Scribd
Upload
4 views

Cardiac Cycle 1

The document outlines the cardiac cycle, detailing the electrical events during a heartbeat, including the roles of the S-A and A-V nodes, and the propagation of action potentials. It describes the functional syncytium of the heart, the conduction system, and the electrical properties of both noncontractile and contractile cardiocytes. Additionally, it covers the electrocardiogram (ECG) and its conventions for monitoring heart activity.

Uploaded by

chiumiawanangwa3
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
4 views

Cardiac Cycle 1

The document outlines the cardiac cycle, detailing the electrical events during a heartbeat, including the roles of the S-A and A-V nodes, and the propagation of action potentials. It describes the functional syncytium of the heart, the conduction system, and the electrical properties of both noncontractile and contractile cardiocytes. Additionally, it covers the electrocardiogram (ECG) and its conventions for monitoring heart activity.

Uploaded by

chiumiawanangwa3
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 38

Cardiac cycle

Electrical
Cardiac cycle
 all events that occur during one
complete heart beat – including;
 filling of atria & ventricles,
 generation of a depolarisation wave,
 cardiac contraction,
 pressure changes,
 opening and closure of valves,
 ejection of blood, etc.
Electrical activity:

 from an electrical point of view, heart


is thought of having only 2 chambers
since 2 atria contract together & then
2 ventricles

 Resting potential
 -50 to –60 mV in S-A & A-V node:
unstable
 -80 to-90 mV in contractile muscle;
stable
Electrical activity cont.
 Action potential:
 Triggered by impulses discharged
spontaneously & rhythmically by S-A
node
 Spread: S-A node  atria  A-V node 
A-V bundle branches  myocardiocytes
 Characterised by prolonged AP
 Long plateau phase & long refractory
period
Functional syncytium
(2 syncytia: atria and ventricles)
 Intercalated discs
contain two types of
specialized
junctions
1. desmosomes (hold
cells tightly
together)
2. gap junctions
 combined
properties of both
skeletal & smooth
muscles
 if any cell is stimulated within a syncytium,
impulse spread to all cells coz of gap junctions
 2 atria always function as a unit & 2 ventricles
always function as a unit.
 no gap junctions btwn atrial & ventricular
contractile cells.
 atria & ventricles are separated by electrically
nonconductive tissue that surrounds valves.
 special conducting system is needed to permit
transmission of impulses from atria to
ventricles.

 essential for pumping action


Noncontractile cardiocytes (conducting
system)
 S-A & A-V nodes, A-V bundle (His),bundle branches, Purkinje fibres,
etc.
0.05 m/s

9 Delay

0.3 m/s

Ventricular
Muscle
3.0 m/s 0.5 m/s

Mc-Graw-Hill Companies, Inc.


9
Noncontractile cardiocytes cont.
1. S-A node
 Normal (dominant) pacemaker
 has highest or fastest rhythm &, ,
sets pace or rate of contraction for
entire heart.
 RMP: -50 to –60 mV
 Unstable RMP
 Depolarises spontaneously
 Discharges impulses rhythmically
 60 – 100/ min (usually 70 – 80/min)
Noncontractile cardiocytes cont.

2. A-V node
 Structurally & functionally similar to
S-A node
 Reserve pacemaker
 discharges impulses more slowly
 40 - 60 per minute
 Delays impulses discharged by S-A
node
Noncontractile cardiocytes cont.

3. A-V bundle
 The only functional connection btwn
atria & ventricles
 Conducts impulses rapidly
 Discharges 40 – 60 impulses per
minute

 Bundle branches & Purkinje fibers


- discharges 20 - 40 per minute
Electrical properties of
Noncontractile cardiocytes
 RMP is - 50 to - 60
mV
 Unstable RMP due to
 ↓ permeability of
K+ leak channels
 partial closure of
Na+ channels that
allows slow inward
leak of Na+
 Diastolic
depolarization of
pacemaker cells, SA
node, is mediated by
at least 3 currents
i. hyperpolarization
induced inward
current, if,
ii. inward calcium
current, iCa
iii. outward potassium
current, ik
1. inward current, if
 induced by hyperpolarisation
 Carried mainly by Na+
 specific channels different
from fast Na+ channels
conduct current
 Activated during
repolarisation phase of AP,
 as MP becomes more
negative than about – 50
mV i.e. the more negative
the MP at end of
repolarisation, the greater
the activation of if current
2. inward calcium current, iCa
 activated toward end of phase 4,
as transmembrane potential
reaches – 55 mV
 once activated, Ca++ influx into
cell 
 Ca++ influx accelerates rate of
diastolic depolarization 
upstroke of AP
  in [Ca++]e or addition of Ca++
channel antagonists diminishes
amplitude of AP & slope of
pacemaker potential in SA node
cells
3. outward potassium current,
ik if and iCa
 opposes
currents
 repolarise the cell
after the upstroke of
AP
 continues well beyond
time of maximal
repolarisation, but it
diminishes throughout
phase 4
Excitation and automaticity
1. Prepotential (pacemaker
potential) (1)
 slow depolarization of PM btwn
AP
 called diastolic depolarisation
 due to slow spontaneous and
progressive ↓ in K+ permeability
 ↓ of efflux of K+ from cytoplasm
(+ small progressive ↑ in Na+ &
Ca++ permeability) → slow ↓ in
electronegativity of PM

