Interpretation of EKG's
Five Cardinal Features

(1) Rate

(2) Rhythm – including intervals

(3) Axis

(4) Hypertrophy

(5) Infarction

Rate

Three ways to determine rate:

(1) count number of thick lines that occur between QRS complexes: 300 if next QRS on thick lines, 150 if 2^nd, 100 if 3^rd, then 75, 60, 50

say: "300, 150, 100" "75, 60, 50" as counting thick lines
can also use thin lines (thick lines bolded): 300, 250, 214, 187, 167; 150, 136, 125, 115, 107; 100, 94, 88, 83, 79; 75, 71, 68, 65, 62; 60

(2) if bradycardic (less than 60 bpm) or irregular: count 6 second strip (2 3-second marks) and multiply by 10

can also count entire strip (10 seconds) and multiply by 6

(3) calculate: 1500/number of small lines between similar waves

must determine coexisting independent rates if there are more than one

Rhythm

Automaticity – heart has automaticity foci that respond at different rates and produce different morphology on EKG

atrial – preceeded by P wave (shape of P wave changes depending upon originating focus), narrow complex QRS, normal rate 60-80/min
junctional – no P wave, narrow QRS, normal rate 40-60/min
ventricular – no P wave, wide QRS, normal rate 20-40/min

Intervals

PR should be less than 0.2 seconds (one large square)
QRS should be less than 0.12 seconds (three small squares)
QT interval – must be corrected for rate (QTc); in general, QT should be less than half R-R interval

Sinus Rhythm – P before each QRS, QRS after each P, P in correct orientation (up in II)

normal sinus rate is 60-100 bpm; if sinus rhythm but greater than 100 bpm, it is sinus tachycardia; if less than 60 bpm, it is sinus bradycardia

Irregular Rhythms

Sinus Arrythmia – varies with respiration, P waves identical; not pathological

Wandering Pacemaker – irregular rhythm, P waves change shape, rate less than 100 bpm

Multifocal Atrial Tachycardia – same as wandering pacemaker with rate greater than 100 bpm

Atrial Fibrillation – irregular ventricular rhythm without P waves; may see erratic atrial spikes or wavy baseline

Escape – lower level of heart will automatically respond if not driven with faster rate from above (automaticity)

Escape Beat – single beat after a pause; can be atrial, junctional, or ventricular

ventricular escape beats can be caused by burst of excessive parasympathetic activity (parasympathetic innervation inhibits SA node and AV junction but NOT ventricular tissue)

Escape Rhythms – persistent escape beats (sinus node not active or not conducting); can be atrial, junctional ("idiojunctional" rhythm), or ventricular ("idioventricular" rhythm)

idiojunctional rhythms can produce retrograde atrial depolarization with an inverted P' before, during, or after the QRS
idioventricular rhythms caused by complete block below AV junction (P waves present but not associated with QRS) or total failure of all tissue above ventricles (downward displacement of the pacemaker)

idioventricular rhythms can cause loss of consciousness due to insufficient cardiac output (Stokes-Adams Syndrome)

Premature Beats – from an irritable automaticity focus; can be atrial (PAB), junctional (PJB), or ventricular (PVC; 6 PVC's per minute is pathological)

PAB/PJB – irritable atrial and junctional foci are caused by sympathetic stimulation, caffeine, amphetamines, cocaine, digitalis, toxins, ethanol, hyperthyroidism, and stretch receptors

PAB resets from the new P' wave at previous rate (first cycle slightly lengthened due to transient baroreceptor reflex)
PAB's can cause wide QRS (aberrent ventricular conduction)
PAB and PJB still depolarize the SA node (either directly or through retrograde atrial depolarization) and reset the pacing, so rhythm begins again in phase with the premature beat
if the beat is not conducted (due to refractoriness), the missed QRS in produces a long empty baseline (harmless)

can occur every other beat (atrial or junctional bigeminy) or every third beat (atrial or junctional trigeminy)

PVC – irritable ventricular foci are caused by low oxygen, hypokalemia, or muscle pathology (mitral valve prolapse, myocarditis, etc.)

