ECG etc.

ECG – Investigating PE
- Small/medium pulmonary embolism
· Usually normal, except for sinus tachycardia
· Sometimes atrial fibrillation another tachy-arrhythmia occurs
· May be evidence of right ventricular strain
- massive pulmonary emboli
· Show right atrial dilation with tall peaked P waves in lead II
· Right ventricular strain and dilation give rise to right axis deviation, some degree of right bundle branch block, and T wave inversion in the right precordial leads
- multiple recurrent pulmonary emboli
· Can be normal or show signs of pulmonary hypertension
- acute pulmonary embolism
· S wave in lead I
· A Q wave in lead III
· An inverted T wave in lead III
· Sinus tachycardia
· Incomplete right bundle branch block pattern (R wave in aVR and V1 and an S wave in V6)

P Wave
- An impulse that begins in the SA node is not recorded on the ECG, however –
- The spread of depolarisation through the atria (atrial depolarisation) is observed
- First phase of P wave – electrical stimulation from the SA node stimulates the right atrium and reaches the AV node
- Downslope of P wave – stimulation of the left atrium
- Atria begin to repolarise at the same time the ventricles depolarise
- Wave of atrial repolarisation is lost in the QRS complex
- Normal Characteristics of a P Wave
o Smooth and rounded
o No more than 2.5mm in height
o No more than 0.11 sec in duration
o Positive in leads I, II, aVF and V2-V6

QRS Complex
- Spread of electrical impulse through the ventricles (ventricular depolarisation)
- Depolarisation = contraction, thus, ventricles contract shortly after QRS complex begins
- Much larger as there is a considerably larger muscle mass being depolarised
- QRS duration – measurement of the time required for ventricular depolarisation
- Adult – normal duration – 0.06 – 0.10 seconds
- If conduction is delayed, QRS complex produced by the ventricle is wider
- Normal characteristics of the QRS complex
- Normal duration of the QRS complex in an adult varies between 0.06 and 0.10 sec
- A normal Q wave is less than 0.04 sec in duration and less than 1/3 the amplitude of the R wave in that lead

T Wave
- Ventricular repolarisation
- Slightly asymmetric – peak is slightly closer to the end than the beginning
- Normal characteristics of T wave
- Slightly asymmetric
- T waves are not normally more than 5mm in height in any limb lead or 10mm in any chest lead; T waves are not normally less than 0.5mm in height in leads I and II

U Wave
- Not always seen, cause not known
- Normal characteristics
- Rounded and symmetric
- Usually less than 1.5mm in height and smaller than in the preceding T wave
- In general, a U wave more than 1.5mm in height in any lead is considered abnormal

Segments
PR Segment
- Horizontal line between the end of the P wave and the start of the QRS complex
- Activation of the AV node, the bundle of His, the bundle branches and the Purkinje fibres

ST segment
- ST segment is between the QRS complex and the T wave
- Early part of repolarisation of the right and left ventricles
- ST segment deviation
- Myocardial Ischaemia
- Injury
- Infarction
- Normal characteristics of an ST segment
- Begins with the QRS complex and ends with the onset of the T wave
- In the limb leads, the normal ST segment is isoelectric (flat) but may normally be slightly elevated or depressed
- In the chest leads, ST segment deviation may vary from -0.5 to +2mm

TP Segment
- Between T wave and P wave
- Isoelectric when the heart rate is within normal limits
- With rapid heart rates, the TP segment is often unrecognisable because the P wave encroaches the preceding T wave

Intervals

An interval is a waveform and a segment

PR Intervals
- P wave + PR segment = PR interval
- PRI changes with HR but normally measures 0.12 to 0.20 sec in adults
- As HR increases, the duration of the PR interval shortens
- A conduction problem above the level of the bundle branches will largely affect the P wave and PR interval
- Normal characteristics of the PR interval
- Normally measures 0.12 to 0.20 sec in adults; may be shorter in children and longer in old people
- Normally shortens as heart rate increases

