Supraventricular Arrhythmias [classification, treatment]; Obliterative arterial disease of the lower limbs [risk factors, stages, dx] Flashcards
Supraventricular Arrhythmias classification
Supraventricular Arrhythmias are Tachyarrhythmias causing narrow QRS tachycardias with regular or irregular rhythms
Classified into AV node dependent and AV node independent
AV node Dependent:
- AVNRT
- AVRT
- “True” junctional Tachycardia
AV node Independent:
- Atrial Fibrillation
- Atrial Macrorentry [Isthmus dependent A. flutter; Non-isthmus dependent]
- Focal Atrial tachycardias [Ectopic, SA node origin]
Different broad etiologic factors causing Supraventricular Tachyarrhythmias
- Increase in Automaticity [aka Increased Sympathetic tone]: Decreased BP, Hypoxemia, Decreased O2 sat, Hyperthyroidism, Fevers, Sympathomimetic drugs
- Increase in Reentry pathways [Anatomical or Pathological]: Pathologic reentry pathway formation is due to Atrial and Ventricular remodelling. Atrial remodelling caused by Congestive HF, HTN, MS. Ventricular remodelling caused by MI scarring, Fibrosis, Systolic HF with reduced EF
- Increased Triggered activity [Atrial or Ventricular Ectopy]: Early After Depolarizations or Late After Depolarizations. Aided by Hypokalemia, Hypomagnesemia
Each Supraventricular tachyarrhythmia is caused by either one of the above or a combination of all three of the etiologies
Etiology of each of the Supraventricular Tachyarrhythmias
PSVT divided into AVNRT, AVRT and WPW
AVNRT:
- Anatomical Reentry pathway from Fibrosis in AV node, forming two separate paths of impulse conduction [Slow-Fast or Fast-Slow and Slow-Slow]
- Presence of retrograde ‘p’ waves or even indistinguishable from QRS complex, can also be after QRS complex
AVRT:
- Anatomical or Pathological accessory pathway allowing reentry of impulse from ventricles to atria
- Orthodromic where impulse moves in antegrade direction via AV node
- Antodromic where impulse travels in retrograde direction
WPW:
- Type of AVRT where the accessory pathway is the Bundle of Kent [lateral LA between Atria and Ventricle, can bypass AV node entirely; Decreased PR distance, wide QRS, Delta waves]\
Multifocal Atrial Tachycardia:
- Due to increase in Automaticity [aka Increased Sympathetic tone], especially Chronic Hypoxemia in COPD patients
- 3 morphologically distinct ‘p’ waves
- HR ~ 100 bpm is called ‘Wandering Atrial Pacemaker’
Atrial Fibrillation:
- Combination of Increased Sympathetic tone, formation of pathologic Reentry pathways and Increased EAD triggered activity
- Reentry mainly occurs via Pulmonary veins
- Reentry pathway develops due to Atrial remodelling from HTN, CHF, MS
Atrial Flutter:
- Combination of Increased Sympathetic tone, formation of pathological Reentry pathways and Increased EAD triggered activity
- Reentry mainly occurs via Cavotricuspid Isthmus
- Reentry pathway develops due to Atrial remodelling from HTN, CHF, MS
Acute and Long term management
AVNRT Treatment
Acute Management:
- Unstable tachycardia with pulse: Electric Cardioversion
- Stable with Narrow QRS: Vagal maneuvers [Carotid massage, Valsalva] | Persistant SVT treated with Adenosine; Other options are CCBs and Beta Blockers
- Stable with Wide QRS [indicates abhorrent conduction]: If AVNRT is established, AV nodal blocking agents continues | If AVNRT not established, AV nodal blocking agents not continued
Long term Management:
- Vagal maneuvers for infrequent episodes [self administered]
- Percutaneous Catheter Ablation of Slow pathway [as fast pathway ablation can easily lead to AV blocks]
- Pharmacological therapy if frequent episodes: Beta Blockers, Verapamil, Diltiazem as Daily | Propranolol + Diltiazem for single pill option [off label]
Acute and Long term Management
AVRT Treatment
Acute Episodes:
- Unstable tachycardia with pulse: Electric Cardioversion
- Stable Orthodromic AVRT: Vagal maneuvers [Carotid massage, Valsalva] | Persistant SVT treated with Adenosine; Other options are CCBs and Beta Blockers
- Stable Antidromic AVRT: If AVRT is established, AV nodal blocking agents continues | If AVRT not established, AV nodal blocking agents not continued
Long Term Management:
- Catheter Ablation first line
- Pharmacotherapy based on presence or absence of preexitation patterns
- Preexitation pattern present [Antegrade direction conduction]: Known Heart disease give Sotalol OR Dofetilide | No known heart disease give Flecainide OR Propafenone
- Preexitation pattern not present [Retrograde direaction conduction]: CCBs like Verapamil OR Diltiazem | Beta Blockers like Propranolol OR Metoprolol
Acute and Long term management
WPW Treatment
Acute Episodes:
- Unstable with a pulse: Electric Cardioversion
