Carditis (Cardio 1) Flashcards
Pericarditis
- inflammation of the pericardial sac
- most common disorder involving pericardium
- 0.1% of hospitalized pts and 5% of pts in ED w/ non ischemic chest px
- may be first sign of underlying systemic dz
Major Causes of Pericardial Dz
- 85% idiopathic
- infectious: prodrome of flu-like illness (cocksackie, echovirus, CMV, herpes, HIV, staph, strep, pneumococcus)
- radiation
- neoplasm
- trauma
- metabolic: hypothyroid, uremia
- cardiac: Dressler’s syndrome, myocarditis, dissecting AA
- autoimmune
- drugs: phenytoin, procainamide, INH, penicillins
Uremic Pericarditis
- occurs in 6-10% of advanced renal failure pts not yet on dialysis
- 13% of dialysis pts due to no/inadequate dialysis
- EKG dos NOT usually show the typical diffuse STE
Major Clinical Features of Pericarditis
- chest pain: 95%+, sudden onset, sharp, pleuritic, improved by sitting up/leaning forward
- pericardial friction rub: 35-85%, scratchy/squeaky sound heard with diaphragm over LSB when pt holds breath and leans forward
- EKG changes: 60%, widespread STE or PR depression
- pericardial effusion: 60%; inflammatory cells and serum accumulate in pericardial space
Pericarditis on EKG
- EKG changes signify inflammation of epicardium
- some causes of pericarditis don’t result in inflammation of epicardium so may not change EKG at all
- 4 stages of EKG progression: highly variable, tx can alter the stages
Pericarditis Stage 1 EKG Changes
-first hours to days
Pericarditis Stage 2 EKG Changes
- 1-3 weeks
- normalization of ST and PR segments
Pericarditis Stage 3 EKG Changes
- 3 to several weeks
- diffuse TWI, not seen in some pts
Pericarditis Stage 4 EKG Changes
- several weeks onward
- normalization of EKG or indefinite persistence of TWI
Lab Evaluation - Pericarditis
- CBC, inflammatory markers, troponin
- can see general serum markers of inflammation (eg leukocytosis) but does not make a dx
- CXR: typically normal; cardiomegaly not a common finding
- echocardio: often normal
Causes of Pericarditis
- specific etiology in only 17% patients
- most cases in immunocompetent pts are idiopathic or viral
- course associated with common pericarditis causes is benign
Tx of Pericarditis
- viral: ibuprofen, colchicine
- post-MI: ASA, colchicine
- refractory or CIs to NSAIDs or ASA: prednisone, colchicine
Beck’s Triad of Cardiac Tamponade (3 Ds)
- decreased BP
- distended neck veins
- distant or muffled heart sounds
Symptoms of Cardiac Tamponade
- dyspnea
- tachypnea
- tachycardia
- elevated JVD
- hypotension
- pulsus paradoxicus
- electrical alternans
Pulsus Paradoxicus in Cardiac Tamponade
- drop in systolic BP during inspiration; weaker peripheral pulses during inspiration
- R side of heart expands, but no room for L heart to expand outward –> exaggerated septal shift = severe drop in stroke volume
Electrical Alternans in Cardiac Tamponade
- consecutive, normally conducted QRS complexes alternate in height
- heart is essentially wobbling back and forth in pericardial sack
Tamponade Tx
- pericardial drainage: catheter placed to drain effusion
- pericardiotomy/pericardial window: surgical removal of all or part of pericardium (rare!)
Myocarditis
inflammation of heart muscle
Infectious Causes of Myocarditis
- viral: parvo B19, HHV 6, cocksackie, adeno, CMV, EBV, HCV
- bacterial: staph, strep, TB
- spirochetes, mycotic, rickettsial, protozoal, heminthal
- developed countries = viral
- undeveloped = rheumatic fever, chagas dz, advanced HIV
Non-Infectious Causes of Myocarditis
- cardiotoxins: EtOH, CO, cocaine, catecholamines, heavy metals
- hypersensitivity rxns: abx, clozapine, diuretics, lithium
- systemic disorders: celiac, CVD, Wegener’s, SLE, HE, IBD, Kawasakie dz, sarcoid
- radiation
Clinical Presentation of Myocarditis
- highly variable; many cases can go undetected
- usually 20-50 yo
- some pts have viral prodrome or rash
- myocardial inflammation may be focal or diffuse
- fatigue
- chest px, heart failure
- cardiogenic shock
- arrhythmias (tachy or brady)
- sudden death
Myocarditis Virus-Immune Hypothesis
- for acute viral myocarditis, pts NOT predisposed to autoimmunity develop self-limited dz and recover fully
- genetic predisposition to autoimmunity may initiate a chronic autoimmune myocarditis leading to DCM
Myocarditis Physical Exam
- signs of fluid overload, CHF
- occas S3 and S4 heard
- new murmurs
- friction rub
Myocarditis Lab Evaluation
-EKG, troponin, NT-pro-BNP, CXR
Echocardiogram for Myocarditis
- key method of detecting impaired ventricular function
- may have focal or global wall motion abnormalities, LV dilation, MR or TR
Diagnosing Myocarditis
-gold standard is endomyocardial biopsy, but most pts can be diagnosed based on clinical presentation and non-invasive diagnostic findings
