Diseases of the peri/myocardium Flashcards
Discuss clinical signs of pericarditis
Discuss clinical criteria for pericarditis (two or more of the following)
1) chest pain - typically sharp and pleuritic improved by sitting up and leaning forward
2) ECG changes new widespread ST eleavtion and PR depression
3) Pericardial friction rub
4) pericardial effusion
History
Chest pain – sharp in nature, pleurtic relieved sitting up worse on lying supine, deep breathing or swallowing, Retrosternal pain radiating through to the trapezius
Signs
Pericardial rub
ECG changes
Discuss Aetiology of pericarditis
INfection
- vrial (coxsackie, echovirus, adenovirus, EBV, CMV, varicella)
- bacterail (TB, staph, strep, haemophilus, chlamydia, legionella, salmonella, mycoplasm)
- fungal (histoplasma, aspergillus, coccidiodes, candida)
- parasite
- rickettsia
Post injury
- penetrating
- blunt
- surgery
- MI
- Radiation
- Medications
Systemic disease
- uremia
- metastatic cancer
- rheumatoid arthritis
- SLE
- sarcoidosis
- scleroderma
- dermatomyositis
- amyloidosis
Primary tumours
aortic dissection
Cardiac
- Early and late (dresslers) post MI syndrome
- myocarditis
Discuss IX for pericarditis
ECG
- first stage occurs in the hours to days of illness and includes diffuse ST elevation and reciprical ST depression
- PR depression and reciprical PR elevation
- Next stage ST segment and PR changes resolves and deep symmetrical t-wave appear
- Resolution is the last stage however t-waves can persist
ECG vs STEMI
- nil particular distribution
- Concave rather then convex
- nil q-wave
- not progressive
- simultaneous t-wave inversion are not seen
ECHO - normal does not exclude pericarditis
- pericardial effusion
- thickened pericardium
- tamponade
- cysts
- tumours
- absence of pericardium
BLoods
- TNI –> myocarditis
- WBC
- ESR
Discuss MX and disposition percarditis
NSAIDS – if chosen NSAID is not useful in the 1st week a second calls should be used – ibuprofen has best symptom profile – 600-800 mg TDS
Colchicine – treatment of choice for recurrence
-recurrent pericarditis is often due to an immune or rheumatoological etiology - 0.5-0.6mg BD >70 or OD<70kg
Most HD stable patient can be managed as in OPD setting unless significant pericardial effusion or diagnostic uncertainty. Features of acute pericarditis associated with higher risk who may need hospitalisation include
- fever >38
- Subacute course
- evidence of tamponade
- large pericardial effusion
- immunosuppression
- history of therapy with warfarin or NOAC
- active trauma
- failure to improve following 7 days of NSAIDs and colchicine
- elevated TNI
Discuss uremic pericardial disease
Seen in patient with CKD on HD – can occur with PD but less common –is associated with occult infection and should prompt investigation for the same
Clinical features are typical – ECG however is usually NAD as litte epicardial inflammation occurs.
CXR showing cardiac enlargement wihtout signs of overload or CCF should prompt thoughts of uremic pericarditis
US definitive
Uremic pericarditis treatment is with intensive dialysis- NSAIDS are ineffective and often contrindicated. Systemic steroids can be used for those few who do not respond to dialysis
Discuss post MI pericarditis
Aproximately 20% of patients with transmural MI experience a different quality of chest pain 2-4 days after infarct. There is often fever and a transietn pericardial friction rub.
Early post mi pericarditis is often short lived and treated with aspirin ECG changes are masked by the MI
In contrast to early post MI pericarditis dressler reported a syndroe of fever pleurtisis, leukocytosis, friction rub and CXR evidence of new pericardail or pleural effusion. Frequent relapses are associated with this. May be immunological aetiology.
Treated with NSAIDs
Anticoagulants should be discontinued to reduce the risk of haemorrhage
Discuss Post injury pericarditis
Defined as pericardits after MI cardiac surgery or trauma. Incidence ranges from 5-30% after thoracic surgery or trauma. Can aslo occur in chest truama that does not involve the heart of the pericadium.