 slope of prepotential determines


rate of AP generation & it can be
modified by chemical agents and
ANS activity.
2. Slow depolarisation 2):
 prepotential slowly reaches
the firing level
 opening of slow voltage
sensitive Na+-Ca2+ channels
 ↑ permeability for Ca2+ &
Na+
 depolarization of PM
 overshoot is up to + 10 mV,
spike is absent → amplitude
of AP is less than in
contractile cells
 Slow
repolarisation
(3)
 Hyperpolarisatio
n (4)
Spread of cardiac excitation
Electrical properties of Contractile cardiocytes

 RMP is minus 85 to minus 95 mV


 stable due to stable conductance for Na+ & K+
 Excitation – AP generation
 Phases of AP generation
i. Depolarisation (0 phase)
ii. Early repolarisation [initial rapid
depolarisation] (1)
iii. Plateau phase (2)
iv. Repolarisation (3)
Contractile cardiocytes cont.
 Force of contraction depend partly on
amount Ca++ that enters cells
 Prolonged AP (150 ms in atria, 300 in
ventricles)
 Prolonged plateau phase
 Prolonged refractory period
 Nervous supply - ANS
 Blood supply: coronary arteries
 Coronary veins drain into coronary sinus
1. Depolarisation (0 phase)
 caused by transmission of AP
from source of initial generation
(SA node)
 transmission of AP→electrotonic
depolarization of PM to threshold
 (-70 to -60 mV)
 activation of voltage-gated
Na+ channels (self-
regenerating process)
 rapid & brief depolarization &
overshoot to positive
potential of plus 20 to 30 mV
Early repolarisation (initial rapid depolarisation) (1)

1. cessation of
Na+ influx
(inactivation
of voltage-
gated Na+
channels)
2.  permeability
for K+ and Cl-
ions
Plateau phase (2)
 membrane remains
depolarised (0 to – 20 mV) for
relatively long period of time
 opening of slow voltage gated
Ca2+ -Na+ channels & K+
permeability is below resting
value.
 Small but sustained inward
current of +ve ions
prevents myocytes from
repolarizing rapidly →
plateau
 influx of Ca2+ directly
influences strength of
myocardial contraction
([Ca2+]i)
Repolarisation (3)
1. closing of slow
Ca2+-Na+
channels
2. reopening of K +
channels ( K +
efflux through
voltage gated
and leak
channels).
 in excitability during AP
1.
generation.
absolute refractory
period (corresponds
to phases 0,1,2 and
half of phase 3)
2. relative refractory
period (half of
phase 3)
3. supernormal
excitability period
(is almost absent)
Electrocardiogram (ECG)
 record of spread of electrical activity thru heart
Einthoven’s triangle
Segments are “baseline

32 Intervals have waves

4.1 MH

Mohrman and Heller. Cardiovascular Physiology. McGraw-Hill, 2006. 6th ed.


Some information about ECG
Conventions for 6 Frontal Lead ECG
35 Name
Lead Positive Electrode Negative Electrode
+ -
Lead I Left Arm Right Arm
Lead II Left Leg Right Arm
Lead III Left Leg Left Arm

aVR Right Arm Indifferent (1)


aVL Left Arm Indifferent (1)
aVF Left Leg (Foot) Indifferent (1)

Indifferent lead (1)


is the remaining two limb leads combined.
Augmented
36 (unipolar) limb leads
 To gain increased sensitivity and additional
electrical perspective three “Augmented Voltage”
leads have been devised from original
RA, LA and LL leads.

 They are aVR, aVL and aVF. The abbreviation


defines the positive electrode.
aVR has Right arm +
aVL has Left arm +
aVF has Foot +
Supraventricular arrhythmias

High HR

Slow A to V

Some blocked A to V

All blocked A to V

No P wave

MH Fig 5.1
37
Mohrman and Heller. Cardiovascular Physiology. McGraw-Hill, 2006. 6th ed.

You might also like