Cardiac Dysrhythmias

• 1. Atrial fibrillation/flutter
• 2. Narrow-complex tachycardia
• 3. Stable wide-complex tachycardia, unknown type
• 4. Stable monomorphic VT and/or stable polymorphic VT

Atrial Fibrillation/Flutter

• 1. Is patient clinically unstable?
• 2. Is cardiac function impaired?
• 3. Is WPW present?
• 4. Is duration of AF <48 or >48 hours?

• 1. Treat unstable patients urgently
• 2. Control rate
• 3. Convert rhythm
• 4. Provide anticoagulation if indicated

Atrial Flutter 

Paroxysmal Supraventricular Tachycardia

Sinus Tachycardia

Ventricular Tachycardia

• 1. Atrial fibrillation/flutter
• 2. Narrow-complex tachycardias
• 3. Wide-complex tachycardias of unknown type
• 4. Ventricular Tachycardia

• Paroxysmal supraventricular tachycardia (PSVT)
• Junctional tachycardia
• Multifocal atrial or ectopic atrial tachycardia

• Wide-complex tachycardia - not specified
• Aberrant conduction of an SVT

• Stable monomorphic VT
• Stable polymorphic VT (baseline QT interval normal)
• Stable polymorphic VT (baseline QT interval prolonged = torsades de pointes)

Sinus Tach: PSVT (Paroxysmal Supraventricular Tachycardia)

Atrial Flutter:

• Atrial Rate = 250 bpm
• Ventricular Rate = 125 bpm

Sinus Bradycardia

• 1st Degree
• 2nd Degree type 1
• 2nd Degree type 2
• 3rd Degree

Cardiac Conduction System 2:

Relationship of ECG to anatomy

Approximately 80% of wide-complex tachyarrhythmias are V. Tach

• Lidocaine
• Procainamide
• Bretylium

• 1. Find where the R-S junction of a QRS complex fall on one of the darker 5-mm lines
• 2. Note the next R-S junction; mark it
• 3. Label each of the darker 5-mm lines between the first R-S junction and the next one in the following sequence:  300 - 150 - 100 - 75 - 60 - 50
• This number is the rate of beats per minute

• Are QRS complexes present?
• Are P waves present?
• How is the P wave related to the QRS complex?

• Every P wave is followed by a QRS complex w/ normal P-R interval
• Every P wave is followed by a QRS complex but the P-R interval is prolonged
• Some P waves are NOT followed by a QRS complex; more P waves than QRS complexes

Slow rates and more P waves than QRS complexes

First-Degree AV Block

P-R interval is equal to or greater than 0.2 seconds

The P-R interval is prolonged. It is 0.31 seconds

The impulse is slowed getting through the AV node

Rate = 48 bpm; regular

Pathology:

is a decrease in the rate of atrial depolarization secondary to sinus node disease, increased parasympathetic tone, or the effects of drugs such as digoxin, β-blockers, or calcium channel blockers.

Second-Degree Type 1 AV Block

• Progressive lengthening of the P-R interval until a P wave is NOT followed by a QRS complex
• Atrial rhythm is regular
• Ventricular rhythm has pauses b/c every 4th P wave fails to conduct into the ventricles. (4 P waves to 3 QRS complexes = a 4:3 cycle)

Increasing conduction delay in AV node before the non-conducted beat

Lengthening of the P-R interval

Second-Degree Type 2 AV Block

• 3 conducted beats are followed by 2 non-conducted P waves
• The P-R interval of conducted beats remains constant
• Block is usually located at the level of the bundle branches
• QRS is wide because of the block location near the bundle branches

Cause: A serious organic lesion in the conduction pathway

Prognosis: Usually poor

Risk: High risk for complete heart block to develop

Fixed P-R interval until a beat is dropped

More P's than QRS's? → YES → PR fixed? → YES → 2nd-degree AV block, Fixed Mobitz II

PR fixed? → NO → QRS's that look alike regular? → YES → 3rd-degree AV Block

QRS's that look alike regular? → NO → 2nd-degree AV Block, Variable, Mobitz I Wenckebach

Do NOT treat a slow heart rate in a Stable patient

Treating the symptoms is the most important concept

Relative bradycardia exists when a hypotensive patient "needs" a faster HR. but the rate cannot accelerate due to sinus node disease, conduction system disease, or β-blockers

Resting Athletes may have sinus rate <40 bpm and still be completely asymptomatic

Patients with inferior MI frequently have sinus bradycardia w/ or w/out chest pain

Usually the bradycardia is NOT the cause of the chest pain.

