Lecture 1: Dysrhythmias Flashcards

1
Q

define depolarization

A

process where resting membrane potential of heart becomes more positive. occurs when Na and Ca2+ ions flow into cells leading to rapid change in cell’s electrical charge.

heart sends signal, causing cells in atria and ventricles to depolarize. causes the muscle fiber to contract.

this initiates the contraction of heart muscle, which pumps blood through the chambers.

inside of cell becomes more positive (sodium, potassium and chloride needs to move for contraction for heart to beat)

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2
Q

Ectopic

A

(SA node is the beginning point of domino effect) we have a coordinated contraction and if the impulse starts in a different locations then it is ectopic (still falls but not right sequence and not as effective)

when heart beats out of its usual rhythm or place.

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2
Q

repolarization

A

is the process where cell’s membrane potential returns to its resting, negative state after depolarization. during repolarization, K ions move out of cell restoring internal -‘ve charge.

after heart muscle contracts, electrical charge within cells begins to return to baseline. Preparing cells for next depolarization.

allows heart muscle to relax after contraction, so it is ready to contract again.

(all electrolytes move back to where they need to be so it can happen again) happens very quickly

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3
Q

permeability

A

(sodium, potassium, and chloride needs to pass) changing permeability affects this cycle (meds can alter this cycle)

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4
Q

absolute refractory period

A

(when sodium and potassium move back to where they need to be (there has not been enough electrolyte movement of electrolytes for depolarization to happen again)

“no entry zone”. time after heart muscle cell has depolarized when it cant fire again no matter what. gives heart time to rest and recover.

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5
Q

relative refractory period

A

(it could be set off, but not the same magnitude of depolarization if we are only part way through repolarization)

like a “half open door” for heart cells. heart cells can fire again, but only if signal is strong enough. time when heart is still recovering but if the heart gets a big enough push it could beat again.

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6
Q

describe to me how blood moves thru the heart (this is a horrible cue card going to have to whiteboard + look at notes)

A
  1. R atrium: blood comes from body, low in o2 into R atrium
  2. R ventricle: blood moves to the right ventricle
  3. lungs: r ventricle pumps blood into lungs to get oxygen
  4. L atrium: oxygen-rich blood returns to heart, entering the L atrium
  5. L ventricle: blood moves to the L ventricle
  6. Body: L ventricle pumps oxygen - rich blood out to the body

R atrium -> R ventricle -> lungs -> L atrium -> L ventricle -> body

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7
Q

describe the hearts automaticity

A

heart can contract by itself, independently of any signals or stim from body. heart contracts in response to electrical current conveyed by conduction sys.

heart attacks SA node
every cell in the heart can start the domino effect

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8
Q

3 main parts of the conduction system for the heart

A
  1. (sinoatrial) SA node
  2. AV node
  3. conduction fibers within the ventricle, specifically the bundle of His, bundle brances, and Purkinje fibres
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9
Q

describe to me the intrinsic pacemaker rates of cardiac conduction tissue

A
  • If everything is good, SA node is the pacemaker (60-100 beats per minute)
  • SA node sends signals to depolarize, the other parts won’t have a chance to take over because everything is synchronized and beautiful
  • No SA node, then AV node will say (hey this is not good (less than 60 beats a min), it will start depolarizing at a rate of 40-60
  • Less than 40 per minute, then the Purkinje fibers will start (40-15)
  • It is a failsafe method
    This is dysrhythmia
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10
Q

describe cardiac monitoring and telemetry (6 lead)

A
  • Top is cardiac monitoring strip (usually they have 2)
  • Connected straight to wall and monitored at bedside
    Portable units around their neck (wires connect to stickers on chest)
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11
Q

describe an ECG

A
  • Heart from different views
  • Tracings of electrical energy as it moves towards a lead
  • Looking from a different view of the heart
  • Energy moves as it depolarizes (energy coming towards me is more positive)
  • Going up means net energy is moving towards it
  • Positive when coming towards the lead (positive deflection), then drops when it goes away (negative deflection)
  • Ventricles (bigger QRS) is representative of the current as it goes through (bigger whether positive or negative)
  • Think of the lead as an eye
    Lead 2 is most easy to read
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12
Q

describe cardiac monitoring

A
  • Emergency (chest pain, SOB) to see changed (shows PQRST)
  • Quick view to show us anything obvious with the heart
  • Lets us know HR, disease or injury, pacemaker function, evaluates if a med is working
    Evaluate if a patient is having an MI
    3 lead or 5 lead
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13
Q

describe a 12 lead ECG

A

One is bisecting and the other looks at planes (look at the diagrams)