PVC's do not depolarize the SA node, so there is a "compensatory" pause after them (except for "interpolated" PVC's, where they occur exactly where the ventricular contraction would have)

P waves continue unaffected and the next QRS occurs where it would have if there had been no PVC

a PVC that falls on a T wave ("R on T phenomenon") can cause sustained ventricular tachycardia

ventricular parasystole – ventricular tissue with entrance block (NOT an irritable focus) that starts PVC's at its own automatic firing rate

Tachyarrhythmias

Paroxysmal tachycardia – 150-250 bpm; can be atrial (PAT), junctional (PJT), or ventricular (PVT)

atrial (PAT) or junctional (PJT) are also called paroxysmal superventricular tachycardia (PSVT)

paroxysmal atrial tachycardia with block (PAT with more than one P wave before each QRS) – caused by digitalis

AV nodal reentry tachycardia (AVNRT) is a type of PJT
PJT may still have retrograde atrial depolarization and inverted P' waves
PJT may involve somewhat widened QRS since one bundle branch may still be refractory when next beat arrives (aberrent ventricular conduction)

PVT:

during PVT, if the P wave appears at just the right time, can see normal QRS (capture beat) or QRS that degenerates into a PVC (fusion beat)
PVT can be distinguished from PSVT with wide QRS (caused by BBB, etc.) by the following:

presence of coronary artery disease
very wide QRS (more than 0.14 sec)
extreme RAD
AV dissociation (see capture or fusion beats)

Torsades des Pointes – "party streamer"; caused by two competitive, irritable foci in different ventricular areas

Flutter – 250-350 bpm; can be atrial (sawtooth baseline with QRS's) or ventricular (sine wave; almost always leads to fibrillation unless treated)

Fibrillation – greater than 350 bpm; can be atrial (jagged baseline with QRS's) or ventricular (no identifiable waves)

no pumping occurs
atrial fibrillation can produce a narrow-complex tachycardia (rapid ventricular response)

Block – identify by pauses (sinus block), abnormal PR intervals (AV blocks), abnormal QRS interval (bundle branch block), or axis deviation (hemiblock)

Sinus Block – spontaneous pause in electrical activity; can restart automatically or have an escape beat (see above)

AV Block – causes abnormal PR interval

1^st degree block – PR too long (greater than 0.2 seconds, or one large square)

2^nd degree block – some P waves without QRS:

Wenkebach (Mobitz I) – block at the node itself; PR gradually lengthens until a P does not produce a QRS

Mobitz II – block beyond the node; PR length constant, but some P waves do not produce QRS (can be 2:1, 3:1, etc., or even intermittent)
2:1 block can be either of above; can use vagal maneuvers to differentiate (see below)

3^rd degree block – none of the P waves get through; there is an idioventricular or idiojunctional rate instead

Bundle Brach Block – basically two out of phase QRS's (R R'); requires wide QRS for diagnosis (at least 3 small squares; best to use limb leads since low voltages allow for more accurate measurement)

Right Bundle Branch Block (RBBB) – QRS has two peaks (R R') in V₁ or V₂ usually returning to lower than baseline between them

Left Bundle Branch Block (LBBB) – QRS has two peaks (R R') in V₅ or V₆ with slight depression between them
BBB makes ventricular hypertrophy criteria unreliable
LBBB makes infarction difficult to determine
BBB can cause SVT to degenerate more easily into VT

Hemiblock – block of anterior or posterior fascicle of LBB; causes axis deviation and widened QRS

Anterior hemiblock – left axis deviation with a Q wave in I and a prominent S wave in III

Posterior hemiblock – right axis deviation with a prominent S wave in I and a Q wave in III
can have bifascicular blocks (RBBB + hemiblock)
must have previous EKG to diagnose so that other causes of axis deviation can be ruled out

Vagal Maneuvers (gagging or carotid sinus massage) – inhibit irritable atrial or junctional foci or increase the refractoriness of the AV node

abolishes PSVT, identifies 2:1 AV block (no effect if Mobitz II), and reveals flutter waves in atrial flutter

Axis

find axis quadrant using below diagram (QRS above or below baseline in each lead):

axis is also 90 degrees from isoelectric QRS (same up as down) or in the direction of a QRS that only goes up (opposite direction of QRS that only goes down)