QT Interval
- This represents total ventricular activity à the time from ventricular depolarisation (activation) to repolarisation (recovery)
- Start of QRS Complex + End of T Wave = QT Interval
- Varies according to age, gender and heart rate

Analysing a Rhythm Strip

Assess the rate
- 6 Second Method
o To determine ventricular rate
o Count the number of QRS Complexes within a 6 second period
o Multiply this by 10 to find the number of complexes in a minute
o Can be used for regular and irregular rhythms
- Large Boxes
o To determine ventricular rate
o Count number of large boxes between two consecutive R waves (R-R interval)
o Divide this number into 300
o To determine atrial rate
o Count number of large boxes between two consecutive P waves (P-P interval)
o Divide this number into 300

Assess rhythm
- Rhythm indicates the site of origin of an electrical impulse (eg sinus rhythm, junctional rhythm)
- Also used to describe the regularity or irregularity of waveforms
- We assess regularity by measuring the distance between the QRS waves

Identify and examine P waves
- To locate P waves, look to the left of the QRS complex
- Normally, P waves looking similar in size, shape and position
- If no P wave is present, the rhythm originated in the AV junction or the ventricles
- If one P wave is present before each QRS and the QRS is narrow:
o Is the P wave positive? If so, the rhythm probably began in the SA node
o Is the P wave negative or absent? If so, and the QRS complexes occur regularly, the rhythm probably started in the AV junction

Assess Intervals (Evaluate Conduction)

PR Interval
- Measured from where the P waves leaves the baseline to the beginning of the QRS Complex
- Normal – 0.12 to 0.20 seconds
- If they are the same – ‘constant’
- ‘lengthening’ – dysrhythmia
QRS Duration
- Narrow (normal) if less than 0.10 seconds
- Wide – more than 0.10 seconds
QT Interval
- Measure the QT interval in the leads that show the largest amplitude T waves
- Measured from beginning of QRS complex to end of T wave
- Duration varies according to age, gender and heart rate
R-R and P-P Intervals
To determine the rate and regularity of a cardiac rhythm, the intervals are used
o R-R interval – measure and compare distance – ventricular rhythm
o P-P – atrial rhythm


· T wave
o Negative – MI
o Tall, pointed – hyperkalemia

Investigations & Prognosis

DVT Investigations
1) ultrasound (doppler) - transducer is placed over leg and send sound waves through the tissue, reflect back and waves is shown as a moving image on the screen. clot maybe visible. series done over a few days to see if the clot is growing or new one is developing

2) CT/MRI scans. computerized tomography (CT) and magnetic resonance imaging(MRI) - visual images of veins and show clot present. usually for pregnant ladies & renal problem people with dye-related problems.

3) blood test - elevated level of D-dimer (clot-dissolving substance). however, D-dimer is elevated in other things too. used for RULING OUT dvt or identifying those at risk of recurrence. look for inherited defects in clotting system as well.

4) venography - dye injected into large vein @ foot/ankle. x-ray creates image of veins to look for clots. abit invasive, so not less used.

DVT Prognosis
1) PE! 3% fatal!

2) 15% people get postphlebitic syndrome(post-thrombotic synd) - syndrome used to describe a collection of signs & symptoms
(a) oedema in legs (usually medial lower leg)
(b) pain
(c) skin discolaration
(d) dermatitis
(e) venous claudication
(f) nocturnal cramping
(g) ulceration
due to damage of veins from blood clot. this reduces blood flow to damaged areas. can occur a few years after DVT. (Rx: aspirin, diuretics, compression stockings)

PE Investigations
1) CXR - cannot diagnose PE but can rule out other conditions

2) V/Q scan - use small amts of radioisoptopes (SMALL AMT!) attached to radiopharmaceuticals which is inhaled to take pictures of movement of air in lungs. different radiopharm is injected into vein in arm & pictures of blood flow in blood vessels of lungs are taken. results are compared. normal lung scan can rule out PE but not DVT. thus not used much now.

