Cardiovascular history and examination Flashcards
Cardiovascular history: chest pain
SOCRATES.
Site- central?
Onset- sudden? what was the patient doing?
Character- ask patient to describe pain, crushing? heavy?
Radiation- ask specifically if it moves to the arm, neck, or jaw.
Associations- ask specifically about SOB, nausea, sweating.
Timing? Duration?
Exacerbating and alleviating factors- worse with respiration or movement (less likely angina)? relieved by GTN? worse on inspiration and better leaning forwards (pericarditis)?
Severity- out of 10?
Is patient known to have angina or chest pain? better/worse/same as usual pain? more frequent? decreasing exercise tolerance?
‘Heartburn’ more likely if ‘burning’, onset after eating/drinking, worse lying flat, or associated with dysphagia.
Cardiovascular history: palpitations
‘Ever aware of your own heartbeat?
When and how did it start/stop?
Duration?
Onset sudden/gradual?
Associated with blackout (how long)?
Chest pain?
Dyspnoea?
Food related, e.g. caffeine?
Regular fast palpitations may reflect paroxysmal supra ventricular tachycardia (SVT) or ventricular tachycardia (VT).
Irregular fast palpitations are likely to be paroxysmal AF, or atrial flutter with variable block.
Dropped or missed beats related to rest, recumbency, or eating are likely to be atrial or ventricular ectopics.
Regular pounding may be due to anxiety.
Slow palpitations are likely to be due to drugs such as beta-blockers, or bigeminus.
Reassurance is vital and can be therapeutic.
Check a TSH and consider a 24hr ECG (Holter monitor).
Cardiovascular history: dyspnoea
Duration?
At rest?
On exertion?
Determine exercise tolerance (and any other reason for limitation, e.g. arthritis).
NYHA classification?
Worse when lying flat, how many pillows does the patient sleep with (orthopnoea)?
Does the patient ever wake up in the night gasping for breath (paroxysmal nocturnal dyspnoea), and how often?
Any ankle swelling?
Cardiovascular history: dizziness/blackouts
Did they lose consciousness? for how long? short duration suggests cardiac while long duration suggests neurological cause. Any warning (pre-syncope)? What was patient doing at the time? Sudden/gradual? Associated symptoms? Any residual symptoms, e.g. confusion? How long did it take for patient to return to 'normal'? Tongue biting, seizure, incontinence? Witnessed? Memory loss pre/post event?
Cardiovascular history: claudication
SOCRATES.
Foot/calf/thigh/buttock?
Claudication distance- how long can the patient walk before onset of pain?
Rest pain?
Cardiovascular history: past history
Angina? Any previous heart attack or stroke? Rheumatic fever? Diabetes? Hypertension? Hypercholesterolaemia? Previous tests/procedures (ECG, angiograms, angioplasty/stents, echocardiogram, cardiac scintigraphy, coronary artery bypass grafts)?
Cardiovascular history: drug history
Aspirin GTN Beta-blocker Diuretic ACE inhibitor Digoxin Statin Anticoagulant
Cardiovascular history: family history
First degree relatives having had cardiovascular events, especially if <60 years.
Cardiovascular history: social history
Smoking Impact of symptoms on daily life Alcohol (number of units) Hobbies Exercise
Cardiovascular history: ischaemic heart disease risk factors
Hypertension Smoking Diabetes mellitus Family history (1st degree relative <60yrs old with IHD) Hyperlipidaemia
Cardiovascular examination: introductions
Introduce yourself. Obtain consent to examine. Position the patient appropriately- lying on the bed at 45 degrees. Expose them to the waist. Explain what you are doing throughout.
Cardiovascular examination: general inspection
Assess general state (ill/well). Look for clues (oxygen, GTN spray). Colour (pale, cyanosed, flushed). Short of breath? Scars on chest wall?
Cardiovascular examination: hands
Temperature: capillary refill time.
Inspect skin: tobacco staining, peripheral cyanosis, tendon xanthomata (hyperlipidaemia), Janeway lesions, Osler’s nodes (signs of infective endocarditis).
Inspect nails: clubbing, splinter haemorrhages, nail bed pulsation (Quincke’s sign of aortic regurgitation), nail fold infarcts (vasculitis).
Clubbing = congenital cyanotic heart disease and endocarditis.
Splinter haemorrhages, Osler’s nodes (tender nodules, e.g. in finger pulps) and Janeway lesions (red macules on palms) are signs of infective endocarditis- if found, examine the fundi for Roth’s spots (retinal infarcts).
