CARDIOVASCULAR Last edited: 3/9/2024

10. AORTIC DISEASES

I. PATHOPHYSIOLOGY III. DIAGNOSTIC APPROACH TO IV. TREATMENT OF V. DIAGNOSTIC APPROACH TO AORTIC ANEURYSMS
A. AORTIC DISSECTION AORTIC DISSECTION AORTIC DISSECTION A. AAA SCREENING
B. AORTIC ANEURYSM A. INITIAL EVALUATION A. STANFORD TYPE A B. TAA SCREENING
B. DIAGNOSTIC TESTS B. STANFORD TYPE B C. SYMPTOMATIC ANEURYSMS
II. COMPLICATIONS C. HEMODYNAMICALLY STABLE OR
A. AORTIC DISSECTION D. (+) RISK OF CIN? VI. TREATMENT OF AORTIC ANEURYSM
B. AORTIC ANEURYSM A. MEDICAL MANAGEMENT
B. SURGICAL MANAGEMENT

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I. PATHOPHYSIOLOGY
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A. Aortic Dissection
1. Pathophysiology:
o Tear in the tunica interna → Blood dissects between tunica
interna and tunica media → Accumulation of blood occurs in
the false lumen → Blood in the false lumen can compress/block
a blood vessel branch → Leads to malperfusion syndromes
discussed below

2. Causes of Intimal Tear

a) ↑Aortic Pressure
o Chronic Hypertension
 ↑BP → ↑Shearing forces → Intimal tear

b) Weak Aorta
1) Vasculitis (e.g., Syphilis or Takayasu’s)
• Vasa vasorum inflammation → ↓O2 supply to blood vessel →
weakening of blood vessel → ↑ susceptibility to injury
2) Ehlers-Danlos Syndrome
• ↓ Collagen in blood vessel → ↑ susceptibility to injury
3) Marfan Syndrome
• ↓ Fibrillin in blood vessels → ↑ susceptibility to injury
4) Aneurysms
• Thin aortic walls → ↑ susceptibility to injury

3. Types of Aortic Dissection

a) Stanford A
Originates at the Ascending Aorta

b) Stanford B
Beyond or after the Left Subclavian Artery

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B. Aortic Aneurysm
1. Pathophysiology:
Aortic wall destruction → weakening of aortic vessel→ dilation
(≥ 3cm) of the aortic vessel occurs as a result.

2. Causes of Aortic Aneurysm

Weak Aorta AND ↑Aortic Pressure

Weak Aorta Caused by:
o Vasculitis
• Vasa vasorum inflammation → ↓O2 supply to blood vessel →
weakening of blood vessel → ↑ Susceptibility to injury
o Ehlers Danlos Syndrome
• ↓ Collagen in blood vessel → ↑ Susceptibility to injury
o Marfan Syndrome
• ↓ Fibrillin in blood vessels → ↑ Susceptibility to injury
o Smoking
 Can cause proteolytic activation → Vessel wall destruction→
↑ susceptibility to injury.
o Atherosclerosis
• Inflammation of blood vessels → Vasa vasorum inflammation →
↓O2 supply to blood vessel → Weakening of blood vessel → Smoking and atherosclerosis, in combination with
↑ Susceptibility to injury hypertension, are the most common cause of aortic aneurysm
↑Aortic Pressure Caused by:
o Hypertension
 ↑BP → ↑Shearing forces → Weakening of the aortic vessel

3. Types of Aortic Aneurysm

a) Thoracic Aortic Aneurysm (TAA)

Dilation of the aorta above the diaphragm
Most commonly, it involves the ascending aorta

b) Abdominal Aortic Aneurysm (AAA)

Dilation of the aorta below the diaphragm
Most commonly, it involves the infrarenal aorta (inferior to
kidneys)

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II. COMPLICATIONS
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A. Aortic Dissection
Aortic Dissection Presents with:
o Most often presents with Ripping or tearing chest pain
o May present with complications such as shock or malperfusion syndromes listed below

1. Shock

a) Hemorrhagic Shock from Aortic Rupture
Pathophysiology of Hemorrhagic shock:
o Blood travels through false lumen → Blood can then track
through the vessel wall and break through tunica externa →
Blood can then leak out of the vascular system (rupture) →
↑Blood loss → ↓BP → Hemorrhagic Shock
Hemorrhagic Shock Presents with:
o Hypotension/Shock
o Tachycardia
o Multisystem organ failure (e.g. AKI or AMS)
b) Obstructive Shock from Cardiac Tamponade
Pathophysiology of Cardiac tamponade:
o Blood travels through false lumen → Blood can then track
through the vessel wall and break through tunica externa →
Blood can then leak out of the vascular system (rupture
through pericardium) → Hemopericardium →
Cardiac tamponade → Obstructive Shock
Cardiac Tamponade Presents with:
o Hypotension/Shock
o JVD
o Muffled Heart sounds

