Week 1: Dysrhythmias Flashcards
(75 cards)
1
Q
Depolarization - what does it cause
A
movement of ions across cell membrane, causing inside of cell to be more positive resulting in contraction
2
Q
Repolarization
A
Movement of ions where inside of cell is restored to negative charge
3
Q
Ectoic
A
impulse originating from a source other than SA node
4
Q
Permeability
A
ability of membrane channel to allow passage of electrolytes once it is open
5
Q
Absolute refractory period - when is it? what happens to cardiac cells?
A
corresponds with onset of QRS complex to approximately the peak of T wave
- cannot be stimulated to conduct electrical impulse no matter how strong the stimulus
6
Q
Relative refractory period - when is it? what happens to cardiac cells?
A
downslope of T wave
- can stimulate to depolarize if the stimulus is strong enough
7
Q
Explain the hearts automaticity
A
- can contract by itself, independently of any signals or stimulation from body
- contracts in response to an electrical current
8
Q
what are the areas of conduction
A
- Sinoatrial node (SA)
- Atrioventricular node (AV)
- Conduction fibers within ventricle - bundle of His, bundle branches, Purkinje fibers
9
Q
What are the rates of intrinsic pacemakers
A
- SA node - 60-100bpm
- AV node - 40-60bpm
- purkinje fibers - 15-40bpm
10
Q
what are 3 examples of impairments that can impact the hearts system?
A
- ventricular hypertrophy
- valve impairment
- structural integrity (primary cause of weakening)
11
Q
Cardiac monitoring - what is it? settings where we may use it?
A
- non-invasive, quick, effective diagnostic tool
- can be 3 or 5 lead: continuous monitoring
- emergency, intensive care units, telemetry units, medical procedures
12
Q
Cardiac monitoring - what are the 6 things we use it for?
A
- monitor heart rate
- evaluate effects of disease or injury on heart function
- evaluate pacemaker function
- evaluate response to medications (ex. antiarrhythmics)
- obtain baseline recording before, during, annd after medical procedure
- evaluate for signs of myocardial ischemia, injury, infarction
13
Q
Where do we place each lead on a 5-lead cardiac monitoring system?
1. Chest: Brown
2. RA: White
3. LA: Black
4. LL: Red
5. RL: Green
A
Chest: Right sternal border, 4th ICS
Right arm: 2nd ICS
Left arm: 2nd ICS
Right leg: 7ish ICS
Left leg: 7ish ICS
- Remember: white to the right, smoke (black) over fire (red), brown i <3 chocolate (chest), green is last
14
Q
Afterload
A
pressure/resistance against which the ventricles must pump to eject blood
(volume pumping against)
15
Q
preload (end-diastolic volume)
A
force exerted by blood on walls of ventricles at the end of diastole
- helps determine how effective our contraction is going to be
16
Q
contractions
A
cardiac cells shorten, causing muscle contraction in response to electrical stimulus
17
Q
venous return
A
amount of blood flowing into right atrium each min from systemic circulation
18
Q
stroke volume
A
amount of blood ejected from ventricles with each heartbeat
19
Q
ejection fraction
A
% of blood pumped out of a heart chamber with each contraction
- 50-80% is normal
20
Q
cardiac output
A
amount of blood pumped into aorta each min by heart (SVxHR)
21
Q
Diastole
A
phase of cardiac cycle where atria and ventricles are RELAXED
- blood enters chambers
22
Q
Systole
A
Contraction of the heart where blood moves into pulmonary artery and aorta
23
Q
blood pressure
A
force exerted by the circulating blood volume on the arterial walls
24
Q
Heart failure
A
condition where heart is unable to pump enough blood to meet metabolic needs of the body
- results from any condition that impairs preload, afterload, cardiac contractility, or heart rate
25
shock
inadequate tissue perfusion that results from failure of cardiovascular system to deliver sufficient oxygen and nutrients to sustain vital organ function
26
cardiac cycle
one complete mechanical cycle of the heartbeat - beginning with ventricular contraction and ending with ventricular relaxation
27
What are the 5 phases of the cardiac cycle and what happens
1. Atrial systole: atrial kick - atrial contraction sends last bit blood from atria to ventricles, AV valves open, Semilunar valves closed
2. Isovolumetric contraction: AV valves close (LUB), stable volume in ventricles bc wave of depolarization is increasing to overcome pulmonary and systemic pressures, no blood leaving ventricles yet
