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PACES - Instruments > Acute care > Flashcards

Acute care Flashcards

1
Q

Once pulmonary embolism is confirmed, how do you treat- give dosage

A

Apixaban - 10 mg BD for 7 days

then 5mg BD untill 3 months (or 6 months) - depending if it was provoked or unprovoked

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2
Q

If a patient in pulmonary embolism has renal impairment, what treatment would you give instead of apixaban?

A

Warfarin with lead in therapy of LMWH

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3
Q

If a patient has a massive pulmonary embolism and is haemodynamically unstable- what is the treatment?

A

Thrombolysis - Alteplase
10mg to be given over 1-2 mins
then 90mg given over 2 hours

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4
Q

What scoring system can be used to determine if the patient with pulmonary embolism should be managed as an outpatient?

A

Pulmonary embolsim severity index (PESI)

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5
Q

What features in a patient are considered low risk on the pulmonary embolism severity score- i.e.can be managed as outpatient?

A

Haemodynamically stable
No co-morbidities
Support at home

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6
Q

What can you give to patients with recurrent Pulmonary embolism?

A

IVC filter

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7
Q

Outline the 2-level Wells score of Pulmonary embolism

A
  1. Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) = 3 points
  2. Alternative diagnosis less likely than PE = 3 points
  3. Tachycardia > 100bpm = 1.5 points
  4. Immobilisation for 3 days / surgery in the last 4 weeks = 1.5 points
  5. Previous DVT/PE = 1.5 points
  6. Haemoptysis = 1 point
  7. Malignancy (on Rx, Rx in the last 6 months, palliative) = 1 point
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8
Q

What is the interpretation of the 2 -level Wells score for PE?

A

< or = 4 points - PE unlikely

> 4 points - PE likely

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9
Q

If PE is likely according to Wells score, what do you do?

A

Arrange an immediate CTPA (if unable to occur soon then start anticoagulation)

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10
Q

If CTPA for PE is negative what do you do?

A

Proximal leg vein US if DVT is suspected

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11
Q

If PE is unlikely according to Wells score what do you do?

A

Arrange a D-dimer test (if it cannot be attained within 4 hours then start anticoagulation)

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12
Q

If the D- dimer for PE is positive, what do you do?

A

Arrange an immediate CTPA (if unable to occur soon then start anticoagulation)

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13
Q

If the D- dimer for PE is nagative, what do you do?

A

PE is unlikely, consider other diagnosisx

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14
Q

If a patient has renal failure, which is used CTPA or V/Q scan in ?PE and why?

A

V/Q scan as you avoid the contrast which is used in CTPA

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15
Q

What are the ECG findings of PE?

A

S1Q3T3
S1 = Large S wave in lead 1
Q3 = Large Q wave in lead 3
T3 = T wave inversion in lead 3

RBBB
Right axis deviation
Sinus tachycardia

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16
Q

In ?PE, which patients should have a CXR?

A

All patients - important to exclude other pathology

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17
Q

What are the 8 criteria in the Pulmonary Embolism rule out criteria (PERC)?

A
  1. Age > or = 50
  2. Heart rate > or = to 100 bpm
  3. Oxygen < or = to 94%
  4. Previous PE or DVT
  5. Recent trauma or surgery in the last 4 weeks
  6. Haemoptysis
  7. Unilateral leg swelling
  8. Oestrogen use (COPC or contraceptives)
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18
Q

When should PERC be used?

A

When there is a low pre-test probability of PE but you want to be sure

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19
Q

How is PERC interpreted?

A

Negative means all 8 are negative - meaning less than 2% chance of PE
(if positive then do 2 level Wells score)

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20
Q

If a patient is unstable how do you investigate for PE?

A

CTPA

But if not able to get an urgent CTPA, you can get a bedside echo instead (RV dysfunction)

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21
Q

What is the management of PE in an unstable patient?

A

if PE found on CTPA/ RV dysfunction detected on echo
then pt needs URGENT REPERFUSION
1. UFH 10,000 Units IV - bolus
2. UFH continuous infusion
3. Consider if they need fluid resus (if SBP <90mmHg)
4. +/- vasoactive agents e.g. Noradrenaline if fluid resus is not successful
5. Consider if they need Oxygen
6. Whilst Heparin is still running, do pharmacological thrombolysis to break down the clot:
- Alteplase, Streptokinase, Urokinase (all IV)
7. Later on switch to anticoagulant (DOAC, LMWH, VKA)

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22
Q

What is the management of a primary pneumothorax?

A

> 2cm/SOB?
If NO –> consider discharge and outpatient review in 2-4 weeks
If YES –> Aspirate - if aspiration doesn’t work then chest drain

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23
Q

What is the management of a secondary pneumothorax?

A

> 2cm/ SOB?
If NO –> then;
- 1-2cm –> aspitate, if aspirate successful then admit for 24 hours + oxygen (if aspiration fails then chest drain)
- <1cm admit for 24 hour observation and oxygen

If YES –> straight to chest drain

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24
Q

Which set of bloods need to be taken for pulmonary embolism?

A

FBC, U and E and LFT, Clotting profile

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25
Q

What investigations do you want for acute heart failure?

A 
FBC - looking for anaemia/infection 
U and E - renal function 
CXR 
Echo  
BNP
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26
Q

What is the stepwise management for acute heart failure?

A
  1. Sit the patient upright
  2. High flow oxygen - 15L via a non-rebreathe mask
  3. IV access - 2 wide bore cannulae and monitor ECG
  4. Treat any arrhythmias e.g. AF
  5. IV furosemide 40-80mg SLOWLY
  6. other medications to consider: diamorphine, GTN 2 puffs
    (if SBP <100mmHg then treat as cardiogenic shock)
  7. If furosemide is not working - consider CPAP
  8. Discontinue Beta-blockers in the short term as they can make acute heart failure worse
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27
Q

What are the features of a moderate asthma attack? (4)

A
  1. PEFR 50-75% best or predicted
  2. Speech normal
  3. RR < 25 / min
  4. Pulse < 110 bpm
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28
Q

What are the features of a severe asthma attack? (4)

A
  1. PEFR 33-50% best or predicted
  2. Can’t speak in full sentences
  3. RR > 25/ min
  4. Pulse >110 bpm
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29
Q

What are the features of life-threatening asthma attack? (5)

A
  1. PEFR < 33% best or predicted
  2. Oxygen sats < 92%
  3. Silent chest, cyanosis or feeble respiratory effort
  4. Bradycardia, dysrhythmia or hypotension
  5. Exhaustion, confusion or coma
    NOte: normal CO2 indicates life threatening also
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30
Q

CXR is not routinely done in an asthma attack, but when would you get one?

A
  1. Life threatening
  2. Not responding to treatment
  3. Suspected pneumothorax
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31
Q

In acute asthma attack, what is the criteria for admission to hospital?