*3) Spiral (helical) CT scan
CT: 2-d slices seen of organ by thin x-ray beams passing through organs. dye is used to visualize.
spiral CT: scanner rotates continously around body, to create 3-d images! faster - scan pulm arteries in <20secs. however, exposes to slightly more radiation then standard x-ray + allergic reaction to contrast medium.

4) Pulmonary angiogram - blood flow in lung arteries. most accurate diagnosis but requires high degree of skills & risks. usually performed when other tests fail to give Dx. catheter is inserted into femoral vein to pulm arteries. dye is injected and x-ray is taken.
risk: change in heart rhythm. dye may cause kidney damage with ppl with decrease renal function (usually temp). developing a hematoma at puncture site.

PE Prognosis
1) 1/3 undiagnosed - fatal

2) once had, increase recurrence risk

3) pulmonary HPT - large number of clots obstruct blood flow in lung blood vessles for long time causing right heart to be overworked

4) cor pulmonale - right ventricle enlarged & fails.

Veins of the lower limb!-Anat

Full Blood Examination + INR, APTT D-Dimer

Haemoglobin (Hb)

Haemoglobin is an iron-containing compound found in the red blood cells, which transports oxygen around the body. Measuring the concentration of haemoglobin in the blood can help diagnose anaemia, a condition caused by a deficiency of haemoglobin. Anaemia can arise due to:
too few red blood cells;
inadequate iron intake;
inadequate folate or vitamin B12 intake;
microscopic bleeding or other blood loss;
blood cell destruction;
a chronic illness; or
a defect in the haemoglobin molecule itself.
This measurement may also detect abnormally high concentrations of haemoglobin. This may occur in people with chronic lung disease, as an adaptation to high altitudes, or because of an abnormal increase in red cell production by the bone marrow (polycythaemia vera).

The normal haemoglobin level for adult males is 130-170 g/L, and 120-150 g/L for adult females.

Red cell count (RCC)

Red cell count is an estimation of the number of red blood cells per litre of blood.
Abnormally low numbers of red blood cells may indicate anaemia as a result of blood loss, bone marrow failure, malnutrition such as iron deficiency, over-hydration, or mechanical damage to red blood cells.
Abnormally high numbers of red blood cells may indicate congenital heart disease, some lung diseases, dehydration, kidney disease or polycythaemia vera.

The normal red cell count for adult males is 4.5-5.5 x 1012/L, and 3.8-4.8 x 1012/L for adult females.

Packed cell volume (PCV) or haematocrit (Hct)

Haematocrit is a measure of the percentage of red blood cells to the total blood volume.
A low haematocrit may indicate anaemia, blood loss, bone marrow failure, leukaemia, multiple myeloma, nutritional deficiency, over-hydration or rheumatoid arthritis.
A high haematocrit may indicate dehydration (for example, due to burns or diarrhoea), eclampsia (a serious condition that can occur during pregnancy) or polycythaemia vera.

The normal haematocrit range for adult males is 40-50 per cent, and 36-46 per cent for adult females.

Mean cell volume or mean corpuscular volume (MCV)

Mean cell volume is an estimate of the volume of red blood cells. It is useful for determining the type of anaemia a person might have.
A low MCV may indicate iron deficiency, chronic disease, pregnancy, anaemia due to blood cell destruction or bone marrow disorders.
A high MCV may indicate anaemia due to nutritional deficiencies, bone marrow abnormalities, liver disease, alcoholism, chronic lung disease, or therapy with certain medications.

The normal MCV range for adults is 83-101 fL.

Mean cell haemoglobin (MCH) and mean cell haemoglobin concentration (MCHC)

These measures, also known as mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration, are further guides to the investigation of anaemia.
The MCH is the haemoglobin content of the average red cell. The MCHC is the average haemoglobin concentration in a given volume of packed red cells.
The MCH may be low in types of anaemia where the red blood cells are abnormally small, or high in other types of anaemia where the red blood cells are enlarged (for example, as a result of folic acid or vitamin B12 deficiency).
The MCHC is low in iron deficiency, blood loss, pregnancy and anaemias caused by chronic disease.

