ECG Rules Flashcards
Tall, peaked T wave
K+ is too high or myocardial ischemia is present
U wave may represent
- low K+
- abnormal Mg+ levels
- normal repolarization of purkinje fibers
Slowed conduction (>0.20) in the PR interval is indicative of…
1st degree AVB (AV block)
QRS complex >0.12 represents
-R or L bundle branch block and a slowing of normal conduction through the ventricles
a deep Q wave signifies…
myocardial infarct
what creates a slight variance in normal RR intervals?
respiration
Normal QT interval
less than one-half the RR interval and should not vary from one complex to another
problem with a long QT interval
it presents an extended opportunity for stray irritable impulses to excite the muscle and may trigger dangerous ventricular rhythms
medications that prolong the QT interval
quinidine and pronestyl
elevated ST segment
- more than 1mm above baseline
- indicates myocardial ischemia: lack of oxygen to cardiac muscle (STEMI)
normal sinus rhythm (NSR)
- regular rhythm
- 60-100 bpm
- each complex is complete
- intervals are within normal limits
- nothing looks off
treatment of sinus bradycardia if pt is symptomatic
atropine
significance of sinus tachycardia
- depends on pt’s tolerance of increased HR- some have dizziness and hypotension
- increased HR = increased myocardial O2 consumption
- MI pts with consistent tachy have increased risk for angina and increased infarct size
treatment of sinus tachycardia
- treat underlying cause
- beta blockers (Inderal)
sinus arrhythmia
- RR intervals vary; rate changes with respirations
- usually no significance and no treatment
Premature atrial contractions (PAC)
- early complex
- atrial because it still has a p-wave
- t-wave might be bigger because p-wave is sitting on top of it
PAC associations
- usually from stress, caffeine, tobacco, alcohol
- could be infection, inflammation, hyperthyroidism, COPD, heart disease, valvular disease
- enlarged atrium
treatment of PAC
- start with getting rid of caffeine, tobacco, alcohol
- meds: dig, quinidine, procainamide, beta-blockers
atrial flutter
- p-waves have saw-tooth appearance
- SA node constantly firing
- if >100 bpm, significantly decreased CO and could go into HF
problems with atrial flutter
- decreased CO because atria can’t refill with blood (decreased preload)
- at risk for clots because of sitting blood… they’ll be on an anticoagulant
treatment of atrial flutter
- cardioversion: reads QRS so it shocks when its supposed to
- meds: verapamil, diltizem, dig, quinidine, procainamide, beta-blockers
atrial fibrillation
- *hallmark sign is regularly irregular QRS complexes
- syncope is often caused by an otherwise healthy person going into AFib
significance of AFib
- decreased CO because lose “atrial kick”
- thrombi
- stroke
treatment of AFib
- will need to be on anticoagulants
- if fast: digoxin
- if slow: pacemaker
- emergency situations: cardioversion
- other meds: verapamil, diltizem, quinidine, beta-blockers
atrial tachycardia
- R-R is constant and rate is regular
- rate is 150-250 bpm
- patient will say “my heart is racing” or “pounding out of my chest”
atrial tachycardia associations
- overexertion and emotional stress
- DIG TOXICITY
- changes in position, deep insporation, caffeine and tobacco
- Will Parkinson Wright
- RDH
treatment of atrial tachycardia
- Adenosine doesn’t treat, just slows HR so you can see rhythm and have paddles ready
- vagal stimulation
- Meds: adenosine, verapamil, diltiazem, digitalis, propanolol
premature junctional contraction (PJC)
- premature beat (irregular rhythm)
- no p-wave
- fired from the AV node
- QRS
treatment of PJC
- rarely causes s/s
- MAY medicate with procainamide or quinidine
treatment of junctional escape rhythm
- only medicate if symptomatic
- if symptomatic, give atropine
associations of accelerated junctional rhythm
- acute inferior MI
- Dig toxicity
- acute rheumatic fever
- open heart surgery
treatment of accelerated junctional rhythm
- if Dig tox: hold Dig
- atrial pacemaker
junctional tachycardia
- no p-wave
- regular rate and rhythm
- rate >100 bpm (usually 100-180)
- QRS
junctional tachycardia associations
-*ACUTE INFERIOR MI
-Dig tix
acute rheumatic fever
-open heart surgery
(rapid HR can cause s/s of low CO)
treatment of junctional tachycardia
- vagal stimulation
- verapamil
- cardioversion
premature ventricular contractions (PVC)
- ectopic beat
- no p-wave
- wide QRS >.12
- associated with irregular pulse
bigeminy
every other beat is early
trigeminy
every 3rd beat is early
couplet vs run
- couplet is a PVC that comes in pairs