Normal axis is "up in I and aVF" (some say "up in I and II")

if I is down: right axis deviation (RAD)
if aVF is down: left axis deviation (LAD)
if both are down: extreme RAD

Axis Rotation – find isoelectric QRS (same up as down) in chest leads (V₁ to V₆); normally occurs in V₃ or V₄

if isoelectric in V₁ or V₂: rightward rotation
if isoelectric in V₅ or V₆: leftward rotation

Hypertrophy

Atrial Hypertrophy – diphasic P wave in V₁

right atrial hypertrophy – large initial component of diphasic P wave in V₁

left atrial hypertrophy – large terminal component of diphasic P wave in V₁

Ventricular Hypertrophy – tall R wave in V₁ for RVH, deep S wave in V₁ and tall R wave in V₅ for LVH

right ventricular hypertrophy – widened QRS with RAD, rightward rotation, and:

R greater than S in V₁ but R gets smaller in V₂ through V₆
S wave persists in V₅ and V₆

left ventricular hypertrophy – widened QRS with LAD, leftward rotation, and:

sum of depth of S in V₁ and height of R in V₅ is more than 35 small squares
inverted T wave with gradual downslope and rapid upslope

Infarction – always requires previous EKG for comparison

Identifying Injury

(1) ischemia – inverted T waves (earliest sign) – symmetrical down- and upslope, opposite direction of QRS

(2) acute injury – ST elevation

can occur without Q waves: "non Q-wave MI"
ST depression may indicate "subendocardial infarction" (small shallow area as opposed to entire wall of heart)

(3) necrosis (non-conductive tissue) – Q-waves

significant if more than one small square wide or greater than 1/3 the amplitude of the QRS
remain even after acute infarction is over (unlike other two)

Localizing Injury – leads where the above occur; also remember that axis points away from infarction

Anterior – left anterior descending artery – V₁ to V₄

Lateral – circumflex artery – I, aVL

Inferior – right or left coronary artery – II, III, aVF

Posterior – right coronary artery – V₁ and V₂, but changes are mirror image (R instead of Q, ST depression instead of elevation, etc.)
for blocks and hemiblocks: AV node is supplied by the right coronary artery, RBB and anterior LBB is supplied by LAD, posterior LBB is supplied by either

Effects of Other Medical Conditions on EKG

Pulmonary Embolism

prominent S wave in I
Q wave in III
inverted T waves in III and V₁ through V₄
ST depression in II
acute incomplete RBBB
RAD with rightward rotation

Electrolyte Disturbances

hyperkalemia

wide flat P – P disappears entirely with severe hyperkalemia
wide QRS
peaked T wave

hypokalemia

flat T wave
U wave (after T wave; represents Purkinje cell repolarization) – prominent with severe hypokalemia
can cause torsades des pointes if extreme

hypercalcemia – shortened QT interval

hypocalcemia – prolonged QT interval

Drugs

Digitalis

therapeutic – ST slopes below baseline, inverted T waves, shortened QT
excessive – blocks: SA block, paroxysmal atrial tachycardia (PAT) with block, AV block (can be 3^rd degree)
toxic – atrial fibrillation, junctional or ventricular tachycardia, frequent PVC's, ventricular fibrillation

Quinidine (blocks potassium channels)

wide notched P wave
wide QRS
very deep ST
U wave
long QT interval

Pericarditis

flat or concave downward ST segment elevation in leads where QRS is mainly negative (right chest leads – V₁ to V₃)
elevated ST segment with T wave off baseline in leads where QRS is mainly positive (lateral/inferior limb leads – aVL, I, II, aVF, III)

COPD

all waves of minimal amplitude; often leads to RVH with RAD; MAT in some cases

Effect of Cardiac Syndromes on EKG

Wolff-Parkinson-White Syndrome – caused by accessory bundle of Kent that bypasses the AV node to allow ventricular pre-excitation

delta wave with apparently shortened PR interval
can cause tachycardia through three mechanisms:

(1) rapid conduction of rapid atrial beats (PSVT, atrial flutter, or atrial fibrillation)
(2) automaticity foci within the bundle
(3) re-entry of ventricular depolarization

