Chapter 2 – Symptoms and Signs of Cardiac Disease




Abstract




Despite the widespread availability of investigational tests and imaging techniques for the diagnosis and management of cardiac disease, eliciting a comprehensive history and performing a systematic physical examination remain essential clinical skills.





Chapter 2 Symptoms and Signs of Cardiac Disease



Joseph E. Arrowsmith


Despite the widespread availability of investigational tests and imaging techniques for the diagnosis and management of cardiac disease, eliciting a comprehensive history and performing a systematic physical examination remain essential clinical skills.



Symptoms


The presence or absence of specific symptoms should be sought in a systematic fashion. Symptoms should be described in terms of their nature (using the patient’s own words), onset, duration and progression, as well as any modifying factors or associations.




  • Overall functional status: The NYHA functional capacity classification provides an assessment of the impact of symptoms (dyspnoea, angina, fatigue, palpitation) on physical activity. An objective assessment of severity of cardiovascular disease, added in 1994, recognizes the fact that severity of symptoms (i.e. functional capacity) may not reflect the severity of the underlying cardiovascular disease.



  • Dyspnoea: The sensation of uncomfortable breathing. It is essential to make the distinction between cardiac and respiratory causes. Mechanisms include: hypoxia, hypercarbia, bronchoconstriction, bronchial mucosal oedema, reduced lung compliance (increased work of breathing), reflex hyperventilation and reduced vital capacity (hydrothorax, ascites, pregnancy).




    • Cardiac causes include: Elevated pulmonary venous pressure, reduced pulmonary blood flow (right-to-left shunt), and a low CO (RV failure). An acute onset may suggest papillary muscle or MV chordal rupture, whereas a more insidious onset may suggest gradually worsening ventricular function.



    • Associated symptoms: Especially chest pain, palpitation, diaphoresis and (pre)syncope.



    • Postural: Supine (orthopnoea, paroxysmal noctural dyspnoea), other (atrial myxoma).



  • Haemoptysis: Not uncommon in cardiac disease. Frank haemoptysis may occur in MS (bronchial or pulmonary vein rupture) and pulmonary infarction. In pulmonary oedema the sputum is frothy and often streaked with blood. Pulmonary causes include: TB, bronchiectasis and cancer.



  • Chest pain: Aetiology may be cardiac (ischaemic and non-ischaemic) or non-cardiac. Enquiry should be made about the quality, location, radiation, timing and duration of pain, as well as any provoking, exacerbating or relieving factors and associated symptoms.




    • Non-ischaemic cardiac causes include: aortic dissection (‘tearing’ central pain, radiating to back), MV prolapse (sharp infra-mammary pain), pericarditis (dull central chest pain, worsened on leaning forward) and PE (pleuritic pain worse on inspiration).



    • Non-cardiac causes include: oesophagitis and oesophageal spasm (relieved by nitrates), biliary and pancreatic disorders, pleural inflammation and musculoskeletal disorders of the chest wall and spine.



  • Angina pectoris: Typically described as ‘choking’, ‘tightening’ or ‘heaviness’. Levine’s sign (hand clenched against the chest) may be present. Usually diffuse in nature, located to mid chest or xiphisternum with radiation to the left chest and arm, epigastrium, back or jaw. Typically lasting <10 minutes (duration >20 minutes may indicate ACS – infarction or unstable angina). Provoked by exertion, cold exposure, eating and emotional stress. May be worsened, or paradoxically relieved, by continuing exertion. Relieved by cessation of activity or nitrates. Typically graded using CCS angina scale.



  • Syncope: Transient loss or near loss (pre-syncope) of consciousness secondary to reduced cerebral blood flow – a low CO or cerebral perfusion pressure. The patient may describe ‘drop attacks’, a ‘funny turn’, dizziness or tinnitus. The presence of associated symptoms, such as a premonitory aura, palpitation or chest pain should be actively sought. The differential diagnosis includes: postural hypotension, neurological disorders and cardiac disease.




    • Postural hypotension may be drug-induced (e.g. β-blockers, vasodilators), vasovagal (e.g. micturitional), orthostatic (>20 mmHg fall in systolic BP on standing) or secondary to aortocaval compression when supine in pregnancy. DM and Parkinson’s disease may cause autonomic dysfunction.



    • A witnessed seizure may indicate epilepsy as the cause, whereas pre-syncope associated with transient dysphasia, blindness (amaurosis fugax) or paresis suggests a thromboembolic or vasculopathic cause.



    • Stokes–Adams attacks: Causes include sinus arrest, heart block and VT.



