Critical care medicine

Question 1

What is acute respiratory distress syndrome?

Answer 1

Acute inflammatory lung disease of multifactorial aetiology. Characterised by hypoxia, tachypnoea, refractory hypoxaemia and diffuse opaciteis on CXR and CT. Fluid overload appears to play a role.

Question 2

What treatments (underlying cause agnostic) reduces mortality in ARDS?

Answer 2

1) Invasive mechanical ventilation with lower tidal volumes and airway pressures. 2) minimising IV crystalloid administration improves outcomes. Albumin had no impact.
3) proning the patient may improve mortality

Question 3

What is the pathophysiology of ARDS?

Answer 3

Alveolar macrophage activation -> recruitment of neutrophils and monocytes. This causes alveorla injury and alveolar flooding. Tissue factor expression is mediated by TNF which then promotes platelet aggregation and intra-alveolar coagulation with hyline membrane formation. Permanent reduction in lung capacity is observed in patients who survive ARDS.

Question 4

What is the most common ECG finding in cardiac tamponade?

Answer 4

Sinus tachycardia. Second most common is electrical alternans - alternating high and low voltage QRS complexes.

Question 5

What are the management options of pericarcdial tamponade?

Answer 5

Bedside pericardiocentesis +/- echo guidance or cutting a pericardial window surgically, or completely removing the pericardium.

Question 6

Carbon monoxide binds with greater affinity to heme in red blood cells than O2. How else does it cause issues?

Answer 6

It binds to heme moieties everywhere. This includes in cycochrome C in the electrol transport chain in mitochondria - interfering with cellular respiration. Because of this, there is a sharp increase in oxidative stress body wide. Notable problems related to this:
1. platelet dysfunction 2. inflammation globally 3. Central deymelination and global brain ischaemia.
Pts often present with headaches, chest pain, syncope.

Question 7

What’s the thing about carbon monoxide poisoning and pulse oximetry?

Answer 7

Pulse oximeter can’t distinguish between heme saturated with O2 or CO - so good SpO2 saturations will be seen on pulse oximetry.

Question 8

What are the typical laboratory features of DIC? What is required for diagnsois?

Answer 8

Consistent with excess clotting and depletion of clotting factors. So, decreased (consumed) platelet count, increase PT (due to consumption of coag products), increased D-dimer (made excessive through thrombin cleavage), decreased fibrinogen (through consumption).

Question 9

Is fibrinogen always low in clinically significant DIC?

Answer 9

No - it’s only reduced in 30% of sepsis related DIC for example. The diagnosis is better made with a scoring tool like the International Society of Thrombosis and Haemostasis score that weights each DIC associated abnormality.

Question 10

What are the Sgarbossa criteria used for?

Answer 10

A set of criteria that are used to identify ST elevation myocardial infarctions from ECG in the setting of suspected new LBBB and chest pain.

Question 11

With regards to the Sgarbossa criteria, what is appropriate discordance?

Answer 11

This refers to when there is appropriate discordance between the charges of the QRS complex and the T wave. In the septal leads in LBBB this is often a downgoing QRS complex with an upgoing T-wave, and it lateral leads it’s often an upgiong QRS and downgoing T-wave.

Question 12

What are the smith modified Sgarbossa criteria?

Answer 12

In a patient with chest pain, raised cardiac damage markers, and LBBB, a STEMI can be considered likely if: 1. there is concordant ST elevation of 1mm in at least 1 lead (concordant means QRS and ST segment in the same direction) OR concordant ST-segment depression in V1-V3 OR in the Smith modified form, any single lead with at least 1mm of discordant ST elevation that is >25% of the preceding S-wave.

Question 13

What are the indications for VA and VV ECMO?

Answer 13

VA ECMO is for support of patients with reversible cardiogenic shock refractory to other treatments. VV ECMO is for patients with reversible respiratory failure for which other options have failed.

Question 14

What are intraaortic balloon pumps used for?

Answer 14

They provide better coronary artery blood flow during diastole. It inflates during diastole, pushing blood back through the coronaries, but deflates during systole so as not to increase afterload on the LV. It also has a slight vaccuum effect when it deflates improving forward blood flow. the end sresult is a decrease in systolic BP by about 20%, with an increase in diastolic pressure, and a stable MAP.

Question 15

What are the indications for an intraaortic balloon pump?

Answer 15

MI with decreased LV function leading to cardiogenic shock
MI with mechanical issues (e.g. papillary muscle rupture) leading to shock.
APO with hypotension
Prophylaxis in high risk PCI
Low cardiac output states after CABG
As a bridge to in patients with intractable myocardial ischaemia, refractory HF, inctractable ventricular arrythmias.

Question 16

What are the three types of necrotising fasciitis?

Answer 16

Type 1 - polymicrobial. Type 2 - group A strep. Type 3 - clostridial myonecrosis.

Question 17

What is the management of necrotising fasciitis?

