Aortic dissection resident survival guide

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D.; Chetan Lokhande, M.B.B.S [2]; Pratik Bahekar, MBBS [3]

Aortic dissection resident survival guide Microchapters


Aortic dissection (AD) is a disruption of the medial layer of the aorta triggered by intramural bleeding. It is commonly due to an intimal tear that causes tracking of blood in a dissection plane within the media. Blood accumulation results in a separation of the aortic wall layers with ensuing formation of a true lumen and a false lumen with or without communication between the two. Aortic dissection is a medical emergency and can quickly lead to death if not treated urgently. Patients classically present with abrupt onset of severe, knife-like chest (most common), back, or abdominal pain. Other important features that increases the probability of aortic dissection include pulse deficits, systolic blood pressure differences between limbs, focal neurologic deficits, new aortic murmurs, shock, and a history of connective tissue disease and aortic valve disease. CT, MRI, or transesophageal echocardiography (TEE) may be used for the diagnosis AD, although CT is preferred because of it's speed, excellent sensitivity, and superiority in diagnosing arch vessel involvement. Serial imaging is recommended to monitor for progression of the dissection. After excluding possible aortic regurgitation, intravenous beta-blockers should be initiated in all patients to reduce the systolic blood pressure (SBP) to 100 to 120 mmHg and controlling the heart rate, to minimize the shear stress on the aortic wall. Treatment depends on the anatomic location of the dissection and complications. Uncomplicated type B dissections should be treated medically whereas type A dissections and complicated type B dissections should be treated surgically. Complications of AD include aortic regurgitation, myocardial ischaemia or infarction, pleural effusion, stroke, mesenteric ischemia, and acute kidney injury.[1]


DeBakey and Stanford systems are the commonly used systems to classify aortic dissection.[2][3][4][5]

Proximal Dissections

Originate in the ascending aorta and may propagate to involve the aortic arch, and possibly part of the descending aorta (include Debakey type I and II, and Stanford type A)[6]

Distal Dissections

Originate in the descending aorta (distal to left subclavian artery) and propagate distally, rarely extends proximally (include Debakey type IIIa and IIIb, and Stanford type B)

Click here for the detailed classification schemes.


Life Threatening Causes

Aortic dissection is a life-threatening condition and must be treated as such irrespective of the underlying cause.

Common Causes

Click here for the complete list of causes.

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.[7]
Boxes in red signify that an urgent management is needed.

Abbreviations: AVR: Aortic valve replacement; BP Blood Pressure, CCU: Coronary care unit; CHF: Congestive cardiac failure; CXR: Chest X-ray; EKG: Electrocardiogram; MI: Myocardial infarction; OR: Operating room; TAVR: Transcatheter aortic valve replacement; TEE: Transesophageal echocardiogram; TTE: Transthoracic echocardiogram; HEENT: Head eye ear nose throat

Identify cardinal findings that increase the pretest probability of acute aortic dissection
Chest pain or back pain or abdominal pain
❑ Sudden in onset
Tearing or sharp in quality
❑ Increasing in intensity

Associated with any of the following:
❑ Unexplained syncope
❑ Focal neurological deficits
Unequal pulses or BPs in the limbs
❑ Perfusion deficits

Refractory hypertension (decreased renal perfusion)
❑ Tensed abdomen
❑ Progressive metabolic acidosis
❑ Increasing liver enzymes[8]
Does the patient have the following findings which require urgent management?
❑ Hypotension or shock
❑ Perfusion deficits
Attempt to stabilize patient
❑ Attend to the patient's ABCs (Airway, Breathing, Circulation)
❑ Consider intubation if the patient's airway is compromised, has a glasgow coma scale (GCS < 8) or profound haemodynamic instability
❑ Administer oxygen and maintain a saturation >90%
❑ Secure 2 large-bore intravenous lines (IVs) and initiate fluid resuscitation
❑ Titrate fluids to a mean arterial blood pressure of 70 mm Hg, overzealous fluid administration may lead to progression of the dissection
❑ Consider vasopressors only if patient remains hypotensive despite fluids

❑ Obtain 12 lead ECG and place the patient on a cardiac monitor
❑ Consider intra-arterial BP monitoring
❑ Place an indwelling urethral catheter and monitor urine output
❑ Frequently assess mental status and check for focal neurologic deficits
❑ Monitor development or progression of carotid, brachial, or femoral bruits
❑ Type and crossmatch patient for possible blood transfusion

