module 4 osce notes · 2021. 1. 14. · module 4 osce notes sarah carlton 3 (“i’m now checking...

Module 4 OSCE Notes

Examination Skills ● Cardiovascular Examination ● Peripheral Vascular Examination

Procedures ● ECG ● ABPI ● Defibrillation

Investigation Interpretation ● ECG including Exercise ECG ● Cardiac Enzymes ● Stroke on CT Head Scans ● Arteriogram

Module 4 OSCE Notes Sarah Carlton

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Examination Skills

Cardiovascular Examination


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Part What to say What you’re looking for/additional information

Introduction “Hello, I’m … and I’m a … year medical student at the University of East Anglia, could I start by

confirming your name and date of birth please?”

“And I’ll just quickly check your wrist band”

“Today, I’ve been asked to do a cardiovascular examination on you which will include me looking at you in general, your hands and face, assessing your

pulses and then listening to your heart, is that okay?”

“Please could you take off your shirt?”

“Are you comfortable for me to begin?”

“I’ll be talking to the examiner throughout the examination if that’s okay”

Wash hands

Check name and date of birth on wrist band

Ensure the patient is appropriately exposed – nothing on upper half. If it’s a woman, allow her to leave her bra on apart from in

auscultation when it should be loosened to allow proper positioning of the stethoscope

General Inspection

“On general inspection, I’m looking if the patient is comfortable; if there are any obvious signs of distress, breathlessness, pallor or cyanosis”

Distress and breathlessness – suggestive of (s/o) MI

Hands “Could I take a look at your hands please?”

“On inspection of the nails, I’m looking for splinter haemorrhages and clubbing – please could you put

your nails together like this” (show them Schamroth’s window)

“Could you turn your hands over please”

“Looking for Osler’s nodes and Janeway lesions. Also checking capillary refill”

Splinter haemorrhages1 – reddish/brown streaks of the nail bed – s/o infective endocarditis

Clubbing2 – s/o cyanotic congenital heart disease (deoxygenated blood bypasses lungs and goes into body) and infective

endocarditis

Osler’s nodes3 – painful raised erythematous lesions found on pads of fingers – s/o infective endocarditis

Janeway lesions4 – painless, blanching red spots on thenar/hypothenar eminences or soles of feet – s/o infective

endocarditis

Capillary refill – press on fingertips for a few seconds and then release – colour should return within about 2 seconds – if not, s/o

poor perfusion

Pulses and Blood

Pressure

“I’m now just going to check your pulse”

“The heart rate is … and the rhythm is …”

Radial pulse – count for 15 seconds and times by 4 to get beats/minute.

Rate – bradycardia < 60 < normal < 100 < tachycardia


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(“I’m now checking for a radial-radial delay”

“I’m going to check for something called a collapsing pulse that’ll involve me lifting your arm above your

head, is your shoulder painful at all?”)

“There is/isn’t a collapsing pulse”

“Would the examiner like me to do blood pressure?”

Rhythm – Irregularly irregular – Atrial fibrillation or ventricular ectopics (premature ventricular contraction)

- Regularly irregular – 2nd degree heart block

Probably won’t have to do in OSCE but good to know:

Radial-radial delay – palpate both radial arteries simultaneously, to see if there’s any difference between the two – if there is, s/o atherosclerosis, aortic dissection and aortic arch aneurysm

Collapsing pulse – feel radial pulse with bottom of fingers then raise the patient’s arm vertically above their head – if (+) – first 3/4

pulsations feel much stronger - s/o severe aortic regurgitation

Face “So now moving onto the face, could you pull your lower eyelids down for me please?”

“Looking for conjunctival pallor, corneal arcus and xanthelasma”

“Looking at the cheeks for malar flush”

“Please could you open your mouth and lift your tongue up?”

“Looking for central cyanosis, poor dental hygiene and a high arched palate”

Conjunctival Pallor5 – s/o anaemia

Corneal arcus6 – creamy yellow discoloration at the boundary of the iris and cornea caused by the deposition of cholesterol. Often

seen in healthy people over 50 but s/o of dyslipidaemia

Xanthelasma7 – soft, yellowish plaques periorbitally and on the medial aspect of the eyelids – s/o hyperlipidaemia

Malar flush8 – rosy cheeks with a bluish tinge – s/o mitral stenosis

Central cyanosis9 – blue discoloration under the tongue - hypoxia/poor perfusion

Poor dental hygiene – Tooth infection can precede infective endocarditis

High arched palate10 – top of mouth is unusually high and narrow - s/o Marfan’s Syndrome (genetic disorder affecting body’s

connective tissue – affects aorta eg. Causes aortic regurgitation)

Jugular Venous Pressure

“I’m just going to make sure the bed is at 45⁰”

“Could you turn your head slightly to the left for me please?”

“Looking for a raised JVP”

“Is your stomach painful at all? Is it okay if I press on it?”

“Testing to see if the JVP rises with the hepato-jugular reflux”

Normal = see a double pulsation just above the clavicle, along the border of the sternocleidomastoid. When you test the

hepatojugular reflux, the JVP may increase for a few beats but should then return to normal

Abnormal1 = an elevated JVP or a JVP that remains elevated when you do the hepato-jugular reflux - s/o fluid overload eg. Heart

failure or right heart dilation eg. PE, COPD. Can also be s/o obstruction of the vena cava due to eg. Lung cancer

Carotid Pulse “I’m now going to feel for a pulse in your neck”

“The volume of the pulse is… and the character is…”

Assessing volume and character, do each side individually

Volume – Reduced in people with low cardiac output


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Increased – Aortic regurgitation, aortic stenosis

Character –slow-rising pulse (gradual upstroke with a reduced peak) – s/o aortic stenosis

Very rapid upstroke and down-stroke – s/o aortic regurgitation

Inspection of Praecordium

“Inspecting the praecordium, I’m looking for any chest wall abnormalities or scars from

surgery or pacemaker implantation”

Praecordium = the surface region of the heart and the lower thorax

Chest wall abnormalities – pectus excavatum11 – funnel chest or pectus carinatum12 - pigeon chest – can both displace heart and

affect palpitation

Scars – Midline sternotomy scar13 – s/o previous CABG or aortic valve replacement - can get mini sternotomy scars

Left sub mammary scar14 – s/o mitral valvotomy (opens up a valve, often using a balloon)

Infraclavicular scars15 – s/o pacemaker or defibrillator implantation – bulge of device may be obvious – can also get a larger defibrillator

device inserted under the axilla

Palpation

Apex Beat “I’m now going to feel for the apex beat”

“The apex beat is/isn’t palpable in a normal/abnormal position”

Apex beat = most lateral and inferior position where the cardiac impulse can be felt – cardiac impulse results from left ventricle

moving forward and striking the chest wall in systole

Normally found in 5th left intercostal pace at, or medial to, the mid-clavicular line16

Often not palpable but start more laterally and work your way in so you don’t miss any displacement

Abnormal findings = displaced inferiorly or laterally – s/o left ventricular dilatation eg. After MI, aortic stenosis, severe

hypertension and dilated cardiomyopathy (heart muscle thins and stretches)

Forceful, undisplaced apical impulse – left ventricular hypertrophy eg. Hypertension or aortic stenosis

Heaves “I’m going to press down quite firmly in the middle of your chest, is that okay?”