3. Ventricular systole: pressure in ventricles overcomes aortic and pulmonary pressure, semilunar valves open, blood ejected into arteries
4. Isovolumetric relaxation: Semilunar valves shut (DUB), AV valves are closed, ventricles relax, no blood enters until AV valves open when Atrial pressure > Ventricular pressure
5. Ventricular diastole: Atrial pressure > ventricular pressure = AV valves open allowing for passive filling into ventricles. Phase continues until atrial systole
28
Potassium resting state concentrations (extracellular/intracellular)
Extracellular: 4 mEQ/L
Intracellular: 135 mEG/L
29
Sodium resting state concentrations (extracellular/intracellular)
Extracellular: 145 mEQ/L
Intracellular: 10 mEG/L
30
Calcium resting state concentrations (extracellular/intracellular)
Extracellular: 2 mEQ/L
Intracellular: 0.1 mEG/L
31
Contraction vs. Depolarization
Depolarization is electricity going through muscle and DOES NOT MEAN that heart is contracting
- Depolarization can cause contraction
32
What happens during phase 0 of an action potential (ionic movement and mechanisms)
- upstroke
- Ionic movement:
- Na+ into cell
- K+ leaves cell
- Ca2+ moves slowly into cell
- Mechanisms: Fast Na+ channels open
33
What happens during phase 1 of an action potential (ionic movement and mechanisms)
- Overshoot
- Ionic movement:
- Na+ into cell slows
- Cl- into cell
- K+ leaves cell
- Mechanisms: Fast Na+ channels close partially
34
What happens during phase 2 of an action potential (ionic movement and mechanisms)
- Plateau
- Ionic movement:
- Na and Ca into cell
- K out
- Mechanisms: multiple channels (Ca, Na, K) open to maintain membrane voltage
35
What happens during phase 3 of an action potential (ionic movement and mechanisms)
- Repolarization
- Ionic movement:
- K out of cell
- Mechanisms:
- Ca and Na channels close
- K channel remains open
36
What happens during phase 4 of an action potential (ionic movement and mechanisms)
- Resting membrane potential
- Ionic movement:
- Na out
- K in
- Mechanism: Na-K pump
37
What is a rhythm strip
- graphic tracing of electrical impulses
- movement of charged ions across membrane of myocardial cells creating waveforms that represent depolarization and repolarization
38
What does the P wave represent and how long should it last
Atrial depolarization / contraction
0.06-0.12 seconds
39
What does the PR interval/segment represent and how long does it last?
electrical impulse traveling from the SA node to the AV node
0.12 to 0.20 seconds
40
What does the QRS complex represent and how long does it last?
Ventricular depolarization/contraction
0.06-0.12 seconds
41
What does the ST segment represent
period between ventricular depolarization and repolarization
42
What does the T wave represent and how long should it be?
Ventricular repolarization
0.10-0.25 seconds
43
What does the QT interval represent and how long does it last?
time for ventricular depolarization and repolarization
0.34 to 0.43 seconds
44
When does S1 and S2 occur on the ECG
S1 at QRS peak
S2 end of T wave
45
What is the standard paper speed?
what are the measurements of 1 little box?
what are the measurements of 1 big box?
what time does the little triangle dash represent?
22mm/s
- little box: 0.04 sec
- big box: 0.2 sec
- dash: 3 seconds
46
What are the 7 steps of EKG analysis
1. determine heart rhythm
2. measure heart rate
3. P-wave evaluation
4. PR-interval evaluation
5. P-QRS ratio
6. QRS complex evaluation
7. Interpret the rhythm
47
Explain the 3 rhythm determinations
1. regular: QRS spaces are equal
2. Irregular: QRS distances are not equal
3. Irregularly regular: Irregular pattern of QRS
48
How do you calculate heart rate via rhythm strip? *will be on midterm
6-second method
- the R-R intervals in 6 seconds, multiply by 10
- determine 6 seconds, count the amount of QRS complexes in 6 seconds, and multiply by 10
NOTE: 5 large boxes = 1 sec, 15 = 3 sec, 30 = 6 sec
49
P-wave/P-R interval evaluation: time, representation, clinical significance
ensure upright and uniform
- P: 0.6-0.12 sec
- P-R Interval: 0.12-0.20 sec
- atrial depolarization
- time for impulse to travel from atria to AV node, bundle of His, and Purkinje Fibres
- if beyond normal time, we can have dead tissue, heart attack, electrolyte imbalances
50
P-QRS Ratio - is there a P for every QRS? what happens with P no QRS and no P and QRS
There should be!