❑ Obtain blood for CBC, electrolytes, BUN, creatinine, LFTS, and troponin I, and CK-MB

Control blood pressure
❑ Beta blockers are first-line agents, as they circumvent the reflex tachycardia associated with blood pressure lowering
❑ 500 micrograms/kg intravenous push initially, followed by 50 micrograms/kg/min for 4 min
❑ If necessary increase infusion up to 200 micrograms/kg/min
❑ 5 mg intravenously every 5-10 minutes
❑ If necessary increase up to a maximum dosage of 15 mg/total dose
❑ 1-5 mg/min IV infusion

❑ Substitute with non-dihydropyridine calcium channel blockers if beta-blockers are contraindicated

❑ 0.25 mg/kg intravenous bolus initially then 5-10 mg/hr infusion
❑ If necessary increase dose to 15 mg/hr
❑ 0.05 to 0.1 mg/kg IV bolus

Control pain
Morphine sulphate
❑ 2.5-5 mg every 3 to 4 hours, infused over 4-5 minutes
Urgent imaging required
TEE (preferred in hemodynamically unstable) or CT looking for the following:
❑ Location and features of dissection
❑ Proximal vs. Distal
❑ Involvement of aortic branches
❑ Associated complications
Pericardial effusion
❑ Regional wall motion abnormality
Severe aortic regurgitation (AR)
Can aortic dissection be confirmed?
Obtain a secondary imaging study, if there is high clinical suspicion

Complete Diagnostic Approach

A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.[9]

Characterize the symptoms:
Chest pain
❑ Tearing, ripping, sharp. stabbing, or knife-like
❑ Sudden onset and increasing in intensity
❑ Worsened by deep breathing or cough and
relieved by sitting upright (suggestive of hemorrhage into the pericardial sac).

Neck, throat, and jaw pain
Abdominal pain or back pain (think of associated mesenteric ischemia)
Syncope in 50% of cases (suggestive of hemorrhage into the pericardial sac causing pericardial tamponade)
❑ Rapid, weak pulse
Rapid breathing
Hemoptysis (suggestive of compression of and erosion into the bronchus)
Stridor (suggestive of compression of the airway)
Flank pain
Oliguria/ anuria (suggestive of involvement of the renal arteries causing pre-renal kidney injury).[10] [11] [12] [13]
Nausea and vomiting
Dysphasia(suggestive of pressure on the esophagus)
Gastrointestinal bleeding
Altered mental status
❑ Symptoms suggestive of stroke e.g. paraplegia, numbness and tingling (suggestive of involvement of cerebral or spinal arteries)
Horner's syndrome (suggestive of compression of the superior cervical ganglia)

Drooping of eyelids (ptosis)
Decreased or no sweating (anhidrosis)

Hoarseness of voice (suggestive of compression of the recurrent laryngeal nerve)
Claudication (suggestive of iliac artery occlusion)

❑ Painless dissection (15 – 55 %)(unexplained syncope, stroke or congestive heart failure (CHF))
Obtain a detailed history:
❑ Past medical history
Hypertension (most important risk factor present in >70% of patients)

❑ Family history
Connective tissue disorder

❑ Marfan syndrome
❑ Ehlers-Danlos syndrome
❑ Loeys-Dietz syndrome
❑ Polycystic kidney disease

❑ Anatomic defects

Biscuspid aortic valve
❑ Aortic valve disease
❑ Aortic root disorders
Aortic aneurysm
Coarctation of aorta

❑ Iatrogenic

❑ Recent aortic manipulation
Chronic steroid usage
Immunosuppressive therapy

❑ Social history

Cocaine abuse
❑ Heavy weight lifting

❑ Other genetic disorders

Turners syndrome (usually due to bicuspid aortic valve)
Familial thoracic aneurysm and dissection syndrome

