Lecture 2 - arrythmias Flashcards
components of telemetry (electrodes, applying, location, lead analysis (2))
1) electrodes:
- disposable disks consisting an adhesive ring with a conductive substance in the center (conducts electricity)
- conductive media conducts skin surface voltage changes through color coded wires
2) applying:
- dry skin
- remove dead/dry skin before application with a rough paper or cloth
- clip hair (if needed)
- place on skin over areas with MINIMAL muscle activity to avoid artifact (leads CANNOT tell difference between skeletal/cardiac muscle)
- change PRN or QD
- change batteries for portable monitors PRN
3) location of labels:
- clouds (white) over grass (green)
- smoke (black) over fire (red)
- chocolate (brown) to heart
4) cardiac monitor lead analysis for telemetry
- Lead 2: R posterior heart
- V1/MCL1: L anterior/R posterior heart
TIP: leads in V1 can detect major heart attacks
5) wave deflection:
(-) -> (+) = up spike
(+) -> (-) = down spike
tip: some disease processes cause wave inversion so MAKE SURE PUT ON CORRECT
A & P review: cardiac (3)
1) myocardial cells exist in a NEGATIVE mili-volt state (AKA polarized)
- calcium (Ca2+) moves IN myocardial cells
- potassium (K+) moves OUT myocardial cells
- increases positive charge of the cell -> depolarizing the cells, allowing for CONTRACTION
2) properties of myocardial cells (6):
- automaticity (automatic functions)
- excitability (acts on impulse, stimulated)
- contractility (contract)
- rhythmicity (defined cadence)
- refractoriness (rest and return to baseline)
3) automaticity/pace maker potential changes depending on LOCATION:
- SA node: 60-100
- AV node: 40-60
- Bundle: 25-40/30-40
- Purkinje: 20-40
EXAM: the rate of impulse gets slower as we get deeper into the heart
- ex: if theres a block in the SA node, the AV node will take over and act on that. It will NOT be as strong, and it continues to get weaker as we get deeper into the heart and NOT sustainable for long life functioning
heart electrical conduction review:
P wave - atrial depolarization
QRS - ventricle depolarization
T - ventricle repolarization
tip:
- atrial repolarization is hidden in ventricle depolarization
- not everyone has a Q wave!! if it suddenly appears, that is area for concern
- depolarization = contraction
- repolarization = relaxation
ECG analysis summary (6 steps)
1a) heart rhythm:
- regular OR irregular
- slightly irregular? (PAC)
- basically regular (premature ectopic beats, escape ectopic beats, regularly irregular (PVCs), irregularly irregular (AFIB)
1b) heart rate (60-100):
- 1500/ # small boxes between QRS complex = rate (only works for regular)
- count # big boxes in 6 seconds x 10
tip:
- 1 small box = 0.04
- 1 large box = 0.20
- 5 large box = 1 second
2) p wave evaluation (atrial depolarization):
- is p wave present? what does it represent?
- are there p waves for each QRS?
- are the p waves before OR after QRS?
- what is the shape of the p wave? do they look alike? (should be but if NOT, coming from different spot in the atrium)
- are there more p waves than QRS?
- ectopic beats? abnormally shaped p waves in relationship to the beats?
- are p waves buried (svt, 3rd degree block)
3) PR interval evaluation (atrial KICK):
- is PR interval normal? 0.12 - 0.20 ms
- are all PR intervals the same?
- if PR intervals different -> pattern?
- TIP: ventricles passively fill at a slow rate with no contraction. atrial contraction allows for MAX ventricle filling. AV node is delayed in electrical conduction because electricity moves at a faster rate than fluid
4) QRS evaluation (ventricle depolarization):
- are QRS complex normal? 0.06 - 0.12 ms
- are all QRS complexes same duration?
- do all QRS complexes look the same ?
