A rapid response event was initiated by the bedside nurse for acute onset hypotension. On prompt arrival of the rapid response team, it was noted that the patient was a 66-year-old female with a known history of ST-elevation myocardial infarction (STEMI) status post coronary artery bypass grafting a year ago, hypertension, and type 2 diabetes. She initially presented to the hospital for right flank pain and was being treated for a urinary tract infection. Upon further questioning at the bedside, the patient mentioned that she had been having substernal chest pain for the past 1 h. Her chest pain had continued to worsen, and she now had associated diaphoresis and tachypnea.
Temperature: 37.4 °F, axillary
Blood Pressure: 90/40 mmHg
Pulse: 105 beats per min (bpm), sinus tachycardia on telemetry (see Fig. 1.1 )
Respiratory Rate: 22 breaths per min
Pulse Oximetry: 99% on room air
Focused Physical Examination
The patient was an elderly female who was in moderate distress, holding her chest and appeared diaphoretic. She responded briefly to her name but swiftly stopped responding to further commands. She was moving all her limbs spontaneously. The heart rate was 105-110 bpm, with a regular rhythm and no murmurs. The abdominal exam did not elicit any tenderness, and the rest of her physical exam was benign.
The patient was given a 1 L fluid bolus which increased her blood pressure to 120/70 mmHg. A complete metabolic panel, troponin level, and magnesium levels were ordered. An EKG was done, which showed sinus tachycardia, with no acute ischemic findings. Chest X-ray at bedside showed no evidence of pneumothorax, consolidation, widened mediastinum, or enlarged aortic knob and no evidence of fluid overload. The pretest probability of PE was low, so a d-dimer test was ordered, which was normal. The patient was given one dose of 0.3 mg sublingual nitroglycerin (NTG), which improved her chest pain. Based on her cardiac history and current presentation, she was loaded with 325 mg of aspirin and 600 mg of clopidogrel and started on a therapeutic dose of enoxaparin after consultation with cardiology.
Final Diagnosis: Unstable AnginA
Generalized Approach to Acute Severe Chest Pain
There is a wide range of causes of chest pain in a rapid response setting, but the differential can be narrowed down with an organized history, physical, and appropriate workup. Chest pain is the second most common presenting complaint in the United States, with 7.6 million emergency department visits yearly. Prompt recognition and exclusion of the life-threatening differentials of chest pain are of paramount importance. However, it can be tricky at times as patients may appear deceptively well ( Table 1.1 ). This emphasizes the importance of appropriate workup.
|Acute coronary syndrome||Lung infection|
|Acute aortic dissection||Pericarditis|
|Pulmonary embolism||Gastroesophageal reflux disease|
|Pericardial tamponade||Panic attack|
|Esophageal rupture||Aortic stenosis|
Acute Coronary Syndrome (ACS)
ACS results either from rupture of atherosclerotic plaques or formation of intramural thrombus, which reduces blood flow to the myocardium causing ischemia via mismatch in the oxygen supply vs. demand. If this mismatch is reversible and not significant enough to cause myocardial necrosis, it is called unstable angina. If the myocardial ischemia is irreversible with associated myocardial injury, it is called a myocardial infarction (STEMI vs. non-STEMI, discussed in detail in later chapters). EKG is the diagnostic investigation of choice, aided by elevated cardiac enzymes in the appropriate setting.
Acute Aortic Dissection
Aortic dissection begins with a tear in the inner layer (tunica intima) of the aortic wall. This causes blood to travel between the intimal and medial layers of the vessel. The pulsatile blood flow causes the dissection to spread and subsequently causes obstruction of the branch arteries leading to end-organ ischemia. The type of chest pain is typically stabbing chest pain radiating to the back. Computed tomography (CT) angiogram is the diagnostic investigation of choice.
Pulmonary Embolism (PE)
PE occurs when a distal deep venous clot gets dislodged, travels through the right side of the heart, and gets lodged at the branch point in the main pulmonary artery (saddle embolus) or one of its distal branches (segmental or sub-segmental clots). This occlusion can cause acute pulmonary hypertension, dysfunction of the right ventricle leading to right-sided heart failure, a mismatch in gas exchange, and possibly infarction of lung parenchyma. CT angiogram is the diagnostic investigation of choice.
Pneumothorax is the presence of air in the pleural space. It typically occurs because of an abnormal connection between the pulmonary parenchyma and pleural space. Tension pneumothorax is a life-threatening form of pneumothorax that occurs because of a one-way valve opening into the pleural space that allows air to enter this space but does not allow it to move back into the lung. This leads to increased pressure within the pleural space that can displace mediastinal structures and cause hemodynamic compromise. Primary spontaneous pneumothorax occurs typically in younger males that are thin and tall. Secondary spontaneous pneumothorax typically occurs in patients with chronic obstructive lung disease, cystic fibrosis, and asthma. Chest X-ray is the diagnostic investigation of choice.
Mediastinitis is either inflammation or infection of the mediastinal space. Common causes include esophageal perforation (Boerhaave’s syndrome), odontogenic infections, and iatrogenic causes secondary to cardiac, upper gastrointestinal, or airway procedures. The mortality rate is high, ranging from 14% to 42%, despite surgical or medical management, and delays in diagnosis can further increase mortality. Chest CT is the diagnostic investigation of choice.
Pericardial tamponade occurs when fluid around the heart accumulates under pressure, causing impaired filling of the heart. Severely compromised cardiac filling presents as cardiogenic shock and requires an immediate reduction in pericardial pressure via pericardiocentesis. Causes of tamponade can include aortic dissection, thoracic trauma, ventricular free wall rupture after myocardial infarction (refer to Chapter 13 for further reading), or as a complication of acute pericarditis secondary to an infection, malignancy, or uremia. An EKG is the diagnostic investigation of choice.
Suggested Approach to Chest Pain in a Rapid Response Setting
The following protocol can be used for immediate risk assessment and management in inpatient scenarios where chest pain is being evaluated. This stepwise approach can be used to evaluate emergency room patients. The usual sequence of history taking, physical exam, investigations, and resuscitative interventions is rarely followed during a rapid response. Instead, these measures often run parallel to each other in a code situation. The following components of the rapid response are discussed in the traditional sequence only to ease understanding. For a flowchart of evaluation and management of chest pain, see Figs. 1.2 and 1.3 .