QS wave
when there is no upward deflection in the QRS complex- therefore you cant say if the downward wave is Q or S
.2 sec
amount of time between two HEAVY black lines
.04 sec
amount of time in one small square
limb leads
-uses electrodes on R and L arms and L leg
-lie on flat/frontal plane
INCLUDES:
- bipolar: I-III
-unipolar(augmented) (capital letter indicates where the + lead is): avR, avL, avF
draw the 6 different limb leads
see from + to - ....positive charges moving toward positive electrode (each in slightly a different position seen here) produce upward deflection on EKG
lateral leads
I and avL
-these have + electrodes on L arm
(also V5/V6)
inferior (limb) leads
II,III, and avF
-all these have + electrodes on L foot
chest (precordial) leads
-uses positive electrodes only on the front of the chest over the heart starting at the R sternal border (along the R ventricle) and ends near mid axillary line in line with the apex
-oriented through the AV node and projected toward the patients back whi
Normal EKG
1. RATE--> between 60-100 BPM
2. RHYTHM
--> NSR: <10% variability with respiration but pretty much constant rate between similar waves; P wave before each QRS and 'normal' for that individual ;
-P waves: upright in leads I, II and avF (+V3-V6); inverted i
U wave
a small hump past T wave that may be present that represents final phase of purkinje repolarization
-present in hypokalemia and Quinidine (and other K+ blocking agents)
Sympathetic system effects on cardiac Beta 1 adrenergic receptors
EXCITATORY effects
-increase SA node PACING RATE(^ HR)
-increase RATE OF CONDUCTION through AV node+ atrial/ventric myocardium
-increase FORCE OF myocardial CONTRACTION
-increase IRRITABILITY OF atrial/ AV junctional automaticity FOCI (can cause spontaneo
Parasympathetic system effects on cardiac muscarinic cholinergic receptors (via vagus n.)
INHIBITORY effects
-decrease SA node pacing rate (decrease HR)
-decrease rate of conduction
-decrease force of contraction
-decrease irritability of foci
Vagal maneuvers (PS reflexes)
used to counteract S effects on the heart
for example:
- to inhibit AV node or increase AV refractory (used as diagnostic aid in 2:1 AV block and atrial flutter)
-to inhibit irritable focus (used to convert SVT to sinus rhythm)
INCLUDES;
1. induced gaggin
Neuro-cardiogenic syncope
in some elderly its after prolonged standing--> they have failure of S vasoconstriction but still have the increase heart effects --> transient tachycardia with poor cardiac volumes-->partially filled ventricles contract vigorously--> stim of LV PS mechan
Order of interpretation of EKGs
1. Rate
2. Rhythm
3. Axis
4. Hypertrophy
5. Infarction
Rate
cycles/min
-measure R-R (between large black lines)
-->300,150,100,75,60,50
-if bradycardia (<60 bpm): cycles (R-R)/6 sec strip* 10
- note: a 3 sec strip is between 2 marks above graph
-to figure out more precisely: 1500/mm between similar waves
normal sinus rate
60-100 bpm
-aka sinus rhythm
how to figure out rate with irregular rhythms (arrhythmia)
- the average ventricular rate --> cycles (R-R)/6 sec strip* 10
OR take the pts pulse
Potential pacemakers (automaticity/ ectopic foci= AF) intrinsic rates
*note all have overdrive suppression ( faster pace will suppress all slower ones)
*if they are very irritable they can rapidly discharge @ rate of 150-250 BPM (all of them) which is an emergency rate
1. Atrial AF--> 60-80 BPM
2. (AV) junctional AF (middle
general rhythm interpretation
1. identify basic rhythm (is it regular, is it sinus, etc)
2. scan tracing for pauses, premature beats, irregularity and abnormal waves
3. check for P before each QRS; QRS before each P
4. check for PR intervals (for AV blocks); QRS interval (for BBB)
5.
