ECG wk 2 Flashcards
you have hooked up your hairy pt to telemetry and see on the monitor that it looks like he is in V fib. you rush to check on him and see that he is brushing his teeth and aymptomatic
what happened?
did you set it up wrong and need to reapply?
o If pt is hairy man that is brushing his teeth on telemetry-it will look like he is in v fib….
your pt is exhibiting a weird rhythm and you go to check their radial but its pulseless
why?
what should you do to complete your assessment?
- Know where to check for a pulse in an emergency carotid & femoral. Patient will not be perfusing enough to have peripheral pulses!
what normal and abn things could contribute to sinus bradycardia
20 of them :(
May be d/t lower metb needs (sleep, athlete, hypothyroidism) vagal stim eg from V, suction, severe pain, extreme emotions, meds eg CCB, amiodarone, beta blockers, idiopathic sinus node dysfx, inc ICP, MI Other possible factors that contribute the Hs and the Ts: hypovolemia, hypoxia, H+ acidosis hypokalemia or hyperkalemia, hypoglycemia hypothermia toxins, tamponade tension pneumo, thrombosis, trauma (hypovolemia, inc ICP)
if pt has tachyarrythmia for a prolonged period of time (d/t no intervention) what can happen to their pulse
what kind of HR might do this and why
Pulselessness with a tachyarrhythmia occurs because the ventricles are not effectively moving blood out of the heart and there is therefor no cardiac output. Many tachyarrhythmias of a rate >150 will deteriorate into pulselessness if timely treatment is not given.
your pt has pulseless V tach what does this look like on ECG
what is the HR
how is the QRS complex
o Looking for a bunch of loops, that are narrow, disorganized
Looks like a row of PVCs in configuration, wide and bizarre; very rapid rate of 125-200 beats/min
the rate is usually greater than 180 beats per minute and the rhythm generally has a very wide QRS complex.
pulseless v tach interventions
we dont need to know the ACLS drugs (so basically anytime there are drugs mentioned as Tx) ACLS means advanced cardiac life support
Defibrillate ASAP! (meds: Epinephrine, Amiodarone, possibly Lidocaine these are all ACLS drugs)
what can cause sinus tachy
o psych or physio stress
o Meds that stim sympathetic response eg catecholamines, aminophylline, atropine, stimulants eg caffeine, alcohol, nicotine, illicit drugs eg amphetamines, coke, ecstasy
o Enhanced automaticity of SA node/excess sympathetic tone w dec parasympathetic tone
o Autonomic dysfx which leads to postural orthostatic tachy syndrome
what is the primary cause of V fib and how does it cause v fib
hypoxia which causes hyperirritability in the cardiac muscle tissue.
As a result, multiple muscles cells within the ventricles simultaneously fire as pacemakers causing a quivering or fibrillation that is ineffective for adequate cardiac output.
quality of pulse in v fib
what does v fib generally cause for the heart
Ventricular fibrillation is always pulseless
VF can rapidly lead to heart muscle ischemia and there is a high likelihood that it will deteriorate into asystole.
Tx of v fib
Defibrillate ASAP! (meds: Epi, Amiodarone, possibly Lidocaine)
what is pulseless electrical activity and what forms does it come in
PEA rhythm occurs when any organized heart rhythm that is observed on the electrocardiogram (ECG) does not produce a pulse.
PEA can come in many different forms. Sinus Rhythm, tachycardia, and bradycardia can all be seen with PEA.
PEA gen has a cause that can be treated
which two are most common and which of these causes 40-50% of PEA
hypovolemia and hypoxia
Hypoxia secondary to respiratory failure causes 40-50% of PEA
when you cant det the cause of the pulseless EA what do you do
how to Tx PEA
PEA should be treated in the same fashion as asystole
Priority: Good quality CPR and identifying cause of PEA
t or f aystole is a rhythm
how should it be treated
Asystole is not actually a true rhythm but rather a state of no cardiac electrical activity. The main treatment of choice for asystole is the use of epinephrine and CPR.
Priority: High quality CPR (meds: Epinephrine
your pt arrests what do you do
o assess them eg Check colour, pulse
o Call for help
o Call a code
o Begin CPR
what does acute coronary syndrome include
Unstable Angina
NSTEMI
STEMI
which is more likely to form embolus
thick cap
thin, fibrous cap
Thick cap = stable plaque
Thin, fibrous cap = unstable plaque, could rupture and cause clot to form, may totally block artery, clot could become embolus
what is unstable angina
what is the primary way that unstable angina and NSTEMI are different
UA is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (eg: ST segment depression or transient elevation or new T wave inversion).
UA and NSTEMI differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (ie: Troponin)
why would it often be so hard to distinguish Unstable angina from NSTEMI at the beginning
Since elevated troponin levels may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation.
other than troponin not gen being released with UA what is the other difference between UA and NSTEMI
which part of the ECG is affected
ST segmentand/orT wave changes are often persistent in NSTEMI while, if they occur in UA, they are usually transient.
NSTEMI and UA Tx
meds
Nitroglycerin
Beta-blockers
Clopidogrel (Plavix)
Heparin infusion or LMWH
why is there inc incidence of MI in L ventricle
b/c there’s more muscle on L side more blood flow = more pressure in L coronary artery increased atherosclerosis on L side due to increased pressure
