16.2 Acute Aortic Syndromes & Peripheral Vascular Emergencies

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1 Chapter 1: Exam Structure, Blueprint & Clinical Decision-Making

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7 Chapter 7: Pediatric Health Maintenance & Surveillance

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8 Chapter 8: Behavioral Health & Safety Screening

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9 Chapter 9: Adult Preventive Screening: Cardiovascular & Metabolic

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10 Chapter 10: Adult Cancer Screening: Breast & Gynecologic

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11 Chapter 11: Adult Cancer Screening: Colorectal, Lung & Prostate

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12 Chapter 12: Sexual Health, Infectious Disease Screening & Contraception

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13 Chapter 13: Reproductive Life Planning, Lactation & Preoperative Care

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14 Chapter 14: Emergent Cardiovascular Conditions

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15 Chapter 15: Cardiac Arrhythmias, Heart Failure & Hypertensive Crises

15.1 Acute Atrial & Ventricular Arrhythmias 15.2 Acute Decompensated Heart Failure & Cardiogenic Shock 15.3 Hypertensive Emergency & Urgency Management

16 Chapter 16: Vascular & Thromboembolic Emergencies

16.1 Pulmonary Embolism & Deep Vein Thrombosis 16.2 Acute Aortic Syndromes & Peripheral Vascular Emergencies 16.3 Critical Limb Ischemia & Acute Arterial Occlusion

17 Chapter 17: Neurologic Emergencies: Stroke & Altered Consciousness

17.1 Acute Ischemic Stroke & Intracranial Hemorrhage 17.2 Syncope Evaluation & Status Epilepticus 17.3 Acute Delirium, Encephalopathy & Severe Confusion

18 Chapter 18: Neurologic Trauma & Acute Cranial Emergencies

18.1 Concussion, Moderate-to-Severe TBI & Intracranial Injury 18.2 Thunderclap & Acute Severe Secondary Headaches 18.3 Acute Ophthalmologic Emergencies

19 Chapter 19: Acute Abdominal, Pelvic & Gastrointestinal Emergencies

19.1 Acute Abdominal & Pelvic Pain Triage 19.2 Upper & Lower Gastrointestinal Bleeding 19.3 Acute Hepatic Failure, Cholangitis & Severe Jaundice

20 Chapter 20: Acute Pulmonary & Airway Emergencies

20.1 Acute Hypoxic Respiratory Failure & ARDS 20.2 Severe Community-Acquired Pneumonia & Empyema 20.3 Acute Severe Epistaxis & Airway Obstruction

21 Chapter 21: Acute Traumatic Injuries & Wound Care

21.1 Major Trauma Resuscitation & Initial Assessment 21.2 Burn Assessment, Inhalation Injury & Resuscitation 21.3 Laceration Management, Complex Wounds & Animal Bites

22 Chapter 22: Acute Orthopedic & Musculoskeletal Emergencies

22.1 Acute Ambulatory Fractures & Initial Splinting 22.2 Compartment Syndrome & Major Orthopedic Trauma 22.3 Septic Arthritis & Acute Microcrystalline Crises

23 Chapter 23: Severe Infections, Sepsis & Systemic Emergencies

23.1 Sepsis, Septic Shock & Initial Fluid Resuscitation 23.2 Necrotizing Soft Tissue Infections & Severe CNS Infections 23.3 Anaphylaxis Diagnosis, Epinephrine Dosing & Airway Protection

24 Chapter 24: Metabolic, Endocrine & Electrolyte Emergencies

24.1 Diabetic Ketoacidosis & Hyperosmolar Hyperglycemic State 24.2 Critical Electrolyte Emergencies: Dyskalemias & Dysnatremias 24.3 Severe Calcium Abnormalities & Acute Adrenal Crisis

25 Chapter 25: Hematologic, Urologic & Dental Emergencies

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26 Chapter 26: Psychiatric, Behavioral & Obstetric/Gynecologic Emergencies

26.1 Suicidal Ideation, Acute Agitation & Behavioral Emergencies 26.2 Acute Physical & Sexual Assault Care 26.3 Life-Threatening Vaginal Bleeding & Ectopic Pregnancy 26.4 Environmental Heat Stroke & Severe Hypothermia

27 Chapter 27: Acute Head, Neck & Neurologic Symptoms

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28 Chapter 28: Acute Cranial Nerves, Hearing & Sensory Symptoms

