EKG Flashcards
Order of electrical conductivity
- sa node
- Av node
- bundle of his
- R and L bundle branches
- purkinje fibers
relative refractory phase
- where cardiac gradually recover their excitability
- cardiac muscles will respond to STRONG stimuli
- peak to the end of the T wave
- vulnerable stage
absolute refractory phase
- beginning of depolarization until the fiber can accept another action potential
- cardiac muscle cannot be depolarized by any stimuli
- beginning of the QRS to the peak of the T wave
- as long as it takes for the heart to contract is the length of this phase
time measurement of an ECG
- represents the time it takes for an electrical impulse to pass through a part of the heart
box sizes
- tiny box = 0.04 (5 small will equal one large)
- large box = 0.20
What does the p wave represent
- atrial depolarization
- comes before the QRS
PR interval: normal length
- 0.12 - .20
What does the PR interval represent
the time it takes the original impulse to leave the SA node and travel through the AV node
-tells us how the AV node is functioning
Why does there need to be a delay at the av node
- allows the atria and the ventricles to contract separately from the ventricles
- allows for atrial kick which helps CO
What does the QRS interval represent
- ventricular repolarization
what is the normal length for the QRS interval
- less than 0.12 seconds
What does the ST segment represent
- time btwn completion of ventricular depolarization and beginning of ventricular repolarization
what is a normal ST segment length
isoelectric (not elevated or depressed)
what does an elevated ST mean
- represents myocardial injury/ infarction (irreversible damage)
what does an depression ST mean
- represents myocardial ischemia (reversible)
T wave representation and what does it mean when it is inverted
- ventricular repolarization
- inverted t wave represents any condition that interferes with normal repolarization (ischemia or injury)
What does the QT interval mean
- total duration of combined depolarization and repolarization
- from the beginning of the QRS wave to the end of the T wave
what is normal length of QT
- 0.34-0.43
what is a regular rhythm
- distance between the r waves doesn’t vary more than 3 boxes
what is an regularly irregular rhythm
- if the pattern can be recognized and predicted for the r waves
What is a irregularly irregular rhythm
- if it has no pattern and has no patterns of regularity
Step one:
- figure out the rhythm
- ventricular (count the R x 10) and atrial (count the P x 10) the same
Step two
- calculate HR
- ventricular (count the R x 10) and atrial (count the P x 10) the same
Step 3
- look at the P wave
- are they present?
- are they all the same shape?
- is there one p wave for every QRS
Step 4
- measure the PR interval
- is there consistent PR interval?
- is the measurement normal for PR interval (0.12-0.20)
- is the PR interval measurable?
Step 5
- measure the QRS
- do they all look the same?
- is the measurement normal (less than 0.12)
Normal sinus rhythm
- HR: 60-100
- regular rhythm
- p wave: 1:1
- PRI: normal
- QRS: normal
Sinus bradycardia (SB)
- increased ventricular filling due to firing too slow
- HR: less than 50-60 bpm
- rhythm: regular
- p wave: 1:1
- PRI: normal
- QRS: normal
cause of SB
- variation in athletes
- meds
- MI
- vagal stimulation
TX for SB
- tx only if symptoms of decreased CO ( SOB, hypotension, angina)
- treat the underlying cause
- if s/s of poor perfusion: give atropine
- if atropine is ineffective: transcutaneous pacing, dopamine infusion or epinephrine infusion
Sinus tachycardia (ST)
- decreased ventricular filling due to firing too fast
- HR: > 100 bpm
- rhythm: regular
- P wave: 1:1
- PRI: normal
- QRS: normal
cause of ST
- blood loss
- fever
- anxiety
- meds
- coffee
- hypovolemia
- external influences
TX of ST
- tx only when symptoms present (SOB, hypotension, angina, altered mental status)
- TX underlying cause since brought on by external factors
- stable: diltiazem (ca channel blocker), inderal (B blocker), or vagal maneuvers
General Atrial Dysrhythmias
- p waves differ in configuration for atrial dys.
