DfDx AV nodal reentrant tachycardia. In yellow, is evidenced the P wave that falls after the QRS complex.

LBBB: QRS >0,12 sec, Biphasic R peaks R and R' in leads II and V6, large late negative deflections in V1 Broad monomorphic R waves in I and V6 with no Q waves Broad monomorphic S waves in V1, may have a small r wave conduction in the left bundle is slow delayed depolarization of the LV, especially the left lateral wall.

The late electrical activity in the left lateral wall is unopposed by the usual right ventricular electrical activity. the last activity on the ECG goes to the left or away from V1

RBBB: QRS >0,12 sec, Slurred S wave in lead I and V6, Watch V1: RSR'-pattern where R' > R conduction in the right bundle is slow. As the RV depolarizes, the LV is often halfway finished and little counteracting electrical activity is left.

In RBBB the QRS complex in V1 is always markedly positive. RBBB is a common (13.5% of healthy individuals) The last electrical activity is thus to the right, or towards lead V1.

Hypercalcemia: High blood calcium, speeds repolarization, short QT interval widened T wave suggest hypercalcaemia.

Mild: broad based tall peaking T waves Severe: extremely wide QRS, low R wave, disappearance of p waves, tall peaking T waves. Causes: Primary hyperparathyroidism and malignancy account for about 90% of cases

Significant hypercalcaemia can mimic an acute myocardial infarction. Hypocalcemia: Narrow QRS, Reduced PR interval, T wave flattening and inversion, Prolongation of the QT-interval, Prominent U-wave, Prolonged ST and ST-depression

Hyperkalemia: wide, low amplitude P-waves, slowing of conduction QRS: widening, fusion of QRS-T, loss of the ST segment, Tall tented T waves Causes: acidosis and during Class IC anti-arrhythmic intoxication.

At concentrations > 7.5 mmol/L atrial and ventricular fibrillation can occur Hypokalemia: ST depression and flattening of the T wave, Negative T waves, A U-wave may be visible

Hypothyroidism: characterized by low voltages, ST deviation or T wave inversions across most or all leads,

+sinus bradycardia. presented with profound fatigue Hyperthyroidism: Can be characterized by a sinus tachycardia.

Also in new onset atrial fibrillation, a TSH should be checked as part of the routine workup

Pericarditis: ST elevation in all leads important to distinguish pericarditis from MI

Pericarditis: ST elevation in all leads. PTa depression, inverted T-waves (in early pericarditis STE in all leads except rightward leads (aVR, V1 and III))

MI: has more acute complaints and ST-elevations are limited to the infarct area.

Pericardial Effusion/ Tamponade: Low Amplitude Sinus Tach with Electrical Alterans

= QRS of erratic morphology due to changing fluid impedance

Ischemia: lack of oxygenation, ST depression or T wave inversion (lead specifc)

Injury: prolonged ischemia, ST segment elevation (lead specific)

Infarct: death of tissue, STE + Pathological Q wave

1. Any Q wave (downward deflection) in leads V2V3 0.02 s

2. A Q-wave lasting longer than 0.03 s and > 0.1 mV deep in leads I, II, aVL, aVF, or V4V6

3. R-wave (upward deflection) lasting longer than 0.04 s in V1V2

Quick Diagnostic Findings

Inverted P-Waves: Ectopic Atrial Rhythm

Shortened QT interval: Hypercalcemia, some drugs, certain genetic abnormalities, hyperkalemia Prolonged QT interval: Hypocalcemia, some drugs, certain genetic abnormalities Flattened or inverted T waves: Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs

Hyperacute T waves:1st manifestation of aMI, where T waves become more prominent, symmetrical, and pointed Peaked T wave, QRS wide, prolonged PR, QT short Hyperkalemia, treat with calcium chloride, glucose and insulin or dialysis T-Wave Inversion: coronary ischemia, left ventricular hypertrophy, or CNS disorder, hypothyroidism

Prominent U waves: Hypokalemia Wave Definations Q wave is any downward deflection after the P wave. R wave follows as an upward deflection S wave is any downward deflection after the R wave T-Wave is concordant with QRS (AUC QRS is AUC under T-wave is

U wave is typically small, follows the T wave, repolarization of the papillary muscles or Purkinje fibers

Hypokalemia, Hypercalcemia, Hyperthyroidism

Drugs: Digitalis, Epinephrine, Class 1A & 3 Antiarrhythmics

Congenital Long Qt Syndrome, Intracranial Hemorrhage.

Myocardial ischemia or LV overload.

Acute CNS Event

Ectopic Atrial Rhythm

Severe Hyperkalemia

Mild Hyperkalemia

Pericarditis

II AVB type 2

Non-Sustained VT

LBBB

Ischemia with lead specific T-wave inversion

Hypothyroidism

V5 AVNRT

II AVB type 1

Idioventricular Rhythm

Prolonged QT

Junctional Brady

No Q Waves

Acute Inferior Wall Injury and Infarct

Paced Atrial

III AV Block

Fisrt Degree AV Block

Paced Ventricular

V1 --> looks like letter M Right bundle branch block

Hypothyroidism --> Mild hyperkalemia --> big T waves Severe hyperkalemia --> tall R waves??

Hypercalcemia --> shortened QT interval

T waves are almost as tall as R waves Diagnosis: mild hyperkalemia

R waves are less than 10 small boxes tallRate is fast >120bpmDiagnosis: Pericardial eusionLung cancer in males and breast cancer in females with pericardial eusion until proven otherwise

PVC --> no P wave before that, wide QRS PAC --> narrow QRS following P waveIf rate is slow or ST elevations w smily faces --> early repolarization

Diagnosis: left bundle branch blockV6 --> monophasic predominantly upright Discordant T wave changesV1 --> QS pattern w no R wave

Hypothyroidism and pericardal effusion have same EKG

but hypothyroid is NSR and effusion is tachy

More than 3 in a row and less than 10sec --> nonsustained tachy

Idioventricular rhythm --> typically slower than junctional (can't tell by rate alone)Junctional --> would have narrow QRSRate is slow, QRS is not wide (Ventricular escape rhythm and idioventricular would have wide QRS)

ischemia: T wave inversions (not lead specic) ST elevation

Mobitz 1 Txt --> give atropine

Early activation in WPW --> preexcitationWidened QRS with short PR intervalOriginates in atria and conducted through bypass tract which is why they are wide NOT PVCs

CNS event Prolonged QT with negative T waves

Narrow QRS complexes2 large box btwn R waves --> rate = 150 P waves are after QRSAtrial b --> RR would change Ventricular tachy --> QRS would be wide ANSWER: AV nodal reentrant tachy

AMC ECGs