Cardiovascular examination: radial and brachial pulses
Radial: rate, rhythm, radio-radial delay (palpate pulse bilaterally simultaneously, e.g. from aortic arch aneurysm), radiofemoral delay (palpate ipsilateral pulses simultaneously- sign of coarctation of aorta), collapsing pulse (identify radial pulse, then wrap your fingers around wrist- check for pain in arm/shoulder before elevating arm from the elbow straight up).
Brachial: just medial to tendinous insertion of biceps; waveform character.
Cardiovascular examination: blood pressure
Hyper- or hypotensive? Pulse pressure (wide = aortic regurgitation, arteriosclerosis; narrow = aortic stenosis, dry).
Cardiovascular examination: neck
JVP: ask patient to turn head to the left and look at the supraclavicular fossa- comment on the height of the JVP and waveform, press on the abdomen to check the abdomino-jugular reflex.
Carotid pulse: inspect (visible carotid = Corrigan’s sign of aortic regurgitation), and palpate volume and character on one side then the other.
Cardiovascular examination: face
Colour: pale, flushed, central cyanosis.
Features: corneal/senile arcus, xanthelasma (signs of dyslipidaemia).
Pallor of the conjunctiva (anaemia).
Malar flush (mitral stenosis, low cardiac output).
Dental hygiene.
Exophthalmos or goitre (signs of Graves’ disease).
Dysmorphic face? e.g. Down’s syndrome, Marfan’s syndrome, etc.
Cardiovascular examination: praecordium, inspection
Scars: midline sternotomy, lateral thoracotomy (mitral stenosis valvotomy).
Cardiovascular examination: praecordium, palpation
Apex beat (lowermost lateral pulsation): usually 5th intercostal space in mid-clavicular line; measure position by counting intercostal spaces (sternal notch = 2nd intercostal space)- undisplaced/displaced? character: impalpable (?dextrocardia/COPD), tapping (palpable S1), double impulse, sustained/strong; count rate if pulse irregular.
Heaves and thrills: place the heel of the hand flat on chest to left then right of sternum; left parasternal heave = sustained thrusting usually felt at left sternal edge (right ventricular enlargement, e.g. in pulmonary stenosis, cor pulmonate, ASD); thrill = palpable murmur felt as a vibration beneath your hand.
Heaving: caused by outflow obstruction, e.g. aortic stenosis or systemic hypertension.
Thrusting: caused by volume overload, e.g. mitral or aortic incompetence.
Tapping: mitral stenosis, essentially a palpable 1st heart sound.
Diffuse: LV failure, dilated cardiomyopathy.
Double impulse: hypertrophic cardiomyopathy.
Cardiovascular examination: praecordium, auscultation
Apex (mitral area): listen with bell and diaphragm, identify 1st and 2nd heart sounds- are they normal? listen for added sounds and murmurs; with the diaphragm listen for a pan systolic murmur radiating to the axilla- mitral regurgitation.
At apex with bell, ask the patient to ‘roll over onto your left side, breathe out, and hold it there’ (a rumbling mid-diastolic murmur = mitral stenosis).
Lower left sternal edge (tricuspid area) and pulmonary area (left of manubrium in the 2nd intercostal space)- if suspect right-sided murmur, listen with patient’s breath held in inspiration.
Right of manubrium in 2nd intercostal space (aortic area)- ejection systolic murmur radiating to the carotids = aortic stenosis.
Sit the patient up and listen at the lower left sternal edge with patient held in expiration (early diastolic murmur = aortic regurgitation).
Also listen for bruits over the carotids if there is inequality between pulses or absence of a pulse: atherosclerosis, vasculitis.
Cardiovascular examination: to complete the examination
Palpate for sacral and ankle oedema.
Auscultate the lung bases for inspiratory crackles.
Examine the abdomen for a pulsatile liver and aortic aneurysm.
Check peripheral pulses, observation chart for temperature and oxygen sats, dip urine, perform fundoscopy.
Cardiovascular examination: lungs
Examine the bases for creps and pleural effusions, indicative of heart failure.
Cardiovascular examination: oedema
Examine the ankles, legs, sacrum, and torso for pitting oedema.
Cardiovascular examination: abdomen
Hepatomegaly and ascites in right-sided heart failure.
Pulsatile hepatomegaly with tricuspid regurgitation.
Splenomegaly with infective endocarditis.
Cardiovascular examination: fundoscopy
Roth spots: infective endocarditis.
Cardiovascular examination: urine dipstick
Haematuria.
Cardiovascular examination: presenting your findings
Signs of heart failure?
Clinical evidence of infective endocarditis?
Sinus/abnormal rhythm?
