Pain In Chest Symptoms And Diagnosis
Today we are going to discuss an approach to acute chest pain. There are a huge number of diseases that can present with chest pain. The best diagnostic framework organizes these many ideologies by organ systems. We will go through each one at a time starting with cardiovascular.
We can consider the cardiovascular system to be comprised of:
- endocardium, which is really the valves;
- conduction system;
- blood vessels.
Let's fill in some diagnoses. What are diseases of the pericardium that can present with chest pain? Pericarditis, which is inflammation of the pericardium. With the myocardium, of course, there is myocarditis.
However, also rarely a heart failure exacerbation can present with chest pain. Since oxygen consumption is dependent on wall tension and while tension is dependent upon intraventricular volume. Hypertrophic cardiomyopathy can also be associated with chest pain.
With the valves, you might be tempted to say endocarditis. However, endocarditis does not actually cause pain, at least not directly. But severe aortic stenosis can.
Any sufficiently fast tachyarrhythmia can lead to something called demand ischemia, which the primary problem is not lack of oxygen supply to the organ, but rather is excessive oxygen demand. And last with the vessels, obviously, the acute obstruction of a coronary artery can cause pain.
Acute pain from an occluded artery that is associated with an elevation of troponin is by definition and acute MI. Whereas, acute pain from an occlusion that is not associated with an elevation of troponin is unstable angina. Together acute amide and unstable angina are referred to as an acute coronary syndrome because in the first several hours after pain onset it may not be possible to distinguish them from one another.
An uncommon but very life-threatening etiology in this subcategory is aortic dissection, which is when the layers in the aortic wall start separating. If it spreads to a carotid artery it can lead to a massive stroke. And the dissection, which can also walk a week in the wall to the point of rupture and very rapid exsanguination.
One final etiology that belongs to vessels in the cardiovascular system is a hypertensive emergency of any cause. In this case, a very high afterload increases miocardial oxygen demand and patients can develop demand ischemia
Let's move on to the lungs. The relevant functional components of the lungs include:
- pulmonary vasculature.
Pleuritis also is known as pleurisy can cause chest pain as can a pneumothorax. It is a situation when a tear or hole in one of the pleural layers results in the air getting into the pleural space. Pleural effusions in the absence of concurrent inflammation usually do not cause pain.
Regarding diseases of the airways, asthma attacks frequently cause pain. In the alveoli there is pneumonia and in the vasculature, there is both acute pulmonary embolism and an initial presentation of pulmonary hypertension from any cause.
When it comes to lung cancer, it can cause chest pain. However, it's actually not a very common primary symptom at initial diagnosis. Unless the tumor has spread to the pleural space, invaded other local structures or has metastasized to a rib.
The next relevant organ system to consider is the GI system. In the esophagus, chest pain could be from gastroesophageal reflux disease, better known by its acronym GERD. esophagitis or esophageal spasm.
And in the stomach, although gastritis and peptic ulcer disease more common cause of a gastric pain. They can on occasion present the chest pain instead.
With the musculoskeletal system, rib fractures will obviously cause pain. But there's also a condition called costochondritis, which is local inflammation where a rib joint where a rib joins the sternum.
There are a few remaining miscellaneous causes including severe anemia, which reduces oxygen delivery to the myocardium. We also have herpes zoster, also known as shingles. Zoster has a vesicular rash isolated to a single dermatome that accompanies the pain. However, in a minority of patients the onset of pain may precede the rash by a few hours to a few days.
Acute intoxication of cocaine or amphetamines can cause chest pain. Sickle-cell anemia can cause a complication called acute chest syndrome, which is acute basal occlusion in the pulmonary microvasculature.
Finally, some patients will have psychogenic chest pain as either a manifestation of panic attacks or a manifestation of somatization.
Important Characteristics of Chest Pain
Before getting into the diagnostic algorithm, let's first define a few characteristics of chest pain that are frequently relevant.
First and most importantly - is the chest pain exertional? Meaning either does it start or get worse with exertion? And is it relieved or improved with the rest?
Is it positional? Meaning does it worsen or improve when the patient adopts a particular position such as lying down or sitting up. I
Is it pleuritic?. Pleuritic chest pain is pain that worsens when taking an unusually deep breath. Pleuritic pain can also be that worsened with coughing.
Is pain reproducible?Reproducible chest pain means is that it can be reproduced specifically with physical pressure applied to a focal part of the chest wall. A preferable way to convey that same information is to report focal chest wall tenderness when describing the exam.
Medical Emergencies That Commonly Present With Chest Pain
When approaching the diagnosis of a patient presenting with chest pain, the most important consideration is to determine as quickly as possible if the patient might have an emergent life-threatening problem. For instance:
- acute coronary syndrome;
- pulmonary embolism;
- aortic dissection;
If they are hemodynamically unstable, you need to assume that they have one of those four problems until proven otherwise. How do you differentiate between them? It is based on:
- description of the pain;
- their past medical history;
- physical exam;
- quick bedside diagnostic tests.
Acute coronary syndrom
With acute coronary syndrome, the pain typically comes on over a few minutes and is substernal in location. Although it is classically taught that pain from ACS radiates down the left arm, the evidence suggests that pain rating to the right arm to both arms is as predictive of ACS if not more so.
Pain can also radiate to the jaw. ACS pain is usually exertional and non-pleuritic. It is most often qualitatively described as a pressure or a tightness.
Risk factors the patients may have could include smoking, diabetes, hypertension or hyperlipidemia.
The physical exam is often normal, but on occasion may reveal an S3, elevated JVP and lung crackles if the patient has already developed secondary heart failure.
