ACLS Prep 3

Sinus bradycardia

Originates in the heart’s normal pacemaker, the SA node. It looks like NSR, but at a slower rate.

Sinus brady regular or irregular

Regular

Sinus brady rate

<50

Sinus brady P waves

Precede every QRS, consistent in shape.

Sinus brady PR interval

Usually normal

Sinus brady QRS complex

Usually normal

Sinus brady causes

• Can be normal rhythm in adult athletes and at sleep.

• Hypoxia.

• Vagal stimulation.

  • Carotid sinus massage.

  • Ocular pressure.

  • Vomiting.

• Coronary thrombosis (inferior MI).

• Toxins:

  • Digitalis.

  • Calcium channel blockers.

  • Beta blockers.

  • Antiarrhythmics.

• Can occur with myxedema, obstructive jaundice, uremia, increased ICP, and glaucoma.

Junctional rhythms

An automatic focus in the AV junction begins active pacing in absence of pacing stimuli coming down from atria.

Junctional rhythms regular or irregular

Regular

Junctional rhythms rate

• Junctional rhythm: 40-60.

• Accelerated junctional rhythm: 60-100.

• Junctional tachycardia: >100.

Junctional rhythms P waves

Can precede, follow, or be buried in the QRS.

Junctional rhythms PR interval

Short, <10 seconds when P waves precede the QRS.

Junctional rhythms QRS complex

Usually normal.

Junctional rhythms conduction

Retrograde. thro

Junctional rhythms causes

• Digitalis toxicity.

• Toxins:

  • Beta blockers.

  • Calcium channel blockers.

  • Antiarrhythmics.

• Chest trauma.

• Sick sinus syndrome.

• Myocardial ischemia/infarction.

• Pericarditis.

• Amyloidosis.

• Opioids.

• Cannabinoids.

• Hypothyroidism.

AV blocks

Occurs when there is delayed or failed conduction of impulses from the atria to the ventricles.

1st degree AV block

Every atrial impulse conducts to the ventricles but takes longer than normal to conduct.

1st degree AV block regular or irregular

Usually regular.

1st degree AV block rate

Can occur at any sinus rate.

1st degree AV block P waves

Normal, precede every QRS.

1st degree AV block PR interval

Longer than .20 seconds.

1st degree AV block QRS complex

Usually normal, unless bundle branch block is present.

1st degree AV block conduction

Normal through atria, prolonged through AV junction, normal through ventricle.

1st degree AV block causes

• Coronary thrombosis (inferior MI).

• Rheumatic disease.

• Toxins:

  • Calcium channel blockers.

  • Beta blockers.

  • Digitalis.

  • Antiarrhythmics.

Second degree AV block

One atrial impulse fails to conduct to the ventricles.

Second degree type 1 conduction

• Occurs in the AV node.

• PR interval gradually lengthens in successive cycles, but the last P wave of the series fails to conduct to the ventricles.

• This series repeats.

• Referred to as Wenckebach.

• Sometimes caused by parasympathetic excess.

• Normal through atria, progressively delayed through AV node until one impulse fails to conduct.

Second degree type 2 conduction

• Occurs below the AV node, usually in bundle branches and very rarely in bundle of His.

• No progressive lengthening of the PR interval.

• Intermittent non-conduction of P waves.

• PR interval is fixed with normal conducted beats.

• Referred to as Mobitz type II AV block.

• Normal through atria and AV node but intermittently blocked in bundle branch system so impulse fails to reach ventricles.

Second degree type 1 regular or irregular

Irregular due to blocked P waves. APpears as “group beating”.

Second degree type 1 rate

Can occur at any sinus or atrial rate.

Second degree type 1 P waves

Normal, regular. Some P waves do not conduct to ventricles.

Second degree type 1 PR interval

Gradually lengthens on consecutively conducted beats.

Second degree type 1 QRS complex

Usually normal, unless bundle branch block is present.

Second degree type 1 causes

• Coronary thrombosis (inferior MI).

• Aortic valve disease.

• Toxins:

  • Calcium channel blockers.

  • Beta blockers.

  • Digitalis.

  • Antiarrhythmics.

• Mitral valve prolapse.

Second degree type 2 regular or irregular

Irregular due to blocked P waves.

Second degree type 2 rate

Can occur at any sinus or atrial rate.

Second degree type 2 P waves

Normal or precede each QRS. Some P waves are not followed by QRS complexes.

Second degree type 2 PR interval

Constant before conducted beats.

Second degree type 2 QRS complex

Almost always wide due to associated bundle branch block. Narrow if the block occurs in the bundle of His (rare).

Second degree type 2 causes

• Coronary thrombosis (anterior wall MI).

• Chronic conduction system disease.

• Rheumatic heart disease.

• Mitral valve prolapse.

• Fibrosis or sclerosis of myocardium.

• Ethanol injection hypertrophic cardiomyopathy.

• Collagen vascular disorders.

High grade AV block

Two or more consecutive P waves are blocked when the atrial rate is <135 bpm.

High grade AV block regular or irregular

Regular or irregular, depending on conduction pattern.

High grade AV block rate

Atrial rate <135, ventricular rate depends on conduction ration.

High grade AV block P waves

Normal, present before every conducted QRS.

High grade AV block PR interval

May be normal when block occurs in the AV node and wide when block occurs below AV node.

High grade AV block conduction

Normal through atria. Impulses block either in the AV or in the bundle branch system.

