Chest Pain, Dyspnea, Palpitations

Chest Pain, Dyspnea, Palpitations


I. Causes (see Table 27.1)

Table 27.1 Causes of chest pain.

  1. Cardiac

    1. CAD: stable angina, ACS
    2. Aortic dissection
    3. Acute pericarditis
    4. Secondary ischemia from cardiac causes: acute HF,a acute HTN, AS, HOCM
    5. Secondary ischemia from non-cardiac causes: tachyarrhythmia, anemia

  2. Pulmonary

    1. Pneumothorax
    2. Pneumonia
    3. Exudative pleural effusion
    4. Pulmonary embolism
    5. Pulmonary hypertension (→ chest pain + dyspnea + syncope on exertion)

  3. Gastrointestinal

    1. Esophageal spasm or reflux
    2. Esophageal ulceration after vomiting (Mallory–Weiss syndrome)
    3. Peptic ulcer disease
    4. Acute pancreatitis, cholecystitis, biliary colic

  4. Chest wall

    1. Strain of muscles or ligaments
    2. Costochondritis (“Tietze’s syndrome” is a costochondritis with swollen red costochondral joints)
    3. Shoulder or cervical joint problem (pain is exacerbated by a particular movement of neck/shoulder rather than exertion)

  5. Psychogenic

a The increase in LVEDP reduces the pressure gradient between aortic diastolic pressure and LVEDP, i.e., the coronary perfusing pressure in diastole, and thus reduces coronary flow even in the absence of CAD. Also, elevated LVEDP increases microvascular resistance.

II. Features

A. Angina and acute coronary syndrome

  • Typical angina occurs with exertion and is relieved with rest. It is precipitated by walking uphill, in the cold, or after a meal. Chest pain that occurs at rest and is not reproduced with exertion is unlikely to be angina, the exception being vasospastic angina. Postprandial angina is often a marker of severe, sometimes multivessel CAD; as opposed to biliary colic or peptic ulcer disease, angina occurs immediately after the meal and is exacerbated by postprandial physical activity. Nocturnal angina may imply severe CAD or vasospasm on top of fixed CAD; the increased venous return in the recumbent position increases O2 demands and triggers ischemia in patients with critical, sometimes multivessel, CAD.
  • The duration of angina is typically a few minutes. If chest pain lasts over 20–30 minutes, the cardiac markers should be positive; other- wise, angina is an unlikely diagnosis. If chest pain lasts < 15 seconds, angina is also very unlikely (likely musculoskeletal pain).
  • Severe distress or profuse diaphoresis could mean ACS or another serious illness (aortic dissection). Nausea and vomiting may be seen with severe angina but are not specific. Eructation could mean angina or gastroesophageal disease.
  • Dyspnea may be an angina equivalent and may indicate extensive CAD with a secondary increase in ventricular stiffness and LVEDP. Consider angina in the differential diagnosis of dyspnea with no objective findings (no hypoxemia, wheezes, or pulmonary edema). On the other hand, chronic dyspnea is often a non-specific finding unrelated to CAD, and dyspnea by itself may cause a subjective feeling of chest pressure, unrelated to CAD.
  • Indigestion, deep fatigue, or pain in the arms, neck, or jaw are other atypical presentations for which ACS should be considered.

B. Aortic dissection

Three clinical features point to the possibility of aortic dissection:3

  • Predisposing condition: aortic valve disease, known aortic aneurysm, Marfan, or family history of aortic dissection.
  • Suggestive symptoms: chest, back, or abdominal pain that is either very abrupt (within seconds), severe, or tearing. Note, however, that the pain of aortic dissection is commonly sharp rather than tearing.
  • Suggestive exam findings: AI murmur (in 25–45%), pulse deficit or blood pressure differential between arms (~20%), neurologic deficit concomitant with chest pain (5%).

The presence of two or three features makes aortic dissection highly probable. The probability is intermediate when one feature is present; aortic imaging is warranted in the latter case if symptoms are not clearly explained by chest X-ray (CXR) or ECG. Up to 5% of aortic dissections have none of the features but may be suspected by a widened mediastinum on CXR.

In addition to the classic hypertension, hypotension may be seen with complicated aortic dissection (AI, tamponade). Hypotension may also be a pseudohypotension resulting from the obstruction of flow to one limb. Measuring blood pressure in all limbs may unveil this phenomenon.

