Cardiac Science:
Cardiac Arrhythmias
Physiology Team 436 – Cardiovascular Block Lecture 6
Red: very important.
Green: Doctor’s notes.
Pink: formulas.
Yellow: numbers.
Gray: notes and explanation.
Lecture: If work is intended for initial studying.
Review: If work is intended for revision.
1
Objectives
} From the students’ guide:
} Identify normal rhythm
} Identify the main pathophysiological causes of cardiac arrhythmias
(Arrhythmogenesis) } Identify sinus arrhythmias
} Define different ectopic foci of excitation and the mechanism of re-entry
phenomena } Identify conduction block.
} Identify electrolyte abnormalities (K+, Ca++)
} Enumerate the common arrhythmias and describe the basic ECG changes
2
Study Smart: focus on mutual topics.
The Normal Conduction System ONLY IN FEMALES’ SLIDES
} Develop a systematic approach to reading EKGs
and use it every time.
} The system we will practice is:
} Heart Rate
} Rhythm
(including intervals and blocks)
} Axis
} Hypertrophy
} Ischemia
Interpretation
3
SA node:
cardiac pacemaker
Paces at rate of 60-100 bpm (average of 70 bpm)
AV node: 45-60 bpm
Purkinje: 15-45 bpm
ONLY IN MALES’ SLIDES
Interpretation: Heart Rate
ONLY IN FEMALES’ SLIDES
Rule of 300: Divide 300 by the number of boxes
between each QRS = rate Number of big boxes Rate
1 300
2 150
3 100
4 75
5 60
6 50
— HR of 60-100 per minute is normal
— HR > 100 = tachycardia
— HR < 60 = bradycardia
Heart rate in picture below:(300 / 6) = 50 bpm
Heart rate may vary depending on:
• Age
• Activity
• Time of day
4
BOTH MALES’ & FEMALES’
SLIDES
5
Normal Sinus Rhythm; NSR
} Regular
} Each P followed by QRS with resulting
} PR interval is constant and within normal range
} PP interval is constant.
6
Location Bradyarrythmia Tacharrythmia
SA node Sinus Bradycardia Sinus tachycardia
Sick Sinus Syndrome
Atria Atrial Premature Beats
Atrial Flutter
Atrial Fibrillation
Paroxysmal SVT
Multifocal Atrial Tachycardia
AV node Conduction Blocks (1,2 and 3)
Jxal escape rhythm
Ventricles Ventricular escape rhytm Ventricular premature Beats
VT
Torsades de pointes
Ventricular Fibrillation
ONLY IN FEMALES’ SLIDES
Doctor said we don’t need to memorize all of this.
Classification of Cardiac Arrhythmias
Cardiac Arrhythmias
(According to Mechanism of
Arrhythmia)
2) Arrhythmias due to
alterations or disturbances
of impulse formation
1) Arrhythmias due to
disturbances of impulse
conduction
Cardiac Arrhythmias
(According to Heart Rate)
2) Tachyarrhythmias
1) Bradyarrhythmias
7
Classifications of Cardiac Arrhythmias:
Ø Rate above or below normal (tachy
vs. bradycardia)
Ø Regular or irregular rhythm
Ø Narrow or broad QRS complex
Ø Relation to P wave
Ø SupraventricularVs. ventricular
ONLY IN MALES’ SLIDES
ONLY IN FEMALES’ SLIDES
Blocks at different points
in the spread of impulse
through the heart
Anatomical Classification of Cardiac Arrhythmias
(origin of the arrhythmia)
Cardiac Arrhythmias
Supraventricular
arrhythmias
Atrioventricular (AV)
junctional arrhythmias
Atrial Arrhythmias
(Narrow QRS)
1-Atrial extrasystoles (APC)
2-Atrial Tachycardia
3-Atrial Flutter
4-Atrial Fibrillation
Ventricular arrhythmias
(Wide QRS)
1-Ventricualr extrasystole
2-Ventricular Tachycardia
3-Ventricular Fibrillation
Extrasystole = premature beats= premature complexes= premature contractions
* *
* Also considered as Arrhythmia due to triggered activity and reentry.