28.1 Peripheral Neuropathies: Bell's Palsy, Carpal Tunnel & Radiculopathy 28.2 Acute Tinnitus, Sudden Sensorineural Hearing Loss & Cerumen Impaction 28.3 Acute Dizziness, Benign Paroxysmal Positional Vertigo & Vestibular Neuritis

29 Chapter 29: Acute Upper Respiratory Tract Infections

29.1 Acute Viral Rhinosinusitis vs. Bacterial Rhinosinusitis 29.2 Acute Pharyngitis: Group A Streptococcus & Centor Criteria 29.3 Acute Otitis Media, Otitis Externa & Serous Effusion

30 Chapter 30: Acute Lower Respiratory Infections & Cough

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31 Chapter 31: Allergic, Nasal & Non-Infectious Pulmonary Conditions

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32 Chapter 32: Acute Chest, Cardiac & Vascular Symptoms

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33 Chapter 33: Acute Upper Gastrointestinal Conditions

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34 Chapter 34: Acute Lower Gastrointestinal Conditions

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35 Chapter 35: Inflammatory, Functional & Malabsorptive GI Disorders

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36 Chapter 36: Acute Abdominal, Hepatic & Biliary Disorders

36.1 Ambulatory Abdominal & Pelvic Pain Triage 36.2 Acute Cholecystitis, Biliary Colic & Pancreatitis 36.3 Acute Liver Injury & Viral Hepatitis

37 Chapter 37: Acute Abdominal Wall, Hernias & Dental Conditions

37.1 Abdominal Wall, Inguinal & Ventral Hernias 37.2 Acute Dental Pain, Odontogenic Abscess & Aphthous Ulcers 37.3 Acute Edema: Unilateral vs. Bilateral Diagnostic Evaluation

38 Chapter 38: Acute Infectious Dermatoses

38.1 Bacterial Skin Infections: Impetigo, Cellulitis & Cutaneous Abscesses 38.2 Fungal Skin Infections: Tinea Corporis, Cruris, Pedis & Onychomycosis 38.3 Viral Cutaneous Infections: Herpes Simplex, Zoster & Molluscum Contagiosum

39 Chapter 39: Inflammatory, Allergic & Autoimmune Dermatoses

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40 Chapter 40: Acute Shoulder, Elbow & Upper Extremity Injuries

40.1 Rotator Cuff Pathology, Tendinopathy & Shoulder Impingement 40.2 Lateral & Medial Epicondylitis, Olecranon Bursitis & Elbow Sprains 40.3 Wrist & Hand Soft-Tissue Injuries: De Quervain, TFCC & Finger Sprains

41 Chapter 41: Acute Knee, Ankle & Lower Extremity Injuries

41.1 Meniscal Tears, Ligamentous Knee Injuries & Patellofemoral Pain 41.2 Ankle Sprains, Ottawa Ankle Rules & Achilles Tendinopathy 41.3 Plantar Fasciitis, Shin Splints & Overuse Syndromes

42 Chapter 42: Acute Ambulatory Fractures & Dislocations

42.1 Distal Radius, Scaphoid & Common Upper Extremity Fractures 42.2 Metatarsal, Clavicle & Common Lower Extremity Fractures 42.3 Joint Dislocation Management: Nursemaid's Elbow & Shoulder Subluxation

43 Chapter 43: Acute Axial Musculoskeletal Pain & Falls

43.1 Acute Low Back Pain: Red Flags, Strain & Disc Herniation 43.2 Acute Cervical Strain, Whiplash & Axial Neck Pain 43.3 Evaluation of Falls in Ambulatory & Older Patients

44 Chapter 44: Acute Inflammatory Arthropathies & Generalized Pain

44.1 Acute Inflammatory Arthritis & Spondyloarthropathies 44.2 Myalgias, Rhabdomyolysis & Post-Viral Pain Syndromes 44.3 Acute Non-Headache Pain Management Strategies

45 Chapter 45: Acute Renal, Urinary & Genitourinary Conditions

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46 Chapter 46: Acute Male Genitourinary & Prostatic Conditions

46.1 Acute Prostatitis, Epididymitis & Orchitis 46.2 Acute Scrotal Pain: Torsion vs Appendage, BPH & Male Genital Emergencies 46.3 Acute Urinary Retention & Incontinence Evaluation

47 Chapter 47: Acute Women's Health & Early Pregnancy Care

47.1 Early Pregnancy Diagnosis, Dating & Initial Complications 47.2 Abnormal Uterine Bleeding & Acute Menstrual Disorders 47.3 Premenstrual Syndrome & Premenstrual Dysphoric Disorder

