Coronary Artery Diseases Continued Flashcards Preview

Post Midterm Patho > Coronary Artery Diseases Continued > Flashcards

Flashcards in Coronary Artery Diseases Continued Deck (56):
1

What is Endocarditis?

Bacterial infection in the endocardium and the valves

2

What are the 2 Requirements for endocarditis to occur?

1. Microbe must be able to get into Cardiovascular System
2. Microbe must be able to adhere to the endocardium

3

Why is it difficult for the microbe to enter the Cardiovascular system?

Because of the defence cells circulating in the blood.

4

What are two ways that adherence of the microbe to the endocardium/valve is made possible?

1. Sutures, post surgery
2. Valvular dysfunction

5

The bacteria in endocarditis colonizes amongst what 2 things?

Platelets and fibrin.

6

What are the Local Manifestations of Endocarditis? (4)

What are the systemic manifestations? (2)

1. Dysfunction of the Heart
2. Possible distal emobolization if an emblous breaks off from the colony that has formed.
3. Can cause Valvular Dysfunction
4. Murmur heard

1. fever
2. chills

7

Diagnosis of Endocarditis?

1. Echocardiogram
2. C & S

8

Tx for Endocarditis?

1. Antibiotic for the infection (ex. penicillin, vancomycin)
2. Treat the Cardiac Complications

9

What is Rheumatic Fever?

Immune Mediated Inflammation that effects multiple organs.

10

What do the Antibodies and T Cells do in response to Rheumatic Fever which is problematic?

They mistarget integument, CNS, Joints and the Heart.

11

What does mistargeting of the antigens in the heart cause to happen to the heart?

inflammation of the pericardium, myocardium and the valves.

12

Is Rheumatic Heart Disease an Infection in the Heart?

No. It is caused by an infection but what happens to the Heart is inflammation.

13

What is the treatment for Rheumatic Heart Disease?

1. Antibiotic for the infection (not in the heart, penicillin or erythromycin)
2. Anti-inflammatory drugs
3. Bed rest
4. Symptomatic Management (management of pain / swelling joints)
5. Avoid cardiac failure, deal with the complications.

14

Is acute RHD life threatening?

No, it is self limiting. Chronic can cause severe heart damage.

15

Define Congestive Heart Failure.

NOT A DISEASE. It is a group of manifestations related to dysfunction of the heart.

16

Congestive Heart Failure , what does the word congestion refer to?

Pooling of blood in the vessels

17

CHF is the end point of what?

Serious Heart Disease
- Cardiomyopathy
-MI

18

What is the Etiology of CHF?

1. Cardiomyopathy
2. MI
3. ^^ excessive workload on the heart
4. Valvular Disease
5. Hypervolemia
6. Uncontrolled HTN

19

What does L sided Heart failure lead to?

R sided Heart Failure.

20

Describe Left Sided Heart Failure beginning in the Left Ventricle.

L Ventricle not able to eject all the blood -- Residual Blood in Left ventricle. L Atria works harder to eject all its blood to the LV. Unable to do so, therefore can't receive all of the blood from the Pulmonary Circuit. Pulmonary Congestion occurs (pooling of blood in the vessels) -- Leads to ^^ Hydrostatic Pressure -- leads to Increase fluid in the interstitial spaces (Pulmonary Edema occurs). Right Ventricle now tries to work harder to pump into the Pulmonary circuit, result in the R Ventricle being hypertrophied.

21

What are the 3 main signs of R sided heart failure?

Systemic congestion
- Jugular Venous Distension
- Abdominal Organ Distention
- Peripheral Edema

22

What is the main sign of L sided heart failure?

Pulmonary edema

23

Why does the heart not initially fail when it begins to become congested?

Compensatory mechanisms kick it.

24

Does compensated Heart Failure show any symptoms?

No, it is asymptomatic until the compensation fails.

25

What are the 6 mechanisms of Compensated Heart Failure?
V
S
R
N
E
C

1. Ventricle Dilation
2. SNS
3. RAAS
4. Natuertic Peptides
5. Endothelins
6. Cardiac Hypertrophy / Remodelling

26

Describe the mechanism of Ventricular Dilation

Increase of ED volume -- Increase stretch of ventricles -- Increase preload -- Increase cardiac output

Long term: overstretch / ^^ 02 requirement for heart because it requires more ATP.