- AV node replaces the SA node as the gatekeeper (pacemaker)
- the atrial pacemaking sites replace the SA node as pace maker
- conduction pathway is the same through the AV node and it acts as the gatekeeper to control how many impulses reach the ventricles
- protective mechanism
What is most concerning about atrial fib and flutter
- risk for thrombi formation and low CO
- thrombi can form due to the incomplete emptying of the atrium since the AV node is acting as the gatekeeper
- low CO due to: loss of atrial kick, ventricular rate is too fast or too slow, one or both
what is atrial flutter
- rapid discharge of one single ectopic foci causing the atria to contract but not all impulses make it to the ventricles causing a protective block at the AV node
- atrial kick becomes compromised by the multiple atrial contractions each time the ventricles contract so CO is affected
what happens if too many impulses get through the AV node
- the ventricles will respond, the pt will have symptoms due to the increased HR, decreased ventricular filling time, and resulting in low CO
what happens if too little impulses get through the AV node
- the pt will have symptoms of low CO
Atrial flutter
- Atrial rate: 250-350 Ventricular rate: 75-150 –> if vent is less than 100= controlled
- rhythm: regular or irregular
- p wave: saw tooth pattern- called F waves
- PRI: not measurable
- QRS: NORMAL
causes of A flutter
- disease (cardiomyopathy, Coronary heart disease, vulvular disease, HTN
tx for A flutter
- treat underlying cause
- reduce fast HR
- reduce risk of stroke
- convert to or maintaining NSR
- difference between if they are stable or not
Atrial flutter when Pt is unstable
- synchronized cardioversion
atrial flutter if Stable
- look for cause, may not need tx
Atrial flutter and stable but has high ventricular rate or some symptoms
- slow vent rate with meds (diltiazem or verapamil, inderel, digoxin
- then restore NSR with chemical or electrical cardioversion
cardioversion
- giving electrical shock so the SA node can take over
- load with amioderone 150 mg IVP slowly (over 10 minutes) before
steps for synchronized cardioversion
- needs to be delivered to heart during R wave
- shock 50-360 J
- Use defib in sync mode
- is do it when in the T wave then VT or VF could happen
- done with sedation and analgesics
anticoagulation prior to cardioversion
- based on TEE
- If stable w/out clots: cardioversion
- if stable w/clots: send home on anticoag like coumadin or lovenox or heparin before cardioversion occurs
- if unstable (with or without clots): immediate cardioversion and don’t give amioderone prior
Atrial flutter and anticoags
- ppl with chronic a flutter will be on anticoag therapy for ever (warfarin or aspirin)
what is A fib?
- rapid discharge of multiple atrial ectopic foci; each electrical impulse results in depolarization of a small part of the myocardium and not the entire atrium
- the atria cannot contract effectively and empty into the ventricles
- the atria are twitching
- AV node will randomly conduct the impulse to the ventricles
Atrial fib
- atrial rate: 350-600 –> irregular and not measured normally ventricular rate: irregular at 100-150 –> less than 100 = controlled
- rhythm: irregularly irregular
- p wave: f waves (squiggly and cant tell P wave)
- PRI: not measurable
- QRS: normal
causes of A fib
- a flutter, high alcohol intake, idiopathic, COPD, cardiac valve disease, CHF
Tx for A fib
- treat underlying cause
- reduce fast HR
- reduce risk of stroke
- convert to or maintaining NSR
- difference between if they are stable or not
what is a first degree AV block
- delay in normal conduction of the impulse from the atria to the ventricles
- p wave for every QRS but the PRI is long
- could lead to other blocks but usually not a big deal and dont worry about
First degree Av block
- constant prolonged PRI
- rate: normal
- rhythm: regular
- P wave: 1:1
- PRI: constant greater than .20
- QRS: normal
causes of first degree AV block
- athletes and children
- lesions along the conduction pathway, MI, myocarditis
TX for first degree
- monitor pt and tolerance
- monitor for progression to 2ND
- no tx if tolerating
second degree AV block type 1
- progressively long PRI and not p wave for every QRS
- prolonged
- Atrial: normal Ventricular: normal but slower than atrial
- rhythm: regularly irregular
- P wave: normal
- PRI: progressively lengthens until QRS is dropped
