Endo/myocarditis And Sepsis

Front 1

In infective endocarditis, what parts of heart are involved?

Back 1

1. Valves
2. Mural (heart wall) endothelium
3. Vascular endothelium
4. Intracardiac devices - wires, catheters, ventricular assist devices etc

Front 2

What is acute endocarditis?

Back 2

Fulminant (acutely) course w/systemic toxicity and high mortality

Normal valves
Prosthetic valves
Hospital acquired
IV drug abusers = staph aureus

Front 3

Organisms mostly involved with acute endocarditis -

Back 3

Staph aureus
Strep pyogenes
Strep pneumoniae
Neisseria gonorrhea

Front 4

Subacute endocarditis -

Back 4

Develops slowly over longer time (weeks)
Prior valvular disease (MVP, congenital valvular dz, or rheumatic valve dz)

Front 5

Organisms mostly involved with subacute endocarditis -

Back 5

Strep viridans
Strep bovis
Enterococci

Front 6

Si/Sx of subacute endocarditis -

Back 6

Very vague and nonspecific
Low fever
Night sweats
malaise

Front 7

Si/Sx of acute endocarditis -

Back 7

Very high fever
Toxic
High mortality

Front 8

Classification of acute/subacute endocarditis -

Back 8

classifying by organisms is not absolute and has implications for likelihood of preexisting dz, course of dz and treatment

Front 9

Epidemiology of Infective endocarditis -

Back 9

M>F 2:1 except under age 35
Age >50
> 65 almost have 4.6x the risk

Front 10

Valves involved in infective endocarditis -

Back 10

MV/AV > Mitral and aortic > congenital > tricuspid (IV users)

Front 11

Predisposing factors to infective endocarditis -

Back 11

Valvular disease
Potential bacteremia:
Catheters, CV devices, Dental work, bowel injury, GI bleed

Trauma/ skin lesions
IV drug abuse

Front 12

Pathogenesis of Endocarditis -

Back 12

Turbulent blood flow/endothelial damage
Increased platelet agg/fibrin dep. -> Non-bacterial thrombolytic endocarditis
Bacteremia insult by trauma -> adhere to NBTE -> grow under the protection of vegetation

Double diff in treating with Abs as decreased blood flow to the valves and also protection from vegetation

Front 13

Symptoms of infective endocarditis -

Back 13

Remittent fever - does not return to nL
Constitutional sx - anorexia, wt loss, fatigue, myalgias, neuralgias
Malaise N/V

Backpain - typically with s. aureus

Front 14

Physical findings for infective endocarditis -

Back 14

Heart murmur - old or new
Clubbing
Splinter hemorrhages, petechiae, peripheral emboli
Roth spots
Olser's nodes (Arterial proliferation on finger/toe pads)
Janeway lesions (non tender) - subQ painless plaques palms and soles

Roth spots in eyes (Retinal hemorrhages)

Splenomegaly
Lymphadenopathy

Front 15

Lab tests for infective endocarditis -

Back 15

Blood culture - MOST IMP
Anemia
Elevated rheumatoid factor
Elevated Sed rate
Positive VDRL
Thrombocytopenia
Hematuria/Proteinuria (from RF)

TTE
TEE - neither are a screening tool

Front 16

Treatment of infective endocarditis -

Back 16

Eradication of infection takes weeks - because of impaired host defenses, high density of organisms, and slow metabolic rate of organisms

IV Bactericidal Abx for sustained activity - synergistic combinations when appropriate

Surgical interventions in acute IE

Front 17

Prevention of Infective endocarditis -

Back 17

Recognition of cardiac disorders of high risks - prosthetic valves, previous IE, certain congenital heart disease, cardiac transplantation

Recognition of procedures with significant risk of bacteremia (dental procedures)

Prophylactic Abx

Front 18

Diff. diagnosis of Infective endocarditis -

Back 18

SLE (Lupus): Libman Sacks endocarditis
Malignancy associated: Thrombotic Non-bacterial Endocarditis (Marantic endocarditis)
Thrombotic Thrombocytopenic Purpura
Vasculitis
Atrial Myxoma
Acute Rheumatic Fever


All have systemic symptoms and multisystemic presentations

Front 19

Addict Endocarditis -

Back 19

2/3rd - no underlying heart dz
R sided in 50% -> tricuspid vavle

S. aureus, P. auerginosa, candida and polymicrobial infections are more common

Response to Rx better than non-addicts

Front 20

Prosthetic valve endocarditis -

Back 20

Early onset: intraoperative contamination or postop infection
Coag neg staph, S. aureus, gm. neg, candida -> high mortality and very ill

Late onset - source similar to native valve endocarditis
Strep, s. aureus, coag neg staph
Need for surgery

Front 21

Most cases of hospital onset bacteremia do/don't lead to endocarditis -

Back 21

don't

IV catheters, pacemakers, dialysis, fistulas, burns.