27

Describe the mechanism of SNS

Sympathetic Nervous System causes:
- Vasoconstriction
- Tachycardia
- Increase contractility

*all aiming to increase CO

28

Describe the mechanism of RAAS

Aiming to increase Blood pressure

29

Describe the mechanism of Nateuretic Peptides

ANP/BNP
-both produced by the heart

-Causes diuersis and natriuresis
- Affects Smooth Muscle (vasodolation to decrease pressure)

30

Describe the mechanism of Endothelins.

Vasoconstrictors
Smooth muscle proliferates (^^ in numbers, and hypertrophies)

31

Describe the mechanism of Cardiac Hypertrophy/ Remodelling.

- ^ workload of failing heart leads to... Hypertrophy
- eventually will cause a decrease in contractility
- Requires more 02, myocardial dysfunction will occur

32

Can the heart continue to compensate for the failure forever?

No, Uncompensated Heart Failure will occur

33

Can the heart compensate for years?

Yes

34

What are the manifestations of Uncompensated Heart Failure?

1. Decreased HR, Decreased CO
2. Effects of Impaired Pumping

(SNS mediated)

35

Dx of CHF? 3 subgroups.

1. Risk Factors (Hx, Px)
2. Labs (CBC, Hgb, (looking for anemia), Liver Function Tests
3. ECG/ Echocardiogram

36

Tx of Acute CHF

Stabilize and correct cause:
- Inotrope
- Diuretics
- Vasodilators

37

Tx of Chronic CHF

- Try to help the symptoms
- Try to decrease risks
- Try to improve the Fx

38

For CHF... ejection fraction

ACEI & BetaBlocker

39

For CHF... if ejection fraction is equal to or >40%, how do you treat?

- Tx the cause
- ACEI & BetaBlocker
-Angiotensin Receptor Blocker (if symptom is w/ activity)
- ^^ dose or add diuretic if symptom is at rest
- Sx for repairable defect

40

What is Pericarditis?

Pericardial Inflammation
(membrane that lines the heart, not part of the heart wall)

41

What causes pericarditis?

Infection or injury

42

Inflammation cause an increase of capillary permeability and exudate to form, in the case of pericarditis, where does this exudate shift to?

Exudate will be in pericardial space.

43

What type of exudate is there in Pericarditis?

Fibrinous or fluid.

44

What does this exudate cause to happen in pericarditis?

Restricts the filling of the heart, therefore restricts cardiac function.

45

Which exudate is considered "worse" in pericarditis? Why?

Fibrinous. The fluid can't be displaced, where as the fluid exudate could be displaced depending on the A or V filling.

46

What is the triad manifestations of Pericarditis?

1. Chest pain (^^ by resp movement, aggravated by moving torso or breathing.)
2. Pericardial rub (sound heard through stethoscope when patient breathes)
3. ECG changes (emptying / filling of the heart altered)

47

What is the treatment for pericarditis?

- Based on the cause
- Antiinflammatory drugs
- Abx? If it is caused by bacterial infection

48

What can pericarditis lead to?

Cardiac Tamponade

49

Define Cardiac Tamponade.

External compression of the heart.

50

What is cardiac tamponade caused by?

D/t accumulation of fluid, pus, or air in pericardial space (this restricts filling and emptying of the heart)

51

Is cardiac tamponade life threatening?

Yes.

52

What type of shock is cardiac tamponade an example of?

Obstructive shock.

53

What are the manifestations of cardiac tamponade?

Decrease C0 --> decreased arterial pressure --> compensatory response --> tachycardia (temporary) -- body realizes this is not working/ helping so will stop

54

What is the treatment for cardiac tamponade?

Stat pericardiocentesis

55

What is pericardiocentesis?

Remove the fluid from the pericardial space! Quickly!

56

What happens if fluid is not removed quickly from the pericardial space in treatment for cardiac tamponade?

Fluid could become solid (ex. blood clot) this would mean you could not aspirate the fluid, and would need to be surgically removed.