Treatment of Cardiac Dysrhythmias

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Treatment of Cardiac Dysrhythmias

Bradycardia

Tachycardia

  • Most tachycardias are due to
  • re-entry circuits of some form

Sinus Tachycardia

  • Rate 100-150bpm, normal P waves and PR interval
  • Treat underlying cause e.g. pain, anxiety, left ventricular failure, asthma, thyrotoxicosis

Supraventricular Tachycardias

  • Rapid narrow complex tachycardias at rates of approx. 150bpm
  • In older patients, rapid rate commonly
    • → failure of conduction in a branch bundle
    • → broad complexes because of the rate-dependent BBB - can be difficult to distinguish from ventricular tachycardia

Atrial Fibrillation

  • Multiple re-entry circuits in different parts of the atria
  • As person ages
  • scarring in the heart →
  • more re-entry circuits →
  • AF
  • rate >350 bpm
  • variable AV conduction leading to irregular pulse
  • most important modes of treatment convert to sinus rhythm or slow conduction through AV node

Digoxin

  • used acutely if patient not in shock
  • ~50% patient revert to sinus rhythm
  • slows AV node conduction by ~10%
  • used to treat rapid AF

DC cardiversion

  • when patient hypotensivew and poorly perfused
  • dangerous if patient digoxin levels too high
    • measure digoxin levels and leave 24 hours after last dose
  • may be innappropriate if unlikely to remain in sinus rhythm

Verapamil

  • Slow IV
  • but is negative inotrope
  • can provoke acute heart failure
  • may be used with digoxin

Amiodarone

  • very effective but only used when other drugs have failed due to toxicity

Atrial Flutter

  • single re-entry circuit
  • ~300 bpm can lead to VF
  • Treatment same as AF but more resistant
  • responsive to DC cardioversion

AV Nodal Tachycardia

  • re-entry circuits
  • need to influenced conducting properties of re-entry circuits be reducing rate of depolarisation or conduction or increasing refractory period

Targets in treating SVTs

  • conduction within re-entry circuits
  • block AV node
  • carotid sinus pressure / facial immersion in cold water,etc.
    • increases vagal tone
  • adenosine bolus
  • DC cardioversion
  • prophylaxis with oral beta-blocker or verapamil

Adenosine

  • IV bolus
    • metabolised in stomach
  • short-lived AV block (few seconds)
    • cures nodal tachycardia
  • achieves 80% AV node block
  • negatively inotropic but cleared rapidly so effect is brief
  • used as diagnostic test between nodal tachycardia and atrial flutter

Mechanism

  • acts via phosphodiesterase systems

Side Effects

  • flushing
  • headaches
  • histamine degranulation
    • asthmatics get bronchospasm

Interactions

  • won't work with theophyllines or phosphodiesterase inhibitors

Beta-blockers

  • reduce conduction rate through AV node by ~20%

  • reduce rate of pacemaker potential

  • contraindicated in presence of haemodynamic compromise / following verapamil

Calcium Channel Blockers

  • verapamil

    • voltage dependent L-type

    • particular affinity for those in cardiac AV conducting tissue

  • given acutely to terminate SVT

  • recent use replaced by adenosine

  • given IV or oral

  • useful in chronic prophylaxis

  • controls rate in rapid AF

  • 20-30% AV block

Side Effects

  • constipation

  • leg swelling

  • headaches

Interactions

  • strong interaction with beta-blockers leading to heart block

    • can give diltiazem + beta blocker

Contra-indications

  • VT

    • as negatively inotropic

Amiodarone

  • effective in SVT as well as VT

  • can be given slowly IV

  • less negatively inotropic than verapamil or beta-blockers but has risks

Lignocaine

  • sodium channel blocker
  • almost purely selective for ventricles
    • no use in atrial disorders
  • dissociates rapidly very rapidly from sodium channels and slows depolarisation, no prolongation of repolarisation
  • only acts on active channels
  • very selective for fast acting channels
  • most effective in tachycardias >180bpm
  • ineffective <140bpm
  • only given IV due to first pass metabolism
  • used to be important in treatment of VF/VT often as adjunct to DC cardioversion
  • Effective plasma concentration rapidly achieved by giving bolus of 50-100mg iv over 1min followed by infusion of 4mg/min for 1hr, reducing to 2mg/min for 1hr and to 1mg/min thereafter for usually not longer than 36-48hrs
  • Lower doses required in patients with shock or severe hepatic dysfunction in whom initial infusion should not >1mg/min
  • Selectively blocks open or inactivated Na+ channels (use-dependent block) Þ¯rate of ­ of action potential and ­ effective refractory period
  • Metabolised in liver
  • heart failure reduces clearance & predisposes to toxicity unless dose reduced
  • therapeutic plasma concentration range is 1.5-4mg /l difference between therapeutic and toxic concentrations small

Interactions

  • negative inotropes reduced clearance

Side Effects

  • CNS
    • drowsiness
    • twitching
    • nausea and vomiting
    • focal → general seizures
  • CVS
    • bradycardia
    • cardiac depression
    • asystole

¥   Target Conduction processes within myocardium:

¥   Na+-channel blockers e.g. Lignocaine (Ib) (fast-acting channels), Quinidine-like agents (Ia), Flecainide-like agents (Ic).

