40) Inflammatory heart diseases. Cardiomyopathies. Flashcards
What are the risk factors for infective endocarditis
Congestive heart failure
Central venous catheters
Surgery
Rheumatic heart disease
Where are mostly the bacteria set to colonise in the heart for IE
If not operated for congenial malformation - SMall infection in VSD,AS, TOF, PAD
AFTER surgery for congestive heart disease
What are the pathogens for infective endocarditis?
Gram positive
Streptococcus viridans (most common
Subacute
Pre damaged native valves )
Staphylococcus aureus ( prosthetic valves - acute- fatal with 6 weeks Usually mitral)
Enterococcus
HAECK and diphtheroids
Frequently affect damaged valves
Gram negative bacilli ( neonates and immunocompromised )
Strep pneumonia
Fungal endocarditis
Others- strep pyogenes associated with erysipelas
What are the clinical features of IE
Fever Weight loss Chills Weakness Tachycardia
Congestive heart failure may develop
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Extra cardiac manifestations
Petechiae- splinter hemorrhages
Jane-way lesions - small NON tender erythematous macules on palms and some (microabcess)
Osler nodes - nodes on pads pod fingers and toes caused by immune complex deposition
Roth spots - retinal haemorrhages
Acute renal injury - due to renal artery occlusion or glomerulonephritis hematurea
Neurological - stroke due to septic emboli , or meningitis, intracranial haemorrhage
Pulmonary embolism
Physical findings of infective endocarditis
Appearance of a new murmur
Tricuspid valve regurgitation
Holosystolic murmur that is loudest at the left sternal border immunocompromised ndividuals, patients with congenital
Central venous catheters in the right heart
Aortic valve regurgitation: early diastolic murmur that is loudest at the left sternal border
Mitral valve regurgitation: holosystolic murmur that is loudest at the heart’s apex and radiates to the left axilla
Heart failure (e.g., dyspnea, lower limb edema) due to valve insufficiency
Arrhythmias: Suspect a perivalvular abscess
Diagnosis of IE
Elevated ESR AND CRP
EchoCG - vegetation’s are seen - hyperechoic
Blood culture- organism can be obtained. Atleast six blood cultures within 24 hours
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Dukes criteria
Major - positive blood culture for two separate occasions
Or echo findings of IE
Minor - predisposing conditions to IE
Fever of more than 38
Vascular abnormalities - emboli
Immunological -( glomerulonephritis, osler, Roth, rheumatoid factor)
Positive blood culture
Pathology- microprganism detected by tissue culture or biopsy
===== Definitive two major One major and three minor Five minor One pathology
What are the dd of endocarditis
Rare non infective form of endocarditis causing sterile platelet thrombus formations on heart valves -libman sack endocarditis seen in SLE or antiphospholipid syndrome
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Rheumatic fever - group a beta haemolytic strep
( anti streptolysin o titre, penicillin g)
Constitutional symptoms: fever, malaise, fatigue
Joints: migratory polyarthritis
Heart -Pancarditis (endocarditis, myocarditis, and pericarditis)
Valvular lesions:
Early mitral regurgitation or prolapse
Late mitral stenosis: Rheumatic fever is the most frequent cause of mitral stenosis.
Aortic valve (∼ 25% of cases) Aortic regurgitation Aortic stenosis (late cases)
CNS: Sydenham chorea (involuntary, irregular, nonrepetitive movements of the limbs, neck, head, and/or face)
Sometimes asymmetrical or confined to one side (hemichorea)
Additional motor symptoms muscle weakness) and speech disorders (slurred or “jerky” speech)
Neuropsychiatric symptoms (e.g., inappropriate laughing/crying, agitation, anxiety,) structures → reversible
Subcutaneous nodules
Erythema marginatum: centrifugally expanding pink or light red rash with a well-defined outer border and central clearing.
Painless and nonpruritic
Location: The trunk and limbs are affected;
Confirmation of GAS infection [10]
Used to rule out differential diagnoses
Any of the following test results can confirm recent GAS infection:
Tests showing elevated or rising antibodies
↑ Antistreptolysin O titer (ASO)
↑ Antistreptococcal DNAse B titer (ADB)
Positive throat culture
Positive rapid GAS carbohydrate antigen detection test
GAS eradication [
First-line: penicillin V
Cephalosporib
Symptomatic treatment of arthritis and fever
First-line: nonsteroidal anti-inflammatory drugs (NSAIDs)
———- ‘
Malignancy
Hypercoaguble state
What is the treatment of infective endocarditis?
