Emergency Medicine Flashcards
Aspects of A-E assessment
Identify a problem and deal with it as going along…
Airway - patent? look, listen and feel –> head tilt + chin lift, jaw thrust, airway adjunct
Breathing - RR, O2 Sats (>94% - scale 1, 88-92% - scale 2 if COPD), resp exam, ABG –> Oxygen (15L/min O2 non-rebreather mask)
Circulation - HR, BP, CRT, cardio exam –> IV fluids
Disability - BM, pupils (PEARL - pupils equal and reactive to light), GCS/AVPU, abdo/neuro exam
Exposure - calf tenderness, bleeding, bruising, rashes etc.
COPD breathing problem Ix? Mx?
Ix: ABG, ECG, CXR, FBC, U&E
Infective exacerbation of COPD Oon CXR: emphysematous changes, opacity, flattened diaphragm + hyperexpanded chest
Acute Mx:
- 15L/min O2 non-rebreather mask (despite COPD)
- Salbutamol NEB - back to back
- IpB NEB - 6 hourly
On discharge:
- Pred for 7 days
- PO Abx (e.g. co-amox)
Reassess:
- If O2 sats increasing, RR decreasing and HR decreasing
- Continue abx/steroids, wean off nebs + O2
PaO2 (Partial Pressure of Oxygen) normal range?
Normal: ≥10 on room air
On Oxygen: PaO2 (kPa) should be 10 less than FiO2 (level of oxygen they are on %)
Reading an ABG?
Low O2 = T1RF
Low O2 + High CO2 = T2RF
Low pH + high CO2 = Respiratory acidosis (low CO2 = metabolic)
High pH + low CO2 = Respiratory alkalosis (high CO2 = metabolic)
NOTE: if bicarb is high in RA = chronic RA (compensation by bicarb is slow) –> this determines if should be on scale 1/2 O2 (scale 2 = 88-92%)
When to do ABG vs VBG?
ABG (radial artery) - acute breathing problem
VBG (venous) - check lactate, glucose, elctrolytes FAST
Oxygen therapy principles
Oxygen from wall = 100%
Peak inspiratory flow - the maximum rate of drawing in O2 normally is 20L/min (not normally measured unless ITU)
O2 therapy goal is increasing conc grad between alveoli and blood - done by increasing FiO2 (fraction of inspired O2)
Devices types: 1) variable (can’t guarantee FiO2, depends on PIF) - nasal cannula, hudson mask, non-rebreather mask 2) fixed - venturi mask (useful if COPD as need to know exactly how much O2 giving)
NOTE: If PIF increases (breathing harder) –> FiO2 decreases so more device O2 is required
High-flow nasal oxygen therapy - humidifies + warms O2 = well-tolerated –> very high flow rate can be achieved - finely controlled FiO2
O2 therapy vs ventilation
O2 therapy - increase FiO2 so bigger conc gradient between alveoli and bloodstream (of part of the lung that is working)
Ventilation - pressure increases SA of lungs available for gas exchange e.g. if part of the lung is blocked off (e.g. mucus, collapse)
SO COMBO IS NORMALLY USED
AKI - key things to do?
1) Check trend
2) Check drug chart (any nephrotoxic?) –> remove/replace
* Common: Metformin (increases risk of lactic acidosis), ACEi (reduces renal perfusion pressure), NSAIDs, diuretics (unless congestive heart failure - may have AKI from fluid overload)
3) Check fluids (pre-renal - dehydration) –> give fluids
Case 1 Learning points
Bibasal crackles indicates what? Ix? Mx?