Symptoms are reasonably classical.
Interval between onset of pericarditis ranges from 4-12 days post injury,
During hospitalisation purulent pericarditis should be considered as a possible source of febrile illness in a trauma patient with multisystem organ failure
Discuss Neoplastic pericardial disease
Malignant pericardail tumors typically manifest late. Malignant involvement of the pericardium is observed in up to 31% of cancer autopsies
Most common associated cancers are
1) lung (30%)
2) breast 23%
3) lymphoma 17%
4) leukaemia
Prinary cardiac neoplasms initially cause symptoms consistent with pericarditis
Malignant pericardial disease is difficult to diagnosises with asymptomatic patient or nonspecific symptoms such as SOB cough palpitaiton and illdefined chest pain
CT, MRI and US are diagnsotic
Pericardail fluid cytology is recommended if the underlying malignancy is undiagnosedn
Treatmnet may include
pericardiocentesis, local instillation of sclerosing or chemotherapeutic agemt systemic chemo, caridac radiation and pericardial window
Discuss pericardial disease and connective tissue disorders
Occurs in approximatly 1/3 of patient with rehumatoid arthirits, usually within 3 years of diagnosis but is rarely clinically significant. These patient can develop effusions, constrictive pericarditis
Discuss cardiac tamponade
Ten percent of all patient with cancer develop caridac tamponande.
tamponade is the result of compression of the myocardium by the contents of the pericardium. Usually is caused by fluid but can be cuased by blood, pus or air.
Cardiac tamponade occurs in a physiological continuum reflecting the amount of fluid, the rate of accumulation and the natuer of the heart. THe most important factor in the development of tamponade is the rate of fluid accumulation.
There are three factors involved in the development of cardiac tamponade
1) fluid filling the recesses of the parietal pericardium
2) accumulation of fluid faster than the parietal pericardiumis able ot stretch
3) fluid accumulation that exceeds the bodies ability to increase blood volume to support right ventricle filling pressures
The result is increased pericardial pressure whcih decrases ventircle compliance and decreases flow of blood into the heart. THe heart increases rate to compensate for poor SV until late in clinical course
Discuss clinical features and diagnositic testing of tamponande
Symptoms are often non specifc and include chest pain, cough or dyspnoea any of which may be progressive or severe
Becks triad - muffled heart sounds, distended neck veins and hypotension
CXR- cardiomegaly if more than 250 mls accumulation
ECG: small amplitude with electrical alternans
US- large effusion and right chamber collapse in diastoly, -Systolic right atrial collapse
Discuss management of cardiac tamponade
Initial treatment is IV fluids to increase right sided filling pressure to overcome pericardial constriction
Pericardiocentesis or window is the treatment of choice.
If recurrent a drainage catheter may be left in the pericardial space, Pericardioectomy may be ultimately necessary
Discuss purulent pericarditis
Life threatening process most commonly seen in a hospitalized patient with systemic illnesses who develop sepsis. Can occur in any age group and can be cuased by any type of infectious agent. Strep and staph are most common
Can occur by many mechanisms
1) spread from adjecent infection such as pneumonia or empyema
2) Haemategnous spread from a distal site
3) direct inoculation of bacteria (trauma or procedure)
4) Spread from intraarticular source
Features include
tachycardia, dyspnoea, hepatomegaly, elevated central venous pressure, chest pain, friction rub and leukocytosis
Pericardiectomy is the treatment of choice. Indwelling catheters coupled with lavage antibiotics and fibrinolytics may avoid the need for surgery.
Required admit for IVABs or antifungals and monitoring. Fibrinolytics may reduce the rate of contrictive pericarditis when surgery is not an option.
Discuss pneumopericardium
Can be caused by formation fo a fistula between the pericardail and pleural spaces, bronchial tree or upper GIT.
It may result from broncial carcinoma or gas forming purelent pericaritis.
Spontaneous
Hamman’s sign and mediastinal cruncha re the terms used for a loud curnching sound associated with pneumopericardium or pneumomediastinum
Stable patient with spont can be observed
Discuss constrictive pericarditis
May be a late consequence of acute pericarditis of virtually any aetiology. Occurs as a result from fibrous reaction of the pericardium. The key feature is impaired diastolic filling from external cardiac compression caused by a the thickened pericardium.