The normal MCH range for adults is 27-32 pg, and the normal MCHC range is 315-345 g/L.

White cell (leucocyte) count

White cell count estimates the total number of white blood cells per litre of blood.
An abnormal high or low white cell count can indicate many possible medical conditions and a leucocyte differential count, which provides numbers of the different types of white cells, is usually needed to help make any diagnosis.
Abnormally low numbers of white blood cells may indicate liver or spleen disorders, bone marrow disorders, or exposure to radiation or toxic substances.
Abnormally high levels of white blood cells may indicate infection, tissue damage, leukaemia, or inflammatory diseases.

The normal white cell count for adults is 4.0-10.0 x 109/L.

Leucocyte (white cell) differential count

Leucocyte differential count provides an estimate of the numbers of the 5 main types of white blood cells. These are: neutrophils; monocytes; lymphocytes; eosinophils; and basophils.
Each of the 5 types has a specific role in the body.
Neutrophils and monocytes protect the body against bacteria and eat up small particles of foreign matter.
Lymphocytes are involved in the immune process, producing antibodies against foreign organisms, protecting against viruses and fighting cancer.
Eosinophils kill parasites and are involved in allergic responses. High numbers of eosinophils may be associated with worm infections or exposure to substances that cause allergic reactions.
Basophils also take part in allergic responses and increased basophil production may be associated with bone marrow disorders or viral infection.

The normal ranges for the number of the different types of white cells in adults are:
Neutrophils: 2.0-7.0 x 109/L
Eosinophils: 0.02-0.5 x 109/L
Basophils: 0.05-0.1 x 109/L
Monocytes: 0.2-1.0 x 109/L
Lymphocytes: 1.0-3.0 x 109/L

Platelet count

Platelet count is an estimation of the number of platelets per litre of blood. Abnormally low numbers of platelets is known as thrombocytopenia, while an abnormally high level of platelets is known as thrombocytosis.
Platelet counts are often used to monitor medications such as heparin, which may cause low numbers of platelets, as well as medications that can have toxic effects on bone marrow. They may also be used to help diagnose problems associated with abnormal bleeding or bruising.

The normal platelet count for adults is 150-400 x 109/L.


The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. They are used to determine the clotting tendency of blood, in the measure of warfarin dosage, liver damage, and vitamin K status. The reference range for prothrombin time is usually around 12–15 seconds; the normal range for the INR is 0.8–1.2. PT measures factors II, V, VII, X and fibrinogen. It is used in conjunction with the activated partial thromboplastin time (aPTT) which measures the intrinsic pathway.

The prothrombin time is the time it takes plasma to clot after addition of tissue factor (obtained from animals). This measures the quality of the extrinsic pathway (as well as the common pathway) of coagulation.

The speed of the extrinsic pathway is greatly affected by levels of factor VII in the body. Factor VII has a short half-life and its synthesis requires vitamin K. The prothrombin time can be prolonged as a result of deficiencies in vitamin K, which can be caused by warfarin, malabsorption, or lack of intestinal colonization by bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver disease) or increased consumption (in disseminated intravascular coagulation) may prolong the PT.
A high INR level such as INR=5 indicates that there is a high chance of bleeding, whereas if the INR=0.5 then there is a high chance of having a clot. Normal range for a healthy person is 0.9–1.3, and for people on warfarin therapy, 2.0–3.0, although the target INR may be higher in particular situations, such as for those with a mechanical heart valve, or bridging warfarin with a low-molecular weight heparin (such as enoxaparin) perioperatively.