48 Chapter 48: Breast Disorders, STIs & Pediatric Elimination

48.1 Palpable Breast Mass, Mastitis & Nipple Discharge 48.2 Sexually Transmitted Infections: Diagnosis, Staging & CDC Guidelines 48.3 Pediatric Enuresis & Encopresis

49 Chapter 49: Systemic Signs, Metabolic Dysregulation & Miscellaneous Infections

49.1 Acute Fever, Sepsis Screening & FUO in Primary Care 49.2 Acute Hyperglycemia & Symptomatic Hypoglycemia 49.3 Electrolyte Abnormalities: Mild-to-Moderate Disturbances 49.4 Vector-Borne, Tick-Borne & Rickettsial Illnesses

50 Chapter 50: Chronic Cardiovascular Diseases: Hypertension & Ischemia

50.1 Essential Hypertension Management: 2025 AHA/ACC Guideline & JNC Strategies 50.2 Chronic Coronary Artery Disease & Post-MI Secondary Prevention 50.3 Chronic Heart Failure: HFrEF, HFpEF & Quadruple GDMT

51 Chapter 51: Chronic Vascular, Valvular & Dyslipidemic Diseases

51.1 Peripheral Arterial Disease & Claudication 51.2 Chronic Valvular Heart Disease & Murmur Evaluation 51.3 Lipid Disorders & ASCVD Risk-Based Statin Therapy

52 Chapter 52: Chronic Respiratory Diseases: Asthma & COPD

52.1 Chronic Asthma Management: GINA Stepwise SMART Therapy 52.2 Chronic Obstructive Pulmonary Disease: GOLD Recommendations 52.3 Solitary Pulmonary Nodule Evaluation & Fleischner Society Criteria

53 Chapter 53: Chronic Metabolic Diseases: Diabetes Mellitus

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54 Chapter 54: Obesity, Nutrition & Metabolic Bone Diseases

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55 Chapter 55: Chronic Endocrine Disorders

55.1 Primary & Subclinical Hypothyroidism, Hyperthyroidism & Nodules 55.2 Adrenal Disorders: Addison's Disease & Cushing's Syndrome 55.3 Hypercalcemia, Hyperparathyroidism & Pituitary Disorders

56 Chapter 56: Chronic Kidney Disease & Venous Disorders

56.1 Chronic Kidney Disease: KDIGO Staging & Renoprotective Therapy 56.2 Chronic Venous Insufficiency, Stasis Dermatitis & Lymphedema 56.3 Chronic Electrolyte & Acid-Base Management in CKD

57 Chapter 57: Chronic Gastrointestinal & Hepatic Diseases

57.1 Gastroesophageal Reflux Disease, Barrett's Esophagus & Dyspepsia 57.2 Chronic Liver Disease: MASLD/NAFLD, Cirrhosis & Portal Hypertension 57.3 Viral Hepatitis B & C: Long-Term Monitoring & DAA Therapy

58 Chapter 58: Colorectal Surveillance & Chronic Pancreaticobiliary Care

58.1 Post-Polypectomy Colorectal Polyp Surveillance Guidelines 58.2 Chronic Pancreatitis & Exocrine Pancreatic Insufficiency 58.3 Chronic Nausea, Gastroparesis & Functional GI Disorders

59 Chapter 59: Chronic Musculoskeletal & Rheumatologic Disorders

59.1 Osteoarthritis: Hip, Knee & Hand Management 59.2 Spinal Conditions: Spinal Stenosis, Spondylolisthesis & Compression Fractures 59.3 Chronic Myopathies & Fibromyalgia Syndrome

60 Chapter 60: Chronic Neurologic & Neurodegenerative Disorders

60.1 Dementia: Alzheimer's, Vascular & Lewy Body Disease 60.2 Parkinson's Disease & Essential Tremor 60.3 Epilepsy: Chronic Antiseizure Medications & Post-Stroke Care

61 Chapter 61: Chronic Peripheral Nerves, Pain & Sensory Disorders

61.1 Diabetic & Chronic Peripheral Neuropathies 61.2 Chronic Pain Syndromes & Chronic Daily Headaches 61.3 Chronic Tinnitus, Presbycusis & Persistent Dizziness

62 Chapter 62: Chronic Psychiatric Disorders

62.1 Major Depressive Disorder & Generalized Anxiety Disorder 62.2 Bipolar Disorder: Maintenance Pharmacotherapy & Lithium Monitoring 62.3 Adult & Pediatric Attention-Deficit/Hyperactivity Disorder