8
ONLY IN FEMALES’ SLIDES
Arrhythmias Due to Alterations or Disturbances of Impulse Formation
Arrhythmias due to alterations or
disturbances of impulse formation
Arrhythmias due to
alterations in SA node
pacemaker activity
Arrhythmias due to
enhanced automaticity of
the AV junction
Arrhythmias due to
triggered activity and
reentry
} Mechanisms:
1. Enhanced automaticity.
2. Triggered activity.
3. Reentrant circuits (circus movement).
9
ONLY IN FEMALES’ SLIDES
Other mechanism
• Abnormal rhythmicity of the
pacemaker
• Blocks at different points in the
spread of impulse through the
heart
Mechanisms of Arrhythmias Due to Alterations or Disturbances of
Impulse Formation EXTRA
1. Enhanced automaticity 2.Triggered activity
3. Re-entry
(Lewis circus movement)
Enhanced automaticity is defined
as an inappropriate increase in
the rate of discharge of a tissue
having physiological pacemaker
properties (i.e., sinus node,
atrioventricular node or Purkinje
fibers).
The term triggered activity is
used to define the appearance of
automaticity as a result of
external stimulation, and may
arise in tissues that do not
demonstrate physiological
automaticity.
Re-entry (reentry): occurs when a
cardiac impulse re-excites some
region of the heart through which
the impulse has already passed in
that heart beat.
Unidirectional or partial
conduction block is required to
initiate re-entry.
10
Causes of Cardiac Arrhythmias
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker from the sinus node to another place in the heart
3. Blocks at different points during the spread of the impulse through the heart
4. Abnormal pathways of impulse transmission through the heart
5. Spontaneous generation of spurious impulses in almost any part of the heart
— Rate above or below normal
— Regular or irregular rhythm
— Narrow or broad QRS complex
— Relation to P waves
ONLY IN FEMALES’ SLIDES
11
Arrhythmias Due to Alterations in SA Node Pacemaker Activity
1) Sinus Bradycardia
} Heart rate slower than 60 per
minute
1- Physiological Causes:
--Expiration.
2- Pharmacological and pathological Causes:
- Parasympathetic stimulation
12
2) SinusTachycardia
} Heart rate faster than 100
per minute
Causes:
1- Physiological:
-During exercise, sympathetic stimulation, increased body
temperature
-Inspiration
2- Pharmacological and pathological:
-Sympathetic stimulation
- Digoxin drug.
Differential Diagnosis of Tachycardia
Tachycardia Narrow Complex Wide Complex
Regular Sinus Tachy
SVT
Atrial flutter
ST w/ aberrancy
SVT w/ aberrancy
VT
Irregular A-fib
A-flutter w/ variable
conduction
MAT
A-fib w/ aberrancy
A-fib w/ WPW
VT
ONLY IN FEMALES’ SLIDES
13
Arrhythmias Due to Alterations in SA Node Pacemaker Activity
} 3) Respiratory sinus arrhythmia
} Sinus arrhythmia is an increase in heart
rate during inspiration and a decrease
during expiration
} It is a normal finding in children and
young adults and tends to diminish or
disappear with age.
Causes:
1- Sinus arrhythmia is due to variations in
the vagal tone that affects the SA node.
14
Sinus Arrhythmia: Result from spillover of signals from the medullary respiratory center into the
adjacent vasomotor center during inspiration and expiratory cycles of respiration.The spillover
signals cause alternate increase and decrease in the number of impulses transmitted through the
sympathetic and vagus nerves to the heart
ONLY IN MALES’ SLIDES
Atrial and Ventricular
Extrasystoles
} Extrasystoles = premature beats = premature
contractions = premature complexes
- If the focus is in the ventricles, the premature
beat is called ventricular premature beat.
- If the focus is in the atrial wall, the premature
beat is called atrial premature beat.
- Ectopic foci can also cause a premature beat in
AV junction.