2. Malperfusion Syndrome

a) Ascending Aortic Dissection b) Coronary Artery Compression

Aortic Regurgitation (AR) Myocardial Infarction (MI)
Pathophysiology of AR: Pathophysiology of MI:
o Blood travels through false lumen → Blood can then track o Blood travels through false lumen → Blood can then track
through vessel wall retrograde towards aortic valve → through vessel wall retrograde towards RCA→ Compression of
Compression of aortic valve→ Aortic valve dysfunction → RCA vessel→ ↓Myocardial perfusion→ Acute Inferior MI
Acute AR → Acute Left Heart Failure MI presents with:
Acute AR Presents with: o Angina or epigastric pain
o Hypotension/Shock o ECG with ST↑ and ↑Troponin levels
o Pulmonary edema
o New Onset Decrescendo Diastolic Murmur

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 c) Brachiocephalic Artery Compression e) Renal Artery Compression
Asymmetric BP and Pulses Acute Kidney Injury
Pathophysiology of Asymmetric BP and Pulses: Pathophysiology of AKI:
o Blood travels through the false lumen → Blood can then o Blood travels through false lumen → Blood can then track
track through the vessel wall towards the base of the through the vessel wall towards the base of renal arteries→
brachiocephalic artery → Brachiocephalic artery Renal artery compression → ↓ Renal perfusion →↓GFR
compression → ↓Blood flow through the R. Subclavian AKI Presents with:
Artery → ↓BP and Pulse on R in comparison to the Left side o ↑BUN and Creatinine
which is normally perfused o ↓Urine output
Asymmetric BP and Pulses Presents with:
o SBP Difference of > 20mmHg between Right and Left
o Delayed Pulses on Right in comparison to Left

d) Carotid Artery Compression

TIA or CVA
Pathophysiology of TIA or CVA:
o Blood travels through the false lumen → Blood can then track
through the vessel wall towards the base of Common carotid f) Mesenteric Artery Compression
arteries (CCA)→ CCA compression → ↓Brain perfusion→ TIA or Bowel Ischemia
CVA develops from cerebral hypoxia Pathophysiology of Bowel Ischemia:
TIA or CVA Presents with: o Blood travels through false lumen → Blood can then track
o Neurological deficits (e.g. weakness, dysarthria, sensory loss) through the vessel wall towards the base of mesenteric vessels
Horner’s Syndrome → Mesenteric vessel compression →
Pathophysiology of Horner's syndrome: ↓Bowel perfusion → Bowel ischemia
o Blood travels through false lumen → Blood can then track Bowel Ischemia Presents with:
through the vessel wall towards the base of Common carotid o Abdominal pain
arteries (CCA) near the sympathetic plexus→ Sympathetic o GI bleeding
plexus compression → ↓SNS supply to the ipsilateral face o ↑Lactate
Horners Syndrome Presents with:
o Ptosis: Drooping of eyelid g) Acute Limb Ischemia
o Miosis: Pupillary constriction Pathophysiology of Acute Limb Ischemia:
o Anhidrosis: Lack of facial sweating o Blood travels through false lumen → Blood can then track
through the vessel wall towards the base of aortoiliac
vessels → Aortoiliac compression or narrowing
→ ↓Limb perfusion → Acute limb ischemia
Acute Limb Ischemia Presents with:
o Severe Limb pain
o ↓Distal pulses
o Limb Pallor
o Limb paralysis

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B. Aortic Aneurysm
1. Shock
Pathophysiology of Shock:
o Blood travels across the weak vessel wall→ Aortic rupture →
Massive blood loss → ↓BP → Hemorrhagic shock
Hemorrhagic Shock Presents with:
o Hypotension/Shock
o Sentinel Signs:
 Back or abdominal pain
 Pulsatile abdominal mass
o Flank ecchymosis
 When the abdominal aorta ruptures, it leaks into the
retroperitoneal spaces and produces ecchymosis on the flank

2. Thoracic Aortic Aneurysm

Thoracic Aortic Aneurysm presents with:
o Asymptomatic quite often, but sometimes may present with mild chest pain
o May present with Complications: Thrombo-embolic complications, Aortic regurgitation, Adjacent compression

a) Thromboemboli b) Aortic Regurgitation (AR)