Emperic therapy
naficillin / oxacillin/ flucloxacillin and gentamicin until s aureus is excluded given IV
Mrsa- vancomycin + gentamycin
Viridans strep - a gallolyticus - penicillin G -. Penicillin g + ceftriaxone - Ceftriaxone and gentamicin
Enterococcus- ampicillin or penicillin G
Plus
Gentamicin I
Haeck
First line ceftriaxo ne
Or ampicillin/ ciprofloxacin
The therapy is for four- six weeks
Blood culture should be obtained for eradication
Complications of infective endocarditis
Ruptured chordae tendinae
——-
Embolisation
Neurology
Renal
Splenic Artery occlusion or splenic abscess - may lead to splenic rupture
Supplementally
Possible LUQ
——-
Valvular damage
What is the pathogenesis of infective endocarditis
Damaged endocardial tissue , the endothelium makes thrombus which is a perfect place for bacteria and microorganism to colonise
When do myocarditis usually occur
In neonates and early infants after that it occurs spontaneously
What is the ethology of myocarditis
Infective Viral - coxsackie b1-5 Parvovirus b19 Human herpes 6 Adenovirus HCV HIV
Bacterial Group a haemolytic strep - acute rheumatic fever Corynebacterium diphtheria Borrelia burgdorferi Mycobacterium tuberculosis Mycoplasa pneumonia
Final
Candida
Aspergillus
Parasitic
Toxoplasma Gondii
Trypanosoma cruzi ( chagas)
Heminthic- trichinella
Echinococcus
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Non infectious
SLE , sarcoidosis , deratomyositis.
Vascular is syndromes - kawaski disease
Toxic myocarditis CO positioning Medications - sulfoamides Chemo- anthracycline Radiation therapy
Clinical Features Of myocarditis?
Onset may be abrupt- sudden cardiovascular collapse and death within hours
Or gradual congestive heart failure
Mottled
Weak peripheral pulse/ peripheral capillary refill is delayed
Sinus tachycardia
Dyspnea with feeding
Vomiting
Pallor
Older- decrease in stamina preceding weeks Fly like symptoms
Palpitation
Chest pain - indicates pericardial involvement
Tachypnea
What are the physical findings of myocarditis
Muffled heart sounds
Brief systolic murmur
S3 s4 gallop
If pericarditis then pericardial friction rub
Mitral insufficiency - regurgitate murmur
What is the diagnosis of myocarditis
X-ray- cardiomegaly and pulmonary venous congestion
ECG 24 hours- sinus tachycardia with low qrs voltage and low amplitude t waves
ST segment depression
T wave inversion
Ventricular extrasystole / atrial or ventricular ectopic beats, atrial tachycardia
Heart block - rbbb
Increase in cardiac enzyme - CK CK-MB trining T
Leukocytosis
BNP high
Viral serology,- viral specific antibodies
virus from stool, throat washing
Echo- diffuse hypokinesia
Reduced EF
Pericardial effusion
Dilated LA and LV
Endomyocardial biopsy - PCR
What is the treatment for myocarditis
Some spontaneously resolve
Drugs for congestive heart failure can improve patient status - however it can become chronic
Corticosteroids and immunosuppressives when autoimmune but not beneficial in myocarditis
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Rest avoid physical activity
Fluid and salt intake controlled
More severe disease- monitor drugs such as dopamine and Fontaine
Decrease in areas agent such as nitroprusside can be considered
Antibiotic therapy Of bacterial
Antifungal - fluconazole , amphotericin B
Treatment of cardiac arrythmia
Intravenous gamma globulin / corticosteroids/ azathioprin / cyclosporin
Many patients debilitate - and heart transplant may be the only solution
Dd of myocarditis
Pericarditis
Myocardial infarction
What is the complication of myocarditis
Viral myocarditis can become chronic and lead to dilative cardiomyopathy- and congestive heart failure
Heart failure and sudden cardiac death - due to ventricular tachycardia or vfib
Acute or persistent arrhythmia
Perimyocarditis
Prognosis very poor for infants
What is The ethology of pericarditis
Idiopathic- presumed to be viral coxsackie b virus
Purulent - staphylococcus or streptococcus
TB
Hemophilus
Pneumococcal
Fungal
Toxoplasmosis
More common in adolescents
——- infectious pericarditis uncommon——-
Juvenile RA OR SLE
Uremia - acute or chronic renal failure - third most
Neoplastic disease- hodgkin lymphoma - second most
Postcardiotomy syndrome - most common - after ASD secundum closure surgery
Myocardial infarction - post infraction fibrinious pericarditis
Dressler syndrome - weeks to month following AMI
Clinical features of pericarditis?