❑ Inflammatory vasculitis

Takayasu arteritis
Giant cell arteritis
Behcet's arteritis


Examine the patient:
❑ Obtain vitals:
Tachycardia (suggestive of pain, aortic insufficiency, pericardial tamponade, and aortic rupture if associated with severe hypotension)
Wide pulse pressure (suggestive of acute aortic insufficiency)
Pulsus paradoxus (suggestive of pericardial tamponade)
Pulse deficit involving carotid, femoral or subclavian artery
❑ Absent femoral pulse
Blood pressure
❑ Difference in the blood pressure in both extremities
Hypertension (due to pain and catecholamine surge)
Hypotension (grave prognostic indicator, suggestive of pericardial tamponade, severe aortic insufficiency, or aortic rupture)
❑ Signs of shock (hypoperfusion)
Hypotension (SBP < 90 mm of Hg or drop in mean arterial pressure >30 mm of Hg)
Altered mental status
Cold and clammy extremities
Oliguria (urine output <0.5mL/kg/hr)

❑ Perform a HEENT examination looking for:

❑ Increased JVP (suggestive of heart failure)
Horner's syndrome
Hoarseness due to compression of the left recurrent laryngeal nerve
Swelling of the neck and face (suggestive of superior vena cava syndrome)

❑ Perform a cardiovascular examination looking for:

❑ Faint early diastolic murmur (suggestive of acute aortic regurgitation, vs. loud decrescendo diastolic murmur of chronic AR)[14]
Pericardial friction rub (suggestive of pericarditis)
❑ Clicks (suggestive of pseudoprolapse/true prolapse of mitral and/or tricuspid valve)
Beck's triad (suggestive of cardiac tamponade)
Hypotension (suggestive of decreased stroke volume)
Jugular venous distension (suggestive of venous hypertension due to decrease cardiac output)
❑ Muffled heart sounds (suggestive of fluid inside the pericardium) [15]

❑ Perform a respiratory examination looking for:

Kussmaul's sign (Paradoxical increase in jugular venous pressure with inspiration - Suggestive of tamponade)
❑ Decreased movement of the chest
❑ Stony dullness to percussion (suggestive of hemothorax and / or pleural effusion
❑ Diminished breath sounds
Crackles / crepitations / rales (suggestive of pulmonary edema due to acute aortic insufficiency)
Stridor and wheezing (suggestive of compression of the airway)
❑ Decreased tactile fremitus (suggestive of pleural effusion)

❑ Perform an abdominal examination looking for:


❑ Perform a full neurological examination looking for:

Altered mental status
❑ Extremity tingling and numbness (suggestive of nerve compression)
❑ Focal neurological deficits (signs suggestive of stroke)

❑ Examine the extremities for:

Peripheral edema
Consider alternate diagnosis:
Focused bedside pre-test risk assessment

High risk conditions[16]

❑ Marfan syndrome
❑ Connective tissue disease
❑ Family history of aortic disease
❑ Known aortic valve disease
❑ Recent aortic manipulation
❑ Known thoracic aortic aneurysm
❑ Aortic disorder

High risk pain features[16]

❑ Chest, back, or abdominal pain
❑ Abrupt onset
❑ Severe intensity
❑ Ripping, tearing, sharp, or stabbing

High risk exam features[16]

❑ Perfusion deficits
❑ Pulse deficit
❑ Systolic blood pressure differential
❑ Focal neurological deficit
❑ Murmur of aortic insufficiency
❑ Hypotension or shock
Low pre-test probability
(No features present)
High threshold for aortic imaging
Intermediate pre-test probability
(1 feature present)
Intermediate threshold for aortic imaging
High pre-test probability
(2 or more features present)
Immediate surgical evaluation and expedited aortic imaging
❑ Can an alternate diagnosis be identified?
❑ Order an EKG
❑ Does EKG show ST elevation ?
❑ Consider immediate surgical consultation and do aortic imaging as soon as possible
Treat accordingly
❑ Is there evidence of:
❑ Unexplained hypotension?
Widened mediastinum on CXR?
❑ Can an alternate diagnosis be identified?
❑ Treat like a primary acute coronary syndrome (ACS)
❑ If perfusion deficits are present then consider immediate coronary reperfusion therapy
❑ Identifiable culprit lesion on coronary angiography?
Treat accordingly
❑ Check risk factors for Thoracic aortic disease (TAD)
❑ Advanced age
❑ Risk factor for aortic diseases
❑ Do a detailed aortic imaging for thoracic aortic disease
Detailed and accelerated aortic imaging
❑ Aortic Imaging
Transesophageal echocardiography (TEE) (preferred in unstable patients)
Computed tomography(chest to pelvis; better visualization of aortic branch involvement)
Magnetic resonance imaging(chest to pelvis)
❑ Can aortic dissection be confirmed by imaging study
❑ Start appropriate therapy
❑ Obtain a secondary imaging study if there is high clinical suspicion, even if the initial aortic imaging studies are negative