Mostly by S. aureus

Front 22

What is myocarditis?

Back 22

Inflammatory disorder of myocardium with necrosis of myocytes and assoc inflammatory infiltrate

Front 23

Dx of myocarditis -

Back 23

Requires high degree of suspicion

Sometimes - NO Sx at all!!!

Front 24

What are some of the symptoms assoc with myocarditis?

Back 24

Previous flu like sx - malaise, fever, arthralgia, URI's
New onset OR unexplained Arrhythmia -> lead to sudden cardiac death
Unexplained tachycardia (higher than permitted by fever)
HF - especially in young person
Murmur
Pericarditis (rubbing friction sound)
EKG Changes - can't mistake for MI
Elevated cardiac enzymes
Abnormal echo

Front 25

Major causes of myocarditis in US and Europe -

Back 25

Coxsackie B and Adenovirus by binding to common CAR (Coxsackie-Adenovirus receptor) on myocyte's surface

Front 26

Myocarditis by MMR, polio, HSV, HVZ, influenza?

Back 26

It has gone down over last couple years because of widespread immunization effort

Front 27

Pathophysiology of myocarditis -

Back 27

Likely immune mediated
virus enters myocytes -> body attacks myocytes -> inflammation (poor contraction/conduction = HF)

Front 28

EARLY Histology of Myocarditis -

Back 28

scattered hypereosinophilic myofibers, widesprad edema and only a few inflammatory cells

Front 29

LATE histology of myocarditis -

Back 29

No striation, nuclear degeneration

Fragmented myofibers, inflamm cell infiltration

Acute myocarditis may resolve completely or progress into chronic myocarditis

Front 30

End stage histological manifestations of myocarditis?

Back 30

Interstitial fibrosis, and loss of myofibers

Front 31

Treatment of myocarditis -

Back 31

Aimed against specific agents if known (ganciclovir for CMV)

BED REST ( as exercise increases mortality)
Adequate oxygenation
Avoid fluid overload (to prevent dilated cardiomyopathy)
Monitor for any potential arrhythmias

Captopril or Amlodipine could be given

Front 32

What drugs should def not be used in tx of myocarditis and why?

Back 32

NSAIDs as they increase viral replication and mortality

Steroids - rapid clinical deterioration

Front 33

Prognosis of myocarditis -

Back 33

Most recover completely

Some go in to acute fulminant myocarditis while other into chronic myocarditis

Front 34

What does chronic myocarditis manifest as later on?

Back 34

Dilated cardiomyopathy -> ultimately requiring heart transplant

Front 35

Diff in how coxsackie attacks myocytes as opposed to VZ, CMV and hep b/c?

Back 35

Coxsackie -> infects myocytes themselves

others -> injur vascular endo cell

Front 36

What auto ab is associated with worst prognosis of chronic myocarditis?

Back 36

Auto anti myosin antibody which leads to DCM

Front 37

When should one use Ventriculography in diagnosing myocarditis?

Back 37

Only when TTE and TEE are suboptimum or N/A

Front 38

No more myocarditis from trichinelliosis?

Back 38

because of strict meat inspection

Front 39

What type of viruses are coxsackie b and adeno virus?

Back 39

Coxsackie B -> PicoRNA virus - ss linear RNA

Adeno -> ds DNA virus

Front 40

How does amlodipine help in tx of myocarditis?

Back 40

by reducing myocardial injury and decreasing mortality

Front 41

Definitive diagnosis of Myocarditis can be made by -

Back 41

Biopsy -> safest to get through transvenous endomyocardial biopsy

Front 42

Define bacteremia -

Back 42

presence of viable bacteria in blood stream. Positive blood culture is diagnostic

Front 43

What is SIRS?

