Emergency!

In the ninth part of our emergency series, Sandeep Ghandi, Richard Marshall, Hugh Montgomery, David Howell, and Neil Goldsack tell you how to assess and treat patients who present with chest pain

Chest pain is one of the most common medical presentations to the emergency department. The importance of assessing patients with chest pain is to identify those patients with a high short term risk of mortality or morbidit and to instigate life saving treatment.

In the first of two articles on chest pain, we shall discuss the diagnosis and management of acute coronary events.

A detailed history, problem oriented examination, and electrocardiogram are the most important tools in reaching a diagnosis. The traditional approach of history, examination, investigations, and treatment must, however, be tempered by the clinical urgency of the situation. For example, when you are dealing with a patient with an acute myocardial infarction you will see the electrocardiogram first and start treatment before completing a full history and examination--more on this important concept later.

How to deal with a patient with chest pain

When you are called to see a patient with chest pain you should ascertain basic demographic details of the patient (age, sex, race) and results of vital observations (pulse, blood pressure, temperature, and oxygen saturation). Also ask for an electrocardiogram to be done immediately and for the patient to be attached to a cardiac monitor.

(1) Tell the nurse that you will come and see the patient immediately. On your way to the patient, think about the possible causes of the patient's pain. Armed with the demographic information and the location of the patient, you should be able to reach a "ball park" diagnosis. Thus, if you are asked in a coronary care unit to see a patient with recurrent chest pain the pain is likely to be attributable to recurrent myocardial ischaemia or pericarditis. If, however, you are the surgical house officer summoned to the orthopaedic ward to see a 75 year old woman with chest pain five days after a total hip replacement, acute pulmonary embolus should be high on the list of differential diagnoses.

(2) Immediate assessment. Check the adequacy of the Airway, Breathing, and Circulation (ABC). Breathing may be affected by many causes of chest pain (pulmonary embolus, pneumonia, pneumo-thorax, acute coronary syndrome), so check oxygen saturation and arterial blood gases on air and then give the patient high flow oxygen (provided the patient does not have chronic obstructive airways disease, in which case start off with 2 litres/minute and titrate according to the results of arterial blood gas analysis). If the oxygen saturation is less than 90% call for senior help immediately.

(3) Call for help if necessary. In all the articles in this series we have stressed the importance of calling for help if you are concerned about the patient in any way. With chest pain, the reasons to call are outlined below.

(4) Briefly assess the patient. Your initial assessment should comprise taking the patient's pulse, blood pressure, and state of peripheral circulation. Examine the lungs for a pneumothorax and auscultate the lung bases for pulmonary oedema. Check the arterial oxygen saturation.

(5) Arrange simple urgent investigations: electrocardiogram, chest x ray with a portable machine (to exclude pneumothorax, widened mediastinum seen in dissection of the thoracic aorta, interstitial oedema, and consolidation), full blood count, concentrations of urea and electrolytes (maintain serum concentration of potassium at 4-5 mmol/l to minimise risk of dysrhythmias), glucose, cardiac enzymes, and arterial blood gases (if, however, the patient has acute changes of myocardial infarction on the electrocardiogram, then blood gas analysis should be delayed as there is a risk of local bleeding from the puncture site if thrombolysis needs to be given).

(6) Treat the cause of the chest pain. This management should not be delayed while taking further history, which can be done later.

Arrhythmias

Any arrhythmia can either cause or be triggered by an acute coronary event. The emergency management of these is covered in the guidelines produced by the European Resuscitation Council.

Cardiac pain

Myocardial ischaemia--Transient myocardial pain caused by underlying coronary atheroma. The pain is typically retrosternal and described in any of the following ways.

• Crushing
• Choking
• Squeezing
• Constricting
• Burning or like indigestion

Always enquire about anginal symptoms by using all the above descriptive terms.

