Pericardial Disease Flashcards
Pericardial Diseases
Fluid in peicardium Physiological
Primary Disease of Pericardium
I. Pericardial effusion
a)Hemopericardium
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- b)Hemorragic pericarditis*
- c)Cardiac Tamponade*
Beck’s Triangle:
ECG
II.Pericarditis
Serous
Fibrinous
Sero-Fibrinous
Supurative(pyogenic)
Hemoragic
Fluid in peicardium Physiological
- 30-50 ml clear or strawcolored thin fluid
Primary Disease of Pericardium
- Almost always viral
I. Pericardial effusion
More than 50ml of fluid in pericardium
a)Hemopericardium
If blood leaks to pericardial area without inflamatory exudate (pure blood) => contrast with hemoragic pericarditis
Conditions
1. Traumatic perforation
2.M.I - In day 3 and 4 after MI Neutrophils and Macrophages enzymaticly destroy the deat tissue makeing the miocardium weak…. =>…. STRONG SYSTOLE - produce rupture of myocardiial wall
3. Dissection of Aorta - column of blood may move distaly and eventualy it can rupture the myocardium outwards so bleeding in the pericardial sac may ocur.
4. Infectious Endocarditis - Mostly acute - produce a ring abscess that may go through myocardium. (rupture of ring abscess)
c)Cardiac Tamponade
If excessive ammount of pericardial fluid => Dyastolic Failure. Distant heart sound (muffled heart sound)
200-300 ml can produce tamponade if fluid acumulates fast
Beck’s Triangle:
- Muffeld heart sound
- increased JVP
- Low blood pressure
ECG
Heart will fluctuate in fluid so the Apex electrode will read different QRS morphology => Electrical alternance
II.Pericarditis
Etiology => Immune, Viral
Albumin smaller than globulin, globulin smaller than Fibrin
1) Serous Pericarditis
Mild injury => Mild inflamation => inflamatory mediators => endothelial cell constriction => leak of serous fluid in the pericardial sac (exudate with small amount of protein)
2) Fibrinous Pericarditis
Severe injury => Severe Inflamation =>High amount of inflamatory mediators => Endothelial cell will constrict more => Inter-endothelial spaces bigger => Leak of more brotein + bigger protein (globulin & fibrinogen => Fibrin deposits
3) Sero-Fibrinous Pericarditis
Starts with serous and agravates until fibrin leaks
4) Suppurative (pyogenic) Pericarditis
Pyogenic (pus producing & Verry toxic substances) bacteria reach pericardium Pyogenic pneumonia, pleura involvement => pericardium involvement => destruction of pericardial cells => interepithelial gaps are bigger => Neutrophils will atack bacteria (find living, dying, dead (both imune, bug and pericardial)[CALLED PUS] => more exudate will leak
5)Hemorragic pericarditis
Inflamatory exudate mixed with blood (inflamation creates exudate and as it gets more inflamed vessels are affected and bleeding occurs)
Verry severe inflamation can rupture the blood vessels of pericardium => Blood and exudate is mixed
6) Caseus pericarditis
Caseum formation
Pericardial disease
Complication
**Serous **
Fibrinous
Serous pericarditis
Does not lead to complications (after the viruses are neutralised) the serous fluid resorbs and no adeshions will be formed
Fibrinous pericarditis
Inflamation lead to microvascular damage and exudate with big molecular weight protein (fibrin)=> scar
Fibrin deposits from the pericardium are wiped by plasmin => Complete resolution. If the deposits of fibrin are in big amonuts, than the quantity of plasmin will be overwhelmed and fibrin deposits will remain => deposits will be chemoatrctants for fibroblasts => fibroblasts will colagenise the pericardium called Organised Resolution
Louder Rub
**Acute MI **
Post MI pericarditis (Dressler Syndrome)
**Uremic Pericarditis **
RF
SLE
SD (scleroderma)
Trauma
If not bacteria =>fibrinous
If bacteria => supurative
Cardiac surgery
Produces routinely fibrinous pericarditis
Pericardial disease Fibrinous
Acute MI
Acute MI => will lead to intense inflamation and high amount of chemical mediators that will spread towards the pericardium.
Pericardial Disease - post MI pericarditis (Dressler Syndrome) =>
Post MI pericarditis (Dressler Syndrome) => After postMI myolisis there will be a release of antigen in circulation, antigens that will produce a immune reaction against them, immune reaction against myocardium and it will cross-react lead with pericardium, pleura (2-10 weaks after MI - symptoms includ pleural and pericardial pain (sharp pain, pericardial Rub)- Must distinguish from IHD)
Pericardial disease
Uremic Pericarditis
Radiation Pericarditis
Uremic pericarditis
Patient that have uremia can develop severe pericardial rub
Must be kept on dyalisis until the pericardial rup is gonne
Radiation to the chest
(breast cancer-common)
Injury to pericardium => mild/ severe
Supurative Pericarditis
Pyogenic bacteria
1. Come from neighbouring structure: Lung Heart
2. Hematogenous spread: Tonsilitis / Osteomielitis. Patients at risk are patients that are immunosupresed
3. Surgery
Creamish puss- 200-300 ml
Even if the resolution of infection takes place, colagenisation will ocur and organization of fibrosis => colagenous mass may shrink => constrictive pericarditis
High spyke chills / Fever
ECG
ST segment elevation - (IHD, LV Aneurism)
Hemoragic pericarditis
Fulminant inflamation that will lead to rupture of microvascularisation
Malignancy : => iritate pericardium => C call destroy pericardium => HP
Fibrinous and supurative can convert in HP due to increased tendancy of bleeding ( bleeding diathesis )
Tuberculosis
Caseous Pericarditis
Cause
TUBERCULOSIS
FUNGAL
Fibro - Calcific chronic Constrictive Pericarditis
Chronic Healed Pericarditis
Areas of pericardium are thickened => Soldier plaque
Areas of cross-linked Fibrosis => Adhesive Pericarditis
Pericardium gets fibrosed and extendes to pleura and surrounding tissues => workload on heart increases => Heart Hypertrophy => Dilatation => CHF => Adhesive Mediastinal Pericarditis => Systole Inefficient because of Adesions formed
Fibrosis will produce the retraction of pericardium => Constrictive pericarditis => Diastole Inefficient due to Pericardium scarring => Rx removal of pericardium