5) QT interval (ventricle repolarization/refractory period):
- looking for elevation/depression (can indicate oxygenation issues)
- timing can be PROLONGED with drugs (ex. zofran)
TIP: DO NOT want prolonged QT -> can cause arrythmias/ectopic beats
sinus bradycardia (rhythm, rate, pqrst, clinical considerations (6), possible causes (3), treating (5))
- regular rhythm (R-R equidistant)
- rate: <60 BPM
- normal p wave preceding each QRS
- normal PR, QRS, T wave, QT intervals
clinical considerations of SB:
1) signs of poor perfusion:
- low BP
- decreased LOC
- dizziness
- syncope
- chest pain
- dyspnea
2) possible causes:
- cardiac ischemia
- HR slowing medications (digoxin, BB, CBB, antiarrythmias - amio, betapace)
- non cardiac causes: electrolyte disturbances, vagal responses, hypothermia, hypothyroidism (slow metabolism)
3) treating symptomatic bradycardia:
- assess the ABCs
- assess VS and IV patency
- administer O2 (maximize O2 blood carrying capacity with whats working)
- transcutaneous external pacemaker (SEDATE) -> shocks every second for 60bpm
- meds: atropine (Q3-5min), dopamine gtt (vasopressor), epinephrine gtt (inotrope, beta 1)
TIP:
- don’t treat the number, treat the PATIENT
- athletes have slower HR
- treatment is reserved for symptomatic patients
- occurring with sleep isnt abnormal
vasovagal response (what, how to, how to prevent)
- exaggerate neuro-cardiac response to certain stimuli
- vagus nerve (longest nerve) runs in proximity to the carotid artery to innervate the heart (brain -> anus)
- drop in HR and BP (arterial vasodilation) resulting in LOW blood flow to the brain
how to:
- ask patients to bear down
how to prevent:
- eat -> stimulates PNS
- know triggers (auras)
sinus tachycardia (rate, rhythm, pqrst, clinical significance (2), assess (5), causes (6), tx (3)
- regular atrial/ventricular rhythms
- rate: >100 BPM
- p waves normal, preceding QRS. MAY be superimposed by preceding t wave d/t speed
- PR intervals, QRS complex, T waves are normal
- QT shortened
clinical significance of ST:
1) decreases CO by reducing diastole (filling time, preload)
2) increases myocardial oxygen demands in an unhealthy heart
3) assess:
- ABCs
- VS
- chest pain
- dyspnea
- palpitations
4) causes:
- hypovolemia
- pain
- anxiety
- physiologic stress (ex. infection, sepsis, anemia, shock state)
- fever
- presence of stimulants: caffeine, nicotine, amphetamines OTC, drugs, illicit drugs
5) treatment (treat underlying cause if possible)
- consider slowing rate with BB or CBB, but be careful as it may be compensatory
- provide reassurance and reduce fear/anxiety is possible
- ex: hypovolemic (fluid resuscitation). pain (pain meds)
atrial rhythms: Premature atrial contractions (what, conducted vs. nonconducted, pathway, causes)
extra beats originating in the atria
- conducted (premature P wave, normal QRS)
- nonconducted (p wave showing out of nowhere)
- pathway: where is it coming from? (AV node or somewhere else in atria)
- causes: ICU patients may have more PACs than other patients (caffeine, stress, holding breath, etc.)
TIP:
- decompensating -> throwing ectopy (PAC/PVC) -> something else is going on
- reassess vitals/electrolytes
Superventricular tachycardia (what, rhythm, rate, p wave, presentation, mgmt (4)) vs. paroxysmal supraventricular tachycardia (occurs, mgmt (1))
what is refractory to medication and unstable?
SVT:
1) narrow complex (<0.12ms) tachycardia arising from above the ventricle (SA node)
- narrow complex regular rhythm
- rate: >150 BPM
- p wave buried, slurred, inverted
- presentation is different in ICU than ER (paroxysmal)
2) mgmt:
- medications to limit HR
- ADENOSINE - GOLD STANDARD
- amiodarone
- diltiazem (cardizem)
paroxysmal SVT:
1) usually occurs in the ER
2) mgmt: depends on CO
- valsalva maneuver (stable): breathe through closed straw or flush, bear down
refractory to medication and UNSTABLE: cardiovert (patient still has refractory period and DO NOT want to shock in refractory period)
adenosine (converts, _____/_______ conduction within the heart at the level of the _____ ____, indication, dosing)
converts narrow complex SVT to SR/ST
- reduces/blocks conduction within the heart at the level of the AV node