A
  1. Life threatening
  2. Severe that is not responding to initial treatment
  3. Pregnancy
  4. Previous near fatal asthma attack
  5. Asthma attack despite being on oral corticosteroids
  6. Presentation at night time
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32
Q

Describe the criteria of how to administer SABA e.g. salbutamol or terbutaline in asthma attack

A

Modterate - give SABA via pressurised Metered dose inhaler

Severe - give nebulised SABA

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33
Q

Which patients in asthma attack should be given corticosteroid and what prescription?

A 
All patients
Prednisolone
40-50mg
Oral
for 5 days (or until they recover)
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34
Q

What is a near fatal asthma attack?

A

Raised pC02 and/or requiring mechanical ventilation with raised inflation pressures

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35
Q

Which asthma attack patients should have an ABG?

A

If O2 sats <92% (note- this automatically makes it a life-threatening asthma attack)

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36
Q

Describe oxygen therapy in asthma attack

A

If patients are acutely unwell they should be started on 15L of supplemental via a non-rebreathe mask, which can then be titrated down to a flow rate where they are able to maintain a SpO₂ 94-98%.

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37
Q

What is the quick stepwise INITIAL management of asthma attack (inc doses)

A
  1. Assess severity: PEFR, HR, RR, O2 sats ability to speak, pCO2
  2. If severe or life-theatening –> warn ICU
  3. 15L O2 via non-rebreathe mask (titrate till they maintain sats of 94-98%)
  4. Salbutamol 5mg nebulised with O2 driven by oxygen
  5. Severe/life threatening asthma add in Ipratropium bromide 0.5mg/6hours to the salbutamol nebuliser
  6. Hydrocortisone IV 100mg, oral prednisolone 40-50mg for 5 days (or until recovered)
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38
Q

Which patients in asthma attack receive ipratropium bromide?

A
  1. Severe or Life-threatening asthma

2. Non-responders to SABA and corticosteroids

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39
Q

Whilst the patient is on corticosteroid for asthma attack what is the advice regarding their normal asthma management?

A

Continue as normal - even the inhaled corticosteroid can be taken whilst they are on oral prednisolone

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40
Q

If the Initial management is not working- what should be done?

A

If severe/life threatening asthma attack and the initial management has failed then
IV magnesium sulphate 1-1.2g bolus over 20 minutes

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41
Q

What do you need to do before starting magnesium sulphate?

A

Consult with senior staff

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42
Q

What are the treatment options for asthma patients who need to be treated in HDU?

A

Intubation and Ventilation

Extracorporeal membrane oxygenation ECMO

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43
Q

What is the criteria for discharge after an asthma attack?

A
  1. They have been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
  2. Inhaler technique checked and recorded
  3. PEF >75% of best or predicted
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44
Q

What features would make you inclined to manage a COPD exacerbation in hospital rather than outpatient?

A
  1. Not able to cope at home/ living alone
  2. Cyanosis
  3. Severe breathlessness
  4. Sats <90%
  5. Arterial pH <7.35
  6. Arterial pO2 <7
  7. Impaired consciousness
  8. Already on LTOT
  9. Rapid onset
  10. Worsening peripheral oedema
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45
Q

What investigations do you want in exacerbation of COPD?

A 
Bedside: 
1. ECG - to exclude co-morbidities  
2. Sputum culture - for microscopy and culture 
Bloods: 
1. ABG 
2. FBC 
3. U and E 
4. Blood cultures (if pyrexia) 
Imaging: 
1. CXR
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46
Q

Outline the step wise management of COPD exacerbation:

A
  1. Nebulised salbutamol 5mg/4h
  2. Nebulised ipratropium bromide 0.5mg/6h
  3. Oxygen therapy: initially 15L via non-rebreathe mask until you get the ABG - if chronic retainer then switch to venturi mask
  4. Prednisolone 30mg for 5 days
  5. IV Aminophylline: If no response to nebulisers and steroid
  6. Physiotherapist using positive expiratory pressure devices to aid with sputum clearance
  7. NIV
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47
Q

When would you give antibiotics in a COPD exacerbation?

A

If sputum is purulent

If there are clinical signs of pneumonia

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48
Q

What are the first line antibiotics for COPD?

A
  • Amoxicillin 500 mg three times a day for 5 days.
  • Doxycycline 200 mg on first day, then 100mg once a day for 5-day course in total.
  • Clarithromycin 500 mg twice a day for 5 days.
    Can use any of these three
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49
Q

What prophylaxis should be considered in patients with recurrent COPD infections?

A 
Azithromycin 
Osteoporosis prophylaxis (using
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50
Q

If a patient is started on aminophylline during COPD exacerbation, when do you need to monitor the theophylline levels?

A

Within 24 hours

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51
Q

What must happen before discharge after a COPD exacerbation?

A

Measure spirometry

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52
Q

Give examples of Fibrinolytic drugs and state what they are used for

A 
Used for thrombolysis 
Examples include: 
Alteplase 
Streptokinase 
Urokinase
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53
Q

In STEMI - if a patient is going for planned primary PCI, which drugs should not be given?

A

Fibrinolytics

GPIs

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54
Q

If a patient is not going for primary PCI in a STEMI, what is the medical management (i.e. not for reperfusion therapy)?

A
  1. Most patients: Aspirin + Ticagrelor
  2. Patients with high bleeding risk: Aspirin + Clopidogrel (or Aspirin alone)
  3. The patients can have a cardiology assessment offered
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55
Q

What are the 2 options for reperfusion therapy in STEMI?

A

Fibrinolysis - e.g. alteplase, streptokinase, urokinase
or
Angiography with follow on Primary PCI

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56
Q

What is the criteria for getting Angiography with follow on primary PCI in STEMI?

A
  1. Onset of pain within 12 hours and primary PCI can be delivered within 120 mins (2 hours)
  2. Onset of pain started over 12 hours ago, but continuing myocardial ischaemia or cardiogenic shock
    Note: Radial access is preferred over femoral access
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57
Q

Outline the drug therapy for those going for primary PCI in a STEMI (5)

A
  1. Offer prasugrel and aspirin - if not already on oral anti-coagulant
  2. Offer clopidogrel with aspirin - if already on oral anti-coagulant
  3. If PCI with radial access - UFH with bailout GPI
  4. If PCI with femoral access - Bivalirudin (thrombin inhibitor) with bailout GPI
  5. If a patient is not on oral anti-coagulant and is 75 or older- it is important to consider the bleeding risk with prasugrel - consider giving them clopidogrel or ticagrelor instead which have lower bleeding risks
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58
Q

What does GPI drugs stand for? And give examples of such drugs

A 
Glycoprotein IIb-IIIa inhibitors 
Examples: 
1. Abciximab 
2. Eptifibatide 
3. Tirofiban
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59
Q

What drug class is Bivalirudin?