“Could I ask you to breathe in and out and then hold your breath on the way out

please?”

“Assessing for any right ventricular heave”

Heaves = pulsation over the left parasternal area

Feel for heaves using the heal of your hand on the left parasternal area, keep your fingers off the patient – s/o right ventricular

hypertrophy or dilation, most often accompanying pulmonary hypertension


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Thrills “Assessing for any thrills” Thrills = palpable murmurs

Feel for thrills with your fingertips at the apex and on both sides of the sternum

Aortic stenosis – causes thrill at apex or in the lower sternum

Ventricular septal defect – causes thrill on both sides of sternum

Auscultation

Auscultation with Patient Lying Down

“Now I’m just going to listen to your heart with my stethoscope”

“Listening for normal and abnormal heart sounds, any added sounds and any murmurs”

Patient should be lying down and you should listen with diaphragm (big bit) of stethoscope

Listen to all 4 valves16 – Aortic – 2nd intercostal space, right edge

Pulmonary – 2nd intercostal space, left edge

Tricuspid – 4th intercostal space, left sternal edge

Mitral – 5th intercostal space, mid-clavicular line

Listening for heart sounds, added sounds and murmurs

Heart sounds2: 1st = S1 “lub” – caused by closure of mitral and tricuspid valves at the onset of ventricular systole – best heard at

the apex

2nd = S2 “dub” – caused by closure of the pulmonary and aortic valves at the end of ventricular systole – best heard at left sternal edge – sound can be split since the left ventricle contracts slightly

before the right

There is variation with breathing – splitting of the two heart sounds in S2 is greater in end inspiration

There is also a 3rd heart sound I will talk about below when patient is on their side

Abnormal heart sounds: 1st – mitral stenosis – intensity of S1 is increased due to elevated left atrial pressure

2nd – Quiet/reduced in calcific aortic stenosis and aortic regurgitation

Louder – systemic/pulmonary hypertension

Wide splitting of S23 - with normal respiratory variation – occurs when there’s a delay in right ventricular emptying – right bundle

branch block

- Without normal resp. variation – Atrial septal defect


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Added sounds - Opening snap4 – Mitral stenosis – results from opening of stenosed valve and occurs early in diastole, just after S2

– best heard at the apex

Ejection clicks5 – high-pitched sounds that occur in early systole just after S1 – s/o congenital pulmonary or aortic stenosis – similar

mechanism to opening snap

Mid-systolic clicks6 – high-pitched click – s/o mitral valve prolapse- best heard at apex

Mechanical heart valves7 – can make a high-pitched, metallic sound when they close or open – often audible without

stethoscope

Pericardial rub8 – friction rub – coarse scratching sound – s/o acute viral pericarditis or sometimes heard 24-72hrs after an MI

Murmurs – produced by turbulent flow across the abnormal valve, septal defect or outflow obstruction

“Innocent murmurs” – occurs by increased volume or velocity of flow through a normal valve when stroke volume is increased eg. In

pregnancy, athletes or children with a fever

Systolic murmurs

Ejection murmur – begin after S1 ----------

Auscultate with Patient Lying on

Left Side

“Could I just get you to lie on your left side and put your arm behind your head for me

please?”

“Listening for an S3/S4 sound or a mitral stenosis murmur”

Feel for the apex beat – should be more easily palpable in this position

Put bell over where you palpated the apex beat and listen for:

Heart sounds: Listen for the 3rd heart sound, S3, that I mentioned earlier “lub-dub-dum” – coincides with turbulent, rapid ventricular filling immediately after opening of the AV valves – normal to find in children, young adults and pregnancy, pathological in patients >40y and is s/o left ventricular failure or mitral regurgitation. In heart failure, S3 occurs with a tachycardia, referred to as a gallop

rhythm, and S1 and S2 are quiet

May also hear a 4th heart sound2 – soft and low pitched, occurring just before S1 (da-lub-dub)- very end of diastole – always

pathological and caused by forceful atrial contraction against a non-compliant or stiff ventricle – s/o left ventricular hypertrophy

(due to hypertension, aortic stenosis or hypertrophic cardiomyopathy)


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Mitral stenosis murmur9 – low pitched rumbling sound that may follow an opening snap

Listen to the 4 places on the heart as earlier with the diaphragm to hear any of the earlier mentioned abnormalities

Auscultate with Patient Sitting Up

“Could you just sit up for me please?”

“I’m just going to place my stethoscope on your neck”

“Listening on the carotids to see if there’s any bruits”

“Could you breathe in, then out and hold it on the way out please?”

“Listening for the murmur of aortic regurgitation”

Carotid bruits - Listen with diaphragm to both carotids – just lateral to the Adam’s apple– listening for bruits which is caused by

increased blood flow through the carotids s/o carotid stenosis

Aortic regurgitation murmur10 – systolic also listen with diaphragm – harsh, high-pitched and musical. Usually loud and can often be

heard all over the precordium but best to listen in 2nd-4th intercostal pace on the left sternal edge

Auscultation of Lung Bases

“I’m just going to listen to the bottom of your chest, could you take some deep breaths in

and out for me please?”

“I can/can’t hear any crepitations at the bases of the lungs”

Make sure patient is still sat upright

Listening for crepitations suggestive of pulmonary oedema – s/o left ventricular failure

Inspection and Palpation of Legs

“Finally, I’m going to look at the legs for any oedema or scars”

Roll up trousers and place two fingers in a c shape around the leg and press in – testing for oedema – s/o right ventricular failure

Look for great saphenous vein removal scar17 – used in CABG

Closing “Thank you for allowing me to examine you, you can re-dress if you wish and I’m just going to report my findings back to the examiner”

“On examination, …”

“If I had more time, I would do a full peripheral vascular examination, perform a

12-lead ECG and look at any other investigations that have been done, thank

you.”

