# Rate in beats/min = 60/interval between two beats in seconds - PowerPoint PPT Presentation

PPT – Rate in beats/min = 60/interval between two beats in seconds PowerPoint presentation | free to download - id: 4d3bb4-YzM3M

The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
Title:

## Rate in beats/min = 60/interval between two beats in seconds

Description:

### Rate in beats/min = 60/interval between two beats in seconds A handy shortcut is: Heart rate (beats/min) = 1500/R-R interval (mm) 1500/20 = 75 b/min – PowerPoint PPT presentation

Number of Views:35
Avg rating:3.0/5.0
Slides: 44
Provided by: JamesD114
Category:
Tags:
Transcript and Presenter's Notes

Title: Rate in beats/min = 60/interval between two beats in seconds

1
Rate in beats/min 60/interval between two
beats in seconds  A handy shortcut is
Heart rate (beats/min) 1500/R-R interval (mm)
1500/20 75 b/min
2
(No Transcript)
3
Heart block Heart block results when conduction
between the atria and ventricles is altered.
This often occurs at the AV node which has a low
safety factor.
4
8 x .04 .32 sec
First degree - prolonged PR interval only. The
normal PR interval is 0.12 to 0.21 seconds. A PR
interval gt0.21 would be classified as first
degree block. The injury is above the His
bundle because His conduction is very fast even
when injured.
5
(No Transcript)
6
Second degree - some P waves are not followed by
QRS. Often has a regular sequence, i.e., 21 or
32. The first number is the number of P waves
present and the second is the number of QRSs.
What is this?
7
Mobitz I (Wenckebach) the PR progressively
lengthens with one P wave for every QRS until a
beat is dropped. Usually this block occurs above
His bundle. This is common in coronary patients
and is caused by increased vagal tone and usually
eventually disappears with no problems
8
(No Transcript)
9
Mobitz II 2nd degree heart block missed beats
with no change in P-R It is a dangerous
arrhythmia because the heart may suddenly start
beating very slowly or even stop. The injury is
below the AV node in the fast conducting His
bundle where the pacemaker activity is very slow
10
Complete heart block. Since there is no
conduction down the AV node pathway both atria
and ventricles beat regularly but at different
rates (ventricles always slower).
11
Slow ventricular rate Usually treated with
pacemaker May be temporary or intermittent. Can
be induced by drugs that cause increased
vagotonia (e.g. neostigmine) or slow conduction
in the AV node (e.g. beta blockers or calcium
antagonists)
12
WPW Normally conducting cardiac muscle bridges
the gap between atria and ventricles.
The accessory pathway activates the ventricle
before normal activation via the AV node.
13
The PR interval is lt0.12 sec
Delta waves are usually present
14
If accessory pathway has short antegrade
refractory period, it will cause the ventricle to
beat dangerously fast if atrial fibrillation
occurs. Ventricles pump very poorly at high
heart rates.
Can get retrograde conduction causing reentry and
a tachycardia.
15
(No Transcript)
16
Sinus Tachycardia gt100b/min 1. Normal P waves all
followed by QRS 2. Normal or shortened PR
interval 3. QRS and T vectors are normal 4. ST
segments are normal 5. RR interval is regular but
short lt15mm 1500/15 100
17
Sinus Bradycardia lt60b/min 1. P waves are present
and all are followed by a QRS 2. Normal and
constant PR interval 3. QRS and T vectors are
normal 4. ST segments are normal 5. RR interval
is regular but long gt25mm 1500/ 25 60
18
Premature ventricular contraction (PVC) 1.
Arises from ectopic focus in ventricles 2. Early
QRS not preceded by a P wave (see fig 4) 3. Will
usually have an unusual QRS shape a) odd
vector b) prolonged QRS duration 4. A
compensatory pause
19
Premature ventricular contraction (PVC) 5. The
premature contraction occurs before the ventricle
is completely filled and the contraction may be
two weak to open the aortic valve. 6. The beat is
not felt in the peripheral pulse and can be
mistakenly thought to be a second degree