} Causes:
- Ischemia
- Irritation of cardiac muscle by calcified foci
- Caffeine
15
Abnormal Cardiac Rhythms that Result
from Impulse Conduction Block
Sinoatrial Block
The impulse from the S-A node is blocked before it
enters the atrial muscle à Cessation (no) of P waves
A-V Block
When impulse from the S-A node is blocked
Causes:
Ischemia of the A-V node
Compression of the A-V node by scar formation
Inflammation of the A-V node
Strong vagal stimulation
ONLY IN FEMALES’ SLIDES
Atrial Extrasystoles
— Short P-R interval depending on how far
the ectopic foci from the AV node.
— Pulse deficit if there is no time for the
ventricles to fill with blood.
— The time between the premature
contraction and the succeeding beat is
increased (Compensatory pause).
16
Atrial Flutter
} Atrial flutter occurs when the atria are stimulated to beat at a rate 250 beats per
minute.
} Atrial flutter results in poor atrial pumping since some parts of the atria are relaxing
while other parts are contracting.
} A single large wave travels around and around in the atria
} The refractory period of the AV node causes 2-3 beats of atria for one single
ventricular beat 2:1 or 2:3 rhythm.
17
ONLY IN MALES’ SLIDES
Atrial Fibrillation (AF)
— Same mechanism as ventricular fibrillation.
— It can occur only in atria without affecting the
ventricles.
— It occurs more frequently in patients with enlarged
heart.
— The atria do not pump if they are fibrillating.
— The efficiency of ventricular filling is decreased 20 to
30%
— No P wave, or high frequency of low voltage P wave
— A person can live for years with atrial fibrillation
— Treatment: DC shock
18
} Prolong QRS complex because the impulses are carried out with myocardial fibers with slower conduction rate
than Purkinje fibers
} Increase QRS complexes voltage because QRS wave from one ventricle can not neutralize the one from the
other ventricle
} After PVCs, the T wave has an electrical potential of opposite polarity of that of the QRS because of the slow
conduction in the myocardial fibers, the fibers that depolarizes first will repolarize first
} Causes: drugs, caffeine, smoking, lack of sleep, emotional irritations
Ventricular extrasystoles
19
• The most serious of all arrhythmias
• Cause: impulses stimulate one part of the ventricles, then another, then itself.
• Many part contracts at the same time while other parts relax. (Circus movement)
• Causes: sudden electrical shock, ischemia
} Tachycardia
} Irregular rhythm
} Broad QRS complex
} No P wave
} Treatment : DC shock
Ventricular Fibrillation
20
Abnormal Cardiac Rhythms that Result
from Impulse Conduction Block
— Sinoatrial Block
— Blockade of the S-A node impulse before
entering atrial muscle.
— Cessation of P wave (difficulty of seeing p wave)
ONLY IN FEMALES’ SLIDES
— A-V Block
When impulse from the S-A node is blocked
— First degree block
— Second degree block
— Third degree block
— Causes of SA and AV Block:
— Ischemia of the A-V node
— Compression of the A-V node by scar formation
— Inflammation of the A-V node
— Strong vagal stimulation
21
Other Arrhythmias Due to Disturbances of Impulse
Conduction (impulse conduction block)
Arrhythmias due to
Alterations in impulse
conduction
Bundle branch block
Heart block
= Atrioventricular (AV)
block
1st degree block (partial block): all
impulses pass through the AV node
but with greater than normal delay.
2nd degree block: some, but not all
impulses pass through the AV node.
3rd degree block (complete block):
no impulses pass through AV node
à atria and ventricles beat
independently.
22
Heart Block
23
Heart Block = Atrioventricular (AV) Block
} 1st degree block: all impulses pass through the
AV node but with greater than normal delay.
Every P wave is followed by R wave.
P-R interval is prolonged = 0.2 second
} 2nd degree AV block:
• P-R interval > 0.25 second
• Only few impulses pass to the ventricles
® atria beat faster than ventricles
®“dropped beat” of the ventricles
1. Mobitz I: Progressive increase in P-R interval
until one QRS is dropped.
2. Mobitz II: Constant PR prolongation + dropped
beat
} 3rd degree AV block: (complete heart block).