C. Pulmonary embolism (PE)

1. Clinical features

  • Dyspnea and tachypnea are the most common findings; however, they may not be seen at rest and may be purely exertional.
  • Tachycardia is common and is occasionally an isolated finding. Frequently, however, tachycardia is either transient or relative

    (80–90 bpm).

  • Chest pain is usually a pleuritic pain in patients with distal emboli; angina-like pain may be seen in patients with large central emboli and secondary RV ischemia. Hemoptysis is seen with pulmonary infarction, often resulting from small distal emboli.
  • Hypotension, syncope, and RV failure with increased JVP/RV heave/right-sided S3 are seen with a large PE and imply reduced hemody- namic reserve.
  • Lower extremity edema or tenderness on palpation is seen in 50% of DVTs.

2. The clinical probability of PE is assessed using the Wells criteria, which essentially give weight to three features

  • No alternative diagnosis for the patient’s presentation, whether it is dyspnea, hypoxemia < 95%, chest pain, or tachycardia
  • Clinical signs of DVT or hemoptysis
  • Major risk factors for DVT/PE

The probability is high when two or three features are present, intermediate when only one feature is present, and low when none is present.

3. Initial workup

  • A negative D-dimer rules out PE in low or intermediate probability cases, with an age adjusted cutoff (age/100, in mg/L). D-dimer has however a very low specificity <30%.
  • Arterial blood gas usually shows hypoxia, hypocapnia, and a high A–a gradient (>10 mmHg on ambient air, > 50 mmHg on high-dose O2). O2 saturation and A–a gradient are, however, normal in up to 20% of patients. A–a gradient increases in most pulmonary pathologies as a result of V/Q mismatch, and thus is not specific for PE. Hypercapnia is rare, and only a massive PE with a massive increase in dead space can cause hypercapnia, per se.
  • Chest X-ray is grossly normal.
  • ECG shows sinus tachycardia or relative tachycardia (80–100 bpm). In large PE, it shows more pronounced tachycardia and signs of RV strain in up to 85% of patients: T inversion in the anterior leads V1–V3, RVH/right axis deviation/RBBB, S1Q3T3, and P pulmonale. Atrial arrhythmias may also be seen. Look at the admission ECG, as tachycardia may be transient.

D. Acute pericarditis

Pericarditis is characterized by pleuritic chest pain that increases with recumbency and movements and improves with leaning forward. It typically radiates to the trapezius. It has a rapid onset.

  • On exam, a pericardial friction rub with a systolic and a diastolic component is heard.
  • ECG shows diffuse ST elevation and/or PR depression in 90% of patients. These changes may resolve after one to several days.
  • CRP is highly sensitive for the diagnosis of acute pericarditis.
  • The diagnosis of pericarditis requires two of the following four features:

(1) chest pain; (2) rub; (3) typical ECG findings (widespread ST-segment elevation and/or PR depression); (4) pericardial effusion (which is only present in 40% of pericarditis cases and usually small). CRP is a confirmatory fifth finding.

E. Pneumonia, pleural effusion, pneumothorax

Pleural and pulmonary illnesses are characterized by dyspnea, cough, and pleuritic chest pain, i.e., sharp pain that increases with deep inspiration, cough, or movement.

III. Management of chronic chest pain

See Chapter 3, Section II and Figures 3.1 and 3.2.

IV. Management of acute chest pain


If the ECG shows ST elevation consistent with STEMI, perform emergent reperfusion with primary PCI or fibrinolysis.

If the ECG shows ST depression or deep T inversion consistent with ischemia, especially if dynamic, consider the diagnosis of non-ST elevation ACS, but keep in mind the possibility of aortic dissection, PE, or pericarditis if clinically plausible.

B. CXR, cardiac troponin (sensitive or highly sensitive assay), ± bedside echo during active pain

In ACS, a bedside echo performed during active chest pain typically reveals a wall motion abnormality. In fact, a normal echo during active chest pain reduces the likelihood of ACS. Echo is less sensitive if performed after pain resolution. Conversely, echo is not very specific for ACS, as a wall motion abnormality may correspond to an old infarct. Strain echocardiography (global or regional) improves the sensitivity and negative predictive value of echo for ACS diagnosis in patients with normal initial troponin and non-diagnostic ECG (91%) but is non-specific and has a poor positive predictive value (13% in one study).4

C. If any clinical, X-ray, or ECG feature suggests aortic dissection, PE, pericarditis, or a pulmonary cause of chest pain, proceed to the appropriate workup and therapy. Avoid anticoagulation if the clinical or radiographic likelihood of aortic dissection is more than low. Before starting anticoagulation, verify the lack of mediastinal enlargement on CXR.