63 Chapter 63: Chronic Behavioral Health & Neurodevelopmental Conditions

63.1 Chronic Behavioral Conditions: PTSD, OCD & Somatization 63.2 Autism Spectrum Disorder & Intellectual Disabilities 63.3 Eating Disorders: Anorexia Nervosa, Bulimia & Binge Eating

64 Chapter 64: Chronic Substance Use Disorders & Tobacco Cessation

64.1 Alcohol Use Disorder: Pharmacotherapy & Relapse Prevention 64.2 Opioid & Stimulant Use Disorders: MOUD & Harm Reduction 64.3 Longitudinal Tobacco Cessation Pharmacotherapy

65 Chapter 65: Chronic Dermatologic Conditions

65.1 Acne Vulgaris, Rosacea & Seborrheic Dermatitis 65.2 Chronic Plaque Psoriasis & Biologic Therapies 65.3 Chronic Eczema, Hidradenitis Suppurativa & Cutaneous Lupus

66 Chapter 66: Chronic Reproductive, Infectious & Geriatric Special Care

66.1 Chronic Menstrual Disorders, Infertility & Sexual Dysfunction 66.2 Menopause Management & Hormone Replacement Therapy 66.3 Chronic HIV Infection Management & Primary Care Integration 66.4 Gender-Affirming Primary Care & Hormone Therapy 66.5 Advance Care Planning, Palliative Care & End-of-Life Symptom Control

67 Chapter 67: Continuity Care: Sleep, Fatigue, Cancer, Pregnancy & the Adult Preventive Visit

67.1 Chronic Insomnia & Obstructive Sleep Apnea 67.2 Chronic Malaise, Fatigue & ME/CFS 67.3 Primary Care During Cancer Treatment & Survivorship 67.4 Routine Prenatal Care & Longitudinal Pregnancy Management 67.5 The Periodic Adult Health Examination & Medicare Annual Wellness Visit

16.2 Acute Aortic Syndromes & Peripheral Vascular Emergencies

Key Takeaways Explain This Topic AI

Acute aortic syndromes (AAS) encompass acute aortic dissection, intramural hematoma (IMH, non-communicating medial hematoma without an intimal tear), and penetrating atherosclerotic ulcer (PAU, plaque erosion through the internal elastic lamina); all share high risks of rapid aortic rupture and malperfusion.

Stanford Type A dissections involve the ascending aorta and represent surgical emergencies with untreated mortality increasing 1% to 2% per hour during the first 24 to 48 hours, requiring emergent cardiothoracic surgical repair, whereas uncomplicated Type B dissections involve only the descending aorta and are managed medically.

Anti-impulse therapy requires administering an intravenous beta-blocker (esmolol or labetalol) FIRST to achieve a target heart rate <60 beats/min, followed by an intravenous vasodilator (nicardipine) to reduce systolic blood pressure to 100–120 mm Hg, preventing reflex tachycardia that accelerates aortic wall shear stress (dP/dt).

Physical examination red flags for acute aortic dissection include a systolic blood pressure differential >20 mm Hg between upper extremities, asymmetric pulse deficits, a new early diastolic murmur of aortic regurgitation, and Beck's triad of cardiac tamponade.

Contrast-enhanced CT angiography (CTA) of the chest, abdomen, and pelvis is the gold standard diagnostic imaging in hemodynamically stable patients, whereas transesophageal echocardiography (TEE) is preferred at the bedside in unstable patients or those with severe contrast allergy.

Last updated: September 2026

Spectrum of Acute Aortic Syndromes

Acute Aortic Syndrome (AAS) is an umbrella term encompassing three interrelated, life-threatening pathologies of the thoracic and abdominal aorta characterized by disruption of the aortic wall architecture:

Acute Aortic Dissection (AAD, ~80–90% of AAS) : Characterized by an initial tear in the aortic intima that permits pressurized, pulsatile blood to surge into the aortic media. The driving hemodynamic force cleaves the media longitudinally, creating a true lumen (the original endothelialized channel) and a false lumen (a newly created channel within the aortic media). As blood propagates, it can dissect antegradely down the entire length of the aorta or retrogradely toward the aortic root and coronary ostia.

