Traumatic, Infectious and Inflammatory Heart Conditions

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Last updated 2:18 PM on 4/30/26
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58 Terms

1
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What is the fundamental pathophysiology of Infective Endocarditis (IE)?

An abnormal heart valve or endothelial injury leads to platelet/fibrin deposition, which, when combined with transient bacteremia, results in vegetation formation.

2
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What are the three components of an IE vegetation?

Platelets, fibrin, and bacteria.

3
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What is the stepwise progression of IE?

Abnormal valve or endothelium -> Endothelial injury -> Platelet/fibrin deposition -> Transient bacteremia -> Bacterial adherence -> Vegetation

4
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Which organism is most commonly associated with prosthetic valve endocarditis?

Staphylococcus epidermidis.

5
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What are 2 very common causes of acute IE?

Staph. aureus (MOST common) and IV drug use.

6
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What are 2 very common causes of subacute IE?

Viridans streptococci and dental source.

7
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What is the primary difference in clinical onset between acute and subacute IE?

Acute IE has an explosive onset with high fever and rapid progression, whereas subacute IE is slower and more indolent.

8
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What is a key cardiac presentation of IE?

New or changing murmur.

9
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What are Janeway lesions and what do they indicate?

Small, painless, red-to-bluish-red flat or nodular spots on the palms and soles; they are a sign of acute bacterial endocarditis.

10
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What are Osler nodes?

Tender, raised, purple-pink nodules, often with a pale center, appearing on the fingertips or toes as an immunologic sign of IE.

11
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What are the requirements to meet the Duke Criteria for a diagnosis of IE?

Either 2 major criteria, 1 major + 3 minor criteria, or 5 minor criteria.

12
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What constitutes the 'major criteria' for IE regarding blood cultures?

Typical microorganisms from two separate blood cultures, or microorganisms consistent with IE from persistently positive cultures.

13
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What constitutes the 'major criteria' for IE regarding endocardial involvement?

An echocardiogram positive for endocarditis or the presence of new valvular regurgitation.

14
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List three examples of minor criteria for the Duke classification of IE.

Predisposing cardiac condition/IV drug use, fever >38.0°C, and vascular phenomena (e.g., septic emboli, Janeway lesions).

15
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What are the complications of IE?

Valve destruction, heart failure, septic emboli, abscess formation, death. IE creates or worsens regurgitant lesions.

16
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What is the recommended initial step in the management of suspected IE?

Obtain blood cultures before starting any antibiotics.

17
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What are the three primary indications for surgical intervention in IE?

Heart failure, persistent infection, and large vegetations associated with embolic events.

18
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Which patient populations require antibiotic prophylaxis before dental procedures?

Patients with prosthetic valves, prior history of IE, or certain congenital heart diseases.

19
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Does the presence of a routine heart murmur qualify a patient for IE prophylaxis?

No, routine murmurs do not require prophylaxis.

20
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What are the major systemic complications of IE?

Valve destruction leading to acute regurgitation, heart failure, septic emboli (brain/lungs), abscess formation, and death.

21
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What is the classic triad of symptoms often associated with IE?

Fever, new or changing heart murmur, and embolic/vascular phenomena.

22
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Why is Staphylococcus aureus a common cause of acute IE?

It is highly virulent and capable of causing rapid, destructive infection even on previously normal valves.

23
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What is the significance of a new holosystolic murmur in a patient with fever and history of mitral regurgitation?

It raises high suspicion for infective endocarditis causing valve destruction or worsening regurgitation.

24
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What is the role of echocardiography in the diagnosis of IE?

It is used to identify vegetations and assess for endocardial involvement, serving as a major criterion for diagnosis.

25
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What immunologic phenomena are associated with IE?

Glomerulonephritis, Osler nodes, Roth spots, and positive rheumatoid factor.

26
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What vascular phenomena are associated with IE?

Septic emboli, intracranial hemorrhage, conjunctival hemorrhage, and Janeway lesions.

27
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Which organism is commonly associated with dental sources of IE?

Viridans streptococci.

28
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What is the typical empiric antibiotic strategy for IE?

