regardless of cause, Na replacement should not exceed 10 mmol/L in the first 24 hrs, and 8 mmol/L/24 hrs for subsequent days until Na level is ≥130 mmol/L.
How would you assess a patient with DKA?
(10 steps, 7 lab investigations)
Laboratory Tests:
1. Blood Glucose: Measure blood glucose levels. DKA is typically associated with hyperglycaemia, often exceeding 250 mg/dL (13.9 mmol/L).
2. ABG: Obtain an ABG to assess acid-base status and arterial pH. Patients with DKA typically have metabolic acidosis with a low arterial pH (<7.3), low bicarbonate (HCO3-) levels, and an elevated anion gap.
3. Electrolytes: Check electrolyte levels, including potassium, sodium, chloride, and bicarbonate. Patients with DKA often exhibit electrolyte imbalances, such as hyponatremia, hyperkalaemia (initially, followed by hypokalaemia), and hypophosphatemia.
4. Blood Ketones: Measure blood ketone levels, as elevated ketones confirm the diagnosis of DKA.
5. FBC: Evaluate for leucocytosis, which may indicate an underlying infection triggering DKA.
6. Renal Function Tests: Assess renal function with tests such as serum creatinine and blood urea nitrogen (BUN).
7. Urinalysis: Perform a urinalysis to assess for ketonuria and glucosuria, which are commonly present in DKA.
- What should be calculated in a patient with metabolic acidosis to determine the cause?
- What can help idenitify the cause of metabolic alkalosis?
- In metabolic acidosis, calculation of the anion gap can also help determine the cause and reach a precise diagnosis.
- In metabolic alkalosis, urine chloride (Cl‑) concentration can help identify the cause.
Outline an algorithm for blood gas analysis.
- Causes of High Anion Gap Metabolic Acidosis = MUDPILES?
- Causes of Normal Anion Gap Metabolic Acidosis = HARD-ASS?
SMORE: change in PCO2 in the Same direction as pH → Metabolic disorder; change in PCO2 in the Opposite direction to pH → REspiratory disorder
High anion gap metabolic acidosis
- 3 Step process?
- Aetiology of endogenous organic acids?
- Aetiology of exogenous organic acids?
High anion gap metabolic acidosis
1 - Exclude accumulation of endogenous organic acids.
- Exclude ketoacidosis : Consider measuring ketone levels in urine or serum (e.g., beta-hydroxybutyrate).
- Exclude lactic acidosis: Measure or review lactate levels.
- Exclude uremia: Measure or review BUN and creatinine levels.
2 - Consider accumulation of exogenous organic acids (ingestion) as the cause: e.g., if the cause remains unclear, or initially if the patient is comatose
- Consider obtaining serum or urine toxicology screen.
- Calculate serum osmolal gap: If elevated (≥ 10 mOsm/kg), consider propylene glycol, ethylene glycol, diethylene glycol, methanol, and isopropanol as potential causes.
3 - Calculate the delta gap: to exclude concomitant acid-base disturbances
Normal anion gap metabolic acidosis
1 - Calculate the urine anion gap
- Negative urine anion gap: Acidosis is likely due to loss of bicarbonate.
- Positive urine anion gap: Acidosis is likely due to decreased renal acid excretion.
2 - Consider calculating the urine osmolal gap
- Preferred over urine anion gap if the urine pH is > 6.5 or urine Na+ is < 20 mEq/L
- ↓ Urine osmolal gap (< 80–100 mOsm/kg) suggests impairment in the excretion of urinary ammonium.
Abnormal anion gap without metabolic acidosis
- 2 Causes of low anion gap?
- 2 Causes of high anion gap?
Aetiology of metabolic alkalosis
- 4 Causes of Chloride-responsive metabolic alkalosis (urine chloride < 25 mEq/L)?
- 6 Causes of Chloride-resistant metabolic alkalosis (urine chloride > 40 mEq/L)?
Respiratory Acidosis
- Which rule helps to establish the expected chronicity of respiratory acidosis?
- Causes of Acute Respiratory Acidosis?
- Causes of Chronic Respiratory Acidosis?
