History and Examination of The Cardiovascular System
Presenting complaint The reason the patient has sought medical attention. Most common in
cardiovascular disease are chest pain, dyspnoea (breathlessness), palpitations
and syncope (dizziness).
History of presenting complaint Explore features of the presenting complaint (e.g. onset, progression,
severity; Figure 32a).
· Dyspnoea: the commonest symptom of heart disease. Establish whether it occurs
at rest, on exertion, on lying flat (orthopnoea) or at night. Determine
rate of onset (sudden, gradual). Dyspnoea due to pulmonary oedema (heart failure)
may cause sudden wakening (paroxysmal nocturnal dyspnoea, PND), a
frightening experience in which the patient wakes at night, gasping for breath.
·
Cheast pain ‘SOCRATES’
Site: where is it? Onset:
gradual, sudden? Character: sharp, dull, crushing? Radiation: to
arm, neck, jaw? Associated symptoms: dyspnoea, sweating, nausea, syncope
or palpitations? Timing: duration of the pain? Is it constant or does it
come and go? Exacerbating and relieving factors: worse/better with
breathing, posture? Severity: does it interfere with daily activities or
sleep? Angina is described as crushing central chest pain, radiating to
left arm/shoulder, back, neck or jaw. Pain due to pericarditis is sharp
and severe, aggravated by inspiration, and is classically relieved by leaning
forward.
• Palpitations: increased awareness of the heart beat. Ask patient to tap out the
rhythm. Premature beats and extrasystoles give sensation of missed beats.
·
Syncope: commonly vasovagal, provoked by anxiety or standing for
extended periods of time. Cardiovascular syncope is usually due to sudden
changes in heart rhythm; for example, heart block, paroxysmal arrhythmias (Stokes Adams attacks).
· Others: fatigue – heart failure, arrhythmias and drugs (e.g. β-blockers).
Oedema and abdominal discomfort – raised central venous pressure (CVP), heart
failure. Leg pain on walking may be due to claudication secondary to
peripheral vascular disease.
Past medical history Previous and current conditions. Ask about myocardial infarction
(MI), stroke, hypertension, diabetes, rheumatic fever. Also recent blood
pressure measurements and lipid levels, and any investigations.
Drug history Prescribed
and over-the-counter medications. Ascertain compliance. Ask about drug
allergies and their effect(s). Family, occupational and social
history Family history of MI, hypertension, diabetes, stroke or sudden
death? Smoking including duration and amount and alcohol consumption. Occupation: stress,
sedentary or active.
General examination (Figure
32a)
Assess general appearance: obesity, cachexia (wasting),
jaundice. Note the presence of scars; for example, a sternotomy scar in the
midline (coronary artery bypass graft, CABG; valve replacement). NB: if a
midline sternotomy scar is present, inspect the legs for a saphenous vein graft
scar.
· Hands: warm and well-perfused or cold? Peripheral cyanosis (dusky blue
discoloration, deoxyhaemoglobin >5 g/dL, e.g. vasoconstriction, shock, heart
failure; not seen in anaemia); assess capillary refill by pressing on the
nail bed for 5 s and releasing. Normal capillary refill is <2 s. Inspect
nails for clubbing (Figure 32a), tar stains, splinter haemorrhages (infective
endocarditis). Inspect the finger pads for Janeway lesions and Osler’s nodes
(infective endocarditis).
·
Pulses: radial pulse; assess rate and character (regular or irregular). Feel
for a collapsing pulse (aortic regurgitation).
·
Blood pressure: measure the blood pressure over the brachial artery (ideally in both
arms and take the highest reading).
·
Face and neck: determine whether or not the jugular venous pressure (JVP) is
raised. It is raised if the tip of the pulsation in the internal jugular vein
is >3 cm above the angle of Louis. Feel the carotid pulse and assess its
volume and character. Inspect the conjunctivae for pallor (anaemia);
cornea for corneal arcus (hyperlipidaemia, although normal in old age); eyelids
for xanthelasma (soft yellow plaques: hyperlipidaemia); tongue for central
cyanosis; dental hygiene (infective endocarditis); cheeks for malar flush (mitral
valve disease); retinae for hypertensive or diabetic retinopathy.