A

Thrombin inhibitor

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60
Q

In primary PCI, what type of stent should be used?

A

A drug-eluting stent

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61
Q

When should complete revascularisation be offered in primary PCI?

A

If there is multi-vessel coronary artery disease + NO cardiogenic shock

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62
Q

What is the criteria for receiving fibrinolysis (aka thrombolysis) in a STEMI?

A

Presenting within 12 hours of onset of symptoms + PCI cannot be delivered within 120 minutes (2 hours)

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63
Q

If a patient having a STEMI is having fibrinolysis what medication needs to be delivered at the same time?

A

Anti-thrombin

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64
Q

What needs to happen 60-90 minutes after fibrinolysis in STEMI?

A

An ECG

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65
Q

Outline the drug therapy for those having fibrinolysis in a STEMI (2)

A
  1. Offer ticagrelor + aspirin for those without a high bleeding risk
  2. Offer clopidogrel + aspirin (or aspirin alone) for those with a high bleeding risk
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66
Q

How many times can you do do fibrinolysis in a STEMI?

A

Once

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67
Q

Describe the management of STEMI once you have given fibrinolysis and anti-thrombin

A

After 60-90 minutes take an ECG

If the ECG indicates it was unsuccessful, then offer IMMEDIATE angiography with follow on PCI

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68
Q

What should happen during the admission of a STEMI patient who has had successful PCI?

A

Consideration for angiography with follow on PCI

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69
Q

What assessment should all patient with STEMI (regardless of how it was treated) have done?

A

Assessment of LV function (using echocardiogram)

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70
Q

What follow on management should all STEMI patients (regardless of treatment) receive after the event?

A

Cardiac rehabilitation

Secondary prevention

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71
Q

What is the initial therapy for NSTEMI patients?

A

Aspirin 300mg loading dose

Fondapariux

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72
Q

When would you not give the fondaparinux in an NSTEMI patient?

A

If high bleeding risk

If they are going for IMMEDIATE angiography

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73
Q

What do you use to risk assess NSTEMI patients? (6)

A
  1. GRACE score
  2. Clinical history
  3. Physical examination
  4. 12-lead ECG
  5. Blood tests - troponin, creatinine, glucose, FBC for Hb
  6. Balance benefits of treatment against bleeding risk
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74
Q

What does the GRACE score predict?

A

6-month mortality and risk cardiovascular events

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75
Q

If an NSTEMI patient has a low risk on the GRACE score what does this mean their predicted 6-month mortality is?

A

< or = 3%

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76
Q

If the NSTEMI patient has an intermediate or higher risk on the GRACE score, what does this mean their predicted 6-month mortality is?

A

> 3%

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77
Q

How do you manage NSTEMI patients with a low risk on the GRACE Score?

A
  1. Consider conservative management without angiography (but be aware some younger patients may benefit from early angiography)
  2. Offer ticagrelor with aspirin unless high bleeding risk (in which case give aspirin + clopidogrel or aspirin alone)
  3. Consider ischaemia testing before discharge and if ischaemia is shown/develops on testing then consider angiography+/- PCI
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78
Q

How do you manage NSTEMI patients with an intermediate or high risk on the GRACE Score?

A
  1. Offer immediate angiography if clinical condition unstable
  2. If stable - consider angiography within 72 hours (if no contra-indications such as comorbidity or active bleeding)
  3. Offer prasugrel or ticagrelor + aspirin (if no separate indication for oral anti-coag), Offer clopidogrel + aspirin if they have a separate indication for oral anti-coag
  4. Only give prasugrel if PCI is intended
  5. Offer systemic UFH in cath lab if having PCI
  6. Offer drug-eluting stent if they are having a stent
  7. In people 75 or older - consider whether bleeding risk with prasugrel outweighs the effectiveness
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79
Q

If a follow-on PCI is not done after angiography in a immediate/high risk NSTEMI patient what should be done after?

A

Management should be discussed with an interventional cardiologist, a cardiac surgeon and the patient

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80
Q

What assessment needs to be done for NSTEMI patients (regardless of treatment)?

A 
LV function 
(+ consider assessing for unstable angina)
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81
Q

What follow on management should all STEMI patients (regardless of treatment) receive after the event?

A

Cardiac rehabilitation and secondary prevention

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82
Q

When should cardiac rehabilitation start after an STEMI or NSTEMI?

A

Before the patient is discharged from hospital

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83
Q

What is involved in the cardiac rehabilitation programme? (4)

A
  1. Physical activity)
  2. Lifestyle advice - inc advice on driving, flying and sex
  3. Stress management
  4. Health education
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84
Q

What are Lifestyle changes a person should make after a STEMI/NSTEMI?

A
  1. Healthy eating - Mediterranean diet
  2. Alcohol - low risk drinking (no more than 14 units a week)
  3. Regular physical activity 20-30 mins a day to slight breathlessness
  4. Stop smoking
  5. Reaching and maintaining a healthy weight
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85
Q

What drug therapy is used for secondary prevention after a STEMI/NSTEMI?

A
  1. ACE inhibitor (continue indefinitely)
  2. DAPT for 1 year, then single antiplate/other anti-coagulant
  3. Beta-blocker (use diltiazem or verapamil if BB is contra-indicated e.g. asthma)
  4. Statin
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86
Q

What monitoring is needed with the ACE inhibitor for secondary prevention of NSTEMI/STEMI?

A

Renal function
Serum electrolytes
BP
Measure before starting and again at 1-2 weeks

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87
Q

If, after an STEMI/NSTEMI, a patient has HFrEF (on assessment of LV function), what additional drug should be added to secondary prevention and when?

A

Aldosterone antagonist e.g. spironolactone

Start 3-14 days after MI, preferably after the ACE inhibitor has been started

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88
Q

What scoring systems are used in acute upper GI bleed and when do you use each?

A

The Blatchford score - at first assessment

The full Rockall score - after endoscopy

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89
Q

If a patient is having a MASSIVE upper GI bleed - what should initial resuscitation be?

A

Transfusion with blood, platelets and clotting factors in line with the major haemorrhage protocol

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90
Q

Which patients should not get platelet transfusion (in upper GI bleed)?

A

If they are not actively bleeding + are haemodynamically stable

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91
Q

During upper GI bleed, what is the criteria for receiving a platelet transfusion?

A

Actively bleeding and platelet count less than 50 x10^9/L

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92
Q

During upper GI bleed, which patients receive fresh frozen plasma?

A

Actively bleeding and have a prothrombin time/INR or APTT >1.5 times normal

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93
Q

When would cryoprecipitate be offered in upper GI bleed?

A

If a patients fibrinogen level remains <1.5g/L despite fresh frozen plasma

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94
Q

When would you offer prothrombin complex concentrate in upper GI bleed?