Treat if clearly detrimental symptoms are present: Hypotension/shock, decreased level of consciousness, sudden increased pain associated w/ decreased rate, CHF, or adrenergic symptoms such as pallor and cool, clammy periphery

Third-Degree AV Block at the level of the AV node

(Supra-nodal or supraventricular level)

Atrial rhythm is irregular due to sinus arrhythmia at a rate of 48-70 bpm

There is no constant P-R interval. The narrow QRS complex indicates that the block is occurring above the ventricles (supraventricular) at an upper level of the AV node.

Rate: Atrial Rate = 45-70 bpm; Ventricular Rate = 44 bpm

Pathology: (A) = increased parasympathetic tone, which can result from drug effects such as digoxin, or β-blockers; 

-OR-

(B) = damage to the AV node

Prognosis: Third-degree AV block with a narrow junctional escape rhythm is usually transient and is associated with a favorable prognosis.

Variable P-R interval w/ regular R-R interval

Look at similar QRS complexes to assess the regularity of the R-R interval

Third-Degree AV Block

Third-Degree AV Block at the infra-nodal (bundle branch) level

The wide QRS indicates that the block is occurring at the ventricular level

• There is no relation between the atrial and ventricular rhythm
• Ventricular rhythm is regular and very slow (38 bpm)
• The QRS is wide b/c block is at the bundle branch level, usually involving both bundle branches. 
• The ventricular pacemaker is downstream from that level

Damage: To both bundle branches indicates extensive conduction system disease below the AV node. 

Cause: This is most often caused by extensive anterior myocardial infarction. The ventricular escape pacemaker is slow (<40 bpm) unstable and may lead to episodes of ventricular asystole

Tx?: New 3rd-degree AV block demands urgent pacing, likely w/ TCP. This is why TCP shoiuld be readied while atropine is tried

Third-Degree AV Block at the Supra-nodal level

Third-degree AV block w/ narrow junctional escape rhythm is usually transient and associated w/ a favorable prognosis

Third-Degree AV Block w/ Ventricular Asystole

Patient has acute anterior myocardial infarction.

He developed right bundle branch block (see wide-QRS complex on left side of strip).

Complete heart block abruptly developed: only P waves seen on right side of strip. P waves are not followed by a ventricular escape focus, resulting in ventricular asystole.

Escape rhythms are less likely w/ Lidocaine

The advantage of TCP over catecholamine infusion is significant.

A transvenous pacemaker often takes too long to place.

The key focus is on the unstable patient and the value of TCP as a bridge while transvenous pacing is organized.

Note the use of pacing to allow the use of lidocaine in stable second-degree AV block with PVC or runs of VT.

This is a good place to reinforce this contraindication to lidocaine for ventricular escape rhythms.

Standby pacing (pads applied but not in pacing mode) is the reason for understanding intranodal AV blocks.

Asystole

A cardiac arrest rhythm associated w/ no discernible electrical activity on ECG "Flat Line"

Successful resuscitation of a person in asystolic cardiac arrest occurs RARELY.

It happens only when rescuers stop, think, and ask “Why did this person have this cardiac arrest at this time?” Only if the cause of asystole is identified and treated in a timely manner will there be any reasonable possibility of survival.

A large % of Pt's will NOT survive.

Severely ill patients.


Often this rhythm represents the terminal rhythm of patients who have deteriorated from organ failure. Cardiac function has diminished until cardiac electrical and functional activity finally stop.

In such scenarios resuscitation fades as a high-priority action.