- P + no QRS = atria depolarize and ventricles don't (can be AV block, ventricle damage)
- no P + QRS = no action in atria but ventricles depolarized
51
When do we shock a defibrillating patient?
we do not want to shock during relative refractory period bc it can cause abnormal rhythm impacting cardiac output
52
what are artifact readings
Environmental factors causing abnormal readings
ex. stickers not sticking properly, sweat/hair
- we need to assess patient so we know it is a real problem or just environmental issue
53
Explain the following for a normal sinus rhythm
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular
Heart rate: 60-100 bpm
P waves: uniform and upright
P to QRS ratio: 1:1
PR interval: 0.12-0.20 sec
QRS complex: narrow, less than 0.12 sec
Treatment: none
54
Explain the following for Sinus Tachycardia
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular as impulse of origin remains in SA node
Heart rate: 100-180bpm
P waves: uniform and upright
P to QRS ratio: 1:1
PR interval: 0.12-0.20 sec
QRS complex: narrow, less than 0.12 sec
Treatment: consider slowing heart rate, look at underlying cause. MEDICATION: metoprolol for rhythm control/BP control
55
what is sinus tachycardia influenced by? what can it do to the cardiac output? what are common side effects and why? what can it lead to?
- influenced by atrial rate, contractile state of myocardium and circulating blood volume
- increase or decrease cardiac output
- dizziness and hypotension due to decreased cardiac output
- increased myocardial oxygen consumption may lead to angina
56
Explain the following for Sinus Bradycardia
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular
Heart rate: less than 60 bpm
P waves: uniform and upright
P to QRS ratio: 1:1
PR interval: 0.12-0.20 sec
QRS complex: narrow, less than 0.12 sec
Treatment: only treat symptomatic!
- atropine to speed up (0.5 mg IVP q3-5min)
- transcutaneous pacing
- consider current medications
57
Impacts of sinus bradycardia on CO and symptoms of sinus bradycardia
CO not significantly decreased until rate under 50 bpm - this is when CO inadequate to meet body's oxygen demands
Symptoms: hypotension, pale/cool skin, weakness, angina, dizziness/syncope, confusion/disorientation, shortness of breath
58
what are atrial dysrhythmias, what do they do
- reflect abnormal electrical impulse formation and conduction in the atria
- most are not life-threatening
- increases in heart rate shorten all phases of cardiac cycle
59
why are most atrial dysrhythmias not life-threatening
because majority of filling into ventricles are passive so as long as we have controlled HR we are okay
- we need to ensure cardiac output and strength with controlled rate
60
Explain the following for Premature atrial contraction
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular except for premature beats (ONE beat)
Heart rate: usually normal
P waves: regular = uniform/upright/smooth, premature = upright, flattened/notched
P to QRS ratio: 1:1 or QRS absent following premature beat
PR interval: 0.12-0.20 sec
QRS complex: narrow, less than 0.12 sec
Treatment: none, assess pt status - significant impact when there is enough that are early and do not cause ventricular contractions
61
Explain the following for atrial fibrillation
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: atrial and ventricular rhythms are irregular (no consistent impulses from SA node)
Heart rate: atrial rate 350-700 bpm, ventricular rates varies usually slower (controlled = less than 100, uncontrolled = more 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 sec
Treatment:
- conversion (1st choice): convert atrial rhythm to normal sinus via meds or electricity
- rate control: keep HR under 100
- anticoagulation: meds to stop blood pooling and blood clots
- ablation: cauterize area that is misbehaving to stop the inappropriate excitability
62
Explain the following for atrial flutter
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
same as Afib but only one spot is excitable rather than many
Heart rhythm: atrial regular, ventricular can be regular or irregular
Heart rate: atrial rate 250-300 bpm, ventricular varies
P waves: flutter waves
P to QRS ratio: more flutter then QRS
PR interval: not measurable
QRS complex: usually narrow, less than 0.12 sec
Treatment: conversion, rate control, anticoagulation, ablation therapy
63
what can atrial fibrillation / flutter result in?
