Shoulder X-Ray Crib Sheet

  1. Usual details
  2. Bones – clavicle, scapula, humerus – #, deformities, sclerosis, degeneration, acromion morphology (hooked implies impingement of supraspinatus)
  3. Joint spaces –  ACJ (in line with small gap), GHJ
    1. In the axillary Y-view (lateral) look for coracoid and humerus. Humerus anterior to coracoid = anterior dislocation. Humerus posterior to glenoid = posterior dislocation. Humerus posterior to coracoid overlying glenoid = normal
  4. Spaces and Lines
    1. Space between humerus and acromion should be >6mm, less implies supraspinatus impingement
    2. Gothic arch line between scapula and humerus – disruption implies #
Gothic Arch

Gothic Arch

Axillary Y-view

Axillary Y-view

Wrist X-Ray Crib Sheet

  1. Usual details of film
  2. Bones – #, sclerosis, cystic degeneration, deformities
  3. Joints – loss of joint space implies OA, increase in joint space implies ligamentous injury
  4. Lines and angles
    1. Radial inclination – normal is 15-25 degrees; loss of radial inclination implies a bad reduction
    2. Volar tilt – normal is 10-25 degrees, a negative volar tilt indicates dorsal angulation of the distal, radial articular surface
    3. Ulnar variance
      1. Ulnar variance refers to the difference between the levels of radial and ulnar articular surfaces
      2. Ulnar variance is said to be neutral if articular surfaces of radius and ulna are at the same level, positive if ulnar articular surface is distal to radial and negative if ulnar articular surface is proximal to radial
      3. Negative ulnar variance is associated osteonecrosis of lunate bone
      4. Positive ulnar variance is associated with, scapholunate instability, ulnar impaction syndrome, triangular fibrocartilage tears lunotriquetral ligament tears and previous excision of radial head

Radial inclination

Volar tilt

Hip X-Ray Crib Sheet

  1. Hedge and play for time
    1. Name, age, film details etc.
    2. Comment on position (testicles should be symmetrical, cocyx and pubic symphysis should have a 2cm gap [impiclication of less gap is pelvic tilt])
  2. Identify the bones – femur, pubis, ischium, illium, acetabulum, sacrum, coccyx, comment on #, sclerosis, osteopenia, deformity
  3. Identify the joints – sacroilliac, pubic symphysis and commment on joint space increase or loss
  4. Lines
    1. Shenton’s line – loss of arch implies NOF
    2. Illioischial line – represents the posterior column, disruption impllies PC#
    3. Illiopectineal line – represents the anterior column, disruption implies AC#

 