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14
Q

describe 5 lead cardiac monitoring (pic on the slides insert later)

A
  • LL left leg
  • RA right arm, etc
  • Colour coordinated
    White to the right, smoke (black) above fire (red), brown at the chest, white clouds over green grass
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15
Q

define afterload

A

what are we pumping against

(pressure or resistance against which ventricles pump to eject blood)

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16
Q

Preload

A

force exerted at the end of diastole (filling), and we are now going to contract, once they are filled that is preload. Preload determines how effective our contraction is going to be

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17
Q

describe contraction

A

mechanical event

ability of cardiac cells to shorten, causing cardiac muscle contraction in response to electrical stim

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18
Q

venous return

A

blood amount going into right atrium

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19
Q

stroke volume

A

amount of volume moved out of ventricles

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20
Q

ejection fraction

A

% of blood pumped out of ventricle with each contraction (each ventricle ejects a % (50-80%) (more volume in ventricle the more volume)

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21
Q

cardiac output

A

stroke volume (that goes out with each contraction) then multiple by contraction (HR per minute)

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22
Q

diastole

A

rest period with filling

term implies ventricular diastole

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23
Q

bp

A

force exerted by circulating blood volume

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24
shock
not getting output we need
25
systole
contraction of heart where blood is propelling into pulm artery and aorta (implied ventricular systole)
26
heart failure
condition where heart is unable to pump enough blood to meet metabolic needs of body, may result from any condition impairing preload, afterload, cardiac contractility, HR
27
define cardiac cycle
1 complete mech cycle of heartbeat, beginning with ventricular contraction and ending with ventricular relaxation
28
describe the cardiac cycle
* Majority of filling in ventricles is passive * Atrial kick at the end, pumps the last bit from the atria into the ventricles * Ventricles are full of blood, there is higher pressure in fill ventricles * AV valves that were open, now snap shut (S1) * Closed system (AV and pulmonary valves shut)-isovolumetric contraction * Ventricular muscles tense and contract, when pressure is at its peak, aortic and pulmonic valve open, and blood leaves-ventricular systole-blood moves forward * Ventricle are now less blood filled, pressure is now greater in aorta and pulmonary system * Aorta and pulmonic valves snap shut (S2) isovolumetric relaxation (closed system) * Atria that fills (pressure is greater), AV valves will open, this is now passive filling into ventricles and depolarization in atria, at the end is contraction and atrial kick Atria empties and ventricles is full, valves shut (isovolumetric relaxation)
29
5 steps of cardiac cycle
1. atrial systole 2. isovolumetric contraction 3. ejection 4. isovolumetric ventricular relaxation 5. passive ventricular filling
30
before depolarization describe the electrolyte concentrations
* Inside of heart is more negative (depolarized state) * Blood levels are the same basically * More potassium, sodium, and calcium in the cells vs outside * Inside of cell is more negative After repolarization we want the electrolytes to return to this so that depolarization can occur
31
describe depolarization
* Depolarization is electricity going through muscle * Does not mean heart contracts * We hope that the heart is contracting * Check pulse to see if they are contracting * If someone's heart does not pump * NOT the same thing * We hope that one causes the other * Depolarization is an electrical event Contraction is a mechanical event
32
describe the phase 0 of action potential 1. description 2. ionic movement 3. mechanisms
1. Upstroke 2. Na+ into cell, K+ leaves the cell, Ca2+ moves slowly into cell 3. Fast Na+ channels open
33
describe the phase 1 of action potential 1. description 2. ionic movement 3. mechanisms
1. Overshoot 2. Na+ into cell slows, Cl- into cell, K+ leaves cell 3. Fast Na+ channel close partially
34
describe the phase 2 of action potential 1. description 2. ionic movement 3. mechanisms