Wash hands

Reporting a murmur: 1) Grade of murmur

Grade 1 – Very faint

Grade 2 – Quiet but heard by very trained ear Grade 3 – Able to hear with stethoscope

Grade 4 – Thrill and able to hear with stethoscope

Grade 5 – Thrill and able to hear the murmur with stethoscope held slightly above chest

Grade 6 – Thrill and no stethoscope needed to hear

2) Timing – e.g. mid-systolic 3) Heard best in… 4) Radiated to…

5) With respiration – right sided murmurs louder on

inspiration and left sided is louder on expiration

Pictures


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Videos 1) Raised JVP - https://www.youtube.com/watch?v=xyvqDrj18js 2) Heart sounds - https://www.youtube.com/watch?v=8lzh9kgnoaU 3) Wide splitting of S2 - https://www.youtube.com/watch?v=3SECQV4T0tE 4) Opening snap - https://www.youtube.com/watch?v=YSg1UDQpr_8 5) Ejection click - https://www.youtube.com/watch?v=6SIZ6xBjF-c 6) Mid-systolic click - https://www.youtube.com/watch?v=eqSM59cmmc4


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https://www.youtube.com/watch?v=xyvqDrj18jshttps://www.youtube.com/watch?v=8lzh9kgnoaUhttps://www.youtube.com/watch?v=3SECQV4T0tEhttps://www.youtube.com/watch?v=YSg1UDQpr_8https://www.youtube.com/watch?v=6SIZ6xBjF-chttps://www.youtube.com/watch?v=eqSM59cmmc4

7) Mechanical heart valve - https://www.youtube.com/watch?v=eKmQ-hzbptw 8) Pericardial rub - https://www.youtube.com/watch?v=EUCp_3_vwtw 9) Mitral stenosis murmur - https://www.youtube.com/watch?v=IycvM5M-Qg4 10) Aortic regurgitation murmur -- https://www.youtube.com/watch?v=dYVDcRFepfo

Peripheral Vascular Examination


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Part of Examination What to Say What You’re Looking For



“Today, I’ve been asked to do a peripheral vascular examination on you which will include me looking at you in general, assessing the pulses and

arteries in your arms, neck, abdomen and legs. Does that sound okay?”

“I’m going to start on the upper body so could you remove your shirt please? And then I’ll ask you to

remove your trousers when I come onto examining the lower body if that’s okay?”

“Are you in any pain at all today?”


“I’ll be talking to the examiner throughout the examination if that’s okay”

Wash hands

Ensure patient is appropriately exposed

General Inspection “Looking at the patient in general to see if they’re well, whether they’re comfortable at rest and

whether there’s any obvious pallor or cyanosis”

“Do you walk with any walking aids/sticks at all?”

“Also looking for any oxygen around the patient”

Pallor/cyanosis – shows poor perfusion

Looking for sticks to give an indication of their ability to walk

Upper Body

Inspection “Could I have your hands please?”

“Looking at the hands, I’m looking for any pallor or cyanosis, any tar staining of the fingers and any

gangrene of the digits”

Tar staining – sign of smoking which is a risk factor for PVD

Gangrene – shows necrosis secondary to inadequate perfusion

Palpation “And checking capillary refill time which is normal/abnormal at about … seconds”

“Comparing the temperature on each side and proximally to distally”

Capillary refill – Normal < 2s

Press on fingertips and then release – should start white and then the colour should return within the 2

seconds Shows poor perfusion if any longer

https://www.youtube.com/watch?v=eKmQ-hzbptwhttps://www.youtube.com/watch?v=EUCp_3_vwtwhttps://www.youtube.com/watch?v=IycvM5M-Qg4https://www.youtube.com/watch?v=dYVDcRFepfo


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Temperature – will be colder with poor perfusion – will normally get reasonably colder the more

peripheral you are though

Pulses and Blood Pressure

“I’m just going to feel all your pulses now if that’s okay”

RADIAL “Feeling the radial pulse for the rate which is … bpm and it’s a regular/irregular rhythm, with

… volume”

“”There is/isn’t any radial-radial delay”

BRACHIAL “And just assessing the brachial artery for volume”

BLOOD PRESSURE “Would the examiner like me to assess the blood pressure?”

CAROTID ARTERY – “I’m just going to press my stethoscope on your neck”

“Auscultating for carotid bruits”

“Since I can/can’t hear a bruit, I’m not going to/going to go on to palpate the carotid pulse…

The character is… and volume is…”

Radial pulse - count for 15 seconds and times by 4 to get beats/minute.

Rate – bradycardia < 60 < normal < 100 < tachycardia

Rhythm – Irregularly irregular – Atrial fibrillation or ventricular ectopics (premature ventricular

contraction)

- Regularly irregular – 2nd degree heart block

Radial-radial delay – palpate both radial arteries simultaneously, to see if there’s any difference

between the two – if there is, s/o atherosclerosis, aortic dissection and aortic arch aneurysm

Blood pressure - >140 systolic and >90 diastolic if hypertensive

Carotid artery – listen for bruits first since if they have this, palpated could cause an emboli

Listen medial to the sternocleidomastoid and next to the trachea

Bruits – shows carotid stenosis

Abdomen

Inspection, Palpation and Auscultation of

the Aorta

“I’m going to move onto the abdomen now”

“Looking at the abdomen, I can’t see any obvious pulsation”

“I’m just going to press in the middle of your stomach, is it painful there at all?”

“Feeling for either side of the aorta. I can/can’t feel the pulsation and it is/isn’t expansile”

“And I’m just going to listen there if that’s okay?”

“I can/can’t hear any bruits”

Obvious pulsation – can see if patient is thin but could also indicate AA

Feel in the midline of the epigastrium for the aorta – may have to press in quite hard

Should feel the pulsation but you shouldn’t see your hands bulging out with each pulsation – if they do

this – this means the aorta is expansile and so indicated AA

Bruits also indicate AA

Lower Limb


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Inspection “Okay, I’m not going to examine your legs and so you can put your shirt back on but if I could ask

you to take off your trousers please?”

“So I’m looking for scars, hair loss, pallor, gangrene, amputations, ulcers or muscle wasting”

Scars – bypass surgery / vein harvest sites Hair loss – PVD

Gangrene – e.g. necrosis Pallor – suggests poor vascular perfusion

Missing limbs / toes – previous amputation Ulcers – venous vs arterial – look between toes and

lift feet up Muscle wasting – may indicate PVD

Palpation “And checking capillary refill time which is normal/abnormal at about … seconds” “Comparing the temperature on each side and proximally to distally”

Same as upper limb

Pulses “I’m just going to feel the pulses in your leg starting with one in your groin, does that sound

okay?”

FEMORAL - “Feeling the femoral pulse, the volume is good/bad.”