A

In patients who are taking warfarin and are actively bleeding

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95
Q

In upper GI bleed - describe the timings of endoscopy

A

Immediately after resuscitation - if pt unstable with severe acute upper GI bleeding

Within 24 hours of admission - to all other patients with upper GI bleed

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96
Q

What are the two features of non-variceal upper GI bleed management?

A

Endoscopic treatment

PPIs

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97
Q

Describe the ENDOSCOPIC management for non-variceal upper GI bleed

A

Use one of the following:
1. mechanical method (e.g. clips) with or withOUT adrenaline
2. Thermal coagulation WITH adrenaline
3. Fibrin or thrombin WITH adrenaline
(DO NOT USE ADRENALINE AS MONOTHERAPY IN NON-VARICEAL)

98
Q

Describe the use of PPIs in the management of non-variceal upper GI bleed

A
  1. Do not offer acid suppression drugs (e.g. PPIs or H2 receptor antagonists) before endoscopy to patients with SUSPECTED non-variceal upper GI bleeding
  2. Offer PPIs to patients with non-variceal UGI bleeding + evidence of recent haemorrhage shown at endoscopy
99
Q

In the management of suspected variceal bleeding, what additional medications are given at presentation (along with the resus)?

A

Terlipressin

Prophylactic antibiotic therapy

100
Q

When do you stop terlipressin used for variceal bleed?

A

After definitive haemostasis or after 5 days

101
Q

If the variceal bleed is oesophageal- what is the management?

A
  1. Band ligation
  2. Consider transjugular intrahepatic portosystemic shunt (TIPS) if bleeding from oesophageal varices is not controlled by band ligation
102
Q

Describe a Transjugular intrahepatic portosystemic shunt and explain why this helps varices

A

Uses imaging guidance to connect the portal vein to the hepatic vein - this reduces the pressure in the portal vein hence helping bleeding varices (as these are often causes by portal HTN in the first place)

103
Q

If the variceal bleed is gastric - what is the management?

A
  1. Endoscopic injection if N-butyl-2-cyanoacrylate

2. Offer TIPS if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate

104
Q

What is the advice for patients with upper GI bleed who are already on any of the following medications: NSAIDS, aspirin, clopidogrel?

A
  1. Low dose aspirin for secondary prevention of vascular events - continue if haemostasis has been achieved
  2. NSAIDs - stop during the acute phase
  3. Clopidogrel - discuss risk/benefits with cardiologist or stroke specialist + with the patient
105
Q

What screening tools are used to help diagnose stroke/TIA a) outside hospital, b) in ED?

A

Outside: FAST (Face, arm, speech, test)

Inside ED: ROSIER (Recognition of Stroke in the Emergency Room)

106
Q

What important rule out test should be done in all people with sudden onset of neurological symptoms?

A

Glucose - need to exclude hypoglycaemia as a cause instead of stroke

107
Q

What is the management of suspected and confirmed TIA?

A
  1. 300 mg aspirin - daily UNTIL diagnosis is established
  2. Refer for specialist assessment and investigation - to be seen within 24 hour of symptom onset
  3. Offer secondary prevention (in addition to the aspirin) as soon as possible after the diagnosis has been confirmed
  4. Do NOT use ABCD2
108
Q

What is the guidance with regards to suspected TIA and imaging?

A
  1. Do not offer CT brain unless there is clinical suspicion of alternative diagnosis that CT could detect
  2. After specialist TIA clinic - consider MRI to determine territory of ischaemia/detect haemorrhage or alternative pathologies
  3. Everyone with TIA who after specialist assessment is considered a candidate for carotid endarterectomy should have urgent carotid imaging
109
Q

If someone has a TIA and has a symptomatic carotid stenosis of 50-99%, what is the guidance?

A
  1. Urgent referral for carotid endarterectomy
  2. Optimal medical treatment - control of BP, anti-platelet agents, cholesterol lowering through diet and and drugs
  3. Lifestyle advice
110
Q

What is the management if someone has TIA and has stenosis of less than 50% what is the guidance?

A
  1. No surgery
  2. Optimal medical treatment - control of BP, anti-platelet agents, cholesterol lowering through diet and and drugs
  3. Lifestyle advice
111
Q

Where should someone having a stroke be managed?

A

Admit everyone with suspected stroke directly to a specialist acute stroke unit (whether from community or ED)

112
Q

Which patients with suspected stroke get a CT brain?

A
  1. If there are indications for thrombolysis or thrombectomy
  2. On oral antigoagulant
  3. Known bleeding tendency
  4. Depressed level of consciousness (GCS <13)
  5. Unexplained progressive or fluctuating symptoms
  6. Papilloedema, neck stiffness or fever
  7. Severe headache at onset of stroke symptoms
113
Q

What type of CT scan should be ordered in stroke?

A

Non-enhanced CT

if thrombectomy indicated - perform imaging with CT constrast angiography after the initial non-enhanced CT

114
Q

For those having a stroke who meet the criteria for CT, within what time frame should they have the CT scan?

A

Within 24 hours

115
Q

What are the indications for getting thrombolysis in stroke and which medication is used?

A
  1. If treatment can be started within 4.5 hours (i.e. get to the stroke unit for within 4.5 hours)
  2. Intracranial haemorrhage has been excluded by imaging
    Use Alteplase for thrombolysis - this should ONLY be done once in the stroke unit
    (look up alteplaase dose)
116
Q

Outline the criteria of who gets thrombectomy (together with thrombolysis):

A

Present within 6 hours of symptom onset:

  1. Acute ischaemic stroke
  2. Confirmed occlusion of the proximal anterior circulation demonstrated by CT angiography or MR angiography

Present within 6-24 hours (inc. wake-up strokes):

  1. acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by CT or MR angiography
  2. There is potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion weighted MRI showing limited infarct core volume
117
Q

Describe aspirin treatment in acute ischaemic stroke

A

Offer as soon as possible within 24 hours once intracerebral haemorrhage excluded
1. Aspirin 300mg orally if no dysphagia
2. Aspirin 300 mg rectally or by enteral tube if they have dysphagia
continue aspirin

Continue aspirin daily 300mg until 2 weeks after the onset of stroke symptoms

118
Q

What is the advice for stroke and statins?

A

Do not start immediate initiation of statin with acute stroke, but continue in people already on statins

119
Q

When should people get oxygen in stroke?

A

If sats <95%

120
Q

What range should blood glucose be maintained at during stroke?

A

4-11mmol/L

121
Q

In which type of stroke is it important to control BP and what is the target?

A

Acute intracerebral haemorrhage

aim for SBP between 130-140mmHg within 1 hour and for at least 7 days

122
Q

What assessment is important for those who have had a stroke?

A

SALT - swallow assessment

123
Q

What investigations should be carried out for meningitis?

