The previous article (Byrne, 2021) discussed cardiac anatomy and many of the conditions that can affect the heart and aorta. The major presentations of cardiac conditions were introduced, and the clinical examination was outlined. In this article, the aim is to examine each of these presenting complaints in more detail and highlight common findings in the history, examination and investigations that may aid diagnosis in the emergency department. The common presentations are chest pain, dyspnoea, syncope, and palpitations (Bickley, 2017).
Chest pain
Chest pain is a common complaint, comprising up to 25% of emergency department attendances (Byrne, 2014). Not all of these will have a cardiac complaint; however, it is crucial to recognise important cardiac presentations such as acute coronary syndromes (ACS), an umbrella term for unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). In addition, aortic dissection, pericarditis, myocarditis and myopericarditis often present with chest pain.
Acute coronary syndromes
These occur when lipid-rich plaques form within the intima of the affected coronary artery. Many factors combine to cause plaque rupture, disrupting the smooth laminar flow of blood and encouraging thrombus formation (Collet et al, 2021). Thrombus may partially or completely occlude the artery, causing myocardial ischaemia, which in turn causes chest pain (Figure 1).
Figure 1. Atherosclerosis of the coronary arteries and various types of acute coronary syndrome
The initial tools in suspected ACS are a clinical history and electrocardiogram (ECG). Blood tests including high-sensitivity troponin T testing (HSTnT) will confirm or refute the diagnosis (Collet et al, 2021).
History
- Location of pain: many people complain of central chest pain, which may radiate to one or both arms, the back, or the jaw (Bickley, 2017)
- Severity and character: usually severe, central, crushing, heavy weight
- Onset: depending on whether unstable angina or NSTEMI/STEMI, it may be sudden onset or have stuttering onset, meaning that there may have been increasing symptoms during the preceding days and weeks. If there are no obvious ECG changes, the patient may be suffering from unstable angina, and intervention at this stage may prevent NSTEMI/STEMI. Pain lasting longer than 20 minutes should be suspected as possible myocardial infarction (MI) (Collet et al, 2021)
- Provocation and palliation of pain: in the case of unstable angina, the pain may come on with exertion and ease with rest or glyceryl trinitrate (GTN) spray. Pain at rest is a red flag. With NSTEMI/STEMI the pain may not relieve until the patient is given intravenous opiates.
Clinical examination
Often there is nothing to find; however, the presence of a new murmur, crackles in the lungs or hypotension are possible indicators of critical illness.
The ECG in ACS
The main signs of ischaemia will be T-wave inversions, ST-segment depression (unstable angina or NSTEMI) (Figure 1), or ST-segment elevation (STEMI) (Figure 2). The location of ECG changes relate to the area supplied by an artery and are described as anterior, inferior, posterior, or lateral (Ramrakha and Hill, 2012). It is beyond the scope of this article to attempt to explain the intricacies of ECG interpretation, however, it is recommended that readers familiarise themselves with the American Heart Association Recommendations for the Standardization and Interpretation of the Electrocardiogram (Kligfield et al, 2007; Mason et al, 2007).
Figure 2. ST-segment elevation: illustration of normal ECG trace (a) and trace showing elevation (b)
Sites of infarction
There are 12 leads, orientated to different areas of the heart.
- V1–V2 are oriented to the interventricular septum
- V3–V4 are oriented to the anterior surface of the left ventricle, therefore changes in these leads may signify anterior ischaemia (left anterior descending artery)
- V4–V6 are oriented to the lateral heart surface (circumflex)
- Leads I and aVL—high lateral view of the left ventricle (circumflex)
- Leads II, III and aVF are oriented to the inferior surface of the heart (right coronary artery).
ST-segment elevation on the ECG is a medical emergency and signifies complete occlusion of a coronary artery. Guidance from the European Society of Cardiology (Ibanez et al, 2018) suggests ST elevation of 2 mm or more in the anterior chest leads (V1-V6) or 1 mm in the limb leads and a history of chest pain within the last 12 hours is diagnostic of STEMI. If no intervention, there will be death of a portion of myocardium with associated poorer patient outcomes (Ibanez et al, 2018). Prompt intervention to the affected coronary artery is required to restore blood flow to the affected myocardium. In this case, HSTnT is irrelevant and waiting for results will slow down treatment. In most of Europe, patients will now go straight to the cardiac catheterisation laboratory for primary percutaneous coronary intervention (Ibanez et al, 2018). In the case of NSTEMI, there may be a rising pattern of HSTnT over several hours whereas with unstable angina, no rise. However, a worrying history of increasing symptoms over a short period of time should prompt cardiology referral, regardless of initial HSTnT results.
NSTEMI and unstable angina tend to present with either ST-segment depression or T-wave inversion on the ECG (Ramrakha and Hill, 2012).
