Cardiac inflammatory disease Flashcards

1
Q

blood flow of the heart

A
  1. right side: un oxygenated
    inferior and superior vena cava –> RA –> Tricuspid –> RV –> pulmonic valve –> pul. artery –> lungs
  2. left side: oxygenated
    Lungs –> pul. veins –> LA –> mitral –> LV –> aortic valve –> body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

endocardium

A

-innermost layer and has heart valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

myocardium

A

-thickest layer between endocardium and pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pericardium

A

-2 layers and the outermost layer of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

infective endocarditis

A
  • infection of the innermost layer of the heart (endocardium) which encompasses the heart
  • treated with ABX but used to be fatal!!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Patho of endocarditis

A
  • blood turbulence within the heart allows organisms (virus, bacteria, fungi) to infect the valves or other endothelial surfaces
  • causes inflammation in response that forms vegetation’s on the surface
  • vegetations form as the microbes stick to the endothelial surface
  • infection spreads and disrupts the electrical conduction of the heart= dysrhythmias and heart blocks and damages the heart valve and supporting structures

*this could spread to the myocardium (thickest layer of the heart= heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

issues with these vegetation’s

A

-they are fragile and can break off = emboli in blood stream and travel to other parts of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

risk factors for endocarditis

A
  • divided into cardiogenic, non cardiogenic, and procedural
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cariogenic risk factors for endocarditis

A
  • make the heart susceptible to pathogens
  • prior endocarditis
  • prosthetic heart valves
  • valvular disease
  • rheumatic heart disease
  • congenital heart defects and pacemakers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

non-cardiogenic risk factors for endocarditis

A
  • hospital acquired infections and IV drug abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

procedural risks for endocarditis

A
  • intravascular devices
  • dental work
  • tonsillectomies
  • wound infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

prophylactic ABX for endocarditis

A
  • may be prescribed for those @ risk for developing endocarditis due to procedure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical manifestations of endocarditis

A
  • fever
  • new heart murmor or change in existing murmur (systolic murmur)
  • flu-like symptoms: arthralgia, anorexia, fatigue, malaise
  • A/V heart blocks
  • vascular manifestations due to of vegetations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why can endocarditis be hard to diagnose

A
  • manifestations are non specific and not present in all cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why do you get a new heart murmur or change in existing one

A
  • as the valves are damaged further = decreased CO and cardiac murmurs worsen = decreased UO and SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the vascular manifestations from microembolism of vegetations

A
  • splinter hemorrhages
  • petechiae
  • oslers nodes (reddened finger tips)
  • janeways lesions (dark small spots on feet)
  • roths spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

embolization

A
  • occurs in 50 % of the pt. with endocarditis
  • vegetations most commonly originate in aortic and mitral valves –> embolization from valves enter arterial circulation and cause symptoms (depending on where its occluded)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Right sided embolization

A
  • rare but could cause PE

- dyspnea, chest pain, hemoptysis, respiratory arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

left sided embolization: spleen

A

-Sharp LUQ pain, splenomegaly, abdominal rigidity, local tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

left sided embolization: kidneys

A

Flank pain, hematuria, renal failure

21
Q

left sided embolization: limbs

A

Ischemia, limb infarction, gangrene

22
Q

left sided embolization: brain

A

Hemiplegia, ataxia, aphasia, visual changes, altered LOC

23
Q

DX of endocarditis

A
  • pt. history and recent procedures
  • blood cultures
  • echocardiography
  • chest x ray
  • ECG
  • cardiac catheterization
24
Q

why is patient history so important for DX of endocarditis

A
  • checking for risk factors

- needs to be in last 6 months

25
Q

why are blood cultures so important in DX of endocarditis

A
  • will be positive in 90 % of people

- shows systemic bacteremia that causes endocarditis

26
Q

Why is echo important for DX of endocarditis

A
  • visualizes the vegetations on the heart valve
27
Q

why is ECG important for dx of endocarditis

A
  • shows 1st and 2nd deg block due to the valves proximity to AV node
28
Q

treatment of endocarditis

A
  1. Antibiotics based on blood culture results:
    - started in the hospital and continued @ home
    - can take 4-8 weeks
    - effectiveness is measured with blood cultures
  2. Valve Replacement
    - ABX not effective with fungal and prosthetic valve endocarditis
29
Q

endocarditis care

A

-Pain assessment and activity intolerance can give insight as to the effectiveness of treatment