APTT - A phlebotomist collects blood samples in vacu-tubes with oxalate or citrate to arrest coagulation by binding calcium. The specimen is then delivered to the laboratory. In order to activate the intrinsic pathway, phospholipid, an activator (such as silica, celite, kaolin, ellagic acid), and calcium (to reverse the anticoagulant effect of the oxalate) are mixed into the plasma sample . The time is measured until a thrombus (clot) forms. This testing is performed by a medical technologist.

A positive D-dimer indicates the presence of an abnormally high level of fibrin degradation products in your body. It tells your doctor that there has been significant clot (thrombus) formation and breakdown in the body, but it does not tell the location or cause.

Necrotising Fasciitis

Definition

Rare but very severe bacterial infection of deep fascia with secondary necrosis of soft tissue (e.g. muscle, skin).

Aetiology

Type I – Polymicrobial

· Mixed aerobic and anaerobic bacteria

Type II - Monomicrobial

· Group A Streptococcus (e.g. Streptococcus pyogenes)

· Staphylococcus aureus (commonly MRSA)

Pathogenesis

Trauma causing the breaking of skin (e.g. surgery, cut, scratch) allows bacteria to enter body. The bacteria colonises soft tissue and spreads in the fascial plane, releasing toxins which destroy the soft tissue. Certain toxins can cause systemic effects (e.g. renal failure, septic shock).

Signs and Symptoms

Symptoms start at site of infection – intense pain in excess of that expected with visual inspection. Signs of inflammation apparent – redness, swelling, heat. Spread of infection leads to a rapidly growing bronze- or purple-coloured patch. Within an hour, the skin may break open and exudation may occur.

Generalised signs and symptoms: malaise, fever, sweating, chills, nausea, dizziness, weakness, shock.

Without treatment, death can occur rapidly (73% untreated mortality rate).

Investigations

CT scan to view extent of necrosis.

Culture to confirm bacteria and determine antibiotic use.

Management

Before culture results, presumptive broad-spectrum aggressive intravenous antibiotic therapy. Intravenous donor antibodies. Targeted antibiotic therapy after identification of pathogenic bacteria.

Surgery to drain infected areas and debridement of necrotic tissue. Consider amputation if infection cannot be controlled. Skin grafting after infection cessation.

Hyperbaric oxygen therapy if bacteria is anaerobic.

Prognosis

Scarring and deformity common.

High death rate even with aggressive treatment.

Complications

Local progressive tissue damage, systemic infection (sepsis, shock), scarring and disfiguration, functional limb loss, death.

Prevention

Proper asepsis following penetrative trauma and surgical incisions.

Signs and Symptoms

DVT
Symptoms can vary with location and size of blood clot, but generally are:
- pain in the affected calf
- difficulty walking due to pain, or pain worsen when walking
Signs
• tenderness
• oedema
• sensation of warmth
• skins appear blue or red
• Engorged superficial veins
• Homan’s sign

PE
Again, symptoms depend on location and size of blood clot:
- shortness of breath
- palpitations
- chest pain, which may radiate to shoulder, arm, jaw or neck
- dizziness
- haemoptysis

Signs
• cyanosis
• tachypnoea
• tachycardia
• hypotension
• raised JVP
• pleural effusion
• pyrexia

Treatment/management DVT

The aims of treatment are to relieve symptoms, reduce the risk of PE or paradoxical embolism to the systemic circulation, prevent post-thrombotic syndrome, and prevent recurrence.

Initial anticoagulation
Anticoagulation is the mainstay of treatment for DVT.
Initial treatment of DVT is heparin, as it is convenient to use and has a favorable side-effects profile. It can be used once or twice daily
LMWH (low molecular weight heparin) has a predictable anticoagulant response, so it can be given in a fixed weight-adjusted subcutaneous dose without laboratory monitoring in most patients. This allows out-of-hospital treatment in more than 80% of patients with acute DVT.
UFH (unfractionated heparin) is the treatment of choice in patients at high risk of bleeding or undergoing invasive procedures, and in patients with renal failure because of its shorter half-life, reversibility with protamine sulfate, and extra-renal metabolism.
In most cases, warfarin can be started on the first day. LMWH or UFH should be continued for at least 5 days and until the international normalised ratio (INR) has exceeded 2.0 on at least two occasions, 24 hours apart. Major bleeding occurs in 1%–5% of patients during initial treatment.
In patients with extensive ilio-femoral DVT and circulatory compromise, LMWH or UFH should be continued for at least 7 days, and initiation of warfarin should be delayed until anticoagulation has been therapeutic for several days.

