Cardiology. There is a separate document introducing the ECG, with test-yourself examples.

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Cardiology

This document is based on the handout from the “Medicine for Finals” course. The notes provided here summarise key aspects, focusing on areas that are popular in clinical examinations. They will complement more detailed descriptions and are not intended to be comprehensive.

Topics covered in these notes

• Examination

• Atrial fibrillation

• Mitral valve disease

• Aortic valve disease

• Coronary heart disease

• Left ventricular failure

These are the core topics of cardiology. Additional topics include: a) arrhythmias

b) cardiomyopathy

c) hypertensive heart disease d) the ECG

There is a separate document introducing the ECG, with test-yourself examples.

There are three types of cardiomyopathy- dilated (the commonest), obstructive (HOCM; causing subvalvular left ventricular outflow obstruction-differential from aortic stenosis) and restrictive (rare). Dilated cardiomyopathy would be suspected in a patient presenting with heart failure who did not have a previous history of angina or myocardial infarction. When angiograms are performed, at least 60% of such patients are found to have “silent” coronary disease (ie previously undetected) and the remainder, with normal coronary arteries, have cardiomyopathy. This may be primary or secondary (for example alcohol-related).

Examination

• It doesn’t matter if you miss a physical sign, so long as your technique is good

• You need to look as though you have a routine, even if it is different from the

examiner’s; “acceptable variation”

• You need to look caring and competent

• Everyone misses diastolic murmurs

It is well recognised that diastolic murmurs are hard to detect, particularly with the added stress of a clinical examination. Cardiologists regularly miss diastolic murmurs too- or else arrange an echo before examining the patient so they know what they are looking for! The important point is to give yourself the best opportunity to hear them. This means lying the patient on the left hand side and listening with the bell for the low-pitched murmur of mitral stenosis. This murmur is probably the most localised of any heart sound, so “inching your way around the apex” is appropriate. Remember that to pick up low-pitched sounds the bell needs to be very lightly applied- too tight and it will convert the patient’s skin into a

diaphragm. Finally, you need to sit the patient forward and listen at the end of expiration with the diaphragm applied to the left sternal edge for the high pitched early diastolic murmur of aortic regurgitation.

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Question stop

What causes the first and second heart sounds?

What are the signs of endocarditis?

(Hint: try to mention the ones without people’s names attached first!)

What are the signs of clubbing?

Heart sounds: lub dub

ventricular systole diastole

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The first and second heart sounds are caused by valve closure. The first sound is caused by closure of the mitral and tricuspid valves and the second sound by the closure of aortic and pulmonary. If heart sounds were single, they would sound “le- de…le de”. The fact that each sound is composed of two valves closing, with a slight separation between them, results in “lub dub…lub dub”).

General examination

• Anaemia, cyanosis, breathlessness

• Hands for clubbing and splinters (the hand signs of endocarditis)

• Signs of endocarditis:

-

2 in the hands (clubbing and splinters)

-

1 in the heart (changing murmurs)

-

2 in the abdomen (splenomegaly, microscopic haematuria)

-

plus a few rarities (Osler, Roth, Janeway etc)

Pay particular attention to the instructions. There is a no win instruction- “examine the heart”. If you start checking the hand and pulse, the examiner could say “No I said the heart”. On the other hand, if you go straight for the praecordium (anterior chest wall for apex etc), the

examiner might say “Oh, don’t you bother with the pulse when you examine the heart?” If you are asked to examine the heart, you might check by saying “Normally I start with the hands and the pulse, is that what you intend me to do now?” This should make the examiner apologetic with either:

“Yes, examine the cardiovascular system” or “No confine your attention to the praecordium”

Stages of clubbing

• Increased fluctuancy (of nail bed)

• Loss of angle

• Increased curvature

• Drum stick appearance (expansion of terminal phalanx)

Stages of Clubbing

Stage 1: normal appearance and angle but increased fluctuancy of nail bed Stage 2: loss of angle between nail and nail bed

Stage 3: increase curvature of nail

Stage 4: expansion of terminal phalanx Drum stick appearance

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Examination

• Anaemia, cyanosis, breathlessness

• Hands for clubbing and splinters

• Pulse- rate, rhythm, character, volume

• Collapsing pulse test

• Ask for or measure blood pressure

• Neck for collapsing pulse; then JVP

Testing for a

Collapsing Pulse

JVP

• Everyone finds it confusing!

• The key is to think separately about the internal jugular (a pulsation) and the

external jugular (a visible superficial vein)

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Jugular venous pulse

• Neck relaxed as internal jugular is behind sterno-mastoid which should be relaxed

• Best to look from in front- you are looking for a pulsation not a visible vein

• JVP usually has a “double pulsation” compared with arterial pulse- may appear to

be “flickering”

• If raised, check for sacral or ankle oedema

The external jugular is best seen from the side, which is why many people look from the side when assessing the JVP. In fact, it is easier to see the pulsation of the internal jugular from the front. If in doubt, check both from the front and from the side- then everyone will be happy!

