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
if pt has obvious ST elevation what do you assume the occlusion is like in their coronary arterie
A patient with obvious ST elevation typically has a total occlusion of at least one coronary artery
how do you diagnose a STEMI
STEMI is diagnosed based on ST-segment elevation (usually greater than 2mm) in two or more contiguous ECG leads
Tx of STEMI d/t occlusion
what is priority
: Percutaneous cardiac catheterization (PCI)
get patient to the cath lab ASAP!
Early reperfusion for STEMI occlusions are treated with fibrinolytics (often tPA) or percutaneous coronary intervention (PCI) (aka: angioplasty)
Some patients may require CABG surgery
MONA
order to do MONA in
when do you give morphine
o Oxygen
o Nitro—check pressure and prime the pump
o ASA
o Morphine (only if pts pain isn’t controlled by nitroglycerin)
what are you worried about with nitro
what to do before giving
remmeber the kitty
drop in BP!
heck their pressure and prime the pump
If you notice ECG changes, or your patient complains of chest pain or discomfort…what are you assessing
what do you do
ASSESS YOUR PATIENT!!! (focused cardiac assessment, PQRST questions, vitals, etc...) Cardiac output (& S/S cardiogenic shock): peripheral pulses, urinary output, decreased LOC, cool peripheries
Order 12 lead ECG
Alert physician, anticipate bloodwork including Troponin level
Consider MONA (Morphine, oxygen, nitroglycerin, ASA)
Initiate IV if not done already
Remain calm!! Your patient will be anxious and you can help by reassuring them
Some patients experience an ‘impending sense of doom
how to differentiate bet heartburn and cardiac pain
2 ways
One way to narrow down what’s happening is to administer a ‘Pink Lady’. This is a combination of an antacid and lidocaine given orally
If the patient’s pain subsides, it’s likely that the cause was non-cardiac, however, if the pain continues, more investigations are needed (ie: 12 lead, bloodwork, etc..)
o If youre pushing on it and it hurts more then it might not be cardiac
which cardiac marker is best and why
when is it released
how long does it stay int he system
Troponin is the preferred test because it is more specific for heart injury than other tests (which may be elevated in the blood with skeletal muscle injury) and it remains elevated for a longer period of time.
Levels can become elevated in the blood within 3 or 4 hours after heart injury and may remain elevated for 10 to 14 days.
what might inc troponin indicate in angina pt
In people withangina, an elevated troponin may indicate that their condition is worsening and they are at increased risk of a heart attack.
which other conditions might lead to elevated troponin
Troponin levels may also be elevated with other heart conditions such as myocarditis, cardiomyopathy, or CHF
which lyte changes lead to ST elevation and which to depression
ST elevation from HYPERkalemia
depression from hypokalemia and HYPERcalcemia
which lyte causes peaked/tall T waves or flattened T waves
peaKed (your K is peaking) HYPERkalemia
flattened hypokalemia
how does hypokalemia and hypocalcemia affect HR
what about HYPER
hypokalemia and hypocalcemia–>faster HR
hyper –>slower HR
what is the hallmark of hypo and hypercalcemia
HYPERCALCEMIA–>QTc is shortened
what are causes of hypokalemia
Use of potassium-wasting diuretics Diarrhea, vomiting, or other GI losses Alkalosis Excess aldosterone secretion Polyuria Extreme sweating Excessive use of potassium-free intravenous solutions Treatment of diabetic ketoacidosis with insulin
causes of HYPERkalemia
Renal failure
Fluid volume deficit
Massive cellular damage such as from burns and trauma
Iatrogenic administration of large amounts of potassium intravenously
Adrenal insufficiency
Acidosis, especially diabetic ketoacidosis
Rapid infusion of stored blood
Use of potassium-sparing diuretics
Ingestion of K+ salt substitutes
hypocalcemia causes
Rapid administration of blood transfusions containing citrate Hypoalbuminemia Hypoparathyroidism Vitamin D deficiency Pancreatitis Alkalosis Chronic renal failure Chronic alcoholism
HYPERcalcemia causes
Hyperparathyroidism Osteometastasis Paget's disease Osteoporosis Prolonged immobilization Acidosis Thiazide diuretics
your pt has sinus bradycardia (HR <60) what do you assess and maybe give
Assess client for tolerance of the rate. If hypotension or decreasing LOC occurs, the rhythm is treated.