Long-term anticoagulation
Warfarin (target INR, 2.0–3.0) is the anticoagulant of choice for long-term treatment of most patients with DVT, because it can be given orally and is highly effective, reducing the risk of recurrent VTE by 80%–90% during treatment.
In patients with provoked DVT, the risk of recurrent VTE after discontinuation of warfarin is 1%–4% per year. Generally, warfarin treatment should be continued for 3 months, although there is some evidence that 6 weeks treatment is as effective as 3 months in patients with provoked distal DVT.
In patients with unprovoked DVT, major chronic predispositions, or active malignancy, the risk of recurrent VTE after discontinuation of warfarin is substantially higher (at least 5%–10% per year) than for provoked events (≤ 4% per year). Decisions regarding the duration of anticoagulant treatment should be individualised by balancing the absolute risk of recurrent VTE with the potential absolute benefits (80%–90% relative risk reduction) and cumulative risks of bleeding associated with anticoagulation.

Thrombolytic therapy and surgical embolectomy
Compared with heparin, thrombolysis improves vein patency and reduces the risk of post-thrombotic syndrome, but increases the risk of bleeding, and there is no evidence of a net clinical benefit. Thrombolysis and surgical embolectomy have been used as limb-saving therapy in patients with extensive proximal DVT and circulatory compromise or venous gangrene.

Vena cava filter
Inferior vena cava filters are indicated to prevent pulmonary embolism in patients with DVT who are ineligible for anticoagulant therapy or who experience embolism despite adequate anticoagulation. Filters do not obviate the need for anticoagulation because they are associated with an increased risk of recurrent DVT. However, the optimal duration of anticoagulation in patients with vena cava filters in whom anticoagulation is deemed safe is uncertain.

Graduated compression stockings
Graduated compression stockings reduce the risk of post-thrombotic syndrome and should be used in the absence of contra-indications (eg, pre-existing leg ulceration or extensive varicosities).
And PE

Acute high-flow oxygen unless significant COPD, bed rest and analgesia. Severe cases IV fluids and ionotropic agents to improve right heart, very ill require ICU.

Prevention of furtheur emboli
• IV heparin, initial large bolus then continue infusion at a lower rate.
• LMWH, UFH have shown no difference in prevention of further emboli
• Oral anticoagulants begun after 48 hours, continue for 6 weeks – 6 months. Heparin is tapered off. Can be continued lifelong.
Dissolution of the thrombus
• Fibrinolytic therapy e.g. streptokinase following major embolism. Hourly up to 12- 72 hours.
• Surgical embolectomy is rarely necessary
Contraindications for anticoagulation and risk factors for anticoagulation-associated haemorrhage

Absolute contraindications

Active bleeding
Relative contraindications
Recent bleeding
Gastrointestinal bleeding within 2 weeks (eg, bleeding peptic ulcer)
Intracranial bleeding within 3 months
Recent major trauma
Bleeding diathesis
Coagulation defect
Severe thrombocytopenia (< 50 × 109/L); inherited or acquired platelet function defect
Uncontrolled hypertension
Endocarditis

Risk factors for anticoagulation-associated haemorrhage
Increasing age
Alcoholism
Cognitive impairment
Chronic corticosteroid use
Liver disease
Peptic ulcer disease
Polymorphisms for the gene encoding the hepatic microsomal enzyme CYP2CP and mutations of Ala-10 in the factor IX propeptide
References
• http://www.mja.com.au/public/issues/182_09_020505/ho10889_fm.html#elementId-1089801
• Kumar and Clarke 5th edition pg, 807 and 832