Fluid overloaded with pulmonary oedema = acute heart failure
HF = pumping of blood by heart isn’t meeting body demands
Ix:
- Bedside - ECG
- Bloods - ABG, troponin, BNP
- Imaging - CXR, Echo (further down the line)
Acute HF Initial Mx:
- Immediate: sit patient up, O2 15L/min NRM
- Medical: IV furosemide (higher dose if on LT Tx), GTN, Morphine IV
- If no improvement: repeat furosemide (after 15mins) –> consider CPAP
Types of Non-Invasive Ventilation
CPAP = fixed IPAP and EPAP
- Holds open/splints airways –> for T1RF –> increase O2
BiPAP = IPAP higher than EPAP
- Gradient allows exhalation more easily –> for T2RF –> excrete CO2
(- If had high CO2 on ABG –> increase IPAP –> more excreted CO2)
CXR for HF
Bilateral opacification
Cardiomegaly
CXR for Infective Exacerbation of COPD (IECOPD)
Emphysematous changes
Opacity
Flattened diaphragm + hyperexpanded chest
ECG Important Considerations
- Make sure to compare to a previous ECG = dynamic changes (acute)
- Coronary infarcts commonly present as T-wave inversion/RBBB/LBBB, not always with ST-elevation/depression
NSTEMI Mx? Scoring? Ix?
Immediate:
- Aspirin PO stat AND Ticagrelor OR Clopidogrel PO stat
- Fondaparinux SC
On discharge (give all despite BP/HR):
- Aspirin for life
- Ticagrelor OR Clopidogrel for 1 year (2 needed for 1 year as stent impregnated with Tacrolimus
- Ramipril (ACEi) - titrate up to 10mg
- Atorvastatin
- Bisoprolol (B-blocker) - titrate up to 10mg
Scoring Risk: GRACE score
Ix if high risk: cathlab for angiogram (will be started on IV unfractionated heparin instead of fondaparinux as procedure is very thrombogenic) –> PCI (stent)
Acute HF vs ACS
Irregularly irregular heart rhythm - Dx? Ix? Mx?
AF - II narrow complex tachycardia with no p-waves
Ix:
- ECG, Echo (valve check)
- Bloods - U&E, Mg (QT interval), Troponin (ischaemic), TFTs
Mx:
- Haemodynamically unstable –> DC cardioversion
- Rate control - Bisoprolol 2.5mg OD (max 10mg, can use rate-lim CCB)
- Rhythm control - if clear reversible cause: <48hrs = DC/chemical cardioversion (flecanide/amiodarone); >48hrs = anticoag 3-4wks (clot may have formed)
- Stroke risk Mx - CHADS-Vasc Vs HAS-BLED/ORBIT - Apixabab 5mg BD (DOAC, can use Warfarin)
Types of anticoagulant
- Heparins
- LMWH (SC) - VTE prophylaxis BUT bad for renal function
- UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring
- DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)
- Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions
EtOH XS (alcohol excess) management?
- Pabrinex (thiamine, B1) - prevent Wernicke’s encephalopathy (ophthalmoplegia, ataxia, confusion)
- Chlordiazepoxide (decreasing regimen + PRN) - prevent alcohol withdrawal Sx (anxiety, shakes etc.) + CIWA scoring (dose increased inf CIWA score increases)
- Bloods - coagulation (injury, bleeds), LFTs
Management of decompensated chronic liver disease?
Ascites
- Dx:
-
Serum Ascites Albumin Gradient (SAAG) - serum albumin conc vs ascites conc - 11.1g/L
- <11.1g/L = exudative cause - infection/inflammation (albumin leaking into ascites) OR nephrotic syndrome (pee out albumin so low serum albumin)
- Otherwise = transudative cause from portal HTN
- >250 neutrophils = spontaneous bacterial peritonitis (SBP) –> Tazocin/3rd gen cephalosporin
-
Serum Ascites Albumin Gradient (SAAG) - serum albumin conc vs ascites conc - 11.1g/L
- Mx:
- Paracentesis –> post-paracentesis circulatory dysfunction SO if >5L drained give human albumin solution (HAS) 8g/L drained
- Spironolactone (2nd line - Furosemide) - prevent reaccumulation
Hepatic encephalopathy (liver not dealing with toxins) - give Lactulose + Rifaximin to prevent
Coagulopathy - OGD (check for varices) + vit K (needed for clotting)
Major hemorrhage GI Mx?