The diagnostic tests include an ECG which may well in an MI by showing ST elevations. It may also show something called dynamic changes, in which the morphology of ST segments and T-waves change with changes in the severity of the patient's pain.
Remember that a significant minority of patients presenting to the IDI with an acute MI will have an unremarkable ECG representation. The chest x-ray is typically normal.
Troponin is also ordered to help diagnose acute IDI. However, they can also be elevated in PE and myocarditis among other diagnoses.
Something that you should notice is not listed as a feature of pain related to ACS is with nitroglycerin. Historically it was thought that a patient presenting to the IDI with chest pain was more likely to have myocardial ischemia if the pain was relieved by Nitro. However, this has been shown to be untrue. A relief with nitroglycerin is useless as a diagnostic test.
Moving on to PE. The pain typically comes on over seconds to minutes. It is non-exertional but is pleuritic. The single most common word to qualitatively describe pain from a PE is sharp, but this is not so consistent as to put much weight on it.
The past medical history may reveal a hypercoagulable state such as recent hospitalization, immobilization or an active malignancy.
The physical exam is usually unremarkable. However, patients can't have evidence of a DBT or very rarely while having a right side at S3 or right ventricular heave if the PE is unusually severe. A chest x-ray is usually normal.
ECG most often shows sinus tachycardia rather than the frequently discussed classic S1Q3T3 pattern. If clinical suspicion of a PE is relatively low, a normal d-dimer test will rule it out completely. However, patients with either high suspicion of PE or those with an elevated d-dimer should undergo a CT angiogram if sufficiently stable enough for the trip to radiology.
In an aortic dissection, the onset of pain is over seconds to minutes. It will be central by location with radiation to the back. It is non-exertional and non-pleuritic. Patients will most often use the word tearing to describe it.
Past medical history may reveal either hypertension or smoking, both of which are significant risk factors for dissection. In patients who have not yet ruptured, the blood pressure is usually extremely elevated. Hypotension in the setting of dissection means either rupture or acute damage of the aortic valve.
The physical exam may reveal discordant blood pressures between the two arms depending on the precise location of the tear. A chest x-ray might show widening of the mediastinum, but this is insufficiently sensitive or specific to be clinically helpful.
ECG is not an all helpful in making this diagnosis. If our dissection is suspected and the patient is sufficiently hemodynamically stable, a CT angiogram should be performed. If the patient is too unstable to leave the emergency department for the scan, an emergent transesophageal echocardiogram can be performed at the bedside.
Finally, with a pneumothorax, the onset of pain is usually very abrupt, often instantaneous. It is non-exertional and is pleuritic and is described as sharp. The patient may have a history of COPD or cystic fibrosis, which are risk factors. The physical exam will reveal unilateral diminished or absent breath sounds and hyper-resonance.
A pneumothorax large enough to be clinically relevant and will always be visible on routine x-ray and further testing beyond this is usually not necessary.
If the patient is humid dynamically stable, remember, that they still might have one of those for diagnosis and you still need to consider them. However, in this situation, you also have more time to consider all those other diagnoses in the framework.
Stable patients should still get an ECG and a chest x-ray. Additional testing beyond this is based on clinical suspicion. Beyond this there is no specific next step in the diagnostic algorithm, but there are features that increase the probability of particular diagnosis.
For example pain from pericarditis may be pleuritic and is relieved by sitting up and leaning forward. The exam may have a pericardial friction rub, but it's usually absent. The ECG commonly reveals two fused ST elevations in more than one vascular territory.
Pain from myocarditis is associated with an elevated troponin, but unlike with ACS is non-exertional and lasts hours or longer.
Pain from pleuritis is feeling on the side and is pleuritic. It may be associated with a pleural friction rub, but as with the pericardial rub, it's usually absent. A chest x-ray usually reveals an associated pleural effusion.
Chest pain that is related to eating or which comes on minutes to a few hours after lying down is suggestive of GERD.
Chest pain that is associated with very focal chest wall tenderness suggested MSK origin.
The pain that is described as burning and which is limited to a single dermatome that wraps around to the back, suggests Zoster.
Frustratingly for both patients and clinicians, if the four most deadly diagnoses are ruled out the patient will more likely to not be discharged home without a specific diagnosis. It is surprisingly common for patients to come to the emergency room with chest pain, get admitted for 24 hours for a so-called chest pain, rule out admission, receive their serial troponin testing and telemetry monitoring and plus or minus an inpatient cardiac stress test with all the data resulting is unremarkable.
There's no standard as to how such emissions should be labeled at the time of discharge. I prefer giving most these patients a discharge diagnosis of nonspecific, noncardiac chest pain implying that it's likely either GI or MSK related and is not life-threatening.
That's not satisfying, but it reflects the reality that further testing beyond what was already mentioned does not have a significant enough yield to justify it. Barring unusual circumstances and provided that the chest pain has self-resolved, which it usually does.
If the chest pain becomes recurrent, then additional testing as an outpatient can be considered including EGD, additional investigations into ischemia or a diagnostic trial of either a PPI or anti-inflammatory medication.
There are many causes of acute chest pain, which range from very benign to imminently life-threatening.
The most important diagnostic step is to rule out these life-threatening ideologies: acute coronary syndrome, pulmonary embolism, aortic dissection and pneumothorax.
To identify the presence of these diagnoses, the most important pieces of data are the characteristics of the pain, the patient's past medical history, vital signs, ECG and chest x-ray.
And a significant portion of human dynamically stable patients presenting with a self-limited episode of chest pain who have no definitive diagnosis made even after a 24-hour stay for observation you.