Atrial fibrillation [pathophysio, causes, dx, manifestations, thromboembolic risk assessment]; Beurger's disease, Great vessel Vasculitis Flashcards
Idea behind trigger of Atrial Fibrillations
Atrial Fibrillation is a poorly understood condition. 15% of all A.fib patients have no other underlying causes that triggers A.fib. However there are certain situations whem A.fib has a higher likelihood of developing. These conditions include:
- Conditions that increase Sympathetic tone aka Automaticity
- Conditions that force Cardial remodelling of atria and formation of Reentry pathways
- Conditions that cause increased Triggered activity [EADs]
- Imbalance in electrolytes
Usually a combination of all 4 has a high likelihood to trigger A.fib
CV risk factors, Intrinsic cardiac, Non-cardiac
Known Etiologies of Atrial Fibrillation
Cardiovascular risk factors:
- Advanced age
- HTN
- DM
- Smoking
- Obesity
- Sleep apnea
Intrinsic Cardiac disorders:
- CADs
- Mitral valve diseases [MS more likely]
- CHF
- Preexcitation Tachycardias [like WPW]
- Sick SInus Syndrome
- Cardiomyopathies
- Pericarditis
- Atrial myxoma
Non-cardiac Disorders:
- Hyperthyroidism
- Pulmonary diseases [COPD, PE, Pneumonia]
- Catecholamine release and Increased Sympathetic tones [Physio stresses, Pheochromocytoma, Cocaine, Amphetamines]
- Electrolyte imbalances
- Adenosine and Digoxin
- Heavy alcohol consumption [in binge or chronically]
- CKD
Pathophysiology of Atrial Fibrillation
Major determinants of new A.fib are cardiac remodelling due to volume and pressure overloads in atria/ventricles, formation of reentrant pathways post MI/injuries or remodelling of myocardium, inflammation and major electrolyte imbalances
A.fib trigger can come from:
- Automatic foci making bursts of electrical activity near Pulmonary vein ostia [Left Atrium] or in fibrotic atrial tissue
- Preexcitation of atria [like in WPW]
A.fib is sustained by:
- Reentrant rhythms which form due to anatomic [WPW] or pathologic [cardiac remodelling] causes
Post A.fib remodelling:
- Forms a viscious cycle
- New A.fib which occurs frequently and goes untreated, causes atrial remodelling by itself
- Electrophysiological changes, fibrosis and dilatations, electrical and structural remodelling ALL increases likelihood of subsequent and chronic A.fib in patients
Diagnosis of Atrial Fibrillation
Dx strategy depends on Hemodynamic stability of newly arrived patient
If patient is hemodynamically unstable, immidiate management protocols are followed [which includes ABCDE survey, ECG, Pulse oxymeter, IV fluids, ventilation support, bedside CXR and TTE, drugs to manage shocks/hypotension, electrolyte imbalances, etc]
If patient is hemodynamically stable AND has a new onset A.fib:
- 12-lead ECG
- Continuous cardiac monitoring or Ambulatory ECG monitoring [for A.fib suspecion without proof in 12-lead ecg]
- ACS and PE diagnostics [reversible and deadly causes of A.fib]
- Routine labs [CBC, Comprehensive metabolic panel]
- TTE
- Tox screen, CXR, CTPA, TFTs on clinical suspecion
- Electrophysiologic Studies
- Sleep studies for sleep apnea evaluation
- Thrombotic complication risk factor assessements
- Bleeding risk assessements
- DM, CAD screening
- AHF and Ischemic stroke screening
Ofcourse, Comprehensive Patient history and Anamnesis is also done
Thrombotic risk assessment strategies
To calculate thrombotic risk associated with Atrial fibrillation [which in turn is due to thrombus formation in blood pooling of spastic atrial walls], we use a scoring system AND Transesophageal Echocardiography
CHA2DS2-VASc Score: the following are part of the scoring
- Congestive Heart failure/Ventricular dysfunction
- Hypertension
- Age [2 points for > 75 years age]
- Diabetes Mellitus
- Prior Stroke/TIA/Thromboembolism [2 points for yes]
- Vascular disease
- Age between 65-74
- Sex [Female is 1 point]
>= 2 for male and >=3 for female in scoring is a HIGH risk for thrombotic events post Atrial fibrillation
Transesophageal Echocardiography:
- To evaluate thrombi and atheroma at ‘‘hotspots’’ for thrombus formation
- Done prior to cardioversion
- Antigcoagulation therapy for >= 3weeks administered on any findings of atheroma or thrombi prior to attempting Rhythm control of A.fib
Beurgers Disease
Also called Thromboangitis Obliterans
It is a recurring inflammation and thrombosis of medium vessel arteries and veins
The biggest risk factor is Tobacco and Non-tobacco Smoking
Typically in young males [< 40 years], Migratory Superficial Thrombophlebitis recurrently seen, Raynauds phenomenon present, Chronic or Acute limb ischemia can also occur
Beurgers Diseases is a diagnosis of exclusion in addition to smoking history. Angiography and Echo could be done in affected areas. Biopsy could be done in atypical presentation of patients. Lab studies for autoantibodies, inflammatory markers, coagulation studies can also be done
Treatments are not absolute other than Smoking cessation. Drugs can provide symptomatic relief or ulcer healing help
Giant cell, Takayasu
Great Vessel Vasculitidies [Etiology, Clinical features, Dx, Treatments]
Great vessel vasculitidies are majorly classified into Giant Cell Arteritis [esp. Carotid and major branches] and Takayasu Arteritis [esp. aorta and major branches, granulomatous and mostly in asian women]
Etiology Giant Cell:
- Genetic predisposition [HLA-DR4]
- Viral infections [like parvovirus B19]
- Polymyalgia Rheumatica association
Clinical Features Giant cell:
- Women > 50
- Blindness severe complication
- New onset headache
- Tender temporal artery
- Jaw claudication
- Polymyalgia Rheumatica
Clinical Features Takayasu:
- Asian women < 40
- Disparity in brachial BP of arms
- Bruit over subclavian artery or abdominal aorta
- Syncope and Angina pectoris could be complaints
Dx:
- ESR, CRP
- Autoantibody testing [negative in Giant cell]
- MR angiography in Takayasu
- Temporal artery biopsy for Giant cell [GOLD standard]
- Granulomatous inflammation on biopsy for Takayasu
Treatments:
- High dose Glucocorticoids for Giant cell
- Glucocorticoids + Glucocorticoid sparing agents [methotrexate/Azothioprin]