Post cardiotomy syndrome occur within 1-2 weeks after the surgery
Infants and children
Distressed
Decrease feeding
Tachycardia
Older
Retrosternal Chest pain- full, sharp, stabbing and is improved when sitting ( caused by inflammation of the parietal pleura)
Aggravated by coughing or deep inspirations
Improves when sitting and leaning forward!!
Can radiate to neck and shoulders
Low grade fever
Dyspnea
Tachypnea
Non productive cough
What are the physical findings in pericarditis?
A pericardial friction rub
Louder when the patient is sitting and leaning forward during expiration - friction between visceral and parietal pericardial tissue
If pericarditis lasts more than 3 months then what are the two different chronic forms of pericarditis that you will see?
Constrictive
Or effusive constrictive
fatigue
Constrictive Fluid overload Jaguar vein distension Peripheral Edema Pericardial knock on auscultation ( caused by sudden stop in diastolic filling in ventricles) Kussmaul sign- unlike normally upon deep inspiration The jugular veins are more distended Hepatomegaly, hepatojugular reflux Ascitis
Decrease cardiac output
Tachycardia
Pericardial knock
Pulsus pardoxus- during deep inspiration blood pressure goes down by Ten mmhg ( also occurs in asthma)
Effusive or constrictive
Large education - symptoms of cardiac tamponade-
Beck triad - hypotension muffled heart sounds and distended neck veins
More comfortable when sitting
Kuasmaul sign
Narrow pulse pressure
Peripheral pulse diminish
What is the diagnostics of pericarditis ?
To diagnose acute pericarditis:
Characteristic chest pain
Pericardial friction rub
Typical ECG changes (see below)
New or worsening pericardial effusion.
X Ray- can be enlarged if effusive
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Stage 1: diffuse ST elevations, ST depression in aVR and V1, PR segment depression
Stage 2: ST segment normalizes in ∼ 1 week.
Stage 3: inverted T waves
Stage 4: ECG returns to normal baseline (as prior to onset of pericarditis) after weeks to months.
In acute MI it is not diffuse
Echo- pericardial effusion
Left ventricular diastolic diameter may be reduced
Cardiac MRI - thickened pericardium and pericardial enhancement
CBC
Increase in leukocytosis
Increase in troponin1 and CK
ESR
CRP
Pericardiocentesis with pericardial fluid analysis
Blood culture
BUN creatinine
Ana and rheumatic factors for autoimmune r
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Constrictive pericarditis
Ec
Increase thickness
Sudden halt during early diastole
Variation in ventricular filling with inspiration : across tricuspid valves velocity of blood flow decreases
Mitral valves - velocity of blood flow decreases
What is the treatment of pericarditis
Often self limited
NSAID therapy - aspirin, ibuprofen
Consider colchine in combo NSAIDS. Consider also gastro protective therapy
Limit the activity
Severe cases of pericarditis caused by items and connective tissue diseases - prednisone
Dialysis / rasbuticase in the case of uremia
Pericardiectomy - purulent pericarditis in the hopes of avoiding restrictive pericarditis
DIGOXIN AND DIURETICS ARE CONTRAINDICATED BECAUSE THE SLE THE HEART RATE
What is the treatment of there is cardiac tamponade
Constrictive or effusive constrictive
Pericardiocentesis
Recent tamponade- thoracotomy with pericardial window
Pericardiectomy