1. Plateau 2. Na+ and Ca2+ into cell, K+ out 3. Multiple channels (Ca2+, Na+, K+) open to maintain membrane voltage
35
describe the phase 3 of action potential 1. description 2. ionic movement 3. mechanisms
1. Repolarization 2. K+ out of cell 3. Ca2+ and Na+ channels close; K+ channels remains open
36
describe the phase 4 of action potential 1. description 2. ionic movement 3. mechanisms
1. Resting membrane potential 2. Na+ out, K+ in 3. Na+-K+ pump
37
define a rhythm stip
- graphic tracing of electrical impulses - movement of charged ions across membranes of myocardial cells creates certain wave forms on the tracings - wave forms represent depolarization and repolarization of myocardial cells
38
describe a rhythm strip
graphic tracing of electrical impulses movement of charged ions across membranes of myocardial cells creating wave forms on tracings wave forms represent depolarization + repolarization of myocardial cells
39
S1
at beginning of ventricular depolarization
40
S2
beginning of ventricular repolarization
41
what is a cardiac monitor paper
graphical display of electrical energy generated by the heart over time * 0.04 seconds (memorize this number) * One little box is 0.04 seconds is 1mm Each dash is 3 seconds between (6 seconds on the image total)
42
define waveforms
standard paper speed - 25mm/s
43
how many seconds is P waves
0.06 to 0.12 sec P Wave: atrial depolarization
44
how many seconds is PR interval
0.12 to 0.20 sec represents the time it takes an impulse to travel from atria to atrioventricular node the bundle of His, and the Purkinje fibres
45
how many seconds is QRS complex
0.06 to 0.12 seconds Longer than that, longer than normal to depolarize through ventricles, something is slowing it down
46
how many seconds is ST segment
deviation from baseline
47
how many seconds is QT interval
0.34 to 0.43 seconds at normal HRs, the QT interval is less than one half of the R-R interval when measured from one QRS complex to the next
48
distance btwn every complex should be _______________
the same (use paper to mark each QRS and then slide to ensure they are equal)
49
look at ipad notes for rhythm determination
50
how do we calculate HR
* Count number of complexes in a 6 seconds strip and multiply by 10 (gives HR per minute) * All test strips will be 6 seconds Irregular rhythms this is just an estimate When on a monitor, this can be consistent if you have a regular HR Look to make sure its staying consistent, and if its inconsistent we can make it into a range on their chart The strip will have pt name, date, time, etc. - quick way to figure out HR Not the best method is HR is irregular On exam they will all be 6 second strips
51
describe P wave
* SA node depolarizes, and goes through atria to beginning of AV node * Time it takes for all that movement should be 0.12-0.20 Want our P waves to all look the same If our Impulses are at the same spot, P wave will look the same P wave is atrial depolarization If P wave is abnormal you know this is a atrial issue
52
what is a controlled HR, brady... etc
HR being controlled means HR less than 100 Brady is less than 50 Athletes run a lower HR 105,110, 120 - this isn't good, there's lots of things that can happen when our HR is too high for too long that’s bad long term Exercise increases HR, BP may also increase, mechanism the body has to meet the needs of the body Overall is not a great thing for our functioning Majority of our atrial filling is passive, systolic kick adds the final bit of blood Need to have good contraction, when the kick happens we want it at the end Passive filling is time #1 factor If a HR too fast, not enough blood can enter atria before it closes Have to think about the "backroom" why is tachy bad
53
what is diastole
when there's rest: we lessen diastole if HR is really fast, means less blood flow to the heart vessels
54
what is systole
when there's contraction
55
if P wave is prolonged what does this mean
If P is prolonged the depolarization is slowed down, something is going on If tissue is dead, if someone had a heart attack affecting the AV node, if they have a lytes imbalance
56
1.describe what a P-QRS ratio should look like 2.what happens if there is P without QRS 3.and QRS without P
1. every P for every QRS 2. P without QRS means it did not go thru AV node 3. QRS without P, then it started in ventricles P is SA node
57
What is QRS
ventricular depolarization
58
the R side of our heart is...
pulmonary
59
the L side of our heart is...
systemic
60
if we have P without QRS