A
  1. Full blood count
  2. C-reactive protein (CRP)
  3. Coagulation screen
  4. Blood culture
  5. Whole-blood polymerase chain reaction (PCR) for N meningitidis
  6. Blood glucose
  7. Blood gas
124
Q

What is the initial treatment for suspected bacterial meningitis?

A 
Do not delay!!! 
IV ceftriaxone (look up dose) 
(if cause is Hib - then 10 days, if cause strep pneumoniae 14 days)
125
Q

What corticosteroid do you give in suspected bacterial meningitis and when is it given?

A

Dexamethasone- give before the IV antibiotics or at the same time as the first dose

126
Q

What long term effects/follow up do you need to consider for meningitis?

A
  1. Audiological assessment as soon as possible, preferably before discharge, within 4 weeks of being fit to test.
  2. More than one episode of meningococcal disease - consider complement deficiency
127
Q

What are the public health considerations?

A

Ciprofloxacin single dose prophylaxsis for close household contacts
Inform pulic health england as it is a notifiable disease

128
Q

What are the immediate measures to manage status epilepticus?

A
  1. Positioning the patient to avoid injury,
  2. Supporting respiration including the provision of oxygen,
  3. Maintain blood pressure
  4. Correction of any hypoglycaemia
129
Q

At what point would you give IV lorazepam to the patient in status epilepticus? And what dose?

A

After 5 mins of them seizing

4mg lorazepam

130
Q

After the first IV lorazepam, what is the next management in status epilepticus?

A
  1. repeat dose of IV lorazepam (4mg) after 10 mins
  2. Phenytoin
  3. ITU + propofol
131
Q

If the patient does not have IV access - what are your options in the management of seizures once it gets to 5 mins?

A
  1. Rectal diazepam (10–20 mg, 10mg if elderly)

2. Buccal midazolam (10 mg)

132
Q

When do you use phenytoin in status epilepticus? and what is the loading dose?

A

If benzodiazepine treatment fails and it has been 25 minutes since the onset of the seizure
Loading dose 20 mg/kg

133
Q

What bloods should be taken in Status epilepticus?

A 
FBC 
U and E 
LFT 
Glucose 
Calcium
134
Q

What are the initial investigations in suspected DKA?

A

Beside:
Capillary blood Ketones
Capillary blood Glucose
Urine dip

Bloods:
VBG (or capillary blood glucose depending on age) - pH and bicarbonate
U and E

135
Q

What is the criteria for diagnosing DKA?

A
  1. hyperglycaemia - plasma glucose >11mmol/L
    AND
  2. acidosis - pH <7.3 OR bicarb <15mmol/L
    AND
  3. ketonaemia >3mmol/L OR ketonuria ++ on the urine strip
136
Q

Outline the grading the DKA severity

A

Mild - pH <7.3 or bicarb <15mmol/L
Moderate - pH <7.2 or bicarb <10mmol/L
Severe - pH <7.1 or bicard <5mmol/L

137
Q

When DKA is diagnosed what clinical features need to be recorded?

A
  1. level of conscioussness
  2. HR, BP, temp, RR (look for Kussaml breathing)
  3. Nausea or vomiting - in Hx
  4. Evidence of dehydration
  5. Body weight
138
Q

When DKA is diagnosed, what needs to be recorded from the VBG/CBG? (7)

A 
pH 
CO2 
plasma Na
plasma K
plasma urea 
plasma creatinine 
plasma bicarbonate
139
Q

If a patient has severe DKA, how do they need to be cared for?

A

One to one nursing - in HDU or a paediatric ward

140
Q

In which DKA patients would an NG tube be inserted?

A

Reduced level of consciousness and voming

141
Q

Describe the fluid management in DKA of a child who is clinically dehydrated but not in shock

A
  1. Give IV bolus of 10ml/kg 0.9% sodium cholride over 30 mins
  2. Can give another bolus of step 1- but must be discussed with senior paediatician
  3. When calculating the total fluid requirrment, subtract the initial bolus(es) given from the total fluid deficit
142
Q

What are the signs of shock in DKA?

A
  1. weak, thready pulse

2. hypotension

143
Q

Describe the fluid management in DKA of a child who has signs of shock

A
  1. IV bolus of 20ml/kg 0.9% sodium chloride (NO POTASSIUM CHLORIDE)
  2. Do NOT subtract this from the fluid deficit when calculating the total fluid requirement
144
Q

Which signs elude to shock, but are not actually signs of shock in DKA?

A
  1. prolonged cap refill
  2. tachycardia
  3. tachypnoea
    (they occur as a result of vasoconstriction caused by metabolic acidosis/low Co2)
    (the only signs of shock are weak pulse and hypotension)
145
Q

Outline fluid deficit amount in DKA

A

Mild - moderate DKA - 5% dehydration
Severe DKA - 10% dehydration
Replace the deficit evenly over 48 houra

146
Q

Outline the fluid maintenance requirement in DKA

A 
Use the Holliday Segar formula 
100ml/kg for the first 10kg 
50ml/kg for the second 10kg 
20ml/kg for any weight above 20kg 
REMEMBER for total fluid requirement: 
if clinical dehydration but no shock: 
fluid deficit + maintenance - bolus 
if in shock: fluid deficit + maintenance
147
Q

Which fluid types are used for the fluid deficit (rehydration) and the maintenance?

A

0.9% sodium chloride 1L + 40mmol/L potassium chloride without glucose UNTIL the plasma glucose is below 14mmol/L (then it is 0.9% sodium chloride + 5% dextose) 1L + 40 mmol/L potassium chloride

148
Q

It is important to monitor sodium during DKA - what are you looking out for with the sodium?

A

As DKA is treated - the Na+ should INCREASE (think - increase =good)

A falling Na+ may be a sign of cerebral oedema

149
Q

When is the insulin started in DKA?

A

1-2 hours after starting the IV fluids

150
Q

What should be done if a child in DKA has an insulin pump?

A

Disconnect the pump when starting IV insulin therapy

151
Q

What dose of insulin is given for DKA treatment?

A

0.1 units/kg/hour

152
Q

In DKA, at what point can you think about stopping the IV insulin therapy and switching to subcut insulin?

A
  1. Ketosis is resolving and blood pH has reached 7.3
    AND
  2. they are alert
    AND
  3. they can take oral fluids without N&V
    (Start subcut insulin at least 30 mins before stopping the insulin)
153
Q

When can the insulin pump be started again in DKA?

A

At least 60 mins before stopping IV insulin

154
Q

What do you need to monitor hourly in DKA?

A
  1. Cap blood glucose
  2. HR, BP, temp, resp rate
  3. fluid balance with fluid input/output charts
  4. level of consciousness
155
Q

What continuous monitoring do you need in DKA?