Regular/ normal Rhythm
constant rate - i.e constant distance (duration) between similar waves
-any automaticity foci can have this
-normal sinus rhythm (NSR) is when its SA node pacing
- this tends to have normal variability with respiration (inspir. increase HR slightly (S) ;
Irregular Rhythms
1st type of arrhythmias
-lack constant duration between cycles, usually b/c multiple active automaticity sites (i.e all have cycle length variation)
1. Wandering pacemaker
2. Multifocal atrial tachycardia
3. Atrial fibrillation (also seen under Tachyarrhy
wandering pacemaker
an irregular rhythm produced by pacemaker activity wandering from SA node to nearby atrial automaticity foci (P' waves; so you have different looking P waves from 3+ sites in the atria)
-P wave shape varies in any given lead
-irregular ventricular rhythm
multifocal atrial tachycardia
- wandering pacemaker but rate is >100/min
- usually in pts who are very ill with COPD or sometimes in Digoxin toxicity in pts with heart disease
-atrial automaticity foci show early signs of parasystole (entrance block) so no single focus has pacemaking
parasystolic
when an automaticity focus has an entrance block (any incoming depolarization is blocked) so it paces to surrounding tissue and is not overdrive suppressed by passive depolarization
Atrial fibrillation
an irregular rhythm and can be a tachyarrhythmia due to continuous rapid firing of MULTIPLE rritable atrial foci ALL suffering from parasystole (entrance block) causing rapid pacing all at once producing a jagged/wavy baseline of tiny spikes
-continuous c
Escape
2nd type of arrhythmias
-response of an automaticity focus to a pause in the pacemaking activity
Escape Beat
an automaticity focus escapes overdrive suppression TRANSIENTLY to emit ONE BEAT
-occurs when there is transient SINUS BLOCK (SA node misses one pacing cycle causing a transient pause and then the escape beat will pick up and then go back to normal sinus)
Escape Rhythms
an automaticity focus escapes overdrive suppression to PACE at its inherent rate
-occurs when there is SINUS ARREST (SA node completely stopes pacing -very sick SA)
-usually the next fastest pacemaker will take over (starts with atrial and then goes down)
Idiojunctional Rhythm (junctional Escape rhythm)
occurs if 1. failure of SA node and atrial foci OR
2. complete conduction block of proximal AV node
-40-60 BPM (but occasionally can be accelerated)
-usually only have a series of QRS (+ T) complexes
-can cause retrograde atrial depolarization leading to
Idioventricular Rhythm (Ventricular escape rhythm)
occurs if 1. total failure of SA node and all other automaticity foci (extremely rare and usually fatal; called downward displacement of the pacemaker) OR 2. complete conduction block high in ventricular conduction system (below AV node) causing ventricul
Stokes- Adams syndrome
when pacing from ventricular focus causes significant reduction in blood flow to the brain that it leads to unconsciousness ( syncope )
-
monitor airway
Premature beats
3rd type of arrhythmias
-due to an IRRITABLE automaticity focus that fires spontaneously a single stimulus producing a beat earlier than expected
-if VERY irritable it can cause rapid pacing impulses in succession and can become dominant pacemaker (ex: in
Atrial, junctional or ventricular Bigeminy/ Trigeminy/ Quadrigeminy
irritable atrial focus that produces/repeats PAB's as "couplets" in runs with reset of SA node ( subsequent space - for example: with atrial seen above need to diff with AV block by looking for the P' waves) between couplets
-a couplet is a cycle containi
causes of atrial and junctional foci irritability
usually adrenergic substances (or decrease PS stim)
1. Epi release by adrenals
2. increase S stim
3. adrenergic chemicals that mimic Epi/NE: caffeine, amphetamines, cocaine or other B1- stimulators
4. Excess digitalis, some toxins, occasionally ETOH
5. hy
Premature Atrial Beat (PAB)
Random P' wave
-->may be within a T wave (see a T wave that looks taller than all others in same lead)
--> can be upright (if focus near SA node) or inverted (if focus near lower atrium) in most leads
-usually will cause resetting of SA node pacing (leavi