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ECG Crib Sheet

  • Frequency
    • Number of QRS in the rhythym strip X 6 gives you the rate
    • Dividing 300 by the number of big boxes between QRS also gives you the rate
  • Rhythm
    • SVT
      • AVNRT – reentrant circuit in the AVN. Regular SVT, retrograde P waves in II, III, aVF; possible pseudo R’ wave in V1 or V2, seudo S in II, III or aVF.
      • AVRT – assoc. WPW or LGL; retorgrade P waves in I,II, aVF but occurs a tad later than would see in AVNRT
      • Flutter – Regular, saw-toothed, 2:1, 3:1, 4:1 rtc. block, carotid massage increases block. Note that QRS complexes can be irregular – the atrial flutter is regular, the conduction block may be variable. Note coarse AF in V1 may mimic AFL as the crista terminalis of the RA serves as an anatomic barrier. Inverted P-waves in II provide a useful clue.
      • Fibrillation – Irregular, undulating baseline
      • MAT – Irregular, >3 P wave morphologies, no effect of carotid massage – hallmark of pulmonary disease
      • PAT – Regular, warm-up period, carotid massage inefficacious
    • VT
      • Accelerated idioventricular rhythym  – ‘looks like slow VT’
      • VT – this should be pretty regular. Use your calipers – if irregular consider A-fib with rapid ventricular response and aberrancy (eg. AF + BBB)
      • V-fib, PVCs,
      • Torsade de pointes – QRS spins around the baseline changing axis and amplitude (Mx = Mg)
  • Axis
    • RAD – QRS is positive (dominant R wave) in leads III and aVF, QRS is negative (dominant S wave) in leads I and aVL
      • Right ventricular hypertrophy
      • Things that causes right heart strain – COPD, PE
      • WPW
      • Left posterior fascicular block
      • Lateral MI
    • LAD – QRS is positive (dominant R wave) in leads I and aVL, QRS is negative (dominant S wave) in leads II and aVF
      • LV hypertrophy
      • WPW
      • Left anterior fascicular block
      • Inferior MI
      • LBBB
  • Conductance
    • AV blocks
      • First degree = PR >0.2s
      • Second degree = Mobitz I Weckenbach progressive prolongation until beat is dropped, Mobitz II were bests are dropped with no prolongation
      • Third degree = diassociation
    • BBB
      • RBBB – QRS >0.12, RSR in V1 and v2 with STD and TWI
      • LBBB – QRS >0.12, broad or notched R wave with prolonged upstroke in V5, V6, I and aVL with STD and TWI, reciprocal V1 and V2 changes, LAD
      • Left anterior hemiblock – Isolated LAD between -30 and +90
      • Left posterior hemiblock – Isolated RAD
      • Note that RBBB does not causes RAD so any RBBB pattern plus axis deviation = RBBB + appropriate hemiblock
    • Pre-excitation syndromes
      • WPW – Short PR(<0.12), wide QRS, delta waves; antidromic AVR mimics VT
      • LGL – Short PR (<0.12), normal QRS, no delta wave
  • Hypertrophy
    • LVH
      • R wave in V4, V5 or V6  > 26 mm
      • R wave in V5 or V6 plus S wave in V1 > 35 mm
      • ‘Non voltage criteria’
        • Increased R wave peak time > 50 ms in leads V5 or V6
        • ST segment depression and T wave inversion in the left-sided leads: the left ventricular ‘strain’ pattern
      • RVH – triad of  tall R wave in V1 with marked RAD and tall peaked P wave – pulm stenosis or pulm art HTN
  • Ischemia
    • Bowed upwards elevated ST merging imperceptibly with T-wave >2mm in V2 and V3 or >1mm in 2 other contiguous leads
    • Widespread ST depression + STE in aVR>1mm is LAD or LMCA or 3VD
    • STE in aVR > STE in V1 indicates LMCA over LAD
    • New LBBB = STEMI
    • ST depression = either posterior infarct (reciprocal to posterior STE) or NSTE-ACS
    • STE without the typical rounded, domed appearance of STEMI which returns to baseline with nitroglycerin = Prinzmetal’s
    • TWI with no reasonable explanation = treat as NSTEMI; V1 and V2 acceptable in white people, V3 in black people, always pathological in V4,5 and 6
    • U wave inversion with hx chest pain, specific for MI
    • Wellen’s syndrome = +++ risk for critical stenosis of LAD; risk of anterior MI within a month, can be pain free when ECG taken
      • Deep and symmetrically inverted T waves OR biphasic T waves with the initial deflection positive and the terminal deflection negative in V2, V3
    • Sgarbossa criteria
      • In LBBB, there is appropriate discordant ST changes
      • Concordant STE >1mm in positive QRS leads, concordant STD >1mm in V1-V3 and discordant STE>5mm in negative QRS leads
      • Possibly also applicable in dual-chamber pacing
  • Random other stuff
    • Electrical alterans – tamponade
    • Brugada – coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave
    • Pericarditis – aVR PR elevation and ST depression is pathognomonic. Diffuse STE, PR depression, T wave flattening/inversion
    • PE – RBBB, RAD, sinus tachy, S1Q3T3 (not all that common)
    • Digitalis effect = asymmetric STD with flattening or inversion of T wave
    • Renal failure = triad of “tented” T waves (hyperkalemia) with long QT (ST segment prolongation of hypocalcemia) and LVH (hypertension)
  • Lead-by-lead Review of Non-Obvious Things
    • PQRST
      • Reduced PR of WPW and LGL
      • Long QT
    • II – inverted P wave (AFL), negative QRS in LAD
    • aVR – LMCA/LAD, pericarditis
    • aVL – negative QRS in RAD
    • V1, V2, V3 – Brugada and Wellens

An Astonishingly Applicable Alliterative Approach to the ABG

1.       Determine the pH

pH>7.45                               Alkalosis
pH<7.35                               Acidosis

2.      Determine the primary cause

Bicarbonate pCO2 pH
Metabolic acidosis <7.35
Metabolic alkalosis >7.45
Respiratory acidosis <7.35
Respiratory alkalosis >7.45

The bicarbonate and pCO2 should trend in the same direction. If they do not, this is an indication for a mixed metabolic/respiratory picture. For example, an acidotic patient with decreased bicarbonate and increased pCO2 would lead you to suspect a metabolic acidosis with a respiratory acidosis.

3.     Determine if there has been adequate compensation

If the bicarbonate and pCO2 are trending the same way, there is still the possibility of a mixed acidosis/alkalosis picture. Rule this out by calculating the expected compensations.

Metabolic acidosis pCO2 = 1.5 [HCO3] + 8 mmHg +/- 2
Metabolic alkalosis pCO2 = 0.7 [HCO3] + 20 mmHg +/- 5

For respiratory alkalosis/acidosis, use the 1,2,3,4,5 rule of thumb

 10 mmHg change in pCO2

HCO3

Acute

Chronic

1

4

2

5

4.      Calculate the anion gap

The anion gap is useful in cases of metabolic acidosis
It is calculated by Na+ K– Cl– – HCO3

Since organic acids are anions, any increase in an organic acid will result in a high-anion gap metabolic acidosis (HAGMA)
A normal anion-gap metabolic acidosis, on the other hand, is likely due to excessive loss of bicarbonate

The mnemonic for HAGMA causes is MUDPILES (Methanol, uremia, DKA, propylene glycol, infection, lactic acidosis, ethylene glycol, salicylates)

The mnemonic for NAGMA causes is HARDUP (hyperalimentation, acetazolamide, renal tubular acidosis, diarrhoea, uretoenteric fistula, pancreaticodudodenal fistula)

5.     Calculate the delta ratio

The delta ratio is given by Change in Anion gap : Change in bicarbonate

The theory is that any change in anion gap due to an organic acid should be reflected by a corresponding change in bicarbonate
The ratio should be used with caution and with corroborative evidence

If the ratio is 0.4-0.8; the implication is that the HAGMA alone is not sufficient to explain the change in bicarbonate and a mixed HAGMA NAGMA may be present.

If the ratio is >2; the implication is that there is a pre-existing elevated bicarbonate which can be due to a concurrent metabolic alkalosis or a pre-existing compensated respiratory acidosis