  1. Education – Prevention is key for those at risk
    -Those at risk must be educated on the importance of good oral hygiene and given information on prophylactic therapy.
    Patients and family should be educated on the symptoms of stroke, pulmonary embolism, and heart failure.
  2. Monitor for fever and assess for skin abnormalities and cardiac murmurs
  3. Maintain perfusion, body temperature, and increase activity tolerance
30
Q

complications of endocarditis

A
  • Myocardial erosion
  • Valvular stenosis
  • Decreased cardiac output due to heart failure
31
Q

Function of the pericardium

A
  • Pericardium is composed of 2 layers

- Anchors the heart to the mediastinum, lubricates to decrease friction, and prevents excessive stretching of the heart.

32
Q

visceral layer “epicardium”

A

-covers the heart

33
Q

parietal layer “pericardium”

A

-Sac that contains the heart

34
Q

patho of acute pericarditis

A
  • Caused by infectious process, Non-infectious injury, or hypersensitive/autoimmune response
  • inflammatory response that increases pericardial vascularity and leads to fibrin deposits on the pericardial sac
  • Acute Pericarditis may occur 48-72 hours post MI
35
Q

causes of acute pericarditis

A
  • can be caused by an infectious injury resulting from invading bacteria, fungus, or a virus.
  • can also be caused by a hypersensitivity reaction such as rheumatic fever.
  • Post MI patients are at increased risk 49-72 hours post injury.
36
Q

manifestations of acute pericarditis

A

-Progressive, sharp chest pain: increases with respiration and when laying supine.
-Pain is relieved by sitting up and leaning forward
Pain may radiate to the back or shoulder

  • Dyspnea: due to the pain with inspiration
  • Pericardial Friction Rub: It is a high pitched grating sound that is best auscultated at the lower left sternal border of the chest while the patient is leaning forward.
37
Q

complications of acute pericarditis

A
  • Pericardial Effusion

- Cardiac Tamponade

38
Q

pericardial effusion

A
  • can occur as the disease process progresses.
  • Fluid collects in the pericardium between the visceral and parietal layers. -This fluid can compress the lungs or phrenic nerve.
39
Q

cardiac tamponade

A
  • As the pericardial effusion increases in volume the fluid begins to compress the heart muscle and leads to decreased cardiac output.
  • The patient will begin to report chest pain and appear confused/anxious.
  • Becks Triad – clinical manifestations
    1. Hypotension
    2. Distended Neck Veins
    3. Muffled Heart sounds
40
Q

DX for pericarditis

A
  • ECG - Widespread ST elevations
  • Echocardiogram
  • Doppler Imaging
  • CT Scan
  • MRI
  • Chest X-ray
  • Elevated Troponin
41
Q

EKG for DX of pericarditis

A

will show widespread ST elevation indicative of pericardial inflammation.

42
Q

echo for DX of pericarditis

A

most helpful in determining the presence of pericardial effusion or cardiac tamponade.

43
Q

CT or MRI for DX of pericarditis

A

make it possible to view the pericardial space

44
Q

chest x ray for DX of pericarditis

A

helpful in the case of an enlarged heart due to pericardial effusion.

45
Q

troponin for DX of pericarditis

A

Elevated troponin levels are indicative of myocardial damage.

46
Q

TX of pericarditis

A
  • Goal = identify and treat the underlying problem
  • Antibiotics for infectious processes
  • NSAIDS for pain and inflammation
  • Corticosteroids: for inflammation
  • Pericardiocentesis
  • Pericardial Window
47
Q

Pericadriocentesis

A
  • a procedure in which a long needle is inserted into the pericardial space to remove fluid and relieve cardiac pressure.
  • This can be a lifesaving procedure and is the definitive treatment for cardiac tamponade.
48
Q

nursing care for pericarditis

A
  • Manage pain and anxiety
  • Bed rest with HOB greater than 45 degrees– provide overbed table to lean on for support
  • Education – provide simple complete explanation of pain
  • Monitor for decreased CO and cardiac tamponade (If tamponade is suspected…immediately notify the provider)