High grade AV block causes

• Coronary thrombosis.

• Chronic conduction system disease.

• Toxins:

  • Calcium channel blockers.

  • Beta blockers.

  • Digitalis.

  • Antiarrhythmics.

Third degree AV block

All atrial impulses are blocked in the AV node or bundle branch system.

High grade AV block regular or irregular

Usually regular.

High grade AV block rate

Atrial rate can be any sinus or atrial rate.

High grade AV block P waves

Normal but dissociated from QRS complexes.

High grade AV block PR interval

There is no relationship between P waves and QRS complexes, no consistent PR intervals.

High grade AV block QRS complex

Normal if a junctional rhythm is in control of ventricles, wide if a ventricular escape rhythm is present.

High grade AV block conduction

No AV conduction takes place.

High grade AV block causes

• Coronary thrombosis.

• Chronic conduction system disease.

• Toxins:

  • Calcium channel blockers.

  • Beta blockers.

  • Digitalis.

  • Antiarrhythmics.

• Open heart surgery.

Idioventricular and accelerated idioventricular rhythms

Escape pacemaker if all other pacemaker sites fail.

Idioventricular and accelerated idioventricular rhythms regular or irregular

Usually regular.

Idioventricular and accelerated idioventricular rhythms rate

• Idioventricular: 20-40.

• Accelerated idioventricular: 40-100.

Idioventricular and accelerated idioventricular rhythms P waves

May be present if sinus node is working, but P waves are not related to QRS complexes.

Idioventricular and accelerated idioventricular rhythms PR interval

Not measures since P waves are unrelated to QRS.

Idioventricular and accelerated idioventricular rhythms QRS complex

WIde and bizarre, >0.12 seconds.

Idioventricular and accelerated idioventricular rhythms conduction

Cell to cell conduction within the ventricles.

Idioventricular and accelerated idioventricular rhythms causes

• Coronary thrombosis (inferior MI).

• Conduction system disease.

• Electrolyte abnormalities.

• Digitalis toxicity.

• Hypertrophic cardiomyopathy.

• Congenital heart disease.

• Arrhythmogenic right ventricular dysplasia.

Signs and symptoms of unstable bradyarrhythmias

• Hypotension.

• Acutely altered mental status.

• Signs of shock.

• Ischemic chest discomfort.

• Acute heart failure.

• Syncope.

Medications for adult bradycardia

• Atropine: 1 mg bolus. Repeat q 3-5 minutes. Maximum of 3 mg.

• Dopamine IV infusion: 5-20 mcg/kg/min.

• Epinephrine IV infusion: 2-10 mcg/min.

Atropine

• First line treatment for bradyarrhythmias.

• Acts by reversing cholinergic-mediated decreased in the heart and AV node conduction.

• Leads to parasympathetic inhibition, allowing sympathetic stimulation to predominate.

  • Few parasympathetic fibers below AV node, primarily in atria and AV node.

• 1 mg IV bolus.

  • Can repeat every 5 minutes for total of 3 mg.

• In crash cart.

• Use cautiously in presence of acute coronary ischemia or myocardial infarctions.

• Do not delay transcutaneous pacing.

Dopamine

• beta adrenergic infusion.

• Not first line, but can be used as alternative.

  • In crash cart.

• Use as a temporary measure while preparing for transvenous pacing.

• 5-20 mcg/kg/min.

  • Titrate and taper slowly.

  • 2-10 mcg/kg/min stimulates myocardial contractility and increases electrical conductivity in heart leading to increased cardiac output.

  • 10-20 mcg/kg/min causes vasoconstriction via alpha and beta stimulation.

Calcium channel blocker overdose meds

• 10% calcium chloride.

  • 1-2 g IV q 10-20 minutes or infusion 0.2-0.4 mL/kg/hr.

  • Administer boluses over 5 minutes to prevent hypotension, AV dissociation, Vfib.

  • Administer in central line to prevent tissue necrosis and extravasation.

• 10% calcium gluconate.

  • 3-6 g IV q 10-20 minutes or infusion 0.6-1.2 mL/kg/hr.

  • Administer boluses over 5 minutes to prevent hypotension, AV dissociation, Vfib.

Beta blocker overdose meds

• Administer sodium bicarb and magnesium.

• Glucagon:

  • 3-10 mg IV with infusion 3-5 mg/hr.

  • Premedicate with antiemetic (can induce vomiting).

• Insulin:

  • IV bolus 1 u/kg and infusion of 0.5 u/kg/hr.

  • Monitor K+ and BGL.

Digoxin overdose med

• Digoxin specific antibody antigen-binding fragments (DSFab).

  • Infusion lasts over 30 minutes.

  • Can be given as a bolus in critical patients.

  • Onset of effect is 20 minutes, complete effect in 90 minutes.

Transcutaneous pacing

• Noninvasive and can be performed by ACLS providers.

• Indications:

  • No response from atropine.

  • Hemodynamically unstable.

  • Bradycardia with stable ventricular escape rhythms.

• Contraindicated in severe hypothermia.

• Cautious use in setting of acute coronary syndrome, pace at lowest possible rate that achieves stability.

• Unstable Mobitz II, third degree AV block, idioventricular escape rhythms.

• Pace at lowest effective rate based on clinical assessment and symptom resolution.

• Limitations:

  • Painful (consider analgesics and sedative medications if patient’s condition allows).

  • May not produce effective electrical and mechanical capture.

• Emergent bridge to transvenous pacing.