• Complete dissociation of P wave and QRS waves
— Ventricle escape from the influence of S-A node
} Atrial rate is 100 beats/min
} Ventricular rate is 57 beats/min. (40 in females)
} Stroke-Adams Syndrome::AV block comes and
goes
Mobitz I:
Mobitz II
24
Diseases in ECG:
1. Ischemia: common use of ECG is acute chest pain.
Cause: restriction of blood flow to the myocardium due to
- reversible: angina pectoris
- Irreversible: myocardial infarction.
- Ischemia ® injury ® infarction
2. Reversible Ischemia: Inverted T wave - ST segment depression.
3. Myocardial infarction: ST segment elevation – Deep Q wave. Complete
loss of blood supply to the myocardium resulting in necrosis or death of tissue.
4. Hypokalemia: FlatT wave
5. Hyperkalemia: Tall peak T wave.
ONLY IN FEMALES’ SLIDES
25
Link to Editing File
(Please be sure to check this file frequently for any edits or updates on all of our lectures.)
References:
• Girls’ and boys’ slides.
• Guyton and Hall Textbook of Medical Physiology (Thirteenth Edition.)
Quiz
} https://www.onlineexambuilder.com/arrhythmias/exam-139189
26
Thank you!
Contact us:
Physiology436@gmail.com
@Physiology436
The Physiology 436Team:
Team Leaders:
Qaiss Almuhaideb
Lulwah Alshiha
‫ﻋﻣﻼ‬ ‫أﺣﺳن‬ ‫ﻣن‬ ‫أﺟر‬ ‫ﯾﺿﯾﻊ‬ ‫ﻻ‬ ‫ﷲ‬ ‫أن‬ ‫ﺗﻌﻠم‬ ‫أﻧت‬ ‫و‬ ‫اﻋﻣل‬ ،‫دﻣﻌﺔ‬ ‫ﻟﺗﻣﺳﺢ‬ ‫اﻋﻣل‬ ،‫ﺑﺳﻣﺔ‬ ‫ﻟﺗرﺳم‬ ‫اﻋﻣل‬
.
Female Members:
Amal AlShaibi
Rana Barasain
27
Male Members:
Mohammed Almutllaq

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6- Cardiac Arrhythmias .pdf is a disease

  • 1. Cardiac Science: Cardiac Arrhythmias Physiology Team 436 – Cardiovascular Block Lecture 6 Red: very important. Green: Doctor’s notes. Pink: formulas. Yellow: numbers. Gray: notes and explanation. Lecture: If work is intended for initial studying. Review: If work is intended for revision. 1
  • 2. Objectives } From the students’ guide: } Identify normal rhythm } Identify the main pathophysiological causes of cardiac arrhythmias (Arrhythmogenesis) } Identify sinus arrhythmias } Define different ectopic foci of excitation and the mechanism of re-entry phenomena } Identify conduction block. } Identify electrolyte abnormalities (K+, Ca++) } Enumerate the common arrhythmias and describe the basic ECG changes 2 Study Smart: focus on mutual topics.
  • 3. The Normal Conduction System ONLY IN FEMALES’ SLIDES } Develop a systematic approach to reading EKGs and use it every time. } The system we will practice is: } Heart Rate } Rhythm (including intervals and blocks) } Axis } Hypertrophy } Ischemia Interpretation 3 SA node: cardiac pacemaker Paces at rate of 60-100 bpm (average of 70 bpm) AV node: 45-60 bpm Purkinje: 15-45 bpm ONLY IN MALES’ SLIDES
  • 4. Interpretation: Heart Rate ONLY IN FEMALES’ SLIDES Rule of 300: Divide 300 by the number of boxes between each QRS = rate Number of big boxes Rate 1 300 2 150 3 100 4 75 5 60 6 50 — HR of 60-100 per minute is normal — HR > 100 = tachycardia — HR < 60 = bradycardia Heart rate in picture below:(300 / 6) = 50 bpm Heart rate may vary depending on: • Age • Activity • Time of day 4 BOTH MALES’ & FEMALES’ SLIDES
  • 5. 5
  • 6. Normal Sinus Rhythm; NSR } Regular } Each P followed by QRS with resulting } PR interval is constant and within normal range } PP interval is constant. 6 Location Bradyarrythmia Tacharrythmia SA node Sinus Bradycardia Sinus tachycardia Sick Sinus Syndrome Atria Atrial Premature Beats Atrial Flutter Atrial Fibrillation Paroxysmal SVT Multifocal Atrial Tachycardia AV node Conduction Blocks (1,2 and 3) Jxal escape rhythm Ventricles Ventricular escape rhytm Ventricular premature Beats VT Torsades de pointes Ventricular Fibrillation ONLY IN FEMALES’ SLIDES Doctor said we don’t need to memorize all of this.