- slows rate to allow for analysis of conduction behind QRS complex
dosing:
- 6mg IVP (starting dose, central line preferred)
- 12 mg IVP for refractory/ 12 again for third dose
atrial flutter (rate, rhythm, p wave, qrs, pr interval, QT, mgmt (depends on, pharm (2), nonpharm, surgery))
- rate: atrial -> 200-400 BPM (will be greater than ventricular rate)
- abnormal p waves (AKA SAW TOOTH WAVES)
- QRS complex usually normal
- PR interval: atrial (regular), ventricular (irregular)
- QT: indiscernible
1) mgmt:
- dependent on ventricular response rate (need to control ventricle) -> either 1:1 or 1:2
- pharmacologic CARDIOVERSION: ilbutilide, sotalol, procainamide, amiodarone (GOLD STANDARD)
- pharmacologic RATE CONTROL: CCB (diltiazem), BB, digoxin
- non pharm: cardioversion, overdrive atrial pacing (speed atrial rate, then slow down gradually)
- permanent termination: radiofrequency ablation (lithmus -> burn myocardium)
atrial fibrillation (rate, rhythm, p wave, pr, qrs, t wave/qt, _____ ______ acts as a buffer zone to the _______, coordinated _____ ______ during _______ is impaired, effects (3), risk factor (7), complications (3), mgmt - goal is to convert within _____ hours, (3), medical tx - consider?, (2), overall, look at (3))
-irregularly irregular
- rate: atrial -> 350-600 BPM (disorganized chaotic stimulus), vent -> <100 or >150 (guidelines: >120 = RVR)
- p waves absent, PR interval indiscernable
- QRS: <0.12 ms, T wave/QT interval indiscernible
- AV node acts as a budder zone to the ventricles (keeps impulse out vents)
- coordinated atrial emptying during diastole is IMPAIRED
1) effects include:
- loss of “atrial kick” (30% CO, diastole fill)
- pooling and clotting of blood in the atria (if blood doesn’t move forward)
- subsequent thromboembolism (70,000 strokes annually)
2) RF:
- HTN
- advancing age
- dilated L atrium
- valve disease (aortic stenosis/mitral regurg) -> blood can’t get through aorta, causing back flow and mitral regurgitation
- CAD
- elevated glucose
- thyroid disease (hyper/hypo)
3) complications: loss of ventricular regulation (RVR)
- too much impulse going towards the AV node can cause “rapid ventricular response”
- rates exceed NSR and diminish diastolic filling
- treatment: rate/rhythm control drugs
4) complications: loss of coordinated emptying (risk of clot formation in the atria)
- treatment: DOACs (or heparin gtt in acute setting)
- TIP: stable -> DOAC, inpatient -> heparin gtt
5) complications: loss of atrial systole (30% CO)
6) mgmt: goal to convert in 48 HOURS
(a) rhythm control: conversion to SR
- antidysrhythmic drugs: amiodarone, ibutilide
- cardioversion: must be anti-coagulated if done outpatient
(b) rate control: control ventricular rate
- CCB, BB, digoxin (adjunct)
- slow ventricles after 48 hours -> to keep diastolic filling time normal
(c) anti-coagulation (post 48 hours):
- significant threat of emboli
- heparin IV gtt (FIRST)
- NOACs, coumadin (LT, outpatient)
7) medical treatment atrial fibrillation:
- consider duration of onset (48 hours is window of opportunity for un-anticoagulated cardioversion/conversion to NSR)
(a) rate control: slow ventricles
- IV/IVP diltiazem (cardizem)
(b) rhythm control: prevent blood clots
- IV amiodarone (rapid infusion, convert to PO)
- may cause profound vasodilation and hTN, may see pauses as convert to NSR
8) overall: look at precipitating factors (sepsis, hypoxia, increased CO2, DKA?)
cardioversion (electrical) (_____ may be converted with cardioversion within _____ hours, joules, which rhythm may be cardioverted and should be, delivers shock ________ from _______)
when would defib?
1) atrial fibrillation may be converted with cardioversion WITHIN 48H of onset
2) 200 -> 300 -> 400 joules (some cardiologists may start with 100)
3) stable VT MAY be electrically cardioverted
- unstable VT SHOULD be cardioverted
4) delivers shock AWAY from the QT (refractory period)
- pulseless VT = defibrillation
tip:
- stable vt: maybe cario
- unstable vt: cardio
- pulseless vt: defib
- adenosine inhibits breakdown epi/norepi
- caffeine inhibits adenosine
stroke prevention a fib (CHA2DS2VASc)
if patient is cardioverted in ____ hours, continue what?
if over ____ hours, what are the 2 options?
