Electrical System of Heart Flashcards
1st Type of Heart Cell and 4 Properties
Electrical/Pacemaker
Automaticity: property of cardiac cells to generate spontaneous action potentials; initiation
Excitability: the ability of a cardiac cell to generate an action potential at its membrane in response to depolarization and to transmit an impulse along the membrane.
Refractoriness: cannot fire another action potential even if a stimulus is received.
Conductivity: electrical signals travel through your heart. These signals cause different parts of your heart to expand and contract; transmission
2nd type of heart cell and 2 properties
Mechanical
- Contractibility: the ability of the cell to shorten/lengthen fibres
- Extensibility: the ability of the cell to stretch
Explain the hearts normal conduction pathway
- SA Node generates impulse and spreads from cell to cell from right to left atria
- Bachmann’s bundle: electrical connection between right and left atria
- 3 Internodal pathways transmit impulse from SA to AV node
- AV node slows impulse to allow for delay between atrial and ventricular contraction
- Bundle of his leaves AV and splits into purkinje fibres to supply rest of cardiac muscle
Intrinsic rates of SA, AV, and Purkinje Fibres
SA Node 60 – 100
AV Junction 40 – 60
Purkinje Fibres 20 – 40
What electrolytes are responsible for the electrophysiology of the heart?
Calcium, Magnesium, Potassium, Sodium
What is seen on the ECG of a patient with hypocalcemia or hypomagnesemia
Prolonged QT Interval
Phase 4, Phase 0, Phase, 1, Phase 2, and Phase 3 of Electrophysiology of the heart
Phase 4: resting, net negative
Phase 0: rapid depolarization - sodium influx and calcium channels open
Phase 1: fully depolarized - net positive
Phase 2: plateau - calcium entry and potassium diffussion slows
Phase 3: repolarization - calcium channels close and sodium is pumped out
Each small box on an ECG is
0.04 seconds
Each big box on an ECG is
0.2 seconds
Vertical and horizontal meanings of ECG
vertical: amount of depolarization
horizontal: time
P Wave normal length
0.08-0.11 seconds (2-3 boxes)
PR interval normal length
0.12-0.2 seconds (3-5 boxes)
QRS normal length
< 0.12 seconds
Normal ST segment
On isoelectric line
Normal T Wave
should begin in the same direction as the QRS
Normal QT interval
we use QTc (QT corrected interval because it is closely related to HR)
* Normal <0.41 seconds
P Wave represents
atrial depolarization and diastole - followed by atrial systole
0.08-0.11
PR Segment Represents
time that it takes for impulse to travel from atria to ventricle; period of delay
PR Interval represents
Inclusion of both the PR Segment (contraction + impulse travel time) and P Wave (atrial depolarization)
Total time depolarizing atria
0.12-0.2
QRS Complex represents
Ventricular depolarization + diastole followed by ventricular systole
< 0.12
J Point Represents
Junction of QRS Complex (ventricular depolarization) ends and ST segment (ventricular repolarization) begins
ST Segment Represents
early ventricular repolarization + ventricular contraction
T wave represents
ventricular repolarization + ventricular contraction ends (at end of T wave)
U Wave represents
late ventricular repolarization
QT Interval represents
Total time for ventricular depolarization and repolarization; dependent on HR. Interval increases with decreased HR, decreases with increased HR.
9 Step Method of ECG Analysis
Left to right:
P wave
- present?
- regular?
- P-P rate?
- PR interval?
QRS
- regular?
- R-R rate?
- Complex length?
Repolarization
- QTc Interval (refraction)
- ST Segment (ischemia/electrolyte changes)
If no P wave is present:
SA/AV not stimulating QRS or P wave hidden in other electric activity
You need to see a P wave to know
SA stimulated AV
Method to determine rate on ECG
1500 / no. of small boxes between each R wave
How do you calculate QRS Complex?
Normal < 0.12 (3 boxes)
of small boxes x 0.04 seconds
What does the QT Interval represent
The refractory period; beginning of Q to end of T
Cells are busy
Normal < 450 ms
ST Segment and T Wave Changes are associated with
- Myocardial ischemia/injury/infarction
- Electrolyte changes
How does hypokalemia change ECG?