This is probably all you need to do as a medical student or junior doctor. If you haven’t seen the JVP, it is usually reasonable to assume the central venous pressure isn’t elevated. However, some clinicians want to be sure the JVP is not high, even when they haven’t seen it, and this is where, for many of us, things start to feel confusing.

If JVP not seen, 3 options to prove pressure not high

• Hepato-jugular reflux- painful and many false positives and false negatives

• Move patient slowly, step-by-step, into more horizontal position, noting angle at

which JVP seen (laborious)

• Fill and empty external jugular vein (light pressure just behind sternomastoid)

The first approach involves pressing on the abdomen, which transmits pressure via the inferior vena cava to the superior vena cava. This may make the JVP become visible in the neck. Removing the abdominal pressure should then result in a return to the initial situation- with no JVP visible. The problem is that there are both false positive and false negatives with this manoeuvre and it causes significant discomfort to the patient (“The last doctor punched me in the guts and looked at my neck- I don’t understand why they do that”).

The second approach is ideal for obsessionals. You move the patient into a progressively more horizontal position until the JVP becomes visible. If this is less than 45 degrees, the JVP is not elevated. This procedure involves so much wrestling with the pillow-rest that most people do not bother with it.

The third approach is quick and easy and where it works can be additional good evidence that the JVP is not elevated. Light pressure with one finger behind sternomastoid at the base of the neck, will lead, after a few seconds, to filling of the external jugular vein by blood draining from the head and neck. Then the examining finger is removed and the vein should empty again. This confirms that the “manometer pressure” is not high. Compressing the vein is the equivalent of filling the manometer of a CVP device (by connecting the fluid supply to the vertical measuring tube). Removing the finger is the equivalent of turning the three-way tap to connect manometer and patient.

External jugular vein

• Often distended and pulsatile when internal jugular pressure raised

• But false positives- may be distended if vein kinks as it pierces fascia in neck

• And false negatives: not visible if low flow or situated deeply or excess fat

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JVP: the evidence

• Poor validity- correlation with right atrial pressure from cardiac catheter data

• Poor reliability (McGee, S. 1998. American Heart Journal 136:10-18)

• Pulsation 3cm above sternal angle in either external or internal vein is significant

If anyone gives you a hard time about the JVP, it may be worth mentioning that it is one of the worst physical signs in the whole body- both in terms of reliability and validity. If it is obviously elevated, this can help, but if it is hard to assess, you may need additional

evidence of heart failure from echocardiography or cardiac catheterisation. This brings us full circle and is an argument for looking once only with the patient lying relaxed at 45 degrees and to forget the three manoeuvres to prove the pressure is not high!

Praecordium

• Apex beat (look for scars as well as feel)

• Left parasternal (for right ventricular impulse)

• Aortic and pulmonary areas for thrills

• Auscultation- bell and diaphragm from apex to neck

• Patient on left side with bell for mitral stenosis

• Patient sitting forward, at the end of expiration, with diaphragm (for aortic

regurgitation)

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Case 1: irregularly irregular pulse

Atrial fibrillation

• Loss of atrial contraction reduces cardiac output- often triggers heart failure

• Relative stagnation within atria gives high risk of thrombo-embolism

• Fast ventricular rate may occur; loss of diastolic filling time worsens heart failure

• Digoxin and verapamil slow rate by increasing delay at a-v node

• What are the main two possible explanations and how would you distinguish

them?

• What are the causes of atrial fibrillation?

• How would you assess whether atrial fibrillation is well controlled?

• Why is there sometimes a difference between the pulse rate taken at the wrist

and the apex?

• In a patient with atrial fibrillation taking warfarin, what level of INR would you

aim for?

• What level would you aim for if the patient had a prosthetic valve?

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Atrial fibrillation is probably the commonest case in clinical exams at undergraduate level. The other cause of an irregularly irregular pulse is the presence of multiple ventricular ectopic beats. This can be distinguished without an ECG because multiple ectopics should be

abolished by exercise, making the pulse become regular, whereas exercise simply increases the rate in atrial fibrillation. With an ectopic ventricular focus, beats are transmitted to the ventricle only occasionally when the refractory period allows. Increasing the sinus node rate by exercising the patient will make it less likely that the ectopic focus can “drive the ventricle”

Case 2: Mitral stenosis

• Malar flush

• Atrial fibrillation

• JVP not raised

• Apex beat not displaced

• Apex beat tapping in quality

Mitral stenosis: LUB de de

• Loud first heart sound (high left atrial pressure keeps valve open until late in

diastole; systole then slams it shut)

• Opening snap (high pitched sound just after second heart sound- best heard at

lower left sternal edge with diaphragm)

L U B D e D e

v e n tric u la r s y s to le d ia s to le

D e D e L U B

Now add a mid-diastolic murmur: LUB de derrr

•

LUB de-derrr

•

Rumbling low pitched and mid-diastolic if mild stenosis

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L u b D e D e rrrr

v entricula r systo le diastole

D e D e rrrr L U B

Mitral stenosis: the problem

• If severe, the murmur may become the dominant sound and the

ear plays tricks on you!