CHA2DS2VASc scoring system (higher score, more aggressive with anticoags)
- C = congestive HF
- H = hypertension
- A = age 75y
- D = diabetes
- S2 = stroke
- V = vascular disease
- A = age 64
- Sc = female
1) if patient is cardioverted WITHIN 24-48 hours of onset -> continue IV heparin gtt during hospitalization until decision is made regarding outpatient anticoagulation
2) iv OVER 48 hours, either delay DCCV until INR >2.0 (on coumadin), or dabigatran (pradaxa), eliquis, or xarelto for 3-4 weeks or TEE DCCV followed by anticoagulation
score risk recommendation for LT anticoagulation (0, 1, 2)
0 = 1.9% adjusted stroke risk, no therapy indicated
1 = intermediate
- anticoagulation recommended risk vs. benefit discussed with patient
- ASA strongly advised at very least
2 or more (3 women)
- anticoagulation highly recommended
- high (CHA2DS2VASc) or intermediate (CHADS2 classic)
- NOAX unless there are reasons to avoid it
- coumadin if valvular disease present
DOACs (3)
apixiban (eliquis)
dabigatran (pradaxa)
rivaroxaban (xarelto)
afib definitive treatment (4)
1) electrical cardioversion
- must be on anticoagulants for minimum 4 weeks, with TEE to r/o clot
2) catheter ablation therapy (similar invasiveness as cardiac cath)
3) cox maze procedures (requires open heart approach)
4) left atrial appendage occlusion (watchman device)
ventricular rhythms (charaterized by.., initiates.., mgmt (3))
characterized by regular ventricular rate WITHOUT a “p” wave or very short “RR” interval
- initiates at or below the AV NODE (junction)
mgmt:
- monitor BP
- Avoid BB/CCB
- pace if hemodynamically compromised (pace)
tip: slow, no p wave
- meds don’t help d/t SA node not functional
premature ventricular contractions (PVCs) (originates…, p wave, t wave/QRS complex, QRS complex, can be normal with.., types (2), mgmt (assess (2), treat, pharm) (4))
- originates in the ventricles below the BOH from a different pathway (Benign) -> doesn’t follow normal pathway
- P waves: absent d/t NO atrial depolarization
- T waves/QRS complexes: deflect in opposite direction
- QRS complex: WIDER than normal (bizarre)
- can be normal with no tx. or a warning of ventricular irritability
1) types:
- unifocal
- multifocal (2 PVC from 2 different spots, bigeminy/trigeminy)
2) mgmt:
- assess need for treatment
- assess for symptoms
- treat cause: assess electrolytes, assess for drugs that cause ventricular ectopy
- pharmacologic mgmt: BB to reduce sympathetic stimulation (intrinsic), antidysrhythmic drugs
tip: epi will cause ectopy/PVCs
ventricular tachycardia (VT) ( 3 or more _____ in a row, atrial rate, ventricular rate, _________ rhythm may or may not be regular, p wave, pr interval, qrs, t wave, mgmt depending on patient condition(3))
- 3 or more PVCs in a row (continuous -> concern)
- unable to determine atrial rhythm; ventricular rate >100 BPM
- ventricular rhythm may or may not be regular
- no p waves, unmeasurable PR intervals
- QRS complex is wide/bizarre with T wave in the opposite direction
mgmt: dependent on patient condition
(a) pulseless vt: life threatening, unsynchronized defibrillation
(b) unstable VT: electrical conversion (decreased BP, unconscious, pulse)
(c) stable VT: no loss of CO, meds: amiodarone or CCB (cardizem)
tip: causes low CO
torsades de pointes (what, looks like, cause (2), treatment)
polymorphic VT occurring with prolonged QT
- outline looks like a party streamer
- cause: antipsychotics, antiemetics
- treatment: 1-2gm of Mg, over 5-60 minutes (stable)
tip:
- no pulse -> ACLS
- unstable -> cardiovert
ventricular fibrillation (what, rhythm, rate, p wave, pr, t wave, waveform, primary _____ _________, mgmt (2))
life threatening dysrhythmia (no functional contraction)
- chaotic rhythm
- rate: indeterminate
- no p waves; immeasurable PR
- indiscernible t waves
- waveform may appear as wavy baseline
- PRIMARY LETHAL ARRHYTHMIAS
(no blood moving forward)
mgmt:
- defibrillation
- CPR (CODE)
clinical significance of VT/VF (5) (stable patients, unstable, pulseless, in vfib the ____ is _____ instead of contracting, _________ ___ to 0, steps for code)
1) stable patients in vt may convert with amiodarone 150mg over 10 minutes
2) unstable patients in vt require cardioversion
3) pulseless patients in vt require defibrillation
4) in vfib, the ventricles are QUIVERING instead of contracting, reducing CO to 0
5) ABCs are vital importance
- check pt responsiveness