Aortic dissection
Aortic dissection is uncommon but devastating if missed. It is caused by tearing of the intimal layer of the aorta and the formation of a false lumen, which then fills with blood, causing bulging, weakening of the vessel wall and eventually rupture. Symptoms can progress over 2 weeks from start of the dissection to aortic rupture and sudden death, which is the most important thing to rule out in the emergency department. Death may occur rapidly due to haemothorax (Erbel et al, 2014). Therefore, it is important to be mindful of patients re-presenting with severe chest pain within this time frame. The gold standard investigation is a computerised tomography (CT) scan of the aorta (Provan, 2018).
History
- Patients often complain of ripping/tearing pain radiating to the back, usually the interscapular area—it may be described as ‘the worst pain ever’
- Pain tends to be sudden onset and worst at onset
- There may be neurological signs/symptoms as the tearing of the aorta may impinge on other blood vessels, for example, loss of power or sensation in a limb or stroke-like symptoms
- There may be a background history of aortic syndromes personally or within the family
- There may be a personal or family history of connective tissue diseases that increase the incidence of aortic dissection such as Marfan's syndrome (Erbel et al, 2014).
Examination
Findings may include:
- New murmur (aortic regurgitation)
- Radio-radial delay, a loss of synchronicity between the two radial pulses (these would normally be felt at the same time)
- Radio-femoral delay
- A difference of 20 mmHg or more in bilateral blood pressures.
- Examination may be normal, with no physical findings (so a history suggestive of aortic dissection should be followed up).
Investigations
- Blood tests may be normal
- Chest X-ray may show a widened mediastinum with or without effusions, which may be blood
- ECG can be normal or can show ischaemic changes if the dissection involves the coronary arteries
- Gold standard investigation is CT scan of the aorta for definite rule in/out.
Pericarditis, myocarditis and myopericarditis
Pericarditis is inflammation affecting the pericardium, the outer serous membrane surrounding the heart. As the pericardium is a double serous membrane, inflammation causes irritation as the heart contracts, causing chest pain. Myocarditis affects the myocardium and myopericarditis affects both layers. Both these conditions may follow a viral illness (typically Coxsackie virus), may be associated with auto-immune conditions, with malignancy or idiopathic (Adler et al, 2015).
History
- Often sudden onset chest pain
- May be described as pleuritic (worse on inspiration)
- Often radiates to the shoulder and neck
- May be worse lying down and relieved by sitting forward.
Examination
- There may be a pericardial rub heard on auscultation, caused by the two layers of pericardium rubbing together. Present in less than 33% of cases (Adler et al, 2015)
- Examination may be entirely normal.
Investigations
As with ACS, the key investigations are ECG and HSTnT. In addition, C-reactive protein, erythrocyte sedimentation rate, and white cell count may be elevated. HSTnT is not usually elevated in pericarditis that is uncomplicated, but will be elevated if there is myocardial involvement such as myocarditis/myopericarditis (Provan, 2018).
The ECG may show characteristic widespread ST-segment elevation in 60% of cases (Adler et al, 2015). This can present as a STEMI mimic; however, in pericarditis, there will not be reciprocal depression in opposite leads and there may be depression of the PR segment. Other changes include T-wave inversion and subtle ST-segment elevations. History and inflammatory markers are key in differentiating between pericardial disease and ACS (Adler et al, 2015).
Dyspnoea
Dyspnoea is a common presenting complaint in cardiac illness and may be associated with other symptoms such as chest pain or palpitations. However, if acute shortness of breath is the chief complaint prompting presentation to the emergency department, some of the conditions that predispose to heart failure are worth exploring (Ponikowski et al, 2016). These include (but are not limited to)
- Previous MI (leading to impairment of left ventricular pumping due to damage)
- Valvular disease, either stenosis or incompetence of valves.
- Cardiomyopathies
- Tachyarrhythmias and bradyarrhythmias in an already compromised patient, such as fast atrial fibrillation, which may not be symptomatic but over time causes heart failure symptoms.
History
- Is there shortness of breath on exertion or at rest?
- Has the patient had to increase the number of pillows (orthopnoea)? Does the patient feel more breathless lying flatter?
- Has the patient ever woken in the night unable to breathe (paroxysmal nocturnal dyspnoea)?
- Has there been an increase in weight?
- Has the patient noticed difficulty in getting shoes and socks on or had to loosen their belt?
- Have there been any symptoms of palpitations or chest pain?
Examination
- Weight: increase may suggest fluid overload and weight loss can help to show if diuretic therapy is helping (1 litre of fluid retained = 1 kg weight gain; 1 kg lost = 1 litre of fluid lost) though this must be interpreted in the context of other clinical signs of heart failure)
- Pulses: regularity, and rate. May find atrial fibrillation, which is irregularly irregular
- Jugular venous pressure (JVP): there may be elevation of the JVP if the patient is fluid-overloaded
- Palpate the precordium for heaves and thrills (indicating valve problems or right ventricular enlargement)
- Heart sounds: it is important to listen carefully for any new murmurs or a change in a pre-existing murmur as this can signify new or advancing valvular disease
- Lung sounds: listen to the chest for crepitations; heart failure presents with fine crackles bilaterally
- Check for sacral oedema
- Check for pitting oedema from the feet up to the tops of the legs. If this is present to tops of legs, check for scrotal oedema.