High risk of variceal bleed:
- MASSIVE –> balloon tamponade
- Assess - A-E approach:
- Circulation –> blood transfusion (Hb <70) but if haemodynamically unstable and waiting give IV fluids
- Drugs
- IV Terlipressin(/Somatostatin) - blanked vascoconstriction
- Ceftriaxone/Norfloxacin (apparently helps outcomes)
- Intervention - endoscopic band ligation
F1 essentials: 2x large bore cannula, VBG, G&S + X-Match, bleep the bleed registrar (arrange endoscopy)
How does lactic acidosis appear on VBG? Lactate physiology/pathology?
Acute metabolic acidosis - low pH, low cHCO3/low BE, high lactate
Physiology:
- Glucose –> Pyruvate –O2–> mitochondria –> ATP
- Glucose –> Pyruvate –NO O2–> Lactate (+ small ATP) –> excreted by kidney or liver/muscle –gluconeogenesis –> glucose
Pathology:
- Hypoxia
- Reduced oxygen delivery - from reduced circulating volume (bleed), vascular compromise (clot)
- Reduced oxygen carriage - reduced gas exchange, anemia
- Mitochondrial toxicity - mitochondria can’t aerobically produce ATP
- Drugs - metformin, propofol, cyanide
- Inherited - MELAS
- Reduced metabolism (of lactate) - liver/renal impairment, muscle compromise
- Increased glycolysis (more pyruvate) - both paths increase
- Increased glucose uptake from adrenergic stimulation e.g. salbutamol use
- Increased energy demand of cells - exercise
How to think about inf for abx? What are the best broad-spectrum abx? Abx for pseudomonas cover?
- where is the infection? e.g. resp, skin, cardio etc.
- what are the common organisms that cause these infections? mainly G+ve or -ve?
G+ve: staph, strep, C. diff –> pneumonia, skin inf, colitis, sepsis
- B-lactams:
- Penicillins (peptidoglycan cell wall) - amox, co-amox, fluclox, tazocin
- Cephalosporins (cover -ve’s as well) - ceftriaxone, cefuroxime, cefalexin
- Carbapenems (holy grail) - meropenem
- NOTE: ESBL (extended spectrum b-lactamase) - bacteria that are not sensitive to Pen + Cephalosporins
- NOTE: Carbapenemase - resistant to carbapenems as well
- Macrolides - for pen allergic = Clari, erythromycin
- Glycopeptides - vancomycin, teicoplanin (good if pen allergic)
- Oxazolidinones - linezolid (rarely used)
G-ve: E.coli, P. aeruginosa, K. pneumo, salmonella –> UTI, pneumonia, GI inf
- Aminoglycosides (nephrotoxic –> monitoring) - gent, amikacin
- Fluoroquinolones - cipro/levo/moxifloxacin
- NOTE: broad spectrum so some +ve cover
Other antibiotic types:
- Tetracyclines - doxy
- Broad-spectrum intracellular pathogens (chlamydia, mycoplasma) –> STIs, pneumonia
- Nitroimidazoles - metro
- Anaerobes (c. diff, bacterial vaginosis) –> aspiration pneumo, abscesses
- NOTE: nitrofurantoin (related compound) - concentrates in bladder –> UTI
Best broad-spectrum abx:
- Co-amox: most G-ve AND +ve AND anaerobes
- Does not cover pseudomonas + Neisseria spp.
- Tazocin: as above AND pseudomonas
- Does not cover Neisseria gonorrhoea
- Meropenem: EVERYTHING (bar carbapenemase bacteria)
Abx for pseudomonas cover: gentamicin, amikacin, ciprofloxacin, ceftazidime