- Stable: Assess underlying rhythm | NCT - Vagal maneuvers and Adenosine | WCT regular or irregular rhythm - do not perform Vagal maneuvers or AV nodal blockers, provide cardioversion or IV procainamide
Long term Management:
- High risk patients [ie patients with concerning clinical features]: Catheter ablation of accessory pathway
- Low risk patients [ie patient with no concerning clinical features]: Symptomatic - Catheter ablation | No structural heart disease - Flecainide or Propafenone | Structural heart diease - Dofetilide or Sotalol, use AV nodal blockers with caution
First line, Rate control and ablation
Multifocal Atrial Tachycardia Treatment
First Line Treatment:
- Manage exacerbations of Chronic diseases [like COPD]
- Correct reversible causes like acidosis, hypoxemia, electrolyte abnormalities
- Potassium and Magnesium replacement therapies
- IV mangesium is beneficial even in normal Mg levels
- Discontinue potential offending medications
Rate Control: Used with continuous ECG and BP monitoring
- Beta Blockers: Metroprolol
- Calcium Channel Blockers: Verapamil [prefered in asthma and COPD patients]
AV node radiofrequency Ablation: Consider in refractory Multifocal Atrial Tachycardia
AVOID cardioversion and antiarrhythmic drugs in MAT as they are not affective
Rate and Rhythm control, Long term anticoagulation
Atrial Fibrillation Treatments
Rate Control: Controls number of impulses reaching ventricles to improve symptoms and quality of life
- First Line: Beta Blockers like Metroprolol, Atenolol, Propranolol [avoid in COPD and Acute decompensated HF patients] | ndHP CCBs like Verapamil, Diltiazem [avoid in ADHF patients, prefered in HF with preserved LV function]
- Second Line: Digoxin [preferred in ADHF]
- Third Line: Amiodarone [has both rate and rhythm control, reserved for non responsive to above patients]
- AV nodal ablation and permanent Ventricular pacemaker implantation
- DO NOT GIVE NODAL BLOCKERS in WPW and preexcited A.fib conditions as this will kill the patient
Rhythm Control: Controls atrial rhythm to prevent excess impulse generations and maintain Sinus rhythm
- Planned Electrical Cardioversion
- Pharmacological Cardioversion: Flecainide, Dofetilide, Propafenone, Ibutilide, Amiodarone
- Interventional Cardioversion: creating scar tissue in atria [Radiofrequency ablation aka Pulmonary vein Isolation or Maze ablation]
Long Term Anticoagulation:
- Calculate CHA2DS2-VASc score [Thrombotic risk]
- Calculate HAS-BLED scores [Bleeding risk]
- DOACs: Dabigatran | Rivaroxaban | Apixaban | Edoxaban
- VKAs: Warfarin
- Heparin: Unfractionated | LMWH
Maze Ablation - making multiple incision cuts in atria to prevent macrorentry
Same as Afib
Atrial Flutter Treatments
Atrial Flutter acute management is similar to AFib with RVR, most patients get Emergency cardioversion while WCT Atrial flutter gets desynchronized cardioversion
Atrial flutter pharmacological therapy also has Rate and Rhythm control similar to AFib
Rate control is more difficult to achieve in Atrial flutter than Afib
Rhythm control has better results than Afib and Catheter ablation is the most effective rhythm control treatment
Anticoagulation recommendations same as Afib
Obliterative Arterial Disease of the Lower Limb major cause
Atherosclerosis in Limb arteries
PAD risk factors and incidence increase of MI
Risk Factors:
- Hypertension
- Hyperlipidemia
- Smoking
- Diabetes Mellitus
PAD leads to a 4 fold increase in MI incidence and 2-3 fold increase in risk of stroke
Clinical Stages from Fontaine
PAD classification
Stage 1 - Asymptomatic
Stage 2a - Mild claudication
Stage 2b - Moderate to Severe claudication
Stage 3 - Ischemic rest pain
Stage 4 - Ulcerations and/or Gangrene in limbs
Dx of PAD
- Thorough patient history asking about risk factors, claudication
- Physical exam: Inspection of foot, muscle atrophy, hypertrophoed and slow growing nails | Palpation of femoral, popliteal, dosalis pedis and posterior tibial pulses
- Ankle-Brachial Index [Systolic pressure comparison between brachial and ankle | If ankle pressure lower, some form of obstruction is present]: ABI range 0,9 - 1,4 NORMAL | ABI < 0,9 PAD | ABI < 0,5 CRITICAL LIMB ISCHEMIA
- Abnormal ABI - Doppler US to find site of obstruction and extent of Atherosclerosis
- Gold Standard for evaluation of PAD is Angiography
Treatments for PAD
- Lifestyle changes: Cessation of smoking | Increased physical activity | Control of other risk factors
- Diabetes Management [metformin]
- HTN Management [ACEis, Beta blockers, ndHP CCBs, ARBs]
- Hypercholesterolemia Management [statins]
- Antiplatelet drugs [aspirin, clopidogrel]
- Cilostazol [Phosphodiesterase III inhibitor, improving walking distance for claudication]
- Revascularization [Angioplasty, Vascular bypass, Amputation in severe gangrene cases]
