Investigations Flashcards

1
Q

Acidosis

A

Metabolic
— increased acid production e.g. ketones (DKA), lactate (shock)
— acid ingestion e.g. salicylates
— failure to excrete hydrogen ions e.g. renal failure, distal renal tubular acidosis, carbonic anhydrase inhibitors
— loss of bicarbonate e.g. proximal renal tubular acidosis, D+V, GI fistula

Respiratory
— increased PaCO2 secondary to alveolar hypoventilation

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2
Q

Anaemia

A

Aetiological Classification
* impaired RBC production
— abnormal bone marrow - aplastic anaemia, myelofibrosis
— essential factors deficiency - iron, B12/folate, EPO (renal disease)
— stimulation factor deficiency - anaemia in chronic disease, hypothyroidism, hypopituitarism
* excessive destruction of RBCs
— intracorpuscular defect - membrane (hereditary spherocytosis), enzyme (G6PD deficiency), Hb (thalassaemia, haemoglobinopathies)
— extracorpuscular defect - mechanical (microangiopathic haemolytic), infective (clostridium titani), antibodies (SLE), hypersplenism
* blood loss
— acute - trauma, acute GI bleed
— chronic - parasitic infection, chronic NSAID use

Morphological Classification
* macrocytic (MCV >94, MCHC >31)
— B12 deficiency - pernicious anaemia
— folate deficiency - nutritional
— drug-induced abnormal DNA synthesis - anti-convulsant, chemotherapy
* microcytic hypochromic (MCV <80, MCHC <31)
— IDA - chronic blood loss, decreased intake, increased demand, malabsorption
— abnormal globin synthesis (thalassaemia, SCD)
* normochromic normocytic
— blood loss
— increased plasma volume (pregnancy)
— hypoplastic marrow
— endocrine - hypothyroidism, adrenal insufficiency
— renal and liver disease

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3
Q

Anion Gap

A
  • (Sodium (+ Potassium)) - (Chloride + Bicarbonate)
  • Normal = 8-16mEq/L

Raised anion gap
— accumulation of organic acids
— impaired hydrogen excretion
— lactate - metformin
— toxins - CO, CN, alcohol, toluene, ethylene glycol, salicylates
— ketones - DKA
— renal - uraemia

Normal anion gap
— loss of bicarbonate from Extracellular fluid (GI causes)
— Addisons
— CA inhibitors (acetazolamide)
— chloride excess

Low anion gap
— decreased unmeasured anions (albumin, dilution)
— increased unmeasured cations (multiple myeloma, increased calcium/magnesium, lithium OD)
— non random analytical errors

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4
Q

C-Spine X-ray

A

A - adequacy
A - alignment
— Atlantic-occipital
— vertebral - anterior vertebral line, posterior vertebral line, spinolaminar line, interspinous line
B - bony landmarks
C - cartilaginous space
D - disc space
S - soft tissue

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5
Q

CPET

A

Dynamic, non invasive assessment of the cardiopulmonary system at rest and during exercise.
Determine the functional capacity of an individual.

  • electromagnetically braked cycle ergometer (with predetermined ramp of pedalling resistance - hand ergometer/treadmill as alternative)
  • rapid gas analyser for breath by breath expired gas concentrations (IR)
  • pressure differential pneumotachograph for spirometry and RR
  • continuous 12-lead ECG
  • continuous SpO2
  • NIBP

Nine panel plot
* cardiovascular system 2, 3, 5
* ventilation 1, 4, 7
* VQ relationships 6, 8, 9

VO2peak = maximum oxygen consumption (<15mlO2/kg/min represents an increased risk of Perioperative complications)
Anaerobic threshold = the point at which the cardiopulmonary system is unable to meet the oxygen demand of the muscles and switches to anaerobic metabolism (AT <11mlO2/kg/min would put the patient into a higher-risk group)