Answer 17

Urgent broad specturm abx. Urgent surgical review for debridement. Consideration of IVIG - evidence in strep A (type 2) necrotising fasciitis.

Question 18

What are the systemic manifestations of necrotising fasciitis?

Answer 18

Capillary leak syndreom causing profound shock - caused by bacterial toxins. Intravascular haemolysis causes by bacterial haemolysins. Stress cardiomyopathy - especially due to strep A - leading to global hypokinesia and severe systolic heart failure. Fortunately this cardiomyopathy is reversible and fully resolves in 3-24months post infection.

Question 19

Under what circumstances would you ignore the plasma paracetamol concentration nomogram and give NAC regardless of the results of blood plasma paracetamol level.

Answer 19

The NAC normogram was developed on the basis of a single - all at once - immediate release paracetamol overdose. Outside of the circumstances, NAC should probably just be given if there is any concern for overdose:
1) if it is not clear when the paractemol was ingested 2) if slow release paracetamol was taken in excess 3) co-ingestion with opiates or anticholinergics.

Question 20

Within what time frame after ingestion of overdose quantities of immediate release paracetamol is taking activated charcoal helpful?

Answer 20

If the overdose quantity is less than 30 grams, then within 2hrs. If the overdose is greater than 30g, then within 4hrs.

Question 21

What are the criteria for a liver transplant in patients with present with acute liver failure secondary to paracetamol overdose unresponsive to NAC treatment?

Answer 21

INR > 3.0 at 48hrs, or >4.5 at any time. Oliguria with serum creatinine >200 micromol/L. Persistent acidsosis with pH <7.3, or arterial lactate >3mmol/L, systolic BP <80mmHg despite fluid resuscitation. Hypoglycaemia, severe thrombocytopoenia or encephalopathy. Alteration in GCS.

Question 22

What’s the most common condition preceding PEA?

Answer 22

Hypoxaemia secondary to respiratory failure

Question 23

Should dialysis be commneced early or in ICU patients with AKI?

Answer 23

No -early or late dialysis (with a trial of more conservative management) made no difference to mortality.

Question 24

In distributive shock, what should be used as a guide for fluid resus?

Answer 24

1) start at 30ml/kg bolus. 2) additional fluids should be given to obtain a) MAP of 65mmHg and and b) a reduction of lactate to normal range.

Question 25

What types of heart block are likely to be associated with haemodynamic compromise requiring external pacing?

Answer 25

Mobitz II (intermittent non-conduction from atria to ventricles - P waves without associated QRS complexes). Complete heart block.

Question 26

How does tanexamic acid work?

Answer 26

Lysine derivative - binds directly to plasminogen and inhibits it. Stops it from activating to plasmin and cleaving fibrinogen.

Question 27

When should adrenaline and amiodarone be administered as part of ALS algorithm?

Answer 27

In shockable rhythms - 1mg adrenaline IV should be administerd after the 2nd shock and then every second CPR cycle. Amiodarone 300mg IV should be adminstered after the 3rd shock.

In non-shockable rhythms - 1mg adrenaline IV should be administered immediately and then every 2nd CPR cycle.

Question 28

Which receptors are activated by noradrenaline?

Answer 28

Primarily alpha-1, but also some beta activity.

Question 29

How does levosimendan work?

Answer 29

Increases sensitivity of troponin C to intracellular calcium (increasing cardiac contractility - positive inotrope)

Question 30

How does milrinone work?

Answer 30

Inhibits enzymes that would ordinarily lead to the breakdown of cyclic AMP. This allows for increased calcium concentration in vascular smooth muscle and cardiac muscle - increasing blood pressure and cardiac output.

Question 31

How does omecamtiv work?

Answer 31

Directly increases actin/myosin cross linking improving cardiac contractility.

Question 32

How does dobutamine work?

Answer 32

A mixed alpha/beta adrenergic receptor agonist with greater beta-1 effect on heart rate.

Question 33

How does phenylephrine work?

Answer 33

It’s a pure alpha-1 receptor agonist

Question 34

During an acute asthma exacerbation that is life threatening - what options do you have outside of beta-agonists and steroids?

Answer 34

Can also give magnesium - smooth muscle relaxant which helps with bronchodilation. It also, when given rapidly, causes hypotension. Don’t forget to also give nebulised ipratropium. Failing all this, they will need IV bronchodilators, adrenaline and mechanical ventilation.

Question 35

If patient collapses with a ventrciular arrhythmia secondary to hyperkalaemia, presuming that CPR has started and someone is getting the defibrillator, what is the next treatment step?

Answer 35

Giving calcium chloride 10% in 10mL (better than calcium gluconate) as a mycoardial cell membrane stabiliser. Then you can look at lowering the potassium with insulin + glucose + salbutamol OR dialysis.

Question 36

Apart from normal ALS +/- defibrillation, what other treatment should be given for torsades de point?

Answer 36

IV magnesium. 2g slow IV push, followed by a 1-4g/hr infusion to keep magneisum levels above 2mmol/L.