    • Exertional syncope: This may suggest AS, coronary artery disease (CAD), PHT or a congenital anomaly of coronary artery anatomy. A family history of syncope may indicate hypertrophic obstructive cardiomyopathy, takotsubo cardiomyopathy or an inherited cardiac conduction defect (long QT syndrome, Wolff–Parkinson–White syndrome).



  • Oedema: ‘Anasarca’, the accumulation of interstitial fluid in dependent areas such as the lower limbs and sacral area. Sodium and water retention may occur in cardiac failure, renal failure and malnutrition. Facial oedema may suggest myxoedema or SVC obstruction.



  • Palpitations: Awareness of heartbeat. ‘Thumping’ sensation in chest, neck or back; ‘missed’, ‘jumping’ or ‘extra’ beats; or ‘racing’ of the heart. A common symptom in the absence of cardiac disease. It may indicate significant dysrhythmia or abnormal cardiac function. Any relationship to exertion or ingestion of alcohol, caffeine or nicotine should be sought, as should symptoms suggestive of thyrotoxicosis.



  • Fatigue: A distinction should be made between lethargy or general malaise, and effort tolerance limited by chest pain, dyspnoea, claudication or leg weakness. As static measures of cardiac (ventricular) performance often give no indication of functional reserve, it is essential to obtain a measure of maximal functional capacity and the rapidity of any decline. The Duke Activity Status Index (DASI) is often used to grade functional capacity.



  • Miscellaneous: These include nausea, anorexia, dry mouth (disopyramide), nocturia and polyuria (diuretics), cough (ACE inhibitors), xanthopsia (digoxin toxicity), tinnitus and vertigo (chinchonism), headache (nitrates), photosensitivity (amiodarone), nightmares (propranolol), abdominal swelling/pain (ascites/hepatomegaly).



Physical Signs


Physical examination is conducted with the patient supine and reclining at 45°. The patient may be required to turn to the left, sit forward, stand or perform isometric exercise.



Observation (Inspection)




  • General appearance: Conscious level, nutritional status, diaphoresis, xanthelasmata, systolic head nodding (de Musset’s sign – AR) and signs of conditions associated with cardiac disease (Marfan, Cushing and Down syndromes, acromegaly, systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, muscular dystrophy).



  • Skin: Cyanosis, orange fingers (tobacco use), anaemia, jaundice (hepatic congestion), malar flush, erythema (pressure sores, cardioversion burns), haemorrhagic palmar/plantar lesions (Janeway lesions – endocarditis), bruising and phlebitis (venepuncture, IV therapy and drug abuse).



  • Surgical scars: These include sternotomy (cardiac surgery), thoracotomy (mitral valvotomy, repair of coarctation or patent ductus arteriosus (PDA)), subclavian (pacemaker or cardiodefibrillator insertion), cervical (carotid endarterectomy), antecubital (coronary angiography), abdominal (aortic aneurysm repair).



  • Nail beds: Clubbing, cyanosis, splinter haemorrhages, arterial pulsation (Quinke’s sign – AR), Osler’s nodes (tender finger-tip nodules – endocarditis).



  • Cyanosis: Cyanosis is blue skin discolouration. May be peripheral (hypovolaemia, low CO) or central (mucous membranes). The latter indicates a deoxygenated Hb concentration >5 g dl−1. May not be manifest in severe anaemia.



  • Respiratory rate: Tachypnoea may indicate anxiety or underlying dyspnoea. Episodic (Cheyne–Stokes) breathing is suggestive of severe cardiac failure.



  • Neck: Goitre, carotid abrupt carotid distension and collapse (Corrigan’s sign – AR), and jugular veins.



  • Jugular veins: Pressure level and waveform. Level rarely 2 cm above sternal angle when patient reclined at 45° and falls on inspiration. Inspiratory rise suggests pericardial constriction (Kussmaul’s sign). Elevated by anxiety, pregnancy, anaemia, exercise, right heart failure and SVC obstruction (non-pulsatile). Giant a-wave (TS, PS, RVH, RA myxoma), cannon a-wave (complete heart block, VT, junctional rhythm, pacing anomaly), systolic cv-wave (TR), slow y-descent (TS), sharp/short y-descent (pericardial constriction), increased x-descent (RV volume overload, tamponade).



  • Mouth: Foetor oris, mucous membrane dryness, state of dentition, palate, systolic uvular pulsation (Müller’s sign – AR).



  • Fundi: Hypertensive and diabetic changes, Roth spots (endocarditis).

Only gold members can continue reading. Log In or Register to continue

Aug 31, 2020 | Posted by in ANESTHESIA | Comments Off on Chapter 2 – Symptoms and Signs of Cardiac Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access