Patterns of Physiological Limitation
* Cardiac - reduced VO2peak, early onset AT, typically limited by leg fatigue/angina, peak HR does not reach max, higher ventilatory equivalent for CO2, BP not increasing normally with exercise
* Respiratory - reduced VO2peak, exhaustion due to ventilatory limitation prior to AT, elevated VE for VO2/VCO2, decreasing tidal volumes, low O2 sats, limited by dyspnoea
* Pulmonary Vascular Disease - reduced VO2peak, elevated HR disproportionate to work rate, desaturation with progressive exercise, low ETCO2, early onset AT

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6
Q

CSF Results

A

Normal:
* clear and colourless
* WCC 0-5 cells/uL (predominantly lymphocytes)
* RBC 0-5/uL
* Protein 0.15-0.45g/L (or <1% of the serum protein concentration)
* Glucose 2.8-4.2mmol/L (or >60% of the serum glucose concentration)
* opening pressure 10-20cmH2O

Bacterial Meningitis
* cloudy/turbid fluid
* elevated WCC >100/uL (primarily polymorphonuclear leukocytes)
* Elevated protein >0.5g/L
* low glucose (<40% serum)
* elevated pressure >25cmH2O
* CSF microscopy, gram stain + culture, PCR, blood cultures, imaging for other pathology?
— gram positive diplococci - pneumococcal
— gram negative diplococci - meningococcal
— gram positive rods/coccobacilli - listerial

Viral Meningitis
* usually clear
* elevated WCC >100/uL (primarily lymphocytes)
* elevated protein > 0.5g/L
* normal glucose >60% serum
* normal or elevated pressure
* viral PCR

Tuberculous Meningitis
* opaque, if left to settle it forms a Fibrin web
* WCC elevated - typically lymphocytes
* protein elevated - 1-5g/L
* low glucose
* elevated opening pressure

Fungal Meningitis
* clear or cloudy
* elevated WCC (typically more modest elevations)
* elevated protein
* low glucose
* elevated opening pressure

SAH
* blood stained initially, with xanthochromia (yellowish appearance) >12hrs later
* WCC elevated
* RBC elevated
* protein elevated
* normal glucose
* elevated opening pressure

MS
* clear
* WCC 0-20/uL (primarily lymphocytes)
* protein mildly elevated 0.45-0.75g/L
* glucose normal
* normal opening pressure
* oligoclonal bands present on electrophoresis

GBS
* clear
* WCC normal
* protein markedly elevated >5.5g/L
* glucose normal
* opening pressure normal or elevated

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7
Q

CXR

A

Projection
Rotation
Inspiration
Penetration

Airway - trace trachea to hila - shifts, foreign bodies, other abnormalities, hilar mass
Breathing - lung from apices to diaphragm, pleura - pulmonary opacifications (air space/interstitial/nodular), air bronchograms, Kerley A/B/C lines
Circulation - heart - trace borders, cardiothoracic ratio, mediastinum - silhouette sign, mediastinal mass (anterior/middle/posterior
Diaphragm - costophrenic and cardiophrenic angles
Everything else
— bone - deposits, fractures
— intervention - tubes, lines, drains, pacemaker, valves
— tissue - surgical emphysema

The trachea is central and the hila are normal. Lung fields are clear with no air or fluid collection. There is no free air under the diaphragm and the angles are clear. The bones and soft tissues appear normal.

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8
Q

Diffusing Capacity of the Lungs for Carbon Monoxide (DLCO)

A

Indirectly measures the ability of the lungs to transfer oxygen to the blood

DLCO = Va x Kco (Va = surface area of the lung available for gas exchange, Kco = rate of alveolar capillary blood CO uptake)

Normal = >75% of predicted (up to 140%)
<60% predicted is associated with increased mortality in thoracic surgery
<80% associated with increased pulmonary complications

  • Causes of increased DLCO
  • exercise, supine, pulmonary haemorrhage, polycythaemia, left to right shunt (e.g. ASD), obesity, mild LVF, asthma, pregnancy, morning
  • Causes of decreased DLCO
  • post exercise, standing, valsalva, lung resection, emphysema, interstitial lung disease, anaemia, evening, drugs (e.g. bleomycin, amiodarone), PAH, PE, CTEPH, cardiac insufficiency