Intramural Hematoma (IMH, ~5–10% of AAS) : Defined as a localized hemorrhage within the aortic media occurring without an identifiable intimal tear or flow-carrying false lumen . IMH is thought to originate from the spontaneous rupture of the vasa vasorum (the microvascular network supplying the aortic adventitia and outer media). IMH is clinically dynamic: in up to 30 % 30\% 30% to 40 % 40\% 40% of cases, it progresses into classic aortic dissection or transmural rupture, particularly when involving the ascending aorta.

Penetrating Atherosclerotic Ulcer (PAU, ~5% of AAS) : Represents deep ulceration of an advanced atherosclerotic plaque that erodes through the internal elastic lamina into the muscular media. Predominantly affects elderly individuals with severe, diffuse atherosclerotic disease and chronic hypertension. PAUs frequently trigger localized intramural hematomas, false aneurysm (pseudoaneurysm) formation, or transmural rupture, most commonly in the descending thoracic aorta.

Pathophysiology & Predisposing Conditions

The initiation and propagation of an aortic dissection require two fundamental biomechanical factors:

High Hemodynamic Shear Stress ( d P / d t dP/dt d P / d t ) : The rate of rise of left ventricular pressure during early systole ( d P / d t dP/dt d P / d t ) generates pulsatile kinetic energy and lateral tensile stress against the aortic wall. The proximal ascending aorta (within centimeters of the aortic valve) experiences the highest shear stress, explaining why the majority of intimal tears occur in the ascending aorta.

Underlying Medial Degeneration (Cystic Medial Necrosis) : Histologically characterized by smooth muscle cell apoptosis, fragmentation and depletion of elastic lamellae, and deposition of amorphous, basophilic proteoglycan matrix within the media, weakening structural tensile integrity.

Clinical Risk Factors & Genetic Syndromes

Chronic Systemic Hypertension : Present in > 75 % >75\% > 75% of patients presenting with acute aortic dissection. Longstanding elevated wall stress accelerates medial elastolysis and arteriosclerosis.

Inherited Connective Tissue Disorders :

Marfan Syndrome : Autosomal dominant mutation in the FBN1 gene encoding fibrillin-1, leading to aberrant TGF-beta signaling and severe medial elastolysis. Accounts for ≈ 50 % \approx 50\% ≈ 50% of aortic dissections occurring in patients < 40 <40 < 40 years of age. Frequently presents with progressive aortic root dilation and annuloaortic ectasia.

Vascular Ehlers-Danlos Syndrome (vEDS, Type IV) : Autosomal dominant mutation in COL3A1 affecting type III procollagen. Causes extreme arterial and hollow organ fragility; spontaneous arterial dissection or rupture can occur without prior aneurysmal dilation.

Loeys-Dietz Syndrome : Autosomal dominant mutations in TGFBR1 , TGFBR2 , or SMAD3 . Features hypertelorism, bifid uvula, and extensive arterial tortuosity, with a high risk of aortic rupture at much smaller diameters than in Marfan syndrome.

Turner Syndrome (45,X) : Associated with bicuspid aortic valve, aortic coarctation, and accelerated aortic root enlargement.

Congenital Vascular Anomalies :

Bicuspid Aortic Valve (BAV) : Present in 1–2% of the population; conveys a 5- to 9-fold increased lifetime risk of aortic dissection due to intrinsic aortopathy independent of valvular hemodynamics.

Coarctation of the Aorta : Localized narrowing distal to the left subclavian artery produces extreme proximal hypertension and structural medial weakness.

Acute Sympathomimetic & Mechanical Stressors : Illicit cocaine or methamphetamine use (induces massive catecholamine release, acute hypertensive spikes, and tachycardia), heavy resistance weightlifting, and intense emotional trauma.

Pregnancy & Puerperium : Elevated circulating estrogen and progesterone alter vascular collagen-elastin composition, combined with the 50 % 50\% 50% increase in cardiac output during the third trimester, predisposing women with underlying aortopathies (e.g., Marfan) to acute peripartum dissection.

Iatrogenic & Prior Cardiac Interventions : Prior coronary artery bypass grafting (CABG), aortic valve replacement, cardiac catheterization, or transcatheter aortic valve replacement (TAVR).