A

ECG monitoring to detect signs of hypokalaemia (ST depression and prominent U waves)

156
Q

What do you need to mointor after 2 hours of starting treatment? (7)

A 
Blood glucose (lab) 
blood pH 
pCO2 
plasma Na+ 
plasma K+ 
plasma urea 
beta-hrdroxybutyrate (ketone) 
(at least every 4 hours - after the 2 hours)
157
Q

At each face-to-face review of children and young people with DKA what do you assess?

A
  1. Clinical status - vital signs / neurological status
  2. Results of blood investigations
  3. ECG trace
  4. Cumulative fluids balance
158
Q

What are the 3 complications of DKA?

A
  1. Cerebral oedema
  2. Hypokalaemia
  3. VTE
159
Q

How do you treat cerebral oedema?

A

Mannitol

Hypertonic sodium

160
Q

What are the signs of cerebral oedema in DKA?

A
  1. headache
  2. agitation or irritability
  3. unexpected fall in HR (cushing’s reflex)
  4. Increased BP (cushing’s relfex)
  5. decreased level of consciousness
  6. Abnormal breathing
  7. Pupil inequality or dilation (sign of raised ICP)
161
Q

What would you do if the potassium drops below ____?

A

Below 3mmol/L

Temporarily suspend the insulin infusion

162
Q

What hollistic advice can I sprinkle in the managment?

A

Discuss with the family what may have led to the event

Advice on how to reduce recurrence

163
Q

Outline the steps of hyperkalaemia treatment

A

1.Elimanate source of hyperkalaemia
2. 10ml of 10% calcium gluconate (if ECG changes are present) -
2.a) - can repeat the calcium gluconate in 5 minutes
3. 10 Units insulin in 50ml of 50% glucose
4. 5mg nebulised salbutamol
Further managment:
- furosemide
If refractory hyperkalamemia: haemodialysis

164
Q

How long is the effect of the calcium gluconate in hyperkalaemia?

A

Starts in minutes but does not last long, hence you can repeat in 5 mins

165
Q

How long does it take for the insulin and salbutamol to start working and how long does their effect last?

A

15 minutes - to start working

The effects last 2 hours

166
Q

What are the causes of hyperkaelamia?

A

DREAD

  1. Drugs (ACEi and MRAs)
  2. Renal failure (AKI/CKD)
  3. Endocrine - Addisons
  4. Artefact - haemolysed blood
  5. DKA
167
Q

What causes Acute Tubular Necrosis?

A

aminoglycosides, rhabdomyolysis,

myeloma

168
Q

What causes interstitial nephritis?

A

pyelonephritis
penicillins
NSAIDs

169
Q

What investigations do you want to Addisonian crisis/ Adrenal insufficiency?

A

Bedside:
ECG
Capillar glucose

Bloods: FBC, U&Es, cortisol

Cultures (if concerned about infection): Blood, urine, sputum

170
Q

What electrolyte imbalance do you get in Addisonian crisis?

A

Hyperkalaemia

Hyponatraemia

171
Q

Why is it important to monitor glucsoe in Addisonian crisis?

A

Risk of hypoglycaemia

172
Q

What are the causes of Addisonian crisis?

A
  1. Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  2. Adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  3. Steroid withdrawal
173
Q

What is the management of Addisonian crisis?

A
  1. Hydrocortisone 100mg IM or IV STAT
  2. IV fluid 1L of 0.9% saline over 30-60 mins) to support BP + dextrose if hypoglycaemic
  3. Monitor blood glucose
  4. Continue hydrocortisone IV, 6-hourly until patient is stable
  5. Antibiotics if concerned about infection
  6. Oral steroid replacement begin after 24 hours and gradually reduced down to maintenance over 3-4 days
  7. Advise about not suddenly stopping steroid
174
Q

What investigations do you want in aortic dissection?

A

Bedside: ECG, uriary catheter to monitor fluid balance
Bloods: FBC, U&E, LFT, Coagulation, Cross match 6 units of RBCs, FFP, Platelets
Imaging: CXR, TOE/TTE, CT angiography

175
Q

When would you use TTE/TOE in aortic dissection?

A

If the patient is too unstable for CT angiography

176
Q

What would the CXR findings be in aortic dissection?

A

Widened mediastinum

177
Q

What is the gold standard investigation for aortic dissection and what do you see?

A

CT angio

  • location and extent of the false lumen
  • useful for planning surgery if needed
178
Q

What is the name of classification system used in aortic dissection and describe it?

A

Stanford classification
Type A - Ascending aorta
Type B - Descending aorta, distal to the left subclavian origin

179
Q

Which type (A or B) is more common?

A

Type A = 2/3 of cases

Type B = 1/3 of cases

180
Q

What is the management of aortic dissection?

A
  1. Invasive monitoring
  2. Reduction in the blood pressure/HR using nitroprusside and labetalol (Both type A and B)
  3. Opioid analgesia - if severe pain
  4. Refer for either endovascular or surgical intervention (if type A)
  5. Conservative management/ bed rest (type B)
181
Q

What should the target systolic BP be in aortic dissection?

A

100-120 mmHg

182
Q

What are the causes of small bowel obstruction?

A

Adhesions (extramural)

Hernias (extramural)

183
Q

What are the causes of large bowel obstruction?

A

Vulvulous (extramural)
Diverticular strictures (mural)
Malignancy (mural)

184
Q

What are the differentials for bowel obstruction?

A

Pseudo-obstrucion (lack of peristalsis), post-op ileus, toxic megacolon

185
Q

What are the investigations for bowel obstruction?

A 
Bloods: 
FBC 
CRP 
U and E 
LFTs 
G and S 
VBG - to identify signs of ischaemia (high lactate) 
Imaging: 
1. CT scan with IV contrast 
of the abdomen and pelvis 
2. ABX 
3. Erect CXR - to check for bowel perforation
186
Q

How can you differentiate between small and large bowel obstruction on ABX?

A

Small

  1. dilated bowel >3cm
  2. Central abdo location
  3. Valvulae conniventes visible

Large

  1. dilated bowel >6cm (or >9cm if caecum)
  2. Peripheral location
  3. Haustra lines visible (halfway = haustra)
187
Q

What is the management in bowel obstruction?

A
  1. fluid resuscitation - 2 wide bore cannulae
  2. NBM + insert a nasogatric tube to decompress the bowel ‘suck’
  3. IV fluids and correct any electrolyte imbalance ‘drip’
  4. Urinary catheter and fluid balance
  5. Analgesia +/- anti-emetics
188
Q

Which Bowel obstruction causes rarely needs sugery?

A

Small bowel obstruction - caused by adhesions

189
Q

Which bowel obstruction tends to need surgery?

A
  1. LBO or SBO in a patient who has not had previous surgery (virgin bowel) - it rarely settles without surgery
  2. Intestinal ischaemia
  3. Strangulated hernia
190
Q

What procedure is usually done for bowel obstruction?

