Download THE HEART

THE HEART
BY
Mohie- Aldien A.Sherief (MD)
Mohie-Aldine A.Sherief
Organization of the Cardiovascular System
Figure 20–
1
Mohie-Aldine A.Sherief
Anatomy of the Heart
Located directly
behind sternum
Figure 20–
2a
Mohie-Aldine A.Sherief
Anatomy of the Heart
 Great veins and arteries at the base
 Pointed tip is apex
Mohie-Aldine A.Sherief
Superficial
Anatomy
of the
Heart
Figure 20–
3
Mohie-Aldine A.Sherief
Heart Structure
Pericardium
Chambers
Coronary vessels
Valves(one-way-flow)
Myocardium
Mohie-Aldine A.Sherief
The Heart Wall
Figure 20–
4
Mohie-Aldine A.Sherief
Left and Right Ventricles
 Have significant
structural differences
Mohie-Aldine A.Sherief
The Heart Valves
One-way valves
prevent backflow
during contraction
Mohie-Aldine A.Sherief
Blood Supply to the Heart(Coronary circulation)
Figure 20–
9
Mohie-Aldine A.Sherief
Extrinsic Innervation of the Heart
Heart is stimulated
by the sympathetic
cardioacceleratory
center
Heart is inhibited
by the
parasympathetic
cardioinhibitory
center
Mohie-Aldine A.Sherief
Autonomic Innervation
Figure 20–
21 (Navigator)
Mohie-Aldine A.Sherief
Cardiac Muscle Cells:
Autorhythmic
Myocardial
Intercalated discs
 Desmosomes
 Gap Junctions
Fast signals
Cell to cell
Many mitochondria
Large T tubes
Mohie-Aldine A.Sherief
Cardiac Muscle Cells
Figure 20–
5
Mohie-Aldine A.Sherief
Cardiac Cells vs. Skeletal Fibers
Table 20-1
Mohie-Aldine A.Sherief
Cardiac cells
Pacemaker(automatic)cells
Non-pacemaker cells
* Depolarization occur spontaneously
*Normally, depolarized by stimulus
* SAN( initiate the impulse) >AVN>AV bundle
> hispurkinije fibers(conduct impulse)
*other cells, normally act as
contractile element
* Short ,AP&RMP less –ve during phase 4
*Long amplitude&duration of AP
The AV-node
action
potential
ascending
phase is
essentially
dependent
on Ca++
entry.
Mohie-Aldine A.Sherief
Ion
Ion Currents
Currents Generating
Generating the
the Ventricular
Ventricular Action
Action Potential
Potential
1 ITo
2 ICa ICl
IKur
INa
Slow inward Ca++ current ICa
Outward Cl- current ICl
0
INa)
3
IKs
Outward K+ currents
(ITo; IKur; IKr; IKs;
IK1)
Rapid inward
Na+ current (
IKr
IK1
Membrane
Na+ /K+
ATPase
Na+
IK1 4
K+
Mohie-Aldine A.Sherief
Effect of ICaT blockade with Ni and tetramethrinon
the pacemaker cell action potential profile
Irisawa et al. Physiol Rev 73: 197, 1993
Mohie-Aldine A.Sherief
Ca antagonist shorten action potential plateau
phase
1,4Dihydropyridines
Ni++, Co++, Mn++
Diltiazem,
Verapami
 Inhibition oft
he“s
l
o
wi
nwar
d”Ca++ channel shorten the
plateau and repolarization phases. Verapamil and diltiazem
block both ICa and IKr repolarization currents.
Mohie-Aldine A.Sherief
Na antagonist decrease the brate of rise of
action potential
Membrane action potentiel (mV)
+ 30
0
Tetrodototox
in
-30
-60
-90
 Inhibition of the fast inward INa with tetrodotoxin leads to
an action potential with a predominat slow inward ICa.
Mohie-Aldine A.Sherief
Ventricular and pace maker cell ionic currents
None or small
1
2
0
3
4
ICaT, but not ICaL plays a role on pacemaker automaticity
Mohie-Aldine A.Sherief
Summary of ionic currents in cardiac cells
Background currents:
1-K inward (Ig)
+30mv
2-Na,Ca inward (Ibi )
(1) Ito1(K)
(2) ICaL
(3) IK1
(0) INa
(0)ICa(L,T)
(4) IKAch,↥Ke
,If
(3) IK1
ARP
RRP
-60mv
-90mv
-90mv
-50mv
-60mv
APD
(4) If (Na),IcaT,/↧Ke↦↧PK
Factors increase slope of phase 4 in nonautomatic cells (RMP less –ve):
a) ischemia(↧IKATP) b) ↧Na/KATPase (digitalise, ↥Cae,↧Ke,)
c)Mohie-Aldine
B1 agonist (↥
Cai)
A.Sherief
Action Potentials in Skeletal and Cardiac
Muscle
Figure 20–
15
Mohie-Aldine A.Sherief
Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and is self-excitable
(automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period
Cardiac muscle contraction is similar to skeletal
muscle contraction
Mohie-Aldine A.Sherief
Mechanical Properties of the Heart
Cardiac output and cardiac contractility may be altered by
many factors.
These can to some degree be conveniently divided into two
groups:
•
Length Independent Factors
•
Length Dependent Factors
Mohie-Aldine A.Sherief
Contractility and Norepinephrine
Sympathetic
stimulation
releases
norepinephrine
and initiates a
cyclic AMP
secondmessenger
system
Mohie-Aldine A.Sherief
Mechanism of Cardiac Muscle Excitation,
Contraction & Relaxation
Mohie-Aldine A.Sherief
Modulation of Contraction
Graded Contraction:
proportional to crossbridges
formed
More [Ca++]: crossbridges,
more force & speed
Autonomic n & epinephrine
modulation
Figure 14-12: Modulation of cardiac contraction by catecholamines
Mohie-Aldine A.Sherief
More Characteristics of Cardiac Muscle Contraction