Heart sounds normal, abnormal, or additional?
Murmurs?
What is postural hypotension?
This is an important cause of falls and faints in the elderly.
It is defined as a drop in systolic BP of >20mmHg or diastolic >10mmHg after standing for 3 minutes vs lying.
What are the causes of postural hypotension?
Hypovolaemia (early sign).
Drugs, e.g. nitrates, diuretics, antihypertensives, antipsychotics.
Addison’s.
Hypopituitarism (low ACTH).
Autonomic neuropathy (DM, multisystem atrophy).
After a marathon run (peripheral resistance is low for some hours).
Idiopathic.
What is the treatment of postural hypotension?
Lie down if feeling faint.
Stand slowly (with escape route- don’t move away from the chair too soon).
Consider referral to ‘falls clinic’.
Manage autonomic neuropathy.
Increase water and salt ingestion.
Physical measures: leg crossing, squatting, elastic compression stockings, careful exercise.
If post-prandial dizziness, eat little and often, reduce carbohydrate and alcohol intake.
Head-up tilt of the bed at night increases renin release, so decreases fluid loss and increases standing BP.
1st-line drug = fludrocortisone, 2nd line = sympathomimetics e.g. midodrine or ephedrine, pyridostigmine.
What are the signs on physical examination of hyperlipidaemia?
Xanthomata are localised deposits of fat under the skin, occurring over joints, tendons, hands and feet.
Xanthelasma = xanthoma on the eyelid.
Corneal arcus = crescentic-shaped opacity at the periphery of the cornea.
Cardiovascular examination: pulses, rate
Is the pulse fast ≥100bpm or slow ≤60bpm?
Cardiovascular examination: pulses, rhythm
An irregularly irregular pulse occurs in AF or multiple ectopics.
A regularly irregular pulse occurs in secondary heart block and ventricular bigeminus.
Cardiovascular examination: pulses, character and volume, types
Bounding pulses. Small volume pulses. Collapsing 'waterhammer' pulses. Anacrotic (slow-rising) pulses. Bisferiens pulses. Pulsus alternans. Jerky pulses. Pulsus paradoxus.
Cardiovascular examination: pulses, character and volume, causes of bounding pulses
CO2 retention.
Liver failure.
Sepsis.
Cardiovascular examination: pulses, character and volume, causes of small volume pulses
Aortic stenosis.
Shock.
Pericardial effusion.
Cardiovascular examination: pulses, character and volume, causes of collapsing ‘waterhammer’ pulses
Aortic incompetence.
AV malformations.
Patent ductus arteriosus.
Cardiovascular examination: pulses, character and volume, cause of anacrotic (slow-rising) pulses
Aortic stenosis.
Cardiovascular examination: pulses, character and volume, cause of bisferiens pulses
Combined aortic stenosis and regurgitation.
Cardiovascular examination: pulses, character and volume, causes of pulsus alternans
– Alternating strong and weak beats –
LVF.
Cardiomyopathy.
Aortic stenosis.
Cardiovascular examination: pulses, character and volume, cause of jerky pulses
Hypertrophic cardiomyopathy.
Cardiovascular examination: pulses, character and volume, causes of pulsus paradoxus
– Systolic pressure weakens in inspiration by >10mmHg –
Severe asthma.
Pericardial constriction.
Cardiac tamponade.
Cardiovascular examination: JVP, overview
The internal jugular vein acts as a capricious manometer of right atrial pressure.
Observe the height and the waveform of the pulse.
JVP observations are often difficult.
Concomitantly palpate the arterial pulse to help decipher patterns.
Cardiovascular examination: JVP, height
Observe the patient at 45 degrees with their head turned slightly to the left and neck relaxed.
Good lighting and correct positioning are key.
Look for the right internal jugular vein as it passes just medial to the clavicular head of the sternocleidomastoid up behind the angle of the jaw to the earlobes.
The JVP is assessed by measuring the vertical height from the manubriosternal angle (not the sternal notch) to the top of the pulse.
Pressure at 0 (sternal angle) is 5cm, so add the height of the JVP with 5cm to obtain the right heart filling pressure in cm of water.
A pressure above 9cm (4cm above the sternal angle at 45 degrees) is elevated.
Cardiovascular examination: JVP, is the pulse venous (and not arterial)?
Usually impalpable, and obliterated by finger pressure on the vessel.
Rises transiently with pressure on abdomen (abdominojugular reflux) or on liver (hepatojugular reflux), and alters with posture and respiration (disappears when patients sits from lying flat).
Usually has a double pulse for every arterial pulse.