Examination of the praecordium
• Palpation: apex beat, usually at fifth
intercostal space, midclavicular line (mitral area). Non-palpable:
obesity, hyperinflation, pleural effusion. Displaced: cardiomegaly,
dilated cardiomyopathy, pneumothorax. Tapping: mitral stenosis. Double:
ventricular hypertrophy. Heaving (forceful and sustained): pressure
overload – hypertension, aortic stenosis. Parasternal heave:
right ventricular hypertrophy. Thrills are palpable (therefore strong)
murmurs (see below).
• Auscultation (Figure 32e; see Chapters
14, 52–54): correlate with radial or carotid pulse. First heart sound (S1):
closure of mitral and tricuspid valves. Loud: atrioventricular valve
stenosis, short PR interval; soft: mitral regurgitation, long PR
interval, heart failure. Second heart sound (S2):
closure of aortic (A2) and pulmonary (P2) valves, A2
louder and preceding P2. Loud A2/P2:
systemic/pulmonary hypertension. Splitting: normal during inspiration or
exercise, particularly in the young. Wide splitting: delayed activation
(e.g. right bundle branch block) or termination (pulmonary hypertension,
stenosis) of RV systole. Reverse splitting: delayed activation (e.g.
left bundle branch block) or termination (hypertension, aortic stenosis) of
LV systole. Others: S3 – rapid ventricular filling,
common in the young but may reflect heart failure in patients >30 years. S4
– precedes S1, due to ventricular stiffness and abnormal filling during
atrial systole. Presence of S3 and/or S4 gives a gallop
rhythm. Ejection click: after S1, opening of stenotic
semilunar valve. Opening snap: after S2, opening of stenotic
atrioventricular valve.
• Murmurs (Figure 32e): added sounds due
to turbulent blood flow. Soft systolic murmurs are common and innocent in young
(∼40% children 3–8 years) and in
exercise; diastolic murmurs are pathological. Most non-benign murmurs are due to valve
defects (see Chapters 53 and 54). Others include a hyperdynamic circulation
and atrial or ventricular septal defects.
• Abdomen: palpate for liver enlargement (hepatomegaly),
ascites (raised CVP, heart failure), splenomegaly (infective endocarditis). The
abdominal aorta is pulsatile in thin individuals but not expansile
(indicates abdominal aortic aneurysm).
• Lower limbs: pitting oedema, peripheral
vascular disease.
Pulse (Figure 32b)
Resting rate 60–90 beats/min, slows with age and
fitness. Compare radial with apex beat (delay: e.g. atrial fibrillation) and
femoral/ lower limbs (delay: atherosclerosis, aortic stenosis). Changes in rate
with breathing are normal (sinus arrhythmia).
• Irregular beats Regularly irregular: e.g. extrasystoles (disappear on exertion), second-degree heart
block. Irregularly irregular: e.g. atrial fibrillation (unchanged by
exertion).
• Character (carotid): thready or weak:
heart failure, shock, valve disease; slowrising: aortic stenosis. Bounding:
highoutput; followedby sharp fall (collapsing): very high
output, aortic valve regurgitation. Alternating weak–strong (pulsus
alternans): left heart failure; distinguishfrom pulsus bigeminus,
normal beatfollowedby weakpremature beat. Pulsus paradoxus,
accentuated weakening of pulse on inspiration: cardiac tamponade, severe
asthma, restrictive pericarditis.
Blood pressure (Figure 32c)
At rest, adult arterial systolic pressure is normally
<140 mmHg, diastolic <90 mmHg. Systolic rises with age.
• JVP (Figure 32d): Indirect measure of
right atrial pressure. Raised in heart failure and volume overload. Large ‘a’
wave (see Chapter 16): pulmonary hypertension, pulmonary valve stenosis,
tricuspid stenosis; large ‘v’ wave: tricuspid regurgitation. Absent ‘a’ wave:
atrial fibrillation.