T wave inversion, ST depression, Prominent U Wave
How does hyperkalemia change ECG?
Peaked T wave, P wave flattening, PR prolongation, Wide QRS complex
How do you put all the information gathered together to interpret the rhythm?
- specify site of origin (sinus, atrial, ventricular)
- specify rate and bpm (ex sinus brady 38bpm)
- evaluate patient presentation (asymptomatic v symptomatic)
Characteristics of SInus Rhythm
- atrial/ventricular rate 60-100
- rhythm: regular
- P waves present, upright
- 1P wave: 1 QRS
- PR interval 0.12-2second
- QRS < 0.12s
Characteristics of Sinus Arrhythmia
Variation in rate regularity, otherwise normal
Cause of sinus arrhythmia
changes in intrathoracic pressure during breathing
Common in athletes, children, can be normal
Characteristics of Sinus Bradycardia
- Rate < 60 beats per minute
- Rhythm regular
- 1:1 ratio
- 1 P wave: 1 QRS complex
- 1 Atrial complex: 1 Ventricular Complex
- Originates in the SA Node
- Causes: pathological, injury, medication, vagal stimulation
Treatment of sinus bradycardia
- Need to look at patient to determine if treatment is necessary
- 0 signs of decreased CO = stable = determine cause (medications/beta blockers, hypothyroidism)
- Signs of decreased CO = unstable = atropine to increase HR, acute transcutaneous pacemaker because SA node too slow; acts as SA node
Characteristics of Sinus Tachycardia
- Rate > 100 beats /minute (<180)
- Rhythm regular
- 1:1 ratio
- 1 P wave:1 QRS
- 1 Atrial Complex: 1 Ventricular Complex
- Originates in the SA Node
Treatment of Sinus Tachycardia
dependent on symptomatic (decreased CO)
* Always response of sympathetic stimulation – FIRST COMPENSATORY MECHANISM – always sign of another problem - (pain, fever, anxiety) therefore treat cause (antianalgesics, antipyretics, antianxiety); as well as beta blockers.
* Stimulation of vagal nerve; bear down like going to bathroom, increase intrathoracic pressure (blowing through straw)
Description of Premature Atrial Contraction
Ectopic focus of atrial tissue fires an impulse before next SA node impulse is due
Normal QRS because random impulse made it to AV
Causes + treatment of premature atrial contraction
stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine, alcohol, certain drugs; usually benign.
Treatment is of cause.
Characteristics of atrial flutter
Rate – ventricular rate regular or irregular
Saw-toothed/flutter waves
Ratio of P Waves:Ventricular Response – 2:1 or 3:1
SA re-entry circuit
Treatment of atrial flutter
- Medications: CCB or BB to slow SA node and hopefully reset (not likely – will ultimately need..)
- Cardioversion: electrical stimulus to stop all activity and stop re-entry circuit
Characteristics Atrial fibrillation
- Rate – difficult to calculate – watch ventricular response
- Rhythm – irregular
- Ratio – Multiple p waves: irregular ventricular response
What dysrhythmia has potential for clots and why?
Potential for clots (irreg rhythm) and HF = venous stasis
Atria contract very rapidly, unable to empty, discharging >400bpm
Unable to refill atrial chambers before contraction; Frank Starling Law
Treatment of atrial fibrillation
anticoagulants, beta-blockers, calcium channels blockers, amiodarone, digoxin
cardioversion: halting of electrical activity
Characteristics of supraventricular tachycardia
- Rate 150-250
- Regular rhythm – originates in or above AV node; somewhere in atria stimulated. AV re-entry circuit
- Undistinguishable p waves
- Normal QRS complex
Treatment of SVT
Unstable: adenosine to stop all electrical activity (cardioversion in medication form – then SA node should begin to fire again)
How do you determine difference between sinus tachy and SVT
Presence of P waves (not in SVT)
What 4 things can cause ventricular rhythms?
- SA node fails
- Impulse from SA is blocked
- Rate of SA is slower than ventricle
- If there is an irritable site in the ventricle
Rate associated with ventricular rhythms
20-40bpm
What is PVC?