** Specific Patterns**
* Normal DLCO with restrictive pattern
* kyphoscoliosis, morbid obesity, neuromuscular weakness, pleural effusion

  • Normal DLCO with obstructive component
  • alpha-1 antitrypsin deficiency, asthma, bronchiectasis, chronic bronchitis
  • Low DLCO with restriction
  • asbestosis, berylliosis, hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, langerhans cell histiocytosis, lymphangitic spread of tumour, miliary TB, sarcoidosis, silicosis (late)
  • Low DLCO with obstruction
  • CF, emphysema, silicosis (early)
  • Low DLCO with normal PFTs
  • CTEPH, CHF, CTD with pulmonary involvement, dermatomyositis/polymyositis, IBD, early ILD, primary pulmonary hypertension, RA, SLE, systemic sclerosis, granulomatosis with polyangitis
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9
Q

ECG Changes

A

ST elevation
- MI
- LBBB
- myocarditis
- hyperkalaemia
- LVH
- pericarditis
- hypothermia
- PE
- cardiac trauma
- SAH/raised ICP
- normal variant (early repolarisation)
- ventricular aneurysm

T wave inversion
- normal in leads III, AVR, V1-2
- MI
- LBBB, RBBB
- SAH/raised ICP
- LVH + RVH
- cardiomyopathies
- PE
- ECT
- drugs
- electrolyte disturbance
- persistent juvenile pattern

Left Axis Deviation (+ve QRS in lead I, -ve QRS in lead II)
- LVH
- LBBB
- mediastinal shift
- LAFB
- inferior MI
- primum ASD
- pre-excitation
- hyperkalaemia

Right Axis Deviation (-ve QRS in lead I, +ve QRS in lead II)
- RVH
- PE/COPD/Cor pulmonale
- mediastinal shift
- LPFB
- secundum ASD
- pre-excitation
- hyperkalaemia
- dextrocardia
- normal variant (tall, slim)

LBBB - widened QRS “WiLLiaM,” LAD, TWI laterally

RBBB - widened QRS “MoRRoW”

Bifascicular Block - RBBB with axis deviation

Trifascicular Block - bifascicular block with prolonged PR interval

AV nodal Block - prolonged PR (I, II Mobitz 1/2, III)

Left anterior fascicular block - small inferior r waves, small lateral q waves, dominant r waves laterally, dominant S waves inferiorly, slightly wide qrs (<120ms) —> exclude inferior MI and other causes of left axis deviation

Left posterior fascicular block - small r wave laterally, small inferior q waves, dominant inferior R waves and lateral S waves, slight prolongation of QRS —> exclude lateral MI and other causes of right axis deviation

Left atrial hypertrophy - notched p in lead II (p mitrale), wide deep negative p wave in V1

Right atrial hypertrophy - tall/peaked p wave (p pulmonale)

Left ventricular hypertrophy - voltage criteria (e.g. S in V1 + tallest R V5-6 >35mm), no voltage criteria (e.g. ventricular activation time >50ms in V5-6 + strain)
- hypertension
- aortic stenosis
- aortic regurgitation
- mitral regurgitation
- HOCM
- coarctation
- normal variant (young/thin)

Right ventricular hypertrophy - increased QRS in V1-3 +/- ST depression or TWI
- chronic lung disease (COPD, pulmonary arterial hypertension, PE)
- pulmonary stenosis
- mitral stenosis
- HOCM
- Right ventricular cardiomyopathy
- CHD

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10
Q

ECGs

A

Hyperkalaemia - tented T wave, prolonged PR, flattened P wave, prolonged QRS, sine wave —> VF

Hypokalaemia - tall, wide P waves, prolonged PR, flattened/inverted T wave, decreased ST segments, U waves, SVT/VEs/AF/VT

Hypercalcaemia - short QT, J waves, VF

Hypocalcaemia - prolonged QTc (long ST), Torsades, AF

Hypermagnesaemia - decreased HR, prolonged PR/QRS/QT, AV block

Hypomagnesaemia - flattened T wave, U waves, prolonged PR/QRS/QT, decreased ST segments, atrial/ventricular arrhythmias