- QRS: normal, wide, dropped
Causes of 2nd degree type 1 AV block
- ischemia
TX of 2nd deg type 1 AV block
- monitor for tolerance
- monitor for progression to third degree (but rare and normally stable)
- No tx if handling well
- if symptoms: atropine or temporary pacer
Second degree type 2 av block
- PR interval constant AND no P for every QRS
- P wave is unconducted without proceeding prolongation of the PR interval ( PR intervals are all the same size and some QRS can be dropped)
- Atrial rate: normal Ventricular: normal but slower than atrial
- rhythm: irregular
- P wave: normal
- PRI: constant
- QRS: normal, wide, or dropped
causes of second degree type 2 AV block
- ischemia, heart disease
TX of second degree type 2 AV block
- atropine may be tried but will probably increase demand on heart by increasing atrial rate
- pacemaker
Third degree AV block
- complete absence of conduction between atrial and ventricles
- atria and vents beat independently
- no impulses get through the AV node
- atrial: may or may not be normal ventricular: may or may not be normal (usually 40)
- rhythm: regular
- P wave: normal, may not be associated with a QRS
- PR interval: not measured, changes randomly
- QRS: normal or wide
- no consistant PRI and p wave may be all over the place
causes of 3rd degree AV block
- ischemia, heart disease
tx of 3rd degree AV block
- follow symptomatic SB algorithm (if signs and symptoms showing do atropine)
- early pacemaker application
what is Premature ventricular Contractions
- QRS will look wide and bizzarre ( > 0.12)
- premature QRS complex due to ectopic foci causing an impulse to start in the ventricle before next sinus impulse
PVC
- rate: any rate
- Rhythm: irregular
- P wave: none
- QRS: WIDE AND BIZZARRE - NOT EVERY ONE HAS TO BE THIS
Sinus rhythym with bigeminy of PVC
- every other beat is going to be upside down
couplet Vent tachy
- there will 2 QRS in a row that are tall
ventricular trigeminy
- every 3rd beat is upside down and looks like a fish hook
when do PVC need TX
- occur frequently ( > 6/min)
- occur on every other beat (bigeminy)
- strike on T wave of proceeding beat (R- on T pattern)
- originate from more than one focus (multifocal)
- occur in consecutive fashion (couplets, triplets)
- occur after MI
Causes of PVC
- with or without cardiac disease
- hypoxia
- ventricular irritability
- caffeine intake
Tx FOR PVC
- look for cause
- monitor pt for tolerance
- consider amioderone 150 mg
V tach
- originates suddenly from very irritable ectopic foci
- ventricles take over as pacemaker
- run of 3 or more PVC’s with rate greater than 100= VT
- Rate: vent- 150-250 atrial: un measurable
- rhythm: regular
- P wave and PRI: not present
- QRS: wide and bizzare (all will look the same)- tall and a lot in a row
cause of V tach
- with or without cardiac disease
- cardiomyopathy
- electrolyte imbalance
tx of v tach
- with pulse and stable:
- medically manage- IV, O2, ECG, echo, cariology consult. load with amioderone and prepare for immediate cardioversion - without pulse: treat like V fib (dfib)
V fib
- ventricles quivering, no effective CO or contractions occurring
- always fatal unless treated
- caused by ischemia and infarction, heart disease
- will convert to a-systole within few minutes
- TX: CRP, defib (see pulseless VT/VF)
- small squiggly line with no obvious QRS
Causes of PEA
- absence of detectable pulse despite evidence of electrical activity
- H’s and T’s ( hypovolemia, hypoxia, acidosis, hyper or hypo K+, hypoglycemia, hypothermia, drug overdose, cardiac tamponode, pneumothorax, thrombosis
tx of PEA
- P-E begin BLS
- P= search for probable cause, push fluids
- E= epi or vasopressin
- not condusive to shock
Asystole
- total absence of ventricular electrical activity
- TX: look for cause, early intubation, epi, don’t attempt to shock, prognosis is poor but exceptions include hypothermia and electrocution
What is cardiac output and what are implications when compromised
CO: HR x SV (volume of blood heart pumps per minute
Implications: SOB, angina, hypotension, altered mental status
When is the use of an ICD warranted?
- when the pt survived VT OR VF, or sudden cardiac death
- experienced syncope with VT/VF
- at high risk for VT/VF after cardiac surgery and cannot tolerate meds or ablation
- prophylactically in pt with ischemic and idiopathic cardiomyopathy with EF 30% or below for prevention of sudden death due to ventricular arrythimias