  • 7. Classification of Cardiac Arrhythmias Cardiac Arrhythmias (According to Mechanism of Arrhythmia) 2) Arrhythmias due to alterations or disturbances of impulse formation 1) Arrhythmias due to disturbances of impulse conduction Cardiac Arrhythmias (According to Heart Rate) 2) Tachyarrhythmias 1) Bradyarrhythmias 7 Classifications of Cardiac Arrhythmias: Ø Rate above or below normal (tachy vs. bradycardia) Ø Regular or irregular rhythm Ø Narrow or broad QRS complex Ø Relation to P wave Ø SupraventricularVs. ventricular ONLY IN MALES’ SLIDES ONLY IN FEMALES’ SLIDES Blocks at different points in the spread of impulse through the heart
  • 8. Anatomical Classification of Cardiac Arrhythmias (origin of the arrhythmia) Cardiac Arrhythmias Supraventricular arrhythmias Atrioventricular (AV) junctional arrhythmias Atrial Arrhythmias (Narrow QRS) 1-Atrial extrasystoles (APC) 2-Atrial Tachycardia 3-Atrial Flutter 4-Atrial Fibrillation Ventricular arrhythmias (Wide QRS) 1-Ventricualr extrasystole 2-Ventricular Tachycardia 3-Ventricular Fibrillation Extrasystole = premature beats= premature complexes= premature contractions * * * Also considered as Arrhythmia due to triggered activity and reentry. 8 ONLY IN FEMALES’ SLIDES
  • 9. Arrhythmias Due to Alterations or Disturbances of Impulse Formation Arrhythmias due to alterations or disturbances of impulse formation Arrhythmias due to alterations in SA node pacemaker activity Arrhythmias due to enhanced automaticity of the AV junction Arrhythmias due to triggered activity and reentry } Mechanisms: 1. Enhanced automaticity. 2. Triggered activity. 3. Reentrant circuits (circus movement). 9 ONLY IN FEMALES’ SLIDES Other mechanism • Abnormal rhythmicity of the pacemaker • Blocks at different points in the spread of impulse through the heart
  • 10. Mechanisms of Arrhythmias Due to Alterations or Disturbances of Impulse Formation EXTRA 1. Enhanced automaticity 2.Triggered activity 3. Re-entry (Lewis circus movement) Enhanced automaticity is defined as an inappropriate increase in the rate of discharge of a tissue having physiological pacemaker properties (i.e., sinus node, atrioventricular node or Purkinje fibers). The term triggered activity is used to define the appearance of automaticity as a result of external stimulation, and may arise in tissues that do not demonstrate physiological automaticity. Re-entry (reentry): occurs when a cardiac impulse re-excites some region of the heart through which the impulse has already passed in that heart beat. Unidirectional or partial conduction block is required to initiate re-entry. 10
  • 11. Causes of Cardiac Arrhythmias 1. Abnormal rhythmicity of the pacemaker 2. Shift of the pacemaker from the sinus node to another place in the heart 3. Blocks at different points during the spread of the impulse through the heart 4. Abnormal pathways of impulse transmission through the heart 5. Spontaneous generation of spurious impulses in almost any part of the heart — Rate above or below normal — Regular or irregular rhythm — Narrow or broad QRS complex — Relation to P waves ONLY IN FEMALES’ SLIDES 11
  • 12. Arrhythmias Due to Alterations in SA Node Pacemaker Activity 1) Sinus Bradycardia } Heart rate slower than 60 per minute 1- Physiological Causes: --Expiration. 2- Pharmacological and pathological Causes: - Parasympathetic stimulation 12 2) SinusTachycardia } Heart rate faster than 100 per minute Causes: 1- Physiological: -During exercise, sympathetic stimulation, increased body temperature -Inspiration 2- Pharmacological and pathological: -Sympathetic stimulation - Digoxin drug.