Establish the expected chronicity of respiratory acidosis based on clinical presentation using the following rule:
- HCO3- increases by 1 mEq/L for every 10 mm Hg increase in PCO2 above 40 mm Hg: suggests acute respiratory acidosis.
- HCO3- increases by 4–5 mEq/L for every 10 mm Hg increase in PCO2 above 40 mm Hg: suggests chronic respiratory acidosis
Respiratory Alkalosis
- Which rule helps to establish the expected chronicity of respiratory alkalosis?
- Causes of Acute Respiratory Alkalosis?
- Causes of Chronic Respiratory Alkalosis?
Establish the expected chronicity based on clinical presentation using the following rule:
- HCO3- decreases by 2 mEq/L for every 10 mm Hg decrease in PCO2 below 40 mm Hg: suggests acute respiratory alkalosis.
- HCO3- decreases by 4–5 mEq/L for every 10 mm Hg decrease in PCO2 below 40 mm Hg: suggests chronic respiratory alkalosis
Treatment of Acid-Base Disorders
- General Principles?
- Respiratory acidosis?
- Respiratory alkalosis?
- Metabolic acidosis: Acute severe?
- Metabolic acidosis: Chronic?
- Metabolic alkalosis: Chloride-responsive?
- Metabolic alkalosis: Chloride-resistant?
Emergency management of hypoglycaemia
- SCGH ED Guidelines?
Oral Hypoglycaemic Poisoning - Acute management?
Discuss and demonstrate how to apply a pressure immobilisation bandage.
How to apply a pressure-immobilisation bandage
1. Call 000
2. Keep the person who has been bitten as still as possible. If possible, lie the patient down to prevent walking or moving around.
3. Apply a firm bandage over the bitten area (preferably use a wide elasticised bandage if available)
4. Then bandage the entire limb (fingers to shoulder or toes to the hip) - the bandage should be as tight as for a sprained ankle.
5. Apply a rigid splint to the limb (piece of wood, branch, or rolled up paper)
6. Keep still await the arrival of the ambulance for transport to the emergency department of the nearest hospital.
Describe the features of acute alcohol withdrawal.
- Alcohol withdrawal syndrome (uncomplicated)?
- Alcohol withdrawal seizures?
- Alcohol-induced psychotic disorder (alcoholic hallucinosis)?
- Alcohol withdrawal delirium (delirium tremens)?
Alcohol-induced psychotic disorder (alcoholic hallucinosis)
- Onset: usually 12–24 hours after cessation of or reduction in alcohol consumption
- Clinical features: Consciousness is usually intact. Vital signs may be normal. Auditory and/or visual hallucinations are common (tactile hallucinations are also possible). Delusions
- Duration: 24–48 hours after onset
- It may be challenging to distinguish alcoholic hallucinosis from the hallucinations associated with delirium; patients with delirium usually have impaired consciousness and abnormal vital signs.
Outline the Timeline of alcohol withdrawal symptoms?
Describe the management of acute alcohol withdrawal.
- Approach? (10 points)
- Pharmacotherapy?
- Supportive Care?
Approach
1. Classify AWS severity using a validated scale, e.g., CIWA-Ar.
2. Adjust pharmacotherapy according to individual symptom severity.
3. Identify and manage any complications without delay.
4. Alcohol withdrawal seizures: Immediately administer IV benzodiazepines.
5. Alcohol-induced psychotic disorder: Consider low-dose antipsychotics (e.g., haloperidol, risperidone) in combination with benzodiazepines (not as monotherapy).
6. Alcohol withdrawal delirium:
7. Consider referral to critical care unit for high-dose IV benzodiazepines and monitoring.
8. Provide supportive care to all patients during the withdrawal episode (e.g., nutritional and metabolic support).
9. Offer treatment of alcohol use disorder.
10. In the event of alcohol withdrawal seizures, benzodiazepines are preferred over other anticonvulsants to prevent further seizures.
Describe 7 psycho-social complications of alcohol dependence.
What are the important features in the assessment of a snake bite?
- History? (4)
- Physical examination? (4)
- Laboratory features? (4)