Investigations
- ECG for abnormalities such as previous or recent MI, cardiomyopathies, left bundle branch block, conduction abnormalities or arrhythmias
- Brain naturetic peptide (NT Pro-BNP) blood test. A good indicator of left ventricular dysfunction; if below the threshold suggested by the ESC (Mueller et al, 2019) it can rule out acute heart failure in the emergency department, while a high result will increase suspicion of acute or decompensated heart failure (a diagnosis of heart failure will need confirmation by echocardiogram). This blood test should be interpreted in light of clinical history and other potential confounders such as body mass index and renal function (Mueller et al, 2019)
- Rule out other causes such as infection
- Patients with suspected heart failure or decompensation of existing heart failure need to be seen by cardiology for further management, echocardiogram and possibly other specialised investigations (Provan, 2018).
Syncope/pre-syncope
Syncope and pre-syncope in cardiology are generally caused by either tachyarrhythmia or bradytachyarrhythmia. This can occur with a structurally normal heart (supraventricular tachyarrhythmias, atrial fibrillation), or in other conditions where the heart is affected by remodelling due to an inherited or acquired condition (Priori et al, 2015; Brignole et al, 2018). Left ventricular dysfunction secondary to ischaemia, cardiomyopathies, conduction system disease, long QT syndrome and others may all predispose to syncope.
History
- Was there any warning? In cardiac syncope there is no prodrome
- Was the patient able to save themselves from injury? Usually, sudden onset of arrhythmia does not allow for warning
- What was the patient doing? Did it happen during exercise? (Likely obstruction of outflow from left ventricle such as aortic stenosis or hypertrophic cardiomyopathy)
- Has it happened before?
- Any history of sudden death in the family? Some conditions that can cause sudden death can be inherited, for example Brugada syndrome, long QT syndrome and some cardiomyopathies. Of particular interest would be drownings, or unexplained death through road traffic collisions (Brignole et al, 2018)
- Does it happen when the patient goes from sitting to standing? (Likely postural hypotension)
- Did anything happen to precipitate event? For example, pain/straining at stool/sight of blood/coughing? (More likely to be vasovagal episode)
- Any tongue biting/tonic-clonic movements/incontinence? Post-ictal phase? (More likely to be a seizure)
- Were there any witnesses? Collateral history can be very useful.
Examination (key points)
- Check pulse for arrhythmias
- Feel for heaves and thrills, which may indicate valvular disease
- Listen for new murmurs or change in previously documented murmurs
- Lying and standing blood pressure (BP) plus standing BP after 3 minutes to check for orthostatic hypotension.
Investigations
- ECG: looking for changes indicating a cardiomyopathy, long QT, Brugada syndrome
- Holter monitoring for arrhythmias
- Echocardiogram
- May undertake exercise stress test.
Palpitations
Palpitations (sensation of being aware of the heartbeat) may be benign. However, palpitations can arise from cardiac arrhythmias, such as supraventricular tachycardias (SVT), atrial fibrillation (AF) and ventricular arrhythmias such as ventricular tachycardia (VT). Patients with underlying structural cardiac disease and those with inherited syndromes such as long QT syndrome or Brugada syndrome may present with palpitations (Priori et al, 2015). In addition, lifestyle factors such as alcohol and obesity can contribute to the onset of AF.
History features
- Sudden or gradual onset/offset? Sudden onset/offset is more likely to be an arrhythmia. Gradual onset/offset is more likely to be a sinus tachycardia (Priori et al, 2015)
- Frequency of symptoms
- Duration of symptoms
- Associated symptoms such as dyspnoea/chest pain/syncope or pre-syncope.
Examination
- May be unremarkable.
Investigations
- ECG: specifically to assess for an arrhythmia or if not present at the time, to check for other abnormalities that may predispose to arrhythmia, for example, prolonged QT duration (may be inherited or drug induced)
- Holter monitoring: This is more valuable if done for longer periods such as 72 hours for arrhythmias or symptoms that are not occurring daily (Priori et al, 2015)
- Echocardiogram
- Blood test for electrolytes such as potassium and magnesium as high or low levels can cause arrhythmias
- Thyroid function tests: hyperthyroidism can cause tachyarrhythmias.
Conclusion
These two articles have provided a brief insight into how the most common complaints from cardiac illness may present and an introduction to the history, clinical examination features and investigations required for diagnosing each one. Further reading around each subject will enhance knowledge and exposure to clinical cases will help develop the skills to assess these patients in clinical practice.
KEY POINTS
- This article outlines the four major presentations of cardiac illness: the common findings in history, examination, and investigations
- Chest pain is a common presenting complaint but acute coronary syndromes are not the only cardiac conditions presenting with chest pain
- Careful questioning is required to elicit subtle findings from the history
- The skill of ECG interpretation is key to developing provisional diagnosis and guiding investigations and further management
CPD reflective questions
- What are the common electrocardiogram (ECG) patterns associated with the spectrum of acute coronary syndromes and what is their significance in clinical practice?
- How would you differentiate between a cardiac syncope and collapse for another reason?
- How would you investigate palpitations and what is the significance of the investigations?