  • 13. Differential Diagnosis of Tachycardia Tachycardia Narrow Complex Wide Complex Regular Sinus Tachy SVT Atrial flutter ST w/ aberrancy SVT w/ aberrancy VT Irregular A-fib A-flutter w/ variable conduction MAT A-fib w/ aberrancy A-fib w/ WPW VT ONLY IN FEMALES’ SLIDES 13
  • 14. Arrhythmias Due to Alterations in SA Node Pacemaker Activity } 3) Respiratory sinus arrhythmia } Sinus arrhythmia is an increase in heart rate during inspiration and a decrease during expiration } It is a normal finding in children and young adults and tends to diminish or disappear with age. Causes: 1- Sinus arrhythmia is due to variations in the vagal tone that affects the SA node. 14 Sinus Arrhythmia: Result from spillover of signals from the medullary respiratory center into the adjacent vasomotor center during inspiration and expiratory cycles of respiration.The spillover signals cause alternate increase and decrease in the number of impulses transmitted through the sympathetic and vagus nerves to the heart ONLY IN MALES’ SLIDES
  • 15. Atrial and Ventricular Extrasystoles } Extrasystoles = premature beats = premature contractions = premature complexes - If the focus is in the ventricles, the premature beat is called ventricular premature beat. - If the focus is in the atrial wall, the premature beat is called atrial premature beat. - Ectopic foci can also cause a premature beat in AV junction. } Causes: - Ischemia - Irritation of cardiac muscle by calcified foci - Caffeine 15 Abnormal Cardiac Rhythms that Result from Impulse Conduction Block Sinoatrial Block The impulse from the S-A node is blocked before it enters the atrial muscle à Cessation (no) of P waves A-V Block When impulse from the S-A node is blocked Causes: Ischemia of the A-V node Compression of the A-V node by scar formation Inflammation of the A-V node Strong vagal stimulation ONLY IN FEMALES’ SLIDES
  • 16. Atrial Extrasystoles — Short P-R interval depending on how far the ectopic foci from the AV node. — Pulse deficit if there is no time for the ventricles to fill with blood. — The time between the premature contraction and the succeeding beat is increased (Compensatory pause). 16
  • 17. Atrial Flutter } Atrial flutter occurs when the atria are stimulated to beat at a rate 250 beats per minute. } Atrial flutter results in poor atrial pumping since some parts of the atria are relaxing while other parts are contracting. } A single large wave travels around and around in the atria } The refractory period of the AV node causes 2-3 beats of atria for one single ventricular beat 2:1 or 2:3 rhythm. 17 ONLY IN MALES’ SLIDES
  • 18. Atrial Fibrillation (AF) — Same mechanism as ventricular fibrillation. — It can occur only in atria without affecting the ventricles. — It occurs more frequently in patients with enlarged heart. — The atria do not pump if they are fibrillating. — The efficiency of ventricular filling is decreased 20 to 30% — No P wave, or high frequency of low voltage P wave — A person can live for years with atrial fibrillation — Treatment: DC shock 18
  • 19. } Prolong QRS complex because the impulses are carried out with myocardial fibers with slower conduction rate than Purkinje fibers } Increase QRS complexes voltage because QRS wave from one ventricle can not neutralize the one from the other ventricle } After PVCs, the T wave has an electrical potential of opposite polarity of that of the QRS because of the slow conduction in the myocardial fibers, the fibers that depolarizes first will repolarize first } Causes: drugs, caffeine, smoking, lack of sleep, emotional irritations Ventricular extrasystoles 19