¥   K+-channel blockers e.g. Amiodarone, Sotalol (both class III), Defetalide (not yet available in UK).

 

 

h   Quinidine

¥               Prolongs medium acting Na+-channel opening Þ disordered slow repolarisation Þ slightly prolonged action potential.

¥               Highly pro-arrhythmic (prolongs QT interval).

¥               Disopyramide used clinically, negative ionotrope.

L                      Atropine-like side effects.

h   Flecainide

¥               Dissociates slowly from Na+-channels and inhibits conduction in the His-Purkinje system Þ prolonging QRS interval.

¥               Given orally or iv.

¥               Mainly used in prophylaxis of AF, WPW syndrome with re-entrant tachycardias.

¥               Negative inotrope

L                      Predisposes to ventricular tachycardia which can degenerate into VF.

L                      Clinical trials show shortens life in some patients.

L                      Can cause heart block

L                      Can't be used safely in IHD: stimulating heart adrenergically breaks through anti-arrhythmic effects and can Þ pro-arrhythmic effect Þ VF. Effective in patients without IHD.

h   Amiodarone

¥               Prolongs plateau phase of cardiac action potential Þ ­QT interval and ­ absolute refractory period.

¥               ¯ likelihood of an ectopic pacemaker capturing the system or of a re-entry pathway becoming perpetuated.

¥               Effective against both ventricular and supraventricular arrhythmias

¥               Takes 3 days to absorb 50% of dose, 7-10 days for first half-life and ~50days for second half life \ if there are side effects e.g. hypothalamus/hyperthyroid, liver problems, photosensitivity, pulmonary fibrosis, they can last months (pulmonary fibrosis may not resolve).

L                      Significant % of patients have reactions.

L                      ­QT interval \ predisposes to VT

h   Sotalol

¥               Prolongs plateau phase of cardiac action potential Þ ­QT interval and ­ absolute refractory period

¥               ¯ likelihood of an ectopic pacemaker capturing the system or of a re-entry pathway becoming perpetuated.

¥               Effective against both ventricular and supraventricular arrhythmias

L                      Also a non-selective b-blocker \ side effects e.g. cold, lack of energy

L                      ­QT interval \ predisposes to VT

ã    K+-channel blockers are relatively safe and can be used as long term therapy in patients who also have IHD and do not promote other arrhythmias.

ã    Na+-channel blockers can not be used as long term therapy in patients who have IHD and do promote arrhythmias.

 

 

Ventricular ectopic beats 

©   Abnormal QRS complexes originating irregularly from ectopic foci in ventricles.

©   Causes include: Electrolyte disturbance, alcohol abuse & excessive caffeine consumption.

©   Treat cause if identified

©   If the ectopics Þ intolerable palpitations or attacks of more serious tachycardia then anti-arrhythmics may be used.

h   Disopyramide (even though treatment may shorten rather than prolong life)

h   Sotalol is an alternative (but SWORD trial showed it may worsen survival).

h   Lignocaine iv bolus followed by infusion may be warranted in acute setting, most commonly after MI treatment, to suppress ventricular ectopics & to try to reduce risk of sustained VT or VF.

Ventricular Tachycardia -

©   Rapid, wide QRS complexes (>0.14s)

©   Patient usually, but not always, hypotensive and poorly perfused.

©   May Þ ventricular fibrillation.

h   DC cardioversion usually.

h   Lignocaine iv bolus of 50-100mg followed by an infusion (1-4mg/min) is an alternative if rate <170bpm and BP is well maintained (constant monitoring in an intensive-care unit needed)

h   If tachycardia is refractory or poorly tolerated DC cardioversion followed by lignocaine infusion is indicated.

h   Amiodarone iv is used for patients who are refractory to lignocaine.

 

ãTREAT THE PATIENT NOT THE ECGã

 

Cardiac arrhythmias, general principles:

In emergencies consider: DC cardioversion (tachyarrhythmia); Pacing (bradyarrythmia)

Correct pro-arrythmogenic metabolic disturbances: electrolytes (especially K+, Mg2+); hypoxia/acid-base; drugs.

Correcting the arrhythmia does not necessarily improve prognosis - anti-arrhythmic drugs can themselves cause arrhythmias.


 

 

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