Cardiology · Aortic Dissection
The facts most likely to be tested
The most significant risk factor for aortic dissection is uncontrolled hypertension.
Patients typically present with sudden-onset, tearing or ripping chest pain that radiates to the back between the scapulae.
A pulse deficit or blood pressure discrepancy between the upper extremities is a highly specific physical exam finding.
Stanford Type A dissections involve the ascending aorta and require emergent surgical repair to prevent cardiac tamponade or aortic regurgitation.
Stanford Type B dissections are limited to the descending aorta and are primarily managed with aggressive blood pressure control using intravenous beta-blockers.
The initial management goal is to reduce heart rate and systolic blood pressure (target 100–120 mmHg) to decrease aortic wall shear stress (dP/dt).
CT angiography is the diagnostic test of choice in hemodynamically stable patients, while transesophageal echocardiography (TEE) is preferred in hemodynamically unstable patients.
Vignette unlocked
A 62-year-old male with a history of poorly controlled hypertension presents to the emergency department with sudden-onset, severe, tearing chest pain radiating to his interscapular region. On physical exam, his blood pressure is 180/100 mmHg in the right arm and 150/90 mmHg in the left arm. A new-onset diastolic decrescendo murmur is heard at the right sternal border. A chest X-ray reveals a widened mediastinum.
What is the most appropriate initial management step to reduce aortic wall shear stress?
Intravenous beta-blockers (e.g., esmolol or labetalol)
The patient presents with classic signs of an aortic dissection; the priority is to reduce the heart rate and blood pressure (dP/dt) using beta-blockers to prevent propagation of the dissection.
Full handout
High yield triage
Etiology / Epidemiology
Hypertension is the primary risk factor; suspect in patients with Marfan syndrome or Ehlers-Danlos.
Clinical Manifestations
Sudden onset tearing chest pain radiating to the back; look for pulse deficits or blood pressure discrepancy.
Diagnosis
CT angiography is the diagnostic test of choice; transesophageal echocardiogram is preferred if hemodynamically unstable.
Treatment
Initiate esmolol or labetalol to target systolic BP 100-120 mmHg and heart rate <60 bpm.
Prognosis
Type A requires emergent surgical repair; Type B is managed medically unless complications arise.
Full handout
Epidemiology & Etiology
Most common in males aged 50-70 with chronic hypertension. Connective tissue disorders like Marfan syndrome predispose younger patients. Other risks include bicuspid aortic valve, cocaine use, and iatrogenic injury during cardiac catheterization.
Pertinent Anatomy
The Stanford A involves the ascending aorta and is a surgical emergency. The Stanford B is confined to the descending aorta distal to the left subclavian artery.
Pathophysiology
An intimal tear allows blood to enter the media, creating a false lumen. This propagation can obstruct branch vessels, leading to end-organ ischemia. The process is driven by high wall stress and pulsatile flow.
Clinical Manifestations
Patients report tearing or ripping chest pain radiating to the interscapular region. Physical exam may reveal a new aortic regurgitation murmur or pulse deficits between limbs. Hypotension suggests rupture or cardiac tamponade.
Diagnosis
In stable patients, CT angiography is the gold standard. If the patient is unstable or has renal failure, use transesophageal echocardiogram. Target systolic BP 100-120 mmHg and heart rate <60 bpm during workup.
Treatment
First-line therapy is esmolol or labetalol to reduce shearing forces (dP/dt). Avoid hydralazine or nitroprusside as monotherapy, as they cause reflex tachycardia. Surgical consultation is mandatory for all Type A dissections.
Prognosis
Mortality increases by 1-2% per hour without intervention. Cardiac tamponade and aortic rupture are the most common causes of death. Long-term management requires strict blood pressure control.
Differential Diagnosis
Myocardial Infarction: ST-segment changes on ECG
Pulmonary Embolism: S1Q3T3 pattern or tachycardia
Pericarditis: Positional pain relieved by leaning forward
Pneumothorax: Absent breath sounds on affected side
Esophageal Rupture: Boerhaave syndrome following forceful emesis