EKG PPT

Paroxysmal Supraventricular Tachycardia (PSVT)

Narrow complex tachycardia (QRS < 0.12 sec) 150-250 bpm Usually no P waves (hidden within T waves) Tx: vagal maneuvers initially; if that doesn't work, tx with adenosine. If THAT doesn't work, try beta blockers or CCBs.

Undersensing

Pacemaker fails to recognize depolarization (does not matter if it is intrinsic or pacemaker mediated). Pacemaker thinks it needs to fire so it does. ECG: Spike seen earlier than it should be. Capture may be present. (sometimes the electricity makes the heart depolarize and you see a wave) Sensitivity threshold too low, pacing catheter on infarcted tissue

Oversensing

Pacemaker is too sensitive and thinks depolarization has taken place when it has not. Does not think it needs to participate. Example: It may think a T wave is depolarization. Use an index card with paced intervals marked to see what pacemaker thought was depolarization. ECG: paced beat that occurs later than expected. -sensitivity is set too high

Failure to Capture

Pacemaker releases stimulus but heart does not depolarize. ECG: Spike seen but there is not an associated p wave (A-pacing) or QRS complex (v- pacing). -output too low, lead out of position, lead on infarcted tissue, electrolyte imbalance

Failure to Fire

Pacer maker does not deliver stimulus ECG: See pattern of firings with QRSs. Then asystole with no impulse. Then previous pattern resumes. -Dead battery, faulty connection, electromagnetic interference (cautery tool), turned off

Sinus Rhythm

60-100 bpm Regular (some variation with respiration) Positive P waves in lead 2 1 P wave preceding each QRS complex PR interval: 0.12-0.20 sec (3-5 little squares) QRS complex < 0.12 sec (3 little squares)

Acute Inferior MI

Acute Inferior MI Diaphragmatic surface of heart Often occlusion of Right Coronary Artery Characteristic EKG changes seen in inferior leads II, III, and aVF

Evidence of Prior Myocardial Infarctions

Acute MI: need to see changes in 2 contiguous lead; changes: ST elevation, inverted T wave, or q waves development

Hypocalcemia Causes:

Anticonvulsants, bisphosphonates, calcitonin, corticosteroids, diuretics, hypoparathyroidism, pancreatitis Class I and III antiarrhythmics cause QT prolongation Amiodarone has the least potential for causing a prolonged QT interval

Ventricular Fibrillation

Chaotic irregular deflections of varying amplitude No identifiable P waves, QRS complexes, or T waves Rate 350 to 500 per minute Amplitude decreases with duration (coarse VF -> fine VF)

RBBB

In RBBB, activation of the right ventricle is delayed as depolarization has to spread across the septum from the left ventricle The delayed right ventricular activation produces a secondary R wave (R') in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads. Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads.

Sinus Tachycardia

Narrow complex (aka QRS complex < 0.12 sec) Narrow Tachycardia can originates from the atria, AV junction or SA node (sinus only comes from SA node) Same as sinus rhythm except rate 100-160 bpm @ rest

Left Bundle Branch Block

LBBB - The overall direction of depolarization (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis deviation. As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched ('M'-shaped) R wave in the lateral leads. The R wave in the lateral leads may be either: M shaped, Notched, Monophasic

MOST MI involve

Left Ventricle (does most work = most vulnerable)

Acute Anterior Lateral MI

Left anterolateral wall of heart Often occlusion of circumflex artery Changes will occur in left lateral leads I, aVL, and V5 and V6 ST elevation in I and aVL Loss general R wave progression across precordial leads

Acute Pericarditis

May cause diffuse ST segment elevation & T wave flattening/inversion Note: MI will NOT have a diffuse ST segment elevation T wave inversion usually only occurs after ST segments have returned to baseline NO Q wave formation PR interval may be depressed

...........................more likely than Wenckebach to progress to a complete heart block

Mobitz type II

Atrial fibrillation

Narrow complex irregularly irregular tachycardia. No P waves. Irregular baseline. Atrial rate greater than 350. Ventricular rate irregular; may be fast (rapid ventricular response), moderate (rate controlled), or slow.

