History and Examination of The Cardiovascular System - pediagenosis
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Saturday, November 10, 2018

History and Examination of The Cardiovascular System

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 and Examination of The Cardiovascular System

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.

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