“Now feeling for radial-femoral delay”

“And I’m just going to listen over them”

“Listening for femoral bruits”

“Now I’m just going to feel the pulse in the back of your knee”

“I can/can’t palpate the popliteal pulse”

“Feeling the dorsalis pedis on both sides.”

“They are/aren’t of equal volume”

“Feeling both posterior tibialis”

“They are/aren’t of equal volume”

Feel at the mid inguinal point - located halfway between the ASIS & the pubic symphysis

Radio-femoral delay – suggestive of coarctation of the aorta

Femoral bruits – shows stenosis

How to feel the popliteal pulse - Flex the knee to 45º. Place thumbs on the tibial tuberosity and curl

your fingers into the popliteal fossa to compress the popliteal artery against the tibia

Dorsalis pedis - Lateral to the extensor hallucis longus tendon - over the 2/3rd cuneiform bones

Posterior tibialis – posterior to the medial malleolus

If they’re not of equal volume – shows PVD in one leg

Sensation “And finally I’m going to test the sensation in your foot so just tell me if you can feel my cotton on

your foot please and whether it feels the same on both sides”

“Sensation if present and equal on both sides”

If the sensation isn’t there, go more and more proximally until they begin to feel it

Use soft touch - cotton

Completing the Examination

“Thank you for allowing me to examine you, you can re-dress if you wish and I’m just going to

report my findings back to the examiner”

“On examination, …”

Wash hands

Procedures ECG Taking Procedure

1) Introduce yourself etc. ASK FOR CHAPERONE IF FEMALE

2) If needed, shave skin on clean with alcowipe

3) Apply limb leads – Ride Your Green Bike

a. Red – Just below shoulder on right arm

b. Yellow – Just below shoulder on left arm

c. Green – Near the ankle on the left leg

d. Black – Near the ankle on the right leg

4) Apply chest leads

a. V1 – 4th intercostal space, right sternal edge b. V2 – 4th intercostal space, left sternal edge c. V4 – 5th intercostal space, mid-clavicular line d. V6 – Mid-axillary line in same horizontal line as V4

e. Then place V3 – Equidistant between V2 and V4

f. Then place V5 – Anterior axillary line same plane as V4

ECG Taking Positioning of Leads

Chest Leads


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“If I had more time, I would do a full cardiovascular examination and peripheral neurological

examination, perform an ABPI and look at any other investigations that have been done, thank

you.”

Precordial Electrode Standard Position

V1 4th intercostal space on right sternal border

V2 4th intercostal space on left sternal border

V3 Exactly midway between V2 and V4

V4 5th intercostal space on the left midclavicular line

V5 Same horizontal plane as electrodes V4 and V6 on the left anterior axillary line

V6 Same horizontal plane as electrodes V4 and V5 on the left midaxillary plane

Limb Leads

Lead Groups ● The ECG leads are grouped into two electrical planes. The frontal leads (Lead I-III, aVR-F) view

the heart from a vertical plane, while the transverse leads (V1-V6) view the heart from a horizontal plane


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Limb Electrode Standard Position

Right Arm (RA) Right arm just proximal to the wrist

Left Arm (LA) Left arm just proximal to the wrist

Right Leg (RL) Right lower leg just proximal to ankle (used for grounding only)

Left Leg (LL) Left lower leg just proximal to ankle

Lead (-) Electrode (+) Electrode View of Heart

Lead I RA LA Lateral

Lead II RA LL Inferior

Lead III LA LL Inferior

aVR LA+LL RA None

aVL RA+LL LA Lateral

aVF RA+LA LL Inferior

V1 Septal

V2 Septal

V3 Anterior

ABPI


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V4 Anterior

V5 Lateral

V6 Lateral

Region Seen Coronary Artery Supply

II, III, aVF Inferior Surface Right coronary artery

V1, V2, V3, V4 Anterior Surface

V1+V2 – Septum

V3+V4 - Anterior

Left anterior descending

I, aVL, V5, V6 Left Lateral Surface Circumflex branch of left coronary artery

aVR The atria Branches of main coronary artery

Part of the Procedure What to Say What to Do



“And I’ll just quickly check your wrist band”

“Today, I’ve been asked to take the blood pressure in your arms and feet. That will include

Wash hands

Prepare equipment – hand-held Doppler, ultrasound jelly and sphygmomanometer

Place meter on bed half way down the bed between the patients arm and feet (so you can

spin it round to take leg readings)


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me inflating a cuff around your arm and then around each of your legs and using a machine to

listen to your blood vessels, does that sound okay?”


“I’m going to start by taking the pressure in your arm if that’s okay”

“Have you got a preferred arm that you’d like me to use?”

“Please could you take off/role up your shirt?”

Ensure the patient is appropriately exposed

Taking Brachial Pressure “Okay, so I’m just going to inflate up the cuff, it might be a bit tight but let me know if it gets too

painful at any point”

“I’m just going to feel for the pulse in your arm”

“I’ll just squeeze on some of this jelly, it might be a bit cold so I apologise for that!”

“Now I’m going to use this machine to listen to the pulse and so I’ll go quite for a minute”

“Okay, that’s done and I’ll just give you some tissue if you want to wipe the jelly off, would the

examiner like me to do the other arm?”

“You can re-clothe”

Put cuff on and ensure everything is ready and easily at hand before putting on the jelly

Feel for the brachial pulse and squeeze a generous amount of jelly onto that area

Place ultrasound in the jelly and then turn it on

Then start moving the probe around to listen for pulse - better to start laterally and make

your way methodically until you find it

Once you’ve heard it, move it around slightly to hear if you can get a better signal

Comment on the sound; whether it’s monophasic (1 sound = poor elasticity of vessels), biphasic (2 sounds = good) or

triphasic (3 sounds = normal)

Once you’ve got the best signal, anchor the probe with your little finger and inflate the

cuff until you can’t hear the pulsation

Then slowly release the pulsation and record the value of the first sound you hear

Interpretation ● If the patient has an ulcer on their leg, provided it’s not too painful, cover with cling-film and

continue as normal ● Once you have the results from the 2 pulses, use the highest reading and insert into the

equation above


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Taking Ankle Pressure “Now I’m going to do the same around your ankles and so do you mind taking off your

trousers/rolling them up please?”

“So again, I’m going to inflate the cuff up and let me know if it gets too painful”

“I’m just going to feel for your pulse in your foot”

“I’m going to squeeze some more jelly on you here”

“And going to repeat the process with the machine”

“And I’m going to inflate it again if that’s okay, are you still comfortable?”

