Emergencies Flashcards
Metabolic acidosis (raised anion gap) - causes
Aspirin – later metabolic compensation for high RR
CAT MUDPILES
C: CO, cyanide, congenital HF
A: Aminoglycosides
T: Theophylline, toluene
M: Methanol
U: Uraemia
D: DKA, alcoholicKA, starvationKA
P: Paracetamol, phenphormin, paraldehyde
I: Iron, isoniazid, IEOM
L: Lactic acidosis
E: Ethanol, ethylene glycol
S: Salicylates/aspirin
DKA - management
Aà E
AIM TO REDUCE KETONES
(1) Fluids (500mL bolus over 15m if SBP <90 until >90 mmHg, otherwise 1L NaCl / hour)
(2) Insulin (0.1U/kg/hr fixed rate IV insulin infusion + patient’s normal insulin regimen) – start after fluids started
(3) Potassium (only if/when low - check K+ on latest VBG, insulin causes hypokalaemia à run 40mmol KCl with second bag of NaCl over 2hrs)
(3) 10% dextrose (when BM <14), 100mL/hour
(4) VTE prophylaxis (very dehydrated)
Throughout: Monitor obs, glucose, ketones, VBG/ABG (pH, HCO3, K+)
Even if the patient is tipping into lower glucose levels, you can still give insulin – just give dextrose as well
DKA - management - K replacement
K>5.5 - nil
K 3.5-5.5 - 40mmol
K<3.5 - higher K concentrations, call ITU for central line
Max 20mmol/hr (therefore add to 2nd bag at the earliest)
HHS - diagnosis
pH >7.3, osmolarity >320mOsm, BM >30 mmol/L – develops over a few days - 1 week
HHS - investigations
Bedside:
ECG
Urinalysis +/- MSU
Urinary pregnancy test
CBG
Bloods: FBC, U&Es, CRP, LFTs, plasma glucose, blood culture, troponin, amylase, CK, Ca
CT Head (if focal neuro)
HHS - management
(1) Slow rehydration over 48hrs (3-6L in 12hrs) as level of dehydration can be massive in HHS; i.e. initial fluids…
Sodium chloride 0.9%, 1L, IV, over 2 hours
½ RATE OF FLUIDS OF DKA
(2) Monitoring (avoid rapid correction Na+, neurological status, every 4hrs: electrolytes, urea, blood glucose)
(3) Insulin (0.05U/kg/hr) sliding scale once BMs stop dropping OR ketones start to rise (i.e. once stabilised)
Fixed rate insulin infusion if evidence of ketonaemia
Replace K+ when UO increases
(4) Specialist review (within 24hrs) + begin prophylactic LMWH
HHS - treatment targets
Plasma osmolality target: falling by 3-8mOsm/kg/hr
Blood glucose/L falling by at least 5mmol/L/hr
Posterior MI - ECG changes + coronary artery
Tall R waves in V1-2
Usually left circumflex, also right coronary
Right coronary artery MI leads to…
Inferior MI
AV/Heart block (supplies AVN) - any degree
STEMI - ECG criteria
ST elevation >1mm in 2 consecutive limb leads,
Or >2mm elevation in 2 consecutive chest leads
Or new LBBB
NSTEMI - ECG criteria
Anything that doesn’t fit STEMI criteria, can have ECG changes i.e. ST depression or T wave inversion.
Silent MI - presentation
Silent MIs = diabetics or elderly à syncope, epigastric pain, vomiting, delirium, post-op oliguria/hypotension
When to do PCI vs CABG
PCI à 1- or 2-vessel disease, not including Left main stem
CABG à 2- or 3-vessel disease, or including Left main stem
If not clear cut –> MDT
ACS - investigations/diagnosis
Basic observations
ECG/Cardiac monitoring
Serial ECGs are useful to monitor for ST segment or T wave changes [dynamic changes]
Bloods
Troponin I/T
FBC, U&Es, glucose, lipids, clotting
CXR à cardiomegaly, pulmonary oedema, widened mediastinum (aortic rupture/aortic dissection)
STEMI - ECG changes sequence
Sequence:
Normal
ST elevation +/- tall T waves
Q waves (full thickness infarcts)
normalisation of ST segments
T wave inversion
Also new LBBB can indicate acute MI
NSTEMI - ECG changes
NSTEMI: ST depression, T wave inversion
ACS - acute management - generic
Admit + cardio review
Medication: MONA (morphine, oxygen, nitroglyceride, aspirin)
M: IV diamorphine 5-10mg (+ IV metoclopramide) = only if severe chest pain otherwise paracetamol
O2: non-rebreather mask if sats <92%, aim sats for 94-98% (if COPD then 88-92%)
N: GTN spray for pain
A: DAPT STAT (300mg aspirin + 300mg clopidogrel/180mg ticagrelor/prasugrel)
Anticoagulation (Fondaparinux 2.5mg SC OD) for 2-8 days until discharge or revascularisation - NOT if PCI possible
Why give ticagrelor over prasugrel?