Treatment: Atropine: If atropine is effective, chronotropic drug infusions are recommended as alternative to external transcutaneous pacing, pacemaker insertion for long-term issues.
sinus tachy what do you assess and do
what could have caused this
Regular rhythm, P waves present, HR 100 – 150 bpm
Assess client for tolerance of the rate. Most often caused by caffeine, alcohol, or physiologic response to stimuli. Treatment based on underlying cause.
Treatment: adenosine, beta-blockers, pain control.
if pt is in a fib after assessing them for tolerance of the rate what do you do
Evaluate client for emboli (pulmonary emboli or an embolic stroke) from clots that can form in fibrillating atrium
A decrease in cardiac output will occur with tachycardia (and loss of atrial kick)
Maintain bed rest until rate is controlled
Anticoagulation before cardioversion if client is in AF for longer than 48 hours
Treatment: digoxin, calcium channel blockers, beta-blockers, cardioversion, amiodarone. Anticoagulants such as warfarin, dabigatran, and rivaroxaban.
what kind of cardioversion might they try for a fib
Chemical cardioversion may be tried first: Medications available for chemical cardioversion of atrial fibrillation include procainamide, ibutilide, and amiodarone
Electrical cardioversion is also a common choice
how does electrical cardioversion work
Cardioversion involves the delivery of a high-energy shock through the chest wall to the heart muscle. This high-energy impulse activates all of the cardiac muscle and conduction tissue simultaneously. Reentrant circuits are interrupted, breaking the repeating cycle and stopping the arrhythmia. When the reentrant circuit is broken and the arrhythmia stops, the sinus node begins to fire again and a normal heart rhythm is restored.
what is prolonged with first degree heart block
what can cause first degree heart block
Tx
Prolonged P-R interval (normal is 0.12 – 0.20 seconds)
All P waves are followed by a QRS complex
May result from digitalis toxicity, electrolyte imbalance, or myocardial ischemia
Identify and treat the underlying cause
what kind of rhythm might occur after MI
what can it lead to
third degree heart block
Symptoms depend on client’s tolerance to rhythm; very unstable and may lead to asystole.
what is occuring with third degree heart block
what is the rate
No correlation between atrial impulses and ventricular response (the atria and ventricles aren’t ‘talking to each other’)
Rate: atrial rate 80-90 beats/min, with ventricular rate around 30 beats/min
Tx of 3rd degree heart block
Treatment: atropine, isoproterenol, and dopamine until pacing can be established with a pacemaker
what is it called when your sinus rhythm alters with respiration
sinus arrythmia
if ECG has these characteristics what is the name of the rhythm
Premature ectopic beats; occur within a basic rhythm; are of ventricular origin; no P waves; wide, bizarre QRS complex
premature ventricular contractions
what does PVC indicate and when should it be treated
Indicative of ventricular irritability; considered to be significant and should be treated if they:
- Occur in excess of 6 beats/min.
- Occur in a consecutive manner or in pairs.
Bigeminy– every other beat.Trigeminy– every third beat.Quadrageminy– every fourth beat - Occur on the T wave of a preceding complex
(“R” on “T” phenomenon)
what do PVCs ofte precede
ventricular tachy
how to treat PVC
Treatment: oxygen, electrolyte replacement, lidocaine, amiodarone, and/or procainamide;
what is the R on T phenomenon and what can it lead to
R on T phenomenon: PVC falls on the T wave of the previous complex can result in V-Fib
