Patho: Infectious Heart Disease

Front 1

Name the 5 functions of the pericardial sac.

Back 1

Fluid
Stabilize
Friction
Overfilling
Barrier

Front 2

If a patient has inpatient pericardial disease, what are the possible causes? (It's serious, inpatient...)

Back 2

Think T.U.M.O.R.
T = Trauma (blunt force- car accident, stabbed in chest
U = Uremia- when patient is in chronic renal failure; see dev. of pericardial friction rub. Correct that by getting patient on dialysis.
M = MI- if you transmural MI then where necrotic tissue is triggers inflammatory response. Dressler’s Syndrome- happens after patient’s MI. This is where areas of necrotic tissue have triggered inflammatory response. Patient complains of chest pain after MI- this is either another MI or inflammatory response.
O = Other infections or MEDs-procainamide and hydralazine; bacterial- c-Dif, diptheria
R = Rheumatoid, Radiation- radiation used in cancer but can’t completely guide radiation exposure so patient develops pericarditis. Radiation destroys healthy tissue and inflammatory response initiates.

Front 3

What are the three main stages of the pathogenesis of pericardial disease?

Back 3

Vasodilation: allows fluid to come out soon

Increased vascular permeability: protein starts to escape also; neutrophils, WBC’s need to get out of circulation into closed system of pericardial sac and take care of invading body.

Leukocyte exudation: need at least 250 cc’s to see on X-Ray. This is not very good. BUT on ECHO, can see fluid start accum. At 25 cc. See right ventricle get pushed in.

Front 4

When considering if a patient w/ pericardial disease will have symptomatic or non-symptomatic tamponade you have to consider what 3 factors about the effusion/sac/heart.

Back 4

Volume: rapid amount of fluid, patient becomes symptomatic very early.

Rate: rate can be fast and heart can’t compensate.

Compliance: if fluid is gathering slowly then compliance increases and a LARGE amount of fluid can accumulate.

Front 5

What two layers of the heart secrete pericardial fluid?

Back 5

visceral and parietal pericardium.

Front 6

What are some indicators that an effusion has progressed to tamponade?

Back 6

JVD, increased venous pressure, pulmonary symptoms, muffled heart sounds, decreased CO, diastolic pressure in both ventricles becomes increased.

Front 7

An analogy to constrictive pericarditis is like putting a __________ around the heart which is made up of _______ ____ ______and _________.

Back 7

...cast around the heart which is made up of (fibrous scar tissue) and (calcification).

Front 8

How does infectious endocarditis begin? What is the best test to diagnosis this?

Back 8

There is turbulent blood flow that causes injury. This leads to platelet formation. Bacteria somehow get introduced to situation when platelets are aggregating (could come from surgery, or other opportunistic entry). Then, calcification of vegetation begins. This calcification essentially protects the bacteria from the body's inflammatory responce.
Patient's temp goes up and down as bacteria reproduce and "seed" into blood stream and sepsis is present.

The bst way to diagnosis this is via ECHO.

Front 9

Infectious pericarditis has two broad classifications of the types of patients involved- either ________ or ________.
What are the major pathogens in each type of patient?

Back 9

IV drug users or non-IV drug users.
nonIVDA: 50-70% strep (viridians and alpha-hemolytic), followed by staph (50%),and enterococci (10%).

IVDA: staph. 50-60% followed by various strep and enterococci (20%) and pseudomonas & serretia (10-15%-not good organism).

Front 10

What are the major valves involved in NonIVDA and IVDA endocarditis?

Back 10

NonIVDA: aortic and mitral
IVDA: tricuspid

Front 11

Within 60 days of perioperative infection, what are the most likely pathogens in a nonIVDA with prosthetic valves?

Back 11

Staph epidermidis 25-30%, Staph. aureus 20-30%, gram negative organisms (20%), and fungi (10-20%).

Front 12

When myocarditis develops, what are the most likely culprites?

Back 12

Cocksackie B virus. Virus or toxic irritant is what causes problem. Alcoholic have high potential for myocarditis. Other causes can be: peripartum (particularly in older women or women having twins- more antigens that are foreign to body), doxyrubison?, cobalt exposure, & tocalytics?(prevent preterm delivery).

Front 13

What are the three types of cardiomyopathies?

Back 13

Dilated, restrictive, and hypertrophic.

Front 14

When looking at an ECHO, how can you tell if a patient has dilated cardiomyopathy of hypertrophic cardiomyopathy?

Back 14

Dilated cardiomyopathy demostrates 4 chambers that are dilated. in hypertrophic myopathy the septum (90%) and the ventricle are dilated. If ventricle dilated then fibers are in disarray. This organizational pattern is different than if the patient had LVH.

Front 15

What is impaired in dilated cardiomyopathy-systole or diastole? What is impaired in hypertrophic cardiomyopathy- systole or diastole?

Back 15

Dilated: systole.
Restrictive: diastole-give CCB and patient feeling better quickly.

Front 16

Which cardiomyopathy is autosomal dominant- which is most likely to result in the sudden death of athletes?

Back 16

Restrictive for both criteria.

Front 17

In restrictive cardiomyopathy, the septum is affected. How does that lead to the problem at hand? What is a kind of drug that you definetely do not want to use in this condition?

Back 17

The enlarged septum cause the mitral valve to be moved from its normal positioning and regurg is now present. Sounds like a "seagull".

No-no drug: positive ionotrope.

Front 18

Amyloid, sarcoid, scleroderma, radiation could all be causes of this cardiomyopathy that results abnormally rigid ventricles and impaired diastolic function.

Back 18

Dilated cardiomyopathy. (not as common as the other 2 cardiomyopathies).

Front 19

What is the differentiates dilated cardiomyopathy from CHF?

Back 19

The two are very similary: JVD, ascities, peripheral edema; but in dilated cardiomyopathy there the pairs of hearts valves begin to seperate from eachother. This seperation can be seen on an ECHO.

Front 20

What is the treatment for dilated cardiomyopathy?

Back 20

heart transplant;

Heart Transplant survival: 74%-5year, 55%-10year
Prognosis if no transplant <50% at 5years.

Front 21

Which cardiomyopathy has genetic roots linked to an autosomal dominant trait?

Back 21

Hypertrophic cardiomyopathy

Front 22

What is the pathophysiology of hypertrophic cardiomyopathy?

Back 22

The patients vary from asymptomatic to marked limitations.

Average age is mid-20s

Interventricular septum affects LF and decreases LV CO. Leaflet of mitral valve gets pulled away from other valves and mitral regurg. results (crescendo-decrescendo heard at left sternal border. When moving the stethoscope toward the apex murmur becomes more blowing pansystolic).

Syncope.

Front 23

What is the treatment for hypertrophic cardiomyopathy?
What is the prognosis?

Back 23

BB or CCB. Stop strenuous activity. Genetic counseling.

Prognosis is sudden cardiac death.

Front 24

Which cardiomyopathy most resembles constrictive pericarditis but in addition has large depositions of iron and amyloid?

Back 24

Restrictive cardiomyopathy

Front 25

What is the prognosis of restrictive cardiomyopathy?

Back 25

Not good.