If we don’t have this we can have P without a QRS, which means atria depolarize but our ventricles did not, or no P but QRS meaning no action in atria, but ventricles depolarized
61
how do we want our SA node, and our ventricles
Every part of heart has its own rate, and own descending values We want our SA node is coordinated and well timed, that follows w atria and ventricular depolarization Our ventricles can do one of two things - they can depolarize early, or they can be waiting and waiting and nothing comes from AV node, we want our ventricle to depolarize itself for C/O
62
tell me about the Q wave. if they are having wide and deep waves what is this vice versa for shallow and narrow
Q wave - many ppl don't have this actually If they are wide and rly deep, they are called pathological which is abnormal - usually means they have had a heart attack and this is the remanence Shallow and narrow is normal If you don’t have a negative deflection, don’t have a Q wave
63
describe T wave for me
0.10 - 0.25 seconds ST segment this is the repolarization of ventricles sodium and potassium return where they should be
64
can you describe to me the difference between absolute and relative
This is super imposing phases of the cardiac cycle over rhythm strip As we come into downward slope we are making K and Na back to where they are supposed to be Flat is when ventricles are repolarized Na or K not enough - absolute refractory period Relative - there is enough for a possible reaction from cell The reason we know this is because later we are going talk about defibrillating patients
65
what happens if u defibrillate a normal person
it could cause an abnormal rhythm and cause something that changes C/O
66
what does the QT interval represent
electrical depolarization and repolarization of the ventricles Electrical depolarization and repolarization of the ventricles Some meds, some abnormalities can expand this period We want to monitor this
67
define artifacts you'd see on a ECG
look at ipad
68
describe to me what a normal sinus rhythm looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex: Treatment:
Heart rhythm: regular HR: 60-100 bpm P waves: uniform and upright P to QRS ratio: 1:1 PR Interval: 0.12-0.20 seconds QRS Complex: narrow, less than 0.12 seconds Treatment: none
69
describe to me what a sinus tachycardia looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex: Treatment:
Heart rhythm: regular (impulse origin remains SA node) HR: greater than 100-180 bpm P waves: uniform and upright P to QRS ratio: 1:1 PR Interval: 0.12-0.20 QRS Complex: narrow, less than 0.12 seconds Treatment: consider slowing HR (looking at underlying cause, metoprolol), consider that increased HR may be in response to decrease stroke volume
70
describe what a sinus tachycardia can cause and potential s/s
- can increase or decrease CO, response is highly individualized and influenced by atrial rate, contractile state of myocardium and circulating blood volume - dizziness and hypotension due to decreased CO - increased myocardial oxygen consumption may lead to angina you want to understand whats going on**
71
describe to me what a sinus bradycardia looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: regular HR: less than. 60 bpm P waves: uniform and upright P to QRS ratio: 1:1 PR Interval: 0.12-0.20 seconds QRS Complex: narrow, less than 0.12 seconds atropine, transcutaneous pacing
72
treatment for sinus bradycardia
- only symptomatic bradycardia needs to be treated - atropine 0.5 mg IVP q3-5 mins up to 3 mg - transcutaneous pacing - consider pt's current medications: example too much metoprolol can make them quite bradycardic
73
describe the C/O of sinus bradycardia
- CO is not significantly decreased until rate falls below 50 bpm. when HR falls below 50 bpm CO may be inadequate to meet the bodies o2 demands
74
s/s of sinus bradycardia
hypotension, pale cool skin, weakness, angina, dizziness, syncope, confusion, disorientation, SOB
75
what are atrial dysrhythmias
- atrial dysrhythmias reflect abnormal electrical impulse formation and conduction in the atria - most atrial dysrhythmias are not life-threatening - increases in HR shorten all phases of the cardiac cycle Most are non-life threatening is bc the majority of filling into the ventricles is passive, so we don’t have a contraction of the atria - as long as we have a controlled HR (less than 100) and lost the atrial kick most people are okay (many ppl have this and aren't in any immediate danger) not perfect we don't love them but not the worst thing When they start having HF,and other CVS issue this is a much bigger issue Shortening of the filling Atrial rhythms can be fast