Most people give ticagrelor because its faster than prodrug clopidogrel
ACS - long-term management - antiplatelets
75mg OD aspirin lifelong
Medically managed - ticagrelor for 12mo
PCI managed - clopi/prasugrel/ticagrelor for 12mo (decreases risk of stent thrombosis)
ACS - acute management - STEMI
PCI available: PCI within 120 mins of presentation (give prasugrel if no AC/clopi if on AC)
PCI unavailable: thrombolysis within 12h of presentation, ECG after 60-90 mins - if STEMI still, rescue PCI/angiography
>12h since symptom onset: specialist advice + anticoagulants (fonda/enox) + angiography + PCI
DAPT - SEs
Dyspepsia - give PPI
GTN spray - SEs
hypotension, headache, tachycardia
ACS - acute management - NSTEMI
Aspirin + serial ECGs + fondaparinoux if no immediate PCI
GRACE >3% - PCI within 72h (give ticagrelor/prasugrel + heparin)
GRACE <=3% - ticagrelor but no PCI
Clinically unstable - immediate PCI
Antiplatelet bleeding risk
Prasugrel > ticagrelor > clopidogrel
If bleeding risk, use clopi
ACS - acute management - UA
Same as ACS treatment = aspirin + clopidogrel and fondaparinux
What does GRACE score measure?
6-month mortality for pts with ACS
Raised troponin I/T - causes
MI, CKD, HF, sepsis, CA spasm, aortic dissection, PE
ACS - acute management - anticoagulant choice
Angiography ± PCI <24 hours - 1st line: enoxaparin (LMWH) OR unfractionated heparin OR bivalirudin
Fibrinolysis - 1st line: enoxaparin (LMWH) OR unfractionated heparin OR fondaparinux 2.5mg SC OD
No intervention (low GRACE) - 1st line: fondaparinux (AKA always give in NSTEMI)
ACS - long-term management
Lifestyle: mediterranean diet, exercise 20-30 mins/day, no sex 4 weeks, no viagra 6 months
Medical: ACEi, BB/RLCCB, DAPT, antiHTN, statin
HF S/S - consider spironolactone
Beta-blockers - CIs
low BP/HR, HF, COPD/asthma, cardiogenic shock, heart block
Suspected MI - GP referral criteria
Pain <12h ago + abnormal ECG à A&E now
Pain 12-72h ago à same day assessment
Pain >72h ago à ECG + troponin
PCI - indications
CAD, valvular disease, congenital heart disease
PCI - complications
haemorrhage, reaction, angina, arrhythmias
CABG - methods
LIMA diverted to LAD post-occlusion
Great saphenous vein harvested + attached to aorta + coronary artery post-occlusion
Both
Heart stopped + blood pumped artificially by bypass
MI - complications
Death
Arrhythmia
Rupture (left ventricular free wall rupture, interventricular septum rupture à VSD)
Thrombus
Haemorrhage
Valvular heart disease
Aneurysm (left ventricular wall; LAD involvement)
Dressler’s syndrome (2-6 weeks), pericarditis (<48 hours)
Embolism
Re-infarct
MI - arrhythmias it can cause
Heart block:
- Inferior MI mx: medical management (atropine; fatigue of AV nodal cells can be reversed)
- Anterior MI mx: temporary TC pacing à permanent pacemaker
Tachy-/brady-arrhythmias (VF = most common cause of death post-MI)
MI - types of rupture
Acute / 3-5 days à acute mitral regurgitation (PAPILLARY MUSCLE RUPTURE; RCA)
Acute / 3-5 days à ventricular septal rupture (LAD or RCA)
5 days – 2 weeks à LV free wall rupture (LAD)
MI - acute MR
Acute / 3-5 days
PAPILLARY MUSCLE RUPTURE; RCA)
S/S: pulmonary oedema, hypotension, new PSM [no thrill, soft murmur]
MI - ventricular septal rupture - presentation + investigations
Acute / 3-5 days
LAD or RCA
S/S: chest pain, biventricular failure (acute HF), shock, new PSM [thrill, harsh murmur]