Stretch-length relationship
-stretch, Ca++ entering

Long action
potential
-contraction force

Long
refractory
period
-No summation
-No tetanus
Mohie-Aldine A.Sherief
More Characteristics of Cardiac Muscle Contraction
Mohie-Aldine A.Sherief
Cardiodynamics
The movement and force generated by cardiac
contractions
Important Cardiodynamics Terms
-End-diastolic volume (EDV)
-End-systolic volume (ESV)
-Stroke volume (SV): SV = EDV — ESV
-Ejection fraction:(the percentage of EDV
represented by SV)
-Cardiac output (CO):the volume pumped by each
ventricle in 1 minute
Mohie-Aldine A.Sherief
Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each ventricle in
one minute:
COP is the product of heart rate (HR) and stroke volume
(SV) CO (ml/min)
= HR (75 beats/min) x SV (70 ml/beat)=
= 5250 ml/min (5.25 L/min)
 HR is the number of heart beats per minute
 SV is the amount of blood pumped out by a ventricle with each beat
 Cardiac reserve is the difference between resting and maximal CO
Mohie-Aldine A.Sherief
Regulation of Stroke Volume
Volume (ml) of blood ejected per beat
SV = end diastolic volume (EDV) minus end
systolic volume (ESV)
EDV = amount of blood collected in a ventricle
during diastole
ESV = amount of blood remaining in a ventricle
after contraction
Mohie-Aldine A.Sherief
Factors Affecting Stroke Volume
Preload –amount ventricles are stretched by
contained blood
Contractility –cardiac cell contractile force due to
factors other than EDV
Afterload –back pressure exerted by blood in the
large arteries leaving the heart
Mohie-Aldine A.Sherief
Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle cells
before they contract is the critical factor controlling
stroke volume
Slow heartbeat and exercise increase venous return
to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease
SV
Mohie-Aldine A.Sherief
Preload and Afterload
18.21
Mohie-AldineFigure
A.Sherief
Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength,
independent of stretch and EDV
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs
Mohie-Aldine A.Sherief
Extrinsic Factors Influencing Stroke Volume
Agents/factors that decrease contractility include:
Acidosis
Increased extracellular K+
Calcium channel blockers
Mohie-Aldine A.Sherief
Factors Affecting Stroke Volume
Changes in EDV or ESV
Figure 20–
23 (Navigator)
Mohie-Aldine A.Sherief
Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex –a sympathetic reflex
initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates baroreceptors in the atria, causing
increased SNS stimulation
Chemical Regulation of the Heart
The hormones epinephrine and thyroxine increase
heart rate

