- Written and Researched: Caleb Dusdal
- Peer Reviewed: Chris Cochrane
Given a patient with undefined chest pain, take an adequate history to make a specific diagnosis (e.g., determine risk factors, whether the pain is pleuritic or sharp, pressure, etc.).
The differential for chest pain is broad. It can be helpful to think about where the pain may be coming from and how that might be experienced by the patient. Pain typically comes in three flavours: Pleuritic, Somatic and Visceral pain. This approach can help localize the source of pain and refine your differential.
What is pleuritic chest pain?
Pleuritic chest pain is a type of sharp, stabbing pain that gets worse when the patient breathes and even worse when they take a deep breath. As the name suggests it is due to pain or irritation at the pleura.
*Include differential for pleuritic pain here??
Some considerations for your differential if your history uncovers a pleuritic chest pain:
|Pleuritic Chest Pain|
The chest wall from the skin down to the parietal pleura, is innervated by spinal nerves, giving rise to somatic pain. Somatic pain can be thought of as the skin, muscle and bones – the things you can touch and break.
Pain from the overlying MSK structures will be specifically localizable by the patient and often feels more ‘sharp’. As you can imagine, this could have similar characteristics to pleuritic pain with changes in breathing, and can make it difficult to differentiate these two.
Tintinalli’s offers a differential for somatic chest wall pain including:
|Somatic, Chest Wall Pain|
Costochondritis or “tietze’s syndrome”
Precordial catch syndrome
Intercostal nerve syndromes
Deeper than this is the visceral pleura innervated by visceral nerves. These often cluster into one area of the spinal cord and share cerebral mapping with somatic nerves.
So if it’s more of a vague, less sharp or poorly localized pain, think about visceral pain.
This is why cardiac pain, for example, can often be felt as radiating to the arms, or neck.
The visceral nerves cause a sensation that is much more difficult for patients to point to and to describe. As a result they’ll often gesture to an overall area, and use words like ‘discomfort’, ‘heaviness’, ‘pressure’, ‘tightness’ or ‘aching.
Some items for your differential here include:
|Visceral Chest Pain DDx|
Acute myocardial infarct
Oesophageal reflux, or spasm
Mitral valve prolapse
The table for this differential from Tintinalli’s will be in the shownotes.
|Visceral Chest Pain DDx||Pleuritic Chest Pain||Somatic, Chest Wall Pain|
|Typical anginaUnstable anginaAcute myocardial infarctAortic dissectionOesophageal ruptureOesophageal reflux, or spasmMitral valve prolapse||Pulmonary embolismPneumoniaSpontaneous pneumothoraxPericarditisPleurisy||Costosternal syndromeCostochondritis or “tietze’s syndrome”Precordial catch syndromeXiphodyniaRadicular syndromesIntercostal nerve syndromesfibromyalgia|
Given a clinical scenario suggestive of life-threatening conditions (e.g., pulmonary embolism, tamponade, dissection, pneumothorax), begin timely treatment (before the diagnosis is confirmed, while doing an appropriate work-up).
Risk factors that should make you suspicious:
- Metastatic malignancy (40% of non-traumatic cases)
- Acute idiopathic pericarditis (15% of non-traumatic cases)
- Uremia (10%)
- Bacterial or tubercular pericarditis
- Chronic idiopathic pericarditis
- Haemorrhagic – on anticoagulants
- Systemic lupus erythematosus
- Trauma, particularly to the cardiac box
Clinical Scenario to consider Cardiac Tamponade
- Dyspnoea at rest and with exertion
- Symptoms due to the cause (refer to above risk)
- Low systolic blood pressure
- Narrow pulse pressure
- Pulsus paradoxus – this is an abnormally large fall, greater than 10mmHg systolic pressure with inspiration
Physical Exam Findings
- Distended neck veins
- Apical impulse is indistinct or ‘tapping’ in quality
- May be RUQ tenderness due to hepatic venous congestion
Assess for using:
- CXR may show enlarged cardiac silhouette, which will look like cardiomegaly due to surrounding fluid that is indistinguishable from the heart itself
- Pulmonary vasculature will usually look normal
- Epicardial fat pad sign may occasionally be seen within the cardiac silhouette (see image in show notes)
- ECG, may show:
- Low voltage (<0.7mV) QRS complexes and
- ST segment elevation, due to inflammation of the epicardium
- PR segment depression, as in pericarditis
- In a large tamponade, may see Electrical alternans in the P and R waves (see this awesome finding in shownotes as well)
- Of course the best way to definitively identify a pericardial effusion that has tamponaded is with ultrasound.