Prolonged efforts are unnecessary, futile, often unethical, and ultimately dehumanizing if not demeaning.

The asystole case therefore provides the most appropriate setting to discuss and understand more about ethics, when not to start resuscitative efforts, and indications for termination of the resuscitation attempt.

• Hypoxia (CNS events)
• Hypokalemia/Hyperkalemia (and other electrolytes)
• Hypothermia/Hyperthermia
• Hypoglycemia/Hyperglycemia
• Hypovolemia (tank/anaphylaxis, gravid)

• Trauma
• Tamponade
• Thrombosis (pulmonary)
• Thrombosis (coronary)
• Tablets (OD's, drugs, etc.)
• Tension (pneumothorax, asthma)

• Electromechanical dissociation (EMD)
• Idioventricular rhythms
• Pulseless asystolic rhythms
• Bradyasystolic rhythms
• Ventricular junctional escape rhythms
• "Pseudo-EMD" (All these terms have been replaced by the term PEA.)

Can be fast or slow, narrow or wide.

Tx approach, and ultimately the patient's prognosis, may vary based on fast V.S. slow and narrow V.S. wide complexes

Any pulseless rhythm that looks as if it could produce a pulse is considered a PEA

THEREFORE, any pulseless rhythm that is not VF, VT, or asystole should be considered PEA. This rhythm—sinus tachycardia with unifocal PVCs and no pulse—is one form of PEA that could be EMD or pseudo-EMD

This rhythm is another form of PEA that could be EMD or pseudo-EMD. This patient also has first-degree AV block.

Another form of PEA.

Epinephrine = administered every 3-5 mins during cardiac arrest

Atropine = used to treat relative bradycardia. One of the standard agents for treating PEA, w/out reference to the rate of the electrical activity. Until specific evidence accumulates otherwise, limit atropine to absolute or relative bradycardia.

The shorter dosing interval (every 3mins) is possibly helpful (Class IIb) in cardiac arrest.

Another form of PEA.

Another form of PEA.

May be due to true EMD. A rapid search for treatable causes is KEY! Only a few reversible causes exist, & must be found and treated quickly.

• Pulsus paradoxus
• Pericardial friction rub may be present
• Heart size on x-ray may be normal or enlarged
• Echocardiogram

PEA

• Chest X-ray:
• 
• Widened mediastinum
• Pneumo- or hemothorax
• Note rounded bottle shape to left side of heart

• Electrical Alternans:
• 

• Impairment of ventricular diastolic filling caused by pressure of pericardial sac
• & by bulging of ventricular septum into LV
• Stroke volume and cardiac output fall

• Air under tension in left thorax
• Pleural margin; partial lung collapse

Although rare, tension pneumo may cause PEA

Hx may include: Trauma, recent CPR, prior chest surgery, central venous lines, or other reason for a pneumo

Air under pressure

• Venous return inhibited
• Mediastinum displaced 
• Vena cava kinked
• Cardiac output decreased
• Cardiovascular collapse developed

• Spontaneous breathing
• Respiratory distress
• Florid face
• Trachea deviation
• Distended neck veins
• Tachycardia
• Hypotension

• Provide as soon as diagnosis is apparent to prevent cardiovascular collapse and cardiac arrest
• Do not wait for x-ray confirmation
• Use large-bore needle tap

Equipment:

• Povidone-iodine solution
• 14-gauge catheter-over-needle device

Technique:

• Cleanse overlying skin
• Insert needle at 2nd or 3rd intercostal space, midclavicular line, over top of rib
• Leave catheter in pleural space open to air

• Misdiagnosis - pneumothorax created
• Lung laceration
• Internal mammary or intercostal vessel laceration
• Hemothorax

Ventricular Fibrillation

• Organized QRS complexes and absent P waves
• Wavy, chaotic, inconsistent baseline
• Irregular rhythm

VF may occur spontaneously or be preceded by VT

Pulseless Ventricular Tachycardia

• Wide, bizarre QRS complexes
• Regular rhythm and mostly uniform in shape
• Absent Pwaves
• Ventricular rate is 150 bpm