Anginal pain often radiates to the neck and down the left arm. Sometimes the pain is felt only in the neck, jaw, or left arm. Angina is precipitated by exertion, cold air, high emotions, or sometimes by a large meal. It is relieved rapidly by rest and within two or three minutes of taking glyceryl trinitrate sublingually.

Your history should conclude by enquiring about the traditional cardiac risk factors as follows.

• Smoking history
• Family history of ischaemic heart disease
• Hypertension
• Diabetes mellitus
• Hypercholesterolaemia

When presenting a patient with angina on a ward round, include these risk factors in the history of presenting complaint.

Examination--Look for signs of aortic stenosis, anaemia, and thyrotoxicosis as these conditions can all cause or worsen angina (by increasing myocardial consumption of oxygen).

Investigations--Electrocardiogram is essential. However, an electrocardiogram when the patient is pain free may be normal. Exercise testing should be employed in all patients with suspected angina (consider a thallium perfusion scan or stress echocardiogram in patients unable to undertake the usual exercise test). Selected patients will need coronary angiography. Check full blood count, concentrations of urea, electrolytes, glucose, and cholesterol, and do thyroid function tests in all patients. Echocardiography may be needed if aortic stenosis or hypertrophic cardiomyopathy are suspected.

Acute coronary artery syndrome--This includes unstable angina, non-Q wave myocardial infarction, and Q wave myocardial infarction.

History--The pain is very similar to that associated with stable angina. It differs in that it is usually more severe and lasts longer (more than 20 minutes). It is not relieved by rest or glyceryl trinitrate, and it comes on at rest (typically in the early hours of the morning). The patient may report autonomic features: nausea, vomiting, and sweating. S/he may also complain of dyspnoea.

Examination--Look for the following.

• Third heart sound
• Raised jugular venous pressure
• Pulmonary crepitations
• Signs of poor cardiac output: cool and clammy skin, pallor
• Low blood pressure
• Murmur of mitral regurgitation

All these may indicate high risk cases.

Investigations--The electrocardiogram is the most important tool. It may be normal in the very early stages of an acute myocardial infarction and therefore should be repeated after half an hour. The earliest sign is the hyperacute T wave (fig 1), followed by ST segment elevation, T wave inversion, and Q waves. The leads that show these changes reflect the anatomical territory of the infarct. Thus an anterior myocardial infarction produces ST elevation in leads V2-V4 (fig 1; this is the electrocardiogram of a man aged 33 years with chest pain, two hours after taking cocaine); an inferior myocardial infarction in leads II, III, aVF (fig 2; this also shows complete heart block). A lateral myocardial infarction is seen in leads I, aVL,V5-V6. Note that new onset left bundle branch block can also signify an acute myocardial infarction (fig 3).

Fig 1 - Hyperacute T waves and ST elevation in anterior chest leads

Fig 2 - Acute inferior myocardial infarction with ST elevation in leads II, III and aVF. There is in addition complete heart block (there is no relation between P waves and the QRS complexes)

Fig 3 - New onset of left bundle branch block. Note the rSr pattern in V5 with widening of the QRS complex

The electricardiogram in unstable angina or non-Q wave myocardial infarction will show ST depression or new T wave inversion.

Finding elevated concentrations of serum creatine kinase (CK) and AST confirm the diagnosis of acute myocardial infarction. Cardiac troponins are new highly sensitive and specific markers of myocardial necrosis. We must emphasise that the acute treatment of myocardial infarction depends only on the history and findings of the electrocardiogram, not on results of cardiac enzymes.

Management of acute coronary syndromes

Acute myocardial infarction

The greatest risk of death is within the first hour (usually a result of ventricular fibrillation or tachycardia), and therefore the priority is to get the patient close to a defibrillator as quickly as possible.

Early attempts to reperfuse infarcting myocardium can dramatically improve survival. Thus the "door to needle" time (time patient enters hospital to time of administration of thrombolytic agent) should be as short as possible: a reasonable time is half an hour.

Initial thoughts

When you are called to see a patient with a suspected myocardial infarction, request the nurse to attach the patient to an electrocardiogram monitor and give oxygen. The vital observations should be recorded.

