Pathophysio 1 ( Exam 2 , Arrhythmias and EKGs)

Dysrhythmias

•Are disturbances of the heart rhythm

•Ranges from an occasional "missed" beat or rapid beats to severe disturbances that affect the pumping ability of the heart

•Can be caused by an abnormal rate of impulse generation or an abnormal impulse conduction

Dysrhythmias Tachycardia

ØAtrial fib/flutter

ØWPW syndrome

ØReentry tachycardia

ØVentricular tach/fib

Dysrhythmias Bradycardia

ØBundle branch blocks

ØAV node block

General Mechanisms of Arrhythmias - 1: Spontaneous impulse generation from a source outside the SA node: ectopy

•AV node and other subsidiary pacemakers have diastolic depolarization, can function as pacemakers

•AV node or subsidiary pacemakers are usually suppressed by faster SA node rate

•Latent pacemakers can generate heart rate if SA node fails (escape rhythms)

•Nonpacemaker cells can develop pacemaker-type characteristics when depolarized, ischemic, under sympathetic stimulation

•Ectopic and triggered activity can generate extra beats in addition to sinus beats

Latent Pacemaker Function

•Failure of SA node impulse generation shifts pacemaker function progressively lower in the conduction system, resulting in slower than normal heart rates

Ectopic Activity Can Generate Extra Beats

•Ectopic beats can be normal, particularly when generated within the atria (premature atrial contraction).

•Ventricular premature contractions can also occur sporadically in the absence of myocardial disease

•Ectopic activity is promoted by hypoxia and ischemia, increased sympathetic tone, hyperkalemia

General Mechanisms of Arrhythmias - 2

•Conduction blocks

•AV node pacemaker cells are vulnerable to aging, hypoxia

•Common site of partial or complete blocks of propagation—can result in bradycardia due to nonconducted beats

•Focal conduction blocks contribute to reentrant arrhythmias

Atrioventricular Block—First Degree

•Prolonged PR interval

Atrioventricular Block—Second Degree

•P waves are not all followed by QRS complex, temporary failure of AV conduction

•Mobitz I shows progressive PR lengthening before nonconducted P wave

Atrioventricular Block—Third Degree

•Complete AV block

•No relationship between P waves and QRS complexes

Mechanisms of Tachyarrhythmias

•Increased automaticity: favored by ischemia, sympathetic nervous system stimulation; common during myocardial infarction

•Triggered activity

•Reentry—facilitated by branching and converging pathways, differing rates of propagation, and ectopic foci

Reentry in AV nodal reentrant tachycardia (AVNRT):

a.Sinus beat is conducted along fast pathway to bundle of His

b.Slow pathway has refractory section, impulse is blocked

c.Ectopic impulse stimulates slow pathway, travels anterograde along His-Purkinje path AND retrograde along fast pathway

d.Also known as "circus rhythm"

Reentry in Wolf-Parkinson-White syndrome

a.Accessory pathway between atria and ventricles can bypass AV node completely, setting up large reentrant circuit

b.Without extrasystole, impulse moves anterograde between atria and ventricles—creating delta wave (early rise of QRS complex)

c.With ectopic beat, circus rhythm creates tachycardia

Atrial Fibrillation Overview

•Most common chronic rhythm disturbance

•No discernible P waves

•Irregularly irregular QRS complexes and pulse

•Associated with aging, atrial enlargement due to hypertension, heart failure, valve disorders

•Common triggers: caffeine, alcohol, lung disease

•Initiated by ectopic foci at junction of atria with pulmonary veins

Atrial Fibrillation: Pathological Consequences

•Inadequate cardiac output—loss of atrial "kick" completing ventricular filling, vulnerability to activity intolerance

•Tachycardia shortens diastole and filling, compromises myocardial oxygenation, vulnerability to ischemia

•Clot formation promoted by atrial blood stasis—major risk factor for transient ischemic attack [TIA] and stroke, managed with anticoagulants

Ventricular Tachycardias

•Short runs may be self-limiting

•If sustained—predisposes to ventricular fibrillation

•Mechanisms: increased automaticity, triggered activity, reentry

•Life-threatening consequence of heart disease, ischemia, infarction

•Can occur as a complication of genetic syndromes of ion channel dysfunction

Brugada syndrome

•Congenital dysfunction of fast sodium channel (SCN5A)

•ECG with varying ST elevation

•Potentially life-threatening, may require implanted defibrillator

Long QT Syndrome

•Arise from genetic mutations affecting fast sodium channel or delayed potassium channel—enhancing excitability or delaying repolarization of nonpacemaker action potentials

•Many subtypes with varying degrees of vulnerability to sudden death

•Can precipitate the torsades de pointes form of ventricular tachycardia

•Contraindication to certain medications

Ventricular Dysrhythmias

PVCs,

Ventricular Tachycardia,

Ventricular

Fibrillation