If aortic dissection is suggested, perform aortic CT or emergent TEE and start aggressive BP control and intravenous β-blockers.

If PE is suggested (clinical probability high, or intermediate with + D-dimer), perform chest CT angiography, PE protocol. The same CT and contrast injection are usually appropriate for the diagnosis of aortic dissection as well (but not vice versa). V/Q scan may be performed instead of CT in renal failure with no severe CXR abnormalities; CXR abnormalities decrease the specificity and the diagnostic yield of the V/Q scan. Anticoagulation is started early on, before the workup, if PE is probable and the bleeding risk is low.

If pericarditis is suggested, the diagnosis will be established by clinical, ECG, and CRP features.

If a pulmonary cause is suggested, the diagnosis will be established by CXR and chest CT if needed.

If cholecystitis or acute pancreatitis is suggested, the diagnosis will be established by a liver function panel, amylase/lipase and abdominal ultrasound.

D. In the absence of aortic dissection, PE, pericarditis, or pulmonary features, use conventional troponin or hs-troponin for MI rule-in and rule-out. A single undetectable or very low hs-troponin (eg, <0.005 ng/ml) is associated with <0.5% risk of acute MI and nearly 0% risk of cardiac death at 30 days. This risk is further reduced in patients whose ECG is not suggestive of ischemia. Therefore, home discharge is safe in those patients.

ESC and multiple European investigators suggest checking hs-troponin at presentation and at 1 or 2 hours after presentation (0/1 or 0/2 strategy). An undetectable hs-troponin, or a detectable hs-troponin with insignificant change at 1 or 2 hours rules out MI with >99.5% confidence (Figure 27.1).514

Most patients who rule out have non-cardiac chest pain, particularly if ruled out with the hs-troponin strategy. Non-invasive testing with CTA or stress testing may be performed after the second negative troponin; it is not definitely required in patients who rule out with the hs-troponin strategy. Yet some of the latter patients have true angina, especially those with exertional chest pain. CTA or stress testing remains necessary in patients with exertional chest pain: a normal or low-risk stress test result suggests no CAD, microvascular disease, or low-risk CAD for which medical therapy is appropriate. Medical therapy is tailored to how much the physician believes the chest pain is anginal based on clinical grounds and is somewhat comparable to the management of chronic CAD; as such, coronary angiography is performed in those patients with significant angina on mild exertion.

In patients with elevated troponin, the most important step is to distinguish type 1 MI from secondary myocardial injury, by clinical context. Up to 50% of patients with mild troponin rise (<0.25 ng/ml) have type 2 MI or injury, rather than type 1 MI.5 ST depression on ECG or more severe troponin elevation (>0.5–1) increases the likelihood of CAD and type 1 MI.


I. Causes (see Table 27.2)


Beside HF, there are two additional causes of nocturnal dyspnea:15

  • Patients with COPD may have mucus hypersecretion, so that, after a few hours of sleep, secretions accumulate and produce dyspnea and wheezing, which are relieved by cough and sputum expectoration.
  • Patients with asthma may have their most severe bronchospasm between 2 a.m. and 4 a.m. and wake up with severe dyspnea and wheezing. Inhaled bronchodilators usually improve symptoms quickly.

In HF, paroxysmal nocturnal dyspnea (PND) usually develops 2–4 hours after sleep and improves after 15–30 minutes of sitting upright or walking. Dyspnea is often accompanied by cough (dry or productive of frothy sputum), wheezing, and diaphoresis.

Schematic illustration of quick rule-in and rule-out algorithm using hs-troponin.

Figure 27.1 Quick rule-in and rule-out algorithm using hs-troponin (in ng/L, which may be divided by 1000 to obtain conventional values in ng/ml).

Delta is the absolute or relative change in troponin value between 0 and 1 or 2 hours. Detection cutoff, MI cutoff, and delta cutoffs depend on the hs-troponin assay. This example uses the cutoff values specific for Roche hs-troponin T assay. Clinical scores (eg, HEART) do not improve the safety of this algorithm and unnecessarily reduce the proportion of patients ruled out.