- volume expansion can help with cardiac output temporarily
- if haemodynaically unstable, emergency pericardiocentesis is necessary, however this is ideally done by your cardiology colleagues in the cath lab using echocardiographic guidance to avoid complications
Risk Factors Include:
- Male sex
- Age over 50 years
- Poorly controlled hypertension
- Cocaine or amphetamine use
- Bicuspid aortic valve or prior aortic valve replacement
- Connective tissue disorders, including: Marfan’s and Ehlers-Danlos
Clinical Presentation to Consider an Aortic Dissection
- ‘ripping’ or ‘tearing’ sensation in chest
- May radiate to interscapular area of back
- Most often sudden onset and maximal at onset
- May migrate above and below the diaphragm, depending on location of dissection
- Secondary symptoms may result from occlusion of branch arteries caused by the dissecting flap
- Acute MI
- Limb ischemia
- Physical Exam Findings
these are insensitive and non-specific
- unilateral pulse deficit of: carotid, radial, femoral artery LR 5.7
- focal neuro deficits can occur in 17% of cases
- new murmur of aortic insufficiency
- A normal CXR ‘lowers’ likelihood of dissection but doesn’t exclude it
- Widened mediastinum or abnormal aortic contour
- Pleural effusions
- Aortic intimal calcification displacement
- Negative D-dimer lower likelihood, but also cannot exclude
- ECG changes are fairly common. Up to 50% have ST or TW changes
- Troponins are non-specific but do suggest worse prognosis
- Need a CT Aortogram or Transoesophageal echocardiogram to definitively confirm
- A normal CXR ‘lowers’ likelihood of dissection but doesn’t exclude it
- Initial Management includes: [Tin Ch 59 pp415]
- Antihypertensives, with negative inotropic agent
- This is to reduce blood pressure without increasing shear forces which can worsen the tearing
- Beta-blockade is the usual with short-acting preferred
- Propranolol, Labetolol or Esmolol
- Usually a sBP 120-130 initially and 100-120 if possible without causing hypotensive symptoms
- Then vasodilators like Nitroprussive may be added after
- They likely need higher level of care, so if you need to ship for this get it going, or upstairs to the ICU
- Antihypertensives, with negative inotropic agent
Classically, a spontaneous pneumothorax occurs in tall, slender males. Of course penetrating trauma is also quite a risk for primary pneumothorax.
Risk Factors are
- Chronic lung diseases, such as asthma or COPD
Up to 3% develop a tension pneumothorax.
Clinical Presentation to Consider a Spontaneous Pneumothorax
- Sharp and/or pleuritic chest pain with dyspnoea
- The pleuritic component may resolve after 24 hours
- Sinus tachycardia is the most common physical finding
- Classic physical findings are:
- Ipsilateral decreased breath sounds
- Hyperresonance to percussion on side with pneumothorax
- Decreased or absent tactile fremitus
- CXR: look for loss of lung markings in the periphery and a pleural line running parallel to the chest wall
- Ultrasound: one of the great uses for bedside ultrasound. Very sensitive and specific, looking for absence of lung sliding in dependent areas of the chest.
- Chest CT of course
If a tension pneumothorax is suspected, based on significant dyspnea, hypotension, tracheal deviation, etc, you may need to intervene more acutely with a needle decompression, followed by a chest tube.
