EKG

SA node

natural pacemaker @ 60-100 bpm

AV node

inherent firing rate 40-60 bpm

his-purkinje

inherent firing rate 30-40 bpm

EKG graph

5 large squares = 1 sec

12 lead EKG

standard most all encompassing, 12 different patterns to determine where problem is

5 lead EKG

white on the right, clouds over grass, smoke over fire, i heart chocolate

p wave

depolarization of both atria

PR interval

p wave and isoelectric line that respresents slight AV node conduction delay to allow atria to eject blood into ventricles

QRS complex

ventricular depolarization, very fast

ST segment

isoelectric line that should run parallel to PR interval, correlates directly to MI

STEMI

ST segment elevated, relaxation not happening
complete occlusion that requires emergent management to reperfuse with thrombolytics/PCI
tombstoning = widow maker

NSTEMI

incomplete occlusion that requires monitoring and non-thrombolytic mgmt to increase perfusion, less emergent

t wave

repolarization of both ventricles, influx of potassium and efflux of sodium

long QT syndrome

most likely congenital but also linked to acquired elongation from meds, electrolyte imbalances, other heart disease, and neuro conditions
longer than normal recovery, can alter myocardial efficiency

RR intervals

distinguishes regularity of rhythm
regular: < .12 sec discrepancy
irregulary: > .12 sec discrepancy, indicator of ventricular depolarization variance

reasons for EKG inaccuracies

muscle contractions or movement, hair or skin conditions, loos electrode placement

sinus tachycardia

> 100 bpm from exercise or stimulant induced

sinus bradycardia

< 60 bpm from physiologic adaptation to high level training, vagal stimulation, sick sinus syndrome

sick sinus syndrome

sinus pause, block, arrest, or dysfunction
temporary cessation of electrical impulse generation by the SA node, resulting in a pause in the heartbeat
regular RR interval but occasional pauses
from meds or congenital

premature atrial complex

extra beat generated by atria prior to normal SA node impulse
p wave different in premature beat, t wave may be buried, RR interval pause or irregularity, HR varies
from imbalances in electrolytes, AV node issue

atrial tachycardia

multiple consecutive PACs in a brief or sustained pattern
abnormal p wave with hidden or merged t wave, RR interval varies, HR 100-200+ BPM
from congenital, stress after surgery

atrial flutter

rapid succession of atrial depolarization due to cyclic electric uptake
p wave sawtooth pattern and multiple before each QRS, RR interval varies, HR 250-350 bpm
from alterations to sympathetic input or electrolyte balance

atrial fibrillation

erratic quivering or twitching of atria without depolarization while AV node determines ventricular response
p wave absent, RR interval irregular
< 100 bpm controlled afib, 100-120 uncontrolled afib, > 120 bpm rapid ventricular response afib
from alterations to sympathetic input or electrolyte imbalance

afib implications

dec CO by 20%, significant inc risk of blood clots due to coagulating of blood in atria

afib mgmt

anticoagulation, surgery, thrombolytics

premature ventricular complex

ectopic focus generated by ventricles prior to normal SA node impulse
p wave absent in premature beat, QRS wide and bizarre, ST segment and T wave slope in opp direction

types of PVC

bigeminy: every other beat
trigeminy: every 3rd beat
unifocal: identical appearance
multifocal: multiple unsimilar PVCs
couplet: two in a row
triplet: 3 in a row

PVC implications

paired together, multifocal, > 6 per min, land on t wave, present in triplets evolving into vtach

ventricular tachycardia

rapid fire from ventricular focus, dec CO and BP
weak, thready pulse associated with lightheadedness, syncope, disorientation
medical emergency, high risk evolving to vfib
wide and bizarre QRS, 100-250 bpm

torsade de pointes

unique vtach configuration, twisting of the points, caused by long QT syndrome

ventricular fibrillation

erratic quivering of ventricular muscle with zero CO, requires immediate defibrillation and CPR

1st degree AV heart block

impulse delay from SA to AV node or prolonged AV conduction time, PR interval > .2 sec
relatively benign

2nd degree heart block type I (Wenckebach or Mobitz)

AV junction disturbance prevents impulse conduction
p wave standalone seen due to dropped QRS, PR interval progressive lengthening, RR interval irregular, HR varies

2nd degree heart block type II (Mobitz)

bundle of his or branch block reduces conduction
2-4 p waves present for every 1 QRS, PR interval normal, RR interval varies, HR brady
risk of evolving into 3rd degree

3rd degree heart block

complete, no impulses conducted to the ventricles
atria and ventricles fire at own inherent rates, no synchronization
p wave no relation to QRS, QRS longer, HR dependent on ventricular firing so 30-50 bpm

paced rhythm

spikes correlate to impulse that initiates depolarization
HR dependent on mode and settings