Heart Blocks: 1st Degree Heart Block

Narrow Complex QRS 1:1 ratio of P waves to QRS complexes Prolonged PR interval >.20

2nd Degree Heart Block: Type 1: Wencheback

Narrow QRS complex Atrial rate regular Ventricular rate irregular Progressive prolongation of the PR interval until QRS complex is dropped The PR interval is shortest immediately after the dropped beat

Accelerated Junctional Rhythm

Originates in an ectopic pacemaker site in the AV junction at a rate of 60 to 100 beats/minute. The term accelerated denotes a rhythm that occurs at a rate faster than the inherent junctional rate of 40 to 60 beats/minute, but that isn't fast enough to be junctional tachycardia. Accelerated junctional rhythm is a regular, continuous rhythm characterized by an inverted P wave that may occur before the QRS, after the QRS, or be hidden within the QRS complex; a short PR interval of 0.10 second or less; and a normal QRS complex.

Junctional Rhythm

P-wave-inverted on lead II,III, aVF QRS complex-normal Rate <60

Premature Atrial Contraction (PAC)

Premature heartbeats originating in the atria Occurs when a region in the atria other than the SA node depolarizes and causes a contraction Usually no tx required and pts are asymptomatic, but can report feeling "skipped beat", "flutter", "jolt" in the chest P wave may appear abnormal (bc originates from somewhere that is not the SA node) Followed by normal narrow complex QRS If aberrantly conducted then the QRS can be wide

Prior MI:

Presence of significant Q waves suggest old MI

EKG Manifestations of Hyperkalemia

Produces a progressive evolution of changes in EKG that can culminate in ventricular fib. And death. Presence of EKG changes is better measure of significant K+ toxicity than the serum K+ level. First sign: T waves across entire EKG begin to peak, changes are diffuse. Continued increase in K+: PR interval becomes prolonged and P wave gradually flattens and disappears (b/c of paralysis of atria). Ultimately -> QRS complex widens merging with T wave forming a sine wave pattern (like ocean waves). VFib. may develop. Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on hamodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements. Difference from peaked Ts in MI: MI: The Ts will only be in the affected leads. In hyperkalemia: they would be widespread.

EKG Manifestations of Hypocalcemia Effects:

Prolonged QT interval (>0.5s) Can lead to Torsades (but more common with low K+ or Mg2+) Rate will frequently be fast: near 300bpm (b/c of Torsades) treated with IV magnesium and increasing the heart rate

Atrial flutter

Regular (usually) or irregular narrow complex tachycardia. If irregular, will have different numbers of flutter waves before consecutive QRS complexes. Atrial rate between 250 - 350. Ventricular rate is a multiple of the atrial rate. Ex: 2:1 conduction would have atrial rate 300 and ventricular rate 150.

Idioventricular Rhythm

Regular rhythm 20-40 bpm Absent P wave Wide QRS

SINUS BRADYCARDIA

Regular rhythm HR < 60 bpm

Acute Anterior Septal MI

ST elevation, Q wave formation, and T wave inversion in V1, V2 +/- V3 A bit of the anterior descending artery

EKG Manifestations of Hypokalemia

ST segment depression Flattened T wave Prolonged QT interval May be a U wave- but not diagnostic Seen in anterior leads

Sinus Rhythm w/Bundle Branch Block (BBB)

Sinus rhythm = rate 60-100 bpm BBB = conduction of electrical impulse through one of the bundle branches is abnormally delayed → wide QRS complex (> 0.10 sec)

PREMATURE VENTRICULAR CONTRACTIONS

Sinus, then wide complex before next scheduled beat w/o a P wave QRS will be much larger than normal

Left Ventricular Hypertrophy

The left ventricle hypertrophies in response to pressure overload secondary to conditions such as aortic stenosis and hypertension R wave in V4, V5 or V6 > 26 mm ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular 'strain' pattern Left Axis deviation (sometimes)

3rd Degree Heart Block

There is no AV conduction Ventricular rate <60 bpm More P waves than QRS complexes P waves are regular P - P will be the same (here the 2nd P wave is in the T wave) PR interval varies QRS complex ----Narrow or wide

2nd Degree Heart Block- Mobitz type II

Ventricular rate is regular & multiple of atrial rate More Ps than QRS complexes PR interval constant QRS Complex ---Narrow or Wide depending on site of block Likely wide b/c block occurs in the His bundle or bundle branches and conduction through the ventricles is slowed

Polymorphic Ventricular Tachycardia (Torsades)

•Regular rate 140-250 beats per min •No P waves •PR interval not measurable •Wide QRS Complexes with different morphologies in the same lead -QRS Complexes "twist" around the isoelectric line •Usually seen in patients with prolonged QT intervals

Monomorphic Ventricular Tachycardia

•Regular rhythm. Rate 140-250 beats per min •No P waves •PR interval not measurable •Wide QRS Complexes with the same morphology in a given lead •ST segment and T wave slope in opposite direction of QRS deflection