• So instead of hearing “LUB de derrr”

• You hear “DurrB de de”

• Particularly likely if atrial fibrillation

• Try to time the murmur with the carotid pulse

E a r p la y s tric k s : D u rrB d e d e

v e n tric u la r s ys to le d ia s to le

D e D e D u rrrrB D u rrrrB

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Aortic knuckle

Pulmonary vessels

Prominent left atrium

Left ventricle

(not enlarged in pure

stenosis)

Mitral Stenosis: x-ray appearance

Case 3: Mitral regurgitation

• More likely to be in sinus rhythm

• Much commoner (eg post myocardial infarction)

• Quiet first heart sound

• Pansystolic murmur

• Radiates LOUDLY to axilla

• Second heart sound not heard separately

M itral regurgitation: “burrr”

P ansystolic m urm ur diastole

lub de

no gap between m urm ur and H S 2

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Case 4: Aortic regurgitation

• Collapsing pulse (Corrigan’s pulse)

• Collapsing pulse in the neck (Corrigan’s sign)

• JVP not raised

• Apex beat displaced

• Diastolic murmur follows second sound

Aortic regurgitation: lub taaarr

lub taaar

Causes of aortic regurgitation

•

Rheumatic heart disease

•

Luetic heart disease (tertiary syphilis weakens aortic wall, causing dilatation)

•

Endocarditis

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Case 5: Aortic stenosis

• Slow rising pulse

• Low volume pulse with low pulse pressure

• JVP not elevated

• Apex beat forceful but not displaced (pressure overload)

• Ejection systolic murmur

Aortic stenosis

lub dub

second sound quiet with severe stenosis audible gap between

mumur and HS2

Coronary heart disease

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Circumflex

Left anterior descending Right coronary artery

Left main stem

Myocardial infarction

Left main stem Large anterior V1-V6 Pump problems Left anterior descending Anteroseptal V1-V4

Left circumflex Anterolateral 1, aVL, V4-6

Right coronary Inferior 2, 3, aVF Bradyarrhythmias

Case 6: Angina vs MI

•

Pain less severe and lasts less than 20 minutes

•

Relieved by nitrates

•

No sweating, nausea, vomiting

•

May get nitrate headache and hypotension

•

No fear of impending doom (poor predictive value)

Complications of MI

•

Sudden death on PRAED Street

•

P- pump failure

•

R- rupture of papillary muscle or septum

•

A- aneurysm and arrhythmias

•

E- embolism

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Investigations

• Temperature chart (often slight fever day 2)

• FBC, U+E (exclude anaemia; avoid low K

+

_{- arrhythmogenic)}

• Blood glucose; lipids (within 24hours as levels fall thereafter)

• Cardiac enzymes- CPK, AST, LDH (false positives with injury, alcohol, exercise)

• Troponins- myofibrillar proteins which link actin and myosin. More specific than

CPK for myocardial injury. Elevated early after 6 hours, peak 24hours; remain

elevated for 2 weeks; good for diagnosis of missed infarct; not for re-infarction)

• CXR- for cardiac size and evidence left ventricular failure

• Serial ECGs- may be normal initially, ST elevation, then q waves if transmural,

later t wave inversion

q waves

imply a full thickness transmural infarct; without them: subendocardial st elevation

Acute Myocardial Infarction

Treatment options: "MORE GAS"

M

Morphine or diamorphine with metoclopramide IV

O

Oxygen- high flow unless COPD

R Reassurance

E Explanation

G GTN

A Aspirin

S

Streptokinase (unless contraindication- local or generalised bleeding risk,

allergic problems etc)

What are the signs of left ventricular failure?

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Case 7: Acute LVF: on inspection

• Patient looks acutely unwell- pale and grey

• Cold clammy peripheries ? cyanosis

• Frothy blood stained sputum in sputum pot

• Orthopnoeic using accessory muscles

• May have wheeze (cardiac asthma)

Third heart sound: lub de dub

lub de dub

Acute LVF

•

Sinus tachycardia or atrial fibrillation

•

Systolic hypotension

•

Signs of cardiomegaly (displaced apex, signs of valve disease)

•

Third and fourth heart sounds

•

Right sided or bilateral pleural effusions

Fourth heart sound: le lub dub

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X-ray changes

• Cardiomegaly

• Upper lobe diversion

• Diffuse mottling of lung fields

• Prominent hilar shadows- bat’s wings

• One bat’s wing= “pseudotumour of heart failure” - usually at right hilum

• Small pleural effusions

• Fluid in fissures

Bat’s wings appearance in pulmonary oedema

Treatment options

• High dose oxygen

• Treat significant arrhythmias

• Intravenous diuretics

• Intravenous diamorphine; if no improvement-

• Repeat diuretics

• Vasodilator eg isosorbide infusion

ECG changes of hyperkalaemia

• Low flat p waves

• Broad bizarre qrs

• Slurring into the st segment

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Low flat P wave Broad bizarre QRS Slurring into the ST segm ent

Tall tented T waves

Treatment of life threatening hyperkalaemia

First arrange ECG monitor and access to resuscitation equipment Intravenous calcium gluconate (stabilises myocardium)

Glucose and insulin (drives potassium into cells) Further options include:

Cation exchange resins eg calcium resonium enema (takes several hours to work) Dialysis