Emergency Medicine: Cardiology 213
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Acute Coronary Syndromes: A Focus on STEMI10 Topics|3 Quizzes
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Pre-Quiz for STEMI Pharmcotherapy
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Background in STEMI
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Diagnostic Evaluation in STEMI
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Antiplatelet Therapy in STEMI
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Glycoprotein IIb/IIIa inhibitors in STEMI
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Anticoagulants in STEMI
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Ancillary Therapies in STEMI
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Reperfusion Therapies in STEMI
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Literature Review: STEMI Pharmacotherapy
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Summary and Key Points in STEMI
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Pre-Quiz for STEMI Pharmcotherapy
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Acute decompensated heart failure10 Topics|3 Quizzes
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Hypertensive Urgency and Emergency Management11 Topics|3 Quizzes
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Pre-Quiz: Hypertensive Urgency and Emergency Management
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Introduction
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Clinical Presentation
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Pathophysiology
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Diagnostic Approach
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Management – Overview
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Hypertensive Urgency Pharmacotherapy
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Hypertensive Emergency Pharmacotherapy
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Literature Review: Hypertensive Urgency and Emergency Management
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Summary
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References and Bibliography
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Pre-Quiz: Hypertensive Urgency and Emergency Management
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Acute aortic dissection8 Topics|2 Quizzes
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Supraventricular Arrhythmias (Afib, AVNRT)10 Topics|2 Quizzes
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Pre-Quiz: Arrhythmias
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Introduction: Supraventricular Arrhythmias
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Clinical Presentation: Supraventricular Arrhythmias
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Pathophysiology: Supraventricular Arrhythmias
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Diagnostic Approach: Supraventricular Arrhythmias
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Management - Overview: Supraventricular Arrhythmias
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Pharmacotherapy: Supraventricular Arrhythmias
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Key Guidelines and Evidence: Supraventricular Arrhythmias
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Summary: Supraventricular Arrhythmias
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References: Supraventricular Arrhythmias
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Pre-Quiz: Arrhythmias
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Ventricular Arrhythmias10 Topics|2 Quizzes
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Pre-Quiz: Ventricular Arrhythmias
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Introduction: Ventricular Arrhythmias
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Clinical Presentation: Ventricular Arrhythmias
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Pathophysology: Ventricular Arrhythmias
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Diagnostic Approach: Ventricular Arrhythmias
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Management - Overview: Ventricular Arrhythmias
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Pharmacotherapy: Ventricular Arrhythmias
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Key Guidelines and Evidence: Ventricular Arrhythmias
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Summary: Ventricular Arrhythmias
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References: Ventricular Arrhythmias
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Pre-Quiz: Ventricular Arrhythmias
Participants 396
Pathophysiology
The aortic wall is composed of three distinct layers: the intima, media, and adventitia. The media layer, which is made up of elastic tissue and smooth muscle, provides the aorta with its properties of distensibility and integrity.
Aortic dissection occurs through a process known as medial degeneration, which is characterized by the loss of smooth muscle cells and elastic tissue. This degeneration is often accompanied by scarring, fibrosis, and hyaline-like changes. Medial degeneration is a precursor to aortic dissection and can be observed with normal aging. However, the progression of medial degeneration is hastened by hypertension.
Although medial degeneration was initially thought to be noninflammatory, more recent evidence has suggested the presence of inflammatory cell infiltration. The repetitive hydrodynamic forces produced by the ejection of blood into the aorta with each cardiac cycle contribute to the weakening of the aortic intima, which can lead to aortic dissection.
Aortic dissection (AD) is a longitudinal cleavage of the aortic media created by a dissecting column of blood. The term “dissecting aortic aneurysm” has been inaccurately applied to this condition. The term “aortic dissection” is preferred because the affected aorta is only rarely aneurysmal.
Dissections that involve the ascending aorta are often more lethal than those limited to the distal aorta and require a different therapeutic approach. Patients with distal dissections tend to be older, smokers with chronic lung disease, and more often have generalized atherosclerosis and hypertension compared with patients who have proximal aortic dissections.
A dissection is classified as acute if it is of short duration, subacute if it lasts for a moderate duration, and chronic if present for longer than 6 weeks. Two other aortic conditions, intramural hemorrhage and penetrating aortic ulcer, are closely related to aortic dissection. Patients with these conditions have clinical symptoms and management recommendations similar to those for patients with aortic dissection.
Analogy
Imagine your aorta as a garden hose. The hose is made up of several layers of material, just like the aorta is made up of layers: the intima, media, and adventitia.
Now, consider the water pressure inside the hose. If the pressure is too high or the hose is old and worn out, the inner layer might tear. This is similar to the aortic dissection, where high blood pressure or degeneration of the aortic wall can cause a tear in the intima layer.
Once the inner layer is torn, water can force its way between the layers of the hose, causing them to separate or ‘dissect’. This is exactly what happens in an aortic dissection. The blood forces its way into the wall of the aorta, causing the layers to separate and creating a new false channel for blood flow.
If the pressure continues to build, the hose might bulge and eventually burst. Similarly, in aortic dissection, if the condition is not treated, the aorta can rupture, leading to life-threatening internal bleeding.
Reference:
Nienaber CA, Clough RE, Hallett, Jr JW, Eagle KA. Aortic dissection: new insights into its pathogenesis, diagnosis, and treatment. J Am Coll Cardiol. 2011;57(11):1195-1207.