Pathophysiology of thromboembolic: Pathophysiology of AR
o Aneurysmal dilation leads to stasis of blood flow → Aortic o Aneurysmal dilation of aortic root→ Aortic valves are pulled
thrombi form → Emboli can break away from thrombus → farther away from another→ Large space occurs between aortic
Emboli lodges in arteries supplying vital organs → ↓Organ valves → ↑Backflow of blood through large space between
perfusion → Organ ischemia aortic valve organ→ Massive regurgitation into LV→ Acute AR →
Thromboemboli Presents with: Acute Left Heart Failure
o CVA Acute AR Presents with:
 Secondary to cerebral artery occlusion o Hypotension/Shock
 May present with neurological deficits o Pulmonary edema
o Acute Mesenteric Ischemia o New Onset Decrescendo Diastolic Murmur
 Abdominal pain
Watch out for Acute Heart Failure!
 ↑Lactate
o Acute Limb ischemia
 Severe Limb pain
 ↓Distal pulses
 Limb Pallor
 Limb paralysis c) Compression
Pathophysiology of Adjacent Compression:
o Aneurysmal dilation of Aortic root and arch → Dilated aorta
compresses nearby structures
Structural compression Presents with:
o SVC compression → SVC syndrome
 Facial plethora and JVD
o Trachea → Stridor or Dyspnea
o Esophagus → Dysphagia
o RLN →Hoarseness of the voice

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3. Abdominal Aortic Aneurysm

a) Thromboemboli b) Upper GI Bleeding (UGIB)

Pathophysiology of Thromboemboli:
o Aneurysmal dilation leads to stasis of blood flow → Aortic
thrombi form → Emboli can break away from thrombus →
Emboli lodges in arteries supplying vital organs→↓Organ
perfusion → Organ ischemia
Thromboemboli Presents with:
Pathophysiology of UGIB:
o Aneurysmal dilation leads to fistula formation between the
duodenum and the aorta (especially if a graft is present) →
Aorto-enteric fistula forms → Massive UGIB ensues
UGIB Presents with:
o Melena: Dark-colored stools

o Acute Mesenteric Ischemia o Hematochezia: Bright red stools

 Hematochezia develops due to rapid hemorrhage that
 Abdominal pain
outpaces the body’s ability to oxidize the blood.
 ↑Lactate
o Anemia
o Acute Limb ischemia
o Hemorrhagic Shock
 Severe Limb pain
 ↓Distal pulses
 Limb Pallor

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III. DIAGNOSTIC APPROACH TO AORTIC DISSECTION

FIGURE 1. DIAGNOSTIC APPROACH TO AORTIC DISSECTION.

A. Initial Evaluation
Evaluate the patient’s blood pressure: Are they hypertensive?
Do they have tearing chest pain?
Do they have asymmetric BP > 20 mmHg?
Do they have any symptoms of malperfusion syndrome?

B. Diagnostic Tests
1. ECG
Indications:
o To rule out MI

2. Chest X-Ray
Indications:
o To assess for alternative pulmonary causes (e.g. PTX)
of new-onset chest pain
Findings suggestive of Aortic dissection:
o May reveal a widened mediastinum ≥ 8cm FIGURE 2. CHEST X-RAY SHOWING A WIDENED MEDIASTINUM.

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 C. Hemodynamically Stable or (+) Risk of CIN?
Are they hemodynamically unstable, or Is there a risk of contrast-induced nephropathy (CIN)?
o Why is hemodynamic stability a decision-making factor?
 In this patient, transport to a CT scanner for a CTA is dangerous and increases the risk of the patient decompensating in an undesirable
location other than in an ICU or ED room where resources and settings are preferred, and as such, a TEE is more preferred.
o Why is CIN a decision-making factor?
 In patients with end-stage renal disease (ESRD), caution is advised when administering contrast media. However, this should not
postpone necessary life-saving diagnostic procedures such as a CTA or the identification of potentially fatal conditions.

1. Transesophageal Echocardiogram (TEE) 2. CT or MRI Angiography

Indications: Indications:
o HD unstable o HD stable
o Risk of severe CIN (e.g., ESRD) o NO risk of severe CIN (e.g., ESRD)
Findings suggestive of Aortic Dissection: Findings suggestive of Aortic Dissection:
o Perform a bedside TEE → Visualize a true and false lumen o Perform a CTA → Visualize a true and false lumen, which also
assists in surgical planning

FIGURE 3. TEE SHOWING BOTH TRUE AND FALSE LUMEN.

FIGURE 4. CT AND MR ANGIOGRAPHY SHOWING BOTH LUMENS.

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IV. TREATMENT OF AORTIC DISSECTION
TABLE 1. SUMMARY OF MANAGEMENT IN AORTIC DISSECTION.