Clinical features are identical to CHF
ECHO
Discuss the pathophysiology of myocarditis
Mycoarditis occurs via
1) necrosis from the direct invasion of an offending infectious agent and its replication within or near the myocytis
2) destruction of cardiac tissue from infiltration of host cellular immune components or from cytotoxic effects of host immunity activity by the infectious agent
3) toxic effect of exogenous or endogenous chemicals produced by a systemic pathogen
Three stages of the disease
- Acute with viral cytotoxicity and focal necrosis
- subacute in whih there is an increase in huoral factors leading to autoimmune injury
- Chronic in which there is diffuse myocardial firbosis and dysfunction that may lead to DCM
Discuss infectious causes of myocarditis
Viral (Adenovirus, Coxsackie, CMV, EBV, hep B and C, HIV, herpes, Flu A and B, Mumps, Varicella)
Bacterial ( Clostridial, staph, strep, chlaymydia, burcellosis, legionella, TB)
Fungal ( asperigillosis, candidiasis, cryptococcus, histoplasmosis, norcardia)
Rickettsial (q fever, rocky moutnain spotted fever, typhus)
Cardiotoxins (alcohol, arsenic, carbon monoxide, catacholamines, cocaine, heavy metals)
Systemic disorders ( coeliac disaese, granulmatosis with polyangitis, IBD, Sarcoidosis)
Discuss clinical feature of myocarditis
Flulike symtpoms including fever, fatigeu, myalgias vomiting and diarrhoea are the first manifestation.s
Most common presentation ins children is dypneoa
In adults it is dyspnoea, chest pain, and dysrhythmias.
Signs incldude
tachycardia, tachypnoea, hypotnesion and fever
TOxic appearance or tachycardia disproportionate to the temperautre may be the only physical finding
In children prominent physical finding include grunting, respirations and intercostal retractions.
Infants can have a fulminant syndrome characterized by fever, cyanosis respiratory distress, tachycardia and cardiac failure.
When children do have ventrciular arryhtmias myocarditis and idiopathic DCM are commonly seen
Discuss diagnosis of myocarditis
ECG - sinus tachycardia, widened QRS and low voltages. May be prolonged QTC and AV block or AMI pattern
TNI may be elevated - can assume that a higher TNI indicates more myocardial damage.
ECHO–> Reduced EF, global hypokinesis, and RWMA
Contrast MRI or nucelar studies may be diagnositc
Endocardial biopsy used to be the gold standard of diagnosis
Discuss the management of myocarditis
Treatment is supportive and aimed at preserving LV function.
This may range from simple limitations of activity to rhythm and CHF treatment, ECMO, ventricular assist devises and eventual cardiac transplant.
Therapy is stage specific
1st stage - anitvirals may be effective such as beta interferon or ribavirin. - the diagnosis is often made after the intitial viral stage
Sub acute –> ongoing research into immunotherapy nil evidence to date. High dose IVIG may be associated with improved recovery of the LV
Chronci stage- CHF treatment, can consider LV assist devices which can be used up to 70 days
All patient should be admitted and those with persistent HD instability should be admitted to ICU
Mortality rate is 20% at 1 year and 50% at 5 years, has not changes in 25 years
5 year survival rate for children is 70%
Discuss complications of myocarditis
Ventricualr dysrythmias, LV aneurysms, CHF and DCM
Discuss Chaga’s disease
Leading cause of myocardial disease in many countires particularly central and south america, Caused by a protozoan trypanosoma cruzi
Most seropositive patients never develop symptoms. acute infection is a non specific viral infection followed by a latent phase and a cardiac phase with DCM and conduction abnormalities
Serum testing for anti igg for T.cruzi
Discuss cocaine use and myocarditis
Cocaine use causes myocardial ischaemia, myocarditis and DCM. Mechanisms are poorly understood but can include sympathetic effect, oxiditave stress and metabolite interiaction with ion channels.
Cocaine also has a direct -ve inotropic effect on cardiac muscle
Discuss DCM
A spectrum of disoriders that have in common dialted and failing heart.