Premature Junctional beat (PJB)
random early QRS/T
+/-retrograde atrial depol==> inverted P' wave either immediately before, disappears within or after the QRS
-if inverted P' wave usually also have SA node reset instep with the P' wave
causes of ventricular focus irritability
most important= LOW O2 (hypoxia) due to either
1. airway obstruction
2. absence of air (suffocation, drowning)
3. poor O2 content in air
4. minimal blood oxygenation in lungs (pulmonary embolus or pneumothorax)
5. reduced CO (hypovolemia, cardiogenic shoc
Premature ventricular beats/ contractions (PVCs)
Giant QRS complex (both height and depth)
-->are usually opposite polarity of normal QRS (i.e if normal is more upright then these are more downward)
--> most often occur just after T wave but can occur during T wave ("R on T phenomenon")
Have normal P wa
Ventricular Parasystole
the specific ventricular automaticity focus suffers from entrance block ( but is NOT irritable)
-see 2 independent rhythms--> SA pacing (with P, QRS, etc) and then ventricular pacing (separate large QRS compelxes)
-interval between the normal cycle and la
R on T phenomenon
when PVC falls on T wave ( peak or initial downslope are vulnerable periods esp in hypoxia or hypoK+)
-may result in dangerous arrhythmias so need to watch closely
Tachyarrhythmias ("rapid arrhythmia")
rapid rhythm/ pacing originating in a VERY irritable automaticity focus
INCLUDES (separated based on rates and then further into the location of irritable focus (atrial/junctional/Ventricular)
1. Paroxysmal Tachycardia --> 125 (150)-250 BPM (note: 250 lin
Paroxysmal (sudden) tachycardia
Suddenly (vs sinus tachy= gradual), a very irritable focus paces rapidly
-can be very irritable for any extreme conditions listed before
-can be initiated by a single premature stimulus from another focus provoking an already irritable focus
-will overdri
Paroxysmal supraventricular tachycardia (SVT)
-may have wide QRS complex (if aberrant conduction or if preexisting BBB) that can cause this to look like VT but its relatively uncommon:
INCLUDES:
A. Paroxysmal Atrial Tachy (PAT)--> P' waves with normal QRS- T following
-if with AV block see >1 P' wave
AV nodal reentry tachycardia (AVNRT)
A different type of Junctional Tachycardia due to a continuous reentry circuit (including lower atria and AV node) that develops and rapidly paces atria and ventricles ("circuit reentry")
-can look exactly like PJT
-need to ablate the focus laden region t
ways to distinguish wide QRS complex SVT vs. VT
in VT commonly:
1. pt with coronary disease or infarct
2. QRS duration greater (>.14 sec)
3. AV dissociation (see captures or fusions)
4. Extreme Right axis deviation (-90--180) (- I and avF)
2. Paroxysmal Ventricular Tachycardia (PVT or VT)
--> enormous consecutive PVC complexes (3+); SA node still paces atria but P waves are only seen occasionally b.c usually hidden in PVCs (independent atria and ventric. depol = AV dissociation); occasionally see normal appearing QRS (capture beat) because
Flutter
rate of 250-350 BPM from a SINGLE rapidly firing irritable foci
INCLUDES:
1. Atrial Flutter
2. Ventricular Flutter
Atrial Flutter
continuous "saw tooth" rapid sequence of atrial complexes from a single rapid firing atrial focus; several flutter waves before a QRS complex because AV node refractory
- in order to see on EKG may need to invert tracing or employ vagal maneuver (increase
ventricular flutter
a rapid series of smooth sine waves from a single rapid- firing ventricular foci
-usually in a short burst --> lead to barely any filling of ventricles and soon--> leading to V. Fib
Fibrillation
350-450 BPM
-totally erratic rhythm due to continuos rapid firing from MULTIPLE foci (that all are parasystolic- ie suffer from enterance block)
INCLUDES:
1. Atrial Fib (see above) -"irregularly irregular" -
2. Ventricular Fib
Ventricular Fibrillation
multiple ventricular foci rapidly discharging producing this totally erratic ventric. rhythm without identifiable waves
-need IMMEDIATE tx (CPR and defib)
-is a type of cardiac arrest b.c lack of pumping action of heart
Types of Cardiac arrest
1. V. Fibrillation