- defibrillate/AED if pt pulseless
- CPR until defibrillator arrives
- initial (10 seconds) -> pulse check -> if not sure if you feel pulse, there is no pulse -> start CPR
- any downtime -> anoxia of the brain
first degree AV block (what, mgmt)
prolonged PR interval (> 0.20 ms)
- mgmt: none, suggest myocardial disease, no acute situation
second degree AV block, Type 1 (mobitz I/wenchebach) (characterized by, mgmt)
characterized by prolongation of PR interval before QRS complex is dropped
- mgmt: continue BB/CCB
tip:
- continues to get longer each time
second degree AV block, Type 2 (mobitz II) (characterized by, can lead to, key, mgmt (4))
characterized by normal PR interval followed by QRS complex with sudden drop of QRS complex
- can lead to complete heart block
- key: RANDOM DROP, something is blocking impulse from SA-> AV node
mgmt:
- transcutaneous pacing (if too slow)
- patient may need temporary transvenous pacemaker
- avoid BB/CCB
- patient has NO RESPONSE to atropine as normal
third degree AV block (characterized by, complete ______ between…, QRS, most?, cause (2), mgmt (4))
characterized by NO “p wave” before QRS complex or “p wave” does not occur before QRS complex
- COMPLETE DISASSOCIATION between atria and ventricles as no impulse is getting through (depolarizing independently)
- equidistant, QRS at slower rate
- most common
cause:
- Right MI
- loss of blood supply to AV node
mgmt:
- transvenous or transcutaneous pacemaker (increased HR to increase CO)
- will NEED permanent pacemaker
- DO NOT give BB, CCB, ANTIARRHYTHMICS
- patient has NO RESPONSE to atropine
bundle branch blocks (similar to AV blocks) (what, delays, leads to, evident by, cause (4))
functional/pathological block in intraventricular conduction pathway
- delays depolarization of ventricle as impulse travels from opposite side (outside of normal pathways) (depolarizes healthy -> unhealthy)
- leads to sequential ventricular depolarization as opposed to simultaneously
- evident by prolonged QRS complex (longer 0.12 ms), may be double peaked
cause:
- MI
- HTN
- HF
- cardiomyopathy
asystole (what, evidenced by, QRS, cause (5), treatment)
cardiac standstill or total absence of ventricular electrical activity
- evidenced clinically by no pulse or CO
- no QRS seen on monitors
- causes: ischemia, hypoxia, drug OD, electrolyte disturbances, traumatic arrest
- think about cause as much as treatment
- tx: CPR Q2min, epi 1mg Q3-5min
KEY: NO SHOCK
causes of asystole (h’s (6) , t’s (6))
H’s
- hypoglycemia (septic/shock state)
- hypovolemia
- hypoxia
- hydrogen ions (metabolic acidosis)
- hyper/hypokalemia
- hypothermia
T’s
- toxins/tablets (OD)
- tamponade (cardiac)
- tension pneumothorax (trauma)
- thrombosis (MI) (bloackage)
- thromboembolism (clot, cyanosis)
- trauma
pacemakers in ICU (what, consist of, may also contain, key)
artificial pulse generators which deliver electrical pulses to stimulate depolarization in the event of inadequate intrinsic heart beats to support CO
- consist of a pacing lead (RA/RV) and pulse generator (battery)
- may also contain AICD lead
key: sits under chest wall
types of pacemaker leads (3)
1) epicardial wires
- wires placed on the surface of the heart and brought through the skin and attached to a pulse generator (cardiac surgery)
2) temporary/transvenous pacing:
- lead wire inserted through a catheter into the right ventricle via Right IJ or femoral vein and attached to a pulse generator
3) permanent pacing:
- lead wires implanted surgically or transvenously and attached to an implanted generator with a lithium battery (lasts average 8-12 years)
types of pace makers (_______ pacing, electrodes place on, location, _____ ______ ____ often causes great discomfort or inability to capture, leading to …)
1) external pacing
- electrodes placed on the chest delivers impulses through the chest wall
- right upper/left lower + anterior/posterior
- chest wall impedance often causes great discomfort or inability to capture (increased resistance)
indications for cardiac pacing -> Drop in ____ (4)
CO
1) unstable bradycardia, AV blocks
- SBP <80
- AMS
- SOB
- chest pain
2) override or “overdrive” unstable tachycardias (cause same sx. as above) in ICU settings
3) brady-asystolic cardiac arrest
4) heart rate support of temporary conduction problems (MI, heart blocks, drug OD)
3 functions of pacemaker
1) (what, pacer delivers, monitor, may prolong, why would we want an atrial lead?