- run is a PVC that is 3 or more in a row
clinical associations of PVCs
- **HYPOKALEMIA
- hypoxia (could happen during suctioning)
- stimulants
- MI, mitral valve prolapse, CHF, CAD
significance of PVCs
- could cause Vtach
- usually benign is pts with normal hearts
- may reduce CO- angina and HF (heart will enlarge to compensate and cause hypertrophy)
indications for treatment of PVCs
- six or more in one minute
- ventricular couplets or triplets
- multifocal PVCs
- R on T phenomenon
treatment of PVCs
- amiodarone is drug of choice
- lidocaine: initial bolus - 0.5-1.5 mg/kg and continuous infusion of 2-4 mg/min
- procainamide
ventricular tachycardia
- regular rate/rhythm
- rate of 150-250 bpm
- QRS >.12
treatment of ventricular tachycardia
- if pulseless: defibrillate
- if they have a pulse: drug of choice is amiodarone
- also lidocaine, pronestyl
torsades de pointes
- type of vtach - “twisting of the points”
- crescendo-decrescendo
treatment of torsades de pointes
-magnesium sulfate
ventricular fibrillation and treatment
- no waves or complexes that can be measured or analyzed
- defibrillate immediately, CPR
idioventricular rhythm
- 20-40 bpm
- no p-wave
- wide QRS and often bizarre looking
treatment of idioventrivular rhythm
- atropine, isuprel (DO NOT GIVE LIDOCAINE)
- pacemaker
asystole and treatment
- flatline, no pulse
- always check leads first
- CPR, ACLS with early intubation and IV epi and atropine
pulseless electrical activity (PEA)
- electrical activity can be observed but there is no mechanical activity and NO pulse
- prognosis is poor unless underlying cause is corrected immediately
causes of PEA
PATCHHH Pulmonary emolus Acidosis Tension pneumothorax Cardiac tamponade Hypovolemia Hypoxemia Hypothermia
treatment of PEA
- treat underlying cause
- CPR with early intubation and IV epi
first degree heart block
- “if the R is far from the P, then you have first degree”
- PR interval will be constant but greater than .20
- AV node is always the one thats blocking it
treatment of first degree
none
wenckebach (second degree heart block type 1)
- “longer, longer, longer, drop, then you have Wenchebach!”
- hallmark: PR is long, next on is longer, longer, then complex is dropped
treatment of wenckebach
if symptomatic: atropine (always start with .5 mg) or pacemaker
classical second degree heart block (Mobitz II)
- “if some p’s don’t get through, then you have Mobitz II”
- some p’s don’t have a QRS, but the ones that do are fixed and regular, they are close to the QRS
treatment of classical 2nd degree heart block
- pacing
- can try atropine, epi, dopamine
complete or 3rd degree heart block
- “if Ps and Qs don’t agree, then you have 3rd degree”
- R-R is regular
- P to P is regular
- But no relationship between P and QRS… complex is all jacked up
treatment of 3rd degree heart block
- priority pt for pacemaker
- may use atropine, epi, dopamine
indications for a pacemaker
- symptomatic sinus bradycardia
- chronic atrial fib with a slow ventricular response
- idioventricular rhythm
- 2nd degree heart block type 2
- 3rd degree heart block
- sick sinus syndrome
failure to pace
- there is no pacemaker spike when there should be one
- pacemaker fails to initiate an electrical impulse when needed
- check battery or MD reposition pacing electrode
failure to capture
- there is a spike and no immediate p wave or QRS
- pacemaker initiates a pulse but fails to get a response (contraction)
- caused by: pacer lead fracture, battery failure, electrode movement, or fibrosis at electrode tip
- may need to increase coltage
failure to sense
- there is a pacemaker pike after a contraction
- pacemaker fails to sense pts heartbeat and initiates an electrical pulse
- caused by: pacer lead fracture, battery failure, movement of electrode
- need to increase the sensitivity of the external pulse generator
Atropine
- increases HR
- always start with 0.5 mg; increase and repeat q 3-5 min in ACLS
digoxin
- slows ventricular rate, increased CO
- give in AFib and AFlutter
- paroxysmal atrial tachycardia
amiodarone
- slows the sinus rate, increases PR and QT intervals, causes vasodilation
- life-threatening ventricular arrhythmias unresponsive to less toxic agents
- VFib and VTach
- supraventricular tachyarrhythmias
adenosine
- slows conduction through the AV node
- conversion of paroxysmal supraventricular tachycardia to NSR when vagal maneuvers are unsuccessful
lidocaine
- suppresses automaticity and spontaneous depolarization of ventricles
- for ventricular arrhythmias
magnesium sulfate
-torsades de pointes