Cardiovascular examination: JVP, abnormalities
Raised JVP with normal waveform. Fixed raised JVP with absent pulsation. Large a wave. Cannon a wave. Absent a wave. Large v waves. Constrictive pericarditis. Absent JVP.
Cardiovascular examination: JVP, abnormalities, causes of raised JVP with normal waveform
Fluid overload.
Right heart failure.
Cardiovascular examination: JVP, abnormalities, cause of fixed raised JVP with absent pulsation
SVC obstruction.
Cardiovascular examination: JVP, abnormalities, causes of large a wave
Pulmonary hypertension.
Pulmonary stenosis.
Cardiovascular examination: JVP, abnormalities, cannon a wave
When the right atrium contracts against a closed tricuspid valve, large ‘cannon’ a waves result.
Causes: complete heart block, single chamber ventricular pacing, ventricular arrythmias/ectopics.
Cardiovascular examination: JVP, abnormalities, cause of absent a wave
Atrial fibrillation.
Cardiovascular examination: JVP, abnormalities, cause of large v waves
Tricuspid regurgitation- look for earlobe movement.
Cardiovascular examination: JVP, abnormalities, constrictive pericarditis
High plateau of JVP (which rises on inspiration- Kussmaul’s sign) with deep x and y descents.
Cardiovascular examination: JVP, abnormalities, absent JVP
When lying flat, the jugular vein should be filled.
If there is reduced circulatory volume (e.g. dehydration, haemorrhage) the JVP may be absent.
Cardiovascular examination: heart sounds, S1
Represents closure of mitral (M1) and tricuspid (T1) valves.
Splitting in inspiration may be heard and is normal.
The intensity of S1 is variable in AV block, AF, and nodal or ventricular tachycardia.
Cardiovascular examination: heart sounds, loud S1
In mitral stenosis, because the narrowed valve orifice limits ventricular filling, there is no gradual decrease in flow towards the end of diastole.
The valves are therefore at their maximum excursion at the end of diastole, so shut rapidly leading to loud S1 (‘tapping’ apex).
S1 is also loud if diastolic filling time is shortened, e.g. if the PR interval is short, and in tachycardia.
Cardiovascular examination: heart sounds, soft S1
Occurs if the diastolic filling time is prolonged, e.g. prolonged PR interval, or if the mitral valve leaflets fail to close properly (i.e. mitral incompetence).
Cardiovascular examination: heart sounds, S2
Represents aortic (A2) and pulmonary (P2) valve closure. The most important abnormality of A2 is aortic stenosis. A2 is loud in tachycardia, hypertension, and transposition.
Cardiovascular examination: heart sounds, splitting of S2
Normal in inspiration, may be due to the variation of right heart venous return with respiration, delaying the pulmonary component.
May be wide, wide fixed, reversed, single S2.
Splitting and P2 are best heard in the pulmonary area.
Cardiovascular examination: heart sounds, causes of wide splitting of S2
Occurs in RBBB, pulmonary stenosis, deep inspiration, mitral regurgitation, and VSD.
Cardiovascular examination: heart sounds, cause of wide fixed splitting of S2
Occurs in atrial septal defect.
Cardiovascular examination: heart sounds, reversed splitting of S2 and causes
A2 following P2, with splitting increasing on expiration.
Occurs in LBBB, aortic stenosis, patent ductus arteriosus, right ventricular pacing.
Cardiovascular examination: heart sounds, causes of single S2
Occurs in Fallot’s tetralogy, severe aortic or pulmonary stenosis, pulmonary atresia, Eisenmenger’s syndrome, large VSD, or hypertension.
Cardiovascular examination: heart sounds, additional sounds
3rd heart sound. 4th heart sound. Triple and gallop rhythms. Ejection systolic click. Mid-systolic clicks. Opening snap. Prosthetic sounds.
Cardiovascular examination: heart sounds, additional sounds, 3rd heart sound
S3 may occur just after S2.
It is low pitched and best heard with the bell of the stethoscope.
S3 is pathological over the age of 30.
A loud S3 occurs in a dilated left ventricle with rapid ventricular filling (mitral regurgitation, VSD) or poor LV function (post MI, dilated cardiomyopathy).
In constrictive pericarditis or restricted cardiomyopathy, it occurs early and is more high pitched (‘pericardial knock’).
Cardiovascular examination: heart sounds, additional sounds, 4th heart sound
S4 occurs just before S1.
Always abnormal, it represents atrial contraction against a ventricle made stiff by any cause, e.g. aortic stenosis or hypertensive heart disease.