Hypothermia - J waves, prolonged PR/QRS/QT, VEs, AF, bradycardia, arrest (VT/VF/asystole), shivering artefact

Digoxin therapy - reverse tick ST depression, biphasic T waves, prominent U waves

ECT therapy - arrhythmia, diffuse T wave inversion

PE - deep S in I, q in III, inverted T in III (20%), RV strain pattern (34% - TWI V1-4 +/- inf leads), sinus tachycardia (44%), ST/T changes (50%)

Pericarditis (4 stages) - diffuse ST elevation with PR depression —> resolution of stage 1 with T wave flattening —> deep T wave inversion —> resolution

STEMI - minutes - hyperacute T waves —> ST elevation; hours - Q waves and TWI; days - ST normalisation; weeks - persistent Q waves, T waves normalise
* LAD occlusion - septal V1-V2, anterior V3-V4, lateral V5-V6+aVL
* LCX (+RCA) occlusion - posterior V7-9 + left axis deviation
* RCA occlusion - inferior II, III, aVF + right axis deviation

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11
Q

ECGs in Pregnancy

A

Normal Findings
* Tachycardia
* Left axis deviation
* Small q waves
* T wave inversion in lead III
* ST depression and TWI/flattening in inferior/lateral leads
* atrial and ventricular ectopics

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12
Q

Hypercalcaemia (Hyperparathyroidism)

A

Malignancy
— primary
— bony metastases

Increased intake
— milk alkali syndrome

Vitamin D metabolic disorders
— hypervitaminosis D (vitamin D intoxication)
— idiopathic hypercalcaemia of infancy
— rebound hypercalcaemia after rhabdomyolysis

Renal Failure

Adrenocortical insufficiency

Disorders related to high bone-turnover rates
— hyperthyroidism
— prolonged immobilisation
— thiazide use
— vitamin A intoxication
— multiple myeloma

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13
Q

Hyperchloraemia

A

Usually associated with Hypernatraemia, and inversely to bicarbonate.

Drugs
* acetazolamide, aspirin OD, steroids, oestrogens
* thiazides, androgens
* IV NaCl replacement

Metabolic
* respiratory alkalosis - decreased C, K, Mg, increased Cl
* metabolic acidosis (normal anion gap metabolic acidosis)

Endocrine
* hypothalamic lesion (increased Na, decreased thirst perception)
* adrenocortical hyper function

Renal
* renal tubular acidosis
* acute renal failure
* diabetes insipius

GIT
* dehydration
* prolonged diarrhoea

Fictitious
* bromide toxicity

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14
Q

Hyperkalaemia

A

Increased intake
— IVI
— oral (potassium supplements)
— blood transfusion
— GI haemorrhage

Decreased renal excretion
— renal failure (acute and chronic)
— adrenocortical insufficiency - hypoaldosteronism, Addisons
— chronic active hepatitis
— obstructive uropathy
— drugs (ACEI, K-sparing diuretics, ARBs, heparin, beta blockers, phenylephrine, digoxin, trimethoprim, amiloride)

Increased release of potassium out of tissues
— trauma/tissue injury
— crush injuries
— malignant hyperthermia
— rhabdomyolysis
— suxamethonium
— intense physical activity
— tumour lysis syndrome
— haemolysis
— burns
— ischaemia

Trans cellular shift
— metabolic acidosis (DKA etc)
— respiratory acidosis

Artefactual
— haemolysed sample
— laboratory error
— leukocytosis, thrombocytosis
— sample taken from IV running potassium containing fluid

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15
Q

Hypermagnesaemia

A

Iatrogenic
— hyperalimentation
— IV and oral magnesium
— laxatives, enemas, antacids (especially in elderly and renal failure)

Renal Failure

Other
— perforated viscus with continued oral intake
— tumour lysis (increased K, Mg, PO4 and decreased Ca)
— rhabdomyolysis
— hypothyroidism, Addisons, adrenocortical insufficiency
— lithium therapy