(1) Go immediately to casualty. On arrival at the patient's bedside, assess the ABC (Airway, Breathing, Circulation) and the vital signs.

(2) Is the patient haemodynamically stable (normal blood pressure, pulse, and oximetry)? Does s/he look well? (Often patients who are having an acute myocardial infarction look extremely unwell with a characteristic sweaty grey appearance). If you are concerned in any way then summon senior help urgently. Again, in the early stages of your medical house job, you should have help with all cardiac cases.

(3) Give the patient high flow oxygen, attach him or her to an electrocardiogram monitor and ensure that a defibrillator is nearby.

(4) Insert intravenous cannula and send blood for full blood count, concentrations of urea and electrolytes, glucose, lipid profile, and cardiac enzymes.

(5) Give 300 mg aspirin chewed.

(6) Give diamorphine 2.5-5 mg intravenously with Maxolon. In this setting opioids act as analgesics, anxiolytics, and vasodilators.

(7) Thrombolytic treatment should be given to the following group of patients with chest pain.

• ;Presentation within 12 hours of typical cardiac pain with ST elevation >2 mm in two or more chest leads
• >1 mm in two or more limb leads

  * New onset left bundle branch block

• Presentation 12-24 hours after onset of cardiac pain, with ongoing pain and acute changes on the electrocardiogram.

(8) Consider referral for immediate coronary angiography and revascularisation if thrombolysis is contraindicated. Discuss with senior doctors.

(9) ß Adrenergic receptor blockers.

Unstable angina and non-Q wave myocardial infarction

Unstable angina and non-Q wave myocardial infarction are triggered by acute disruption of atherosclerotic plaque. This tends to be non-occlusive compared with an occlusive thrombus in acute Q-wave myocardial infarction.

Initially, a non-Q wave myocardial infarction cannot be distinguished from unstable angina. Non-Q wave myocardial infarction is diagnosed on the basis of elevated concentrations of cardiac enzymes. The initial treatment of all these patients, however, is the same.

Initial thoughts

Respond immediately. On the telephone, ask the nurse to give the patient two puffs of glyceryl trinitrate sublingually, give oxygen, attach the patient to an electrocardiogram monitor, and do the vital observations. Order a 12 lead electrocardiogram.

The initial management is identical to steps 1-7 in the management of an acute myocardial infarction.

(1) Briefly assess the risk of the patient. High risk features are older age, ST changes in pain, heart failure, third heart sound, and a new murmur of mitral regurgitation. All high risk patients should be managed on coronary care unit, whereas others can be managed on an acute medical ward. Discuss this point with a senior doctor.

(2) Anticoagulant treatment. Heparin, in its low molecular weight form (enoxaparin), should be commenced in all high risk patients immediately.

(3) Glyceryl trinitrate. Intravenous glyceryl trinitrate should be given for recurrent cardiac chest pain (titrate dose versus chest pain and systolic blood pressure).

(4) ß Blocker treatment. A short acting ß blocker should be given early (as with acute Q wave myocardial infarction).

(5) Coronary angiography. Patients with resistant pain should have urgent coronary angiography with a view to coronary revascularisation.

(6) Antianginal treatment. Add in sequential manner nicorandil (a potassium channel opener), a calcium channel blocker, and nitrate. The order is not critical.

Conclusion

You should now be able to recognise and initiate treatment in a patient with an acute coronary syndrome. Be aware of the high mortality of these patients and ensure that you get senior help at an early stage.

Sandeep Ghandhi, cardiology specialist registrar, North Middlesex Hospital, London

David Howell Medical Research Council fellow

Richard Marshall Wellcome fellow University College and Middlesex Hospital, London

Neil Goldsack respiratory specialist registrar Chest Clinic, North Middlesex Hospital, London

Hugh Montgomery cardiology specialist registrar


studentBMJ 1999;07 October ISSN 0966-6494