“Now I’m going to do the same on the other leg”

Will most likely just have to do one leg

Spin the meter around so you can see it and ensure you’re comfortable

Wrap the cuff around one of the ankles – around the lower calf muscle and above the

ankle joint

Feel for the dorsalis pedis pulse (lateral to extensor hallucis longus ligament)

Once you feel the pulse/if you can’t feel it, squeeze on the gel and repeat the same

process as in the arm, remember to comment on the phasicity

Then try to palpate the posterior tibialis pulse (1.5cm posterior and inferior to the medial

malleolus)

Repeat the same process of gel, inflating the cuff and listening with the probe

After you have recorded these two, move the cuff onto the other leg and repeat the same

pattern

Closing the Station “Okay, that’s the process over, here’s some tissues for the gel and you are free to redress”

Wash hands and clear away equipment

Results ● ABPI normally > 1.0 ● ABPI < 0.95 indicates some peripheral arterial disease ● ABPI > 0.5 and < 0.9 can be associated with claudication and if symptoms warrant a patient

should be referred for further assessment ● ABPI < 0.5 indicates severe arterial disease and may be associated with gangrene, ischaemic

ulceration or rest pain and warrants urgent referral for a vascular opinion

Caution ● The measured ankle cuff pressure may be falsely elevated in patients with calcified arteries

(particularly occurs in diabetic and renal patients).

● An ABPI of >1.3 has been suggested as a strong indicator of calcification ● Local guidance suggests referral for further investigation if the ABPI is > 1.2

Defibrillation

Process 1. Is it safe to approach?

- Reasons why it would not be safe: o Defibrillation could have

already been started o Bed could be sat in a pool of

water/urine – you’d also get

shocked


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ABPI value Interpretation Action Ulcer, if any

Above 1.2 Abnormal. Vessel has been hardened by calcification via PVD.

Refer Venous, so use compression bandages

0.9-1.2 Normal None None.

0.8-0.89 Some arterial disease Manage risk factors Venous, so use compression bandages

0.5-0.79 Moderate arterial disease

Routine specialist referral

Mixed ulcers, so use Stage 1 compression bandaging

Under 0.5 Severe arterial disease Urgent specialist referral

Arterial, so don’t use compression bandaging

2. Confirm the patient is dead

- Shake the dummy lightly and shout “Hello, can you hear me?” - Shout for help - Check in the mouth for obstruction – if obstruction is present, sweep finger in mouth or turn

them on their side - Perform head tilt, chin left - Simultaneously, with ear over the patients mouth, fingers on their carotid pulse and head

tilted to look at chest: o LOOK for chest movements

o LISTEN for breath sounds

o FEEL carotid pulse for 10 seconds

3. If help arrives:

- Tell them to call the cardiac arrest team and say it’s an adult cardiac arrest, specify your location and ask them to come back with the crash trolley

4. Ask the helper/examiner to start chest compressions

- Rate = 100/min - Depth = 1/3 of chest - Ratio = 30 compressions:2 breaths

- Breaths – can be given with a bag mask 5. Set up the defibrillator

- Work around the person doing chest compressions

- Get the pads and say that you’d “connect pads to the test load” – DON’T ACTUALLY DO THIS - The pads will have a photo on them of where to place them

o The 1st one – goes under the armpit – if there’s a pace-maker, it must be at least 8cm away from it

o The 2nd one – goes on right side of chest – better over bony prominences - Must check before placing pads (have a quick, few second look):

o If the chest is wet (from sweat or anything else) – wipe area

o If pacemaker is implanted on the right rather than left, would place pads anteriorly

and posteriorly o Metal – any piercings/necklaces – make sure pads aren’t on top of these

o Chest hair – use razor and shave where you’re putting the pads

o Patches eg. Morphine patches – should take them off and WIPE the area (otherwise

it causes a mini explosion) 6. Put on the pads

- Peel off the cover from the back - Roll on the pads – make sure there are NO AIR BUBBLES

7. Use the machine

- Turn the dial round to 150J - Press the LEAD button twice to select LEAD 2 - When you put the pads on – you will get the heart rhythm

- Stop chest compression for 5 seconds to assess the rhythm – must not do longer than this!


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- If the rhythm is shockable, begin chest compressions again, , tell everyone apart from the

person doing the chest compressions to stand back and charge (by pressing 2) until just before the shock

- Just before the shock, ask the person doing chest compressions to stop and stand back and

remove the oxygen o Do one last check for any oxygen near the bed or anyone holding onto the bed etc.

- Shock by pressing 3 and then immediately restart chest compressions and breaths for two minutes (you do that this time)

o DO NOT LOOK AT THE SCREEN UNTIL THE 2 MINUTES OF CHEST COMPRESSIONS IS

UP o After the two minutes is up, stop chest compressions again for 5 seconds and look at

the screen o If still in shockable rhythm, repeat the process

o After the third shock, give adrenaline

o If they return to non-shockable rhythm

8. Post-Arrest - Request notes

- A – Airway – Should have bag mask on if they’re breathing - B – Breathing - Again, if they’re breathing, use non-re-breathe mask, if not, keep using the

oxygen mask

- C – Circulation – Pulse – check carotid pulse o Blood pressure – take – if systolic < 90 give: 500ml saline IV STAT (if no cardiac

history)

▪ 250ml Saline IV STAT (if they have a cardiac history)

- Blood test – ABG, Troponin, Glucose, FBC, U + E’s, LFTs, clotting

- CXR – to see any damage done to ribs

- 12-lead ECG

Causes of a Cardiac Arrest


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The Four H’s Hypoxia

● Ensure the patient’s airway is open and that there is adequate chest expansion with bilateral breath sounds

● Make sure oxygen supply is connected properly

Hypovolaemia ● Loss of fluid ● Look for obvious blood loss ● Gain IV access ● Give fluid challenge

Hypothermia ● Warming measures should be taken

Hypo/hyperkalaemia ● Hyperkalaemia – will have peaked T waves on ECG ● Hypokalaemia – flattened T waves and prominent U waves

The Four T’s Toxins

● Most common overdoses include: Tricyclics, digoxin, beta-blockers and calcium channel blockers)

● Can also be caused by cocaine and other street drugs ● ECG – shows prolonged PR interval

Thromboembolism ● Coronary/pleural – MI/PE

Tamponade (Cardiac) ● Fluid accumulating in the pericardium ● ECG shows tachycardia and narrow QRS

Tension Pneumothorax ● Air enters pleural space and is unable to escape ● ECG – narrow complex bradycardia ● Tracheal deviation and unequal breath sounds are found on examination


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Investigation Interpretation ECG Interpretation

Interpretation 1) Name

2) Paper speed and calibration

3) Rhythm

4) Rate

5) Axis

6) Waves (P, QRS, T waves)

7) Intervals (PR, ST, QT)

Paper Speed ● 25mm/s ● Each large square represents 0.2 seconds ● Therefore, there are five large squares per second and 300 per minute


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Calibration ● The rectangular peak at the beginning of the ECG should be no more or less than 1cm

Rate ● In regular rhythm – Work out number of large squares in one R-R interval – then do 300/this

number to get the rate.