Broad-spectrum IV antibiotics, such as a vancomycin-based regimen, started after blood cultures are drawn.

29
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Why is it critical to consult both cardiology and infectious disease for IE?

To manage the complex interplay of cardiac structural damage and the need for targeted, prolonged antimicrobial therapy.

30
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What is the fundamental pathophysiology of myocarditis?

Inflammation of the heart muscle leads to impaired contraction and electrical instability.

31
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What is the most common etiology of myocarditis?

Viral infection.

32
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What is the clinical 'rule of thumb' for identifying potential myocarditis in a young patient?

A young patient presenting with a viral prodrome should be considered to have myocarditis until proven otherwise.

33
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What is the pathophysiology of myocarditis?

Viral entry into myocytes -> Immune activation -> Myocyte injury and necrosis -> Decreased contractility and arrhythmias

34
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What phenotype does severe myocarditis often result in?

Dilated cardiomyopathy.

35
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What is the classic triad of myocarditis?

Chest pain, heart failure symptoms and arrhythmias.

36
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What are the common clinical findings in myocarditis?

Dyspnea, tachycardia out of proportion and +/- recent viral illness.

37
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What labs results are seen with myocarditis?

Elevated troponins (due to myocyte injury) and elevated BNP (if HF is present)

38
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Which imaging modality is considered the best noninvasive test for myocarditis?

Cardiac MRI.

39
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What is the primary management approach for myocarditis?

Supportive care, including oxygen, fluids, and guideline-directed heart failure therapy if the ejection fraction is reduced.

40
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What activity restriction is recommended for patients with myocarditis?

Avoidance of intense physical activity.

41
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What are the major complications of myocarditis?

Dilated cardiomyopathy, malignant arrhythmias, cardiogenic shock, and sudden cardiac death.

42
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What is the definition of pericarditis?

Inflammation of the pericardial sac.

43
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What is the most common etiology of pericarditis?

Viral (idiopathic) especially Cocksackie B virus.

44
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What are the timeframes after an MI in which pericarditis can occur?

Fibrinous (1-3 days) or Dressler syndrome (+14 days!!)

45
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What is the classic triad of symptoms for pericarditis?

Chest pain (sharp, pleuritic, worse with inspiration and lying flat, better with leaning forward), fever, and a pericardial friction rub.

46
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What physical exam finding is pathognomonic for pericarditis?

A scratchy, 'sandpaper' pericardial friction rub, best heard while the patient is leaning forward.

47
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What are the characteristic EKG findings in pericarditis?

Diffuse ST-segment elevation and PR-segment depression.

48
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How many of the four diagnostic criteria are required to diagnose pericarditis?

At least 2 of 4 (typical chest pain, pericardial rub, EKG changes, or new/worsening pericardial effusion).

49
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What EKG changes are seen with pericarditis?

Diffuse ST elevation and PR depression.

50
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What is the first-line pharmacological treatment for uncomplicated pericarditis?

NSAIDs.

51
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Which medication is added to NSAIDs in pericarditis to reduce the risk of recurrence?

Colchicine.

52
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What is cardiac tamponade?

External compression of the heart by fluid in the pericardial space that prevents normal filling during diastole.

53
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Why does the right heart typically fail first in cardiac tamponade?

The right heart has lower pressures, making it easier to compress than the left heart.

54
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What is Beck's Triad for cardiac tamponade?

Hypotension, Jugular Venous Distention (JVD), and muffled heart sounds.

55
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What is pulsus paradoxus?

A drop in systolic blood pressure of greater than 10 mmHg during inspiration, often seen in cardiac tamponade.

56
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What is the emergency treatment for cardiac tamponade?

Emergency pericardiocentesis.

57
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How does the chest pain of pericarditis differ from that of ACS?

Pericarditis pain is sharp and pleuritic, and it improves when leaning forward; ACS pain is typically pressure-like and exertional.

58
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When should a patient with suspected pericarditis be referred to the hospital?

If they show signs of hemodynamic instability, elevated troponin, or an abnormal echocardiogram.