Medical Management

Shown below is an algorithm summarizing the medical management of aortic dissection according to the 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for Diagnosis and Management of patients with Thoracic Aortic Disease.[9]

Confirmed aortic dissection
❑ Consider urgent surgical consultation
❑ Consider transfer to other medical facility if resources not available for adequate management
❑ Is patient hemodynamically stable ?
Control rate and pressure
(choose ONE of the following agents)

Beta blockers
Betablockers are contraindicated in bradycardia, heart block, decompensated heart failure, hypotension, asthma, severe chronic obstructive pulmonary disease

❑ 500 micrograms/kg intravenous initially, followed by 50 micrograms/kg/min for 4 min
❑ If necessary increase infusion up to 200 micrograms/kg/min
❑ 5 mg intravenously every 5-10 minutes
❑ If necessary increase up to a maximum dosage of 15 mg/total dose
❑ 1-5 mg/min IV infusion

Substitute with non-dihydropyridine calcium channel blockers if betablockers are contraindicated
Calcium Channel blockers
Calcium channel blockers are contraindicated in hypotension, second- or third-degree atrioventricular block, sick sinus syndrome, left ventricular dysfunction, pulmonary congestion

❑ 0.25 mg/kg intravenous bolus initially then 5-10 mg/hr infusion
❑ If necessary increase dose to 15 mg/hr
❑ 0.05 to 0.1 mg/kg IV bolus

Titrate therapy:
❑ Goal heart rate of 60 beats per minute
❑ Goal systolic BP of 90-120 mm Hg

Control pain

Morphine sulphate

❑ 2.5-5 mg every 3 to 4 hours, infused over 4-5 minutes
Type A dissection

❑ Surgical emergency, expedited transfer to operating room
❑ Intravenous fluid replacement

❑ Maintain euvolemic status
❑ Titrate to mean arterial pressure of 70 mm Hg
❑ Consider vasopressors if still hypotensive
Type B dissection

❑ Intravenous fluid replacement

❑ Maintain euvolemic status
❑ Titrate to mean arterial pressure of 70 mm Hg
❑ Consider vasopressors if still hypotensive

❑ Rule out a possible complication causing hypotension:

❑ Aortic rupture
❑ Severe aortic insufficiency
❑ Pericardial tamponade
❑ Urgent surgical consultation
Systolic blood pressure still >120 mm Hg?
Can hypotension be corrected by surgical intervention?
Add IV vasodilator with SBP goal <120 mmHg
❑ Nitroprusside
❑ 0.3 to 0.5 micrograms/kg/min IV initially then increase by 0.5 micrograms/kg/min
❑ If necessary increase dose to a maximum of 15 mg/hr
Proximal dissection
(involving ascending aorta)?
Proceed to Surgical Management
❑ Continue medical management
❑ Maintain SBP<120 mm Hg
❑ Continue medical management
❑ Maintain SBP<120 mm Hg
❑ Complications that require operative or interventional management?
❑ Limb or mesenteric ischemia
❑ Progression of dissection
❑ Aneurysm expansion
❑ Uncontrolled hypertension
Refer for surgical management

Surgical Management

Surgical management of aortic dissection according to the Guidelines for Diagnosis and Management of patients with Thoracic Aortic Disease.[9]

Is the patient hemodynamically stable?
❑ Age > 40?
❑ Assess need for pre-operative coronary angiography
❑ Known CAD?
❑ Significant risk factors for CAD?
❑ Perform angiography
Significant CAD detected on angiography?
❑ Plan for CABG at the time of aortic dissection repair
❑ Perform urgent operative management
❑ Evidence of any of the following?
Aortic regurgitation
❑ Dissection of aortic sinuses
❑ Perform graft replacement of ascending aorta ± aortic arch
❑ Perform graft replacement of ascending aorta ± aortic arch
❑ Consider repair/replacement of aortic valve


History and Examination

Screening Tests

Initial Management

Definitive Management



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  8. "Predictors of complications in acute type B aortic dissection".
  9. 9.0 9.1 9.2 "". External link in |title= (help)
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