In i

● Irregular rhythm – Count out 30 boxes – then times the number of QRS complexes in these boxes by 6 – this will give you rate per minute

● Normal = 60-100 ● Tachycardia > 100bpm – Causes:

o Atrial fibrillation

o Atrial flutter

o Supraventricular tachycardia

o Ventricular tachycardia

o Ventricular fibrillation

● Bradycardia < 60bpm – Causes: o Post-MI damage to heart tissue

o Hypertension

o Heart block

o Congenital heart defects

o Myocarditis

o Hypothyroidism

o Medications

Rhythm ● Regular – normal sinus rhythm ● Regularly irregular – Sinus arrhythmia (common in young people when breathing in but

pathological in older patients when not breathing in – sick sinus syndrome – when sinus node


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scars and becomes replaced by fibrous tissue) – p intervals are equal distance apart in each fast

and slow section

- Second degree heart block – Wenkenbach heart block – Pulse = regular rate with regular dropped beat. ECG – progressive prolongation of P-R interval with normal QRS complex followed

by an absent QRS complex

● Irregularly irregular – Atrial ectopics/atrial tachycardia (>100bpm) – when depolarisation occurs

from a focus in the atrium rather than in the sinoatrial node. Causes inverted P waves


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- Ventricular ectopics - Ectopic firing of a focus within the ventricles bypasses the His-Purkinje

system and depolarises the ventricles directly. This disrupts the normal sequence of cardiac

activation, leading to asynchronous activation of the two ventricles. The consequent

interventricular conduction delay produces QRS complexes with prolonged duration and

abnormal morphology. ECG – broad, premature QRS complexes with abnormal morphology, ST

segment and T wave changes, usually followed by a full compensatory pause

- Atrial fibrillation – no p waves

- Atrial flutter with variable heart block – ECG shows narrow complex tachycardia, regular atria activity at 300bpm, flutter waves (saw-tooth appearance) best seen in leads II, III and aVF. These

could be seen inverted in V1, normal QRS complexes – atrial rate is 300bpm and the ventricular rate is determined by conduction of AV. Commonest AV ratio is 2:1 – giving a R of 150bpm. Can

get a ratio of 4:1 for example or 1:1 which can lead to ventricular tachycardia.


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Axis ● Considers the average direction of spread of depolarisation wave through the ventricles as seen

from the front

● Normal = the depolarising wave is spreading towards leads I, II and III, and these are therefore normally associated with upward deflection in all these leads – the deflection will be greater in

lead II then in I or III since the depolarisation is heading mainly down the ventricles

● Right axis deviation = if the right ventricle becomes hypertrophied – it has more effect on the QRS than the left ventricle, and the

average depolarisation will swing towards the right. The deflection

in lead I becomes negative because depolarisation is spreading

away from it, and the deflection in lead III becomes more positive.

This is associated with pulmonary conditions that put a strain on the

right heart eg. PE, right ventricular hypertrophy, chronic lung disease and with congenital heart


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disorders. The leads I and II will be reaching for each other.

● Left axis deviation = when left ventircle becomes hypertoprhiped, it exerts more influence on the QRS complex. QRS complex becomes predominanatly negative in lead III and it isn’t

significant until lead II is also predominantly negative. It can also, and more likely, be due to a

conduction defect rather than increased bulk of the left ventircular muscle. Lead I and II will be

pointing in the opposite direction – leaving each other

Waves and Intervals

P wave ● Represents atrial depolarisation – originates in the SA node on the right atrium and spreads

across the right then left atrium

● Amplitude should be less than 2 small squares (0.2mV) and the width should be less than three small squares (0.12s)

● A tall p wave suggests right atrial enlargement ● Left atrial enlargement is associated with

broad and often bifid (split) P waves (second

picture)


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PR Interval

● From beginning of P wave to start of QRS complex ● Reflects conduction through the AV node ● Normal interval is between 120-200ms (3-5 small squares) ● If >200ms = 1st degree heart block ● If

ST Segment

● Normally isometric ie. Shows no deflection from the baseline

T Wave

● Represents ventricular repolarisation ● Normally, the only leads that show negative T waves are aVR and V1

– the rest are positive

● Peaked T waves – tall, narrow, symmetrical T waves – suggestive of hyperkalaemia (1st picture)

● Hyperacute T waves – broad, asymmetrical T waves – seen in early stages of STEMI (2nd picture on left)

● T wave inversion (3rd picture) – Causes: - Normal finding in children

- Persistent juvenile T wave pattern

- Myocardial ischaemia and infarction

- Bundle branch block

- Ventricular hypertrophy (‘strain’ patterns)

- Pulmonary embolism

- Hypertrophic cardiomyopathy

- Raised intracranial pressure

QT Interval

● Extends from the beginning of the QRS complex to the end of the T wave and, therefore, represents time from depolarisation to repolarisation of the ventricles – ie. Action potential

duration

● The duration of the QT interval is dependent upon cycle length ● The upper limit of normal is 0.4s in women and 0.44s in men

Q Waves

● Negative deflection at the beginning of ventricular depolarisation ● Pathological when: - >0.04s (one small square) and more than 25% of the following R wave in depth

- Seen in V1 – V3 - Occur after transmural MI where the myocardium on one side dies – this myocardium has no

electrical activity and therefore, the leads opposite it are able to pick up the opposite side of the

heart’s electrical activity


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- May also occur in patients with hypertrophic cardiomyopathy due to depolarisation of the

thickened septum

U Wave

● An abnormal wave (but can be normal) ● An upright wave that appears after the T wave – causes include - Hypokalaemia

- Hypocalcaemia


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ECG abnormalities in non-cardiac disease

Cause ECG Abnormality

Hypothermia J waves, baseline shiver artefact, bradycardia

Hyperkalaemia Tall peaked T waves, small P wave, gradual widening of QRS, if serum potassium very high – ventricular

tachycardia

Hypokalaemia Decreased T wave amplitude

Hypocalcaemia Long QT interval, U waves

Hypercalcaemia Short QT interval, ST segment depression

Digoxin Downsloping ST segment (reverse tick shape), T wave inversion

Digoxin toxicity AV block, atrial tachycardia with block, ventricular arrythmias

Exercise ECG ● Exercise tolerance testing is an important diagnostic and prognostic tool for assessing patients

with suspected or known ischaemic heart disease.