- decrease in CO due to ineffective atrial contractions (looss of atriall kick) and rapid ventricular response
- precipitate heart failure and angina
- thrombi formation in atria due to blood stasis - can cause stroke if travels
64
Atrial fibrillation/ flutter treatments (5)
1. calcium channel blockers - Diltiazem
2. B-adrenergic blockers - metoprolol
3. Digoxin - only with heart failure elements
4. Antidysrhythmic agents - amiodarone
5. Cardioversion for new onset of Afib or if Afib is not responding to meds or unstable patient
65
What are ventricular dysrhythmias?
- impulse from SA node is generated but blocked (normal activities of atria but ventricles are acting up)
- rate of discharge of SA is slower than the ventricles (ventricles decide to depolarize themselves if no signal from SA)
- an irritable site in either ventricle producing early beat /rapid rhythm (abnormal)
66
Explain the following for a Premature ventricular contraction
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular except for premature beat if origin remains in SA node
Heart rate: normal range, depends on underlying rhythm
P waves: regular = upright and uniform, premature beat = absent p wave
P to QRS ratio: PVC will have no P wave
PR interval: none
QRS complex: greater than 0.12 sec, wide and bizarre
Treatment: none if CO not impacted, frequent PVC's can decrease CO and interrupt diastolic filling
- oxygen therapy for hypoxia
- electrolyte replacement
- drugs: B-adrenergic blockers, procainamide, amiodarone, lidocaine
67
what are the 4 types of premature ventricular contractions
1. ventricular bigeminy (every other is a PVC)
2. multifocal PVCs (happening in more than one place)
3. Coupled PVCs (2 PVCs back to back)
4. Short run of VT (3+ beats) (3 PVC back to back)
68
what is a ventricular escape beat
when the ventricles get stood up by the SA/AV nodes so it decides to leave the party by contracting itself
69
Explain the following for ventricular tachycardia
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: usually regular (impulse origin of VT on ventricles)
Heart rate: 110-250 bpm
P waves: usually absent (bc ventricle is bigger muscle so activity in atria gets buried)
P to QRS ratio: PVC will not have a P
PR interval: none
QRS complex: greater than 0.12 sec, all similar, wide and bizarre (depends on excitable site)
Treatment: CO IS COMPROMISED (no coordination between filling)
- assess for pulse vs pulseless
- stabilize pt - O2, antiarrhythmic drugs to suppress rhythm (procainamide, amiodarone, sotalol), cardioversion if pulse present, defibrillation if pulseless
70
cardioversion vs. defibrillation
cardioversion: same as dfib but we mark QRS, rhythm, and relative refractory period so we do not mess electrical conduction up and make it worse
- given if pulse present
defibrillation: no activity in heart so we have no area to screw up, so we stop the heart completely and hope it restarts
- given is pulse is not present
71
Ventricular tachycardia definition & what can it degenerate to?
- 3 or more ventricular beats that are wide and bizarre, in succession at a rate greater than 100 bpm
- there is usually a severe underlying myocardial disease
- sustained VT ( > 30 beats) can degenerate into ventricular fibrillation, resulting in death
72
what is ventricular fibrillation
very chaotic rhythm that rapidly results in death
- multiple areas within ventricle display variation in depolarization and repolarization resulting in ventricles not contracting as a unit
73
Explain the following for ventricular fibrillation
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: regular or irregular
Heart rate: unable to determine
P waves: undetectable
P to QRS ratio: none
PR interval: none
QRS complex: undetectable
Treatment: no CO - CPR, defibrillation, ACLS protocols & treat underlying cause
74
Explain the following for Asystole
Heart rhythm:
Heart rate:
P waves:
P to QRS ratio:
PR interval:
QRS complex:
Treatment:
Heart rhythm: none
Heart rate: none
P waves: usually none present
P to QRS ratio: none
PR interval: none
QRS complex: none
Treatment: no CO - CPR, ACLS protocol
- no defibrillation bc it can stop the heart and we don't want that
75
Pulseless electrical activity treatment
CPR, ACLS protocol, identify underlying cause
we have conduction but no contraction
