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What is aortic dissection?

A risk associated with HTN. It's dissection of blood along laminar planes of media with the formation of a blood-filled channel within the aortic wall, usually leading to aortic rupture.


Who is at risk for aortic dissection?

1) Men btwn 40-60 with HTN (that is 90 percent of cases)
2) Those with connective tissue disorders (eg Marfan's)
3) Pregnancy (rare)


Where are two places that you are most likely to see aortic dissection?

1) 90 percent of the time in the ascending aorta, in the aortic arch about 10cm of the aortic valve.
2) In the descending thoracic aorta, distal to the left subclavian artery.


A lot of those with aortic dissection also have ______?

Concurrent atherosclerosis.


What are the classifications of aortic dissection?

1) Debakey I - Mostly in ascending aorta, dissection is on both sides but larger area than II. (aka Type A)
2) Debakey II - Mostly in the ascending aorta, dissection is both sides of artery but a small area (aka Type A)
3) Debakey III - Mostly in descending aorta, dissection is mainly on one side (aka Type B)


How the aortic dissection generally presents

A longitudinal or oblique tear about 1-5cm long. The dissection is btwn middle and outer thirds of media. Can happen in a portion or the entire circumference of the arc


What does cystic medial necrosis have to do with aortic dissection?

Happens in about 20 percent of cases. Where muscle wall isn't normal anymore and has spaces and clefts filled with mucus or basophilic material. Happens many times in connective tissue disorders like Marfan's


What can be the outcome of aortic dissection?

1) Blood can continue to dissect proximally to involve the coronary arteries or distally to involve the iliac and femoral arteries.
2) It can rupture into the pericardial sac, pleural or peritoneal cavity.
3) It can re-rupture back into the aortic lumen (double barreled aorta (better outcome)
4)Can cause a collapse in the inner layers of small arteries causing obstruction


What is Marfan's syndrome?

It's a genetic disorder that involved the fibrilin gene (it encodes a protein in elastic connective tissue... like the aorta). About 70-90 percent have HTN. They are at risk for aortic dissection and generally have a thickening of the arterial wall (cystic medial dissection


What is the outside presentation of Marfan's syndrome?

They are generally tall and lanky, chest wall deformities an long double jointed fingers


What are the classic clinical symptoms of aortic dissection?

A sudden excruciating pain in the anterior chest, radiating to the back and moving downward (DDX acute MI)


How do you diagnose aortic dissection?

Aortic angiography, 2D cardiac ultrasound, CT or MRI scan.


What is the prognosis of aortic dissection?

If caught in time, its 65-75 percent salvageable. Anti-HTN therapy works as well


What is the definition of Congestive heart failure?

It's a multisystem derangement when the heart is no longer able to eject blood delivered to it by the venous system.


What are 5 causes of Left Heart failure?

1) HTN
2) Mitral valve disease
3) Aortic valve disease
4) Ischemic heart disease
5) Primary myocardial disease


What are 6 causes of Right heart failure?

1) Left Heart failure (most major cause)
2) Cor pulmonale
3) Pulmonary vascular disease
4) Pulmonic valve disease
5) Tricuspid valve disease
6) Congenital heart disease (left to right shunt)


What are ways that the body compensates for heart failure?

1) It increases sympathetic nervous system activity (catecholamines) (that increase contractility and rate)
2) Hypertrophy, heart muscle can thicken (can contract more forcefully)


What happens after body can no longer properly compensate for heart failure

Forward failure, the CO drops that means an increase in end diastolic volume, EDV (can't pump out all of the blood. That means a rise in end diastolic pressure ,EDP which increases venous pressures and now you have a backward failure (so you have venous congestion). Also increased EDV will stretch fibers and alter contractility


How do you get RHF from LHF?

Left heart is failing as you're not ejecting the blood, that increases congestion in pulmonary circulation and increases pulmonary edema that increases pulmonary resistance and that can lead to RHF and systemic venous congestion


What is the morphology (what can you see) in Left Ventricular Failure?

A dilated hypertrophied heart, boggy lungs with a frothy edema fluid. pulmonary vascular congestion, alveolar hemorrhage, heart failure cells and brown induration of the lung


What is the morphology (what can you see) in Right Ventricular Failure?

Soft tissue edema, abdominal visceral congestion (nutmeg liver), cavity fluid and cardiac cirrhosis (scarring of liver)


What are the clinical features of LHF?

A dyspnea (due to reduced lung compliance) aggravated by lying down, when sleeping and exertion, and enlarged heart, S3, tachy, fine rales in lungs and Afib


What are the clinical features of RHF?

Distended neck veins, an enlarged tender liver, weight gain, dependent edema, cyanosis, acidosis, ventricle arrhythmias and sudden death ( and possibly all of the clinical features of LHF)


What is the morphology of Nonbacterial thrombotic endocarditis

Amalgam of fibrin and platelets at the margins of valve closures.


Where is Nonbacterial thrombotic endocarditis most often found?

Most common on the aortic valve


What is the diagnostic lesion called in ineffective endocarditis.



Where can ineffective endocarditis be found?

In cardiac valves and on the mural surfaces of the endocardium


What is the major cause of ineffective endocarditis?

A bacterial infection


Describe the 2 types of ineffective endocarditis.

1) Acute - caused by highly virulent organisms (like Staph aureus). May infect structurally normal or abnormal valves and progress rapidly. 50% mortality rate
2) Subacute - Caused by less virulent bacteria (a-hemolytic strep). Tends to affect previously abnormal valves. Slow progresssion


What are some of the organisms that can cause ineffective endocarditis?

a-hemolytic strep (50-60% of cases), Staph aureus (10-20%), Enterocci or HACEK group (Haemophilus, Actinobacilli, Cardiobacter, Eikinella, Kingells)