If they are haemodynamically stable we can use some less invasive management options:
- Oxygen administration can help increase resorption of the pleural air
- For small and stable pneumothoraces, we can also elect to just observe and reassess:
- Observe at least 4 hours with repeat CXR for progression/regression
- Should return in 24h for repeat assessment
This is a full-thickness tear of the oesophagus. Classically presents following forceful vomiting.
Clinical suspicion and differentiating from ACS is key to avoiding delay. CT or the chest or emergency endoscopy are the best means for definitive diagnosis.
Usually they are going to appear sick and may also have a few general associated symptoms:
Physical exam may be helpful if you find the specific finding of ‘Hamman’s Crunch’ which is a crepitus, varying with the heartbeat when auscultating the precordium. It is obviously rare and occurs with pneumomediastinum.
- CXR (a normal cannot rule it out, but a few findings might push you to look closer)
- may show a pleural effusion, with the left side being more common than the right
- pneumoperitoneum, or
- subcutaneous air
- If you suspect an oesophageal rupture, you need a CT with water-soluble contrast for definitive diagnosis.
- Resuscitation for shock
- Broad spectrum IV antibiotics
- Emergency surgical consult as soon as you suspect an oesophageal rupture
In a patient with unexplained chest pain, rule out ischemic heart disease.
Risk Factors for Ischemic Heart Disease
Unless they are crashing, you’re likely to have a chance to peruse your incoming patient’s medical history quickly before they arrive. Of course one of the do-not-miss diagnoses for the patient presenting with chest pain is ACS or acute coronary syndromes, in particular an active infarct. For this, it’s useful to remember the usual risk factors for coronary artery disease:
- Age over 40
- Being male, or a post-menopausal female
- Tobacco use
- Central obesity
- Family history of CAD:
- MI in male family member before 55 years of age
- MI in female family member before 65 years of age
- Sedentary lifestyle
Cocaine use can also be associated with acute myocardial infarct due to vasospasm.
Characteristics of cardiac chest pain
JAMA ‘Rational Clinical Examination’ series in 2015 analysed this question regarding history as well as the chest pain symptoms.
Of course, no one item is going to tell us if this is cardiac or not, and so it is presented as Likelihood ratios that are to be taken in summation to determine pre-test probability. These were assessed separately as items that are useful on history and those that are useful on exam.
- Abnormal prior stress test LR 3.1
- Peripheral arterial disease LR 2.7
- Prior CAD or MI, LR 2.0 and 1.6 respectively
- The rest are even lower and include the usual suspects:
- age over 40,
- being male sex or post-menopausal female,
- tobacco use,
- fam hx of CAD,
- truncal obesity,
- sedentary lifestyle
- cocaine use
Obviously none of these likelihood ratios are particularly compelling in isolation. So they need to be taken collectively.
Clinical Exam – Characteristic of ACS Chest Pain
- Radiation to both arms was most convincing with a LR 2.6
- Pain similar to previous ischemic events LR 2.2
- A change in the pain pattern over the past 24h – LR 2.0
- Typical chest pain for them LR 1.9
- Worse with exertion up to LR 1.8
- Then the rest are 1.5 or less, including: radiation to neck or jaw, radiation to L arm, radiation to R arm, diaphoresis, dyspnea, abrupt onset.
Of course, we’re talking about ‘ruling out’ ischemic heart disease. So aside from our awesome history and physical, we are going to need some investigations to feel confident:
- New, or presumably new ST segment deviations, >1mm in at least two anatomically contiguous leads
- T wave inversion in multiple precordial leads
- Any elevation in troponins
- Many authorities will have pathways for this that include repeating the troponin to assess for delta and possibly application of a rule such as the HEART score
The management of a diagnosed STEMI or NSTEMI is covered in Topic 56, but generally this involves ASA chewed, nitroglycerin if they’re not hypertensive or it’s not an inferior infarct, heparin and clopidogrel, and either fibrinolysis or cardiac catheterization. Cocaine associated ACS needs repeat dosing of benzodiazepines.