2. Cardiac standstill ("asystole"): no detectable cardiac activity on EKG due to the SA node and the escape mechanisms of all the foci at all levels being unable to assume pacing responsibility
3. Pulseless electrical activity (PEA): no
Pre excitation syndromes
1. WPW
2. LGL
Wolff- Parkinson- White (WPW)Syndrome
an abnormal, accessory AV conduction pathway (called the Bundle of Kent) causes ventricular pre-excitation (premature depolarization) of a portion of the ventricles
-seen as "delta" wave on EKG just before the normal QRS
--> may appear to "shorten" PR int
Lown- Ganong- Leving (LGL) Syndrome
AV node is bypassed by an extension of the Anterior Internodal Tract called the "James Bundle" which conducts atrial depolarizations directly to bundle of His without delay
-P waves seen directly next to normal QRS with virtually no PR interval
Types of blocks
1. sinus (SA) block
2. AV block
3. Bundle Branch Block
4. Hemiblock (block of either of the 2 subdivision of the L bundle branch)
Sick Sinus Syndrome (SSS)
a wastebasket of arrhythmias caused by SA node dysfunction associated with unresponsive supraventricular (atrial/ junctional) automaticity foci
-usually in elderly with heart disease
-young healthy conditioned athletes (have increase PS at rest) can have
Bradycardia- Tachycardia Syndrome
patients with SSS can have intermittent episodes of SVT (possibly even A flutter or A fib) with sinus bradycardia
AV Blocks
have either decreased or absent conduction from atria to ventricles
-suspect if see prolonged PR (>.2 sec) anywhere in EKG recording
--> can be normal in Mobitz type 2 and variable in 3* block
INCLUDE
1. First degree (1*) AV block
2. Second degree (2*) AV
First degree (1*) AV block
decreased AV node conduction--> lengthens delay between atrial and ventric. depol
-consistently prolonged PR interval (>.2 sec= 1 large square)
-normal P-QRS-T cycle
Second degree (2*) AV block
some atrial depol (P waves) conduct to ventricles (produce QRS) while some are blocked
-->get some areas with P-QRS and then some with P without QRS following it
INCLUDES
1. Wenckebach (Mobitz Type I)
2. Mobitz Type II
NOTE: a 2:1 block in either can look
Wenckebach (Mobitz Type I)
benign type of 2* AV block
- site of block usually WITHIN AV NODE
-progressive prolongation of PR interval until P wave fails to conduct ('dropped' QRS)
-characterized by a P: QRS ratio
(image: 4:3)
Mobitz (Type II)
pathological type of 2* AV block
-site of block actually in PURKINJE FIBER BUNDLES (HIS BUNDLE or R/L BUNDLE BRANCHES)
-have P waves totally blocked then get successful conduction to ventricles for a beat (QRS) (no prolonged PR interval just dropped QRSs)
Third degree (3*; complete) AV block
absence of conduction of atrial impulses to ventricles
*
AV dissociation
: no correspondence between P waves and QRS complexes
(need to look for this to diff from a wide complex bradycardia)
-the atria pace at their own rate ( by SA node)
( sinus-paced P
downward displacement of the pacemaker
failure of all automaticity centers above the ventricles (SA node + supraventricular foci)
- absence of atrial activity with wide QRS complex bradycardia
-bad prognosis
-can also be due to severe HYPER K+
Bundle Branch Block
block of either R or L bundle branch causes delay of conduction (must go through slow muscle) then continuous to conduct rapidly again below the block
-causing one of the ventricles to begin depolarizing before the blocked ventricle --> get 2 "joined" QRS
RBBB
R and R' in V1 or V2 (R chest leads)
-mean QRS vector is within normal range or shows minimal R axis deviation (unless assoc. with anterior hemiblock)
LBBB
R and R' in V5 or V6 (L chest leads)
- infarction is difficult to determine on EKG in a pt with this
Hemiblock
block of either the anterior or posterior division of the L bundle branch (subdivision of L BB= fasicles)
-commonly occur with infarction and can be assoc with RBBB
-usually due to diminished blood supply to one of the 2 divisions
-look for axis deviation
Anterior Hemiblock
due to anterior descending branch of LCA infarct (assoc with MI (anterior) or other heart disease;may also be assoc with RBBB)
-causes delay in conduction to antero-lateral and superior area of LV --> late (unopposed) depol. upward and leftward of LV