Table 27.2 Causes of acute dyspnea.

  1. Cardiac

    1. Acute pulmonary edema due to acutely decompensated HF, or to acute new-onset HF (acute MI, acute hypertension, acute valvular insufficiency, arrhythmia)

      Diagnosis: history (orthopnea, paroxysmal nocturnal dyspnea, recent quick weight gain, and past cardiac history), exam (↑ JVP, S3, ± S4, crackles, peripheral edema), elevated BNP, chest X-ray

    2. Tamponade (↑ JVP, pulsus paradoxus)
    3. Always remember that dyspnea with no objective lung findings or hypoxemia could be an angina equivalent

  2. Pulmonary embolism
    Diagnosed by the following three features: (i) PE/DVT risk factors; (ii) DVT signs; and (iii) absence of other causes of dyspnea (no gross abnormalities on chest X-ray)

  3. Pulmonary

    1. Pneumonia
    2. Asthma attack or COPD exacerbation: asthma may occasionally lead to cough and/or dyspnea in the absence of wheezes on examination (cough-variant asthma or atypical asthma). Wheezing may be uncovered with maximal forced expiration. Also, severe asthma exacerbation may not produce wheezes (airways are so narrow that there is total interruption of airflow and decrease in breath sounds)
    3. Pneumothorax or large pleural effusion
    4. ARDS in the context of pneumonia, aspiration, septic shock, or trauma

  4. Shock of any cause leads to hyperventilation and tachypnea
    +Laryngeal causes (laryngospasm, laryngeal edema [anaphylaxis]) lead to an inspiratory stridor ± urticaria
    +Metabolic causes: Metabolic acidosis (such as diabetic ketoacidosis), hypocalcemia, dyskalemia, severe acute anemia, hyperthyroid storm

Orthopnea is mainly seen in HF but may also be seen with pericardial diseases, advanced asthma/COPD with diaphragmatic flattening and weakness, bilateral diaphragmatic paralysis, severe obesity and severe ascites, all cases where the diaphragm tends be pushed up in a supine position.

Platypnea is dyspnea that worsens in the upright position. Platypnea is seen with pulmonary right-to-left shunts such as pulmonary AV fistulas (including hepatopulmonary syndrome), or the rare case of PFO that allows right-to-left shunting in the upright position.

Trepopnea is orthopnea that mainly occurs in one lateral decubitus position. Patients with HF are typically more comfortable in the right lateral decubitus position, as this position raises the level of the heart (especially the left ventricle), which slows venous return. This position may partly explain the predominance of right pleural effusion in HF.16 Patients with unilateral lung disease are most comfortable lying over the side of the healthy lung, to improve its perfusion and the V/Q matching.

Note that nocturnal or exertional cough, rather than dyspnea, may be the primary complaint of patients with HF, and patients with cough-variant asthma.

II. Notes

A. Differential diagnosis of shock + respiratory distress

Any shock leads to tachypnea (the patient hyperventilates in order to improve O2 supply). Think specifically of:

  • Cardiogenic shock with pulmonary edema
  • Septic shock due to pneumonia or septic shock with ARDS
  • Tamponade
  • Massive PE
  • Anaphylactic shock with bronchospasm, laryngeal edema, urticaria

B. Wheezing

Wheezing may indicate COPD/asthma but may also indicate pulmonary edema (“cardiac asthma”), PE, or pneumonia. In cardiac asthma, cyanosis and diaphoresis occur more often than in bronchial asthma, and adventitious breath sounds are more common (crackles, rhonchi). True asthma has more musical, pure wheezes.15

C. Pulmonary shunt and pulmonary shunt effect

Most of the disorders listed in Table 27.2, A–C, lead to a pulmonary shunt effect in which pulmonary blood is not oxygenated because of obstruction of the airways, or to a true pulmonary shunt in which the alveoli, per se, are obstructed and filled with fluid. A pulmonary shunt or shunt effect initially leads to hypocapnia, hypoxemia, or normoxemia (pO2 may be normal early on), and elevated A–a gradient. A–a gradient increases in most pulmonary pathologies; it implies V/Q mismatch but does not identify it. The more severe the process, the higher the A–a gradient rises.


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

Stay updated, free articles. Join our Telegram channel

Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Chest Pain, Dyspnea, Palpitations

Full access? Get Clinical Tree

Get Clinical Tree app for offline access