Ix: echo (exclude acute mitral regurgitation)
MI - LV free wall rupture - presentation
5 days – 2 weeks
LAD
S/S: HF, tamponade (raised JVP, muffled heart sounds, hypotension, pulsus paradoxus)
MI - aneurysm - presentation + management
left ventricular wall; LAD involvement
S/S: SOB, PERSISTENT ST-ELEVATION, no chest pain, LVF (à thrombus), maybe S3 & S4
Mx: anticoagulation
MI - Dressler’s syndrome/pericarditis - presentation
Dressler’s syndrome (2-6 weeks) (NOTE: pericarditis is <48 hours after MI)
S/S: fever, pleuritic pain, pericardial effusion, raised ESR
MI - Dressler’s syndrome/pericarditis - management
Mx: NSAIDs (ibuprofen) or Aspirin. 2nd line: Colchicine or corticosteroids
MI - reinfarct - investigations
If ?re-infarct 4-10 days after initial MI, use CK-MB (raised for 3-4d) instead of troponin (raised for 10d)
MI - predicting/stratifying prognosis
Killip classification
Acute pulmonary oedema - causes
Cardiovascular (LVF: post-MI, VHD e.g. MR) à elevated PAWP
ARDS (RFs: in trauma, malaria, drugs) à normal PAWP
Fluid overload
Neurogenic (head injury)
Acute pulmonary oedema/acute heart failure - initial management
ABCDE
C/I drugs: STOP BB if HR <50/min, second/third degree AV block or shock
Sit them up à high-flow (15L) O2 (if SpO2 decreased)
IV access + continuous cardiac monitoring + monitor obs + UO + ECG
IV diamorphine (3mg) + IV metoclopramide (10mg) [caution in liver failure and COPD] - venodilator + anxiolytic
IV furosemide (40-80mg) [larger dose in renal failure] - venodilator –> diuretic
SL GTN spray x2 puffs [if SBP ≥100mmHg, use IV GTN] - venodilator
Consider inotropes e.g. dobutamine à vasopressors if unresponsive e.g. noradrenaline
Further management:
Further furosemide [40-80mg]
Further nitrate infusion (isosorbide dinitrate) [maintain SBP ≥90, if it drops <100, treat as per cardiogenic shock]
CPAP / ITU admission
Acute pulmonary oedema - management once stable
Daily weights
Repeat CXR
Manage medications:
Change to oral furosemide
Consider thiazide (if on high doses of furosemide)
ACEi (LV-EF <40%), beta blocker (LV-EF <35%),
Spironolactone
Acute pulmonary oedema - investigations
Ix: ECG –> ABG, BNP –> CXR
Indications for permanent pacemaker
Pacemaker: HB T3, HB T2 MII, HB T2 MI with symptoms, bradycardia, HF, drug-resistant tachy-arrhythmia, bi/tri-fascicular block with symptoms, sick sinus syndrome with symptoms
MI - acute MR - management
Mx: inotropes/vasopressors, surgery*
MI - ventricular septal rupture - management
Mx: analgesia, coronary angio, intra-aortic balloon pump, inotropes/vasopressors, surgery (urgent transfer)
MI - LV free wall rupture - management
Mx: pericardiocentesis + thoracotomy
Cardiogenic shock - causes
MI [tx as per STEMI]
Arrhythmias
Cardiac tamponade
PE, tension-pt
Myocarditis
Valve destruction
Aortic dissection
Cardiac tamponade - management
Senior review
Pericardiocentesis
Cardiogenic shock - investigations
ECG, ABG, CXR, echocardiogram
FBC, U&Es, troponin, BNP, UO [catheterise]
Consider CVP (Swan-Gantz catheter) + arterial lines
Cardiac tamponade - presentation + ECG changes
Beck’s triad = hypotension, raised JVP, muffled sounds
ECG = electrical alternans
Cannot get pulmonary oedema on CXR because the heart will stop before this happens
Cardiogenic shock - management
A-E
Analgesia
Correct arrhythmias, electrolytes, acid-base
