Premature ventricular contractions

(pvcs)

Pathology

-Prematrure depolarization in the ventricles.

-generated by an ectopic stimulus or an irritable foc originating from somewhere below the av junction.

-occure early

-wide and obtuse

-T waves generally opposite of QRS complex

-usually will not see p waves

2 identical pvs in succession.

3 or more pvc's in a row lasting less than 30 seconds

savos- 3 in a row.

ventricular bigeminy

PVCs every other beat

PVCs every third beat

DIfferent ectopic pacemakers

-look different from each otehr but still characteristic of PVCs

-Occurs directly between two normal sinus beats

-PVC exactly whre sinus beat would be

*do not neet to indentify*

Paase between end of pvc and next normal sinus firing of SA node.

-Sinus beat ocurs when it's supposed to after pvc

-idiopathic

-exernal or internal stimuli that increase sypathetic tone

-excssive administration of sypathomimetic drugs

-cardiovascular disorders

-oxygen and electrolyte distrubances

-isolated PVCs without underlying CAD have no significance - no treatment

-when occur with CAD or drug toxicity, may precipitate VT or other life threatening arrhythmia

-search for reversible causes before treating - eliminate caffeine, stress relaxation exercises

-inpresence of AMI w couplets, RonT, increase frequency, treatment with anti-arrythmias.

an arrythmia originating from an ectopic pacemaker in ventricles with a ventricular rate between 110-250

-No p waes

-can beslightly irregular

-wide QRs complex

-all waves look same - same extopic pacemaker

-CAD with prior MI

-abnormal PVC frequencies

-life threatening arrythmia

-low cardiac output

-possible degeneration

-anti-arrythmic drug therapy

-EP studies

-IACD/Cardioeversion

-Anti tachycardic pacemaker

Failure of ventricles to beat in a coordinated fashion

-first stage of cardiac arrest

-very innefective

-no cardiac output

-pt becomes unconscious immediately

-one of 3 major patterns seen with cardiac arrest

very highly unstable ryhtym

-goes quickly to vfib

A premature atrial depolarization arising from an ectopic stimulus in the R or L atrium

-atria depolarized by an ectopic pacemaker

-dollowing atrial depolarization, the stimulus spreads normally through ventricles

-ventricle depolarization is not effected by PACS

-premature

-qrs in PAC is identical to sinus QRS complexes

-P wave

• different shape and size
• Pr interval may be different than sinus beats
• P wave may be lost in preceding T wave

-couplets

-begeminy

-trigeminy

-compensatory pause

-emotional stress

-excessive caffeine

-sympathomimetic agents

-hyperthyroidism

-very common

-patients complain of skipped beats or palpitations

-frequent PACs may precipitate A fib

Series of 3 or more premature supraventricular beats arising from an extopic pacemaker in L or R atrium

-HR between 140 and 250

-P waves lost in preceding T wave

-non sustained (less than 30 seconds)

-sustained (greater or equal to 30 seconds)

Sustained PSVT symptoms

-angina

-light headedness

-syncope

-hypotension

-transeitn PSVT

• increase vagal tone
• electrical synchronized cardioversion

recurrent cases

• radio frequency catheter ablation

inverted P waves or no p waves

-specifically in AV junction

-40 bpm

-qrs complex is usually narrow

junctional rhythm with 60-80 bpm

junctional rhythm with bpm greater than 100

-early beat

-inverted p wave

-no p wave but room for one

-triggered by an ectopic pacemaker

-extremely rapid atrial rate - 300

-no discrete p waves - flutter waves occur in a sawtooth like pattern

-everyhing seen between qrs complexes looks identical

-rarely seen in normal hearts

-atria firing at very rapid rate, about 600x a min

-every once and a while an impulse gets to AV junction and goes through very smoothly

-irregular ventricular rate

-irregular wavy baseline, no p waves, no atrial contraction

-can occur in normal or diseased hearts

-can be chronic or priodic

-atrial depolarization is lost

-pharmacologically

-cardioversion

-ablation

-temporary and reversible reduction in blood supply to the myocardium

-leads to ST segment depression

-transient or chronic

-if chronic it leads to tissue death which leads to myocardial infarction/heart attack

-Complete necrosis of an intire thickness of a portion of LV wall.

-characterized by changes in myocardial repolarization and myocardial depolarization

innapropriate sensing of extraneous electrical signals

-EKG

• PM spikes at a slower rate than the preset rate

-every cycle

-100% capture

-tall peaked T waves, generally taller than qrs comlex

-prolonged QT interval with prominent U wave

-low voltage t waves

-decreased qt intervals

-shorter st segments

-prolonged qt intervals

-prolonged st segments

-CHF

-increase in inoptropic (contractility) of heart

EKG

• decreased qt interval
• scooping of ST-T complex
• fuses st segment and t wave together (hard to tell where one begins and the other ends)

-inflammation of pericardium

• chest pain radiating to the back and relieved by sitting up forward and worsened by lying down (classical presentation)
• st elevation in alll leads except V1 and AVR
• T wave upright in leads with elevation
• often misdiagnosed as an MI

-pre-excitatoin syndrome

• additional conduction pathway (other than SA AV)
• electrical signal may arrive at the ventricles too soon
• delta wave produced on ekg, short pri

tachycardia, dizziness, SOB, chest, palpitations, syncope or rarely cardiac arrest.