A. Stanford Type A B. Stanford Type B

Stanford Type A Treatment Standards:
o Type A Aortic dissection carries a high risk of serious
complications, including aortic regurgitation, myocardial
infarction, cardiac tamponade, and aortic rupture, and as
such, surgical management is the most important and
essential treatment modality
Stanford Type B Treatment Standards:
o Type B Aortic dissection carries a lower risk of serious
complications as compared to type A, and as such, surgical
management should be the second line, and the focus of
treatment should be geared towards medical management as
the most important and essential treatment modality

1. Medical Management
Indications for medical management: Agents used in medical management:
o Stabilization pre-surgical intervention in Type A aortic o Hypertensive? Nitroprusside is administered
dissection  Goal: SBP 100-120 mmHg
o Primary modality for Type B aortic dissection o Tachycardic? β-blockers are administered
Purpose of medical management:  Goal: HR < 60 bpm
o Prevent further propagation of dissection and complications o Shock/hypotensive? Vasopressors and IVF are administered
 Goal: MAP > 65 mmHg

2. Surgical Management
Indications for Surgical Management:
Surgical intervention for Stanford Type B aortic dissection
o All Type A Aortic dissections, given the high mortality rate if
is indicated only in the presence of complications and
not surgically treated
failure of medical management
o Type B Aortic dissections refractory to medical management
or complications such as shock or malperfusion syndromes
develop
Types of Surgical Management:
o Open Surgery with Graft placement
 Preferred more so for patients with Stanford Type A
o Endovascular aortic repair (EVAR) with stent placement
 Preferred for patients with Stanford Type B, given the
improved outcomes
 It can be used in Type A. However, the evidence has shown
higher long-term reintervention rates

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V. DIAGNOSTIC APPROACH TO AORTIC ANEURYSMS

FIGURE 5. APPROACH TO DIAGNOSIS OF AORTIC ANEURYSMS.

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A. AAA Screening B. TAA Screening

Indications for AAA screening: Indications for TAA screening:
o > 65 y/o male with a history of smoking o Bicuspid aortic valve
Modalities used for AAA screening: o Connective tissue disease (e.g. Ehlers-Danlos Syndrome or
o Abdominal US Marfan Syndrome)
Modalities used for TAA screening:
Abdominal Ultrasound o TEE or CTA
Abdominal US findings:
o Abdominal Aorta < 3 cm? → (-) AAA CT Angiogram
o Abdominal Aorta > 3 cm? → (+) AAA and requires follow-up CTA Findings:
 Follow up for > 3cm o Confirms the presence of a TAA and monitors expansion
• Repeat ultrasound every 6-12 months o Should the aneurysm measure 5.5 cm or more OR increase by
• If subsequent ultrasound reveals an aneurysm size of 5.5 cm more than 0.5 cm over a six-month period, the patient should
or greater OR an expansion rate exceeding 0.5 cm over six be assessed for possible surgical intervention
months, surgical evaluation for the patient is indicated.

FIGURE 7. AN ENLARGED AORTIC DIAMETER IN CT ANGIOGRAM.

FIGURE 6. ABDOMINAL U/S SHOWING AN ENLARGED AORTIC DIAMETER.

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 C. Symptomatic Aneurysms
Hemodynamically Unstable?

a) Abdominal U/S for AAA; TEE for TAA b) CT Angiography

Indicated for hemodynamically unstable patients For hemodynamically stable patients
Allows for the visualization of the aneurysm Helpful with:
o Identifying the aneurysm
o Aids In surgical planning
o Monitoring the size of the aneurysm

FIGURE 8. AN ENLARGED AORTIC DIAMETER IN ABDOMINAL U/S.

FIGURE 9. AORTIC RUPTURE IN CT ANGIOGRAPHY.

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VI. TREATMENT OF AORTIC ANEURYSM
TABLE 2. SUMMARY OF MANAGEMENT IN AORTIC ANEURYSM.

A. Medical Management B. Surgical Management

TAA/AAA Medical Treatment Goals: TAA/AAA Surgical Treatment Goals
o Managed medically thus to prevent enlargement of aneurysm o This can be an elective or emergent surgical procedure
and risk of rupture of other complications through the  Patients asymptomatic but presenting with an aortic
following lifestyle modifications and interventions: diameter of 5.5 cm or greater or an increase greater than 0.5
 Smoking cessation cm over six months
 Statin Therapy → Hyperlipidemia → Require urgent evaluation
 Beta-Blockers, ACE Inhibitors, ARBs → BP control  Patients who are hemodynamically unstable or present with
complications
→ Require emergent evaluation
o Surgical modalities include:
 Open surgery (graft)
 EVAR and Stent (preferred)

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