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16
Q

Hypernatraemia

A
  • Sodium excess - high urinary sodium
    — Cushing’s
    — Hyperaldosteronism
    — Iatrogenic e.g. hypertonic saline, poisoning
  • H2O depletion/dehydration
    — diabetes insipidus
    — insufficient H2O intake e.. dementia
    — insensible H2O loss e.g. burns, diarrhoea
  • Sodium deficiency with greater water deficiency
    — renal loss (e.g. osmotic diuresis)
    — diarrhoea and vomiting
    — adrenocortical deficiency
17
Q

Hyperphosphataemia

A

Increased intake
— diet
— IV administration
— excess vitamin D

Increased release from cells/bones
— diabetes
— starvation
— rhabdomyolysis
— malignancy
— renal failure

Fictitious
— haemolysis

Decreased excretion
— hypoparathyroidism
— renal failure
— excess growth hormone secretion

18
Q

Hypocalcaemia

A
  • Decreased PTH
    — parathyroid agensis e.g. DiGeorge syndrome
    — parathyroid destruction e.g. surgery, radiotherapy, infiltration by metastases or systemic disease
    — autoimmune disorder
    — reduced parathyroid secretion - due to gene defects, hypomagnesaemia, neonatal hypocalcaemia
  • Decreased vitamin D activity
    — malabsorption
    — nutritional deficit
    — liver disease
    — CKD
  • Increased calcium loss
    — chelating agents e.g. citrate
    — calcification of soft tissues
    — bisphosphonates
  • Decreased ionised calcium
    — alkalosis
19
Q

Hypochloraemia

A

Usually associated with sodium losses

Drugs
* bicarbonate (inversely proportional to chloride)
* steroids
* diuretics
* laxatives (increased Mg and PO4)
* theophylline

Increased losses (volume contraction and metabolic alkalosis)
* excessive sweating
* excessive diuresis
* prolonged vomiting (pyloric stenosis)or NGT aspiration
* renal salt-losing nephropathy
* adrenocortical deficiency
* acute intermittent porphyria
* SIADH (hand in hand with Na)

20
Q

Hypokalaemia

A

Decreased intake
— poor dietary intake
— starvation

Magnesium depletion - increases renal potassium loss
— poor diet
— increased magnesium loss

Increased losses
— drugs - diuretics, laxatives, liquorice, steroids, antibiotics
— skin - profuse sweating, extensive burns
— GI - diarrhoea, vomiting, ileostomy, intestinal fistula, villus adenoma, laxatives
— renal - tubular disorders, nephrogenic DI, various syndromes
— endocrine (mineralocorticoid excess) - hyperaldosteronism, Cushing’s disease, Conn’s syndrome
— dialysis - haemodialysis on low K+ dialysate, peritoneal dialysis

Movement of potassium into cells
— alkalosis - respiratory and metabolic
— drugs - salbutamol, insulin, beta agonists
— hypokalaemic periodic paralysis

21
Q

Hypomagnesaemia

A

Decreased intake
— starvation
— ETOH dependence
— TPN

Redistribution
— hungry bone syndrome
— DKA treatment
— acute pancreatitis
— re feeding syndrome
— ETOH withdrawal

Increased losses
— D+V
— NG suction
— GI fistulas

22
Q

Hyponatraemia

A

Hypovolaemic - loss of intravascular volume stimulates baroreceptors, triggering an increases release of ADH, despite there being no rise in osmolality. ADH secretion results in increased nephron water reabsorption while thirst stimulates increased water intake, lowering serum sodium concentration.
— renal losses - diuretics, osmotic diuresis (e.g. hyperglycaemia), renal tubular acidosis, mineralocorticoid deficiencies
— upper GI losses - vomiting
— middle GI losses - pancreatitis, bowel obstruction
— lower GI losses - diarrhoea, bowel preparation
— other losses - sweat, bleeding