Myocarditis is the most common cause of DCM in children.
30 -40% of cases have a genetic cause.
DCM affects men more than women, african americans more than whites and may occur in any age group with 40-65 years old being the most common
Discuss risk fractors for DCM
ETOH Pregnancy Tobacco abuse, pregnancy htn infection
Discuss clinical features of DCM
Symptoms are insidious
Onset of left sided failure occurs as the initial manifestation in 75% of cases with orthopnea or exercise intolerance
CHF are the most common presentation in children
Chest pain is the initial symptom in 10% and systemic or pulmonary embolism in 4%
Discuss IX of DCM
ECG- poor R wave progression, intraventricular conduction delay or LBBB
Holter show frequent PVCs and occasional VT
ECHO shows left ventricular dilation, reduced systolic function and variable RWMA. Reduced EF is required for diagnosis of DCM and must be less than 45%
Discuss MX of DCM
Supportive care
ACE inhibitor
ISMN, hyrdalazine, spironolactone and ARBs also prolong survival
B-blockade can reduce symptoms and improve LV funciton ‘
IACD in patient with EF less than 30%
DCM is the leading indication for heart transplantation.
Discuss HCM
The defining anatomical feature of HCM is a hypertrophied left ventricle in the absence of another cause. Ventricle thickening is usaully asymetrical and vaired.
It involves the septum more than the free wall.
HCM is an autosomal dominant disease caused by mutation in genes that encode for sarcomere contractile poteins
Discuss clinical features of HCM
THe average of diagnosis is 30-40.
Often the first presentation is sudden death. For those who do not experience sudden death SOB is the presenting complaint in 90% of cases. Chest pain, syncope, presyncope and palpitations.
Exam – loud s4 and a harsh crescendo-decrescendo midsystolic murmur
splitting of the heart sound
APICAL HCM -Yamaguchi
- giant t-wave inversion in the precordium
- LV criteria
- nil dagger Q
Discuss IX of HCM
ECG
CXR
ECHO/MRI- asymmetrical left ventricular hypertorphy, LV outflow tract narrowing, small levt ventricular cavity and reduced septal motility
Discuss mx of hcm
Beta blocker therapy mainstay of treatment, modualtes the effect of catecholamines on the otuflow gradient- prolongs diastole, increases ventricular filling and result in symptomatic
GTN should not be used as it reduces preload
Amioderone is the drug of choice for dysrythmias
Surgical treatment for large sytolic gradients and severe symptoms with a myomectomy
Dual chamber pacing decrease outflow grad9ient and improves symptoms but not ouctome.
Discuss RCM
Gradual and progressive limitation of ventricular filling secondary to myocardial infilrtration. RCM is the least common of cadiomyopathy.
Most common cause is amyloidosis
Others causes include carcoidosis, haemocrhomatosis, cleroderma, neoplasitc cardiac infiltration.
Discuss clinical features
Worsening diastolic failure. Systolic function is miantianed
Worsening exercise intolerance, elevated central venous pressure, peripheral oedema, pulmonary oedema, S3 and S4 gallops
Discuss MX of RCM
Most of the underlying causes of RCM are untreatable.
Symptomatic treatment with vasodilators and diuretics may help.
Shouold be maintained in sinus rhythm because loss of the atrial contribution to CO results in hypotension.
Discuss peripartum CM
PPCM is uncommon and represents less than 1% of cardiovacular problems assoicted with pregnancy,
PPCM is a idiopathic cardiomyopathy presenting with heart failure towards the end of pregnancy or in the months following delivery.
Risk factors include
- myocarditis
- excessive use of tocolytis
- PET
- advanced maternal age
- multiparity
- twins
- obesitiy
- cocaine use
Clinical features are identical to DCM
Treatment includes
- limitations of physical activity,
- b blocakde
- nitrates and diuretics
ACE and ARB should be avoiding in pregnancy and druing breast feeding
Half of survivors have complete or near complete recovery. THose who dont have persistant left ventircualr dyscunfciotn or continouts cardiac deterioation.
33-50% recurrence rate