Anatomical Classification Systems

Therapeutic decision-making hinges entirely on whether the ascending aorta is involved: STANFORD CLASSIFICATION OF AORTIC DISSECTION

┌────────────────────────────────────────┐ ┌────────────────────────────────────────┐
│ STANFORD TYPE A (65%) │ │ STANFORD TYPE B (35%) │
├────────────────────────────────────────┤ ├────────────────────────────────────────┤
│ • Involves the ASCENDING AORTA │ │ • Involves DESCENDING AORTA ONLY │
│ • Originates proximal to brachiocephalic│ │ • Originates DISTAL to left subclavian │
│ artery (may extend into arch/des- │ │ artery (no ascending aortic involvement)│
│ cending aorta) │ │ • Primarily MEDICAL MANAGEMENT in ICU │
│ • SURGICAL EMERGENCY (Mortality +1-2%/h)│ │ • TEVAR indicated for COMPLICATIONS: │
│ • Immediate Cardiothoracic Consultation│ │ - Malperfusion (renal, bowel, limb) │
│ • DeBakey Types I & II │ │ - Refractory pain / Uncontrolled HTN │
│ │ │ - Rapid expansion / Impending rupture│
│ │ │ • DeBakey Type III │
└────────────────────────────────────────┘ └────────────────────────────────────────┘

Stanford Classification :

Type A : Involves the ascending aorta , regardless of the site of origin or distal extent. (Encompasses DeBakey Type I [ascending and descending aorta] and DeBakey Type II [confined to ascending aorta]). Untreated mortality is approximately 1 % 1\% 1% to 2 % 2\% 2% per hour during the first 24 to 48 hours ( > 50 % >50\% > 50% mortality at 48 hours without surgery). Requires emergent surgical repair .

Type B : Involves exclusively the descending aorta distal to the origin of the left subclavian artery , without involvement of the ascending aorta or aortic arch. (Corresponds to DeBakey Type III). Uncomplicated Type B dissections are managed medically with intensive anti-impulse therapy.

Clinical Presentation & Physical Examination Red Flags
Character and Migration of Pain

Onset : Pain is characteristically abrupt, instantaneous, and reaches maximal intensity at the very onset (unlike the crescendo, waxing-and-waning pain of acute coronary syndromes).

Quality : Described as severe, "sharp," "knife-like," "ripping," or "tearing."

Location : Anterior retrosternal chest pain strongly correlates with ascending aortic involvement (Type A); interscapular, mid-scapular, or lower back pain strongly correlates with descending thoracic involvement (Type B); radiation or migration into the abdomen and flanks reflects distal longitudinal propagation of the dissection flap along the thoracoabdominal aorta.

Cardinal Physical Examination Red Flags

Pulse Deficits & Blood Pressure Differential :

Asymmetric or absent radial, brachial, femoral, or pedal pulses, or a systolic blood pressure differential > 20 >20 > 20 mm Hg between upper extremities (present in ≈ 30 % \approx 30\% ≈ 30% of Type A dissections). Occurs when the expanding false lumen or detached intimal flap compresses or shears the brachiocephalic (innominate) or left subclavian artery.

New Diastolic Murmur of Aortic Regurgitation :

A high-pitched, decrescendo diastolic blowing murmur heard loudest along the right sternal border (present in up to 50 % 50\% 50% of Type A dissections). Mechanism: asymmetrical circumferential dilation of the aortic root, disruption of aortic annular commissural support, or retrograded intimal flap prolapse through the valve leaflets during diastole. Often triggers acute left ventricular volume overload and flash pulmonary edema.

Cardiac Tamponade & Beck's Triad :

The ascending aorta and aortic root are enveloped within the pericardial reflection. Retrograde dissection can rupture into the pericardial space, causing acute hemopericardium and cardiac tamponade —the single leading cause of death in Type A dissection.

Physical findings: Beck's Triad (hypotension, jugular venous distension, and muffled/distant heart tones), pulsus paradoxus ( > 10 >10 > 10 mm Hg drop in systolic blood pressure during normal inspiration), and low-voltage QRS complexes with electrical alternans on ECG.

Neurologic & Malperfusion Syndromes :

Acute Ischemic Stroke / Syncope (~10–15%) : Compression or thromboembolic occlusion of the common carotid arteries, or transient global cerebral hypoperfusion during acute rupture.

Paraplegia / Paraparesis : Acute spinal cord ischemia resulting from dissection flap occlusion of intercostal arteries and the anterior spinal artery (artery of Adamkiewicz) , typically arising between T9 and T12.

Horner Syndrome : Ptosis, miosis, and anhidrosis caused by local compression of the superior cervical sympathetic ganglion by a dilated ascending aortic hematoma.

Vocal Cord Paralysis (Ortner Syndrome) : Hoarseness caused by compression of the left recurrent laryngeal nerve between the aortic arch and the pulmonary artery.