-->
Posterior Hemiblock
-rare to have pure, isolated post. hemiblock b.c it has dual blood supply and is short/thick
-assoc with MI (inferior esp) or other heart disease
-causes late (unopposed) depol. forces toward the right
--> R axis deviation (first hint)
*always R/O pre exi
(Bi) Fasicular Block
BBB+ Hemiblock ("bundles" of purkinje fibers= fasciles; R and L BB and the 2 division of L BB are fasicles)
--> usually referring to RBBB + anterior or post hemiblock
(b.c ant+ post hemiblock = LBBB)
-these are often intermittent (and can have any combina
Intermittent Mobitz (intermittent complete AV block)
due to block of one bundle branch with intermittent block of the other; OR bifasicular block (RBBB with either ant or post hemiblock) with intermittent hemiblock of the other division
--> i.e intermittent complete AV block ; "trifasicular" block
- a conti
differentiate the causes flat baseline
1. 2 (secondary) AV block--> punctual P wave with no QRS response (Wenckebach vs. Mobitz); 3 (tertiary) also missing QRS's (disassociation of P and QRSs)
2. non conducted premature atrial beat--> premature P' with no QRS response
3. Sinus block--> missed
Axis
-aka electrical axis
direction of movement of depolarization that spreads through the heart to stimulate the myocardium to contract
-the mean QRS Vector when located by degrees in the frontal plane
Normal axis: 0 to +90 degrees
Mean QRS Vector
represents the general direction of ventricular depolarization
-the tail / origin is ALWAYS the AV node
-normally the vector points downward and more toward the L (because the depol. vectors are greater due to the thicker LV)
-when described in degrees (p
Axis deviation
determined by mean QRS vector in FRONTAL plane(using limb lead)
Displaced heart and effect on mean QRS Vector
If a person has a displaced heart their 'normal' Vector will be displaced in the same direction
INCLUDES
1. Horizontal Heart: often in obese individuals because the increased abdominal pressure pushes the diaphragm upward so the heart becomes horizontally
Causes of change in direction of Mean QRS Vector (Axis deviation)
1. Displaced (vertical or horizontal) Heart
2. Ventricular Hypertrophy (vector toward hypertrophied side) (RAD if RVH (can be due to things like PE, pulmonary a HTN, COPD), LAD if LVH (MC cause is systemic HTN))
3. Infarction (vector away from infarcted (
how to use thumbs (as lead I and avF) to determine axis quadrant
look at if QRS is primarily upright or downward in leads I and aVF
--> lead I: if +(QRS up) its telling you that the Vector is pointing toward the L side (L arm=+ in lead I) ; if - (QRS down) its telling you that Vector is pointing toward the R (R arm= -
isoelectric QRS
-on EKG seen as equal magnitudes of upward (+) and downward (-) deflection
-due to depolarization moving in a direction that is perpendicular to the orientation of a lead causing minimal deflection toward either electrode
-generally small amplitudes of th
P wave vector
points down and L --> so any leads with + on L foot (inferior leads= II, III, and avF) or L arm (lateral leads= I and avL) will normally have + (upright) P waves
-if see inverted "P wave" in any of these leads--> think its a P' thats depolarizing upward f
Axis rotation
determined by mean QRS Vector in HORIZONTAL plane (using chest leads)
-think direction of QRS moves from V1--> V6 based on the direction of the mean QRS Vector (i.e direction of depolarization which is more posterior) :
--> start at V1 mostly - (downward/
Using lead V2
oriented directly through the person making the front half part of their body + and back half -
==> so the normal mean QRS vector points more backward (toward LV) making normal QRS in V2 - (downward)
-oriented directly through the anterior wall and the po
Steps to Determine Electrical Axis
USE FRONTAL PLANE (Limb leads) to determine exact axis and if there is axis deviation
1. Is QRS +(upright) or - (downward) in leads I and avF? "thumb" signs
--> tells axis quadrant
2. Find limb lead where QRS is most isoelectric (+ parts of QRS= - parts o
Atrial enlargement/hypertrophy on EKG
-best detected by the P wave in lead V1 (+ electrode directly over atria at R 4th ICS)