Euvolaemic - 1) High water intake means the kidneys are unable to excrete urine dilute enough to match, so overall Na is lost. 2) ADH secretion occurs despite normal plasma volume and osmolality.
— SIADH - malignancy, ADH secretion, drugs, CNS disease, hormone deficiency, pulmonary
— drinking excessive water e.g. primary/psychogenic polydipsia, MDMA
— adrenal insufficiency
— hypothyroidism

Hypervolaemic - development of oedema (fluid leak into the interstitium), causing a loss of effective intravascular volume, triggering release of ADH and consequently hyponatraemia.
— IVI (sodium deficient fluids)
— TURP/hysteroscopy syndrome
— CHF (increased hydrostatic pressure)
— cirrhosis/liver failure (both reduced intravascular oncotic pressure and increased hydrostatic pressure)
— nephrotic syndrome (reduced intravascular oncotic pressure)
— pregnancy
— renal failure (impairs kidneys ability to produce dilute urine)

23
Q

Hypophosphataemia

A

Decreased intake
— malnutrition
— phosphate binders
— vitamin D
— malabsorption
— TPN

Redistribution
— re feeding syndrome
— insulin in DKA

Increased output
— urinary - diuretics, osmotic diuresis, hyperparathyroidism, proximal tubular dysfunction
— non urinary - diarrhoea, sweat, burns, sepsis, bleeding

Mild
— hyperparathyroidism
— osteomalacia
— increased carbohydrate metabolism
— haemodialysis
— acute alkalosis

Severe
— ketoacidosis
— TPN and re feeding syndrome after starvation
— chronic alcoholism/withdrawal

24
Q

Interpreting an ECG

A
  • Confirm details
    — patient
    — timing
    — calibration
  • Heart rate
  • Heart rhythm
    — regular vs irregular
  • Axis
    — Normal if QRS positive in leads I and II
  • P waves
    — present
    — followed by QRS
    — morphology
  • PR interval (120-200ms)
  • QRS complex (120ms)
    — width, height, morphology
    — delta waves, q waves
    — R wave progression
  • ST segments
    — elevation/depression
  • T waves
    — tall/flattened
    — inverted
    — biphasic
  • QT interval (corrected to HR 60)
    — M 440ms
    — F 460ms
  • U waves?
25
Q

Interpreting pulmonary arterial catheter

A

Right Heart Failure = increased CVP, increased PVR, decreased CI

Left Heart Failure = increased PCWP, decreased CI, increased SVR

Pericardial Tamponade = increased CVP, increased PCWP, increased SVR

Hypovolaemia = decreased CVP, decreased PCWP, decreased CI, increased SVR

Cardiogenic = increased CVP, increased PCWP, decreased CI, increased SVR

Sepsis (distributive) = decreased CVP, decreased PCWP, increased CI, decreased SVR

26
Q

Investigation of Cardiac Disease

A
  • Exercise stress ECG - modified Bruce Protocol
    — goal is to increase workload of the heart to provoke maximal increase in myocardial blood flow
    — treadmill increases speed/gradient (1 MET) every 3 minutes
    — high risk if systolic BP drops by >10mmHg or positive ST segment changes in 5+ leads
    — high risk if ischaemic changes occur in <3 minutes and take >9 minutes to resolve
    — patient needs to achieve >85% of maximal HR
  • Cardiac catheterisation and angiography
    — confirm sites and severity of coronary artery stenoses
    — mitral and aortic valve function - quantify severity of AS
    — LV morphology and function
  • Transthoracic echo
    — define cardiac anatomy and assess ventricular and valvular function
    — monitor disease progression and aid decision making re: time/type of surgery
  • Stress echo
    — delineate areas of rmwa when the heart is stressed
    — dobutamine used to mimic effects of exercise in those who can’t
  • Trasoesophageal echo
    — relatively minimally invasive imaging modality to look and heart and great vessels from a close proximty in real time
    — aortic dissections/transections, valvular pathologies (and severity), unconfirmed endocarditis, haemodynamic monitoring
  • Nuclear imaging - SPECT/PET
    — administration of radio-labelled isotrope with subsequent imaging of the heart to detect areas of infarct and ischaemia
    — evaluates ventricular wall motion and ejection fraction
    — delineates viable and non-viable myocardium
  • Cardiac MRI
    — diagnosis of pericardial and aortic disease, cardiac masses and congenital heart disease
  • CT
    — contrast enhanced gated CT coronary angiography
    — reliable method of identifying coronary atherosclerosis and severity of blockages
    — can identify early stages of soft plaque formation
27
Q