Sarah

D-dimer tests

D-dimer testing is of clinical use when there is a suspicion of deep venous thrombosis (DVT) or pulmonary embolism (PE).
While a negative result practically rules out thrombosis, a positive result can indicate thrombosis but does not rule out other potential causes. Its main use, therefore, is to exclude thromboembolic disease where the probability is low. – some hospitals wont even carry out the test unless the probability is either low or moderate of thromboembolic disease.
Fibrin degradation products (FDPs) are formed whenever fibrin is broken down by enzymes (e.g., plasmin). Determining FDPs is not considered useful, as this does not indicate whether the fibrin is part of a blood clot (or being generated as part of inflammation).
D-dimers are unique in that they are the breakdown products of a fibrin mesh that has been stabilized by Factor XIII. This factor crosslinks the E-element to two D-elements. This is the final step in the generation of a thrombus.
Plasmin is a fibrinolytic enzyme that organizes clots and breaks down the fibrin mesh. It cannot, however, break down the bonds between one E and two D units. The protein fragment thus left over is a D-dimer.

D-dimer assays rely on monoclonal antibodies to bind to this specific protein fragment. Various kits have 93-95% sensitivity and about 50% specificity in the diagnosis of thrombotic disease.
• False positive readings can be due to various causes: liver disease, high rheumatoid factor, inflammation, malignancy, trauma, pregnancy, recent surgery as well as advanced age
• False negative readings can occur if the sample is taken either too early after thrombus formation or if testing is delayed for several days. Additionally, the presence of anti-coagulation can render the test negative because it prevents thrombus extension.

Chest X-rays and Pulmonary Embolism

General Rules

1. Check patient name, position, technical quality.
2. Soft tissue including breast, chest wall, companion shadow.
3. Review soft tissues and skeletal structures of shoulder girdles and chest wall.
4. Review abdomen for bowel gas, organ size, abnormal calcifications, free air, etc.
5. Review soft tissues and spine of neck.
6. Review spine and rib cage: check alignment, disc space narrowing, lytic or blastic regions, etc.
7. Review mediastinum:
A. overall size and shape
B. trachea: position
C. margins: SVC, ascending aorta, right atrium, left subclavian artery, aortic arch, main pulmonary artery, left ventricle
D. lines and stripes: paratracheal, paraspinal, paraesophageal (azygoesophageal), paraaortic
E. retrosternal clear space
8. Review hila:
A. normal relationships
B. size
9. Review lungs and pleura:
A. compare lung sizes
B. evaluate pulmonary vascular pattern: compare upper to lower lobe, right to left, normal tapering to periphery
C. pulmonary parenchyma
D. pleural surfaces
a. fissures - major and minor - if seen
b. compare hemidiaphragms
c. follow pleura around rib cage


Pulmonary Embolism
• can be done in conjunction with a ventilation-perfusion (V/Q) scan  it is difficult to diagnose pulmonary embolism on the x-ray alone
• VQ scan basically shows the parts of the lungs which are not receiving the air they should be  shows lowered perfusion

What to look out for:
• Small/medium pulmonary embolism
o Is often normal
o Linear atelectasis (partial lung collapse due to blockage)
o Blunting of the costophrenic angle (due to small effusiuon)
o Raised hemidiaphragm – present in some patients
o Wedge-shaped pulmonary infarct, abrupt cut-off of pulmonary artery, translucency of underperfused distal lung zone  rarer
o Previous infarcts – opaque linear scars
• Massive pulmonary embolism
o Pulmonary oligaemia  decrease in the size and number of pulmonary vessels due to vessel blockage or destruction
o Dilation of the pulmonary artery at the hila

- Rushmi
P.s. I have pictures, but it takes to long to stick them all up so, um, if anyone brings a laptop, can i use it? Just let me know before Friday. Thanks!