--> P wave is diphasic (positive and negative)
-if the initial component is larger/tall (is usually +) = RA enlargement
-if the terminal component is larger/wide (is us
Right Ventricular hypertrophy on EKG
R wave: *
characteristic
*
-greater than S in V1--> becoming more + (normally is small r and large S--> mainly -)
-gets progressively smaller from V2-V6 as depol. is away from L sided leads (normally gets larger)
S wave:
-smaller than normal in V1
-persis
Left Ventricular Hypertrophy on EKG
R wave:
-even taller than normal in V5 (normally is large but now even more depol. to V5 toward the L)
S wave:
-even deeper than normal in V1 (normally is deep but now even more depol. going away V1 toward the L)
-->there is LVH if:
**
-mm of S in V1+ mm
Ventricular strain
- (L or R) ventricular hypertrophy may be assoc. with this
-characterized by depressed ST segment (from baseline) which usually humps upward in the middle of the segment
Elements to check for on EKG for MI
Any can occur individually or in combo with each other
1. Ischemia (decreased blood supply) - symmetrical T wave inversion (note this can also occur in LVH - but in LVH is asymmetric typically)
2. Injury - ST segment elevation (or depression)
3. Necrosis
Ischemia on EKG
Inverted T wave (SYMMETRICALLY)
-most pronounced in chest leads (since closest to ventricles)
--> pathologic if in V2- V6 ( inverted or flat T waves can be normal variant in adults in limb leads)
-may indicate ischemia even in the absence of myocardial in
Wellens syndrome
stenosis of anterior descending coronary a. (LAD)
-hallmark is marked T wave inversion in leads V2/V3
-threat of impending MI--> do angioplasty with stenting OR coronary bypass graft to remove this threat
Injury on EKG
ST segment elevation (Seen in image)
-indication of acuteness of infarct (will return to baseline with line) - need to correlate with leads that show Q waves(infarct) to see if that infarct is old or new OR to see if non Q wave infarct
-the earliest consi
Other causes of ST segment elevation
1. Prinzmetal's angina (no infarct): transient ST segment elevation:
2. Ventricular Aneurysm: persistent ST segment elevation (no return to baseline) in most chest leads
3. Pericarditis: ST elevation that is usually flat or concave can also elevate T wave
Brugada Syndrome
-hereditary dysfunction in cardiac Na+ channels that can cause of sudden death in young individuals without structural heart disease/coronary obstruction
-ST elevation (with a peaked downsloping shape- arrows on image) with RBBB pattern QRS (R, R') in V1-
Pericarditis
inflamm of pericardium due to virus, bacteria, cancer, MI or other sources of inflamm.
-can see ST elevation that is flat or slightly concave (middle sags down) that resolves with time
-also takes the T wave with it (elevation of entire T wave off baselin
Necrosis on EKG
Dead tissue (i.e doesnt depolarize- has no vectors- so the + electrode near the area detects no "toward" (+) vectors only away vectors from it
-->so the neg. Q wave which is the initial LV depol. is seen in the electrodes that are + over the area of infar
Anterior infarct ECG findings
L anterior descending a. (LAD) infarct
-Q waves in V1-V4
-if only V1 and V2--> "antero-septal infarct" b.c infarct includes the septum
-if only V3 and V4 (+/-V5/V6)-> "antero-lateral infarct" b.c doesnt include septum (more lat) (can also be from LCX occl
Lateral Infarct ECG findings
L circumflex a. (LCX) infarct
-Q waves in Ieads I and avL (lat . leads)
-may cause R axis deviation (ddx from post. hemiblock)
(may also see on V5/V6 )
Inferior Infarct ECG findings
R or L coronary a. infarct
(depending on which a. is 'dominant'- R is more common)
aka diagphragmatic infarct (b.c inf. wall of LV lies on diaphragm)
-~1/3 also include parts of RV
-Q waves in leads II, III and avF (inferior leads)
-may cause L axis devia
Posterior Infarct ECG findings
R coronary a. infarct
-exact opp. of ant. infarct (in leads V1 and V2+/- V3)
--> large R wave (reversed sig. Q wave; vector is now going toward V1/V2 b.c away from infarct making it +)
-ddx with RVH (also have large R in V1)
--> ST segment depression
-->a
Torsades De Pointes