76
tell me how to identify premature atrial contraction
Heart rhythm: regular except for premature beats (impulse of origin of underlying rhythm remains in SA node) HR: usually in normal range (60-100 bpm) P waves: regular P wave - uniform, upright,smooth, rounded premature beat - upright, flattened, notched P to QRS ratio: 1:1 or QRS may be absent following premature P wave PR Interval: 0.12-0.20 seconds QRS Complex: narrow, less than 0.12 seconds if the irritable site is close to SA node, the atrial P wave will look very similar to P waves initiated by SA node
77
treatment for premature atrial contraction
usually none, assess pt status
78
describe to me what afib looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: atrial and ventricular rhythms are irregular HR: atrial rate 350-700 bpm, ventricular rate varies, usually slower (can be controlled afib [less than 100] or uncontrolled afib [greater than 100]) P waves: no consistently identifiable P wave P to QRS ratio: more fibrillatory waves than QRS PR Interval: not measurable QRS Complex: usually narrow, less than 0.12 seconds
79
treatment for afib
conversion, rate control, anticoagulation, ablation
80
give me the general gist of afib
When someone is in Afib, no depolarization, no consistency, many spots in the atria that are excited depolarizing and causes a wacky rhythm No normal beats, changes the rhythm No coordinated flow, or coordinated contraction No coordinated kick at the end As long as we are controlling their HR, we aren't affecting ventricular contraction All of these impulses are hitting the AV node (gatekeeper) if its letting random bits through Pulse is irreg Treatment: convert back itno normal sinus rhythm, but this is very hard Can use electricity or meds If HR is 60, we don’t need to give the med bc its controlled But if its 100+ obvi give When blood pools it clots, this can cause risk of blood clots, strokes, PE (R side), L side can go anywhere else Treatments are in order of what you should do
81
describe to me what atrial flutter looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: atrial regular, ventricular may be regular or irregular HR: atrial rate 250-300 bpm, ventricular rate varies, usually slower P waves: flutter waves P to QRS ratio: more flutter waves than QRS PR Interval: not measurable QRS Complex: usually narrow, less than 0.12 sec
82
treatment of atrial flutter
conversion, rate control, anticoagulation, ablation therapy
83
give me the sparknotes of atrial flutter
Excitability in one spot - Afib is everywhere Sawtooth P waves bc its coming from the same spot More So likely this will feel reg We control this w medication or conversion Ablation since its in one spot is more useful
84
atrial fibrillation/flutter - describe CO intake and thrombi possibility
- can cause decrease CO due to losing the atrial kick and rapid ventricular response and precipitate HF, angina - thrombi may form in atria as a result of blood stasis -> may develop and travel to brain causing a stroke
85
afib /flutter treatment
- CCBs (diltiazem) - B-adrenergic blockers (metoprolol) - digoxin - antidysrhythmic agents (amiodarone) - cardioversion for new onset afib or afib not responding to meds or unstable pt
86
describe ventricular dysrhythmias sparknotes version
Inherent rate - sometimes w ventricular contractions this can be a defense mechanism, for example damage this could happen so that contraction happens and cardiac output actually happens SA generated but blocked SA nodes fine, but nothing came from above to below, the ventricular would know its not depolarizing so it would do it itself so body can function Rate of SA nodes is slower - for example from damage These are all safety mechanisms!
87
describe ventricular dysrhythmias/when do ventricles become the pacemaker?
- SA node fails to discharge - impulse from SA node is generated but blocked as it exits the SA node - rate of discharge of SA node is slower than that of ventricles - irritable site either ventricle produces an early beat or rapid rhythm
88
describe to me what premature ventricular contraction (PVC) looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: regular except for premature beat if impulse of origin of underlying rhythm remains in SA node HR: usually in normal range (60-100 bpm), depends on underlying rhythm P waves: regular P wave - uniform and upright premature beat - absent P to QRS ratio: PVC will not have a P wave PR Interval: none QRS Complex: greater than 0.12, wide and bizarre
89
treatment for premature ventricular contraction (PVC)
