Emergency care Flashcards
What acid-base imbalance does aspirin overdose initially cause and then turn to?
Starts as respiratory alkalosis (initial respiratory centre stimulation)
Turns to metabolic acidosis (compensation for high resp rate)
Into which categories can shock be classified?
Class 1 - Compensated
Class 2 - Tachycardia
Class 3 - Hypotension
Class 4 - Loss of consciousness
How can cardiogenic, septic and hypovolaemic shock be distinguished clinically?
Cardiogenic: only one with raised JVP
Septic: warm peripheries (others will be cold)
What is the management for cardiogenic vs septic vs hypovolaemic shock?
Cardiogenic: dobutamine, dopamine
Septic: noradrenaline
Hypovolaemic: blood
Define sepsis vs septic shock
Sepsis: life-threatening organ dysfunction caused by dysregulated host response to an infection
Septic shock: sepsis + lactate >2 despite fluid resus OR
patient needs vasopressors to maintain MAP > 65mmHg
Recall the management of sepsis
Cannulate (+ bloods)
Catheterise
3 out: - lactate (VBG) - UO (catheterise) - Blood cultures 3 in: - 15L/min oxygen (even if sats okay) - ABx (as per local guidelines) - Fluids
Investigate for the source of infection
Recall some key elements to ask in the history in suspected sepsis
AMPLE Allergies Medications Past medical history Last meal Events surrounding
Recall the immediate management of anaphylaxis
Secure airway –> remove cause –> raise legs
Then (alphabetical order, (doses on different card)):
- Adrenaline
(insert IV line for following drugs)
- Chlorphenamine IV
- Hydrocortisone IV
Recall the dosing for adrenaline in anaphylaxis in each different age group, and the max dose you can give
> 12y: 500mcg doses, up to 0.5mg
6-12y: 300mcg doses, up to 0.3mg
6m-6y: 150mcg doses, up to 0.3mg
0-6m: same as above
Recall the dosing for chlorphenamine in each different age group given in anaphylaxis
> 12y: 10mg
6-12y: 5mg
6m-6y: 2.5mg
0-6m: 250mcg/kg
Recall the dosing for hydrocortisone in each different age group given in anaphylaxis
> 12y: 200mg
6-12y: 100mg
6m-6y: 50mg
0-6m: 25mg
Describe the changes to the A to E approach in trauma
Before A to E:
- If massive haemorrhage, tamponade the massive bleeding prior to A to E
A
- Never do head tilt (just jaw thrust) because you always assume C spine injury until proven otherwise
B same as usual
C
- If significant haemorrhage, replace with 1-1-1 plasma, platelets and packed rbcs when you get to circulation
- If history of haemorrhage or ongoing bleeding (less massive) then give type O blood
- FAST scan
At what GCS do you intubate?
<8
What is the Canadian C-Spine rule used for?
Criteria that, if any are met, mean you need to immobilise the spine
What are the NEXUS criteria used for?
If any of these criteria are met you cannot clear the C spine clinically
What is the gold-standard form of imaging for investigating a possible cervical spine fracture?
CT neck (or MRI in children <16y)
What is a FAST scan?
A point of care ultrasound scan used to identify intraperitoneal free fluid (assumed to be haemoperitoneum in the context of trauma)
Systematically recall some causes of coma
Metabolic: COMA CAUSES
Cold (hypothermia)
Oxygen (hypoxia)
Medication OD (eg TCAs)
Addisonian…
Crisis Alcohol Underactive thyroid (myxoedema) Sepsis Encephalopathy (uraemic or hepatic) Sugars high/ low
Vascular: THEISM
Trauma Haemorrhage Epilepsy Infection Stroke Malignancy
Recall the elements of the Glasgow Coma Scale in people >5 years old
Eyes: 1: no response 2: open to pain 3: open to voice 4: open spontaneously C = closed by swelling or bandage
Voice: 1: no response 2: sounds 3: words 4: confused 5: orientated T = intubated
Motor:
1: no response
2: abnormal extension (decerebrate)
3: abnormal flexion (decorticate)
4: withdraw from pain
5: localise pain
6: obey commands
What is Cheyne-Stokes hyperventilation?
Type of central sleep apnoea where there are periods of apnoea followed by fast ventilation
If seen when patients are awake it indicates a poor prognosis
What is apneustic breathing?
Regular deep inspirations with an inspiratory pause followed by inadequate expiration
Caused by injury to the pons
What is ataxic breathing?
Completely irregular pattern of breathing that eventually becomes agonal breathing
If pupils are mid-position (3-5mm) and non-reactive (may be irregular or not), what does this indicate?
Midbrain lesion
If pupils are unilaterally fixed and dilated what does this indicate?
3rd nerve compression
If pupils are small but reactive what does this indicate?
Pontine lesion or drugs
How can you test the vestibulo-ocular reflex?
Doll’s head manoevre:
Head is moved laterally quickly
Normal if eyes keep looking at same point in space
Abnormal if eyes turn in opposite direction of rotation
In the most simplistic terms, how do you decide between a PCI or a CABG to manage ACS?