Dallas Criteria for Endomyocardial Biopsy
-inflammatory infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of ischemic damage
Tx of Myocarditis
- treat underlying cause if able: antiviral therapy, immunosuppressive therapy, IVIG
- NO NSAIDs (they can enhance myocarditis and increase mortality)
- restrict activity
- treat for HF if cardiomyopathy has developed
Myocarditis in Kids
- 1:100,000 children, bimodal but avg age 9 yo
- more acute presentation than adults
- viral: recent URI or GI illness, prodrome of fever/myalgia/malaise
- usually more acute and fulminant, usually present with signs of heart failure
- viral titers often drawn
- EMB and cardiac MRI commonly used
Myocarditis F/U
- many require hospitalization
- post-discharge, routine F/U every 1-3 months
- echocardiogram at 1 and 6 mos then annually
Endocarditis
- inflammation of the inner layer of the heart
- can involve septum, chordae tendinae, mural endocardium
- characterized by vegatation: mass of platelets, fibrin, microorganisms, inflamm cells
- 10000 to 15000 new US cases annually
- incidence varies
- survival rate 80% (1/6 doesn’t survive to discharge)
Endocarditis Pathogenesis (3 steps)
- formation of small, noninfected thrombus on abnormal endothelial surface
- 2ary infection with bacteria circulating in bloodstream
- proliferation of bacteria result in formation of vegetations on endothelial surface
Endocarditis Risk Factors
- over age 60: more than 1/2 cases occur in pts >60
- males more common 3:2
- IV drug use
- dental infection
Conditions Associated with Endocarditis
- 75% structural heart dz: valvular dz, congenital heart dz, prosthetic heart valve
- hx of infective endocarditis
- presence of intravascular device (PICC, central line)
- chronic hemodialysis
- HIV infection
Microbiology of Endocarditis
- strep viridans (65%)
- staph (20%)
- enterococcus (10%)
- gram negative bacteria (HACEK, 5%)
- fungus: in immunocompromised pts
- culture negative endocard (8%)
Endocarditis Physical Exam Findings
- new murmur
- new heart failure
- skin findings: petechiae, splinter hemorrhages, Janeway lesions (macular, red non-tender on soles and palms), Osler’s nodes (painful, violaceous nodules fingers and toes), Roth spots: exudative hemorrhagic lesion of retina
Endocarditis Lab and Imaging Work Up
- blood culture prior to giving abx (90% positive)
- CBC, basic metabolic panel
- inflammatory markers
- EKG and CXR
- echocardiogram
Echo in Infectious Endocarditis
- perform as soon as possible in moderate to high suspicion pts
- allows detection and characterization of vegetation on valves or other sites, evaluates valve function, can detect abscesses
- detection of vegetation = positive test, but absence does not rule out endocarditis
Culture Negative Endocarditis
- <10% of pts w/ endocard
- cardiac vegetation in the absence of positive blood cultures in pt w/ persistent fever and other infectious signs
- perhaps from previous abx therapy, inadequate microbio techniques
Treatment of Native-Valve Infectious Endocarditis
- bactericidal therapy
- empiric therapy after blood cultures drawn should cover staph, strep, enterococci
- duration generally 4-6 wks IV
- follow up blood cultures to ensure effective therapy
Tx of Strep Infectious Endocarditis
- strep viridans and bovis account for 40-65% of native valve IE
- most are highly penicillin sensitive
- 4 weeks
Tx of Staph Infectious Endocarditis
- MSSA: nafcillin, cefazolin or vancomycin
- MRSA: vancomycin
- 6 weeks
Tx of Enterococci Infectious Endocarditis
- narrower spectrum of susceptibility than strep species
- can be resistant to pens cephs
- if susceptible, gentamicin plus one of the following penG/ampicillin/vancomycin
- 4-6 wks
Tx of HACEK Infectious Endocarditis
- gram negative bacilli
- 5-10% of all IE cases
- ceftriaxone or ampicillin or ciprofloxacin
- 4 wks
Tx of Culture Negative Infectious Endocarditis
- cover both gram + and - organisms
- amp/sulb + gentamicin
- PCN allergy: vanco + genta + cipro
Antimicrobial Prophylaxis for Bacterial Endocarditis
- standard in most developed countries
- no human study has shown that prophylaxis has prevented endocarditis after an invasive procedure
High Risk Conditions to Prophylax for Endocarditis
- prosthetic heart valve
- prior history of infectious endocard
- cardiac valvulopathy in transplanted heart
- congenital heart defects
Rheumatic Heart Dz
- most severe sequelae of acute rheumatic fever
- usually 10-20 yrs after original illness
- most common cause of acquired valve disease
- mitral stenosis is a classic finding
- no routine abx prophylaxis for RHD unless hx of valve repair
Carditis in Acute Rheumatic Fever
- antimicrobial therapy doesn’t alter course or severity of cardiac complications
- salicylates 4-6 wks then taper
- steroids reserved for severe carditis