Acute Coronary Malperfusion (Inferior STEMI Mimic) : The dissection flap extends retrogradely to obstruct the right coronary artery (RCA) ostium in ≈ 10 % \approx 10\% ≈ 10% of Type A cases, producing ST-segment elevation in leads II, III, and aVF. CRITICAL DANGER : Administering systemic thrombolytics or potent antiplatelet agents for a presumed inferior STEMI without excluding aortic dissection in a patient with tearing chest pain is fatal.

Visceral & Extremity Ischemia : Celiac and superior mesenteric artery obstruction triggers acute mesenteric ischemia (severe abdominal pain out of proportion to exam, lactic acidosis); renal artery compression triggers acute renal failure and refractory malignant hypertension; iliofemoral obstruction produces acute lower extremity ischemia (cold, pale, pulseless leg).

Diagnostic Imaging Strategies ACUTE AORTIC SYNDROME DIAGNOSTIC STRATEGY

┌────────────────────────────────────────────────────────────────────────┐
│ HEMODYNAMICALLY STABLE PATIENT │
│ • Imaging of Choice: Contrast-Enhanced CT Angiography (CTA) │
│ • Coverage: Complete Chest, Abdomen, and Pelvis │
│ • Sensitivity / Specificity: 98–100% │
│ • Demonstrates: Intimal flap, true vs false lumen, branch vessel │
│ malperfusion, extent of dissection, rupture/hemothorax │
└────────────────────────────────────────────────────────────────────────┘
│
┌───────────────────────────────────┴────────────────────────────────────┐
│ HEMODYNAMICALLY UNSTABLE PATIENT (Shock, Peri-arrest, Severe Allergy) │
│ • Imaging of Choice: Bedside Transesophageal Echocardiography (TEE) │
│ • Location: Emergency Department resuscitation bay or Operating Room │
│ • Rapid Assessment: Identifies intimal flap, severe aortic regurgitation│
│ mechanism, pericardial tamponade, and proximal root dilation │
└────────────────────────────────────────────────────────────────────────┘

Contrast-Enhanced CT Angiography (CTA) : Gold standard initial test in stable patients. Triphasic protocol (non-contrast to detect hyperdense intramural hematoma, followed by arterial-phase contrast). Accurately distinguishes the true lumen (smaller caliber, faster contrast transit) from the false lumen (larger caliber, slower opacification, "cobweb signs", "beak sign"). Identifies celiac, SMA, renal, and iliac artery involvement.

Transesophageal Echocardiography (TEE) : Highly sensitive ( > 98 % >98\% > 98% ) and specific ( > 95 % >95\% > 95% ). The definitive modality for hemodynamically unstable patients who cannot safely leave the resuscitation area. Visualizes aortic root architecture, coronaries, aortic valve leaflet coaptation, and hemopericardium. Limited by an anatomic "blind spot" in the distal ascending aorta and arch caused by interposition of the air-filled trachea.

Transthoracic Echocardiography (TTE) : Excellent bedside screening tool (POCUS) to identify pericardial effusion, tamponade physiology, severe aortic regurgitation, and proximal root dilation, but has inadequate sensitivity ( < 60 – 80 % <60–80\% < 60–80% for Type A; < 40 % <40\% < 40% for Type B) to rule out dissection.

Chest Radiography (CXR) : May reveal mediastinal widening ( > 8 >8 > 8 cm on upright PA film), abnormal aortic contour, tracheal deviation, or the "calcium sign" (displacement of intimal calcification > 5 >5 > 5 mm away from the outer aortic soft tissue border). CRITICAL EXAM PEARL : A completely normal chest radiograph is present in 10 % 10\% 10% to 20 % 20\% 20% of acute aortic dissections ; a normal CXR never excludes the diagnosis.

Emergency Medical & Surgical Management
Anti-Impulse Therapy: The Cardinal Sequence

Anti-impulse therapy aims to reduce left ventricular contractility, rate of pressure rise ( d P / d t dP/dt d P / d t ), and systemic arterial blood pressure, thereby halting the propagation of the dissecting hematoma and preventing rupture.

Target Physiological Parameters :

Heart Rate : < 60 <60 < 60 beats/min (target 50 to 60 beats/min) ;

Systolic Blood Pressure : 100 to 120 mm Hg (or lowest blood pressure that maintains adequate cerebral, coronary, and renal perfusion).

THE CARDINAL RULE: BETA-BLOCKER FIRST!