Cardiovascular examination: heart sounds, additional sounds, triple and gallop rhythms
A 3rd or 4th heart sound occurring with a sinus tachycardia may give the impression of galloping hooves.
An S3 gallop has the same rhythm as ‘Ken-tucky’, whereas an S4 gallop has the same rhythm as ‘Tenne-ssee’.
When S3 and S4 occur in a tachycardia, e.g. with pulmonary embolism, they may summate and appear as a single sound, a summation gallop.
Cardiovascular examination: heart sounds, additional sounds, ejection systolic click
Heard in early systole with bicuspid aortic valves, and if raised BP.
The right heart equivalent lesions may also cause clicks.
Cardiovascular examination: heart sounds, additional sounds, cause of mid-systolic click
Occurs in mitral valve prolapse.
Cardiovascular examination: heart sounds, additional sounds, opening snap
Precedes the mid-diastolic murmur of mitral (and tricuspid) stenosis.
Indicates a pliable (non-calcified) valve.
Cardiovascular examination: heart sounds, additional sounds, prosthetic sounds
Caused by non-biological valves, on opening and closing, rumbling sounds = ball and cage valves (e.g. Starr-Edwards), single clicks = tilting disc valve (e.g. single disc: Bjork Shiley; bileaflet: St Jude, often quieter).
Prosthetic mitral valve clicks occur in time with S1, aortic valve clicks in time with S2.
Cardiovascular examination: cardiac murmurs, ejection systolic murmur
Crescendo-decrescendo.
Usually originates from the outflow tract and waxes and wanes with the interventricular pressures.
ESM may be innocent and common in children and high-output states, e.g. tachycardia, pregnancy.
Organic causes include aortic stenosis and sclerosis, pulmonary stenosis, and hypertrophy cardiomyopathy.
Cardiovascular examination: cardiac murmurs, pansystolic murmur
Uniform intensity.
Merges with S2.
Usually organic and occurs in mitral or tricuspid regurgitation (S1 may also be soft in these) or ventricular septal defect.
Mitral valve prolapse may produce a late systolic murmur ± mid-systolic click.
Cardiovascular examination: cardiac murmurs, early diastolic murmur
High-pitched and easily missed.
Listen for the ‘absence of silence’ in early diastole.
Occurs in aortic and rarely in pulmonary regurgitation.
If the pulmonary regurgitation is secondary to pulmonary hypertension resulting from mitral stenosis, it s a Graham Steell murmur.
Cardiovascular examination: cardiac murmurs, mid-diastolic murmur
Low pitched and rumbling.
Occurs in mitral stenosis (accentuated presystolically if heart still in sinus rhythm), rheumatic fever (Carey Coombs’ murmur- due to thickening go the mitral valve leaflets), and aortic regurgitation (Austin Flint murmur- due to fluttering of the anterior mitral valve cusp caused by the regurgitation stream).
Cardiovascular examination: cardiac murmurs, intensity
All murmurs are graded on a scale of 1-6, though in practice diastolic murmurs, being less loud, are only graded 1-4.
Intensity is a poor guide to the severity of a lesion- an ESM may be inaudible in severe aortic stenosis.
Cardiovascular examination: cardiac murmurs, area where loudest
Though an unreliable sign, mitral murmurs tend to be loudest over the apex, in contrast to the area of greatest intensity from lesions of the aortic (right 2nd intercostal space), pulmonary (left 2nd intercostal space), and tricuspid (lower left sternal edge) valves.
Cardiovascular examination: cardiac murmurs, radiation
The ESM of aortic stenosis classically radiates to the carotids, in contrast to the PSM of mitral regurgitation, which radiates to the axilla.
Cardiovascular examination: cardiac murmurs, accentuating manoeuvres
Movements that bring the relevant part of the heart closer to the stethoscope accentuate murmurs (e.g. leaning forward for aortic regurgitation, left lateral position for mitral stenosis).
Expiration increases blood flow to the left side of the heart and therefore accentuates left-sided murmurs. Inspiration has the opposite effect.
Valsalva manoeuvre (forced expiration against closed glottis) decreases systemic venous return, accentuating mitral valve prolapse and hypertrophic cardiomyopathy, but softening mitral regurgitation and aortic stenosis. Squatting has the opposite effect. Exercise accentuates the murmur of mitral stenosis.
Cardiovascular examination: cardiac murmurs, non-valvular murmur
A pericardial friction rub may be heard in pericarditis.
It is a superficial scratching sound, not confined to systole or diastole.
Continuous murmurs are present throughout the cardiac cycle and may occur with a patent ductus arteriosus, arteriovenous fistula, or ruptured sinus of Valsalva.
