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EKG

Terms in this set (58)

Differential diagnosis of ST elevations
1) ischemic heart disease (MI, Prinzmetal angina, ventricular aneurysm)
2) pericarditis
3) left bundle branch block (LBBB) (in V1-V3)
4) normal ("early repolarization") variant (J point elevation)
Pericarditis
1) Diffuseness ST elevations
2) PR segment displacement which has been attributed to subepicardial atrial injury
Wandering pacemaker
Irregular rhythm produced by pacemaker activity from wondering SA node to near by atrial automaticity foci

Produces
- Cycle length variation
- variation in P' wave shapes

Rate is within normal range

Each P' wave have distinct shape related to anatomical location of that focus within the atira
Multifocal atrial tachycardia
Like wandering pacemaker, but rhythm is > 100 bpm

An arrhyhmia of patients who are very ill with COPD
- Also sometimes seen with Digi toxicity
Atrial escape rhythm
When an atrial focus assumes pacing responsiblity in the absence of a sinus rhythm
Junctional escape rhythm
Every paced stimuli will depolarize the ventricles

Pacing may also depolarize the atria from below in a retrograde fashion
- Produces inverted P' waves in EKG lead with an upright QRS
Preventricular beats
Cardiac parasympathetic innervation inhibits the SA node and also inhibits the atrial and junctional foci, but NOT the ventricular foci. Hence, a burst of excessive parasympathetic activity depresses SA Node and also depresses the atrial and junctional foci, but not ventricular foci, leading to these.
Atrial and junctional foci become irritable because of
- Adrenaline released by adrenals
- Increased sympathetic stimulation
- Presence of caffeine, amphetamines, cocaine, or other beta1 receptor stimulants
- Excess digitalis, some toxins, occasionally ethanol
- Hyperthyroidism
- Stretch
- O2 to some extent
Premature atrial beat (PAB)
Because an atrial focus is the origin of this premature atrial depolarization, the stimulus produces a premature and unusually shaped P' wave that does not look like normal P waves
Aberrant ventricular contraction
Premature atrial beat can produce these if one of the Bundle Branches is not completely repolarized, producing a widened QRS
"Non-conducted" PAB
Does not depolarize the ventricles

Does depolerize the SA Note
- Resets pacemaking once cycle length
- Creates harmless, but dangerous-looking span of empty baseline
-- Looks like "some-kind-of-block" but is actually harmless
Atrial Bigeminy
PAB that couples to the end of a normal cycle
- Repeats this process by coupling a PAB to the end of each successive normal cycle
Ventricular foci become irritable because of
Low O2
- Airway obstruction
- Absence of air
- Air with poor O2 content
- Minimal blood oxygenation in lungs (PE, pneumo)
- Reduced cardiac output (Hypovolemic / cardiogenic shock)
- Poor to absent coronary blood supply (MI)

Low K+
Pathology (Mitral valve prolapse, myocarditis)
Premature ventricular contraction
Occur early in cycle
Has enormous amplitude (height and depth)
Usually opposite the polarity of normal QRS's

Does not depolarize the SA node, but usually ventricle is still repolarizing upon firing of sinus node discharge
- "compensatory" pause
Pathological PVC's
> 6 PVC's in one minute

Do not ignore
- Look for reason of poor oxygenation
Ventricular parasystole
Ventricular automaticity focus that suffers from entrance block (but is not irritable)

Not vulnerable to overdrive suppression so it paces at its inherent rate
Sustained VT
A run of ventricular tachycarida that lasts longer than 30 seconds
MVP
Have a mid-systolic click

Can cause PVC's and runs of VT and multifocal PVC's

Considered benign
R on T phenomenon
PVC falls on a T wave
- Can lead to dangerous arrhythmias
-- Especially in situation of hypoxia or low serum potassium
Paroxysmal
Sudden
Paroxysmal Supraventricular Tachycardia
Very irritable automaticity foci that produce both Paroxysmal Atrial Tachycardia and Paroxysmal Junctional Tachycardia originate abotinve the ventricles
Sick Sinus Syndrome
Wastebasket of arrhythmias caused by SA Node dysfunction with unresponsive supraventricular (atrial and Juncitonal) automaticity foci which are dysfunctional and can't employ their normal escape mechanism to assume pacing responsibility
First Degree AV block
PR interval more than one large square (.2 sec)
Wenchkebach (Type II) AV block
Progressive blocking of A node conduction until the final P wave is totally blocked in the AVE node, eliminating the QRS response

Benign
Mobitz (Type II) block
A series of normal PQRST cycles preceded by a series of paced P waves that fail to conduct through the AV node

Pathological
Differentiate 2:1 Wenchkebach from Mobitz
Vagal maneuvers

For mobitz these should eliminate the block

AV node supplied by parasympathetic, so vagal maneuver inhibit the AV node
PR Interval
Increased consistently in first degree AV block