none if CO not impacted, frequent PVC's can decrease CO as they interrupt diastolic filling - o2 therapy for hypoxia - electrolyte replacement - drugs: B-adrenergic blockers, procainamide, amiodarone, lidocaine
90
sparknotes of PVC's
Not a rhythm, it is an isolated beat/complex There is an underlying rhythm (sinus tach/brad/afib/atrial flutter) Then randomly your going to have this wide bizarre looking beat Starts in ventricle so don't have a P wave w it. So usually looks normal. QRS is greater than normal bc the depolarization initiating farther so takes longer (starting in a diff place)
91
4 types of PVC's
1. ventricular bigminy (Bi means 2 means every second one is a PVC) 2. Multifocal PVC's (there are random abnormal beats [one place thats screwed up but these don't look the same so the tracing over it looks different bc the dominos are falling in different ways]) 3. coupled PVC's (2 together) 4. short run of VT (3 or more beats)
92
PVC VS Ventricular escape beat
PVC - premature/early didn't wait escape: late, they depolarize themselves
93
describe to me what ventricular tachycardia looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: usually regular (impulse origin of VT is on the ventricles) HR: 110-250 bpm P waves: usually absent P to QRS ratio: PVC will not have a P wave PR Interval: none QRS Complex: greater than 0.12 sec, are all similar, often wide and bizarre If you have a pulse u have C/O If you see this u get a pulse Stabilize pt, give O2, antiarrhythmic drugs Unstable: quickly convert them, pulse or no
94
treatment ventricular tachycardia
CO is compromised. Pulse vs Pulseless. - stabilize pt - O2, antiarrhythmic drugs to suppress the rhythm (ex: procainamide, amiodarone, sotalol), or defibrillation (pulseless)
95
Big muscle =
bigger wave (ventricles)
96
Smaller muscle
smaller wave (atria)
97
cardioversion
has pulse, VTECH, AFIB, when machine hooked up can mark their rhythm, and where the relative refractory period is, it will delay it so it is not on the relative refractory period Relative refractory period - we do not shock them!! Defibrillation: no pulse (no C/O), no coordinated movement, we just want to hit their heart w electricity
98
ventricular tachy
will come In one spot (one spot is chaotic) need to determine pulse or no pulse
99
describe sparknote version of ventricular tachycardia w pulse
- 3+ ventricular beats that are wide and bizarre, in succession at a rate greater than 100 beats per minute are termed ventricular tachycardia (VT) - there is usually severe underlying myocardial disease - sustained VT (more than about 30 beats) often degenerates into ventricular fibrillation, resulting in death
100
describe to me what ventricular fibrillation looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: reg or irreg (impulse origin of VT is on the ventricles) HR: unable to determine P waves: undetectable P to QRS ratio: none PR Interval: none QRS Complex: undetectable
101
treatment of ventricular fibrillation
No CO - CPR, defibrillation, ACLs protocols = treat underlying cause
102
sparknotes ventricular fibrillation
- is a chaotic ventricular rhythm that rapidly results in death - multiple areas within ventricule display marked variation in depolarization + repolarization, resulting in no organized ventricular depolarization (ventricles do not contract as a unit) Random, no cardiac output CPR and defibrillate NOT GOOD Rapidly goes to death Faster we defibrillate, the better chance at getting them back
103
describe to me what asystole looks like Heart rhythm: HR: P waves: P to QRS ratio: PR Interval: QRS Complex:
Heart rhythm: none HR: none P waves: usually none present P to QRS ratio: none PR Interval: none QRS Complex: none
104
treatment for asystole
no CO - CPR, ACLS protocol fine ventricular fibrillation may look like asystole, it is therefore necessary to check rhythm in more than one lead *do not defibrillate this rhythm
105
pulseless electrical activity treatment
CPR, ACLS protocol, identification of underlying cause Electrical conduction, no mechanical conduction Heart for some reason is not responding to the defibrillation Do CPR Nothing wrong w the electrical conduction, something wrong w the heart muscle pumping itself Check their pulse
106
give the sparknotes of defibrillation
they cant tell if the pt has a pulse, but it can tell if they are in asystole, VTACH, AFIB, etc. So it would tell you no shock but keep doing CPR. Feeling for a pulse, starting CPR, and calling for help, code blue 1. assess pt + check pulse 2. activate code blue 3. start chest compressions 4. defibrillate @120-200 joules 5. administer o2 if pt hypoxic