A

Laparotomy

191
Q

What are the complications of bowel obstruction?

A
  1. Bowel ischaemia
  2. Bowel perforation
  3. Dehydration and renal impairment
192
Q

Name 4 causes GI perforation

A
  1. Peptic ulceration
  2. SBO or LBO
  3. Diverticular disease
  4. IBD
193
Q

What are the clinical signs of perforation (i.e. the signs of peritonitis)?

A
  1. Tachycardia
  2. Postural hypotension
  3. Completely Rigid abdomen
  4. Involuntary guarding
  5. Reduced or absent bowel sounds
  6. Rapid onset of pain
    These patients tend to lay completely still as movement hurts
194
Q

What investigations do you want in GI perforation?

A 
Bedside: Urine sample, pregnancy test 
Bloods:  
FBC 
U and E 
LFT 
CRP
Amylase 
G and S 
Imaging: 
Erect CXR- pneumoperitoneum 
ABX 
Gold standard = CT scan abdomen and pelvis (for diagnosis of cause)
195
Q

Why do you want a urine sample in bowel perforation?

A

To exclude renal pathology and tubo-ovarian pathology

196
Q

What are the signs of bowel perforation on ABX?

A

Rigler’s sign - both sides of the bowel wall can be seen, due to free intra-abdominal air
Psoas sign - loss of the sharp delination of the psoas muscle border, due to fluid in the retroperitoneum

197
Q

What is the management of GI perforation?

A
  1. Broad spec antibiotics (perforation can lead to contamination)
  2. NBM + consider NG tube
  3. IV fluids supportive
  4. Analgesia
  5. Alert surgeons to prepare theatre
198
Q

What may the surgical treatment of perforation be?

A
  1. Treat the underlying cause

2. Thorough washout

199
Q

What is the classic presentation of ruptured abdominal aortic aneurysm? and what is the classic triad of ruptured AAA?

A

Sudden onset abdominal pain radiating to the back

  1. flank or back pain
  2. Hypotension
  3. Pulsatile abdominal mass
200
Q

What investigations would you like for ruptured abdominal aortic aneurysm?

A

Bedside: ECG

Bloods: 
FBC 
U&E 
Clotting 
Crossmatch (minimum 6 units) 
ABG 
Troponin

Imaging: CT angio
(Abdominal US may show free fluid)

201
Q

Where can AAAs rupture?

A
  1. Anteriorly into the peritoneal cavity - 20%, poor prognosis
  2. Posteriorly into the retroperitoneal space - 80%
202
Q

What is the management of ruptured AAA?

A
  1. High flow o2
  2. IV access- x2 large bore cannulae
  3. Urgent bloods (FBC, U and E, clotting, crossmatch for minimum 6 units)
  4. Transfer the patient to the local vascular unit
  5. Inform the blood transfusion lab
203
Q

How would the management of ruptured AAA differ if the patient was stable vs unstable?

A

Stable: CT angiogram to determine whether the aneurysm is suitable for endovascular repair

Unstable: immediate transfer to theatre for open surgical repair

204
Q

What are differentials for a subarachnoid haemorrhage?

A

Meningitis

Migraine

205
Q

What investigations do you want for subarachnoid haemorrhage?

A

Bedside: Continuous cardiac monitoring of BP and ECG (cushing’s reflex)
Bloods: FBC, U and E, LFT, Clotting
Imaging:
Urgent non-contrast CT scan (within 24 hours)
LP (if Hx is negative, but clinical suspicion of SAH - but remember needs be 12 hours for xanthachromia as the blood needs to breakdown
(CT angio or digital subtraction angio can be used in some specialist centres to view the smaller vessels)

206
Q

What is the management of SAH?

A
  1. Fluid resuscitation and analgesia with anti-emetics as necessary
  2. Early neurosurgical involvement and transfer to high-dependency care centre
  3. Start the patient on nimodipine (a CCB)
  4. Close neurological monitoring for complications (cerebral iscaheamia, acute hydrocephalus)
207
Q

What is the purpose of nimodipine in SAH ?

A

To reduce vasospasm

Prevent rebleeding and cereberal ischaemia

208
Q

What are the surgical options for management of SAH?

A
  1. Coiling or clipping of the aneurysm
    - 80% = coiled
    - minority get clipped
209
Q

When is coiling the aneurysm more suitable in SAH than clipping?

A
  1. Presence of multiple cormorbidities
  2. Older age patient
  3. Presence of vasospasm
210
Q

Give examples of some of the complications that can happen in SAH that you should monitor for

A
  1. Rebleeding
  2. Hydrocephalus
  3. Vasospasm
  4. Electrolyte disturbances (hypoatraemia)
211
Q

What is the scale used with SAH to predict survival based on symptoms at presentation? +describe the grades

A

Hunt and Hess Scale (5 grades)
1 - Asymptomatic, mild headache - 70% survival
2 - Moderate to severe headache, neck stiffness, no neurological deficit except cranial nerve palsy - 60% survival
3 - Drowsy - 50% survival
4 - Stuporous, hemiparesis - 20% survival
5 - Coma - 10%

212
Q

What is acute pericarditis?

A

Inflammation of the pericardium

213
Q

What are the causes of acute pericarditis?

A
  1. Idiopathic
  2. Bacterial e.g. TB
  3. Viral e.g. Coxsackie
  4. Autoimmune- SLE, RA
  5. Uraemia
  6. Drugs - isoniazid, hydralazine
214
Q

What are the investigations for acute pericarditis?

A

Bedside: ECG
Bloods: FBC, U and E, LFTs, CRP, Troponin
Imaging:
CXR
All patients with query acute pericarditis should have a TTE (may show pericardial effusion)

215
Q

What is the management of acute pericaditis?

A
  1. Treat the underlying cause
  2. Analgesia and anti-emetics, if necessary
  3. IV access
  4. NSAIDs (1-2 weeks for gastric protection)
  5. Colchicine -
    and colchicine 500 micrograms for 3 months to prevent recurrence
216
Q

During a cardiac arrest check for the reversible causes - what are they?

A

4 Hs:

  1. Hyperkalaemia/Hypokalaemia/Hypocalcaemia
  2. Hypothermia
  3. Hypovolaemia
  4. Hypoxia

4 Ts:

  1. Tension pneumothorax
  2. Tamponade
  3. Toxins and poisons
  4. Thromboembolism
217
Q

At what vertebral level does the spinal cord and the cauda equina begin?

A

L1

218
Q

What exactly is the cauda equina?

A

The nerve roots of L1-S5 pass down the spinal canal as a group - together these nerve roots are called the cauda equina (hence it is LMN)

219
Q

What are the causes of cauda equina?