Paediatric ECGs

A

Normal findings
* HR >100
* marked sinus arrhythmia
* short PR interval and QRS duration
* slightly peaked P waves
* slightly long QTc
* T wave inversion in V1-V3
* Rightward axis >+90
* Dominant R wave in V1
* RSR pattern in V1

28
Q

Polycythaemia

A

Primary
— polycythaemia rubra Vera

Secondary (with appropriately increased EPO)
— high altitude
— respiratory disease
— cyanotic heart disease
— heavy smoking

Secondary (with inappropriately increased EPO)
— renal cell carcinoma
— hepatocellular carcinoma
— massive uterine fibroma

Relative
— stress polycythaemia
— dehydration
— burns

29
Q

Spirometry Results

A
  • FEV1 = volume exhales in the first second after deep inspiration and forced expiration –> normal is >80% predicted
    – low in obstructive lung disease or fixed airway obstruction
    – high in restrictive lung disease or small TLC
  • FVC = total volume of air that the patient can forcibly exhale in 1 breath –> normal is >80% predicted
    – low in restrictive lung disease or poor expiratory effort
    – high in obstructive lung disease or chronic exposure to high altitude
  • FEV1/FVC ratio = ratio of FEV1 to FVC which can indicate obstructive vs restrictive pattern
    – low in obstructive lung disease
    – high in restrictive lung disease
  • DLCO/TLCO = reflects parenchymal lung function and ability of lungs to participate in gas exchange
    – low in interstitial lung disease, pulmonary hypertension, small lung volume, CO poisoning, severe emphysema
    – high in asthma, L–>R shunt, polycythaemia, pulmonary haemorrhage

Restrictive Pattern
* FVC <80% predicted
* FEV1 reduced
* FEV1/FVC normal or increased
* low RV/ERV/IV/TLC

Obstructive Pattern
* FVC normal or decreased
* FEV1 <80% predicted
* FEV1/FVC <70%
* consider reversibility (≥ 12% increase in FEV1 or FVC after inhaled beta agonist or absolute increase in FEV1 of at least 200ml)
* high RV/ERV
* low IC
* TLC may be increased/decreased/normal

COPD
* post bronchodilator FEV1/FVC <70%
* severity graded using FEV1
* FEV1 ≥ 80%
* 50% ≤ FEV1 < 80%
* 30% ≤ FEV1 < 50%
* FEV1 < 30%

Lung Volume Measurement
* measure FRC by body plethysmography, inert gas dilution or nitrogen washout
* once FRC determined, ERV and IC can be determined by spirometry
* TLC can be determined by adding FRC and IC
* RV can be determined by subtracting ERV from FRC

FRC - volume of gas present in the lung at end-expiration during tidal volume
– low in supine position, pregnancy, obesity, ARDS, PEEP, increased intra-abdominal pressure, anaesthesia, paralysis
– high in asthma, emphysema

30
Q

Thrombocytopenia

A

Decreased production
— bone marrow depression (drugs, infection)
— B12/folate deficiency
— PNH
— alcoholism

Shortened survival
— immune (autoantibodies, drugs, cancer)
— non immune (DIC, cardiopulmonary bypass)

Abnormal distribution
— hyposplenism
— hypothermia

31
Q

Thrombocytosis

A

Primary - abnormal bone marrow function
— polycythaemia rubra Vera
— CML
— essential thrombocythaemia
— primary myelofibrosis
— unspecified myeloproliferative disorders

Secondary - reactive thrombocytosis driven by thrombopoietic growth factors in response to inflammation
— chronic inflammation
— drug therapy
— haemolysis
— iron deficiency
— surgery
— trauma
— splenectomy
— severe infection
— some specific cancers