- Result of increased irritability of ventricular cells. Firing prior to stimulation from SA or AV
- Was not stimulated SA/AV therefore no visible P wave
Characteristics of PVC
WIDE QRS WITH NO P
Early ventricular (QRS) complexes followed by compensatory pause
R-T phenomenon - Depolarization occurring before repolarization has fully occurred
Possible patterns of PVC
Couplet/Triplet: 2 or 3 in a row
Bigeminy/Trigeminy: every second QRS is PVC or every third QRS is PVC
Unifocal: look the same
Multifocal: look different
Characteristics of VTach
3 or more consecutive PVCs occurring at a rapid rate
Rate: 100-200 bpm – up to 300
No p-waves (dissociated atrial rate)
May or may not have pulse
Sustained v not
> 0.12s
Treatment of sustained v not sustained v tach
o Stable: short spurts/non-sustained: IV amiodarone/antiarrhythmic/cardioversion
o Unstable (usually quick deterioration): as soon as loose pulse – start CPR, defibrillation and IV Epinephrine (treated same as in VFib)
Description of VFib
- Electrical chaos in ventricles
- Chaotic multifocal firing of ectopic origin in ventricles
- Life-threatening; faster decompensation than VTach
- Coarse vs fine
Treatment of VFib
- CPR, defibrillation, IV Epinephrine
Asystole description
- Cardiac standstill
- Complete cessation of electrical impulses (atrial & ventricular)
- If atrial activity present, called “ventricular standstill”
- No rate, rhythm, CO, or pulse
- Ventricular fibrillation can mimic asystole
- Terminal rhythm; if CPR, defib, and epi did not work
What is PEA
Any organized rhythm present on ECG without ability to palpate central pulse
Explain treatment of symptomatic bradycardia
< 60BPM with S+S
1. Identify and treat underlying cause
- airway, oxygen, cardiac monitor, IV, 12 lead
2. Persistent and symptomatic?
- atropine, dopamine, epinephrine
- consider trancutaneous pacing
Explain treatment of symptomatic tachycardia
<150
1. Identify and treat underlying cause
- airway, oxygen, cardiac monitor, IV, 12 lead
2. Persistent and symptomatic?
No: Wide QRS? > No: vagal stim, adenosine, CCB, BB.
Yes: cardioversion, adenosine
Function of adenosine, amiodarone and atropine
Adenosine: stops heart
Atropine: speeds heart
Amiodorane: AFib
Causes of lethal arrhythmias
Hypoxia
Hypothermia
Hydrogen ions (Acidosis)
Hypovolemia
Hyper/hypokalemia
Toxins
Tamponade
Trauma
Thrombosis
Tension Pneumo
Explain cardiac arrest algorithm for VF/pVT
- help
- CPR
- IV/BVM
- search for and treat causes (Hs and Ts)
- Assess rhythm - if vF/pVT SHOCK
- 2 min CPR
- Assess rhythm - if vF/pVT SHOCK
- 2 min CPR + Epi q3-5min
- Assess rhythm - if vF/pVT shock
- 2 min CPR - amiodorane or lidocaine
Explain cardiac arrest algorithm for asystole/PEA
- Epinephrine ASAP
- CRP q2min epi q3-5min
- Assess rhythm - if shockable move to that algorithm, if not CPR, treat reversible cause
- determine appropriateness of resuscitation
Unstable Angina Description, ECG and Trops
Plaque rupture, thrombus formation around plaque causing partial occlusion of vessel, anginal pain at rest
ECG can be normal, inverted T waves, ST depression
Normal troponin
NSTEMI description, ECG and troponin
Plaque rupture, partial occlusion resulting in injury and infarct
ECG can be normal inverted T waves, ST depression
Elevated troponin
STEMI description, ECG and troponin
Complete occlusion, resulting in injury and infarct
ECG ST elevation
Elevated troponin
ST elevation in V3-V4 shows infarct in
LAD, anterior position
ST elevation in V5, V6, I, of avL shows infarct in
left circumflex (LAD or RCA) lateral position
ST elevation in leads II, III, or aVF shows infarct in
RCA, inferior position
ST elevation in leads V7-V9 show infarct in
RCA, circumflex, posterior position
ST elevation in V1 or V2 show infarct in
LAD, septal position