PCI for 1 or 2 vessel disease, not including LAD
CABG for >2 vessel disease, or including LAD
Recall the reversible causes of cardiac arrest
5 Hs and 4 Ts Hypoxia Hypovolaemia Hypothermia Hypokalaemia/ hyperkalaemia Hypoglycaemia
Toxins
Tamponade
Thrombosis
Tension pneumothorax
Recall the possible complications of an MI
DARTH VADER Death Arrhythmia Rupture (left ventricular free wall, interventricular septum) Thrombosis Haemorrhage Valvular heart disease Aneurysm Dressler's syndrome Embolism Re-infarct
In what time period might LVFW rupture occur post-MI?
5 days to 2 weeks
What are the 2 main differentials for cardiac rupture 3-5days post MI?
1) Acute mitral regurgitation due to papillary muscle rupture
2) Ventricular septal rupture
What are the signs and symptoms of papillary muscle rupture?
Acute mitral regurgitation
Pulmomary oedema
Hypotension
New pansystolic murmur (harsh thrill)
What are the signs and symptoms of ventricular septal rupture post MI?
Chest pain
Biventricular failure
Shock
New PSM
What are the signs and symptoms of LVFW rupture post-MI?
Heart failure
Tamponade
What are the signs of cardiac tamponade?
Raised JVP
Muffled heart sounds
Hypotension
Pulsus paradoxus
How should heart block be managed following an anterior vs inferior MI?
If they had an anterior MI then got heart block:
- Temporary transcutaneous pacing –> permanent pacemaker
If they had an inferior MI then got heart block:
- Medical management with atropine
What is the most common cause of death post-MI?
Ventricular fibrilation
Describe the broad principles of immediate management of MI (this is your big ‘ol card when you turn over warning)
Offer 300mg aspirin loading dose asap
For symptom mx: 10mg IV morphine and 10mg IV metoclopramide (O2 if SpO2 <94%)
Immediately assess suitability for reperfusion therapy
- Can offer reperfusion therapy within 12 hours of symptom onset (or slightly otherwise in some circumstances)
- If it’s >12 hours since symptom onset –> medical mx only
Reperfusion options:
1. PCI - if you can offer within 120 mins (need to add aspirin + one other antiplatelet for this, choice depends on a number of factors)
2. Fibrinolysis - if you can’t offer PCI within 120 mins (1st line is enoxaparin - can also use unfractionated heparin/ fondaparinux)
3. If GRACE score low –> just fondaparinux
Medical mx:
- Aspirin and ticagrelor (180mg PO) unless high bleeding risk
Source: https://www.nice.org.uk/guidance/ng185/resources/visual-summary-stemi-pdf-8900623405
When would beta blockers be contra-indicated in immediate management of an MI?
Bradycardia
Hypotension
Heart failure/ block
COPD/asthma
Recall the long-term management of MI
ACE inhibitor (although consider spironolactine in HF) Beta blocker (OR verapamil/ dilitiazem) Cardiac rehab (diet and exercise) DAPT (aspirin + ticagrelor) Statin
Systematically recall some causes of acute onset pulmonary oedema
Cardiovascular (LVF –> elevated PAWP)
ARDS (normal PAWP)
Fluid overload
Neurogenic (head injury)
Recall the management of acute pulmonary oedema
(1) Sit them up - high flow O2 if sats low
(2) IV diamorphine (3mg) + IV metoclopramide (10mg)
(3) IV furosemide
(4) GTN spray x 2 SL (can use IV if SBP >100)
(5) Continue furosemide and nitrate infusions until stable
How can RA/RV/PAWP be measured?
Swan-Gantz catheter
Inserted through a central vein
What is the management of VF?
Non-synchronised DC shock (no R waves to trigger defib)
What is the management of VT?
Synchronised DC shock (synchronise to R waves)
Medical:
- Amiodarone, lidocaine, procainamide
- VERAPAMIL is a contraindication
How is Torsades de Pointes managed?
Depends on aetiology
Congenital: high dose beta blockers
Drug-induced: MgSO4
How is stable, regular, broad complex tachycardia managed?
IV amiodarone
How is narrow-complex tachycardia managed?
Vagal manoevres –> IV adenosine
How is bradycardia managed?
Give O2 if hypoxic
ECG, IV access, BP
Identify reversible causes (eg electrolyte imbalances)
If adverse signs (shock/ syncope, HF, myocardial ischaemia): IV ATROPINE 500mcg
If no adverse signs: assess risk of asystole (recent asystole? mobitz II? complete heart block?)
If risk –> atropine
If no risk –> continue observation
If atropine does not –> satisfactory response you can repeat it every 3-5 mins (3mg/6 doses max)
When would you admit someone for an acute exacerbation of asthma?
If no response to treatment in A&E or CHEST: Cyanosis Hypotension Exhaustion (PEFR <33%) Silent chest Tachyarrhythmia Near fatal (pCO2 raised) (Asthma management cards in respiratory deck)
How should tension pneumothorax be managed?
