Skip to content

Tachy-Arrythmias

Anti-arrythmics Pharmcology

Causes of Tachyarrythmias

Sinus tachy > Afib > A flutter

Sinus Tachy

  • regular
  • usually narrow- complex tachycardia,
  • with normal P waves preceding each QRS complex alt text

cause of Sinus Tachy

  • physiologic stress
  • compensation to increase cardiac output in lack of perfusion or oxygen delivery.
    • hypovolemia
    • anemia
    • hypoxemia;
  • sympathetic excess
    • whether endogenous (e.g., pain, anxiety, fever, hyperthyroidism)
    • exogenous (e.g., stimulants, other drugs)
  • Treat underlying cause

2.Atrial Tachy

atrial rhythm with more than 100 QRS complexes/min arising from a nonsinus node atrial site(s)

  • common in children and young adults with structural heart disease, often precipitated by the occurrence of a premature atrial contraction (PAC).
    • The rhythm is usually transient and does not require specific therapy. -also in patients with hypoxemia, metabolic disturbances, or drug toxicity.
  • In digoxin, toxicity usuallly 2:1 or higher-grade AV block.

3. Multifocal Atrial Tachycardia

  • Multifocal Atrial Tachycardia (MAT) is a form of AT characterized by:
  • Three or more distinct P wave morphologies
  • Varying PR and P-P intervals from multiple ectopic atrial foci alt text
  • MAT is associated with pulmonary disease (usually chronic obstructive pulmonary disease) in up to 60% or Congestive Cardiac failure

Mng of AT/MAT

  • In hypomagnesemia, give supplemental magnesium (2 g IV over 5 minutes).
  • Vagal maneuvers and adenosine are unlikely to be effective in AT or MAT, although these may help unmask the atrial activity.

A-fib

a narrow- QRS complex tachycardia with an irregular R-R interval and no clear P waves is almost certainly atrial fibrillation.

multiple, small areas of atrial myocardium continuously discharging and contracting 600 beats/min

alt text alt text - Irregualrly Irregualr Ventricle

atrial chaos ⇒ irregularly irregular ventricular rhythm results from variable conduction of impulses through the AV node to the ventricle,@120 to 170 beats/min

  • can be resolve spontaneously in 7days
  • can be permanent
  • cause hemodynamic instability by improper ventricualr filling / COntraction
  • usually 150-170Ventricualr rate

  • 200 indidcates Ventricualr Reentry circiut

Types of A-fib

  • Paroxysmal: spontaneously converts
  • Persistent: requires cardioversion to convert
  • Permanent: when no further efforts to restore sinus rhythm are planned

Pathology

  • M/C ischemic or valvular heart disease cause
  • Left atrial enlargement ⇒ Chronic AFib
  • on Normal Sinus conversion a thrombus in Atrium can reach systemic circualtation

  • 48hrs of Afib ⇒ 10% Thrombolysim

  • So Prophylactic Anti-coagualtion recommended

Mng of A-fib

Goals in A-fib mng

Ventricular rate control

rhythm conversion,

anticoagulation to prevent arterial embolism

Mng based on Pt status and History

  1. New onset ⇒ do Thyroid function 2.prevoius H/O of A-fib ⇒ PT/INR
  2. Clacualte CHADS/CHADS-vasc for embolism risk stratification alt text

Mng based on Cause of A-fib

  • stable low-risk with new-onset atrial fibrillation⇒ rate-control OR rhythm-conversion strategies are appropriate

ventricular rate control <100 beats/min at rest

diltiazem > β-blockers - if both CCB and β-blockers fails use Class-1 Procanimide/ K-blocker Amilorodine

Electro-conversion to normal sinus

150-200J to Normal sinus rhythm - best if Short period A-fib <48hrs ,with no Atrial enlargment

  • Parasymal cause /MI cause ⇒do monitering
  • Acute onset A-fib ⇒ do Sinus rythm conversion in 48-72hrs
  • A-fib + Rapid Ventricualr response + Sepsis /Severe hypo-volumia/Pulmonary embolus/Alcohol withdrawal ⇒ Treat Sepsis and others first

others causing A-fib

Treat the causes of A-fib

  • recent-onset a-fib + rapid ventricular causing hypotension, myocardial ischemia, or pulmonary edema, ⇒urgent electrical cardioversion

A-fib causing complication

Treat A-fib first

  • unstable Long stainding A-fib ⇒ Fluids & Ventricualr rate control
  • unstable pt with embolus risk ⇒ oral anti-coagulatns
  • unstable a-fib pt with prosethic vaulves , Valvualr disease ⇒ LMWM

A-flutter

alt text

  • atrial depolarisation @ regular rate of 250 to 350 beats/min
  • Atrial fultter often accompanies
    • pulmonary disease, structural
    • valvular heart disease, and cardiomyopathies.
  • regular rhythym, rarly irregular due to variable AV nodal block
  • P waves are present and of a single morphology, typically a downward deflection, called flutter waves resembling a saw blade with a “sawtooth” pattern, best seen in the inferior ECG leads and lead V1
  • Normal ventricular rhythm by function of the AV block.

    A:V ratio 2:1 are common and produce a ventricular rate around 150 beats/min, whereas a 3:1 AV ratio will result in a ventricular rate of 100 beats/min.

Mng of A-flutter

  • Atrial flutter is managed same as atrial fibrillation
    • rhythm conversion OR ventricular rate control with β-blockers or calcium channel blockers.
    • Atrial flutter is very responsive to electrical cardioversion; as little as 25 to 50 J is often effective.
  • Anti-coagluation therapy
  • < 50% response to phamacological conversion

why A-fluuter pt stable than A-fib

since most atria is conducting in co-ordination , so most pt are hemodynamically stable

Mng of A-fib & Flutter

alt text

Mng of Ventricular Tachy cardia

  • NO adenosine in Suspected VT
  • Stable patients
    • 1st line 90%sucess Amiodarone 3-5mg/kg OR 250-350mg (stat)
    • SecondlineProcainamide (30 to 50 mg/min IV, up to a total of 18 mg/kg or until VT is terminated)
    • Alternative to AmilodaroneLidocaine (1.0 to 1.5 mg/kg IV bolus, up to 3 mg/kg maximum, followed by an infusion).
  • Unstable patients/No response to pharmacology
    • Sync Cardioversion 100J-200J biphasic

Managment of Torsades de Pointes

  • Congenital Torsades de Pointes => Triggered by sympathetic excess or tachycardia; use beta blockers

  • Stable patient

    • Corect metabolic abnormalities increase HR to shorten Ventricualr repolarisation
    • Class 1A,1C stopping
    • IV magnesium sulfate (1 to 2 g quickly) efefctively treats torsades de pointes, even in the absence of hypomagnesemia
    • maintain 100-120bpm prevent next episode by Beta adrenergic infusion
  • Unstable pt
    • Electrical cardioversion in Non-sync

Management of Ventricular Fibrillation and Pulseless Ventricular Tachycardia

  • Same for Both
    • CPR
    • 1 shock with less pause in CPR
    • 2 min CPR after shock
    • Check rythm and Pulse
    • Still VF/pVT => aminodarone 300mg then second dose 150mg