Optimise filling pressure: fluids if hypovolaemic, inotropes of normo/hypervolaemic
Consider Swan-Gantz catheter
Aim MAP 70mmHg, CVP 8-10mmHg
Central venous line - complications
Immediate: pneumothorax, arrhythmia, failure, air embolus, bleeding, perf., misplacement
Early: bruise, infection, occlusion
Late: thrombosis, Horner’s, phrenic nerve damage, sepsis, venous stenosis
Pericardiocentesis - needle entry points
Left sub xiphisternal/diaphragmatic approach (pointing towards left shoulder/nipple)
Left 5th ICS near sternal border
Cardiac tamponade vs constrictive pericarditis
JVP
Cardiac tamponade: absent Y descent; constrictive pericarditis: X+Y present
Pulsus paradoxus in cardiac tamponade
Kussmaul’s sign in constrictive pericarditis
Broad complex tachycardia - causes
VT
SVT with aberrant conductions (i.e. AF with BBB – likely if patient stable)
Pre-excited tachycardia (i.e. AF with underlying WPW)
Narrow complex tachycardia - causes
Sinus tachycardia
SVT (all of the below):
- AVNRT (most common)
- AVRT (due to WPW)
- AF / flutter
- Atrial tachycardia (usually 2:1)
- Multifocal atrial tachycardia
- Junctional tachycardia
Adult ALS algorithm
Unresponsive + not breathing –> call for help + 2222 + start CPR (30:2)
Shockable rhythm: non-synchronised shock (defibrillation) every 2 mins, IV adrenaline 1mg + IV amiodarone 300mg after 3 shocks. Repeat adrenaline every 3-5 mins. Amiodarone 150mg after 5 shocks.
Non-shockable rhythm: IV adrenaline 1mg immediately. Repeat adrenaline every 3-5 mins
Adult ALS algorithm - hypothermia
Max 3 shocks before warming to above 30C
Withhold drugs until at least 30C
Types of shock to use
Synchronised DC shock (cardioversion): unstable tachycardia (i.e. with shock/syncope/MI/HF - but NOT VF or pulseless VT)
Non-synchronised DC shock (defibrillation): cardiac arrest i.e. VF, pulseless VT
Normal CVP
0-6mmHg
Types of VT
monomorphic VT: usually due to MI
polymorphic VT: e.g. TdP secondary to long QTc
Contraindications in ventricular tachycardia
CI: verapamil (also CI in chronic HF as can precipitate AHF)
Defibrillation - when to give stacked shocks
if the cardiac arrest is witnessed in a monitored patient (e.g. in CCU) then perform ‘up to 3 quick successive (stacked) shocks’ followed by CPR
Adult ALS algorithm - thrombus
If PE –> alteplase
If alteplase given, CPR should be continued for 60-90 minutes
Torsades de Pointes - management
Drug-induced à 2g Mg sulphate over 10mins
Correct any electrolyte abnormalities and stop drugs prolonging QT interval (which leads to TdP)
Differentiation between VT vs [SVT with BBB]
Fusion/capture beats (P waves that have gotten through to the ventricles via the AVN) = VT
If unsure, treat as VT
in SVT with BBB, blocking AVN pauses tachycardia
Bradycardia - causes
Physiological
Cardiac (i.e. post-MI, sick sinus syndrome, aortic valve disease, cardiomyopathy, sarcoid)
Non-cardiac (i.e. vasovagal, hyperkalaemia, hypothermia, raised ICP ‘Cushing’s triad’, hypothyroid)
Drug-induced (beta blockers (if beta blocker OD, give glucagon), amiodarone, verapamil, diltiazem, digoxin)
Bradycardia - management algorithm
A-E
Unstable (shock/syncope/MI/HF) or risk of asystole: IV atropine 500mcg, repeat up to 3mg max
Interim measures: isoprenaline, adrenaline, aminophylline, dopamine, glucagon if BB/CCB overdose, transcutaneous pacing
Senior: transvenous pacing
No risk of asystole: observe