Back 43

Systemic Inflammatory Response Syndrome

inflammatory response to variety of insults, not only infections - pancreatitis, ischemia, burns, blood loss, leukemia

Front 44

Criteria for the SIRS -

Back 44

2 or more of the following -

Temp > 101 or < 97
HR > 90bpm
RR > 20/min
WBC > 12,000 or <4000 or > 10% bands

Front 45

What is sepsis?

Back 45

SIRS presentation due to infection.
May occur without bacteremia

Front 46

Organisms that cause sepsis -

Back 46

Mostly G- rod (LPS endotoxin)

Also G+, fungi, viruses can cause sepsis as well.

Front 47

Sources of infections in sepsis -

Back 47

UT
Lungs
Abdomen
IV devices
Abscess, GI infections

Front 48

Predisposing factors to sepsis -

Back 48

Age
Underlying disease (diabetes for eg)
Indwelling catheters, or IVs
Surgeries

Front 49

Severe sepsis -

Back 49

sepsis w/organ dysfunction or perfusional abnormalities and/or hypotension

Front 50

Septic shock -

Back 50

sepsis with persistent hypotension despite adequate resuscitation - 40 to 70% mortality)

Front 51

What is MODS?

Back 51

Multiple organ dysfunction syndrome - presence of altered organ function in an acutely ill person such that hemostasis cannot be maintained without intervention

Front 52

4 types of shocks -

Back 52

Cardiogenic
Extracardiac obstructive
Hypovolemic
Distributive

Front 53

What is cardiogenic shock?

Back 53

pump failure = decreased cardiac output

Front 54

What is extracardiac obstructive shock?

Back 54

PE, pericarditis = normal pump but unable to perform b/c of limitations around the heart

Front 55

What is hypovolemic shock?

Back 55

hemorrhage, fluid depletion = decreased perfusion of organs (can be corrected with fluid replacement)

Front 56

What is DISTRIBUTIVE shock?

Back 56

blood vessel dilation and ‘leaking’ causes relative hypovolemia (SEPSIS) = hypovolemia as above

Front 57

Pathophysiology of shock -

Back 57

Endotoxin LPS (lipid A) binds proteins in the serum -> form a complex -> which bind to CD14 receptor on monocytes and macros -> initiates release of TNF alpha -> promotes cytokine and self production

Front 58

What cytokines are produced by TNF alpha initiation?

Back 58

IL 1, 6, PAF, and IFN gamma

Front 59

Effects of cytokines on body during shock -

Back 59

act on hypothalamus to produce fever, tachycardia and tachypnea

activation of neutrophils -> free radicals leading to leaky endothelium and more loss of fluids

Also could lead to DIC

Front 60

effect of NO during shock -

Back 60

Vasodilation -> low BP and CO

Front 61

Regulatory step in prodn of NO -

Back 61

NO synthetase levels

Front 62

Types of NOS -

Back 62

2 types

1st -> calcium dependent, constitutive, non inducible enzme responsible for normal regulation of blood pressure

2nd -> inducible NOS -> increased prodn of NO -> vasodilation and hypotension
Cytokines able to induce this form of NOS

Front 63

Effect of chemical inhibitors on NOS?

Back 63

Leads to increase in BP in pts with septic shock

NO change in mortality

Front 64

Complications of Shock -

Back 64

(ARF) Acute Renal Failure (due to ↓ perfusion) but function usually recovers

(DIC) Disseminated Intravascular Coagulation (clotting factors are used up and pt bleeds)

(ARDS) Acute Respiratory
Distress Syndrome (stiff lungs b/c of edema & pulm HTN)
→ most important cause of late death from septic shock

Hepatic Dysfunction (↑ LFT’s) - hyperbilirubinemia

Front 65

Non reversal of vasodilation and increased permeability during shock leads to ->

Back 65

Cellular hypoxia -> lactic acidosis -> death

Front 66

Tx of Sepsis

Back 66

Abx (broad spec)
Fluids
Vasopressors to decrease vasodilation
Tx complications -> dialysis, mechanical vent, surgery
Pulmonary catheters help in managing volume & lung prob

Front 67

Potential new therapies for sepsis in clinical trials -

Back 67

Anti TNF alpha MAb
Anti IL 1 MAB
Anti PAF MAB