● During exercise, coronary blood flow must increase to meet the higher metabolic demands of the myocardium.

● Limiting the coronary blood flow may result in electrocardiographic changes

Normal Changes during Exercise ● P wave increases in height ● R wave decreases in height ● ST segment shops sharply upwards ● Q-T interval shortens ● T wave decreases in height

Changes Suggestive of Ischaemic Heart Disease ● Horizontal ST segment depression of ⩽ 2 mm ● Downsloping ST segment depression ● Early positive response within six minutes ● Persistence of ST depression for more than six minutes into recovery ● ST segment depression in five or more leads ● Exertional hypotension

Cardiac Enzymes ● Despite the fact that cardiac imaging is usually used to confirm a diagnosis, cardiac markers can

give a good idea as to what may be going on; the markers can also be helpful in deciding the appropriate interventions and investigations needed. In some cases, other investigations may not even be required to make a diagnosis.

● For example, patients with a raised troponin but negative creatinine kinase are diagnosed with a NSTEMI (non-ST-elevation MI), even if the ECG does not show abnormal changes. A point to note: previously, if such cardiac marker results were found with a normal ECG, it would be classified as unstable angina or minor cardiac injury.

● It is important to know that cardiac marker tests are not necessary in the case of ischemic chest pain, and with ECG’s with ST elevation (diagnostic of a STEMI). In such case, cardiac markers are not of value since the sensitivity is low in the first 6 hours after symptom onset. More importantly, immediate treatment is needed and testing would cause unnecessary delay.

● The following are some of the key cardiac biomarkers used:


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Troponin test – Normal < 0.01ng/mL ● The most important test; it is the most sensitive and specific test for myocardial injury. It is also

central to the definition of MI as mentioned before; the ECS guidelines suggests that MI is best

described as a rise in troponin in conjunction with clinical symptoms +/- an abnormal ECG ● Troponin is released from the degradation of actin and myosin filaments. There are several

isoforms of troponin, which is found in muscle cells

● Troponin T and I are specific to the myocardium. ● DDx of a raised troponin:

o Acute MI: troponin is released 2-4 hrs after the MI and persists for around 7 days.

The peak is normally between 24-48 hrs, and the value in the 3rd day the value can give an idea to the size of the infarct

o Severe PE (acute right heart overload)

o Heart failure

o Myocarditis

o Renal failure

o Sepsis

o Trauma

Creatine Kinase ● The CK-MB test is a relatively specific test, in the absence of skeletal muscle damage. It was the

main cardiac marker used prior to troponin. ● Creatinine kinase is found in all muscle, the CK-MB isoform of the molecule being the one

expressed in heart muscles. A raised CK-MB can be a false positive, if arising from skeletal muscle.

● CK is found in the cytoplasm and facilitates the movement of phosphates into and out of the mitochondria.

● CK-MB peaks between 10-24 hrs, and normally falls back to normal within 2-3 days. Since it has a short duration relative to troponin, hence cannot be used for late diagnosis of an MI. However, a second peak of CK following a decline can indicate a re-infarction.

● The CK/CK-MB relative index can be used to differentiate a false positive elevation of CK-MB arising from skeletal muscle; a ratio of less than 3 indicates a skeletal muscle source whilst a

ratio of over 5 indicates a cardiac source.

Myoglobin ● Myoglobin is a heme protein found in both skeletal and cardiac muscle. ● It serves as an early marker for MI, rising 2-4 hours after the onset of an MI ● It tends to peak between 6-12 hours and returns to normal within 3 days. ● Although being a test that can be done quickly and early, it LACKS cardio-specificity; it has a

sensitivity of around 90%, meaning that a negative value is not enough to exclude the diagnosis of a MI.

● The sensitivity and specificity of the test can be improved if samples are taken every hour; a 40% rise over a period of 2 hours is highly suggestive of an acute MI, but again is not as specific as other cardiac markers such as troponin.


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● The use of myoglobin as a cardiac marker is slowly beginning to die out, mainly due to the

introduction of troponin, which is a far better test in terms of sensitivity and specificity.

LDH (lactate dehydrogenase) ● LDH catalyses the conversion of pyruvate to lactate in cells. ● The two main types of LDH are LDH-1, which is found in the myocardium, and LDH-2 which is

found in the blood. ● A high LDH-1 to LDH-2 ratio is suggestive of MI ● However, LDH levels are also raised in tissue breakdown/haemolysis, thus may be raised in

malignancies, HIV, meningitis etc. It is therefore not as specific as troponin. ● LDH peaks at around 3 days after the onset of MI and falls to normal levels after 10-14 days.

Stroke on CT Head Scans Basic Principles of Neuroanatomy on CT

● Always describe CT findings as densities - Isodense = anything of the same density of as the brain - Hypodense – lower density – CSF and air are classic examples but

also includes ischaemia - Hyperdense – higher density – skull is the best example but also

includes blood (if acute

● Made up of:

- Dura mater = tough, outermost layer, closely applied to the inner table of the skull

- Arachnoid = thin layer closely applied to the dura mater - Subarachnoid space = space in between the arachnoid mater and the

pia mater which contains connective tissue and CSF - Pia mater = very thin layer applied to the surface of the brain

● Not that obvious on a normal CT scan however, on the right there is a CT of an extra-dural haemorrhage (so between the skull and the dura mater) that shows the classic biconvex shape with sharp attachments (since the dura is so tightly bound to

the skull) – it also shows compression of the ventricles but I’ll come onto that later

Cerebro-Spinal Fluid Spaces ● The brain is surrounded by cerebrospinal fluid (CSF) within

- Sulci – the brain’s surface is formed by folds of the cerebral cortex known as gyri – between these gyri are furrow, known as sulci, which contain CSF

- Fissures - The fissures are large CSF-filled clefts which separate structures of the brain – for example, the interhemispheric fissure separates the cerebral

hemispheres - Basal Cisterns – not on this CT – contains Basilar artery - Ventricles - The ventricles are spaces located deep

inside the brain which contain CSF. You can see the lateral ventricles in this CT (the bright white part is

calcification

Brain Parenchyma and Lobes

● The brain consists of grey and white matter structures which are differentiated on CT by differences in density.