Direct vasodilators (such as nicardipine, nitroprusside, or hydralazine) cause acute peripheral vasodilation, which triggers potent baroreceptor-mediated reflex sympathetic activation and tachycardia . Reflex tachycardia dramatically increases d P / d t dP/dt d P / d t (LV ejection force), accelerating shear stress on the torn aortic media and triggering catastrophic propagation or rupture.

Therefore, intravenous beta-blockade must be fully established to achieve heart rate < 60 <60 < 60 beats/min BEFORE any direct vasodilator is initiated .

Step 1: Intravenous Beta-Adrenergic Blockade :

Esmolol : Preferred first-line agent due to its ultra-short elimination half-life (~9 minutes) and rapid titratability. Loading bolus: 500 mcg/kg IV over 1 minute , followed by a continuous infusion of 50 to 300 mcg/kg/min .

Labetalol : Combined non-selective beta and alpha-1 blocker. Administer 10 to 20 mg IV push over 2 minutes , repeating 20 to 80 mg every 10 minutes (maximum cumulative dose 300 mg), or continuous infusion of 1 to 2 mg/min.

If beta-blockers are strictly contraindicated (e.g., severe acute bronchospasm, severe active asthma, critical bradycardia): administer intravenous non-dihydropyridine calcium channel blockers ( diltiazem or verapamil ) to achieve rate control.

Step 2: Intravenous Vasodilator (Initiated ONLY AFTER Heart Rate < 60 <60 < 60 bpm) :

Nicardipine : Dihydropyridine calcium channel blocker administered as a titratable IV infusion starting at 5 mg/h , titrating by 2.5 mg/h every 5 to 15 minutes to a maximum of 15 mg/h until SBP 100–120 mm Hg is achieved.

Sodium Nitroprusside : Potent arterial and venous vasodilator infused at 0.25 to 5.0 mcg/kg/min. Requires arterial line monitoring; risk of cyanide and thiocyanate toxicity with prolonged infusions.

Contraindicated Vasodilator : Hydralazine is contraindicated because it causes unpredictable, prolonged hypotension and intense reflex tachycardia.

Step 3: Adequate Analgesia :

Intravenous opioids ( fentanyl 25–50 mcg or morphine 2–4 mg IV ) to blunt pain-induced endogenous sympathetic surges.

Definitive Surgical & Endovascular Interventions

Stanford Type A Dissection :

Immediate Cardiothoracic Surgical Consultation and Emergent Operative Repair .

Median sternotomy under cardiopulmonary bypass and deep hypothermic circulatory arrest (DHCA).

Resection of the primary intimal tear, synthetic Dacron graft replacement of the ascending aorta (hemiarch or total arch replacement), and aortic valve resuspension or root reconstruction (Bentall procedure with composite valve-graft conduit if the aortic root or coronary ostia are disrupted).

Stanford Type B Dissection :

Uncomplicated Type B : Managed medically in the intensive care unit with ongoing anti-impulse therapy (oral beta-blockers, ACE inhibitors/ARBs, CCBs). Long-term serial CTA surveillance.

Complicated Type B : Presence of any of the following:

Branch vessel malperfusion (renal failure, mesenteric ischemia, spinal ischemia, or acute limb ischemia);
Refractory or recurrent severe pain despite maximum anti-impulse therapy;
Refractory hypertension resistant to ≥ 3 \ge 3 ≥ 3 full-dose antihypertensive classes;
Rapid aortic expansion ( > 10 >10 > 10 mm/year or diameter ≥ 55 \ge 55 ≥ 55 mm);

Impending or overt rupture (expanding periaortic hematoma, hemothorax).

Management of Complicated Type B : Thoracic Endovascular Aortic Repair (TEVAR) . A covered stent-graft is deployed endovascularly across the primary entry tear in the descending aorta, sealing the entry tear, depressurizing the false lumen, and expanding the true lumen to restore branch vessel perfusion.

The Pericardiocentesis Dilemma in Tamponade :

If hemopericardium and cardiac tamponade complicate Type A dissection, routine large-volume needle pericardiocentesis is strictly CONTRAINDICATED .

Evacuating pericardial fluid removes the intrapericardial tamponading counter-pressure that is temporarily containing the aortic rupture site. The resulting surge in systolic blood pressure precipitates torrential re-rupture into the pericardial cavity and immediate death.

In patients in peri-arrest or PEA, aspirate only the absolute minimal volume of fluid (10 to 20 mL) necessary to restore marginal cardiac output as a temporizing bridge while rolling into the operating room for emergent sternotomy.