block. 7. The following beat has an over-filled
ventricle and is very strong (this is often
perceived by the patient)
20
Multifocal PVCs. Two separate foci are
originating PVCs Irritable ventricle IF all PVCs
are identical it is from only one ectopic site
(Unifocal).
21
(No Transcript)
22
Premature atrial contraction (PAC) 1. Arises from
an ectopic focus in the atria. 2. Will have an
identifiable P wave but the shape of the P wave
may be altered 3. May have a normal QRS 4.
compensatory pause will be small or absent
23
The compensatory pause is lacking because the SA
node was reset. The rhythm has been shifted.
The QRS may be altered if some of the ventricle
is still in its refractory period (the P wave is
the key, not the shape of the QRS).
24
Electrical reentry can cause fibrillations and
tachycardias.
25
Atrial fibrillation 1. Irregularly irregular 2.
No P waves
26
The AV node acts to keep the ventricular rate
low May be treated with drugs to depress AV
conduction and slow the ventricular rhythm Beta
blockers, calcium channel blockers
8 beats in 6 seconds or 80 beats per minute
27
Common will occur in about 1/3 of the
population Lowers cardiac output if ventricular
rate is high Not a life-threatening arrhythmia
unless in WPW Stroke risk - anti coagulation may
be indicated
28
Atrial flutter occurs when the atrium beats very
rapidly rather than fibrillates. The AV note
filters out most beats so the ventricle beats at
a slower rate. Note the presence of multiple p
waves between QRS complexes.
29
1500/9166
Ventricular tachycardia (3 or more sequential
beats) 1. Regularly occurring rapid rhythm
originating from a regularly firing ventricular
ectopic focus. 2. QRS morphology is usually like
a PVC (depending on where the ectopic is located)
30
Because the cardiac output falls due to the fast
rate it often produces (or worsens) myocardial
ischemia which then makes ventricular
fibrillation more likely
31
VF
Ventricular fibrillation (VF) 1. Thought to be a
reentrant excitation of the ventricles premature
impulse may arise during vulnerable period 2.
Irregular baseline with no identifiable waves
32
3. No cardiac output. Usually the cause of
"sudden death" 4. May be the result of ischemia,
lightning strike, electrocution, chest trauma, or
drugs 5. Requires CPR and electrical
defibrillation. Patients do not spontaneously
recover.
33
The defibrillator gives a strong electrical pulse
of current across the chest so that all heart
muscle cells are put into an action potential. A
refractory period follows that usually breaks the
conducted arrhythmia.
34
(No Transcript)
35
Q-T interval is rate- dependent and is an index
of the duration of phase 2 in the ventricular AP
36
In long QT syndrome the QT interval is longer
that the maximal normal value for that heart
rate. Q-T 12 x 40 480 ms Rate 1500/15 100
b/min
37
Long QT syndrome
38
Extended phase two cause long QT syndrome.
39
• Long QT syndrome
• Prolonged duration of phase 2 causes an early
afterdepolarization. That can trigger an early
action potential causing a reentrant tachycardia
• Patients may experience attacks of VT with
torsades de pointes - a waxing and waning of the
QRS morphology (as if circling around a point).

40
3. Long QT is induced by some drugs and can be
due to genetic abnormalities in some potassium
and calcium channels. At present 5 separate
genetic defects have been identified which cause
long QT
41
14 STEPS TO ASSURE A SUCCESSFUL READING AND
UNDERSTANDING OF AN UNKNOWN ECG 1. Is the
ventricular rhythm regular? 2. Are there P
waves? 3. Is the atrial rhythm regular? 4. Is
there one P wave for each QRS? 5. What are the
atrial and ventricular rates? 6. What is the P-R
interval? 7. Is the P-R interval constant? 8. Are
there extra or premature beats? 9. What is the
QRS duration? 10. Does the QRS morphology
indicate presence of a conduction defect?
11. What is the mean electrical QRS axis? 12.
What is the mean electrical P wave axis? 13. Is
there S-T segment deviation? 14. Are there
pathologic Q waves?
42
(No Transcript)
43
(No Transcript)