● White matter has a high content of myelinated axons. ● Grey matter contains relatively few axons and a higher number of cell bodies. ● As myelin is a fatty substance it is of relatively low density compared

to the cellular grey matter. White matter, therefore, appears blacker

than grey matter. ● The lobes of the brain are also shown to the left, but the temporal

lobe is further down so cannot be seen


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Cerebral Vascular Territories ● Different areas of the brain are supplied by the anterior, middle and posterior cerebral arteries

in a predictable distribution. ● The arteries of the brain are not well visualised on conventional CT,

but a knowledge of the areas of the brain they supply is helpful in

determining the source of a vascular insult

Stroke on CT ● Due to its more specific images and ability to pick up an ischaemic stroke early, MRI should be

the investigation of choice for stroke

● However, MRI head takes 45 minutes to perform and when “time is brain” (as is the case if thrombolysis is an option within 4 hours) then doctors need a faster investigation that can assist them with diagnosis

● They do this through CT (CT head takes about 6 seconds) ● Mainly however, a CT is an investigation of exclusion in that it excludes a haemorrhagic stroke or

any other neurological reason for the symptoms (eg. Brain tumour) ● I will first look at haemorrhagic stroke since this is the most obvious on CT, and will then look at

the possible signs of ischaemic stroke

Haemorrhagic Stroke ● Intracranial haemorrhage is a collective term encompassing

many different conditions characterised by the extravascular

accumulation of blood within different intracranial spaces. A simple categorization is based on location: - Intra-axial haemorrhage – these are very localised bleeds

in the specific places mentioned below that I won’t go into as I don’t think we’ll be asked on them but there are some images to the right anyway

o Intracerebral haemorrhage

▪ Basal ganglia haemorrhage (top left)


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▪ Lobar haemorrhage (top right)

▪ Pontine haemorrhage (no picture)

▪ Cerebellar haemorrhage (bottom left) o Intraventricular haemorrhage (IVH) (bottom left)

- Extra-axial haemorrhage o Extradural haemorrhage (EDH) o Subdural haemorrhage (SDH) o Subarachnoid haemorrhage (SAH)

Extradural Haemorrhage ● Collection of blood that forms between the inner surface of the skull and

outer layer of the dura ● Commonly assoc. with trauma and skull fracture ● They are typically bi-convex in shape ● They are hyperdense, somewhat heterogeneous, and sharply demarcated. ● Depending on their size, secondary features of mass effect (e.g. midline shift

which can cause a decrease in the lumen of the ventricles) may be present.

● In the CT above, you can see the large EDH causing midline shift and compression of the ventricles. You can also see the soft tissue swelling of the

skull next to the area of haemorrhage

Subdural Haemorrhage ● Collection of blood accumulating in the potential space between the dura and arachnoid mater

of the meninges around the brain. ● SDH can happen in any age-group, is mainly due to head trauma ● Most often unilateral ● The appearance of SDHs on CT varies with clot age:

- Hyperacute o In most instances patients are not imaged in the hyperacute phase (first hour or so), but

on occasion when this is performed they appear relatively isodense to the adjacent

cortex. There is often underlying cerebral swelling which accentuates the mass effect created by the collection.

- Acute

o Crescent-shaped homogeneously hyperdense collection that spreads diffusely over the

affected hemisphere. - Chronic

o Eventually, the subdural collection becomes hypodense and can reach ~0HU and be

isodense to CSF - Acute on chronic


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o Acute on chronic subdural hematomas refers to a second episode of acute haemorrhage

into a pre-existing chronic subdural hematoma. It typically appears as a hyperdense blood pool posteriorly with a hypodense chronic collection anteriorly (as patient is lying

down when the scan is taken)

Subarachnoid Haemorrhage ● The presence of blood in subarachnoid space ● Has many causes such as infection, trauma, cerebral vasculitis and

cocaine use ● Hyperdense material is seen filling the subarachnoid space. ● Most commonly this is apparent around the circle of Willis

Ischaemic Stroke ● Results from a sudden cessation of adequate amounts of blood

reaching parts of the brain

● Normally use non-contrast CT in acute situations (see James’ PBL from week 4 for different types)

● On CT: - Immediate

o The earliest CT sign visible is a hyperdense segment of a vessel,

representing direct visualisation of the intravascular thrombus /

embolus and as such is visible immediately o Although this can be seen in any vessel, it is most often observed in

the middle cerebral artery o On the CT below, the yellow arrow shows the area of hyperdensity

caused by the thrombus


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- Early (1-3 hours) (also known as hyperacute phase) o Loss of grey-white matter differentiation (this is when the brain

looks the same colour throughout – as in you can’t distinguish

the grey matter from the white (these two are discussed above) – it shows swelling of the brain) – compare one hemisphere to the other and as you can see on the CT to the right, you-re unable to see the sulci very well and there’s less grey-white

matter differentiation

- First week

o With time the hypodensity and swelling become more marked

resulting in a significant

mass effect

Presenting a CT Head ● Obviously up to you how you want to do it but it’s good

having a structure: - This is a non-contrast/contrast etc. CT head Patient’s

name, age, date taken and brief history - Whether it’s a brain/bone window (almost 100% going to

be brain) - What plane it’s in: Axial, sagittal or coronal

- Blood – is there an obvious haemorrhage? - Infarction – Is there an obvious infarct? - Swelling – Is there grey-white matter differentiation and

are the sulci visible? - Mass Effect – Is there midline shift/thinning of the lumen

of ventricles?

- Anything else? – Is there any soft tissue swelling around the skull/fractures?

Arteriograms Coronary Angiography

● Contrast is injected into the left and right coronary arteries to look for any occlusion/stenosis


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Complications of the Procedure

● Average mortality or serious complication is 1/1000 cases due to: - Haemorrhage from arterial puncture site – more common in femoral than radial – firm

pressure should be applied to the site of bleeding

- Formation of a pseudo aneurysm – results from weakening of the femoral artery wall and may require surgical repair

- Infection of the puncture site or rarely septicaemia may occur. Blood cultures should be

taken - Thrombosis – results in a cold blue periphery

- Arrhythmias – may occur during the procedure due to coronary artery spasm

Left Coronary Artery ● Left Main Stem

- Left Anterior Descending Artery (LAD) – Cranial view most useful

- Circumflex – Caudal views are most useful


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Cranial Views ● Best way to view the LAD

Right Anterior Oblique (RAO), Cranial View ● Heart is on the right ● Apex points towards the right ● Ribs go down to the right ● LAD is on the right

Left Anterior Oblique (LAO), Cranial View ● Heart is on the left of the spine ● LAD extends towards the apex ● Ribs go down to the left ● “3 L’s” – in LAO, the LAD is on the Left

Caudal Views ● Best way to view the left circumflex artery

LAO, Caudal

● Left circumflex artery goes diagonal/down the view

Right Coronary Artery ● Obvious since it’s very far left


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Peripheral Angiograms


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module 4 osce notes · 2021. 1. 14. · module 4 osce notes sarah carlton 3 (“i’m now checking...

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