Progressibely increases in each series of cycles with Wenchebach

Totally variable in third degree AV block

Deceases in WPW
Third degree AB block
Total block of conduction to the ventricles, so atrial depolarizations are not conducted to the ventricles. So, automaticity focus below the complete block escapes to pace the ventricles at its inherent rate
Adams-Stokes disease
Sudden collapse into unconsciousness due to a disorder of heart rhythm in which there is a slow or absent pulse resulting in syncope (fainting) with or without convulsions

Third degree AV Block
Right chest leads
V1 & V2
Left chest leads
V5 & V6
Intermittent episodes of complete AV block (Intermittent Mobitz)
RBBB plus intermittent LBBB will record on EKG as continuous RBBB pattern QRS's with _the answer to this question_

Similarly, LBBB plus intermittent RBBB will record on EKG as continuous LBBB pattern QRS's with _the answer to this question_
Short QT
Two chief causes of are
1. hypercalcemia
2. digoxin therapy
Diffuse deeply inverted T wave
1. CNS disease
2. Apical hypertrophic cardiomyopathy
3. Intermittent right ventricular pacing or intermittent LBBB
4. Takotsubo

Pericarditis - relatively low amplitude (usually <5mm)
Axis deviation
Occurs in the frontal plane
Axis rotation
Occurs in the horizontal plane
Right ventricular hypertrophy
Large +ve R wave in V1

S wave in V1 smaller than R wave

qR in V1

The large R wave in V1 becomes progressively smaller in leads V2, V3 & V4
Left ventricular hypertrophy
Tall +ve R wave in V5

Deep, -ve S wave in V1

Add depth of S wave in V1 to height of R wave in V5

mm of S in V1 + mm of R in V5 > 35 mm = LVH

Inverted T wave with gradual downslope and steep return to baseline in V5 & V6 (Asymmetric T wave inversion)
Ventricular strain
Characterized by depression of the ST segment

Right Ventricular Strain - ST depression in V1
Left Ventricular Strain - ST depression in V5
V1 and hypertophy
Check V1 to see if P waves are diphasic

Check R wave in V1 and S wave in V1
Symmetrically inverted T wave
Characteristic sign of ischemia

Can be seen transiently during episodes of angina

Check V1 t0 V6 since these are nearest the ventricles, so changes are most pronounced in them

Minimal inversion can me normal in limb leads, but is always pathological in leads V2 - V6
Brugada syndrome
RBBB and ST elevation in leads V1 to V3

Elevated ST segments have a peculiar peaked downsloping shape (Particularly in V1 and V2)
ST Depression Causes
1. Subendocardial infarction
2. +ve stress test
3. Digitalis
Significant Q wave
One small square wide (.04)
1/3 the amplitude of the entire QRS complex

Look for in all leads except AVR
Always check V1 and V2 for
1. S elevation and Q waves (Anterior infarct)

2. ST depression and large R waves (Posterior infarct)
Posterior infarct
Large R in V1, V2
Maybe Q in V6

RCA
Lateral infarct
Q in I, AVL

Circumflex branch of LCA
Anterior infarct
Q in V1, V2, V3 or V4

LAD
Inferior infarct
Q in II, III, AVF

RCA or Circumflex depending on dominance (90% RCA)
RCA
Renders blood supply to
1. AV Node
2. Bundle of His
3. Variable twig to the posterior division of the left bundle branch
Anterior Hemiblock
1. Left axis deviation
2. Normal/slightly widened QRS
3. Q1S3 (Q in lead I, wide/deep S in lead III)

Must r/o pre-existing sources of left axis deviation
EG. Left Ventricular Hypertrophy, Horizontal heart, Inferior infarction
Posterior Hemiblock
1. Right axis deviation
2. Normal/slightly widened QRS
3. S1Q3 (deep S in lead I, Q in lead III)

Must r/o pre-existing sources of right axis deviation
EG. Slender body (vertical heart), Right ventricular hypertrophy, pulmonary disease
QRS complex
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
Right atrial hypertrophy
Diphasic P wave in V1

Initial component of P wave is the larger one
Left atrial hypertrophy
Diphasic P wave in V1

Terminal component of P wave is the larger one
Rheumatic mitral stenosis
Combination of RVH and marked left atrial abnormality (LAA)
Hypokalemia
Diffuse T wave flattening or inversions, and markedly prominent U waves
Differential diagnosis of tall right precordial R waves
1) Normal/positional variants
2) Right ventricular hypertrophy (RVH) (look for right axis deviation, P pulmonale)
3) Posterior/lateral MI (usually signs of inferior MI, too)
4) hypertrophic cardiomyopathy/idiopathic hypertrophic subaortic stenosis (HCM/IHSS)
5) right bundle branch block (RBBB)
6) Wolff-Parkinson-White (WPW ) variants with posterior/lateral pre-excitation
7) Duchenne muscular dystrophy (young men with myopathy).
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