twisting of points"
form of very rapid ventricular rhythm (rate usually: 250-350 BPM in brief episodes/bursts so ventricles may still pump)
-due to low K+ or Ca++, meds that block K+ channels (like Quinidine) congenital anomalies (like long QT syndrome),
Long QT syndrome
hereditary syndrome where the QT interval is longer than 1/2 the cardiac cycle (R-R interval)
-predisposes to dangerous ventricular arrhythmias
EKG in COPD pts
-low amplitude of all waves in all leads
-RAD (due to RV hypertrophy from increase work against pulmonary resistance) --> - in lead I
-some pts see MAT (multifocal atrial tachycardia)
causes of low amplitude on all waves in all leads
1. COPD
2. Hypothyroidism
3. chronic constrictive pericarditis
ECG in pt with pulmonary Embolus
note: all, some or none of these can be seen in PE
IN LIMB LEADS:
-S1Q3 inverted T3 syndrome--> characterizes acute cor pulmonale from the pulmonary embolus
-large S wave in lead I
-large Q wave in lead III
-inverted T wave in lead III
-RAD (- in lead I)
ECG findings in pt with HYPERkalemia
-P wave:
-as K+ increases P wave becomes wider/ more flat --> extreme cases have no P waves
-QRS: (vent. depol. takes longer)
-as K+ increases QRS becomes wider and wider
-T waves:
-peaked T waves
ECG findings in pt with HYPOkalemia
-T wave:
-as K+ decreases T wave becomes flatter --> extreme cases will become inverted
-U wave appears and becomes bigger the more K+ decreases
-an upright wave that occurs right after the T wave
*makes ventricular automaticity foci very irritable
*can i
ECG findings in pt with HYPERcalcemia
*accelerates both ventricular depol. and repolarization==>
Shortened QT interval
ECG findings in pt with HYPOcalcemia
-slows both ventricular depol. and repol. ==>
Long QT interval
-can initiate Ventricular tachyarrhythmias including torsades, VT, and Vfib
Digitalis "effect" on ECG
-
ST segment depression--> specific gradual downward curve
- classic in pts on digitalis
-look for in lead with no S wave seen to see how it tails off from the R wave
-also can have inverted or depressed T waves and shortened QT interval
-digitalis has PS
'Excess' Digitalis on ECG
supraventricular foci are exceptionally sensitive to digitalis and tends to cause blocks
-Atrial and junctional premature beats
-Paroxysmal atrial tachycardia with block (>1 P' wave spike for every normal QRS-T after)
-transient sinus block
-rate-dependen
Digitalis 'toxicity' on ECG
supraventricular and sometimes ventricular(at really high levels) foci become extremely irritable and fire rapidly
-SVT (PAT and PJT)
-PVC's
-Ventricular Bigeminy, Trigeminy
-VT
-V. Fib
Artificial pacemaker on ECG
each electrical stimuli will capture (depolarize) the myocardial tissue its attached-->
seen as narrow vertical spike on ECG
-have regular pacing stimulus
-have sensing capabilities (Demand Pacemaker) in some==> imitate mech. of automaticity focus ; so it
Delivery Modes of Pacemaker impulses
see the narrow vertical spike whenever the stimulus from the pacemaker occurs
1. Atrial Pacing (atrial pacemaker) --> in pt with SA node dysfunction will
pace atria
and then AV node, etc will conduct to ventricles
2. P wave triggered pacing (aka atrial tr
Locations of pacemaker electrode positions in RV and effect on ECG
* on all will see a paced QRS with a LBBB pattern but axis (lead I and avF) can tell you the exact location
1. mid inflow tract --> normal axis
2. RV apex (ideal)--> L.A.D
3. below pulmonic valve --> R.A.D
ICD (Implantable Cardioverter Defibrillator)
a type of "pacemaker" that can analyze and treat the most dangerous cardiac arrhythmias instantly
-can simulate normal sinus pacin
-can institute overdrive suppression pacing to treat V. tach (suppress the causative ventricular focus)
-can provide cardiov
AED (automated External Defibrillator)
records and analyses the pts EKG and then automatically defibrillates if a deadly arrhythmia is detected (esp V fib or high rate VT)
Quinidine Effect on ECG
*slows depol and repol. through atria and ventricles due to its effects on Na and K+ channels
-P wave widening and notched
-QRS complex widening
-QT interval prolongation (can lead to torsades in toxic amounts)
-ST segment depression
-U waves