NB. these are NEW ATLS GUIDELINES 2018 - it USED to be 2nd ICL at MCL but NOW IS:
Safety triangle - aim for 4th/5th ICS MAL Boundaries: - lateral edge of pec major - 5th ICS - Base of axilla - Lateral edge of lat dorsi
Insert 14-16g needle - plunger removed - partially filled with saline (facilitates a one way valve)
https://www.fortunejournals.com/articles/changing-trends-in-the-decompression-of-tension-pneumothorax.pdf
What score is used to determine if someone is likely to have a PE, and how many points do you need to justify a CTPA?
Well’s score
>4 points
(if <5 points –> D dimer)
What are some possible signs of PE on ECG, and which is the most common?
Most common: sinus tachycardia
Also: RBBB, RAD, S1Q3T3
How will a CXR appear in PE?
Normal
How should pulmonary embolism be managed if a patient is haemodynamically stable?
For all PEs: O2 if hypoxic, morphine/ anti-emetic for pain/ distress, IV fluids if low BP, get IV access
1st line: DOAC
3 months if provoked
Minimum 6 months if unprovoked
2nd line: IVC filter
Recall some provoking factors for PE
Immobility Trauma Surgery COCP/ HRT Pregnancy/ puerperium
How should pulmonary embolism be managed if a patient is haemodynamically unstable?
For all PEs: O2 if hypoxic, morphine/ anti-emetic for pain/ distress, IV fluids if low BP, get IV access
If no contra-indication to thrombolysis:
Unfractionated heparin + alteplase –> DOAC
If contra-indication to thrombolysis:
Unfractionated heparin WITHOUT alteplase –> DOAC
Consider embolectomy
If contraindication to thrombolysis AND anticoagulation:
Noradrenaline OR dobutamine
Consider embolectomy
What are some absolute contraindications to thrombolysis?
Brain things: Previous intracerebral haemorrhage Ischaemic stroke Cerebral malignancy Major trauma/surgery to head
Bleeding things:
- GI bleeding
- Bleeding disorder
- Aortic dissection
- Non-compressible punctures (eg LP/ liver biopsy)
What are the markers of mild, moderate and severe ARDS?
Based on PaO2/FiO2 ratio
Mild: 200-300mmHg
Moderate: 101-200mmHg
Severe <101mmHg
What are some signs and symptoms of ARDS?
BL CXR opacities
Respiratory failure not explained by HF or fluid overload
What are the appropriate investigations for ARDS?
Sepsis 6 Bloods: BC, FBC, U&E, LFT, glucose, clotting, FDPs, D-Dimer, G&S MSU ECG CXR
How should ARDS be managed?
All patients:
- Central venous access –> inotropes
- Peripheral venous access –> broad spec abx, diuretics
- O2
Non-shocked: sit upright
Shocked: colloid infusion
Recall some causes of UGI bleed, and which of these is most common
PUD (most common)
Mallory-Weiss tear
Erosions, oesophagitis, varices, malignancy
What anatomical landmark separates UGI from LGI bleeds?
Ligament of Treitz (suspends duodenal-jejunal flexure)
Recall the headings under which UG bleeds should be managed (other cards will go into each one)
(1) Resuscitation
(2) Risk assess
(3) Endoscopy
(4) Manage
(5) Prophylaxis
How should patients be resuscitated following an UGI bleed?
Packed RBCs
Platelets (if active bleeding or count <50)
FFP (if active bleeding and APTT is normal)
PCC if active bleeding on warfarin (prothrombin complex concentrate)
How can you perform a risk assesment for an UGI bleed?
Pre-endoscopy: Blatchford score
Post-endoscopy (to guide prognosis): Rockall score
When should endoscopy be performed following an UGI bleed?
Immediately if after severe acute resuscitation
Otherwise within 24 hours
How should variceal bleeds be managed?
For all:
IV Terlipressin
IV antibiotics as per local guidelines
For gastric varices:
1st line = endoscopic injection of butyl cyanoacrylate
2nd line = TIPS (transjugular intrahepatic portosystemic shunt)
For oesophageal varices:
1st line: endoscopic band ligation
2nd line: Sengstaken-Blakemore tube and TIPS (definitive)
How should non-variceal bleeds be managed?
Endoscopic options:
- Mechanical clips
- Thermal coagulation
- Fibrin/ thrombin
PPI after endoscopy
How can variceal bleeding with portal HTN be prevented?
PO propranolol
Recall some gram pos cocci and bacilli that may cause meningitis
Cocci:
Staph aureus (coag pos)
Staph epidermidis (coag neg)
Strep (pneumoniae, viridians etc)
Bacilli: ABCDL - Actinomyces - Bacillus - Clostridium - Diptheriae - Listeria
In what type of meningitis would the opening pressure of an LP be normal rather than raised?
Viral
What would the expected glucose be on LP in viral vs bacterial vs TB meningitis?
Viral: normal
Bacterial: low
TB: low