• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/25

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

25 Cards in this Set

  • Front
  • Back

Myocardial Infarction 1

The first muscle to die is at the end of the coronary vascular supply: the subendocardial muscle. If small branch of CA involved

Myocardial Infarction 2

•The infarct gardually enlarges for several hours until it is complete. Transmural MI if large CA branch involved.



•Prompt therapeutic intervention to re-establish coronary flow may stop Necrosis while the infarction is small.

Myocardial Infarction

•Onset and first several hours


-Subendocardial Injury and myocardial ischemia. No cell death (Infarction) yet

Myocardial Infarction

•Before coronary occlusion:


-Heart muscle normal

Myocardial Infarction

•First Day


-Ischemia and Injury extend to epicardial surface. Subendocardial muscle dying in area of most severe Injury.

Myocardial Infarction



Zone of ischemia

•Myocardial ischemia causes ST segment depression with or without. T wave inversion as result of altered repolarization

Myocardial Infarction



Zone of Injury

•Myocardial Injury causes ST segment elevation with or without loss of R wave

Myocardial Infarction



Zone of Infarction

•Myocardial Infarction causes deep. Q waves as result of absence of depolarization current from dead tissue and receding currents from opposite side of heart.

Myocardial Infarction

•Mural (wall) scarring at different levels (cross sections) of heart.

MI: Anatomic Complications of Transmural MI

•Mitral valve papillary muscle connection damaged = mitral valve regurgitation



•Necrotic myocardium oozes substances across endocardium attracting platelets = mural thrombus, cerebral emboli & stroke

MI: Anatomic Complications of Transmural MI

•Blood dissects through and ruptures soft dead myocardium = hemopericardium & cardiac tamponade (smothering)

Myocardial Infarction: Clinical Features

•Electrocardiogram abnormalities (acute, subacute, resolved).



•Blood, total creatine kinase (CK), cardiac creatine kinase (CK-MB), and cardiac troponin are increased.



•Magnitude of increase is related to size of MI.

True

•The most common cause of instantaneous death is ischemic Heart Disease

Hypertensive Heart Disease

•HTN - hypertrophy, Q decrease



•HTN - atherosclerosis



•HTN - increase shearing forces on endothelium

Hypertensive Heart Disease

•Hypertrophic myocardium


-Stiff & high Metabolic requirements, hard to perfuse



•Now susceptible to CHF, MI, Arrythmias

Valvular Heart Disease

Caused by:


•Valvular (Aortic) stenosis


-Incomplete obstructed flow, usually from stiff or fused valve leaflets or age related calcification & degeneration.

Valvular Heart Disease

•Valvular (Aortic) insufficiency -Regurgitation or backflow, usually associated with valves that do not close properly because they are stiff or be deformed by inflammation, or eaten away by bacterial infection.

Valvular Heart Disease



Valvular (Aortic) Insufficiency

-Caused by:


•Syphilitic aortitis


•Papillary muscle Infarction causing mitral valve Chodae tendon tear


•LV heart failure (LV dilation)


•Rheumatic fever (inflamed thick valves)


•Myxomatous degeneration of mitral valve

Valvular Heart Disease



Valvular (Aortic) Stenosis

•Often age-related changes



•Valvular Fibrosis



•Calcification



•Valve deformity


°Causes


-Systolic murmur (Lub-Dub-Swish)


-LVH & Syncope


•Treatment


-Valve replacement

Rheumatic Disease

•Streptococcal pharyngitis (not all strep locations) stimulates production of anti streptococcal antibodies and T cells, which attack the microbe but also attack similar antigens in heart muscle cells, valves (autoimmune) & joints.


-May be chronic and silent resulting in chronic rheumatoid valvulitis

Rheumatic Heart Disease

•Inflammation and scarring produces a stiff, thick valve and short, thick chordae tendineae. Such valves may be stenotic or regurgitant.

Endocarditis



Non-infective thrombotic Endocarditis


(Non-bacterial endocarditis)

Platelets & fibrous material on valve leaflets



Can embolize causing brain Infarction


-Linked to: Cachexia, DVT, Hypercoagulable blood, malignancy or adenocarcinoma

Endocarditis



Infective Endocarditis

•Bacterial Infection



•More Serious


-Erosion of leaflets


-Catastrophic valve insufficiency


-Systemic Infection

Pericarditis

•Viral Infection


-Atypical chest pain


-Audible friction rub


-Can constrict heart and decrease diastolic filling


-EKG changes look like diffuse myocardial Injury

Primary Myocardial Disease

•Myocarditis -Viral Infection (Coxsackie A or B), Or Rheumatic fever (Autoimmune)



•Cardiomyopathy (Intrinsic Myocardial Disease)



•Either can progress to Dilated Cardiomyopathy