Lown-Ganong-Levine Syndrome – caused by James bundle (extention of the anterior internodal tract) that bypasses the AV node directly to the bundle of His

no PR delay (so PR interval is minimal)
QRS immediately responds to any atrial tachyarrythmias, so (for example) atrial flutter produces a rapid QRS response

Brugada Syndrome – familial dysfunction of Na⁺ channels

characterized by RBBB with ST elevation (downsloping) in V₁ through V₃
can cause deadly arrythmias leading to sudden cardiac death with no apparent structural heart disease (responsible for half of all cases)

Wellen's Syndrome – stenosis of LAD

causes marked T-wave inversion in V₂ and V₃

Long QT Syndrome – QT interval more than 1/2 the cardiac cycle

predisposed to ventricular arrythmias

Claude's syndrome is caused by midbrain infarction as a result of occlusion of a branch of the posterior cerebral artery. This lesion is usually a unilateral infarction of the red nucleus and cerebral peduncle, affecting several structures in the midbrain including:

Structure damaged	Effect
dentatorubral fibers	contralateral ataxia
corticospinal tractfibers	contralateral hemiparesis
corticobulbar tractfibers	contralateral hemiplegia of lower facial muscles, tongue, and shoulder
oculomotor nerve fibers	ipsilateral oculomotor nerve palsy with a drooping eyelid and fixed wide pupil pointed down and out; probablediplopia

Bnedikt:
It is characterized by the presence of an CN III oculomotor nerve palsy and cerebellar ataxia including tremor. Neuroanatomical structures affected include CNIII nucleus, Red nucleus, corticospinal tracts, brachium conjunctivum, and cerebellum. It is very similar in etiology, morphology and clinical presentation to Weber's syndrome; the main difference between the two being that Weber's is more associated with hemiplegia (i.e. paralysis), and Benedikt's with hemiparesis (i.e. weakness).

Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as thepons.^[1]

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus.

Millard-Gubler syndrome

Symptoms result from the functional loss of several anatomical structures of the pons, including the sixth and seventh cranial nerves and fibers of the corticospinal tract. Paralysis of the abducens (CN VI) leads to diplopia, internal strabismus, and loss of power to rotate the affected eye outward), and disruption of the facial nerves (CN VII) leads to symptoms including flaccid paralysis of the muscles of facial expression and loss of the corneal reflex. Disruption of the corticospinal tract leads to contralateral hemiplegia of the extremities.

It is a form of "crossed hemiplegia," as the paralysis of muscles controlled by the facial nerve occurs on the same side as the lesion, while the hemiplagia of muscles below the neck occurs on the opposite side as the lesion.

Eye response	4	Eyelids open, tracking or blinking to command
	3	Eyelids open but not tracking
	2	Eyelids closed but open to a loud voice
	1	Eyelids closed but open to pain
	0	Eyelids remain closed with pain
Motor response	4	Thumbs-up, fist or peace sign
	3	Localising to pain
	2	Flexion response to pain
	1	Extension response to pain
	0	No response to pain, or generalised myoclonic status
Brainstem reflexes	4	Normal pupil and corneal reflexes present
	3	One pupil wide and fixed
	2	Pupil or corneal reflexes absent
	1	Pupil and corneal reflexes absent
	0	Absent pupil, corneal and cough reflex
Respiration	4	Not intubated, regular breathing pattern
	3	Not intubated, Cheyne–Stokes breathing pattern
	2	Not intubated, irregular breathing pattern
	1	Breaths above ventilator rate
	0	Breaths at ventilator rate, or apnoea

Internship.preparation

Monday, January 30, 2012

Hypoxemic - Anoxic Brain injury

Interpretation of EKG

Hypertensive Urgency vs Emergrncy

basal cistern

vasogenic vs Cytotoxic Edema

New Onset Atrial Fibrillation

Wednesday, January 25, 2012

VENTILATOR MANAGEMENT

Monday, January 23, 2012

Hypoxemia

Pressors

Tuesday, January 10, 2012

brainstem syndrome

Millard-Gubler syndrome