  • 20. • The most serious of all arrhythmias • Cause: impulses stimulate one part of the ventricles, then another, then itself. • Many part contracts at the same time while other parts relax. (Circus movement) • Causes: sudden electrical shock, ischemia } Tachycardia } Irregular rhythm } Broad QRS complex } No P wave } Treatment : DC shock Ventricular Fibrillation 20
  • 21. Abnormal Cardiac Rhythms that Result from Impulse Conduction Block — Sinoatrial Block — Blockade of the S-A node impulse before entering atrial muscle. — Cessation of P wave (difficulty of seeing p wave) ONLY IN FEMALES’ SLIDES — A-V Block When impulse from the S-A node is blocked — First degree block — Second degree block — Third degree block — Causes of SA and AV Block: — Ischemia of the A-V node — Compression of the A-V node by scar formation — Inflammation of the A-V node — Strong vagal stimulation 21
  • 22. Other Arrhythmias Due to Disturbances of Impulse Conduction (impulse conduction block) Arrhythmias due to Alterations in impulse conduction Bundle branch block Heart block = Atrioventricular (AV) block 1st degree block (partial block): all impulses pass through the AV node but with greater than normal delay. 2nd degree block: some, but not all impulses pass through the AV node. 3rd degree block (complete block): no impulses pass through AV node à atria and ventricles beat independently. 22
  • 24. Heart Block = Atrioventricular (AV) Block } 1st degree block: all impulses pass through the AV node but with greater than normal delay. Every P wave is followed by R wave. P-R interval is prolonged = 0.2 second } 2nd degree AV block: • P-R interval > 0.25 second • Only few impulses pass to the ventricles ® atria beat faster than ventricles ®“dropped beat” of the ventricles 1. Mobitz I: Progressive increase in P-R interval until one QRS is dropped. 2. Mobitz II: Constant PR prolongation + dropped beat } 3rd degree AV block: (complete heart block). • Complete dissociation of P wave and QRS waves — Ventricle escape from the influence of S-A node } Atrial rate is 100 beats/min } Ventricular rate is 57 beats/min. (40 in females) } Stroke-Adams Syndrome::AV block comes and goes Mobitz I: Mobitz II 24
  • 25. Diseases in ECG: 1. Ischemia: common use of ECG is acute chest pain. Cause: restriction of blood flow to the myocardium due to - reversible: angina pectoris - Irreversible: myocardial infarction. - Ischemia ® injury ® infarction 2. Reversible Ischemia: Inverted T wave - ST segment depression. 3. Myocardial infarction: ST segment elevation – Deep Q wave. Complete loss of blood supply to the myocardium resulting in necrosis or death of tissue. 4. Hypokalemia: FlatT wave 5. Hyperkalemia: Tall peak T wave. ONLY IN FEMALES’ SLIDES 25
  • 26. Link to Editing File (Please be sure to check this file frequently for any edits or updates on all of our lectures.) References: • Girls’ and boys’ slides. • Guyton and Hall Textbook of Medical Physiology (Thirteenth Edition.) Quiz } https://www.onlineexambuilder.com/arrhythmias/exam-139189 26
  • 27. Thank you! Contact us: [email protected] @Physiology436 The Physiology 436Team: Team Leaders: Qaiss Almuhaideb Lulwah Alshiha ‫ﻋﻣﻼ‬ ‫أﺣﺳن‬ ‫ﻣن‬ ‫أﺟر‬ ‫ﯾﺿﯾﻊ‬ ‫ﻻ‬ ‫ﷲ‬ ‫أن‬ ‫ﺗﻌﻠم‬ ‫أﻧت‬ ‫و‬ ‫اﻋﻣل‬ ،‫دﻣﻌﺔ‬ ‫ﻟﺗﻣﺳﺢ‬ ‫اﻋﻣل‬ ،‫ﺑﺳﻣﺔ‬ ‫ﻟﺗرﺳم‬ ‫اﻋﻣل‬ . Female Members: Amal AlShaibi Rana Barasain 27 Male Members: Mohammed Almutllaq