A
  1. Disc herniation L5/S1 and L4/L5
  2. Trauma - vertebral fracture
  3. Neoplasm - primary or metastatic
  4. Infection - discitis
220
Q

Which cancers spread to the spinal vertebrae?

A 
Thyroid 
Breast 
Lung 
Renal 
Prostate
221
Q

What are differentials for cauda equina?

A

Radiculopathy

Cord compression

222
Q

What is the difference between cord compression and cauda equina?

A

Same pathophysiology and both surgical emergencies, but cord compression = UMN because it is above L1 where the spinal cord is still running

223
Q

What is the management of cauda equina?

A
  1. Early neurosurgical review for urgent decompression

2. High-dose steroids e.g. dexamethasone - to reduce localised swelling

224
Q

What investigations for cauada equina syndrome?

A

FBC, U and E, G and S

Imaging: whole spine MRI

225
Q

Outline the management of anaphylaxis

A
  1. Secure the airway + give 100% O2
  2. Intubate if resp obstruction = imminent
  3. Remove the cause + raise the feet to help circulation
  4. Give adrenaline 500 micrograms IM 1:1000
  5. Repeat adrenaline every 5 min if needed as guided by BP, pulse and resp function until better
  6. Secure IV access
  7. Chlorphenamine 10mg IV and hydrocortisone 200mg IV
  8. IV fluids - 0.9% sodium chloride 500ml in 15 mins (give fluids according to BP)
  9. If wheeze treat for asthma
  10. If still hypotensive - admission to ICU and IV adrenaline infusion +/- aminophylline + nebulisaed salbutamol
226
Q

What patient counselling details are important after anaphylaxis?

A
  1. ‘MedicAlert’ bracelet naming the culprit
  2. Teach about self-injected adrenaline to prevent fatal attack
  3. Skin prick tests to help identify allergens
227
Q

Define shock

A

Circulatory failure resulting in inadequate organ perfusion

  1. SBP <90mmHg + evidence of tissue hypoperfusion e.g.
    - mottled skin,
    - urine output <0.5ml/kg/h,
    - serum lactate>2 mmol/L
228
Q

What are the types of shock?

A

Septic
Hypovolaemic
Cardiogenic
Anaphylctic

229
Q

How do you differentiate between the types of shock?

A

All of them have low BP

  • Cardiogenic shock will differentiated as JVP will be high
  • Then to differentiate between septic shock and hypovolaemic shock feel the peripheries - warm = septic shock, cool = hypovolaemic shock
230
Q

List a causes of shock for:
Cardiogenic
Septic
Hypovalaemia

A

Cardiogenic: Heart failure, ACS, arrythmia
Septic: Infection
Hypovolaemia: Bleeding, from trauma, ruptured AAA, GI bleed

231
Q

How do you treat sepsis?

A

Mainly in the circulatory part of A-E approach

  1. Fluids- 2 large bore cannulae for IV access (start within 1 hour)
  2. Antibiotics +/- other antimicrobials (start within 1 hour)
  3. Oxygen - target sats 94-98% (or 88-92% if chronic Co2 retainer)
  4. Liaise with other teams: surgical or medial or acute care, ITU (if need of inotropes, ventilation, haemofiltration)
232
Q

How do you treat cardiogenic shock?

A

Check ECG for rate and rhythm and ischaemia

233
Q

How do you definte septic shock?

A

Sepsis in combination with either:
1. lactate >2mmol/L despite fluid resus
or
2. patient is requiring vasopressors to maintain MAP >65mmHg

234
Q

What investigations do you want to get in sepsis?

A

Bedside: ECG, basic obs, urine dip, urine output monitoring
Bloods:
Serial ABG/VBGs for lactate, blood cultures, U and E, CRP, FBC, LFT, clotting screen
Microsamples: Sputum and urine microscopy, culture and sensitivity, swab any wounds, consider LP, send fluid from drains and lines, joint aspirates, ascitic tap
Imaging: CXR

235
Q

How do you treat cardiogenic shock?

A
  1. Oxygen - sats 94-98% or 88-92%
  2. Diamorphine 1.25mg IV for pain/anxiety
  3. Correct arrhythmias, electrolyte imbalance, acid-base disturbance
  4. Monitor urine output + Cardiac monitor
  5. Over-filled (with fluid) - dobutamine 2.5 micrograms/kg/min IV
  6. treat ay reversible cause e.g. thrombolysis for MI/PE
236
Q

What investigations do you want for cardiogenic shock?

A 
Bedside: ECG 
Bloods: FBC, U and E, ABG, troponin 
Imaging: CXR (portable),, Echocardiogram 
Monitor urine output 
Cardiac monitor
237
Q

What is the treatment for hypovolaemic and haemorrhagic shock?

A

Hypovolaemic - raise the legs, fluid bolus 500mL 0.9% sodium chloride

Haemorrhagic - stop the bleeding, blood products (or crystalloid if blood products not available) - cross match, FFP

238
Q

What are the differentials for a broad complex tachycardia?

A

VT (includeing torsades de pointes)
VF
SVT with BBB
AF with wolff parkinson white syndrome

239
Q

What is the initial managment for all TACHYarrhythmia (i.e. both narrow and broad complex tachyarrhythmia)?

A
  1. Check if they have a pulse (if no - then arrest protocol- BLS and ALS)
  2. Give O2 if hypoxic
  3. Monitor: ECG, BP + record 12 lead ECG
  4. Get IV access
  5. Identify and treat reversible causes e.g. electrolyte abnormalities
  6. Check for adverse features
    - Shock (SBP<90, HR >100)
    - Syncope
    - Heart failure
    - Myocardial ischaemia (CP or ischaemia on ECG)
  7. If adverse features proceed to do SYNCHRONISED DC cardioversion shock (up to 3 attempts)

If no adverse features - then treat based on broad or narrow complex

240
Q

Explain the management of TachyArrhythmias with adverse features

A
  1. SYNCHRONISED DC cardioversion shock (up to 3 attempts)
    Broad complex - charge to 120-150J for first shock, then 150-360J
    Narrow complex - charge to 70- 120J for first shock, then 120-360J
  2. Check and correct K+, Mg2+, Ca2+
  3. Amiodarone 300mg IV over 20 mins
  4. Repeat shock
  5. Amiodarone 900mg IV over 24 hours (via central line)
241
Q

What is the management of Regular Broad complex tachyarrhythmia (with no adverse features)?

A
  1. If VT - amiodarone 300mg IV over 20-60 mins, then 900mg over 24 hours (via central line)
  2. If SVT + BBB then treat as narrow complex
242
Q

What is the treatment of Irregular Broad complex tachyarrhythmia (with no adverse features)?

A 
1. Seek expert help 
It could be:  
- AF with BBB 
- Pre-excited AF consider amiodarone 
- Polymorphic VT e.g. torsardes de pointes - Mg2+ 2g IV infusion

PACES - Instruments (2 decks)

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