2) (what, successfully.., if new pacemaker and no ____, what do you do?)
3) (what, the pacer’s ability to …, if the pacer is too sensitive. if the pacer is not sensitive enough)
1) firing/pacing
- pacer delivers an impulse per the programmed rate
- monitor: observable “spike” followed by a p wave (if atria are stimulated) or QRS (if ventricle is the target chamber)
- may prolong QRS
- why would be want an atrial lead? cardiac output
2) capture the target chamber
- successfully depolarizes the target chamber (atria or ventricle) as evidenced on the monitor by a p wave or QRS after the spike
- if new pacemaker and NO CAPTURE -> turn patient on LEFT side
3) sensing
- the pacer’s ability to recognize the presence or absence of intrinsic electrical activity (senses if patients heart beats on own)
- if the pacer is TOO sensitive -> it will recognize inappropriate internal activity (such as skeletal muscle depolarization) and NOT FIRE when necessary (turn off on its own)
- if the pacer is NOT SENSITIVE ENOUGH -> it won’t recognize intrinsic activity and fire on top of one’s own electrical stimulations
automated internal cardiac defib (AICD) (what, indicated for (3), usually used in)
exam: will not?
allows for detection and termination of life threatening arrhythmias
indicated for:
- post MI w/ severe LV dysfunction (40 days post op)
- EF </=35%
- non-ischemic dilated cardiomyopathy w/ low EF
usually used in conjunction with anti-arrhythmic meds to minimize risk of “electrical discharge”
TIP:
- will shock if detects lethal arrhythmias
EXAM: not always immediate candidate for AICD -> will wear life vest first
key interventions of arrhythmias (9)
- assess for chest pain
- evaluate rhythm
- assess/monitor cardiovascular status
- complete assessment of peripheral circulation
- monitor VS frequently
- evaluate client’s response to dysrhythmias
- monitor appropriate lab tests (eg. lytes, mg/phos, cardiac enzymes)
- administer antiarrhythmics
- promote stress reduction
when would we want a 12 lead? (4)
exam: what would you do first for abnormality
new sign/sx:
- SOB (with no associated obvious pulmonary condition)
- chest pain/pressure
- dizziness
- palpitations/fluttering
- hyper/hypotension (sudden)
- nausea
- diaphoresis
when rhythms change:
- looked normal on the monitor, then went into afib
cardiac risk stratification pre-operatively
standard of care for people with cardia conditions
- longstanding history of murmurs/regurgitation
- left ventricular hypertrophy
- previous MI
EXAM: Get a 12 lead FIRST!!
what will warrant further investigation on a 12 lead
ST elevation/depression of 1mm
STEMI treatment (2)
1) emergent PCI:
- unlimited time frame (sooner = better)
- door to balloon goal time = 90 minutes
- arterial access via femoral/radial artery
- catheter advanced retrograde (against flow of blood) into aortic arch
- coronary arteries are illuminated with iodinated contrast (ALLERGY PRECAUTION) and fluroscopy
- atheroma lesions can be: ballooned/stented
- catheter/sheath is removed and “hemostasis” is obtained from accessed artery (patient to lay flat 2-6hours, observe for s/sx blood loss w/ direct manual pressure if needed, monitor pedal pulses for arterial clot, monitor kidney function >1.3 Cr, avoid metformin with diabetic patients, no blood thinners for 6 hours post cath)
2) thrombolytics if PCI is >2.5H away
- signs thrombolytic therapy working: resolution of chest pain, ST elevation GONE
st elevation is seen with
myocardial injury (acute blockage)
st depression is seen with
myocardial ischemia (stress)
stemi, ________ may be seen with opposite leads
depression
q wave development present with
myocardial infarction (damage)
anterior MI (leads) (7)
Leads: V1-V4
- Left anterior descending artery (LAD) -> supplies all of our CO
- V1, V2 may also indicate septal involvement which extends from front to back of the heart along the septum
- L/R bundle branch block
- Acute CHF/Shock
- LV aneurysm (2-3 weeks post MI, atypical chest pain, ECG unchanged)
- major risk arrhythmias
- PCI preferred treatment
inferior MI (leads) (5)
Leads: II, III, AVF
- Right coronary artery (RCA) infarct
- 1-3 AV blocks common (highly preload dependent)
- AVOID NGT/Morphine
- low BP, clear lungs, JVD
- Treatment: PCI, transvenous pacer