Intra- and extracellular ion concentrations must be
maintained for normal heart function
Mohie-Aldine A.Sherief
Factors Affecting Heart Rate and Stroke Volume
Figure 20–
24
Mohie-Aldine A.Sherief
Regulation of Heart Rate: Autonomic Nervous
System
Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation
is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing
heart rate and causing vagal tone
Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate
Mohie-Aldine A.Sherief
Regulators of the Heart: Reflex Controls of Rate
Range: about 50 –near 200
Typical resting: near 70
AP conduction
Muscle Contraction
Parasympathetic slows
Sympathetic speeds
Mohie-Aldine A.Sherief
Regulators of the Heart: Reflex Controls of Rate
Mohie-Aldine A.Sherief
Cardiac Output: Heart Rate X Stroke Volume
Around 5L :
(72 beats/m 70 ml/beat = 5040 ml)
Rate: beats per minute
Volume: ml per beat
 EDV - ESV
Residual (about 50%)
Mohie-Aldine A.Sherief
Cardiac Output: Heart Rate X Stroke Volume
Mohie-Aldine A.Sherief
Regulators of the Heart:
Factors Influencing Stroke Volume
Starlings Law –stretch
Force of contraction
Venous return:
Skeletal pumping
Respiratory pumping
Mohie-Aldine A.Sherief
Regulators of the Heart:
Factors Influencing Stroke Volume
Mohie-Aldine A.Sherief
Regulators of the Heart:
Factors Influencing Stroke Volume
Mohie-Aldine A.Sherief
Factors Involved in Regulation of Cardiac
Output
Mohie-Aldine A.Sherief
Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)
Mohie-Aldine A.Sherief
The Cardiac
Cycle
Figure 20–
11
Mohie-Aldine A.Sherief
Phases of the Cardiac Cycle
Figure 20–
16
Mohie-Aldine A.Sherief
Phases of the Cardiac Cycle
Figure 18.20
Mohie-Aldine A.Sherief
Impulse Conduction through the Heart
Figure 20–
13
Mohie-Aldine A.Sherief
Heart Physiology: Sequence of Excitation
AV bundle splits into two pathways in the
interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex
of the heart
Purkinje fibers carry the impulse to the heart apex
and ventricular walls
Mohie-Aldine A.Sherief
Heart Physiology: Sequence of Excitation
Mohie-Aldine A.Sherief
Heart Physiology: Intrinsic Conduction System
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker
potentials
Use calcium influx (rather than sodium) for rising phase of
the action potentialPacemaker membrane potential
I-f channels Na+ influx
Ca++ channels –influx, to AP
Slow K+ open –repolarization
Mohie-Aldine A.Sherief
Sympathetic and Parasympathetic
Sympathetic –speeds heart rate by Ca++ & I-f channel
flow
Parasympathetic –slows rate by K+ efflux & Ca++
influx
Mohie-Aldine A.Sherief
Heart Excitation Related to ECG
Mohie-Aldine A.Sherief
Electrical Properties of the Heart
Electrocardiograph (ECG)
The ECG is a pictorial representation of the electrical activity in
the heart. It is measured using an Electrocardiogram.
Mohie-Aldine A.Sherief
Electrical Properties of the Heart
Mohie-Aldine A.Sherief
Electrocardiogram (ECG):
Electrical Activity of the Heart
Einthoven's
triangle
P-Wave –atria
QRS- wave –
ventricles
T-wave –
repolarization
Figure 14-20: Ei
nt
hove
n’
striangle
Mohie-Aldine A.Sherief
Electrocardiogram (ECG):
Electrical Activity of the Heart
Figure
14-21: The electrocardiogram
Mohie-Aldine
A.Sherief
ECG Information Gained
(Non-invasive)
Heart Rate
Signal conduction
Heart tissue
Conditions
Figure 14-24: Normal and abnormal electrocardiograms
Mohie-Aldine A.Sherief
Electrical Properties of the Heart
In summary the key components of an ECG are:
P wave
Atrial depolarisation due to SA Node firing
QRS Complex
Contains a mixture of waves
Atrial Repolarisation
Ventricular Depolarisation
T wave
Ventricular Repolarisation
Other features measured in the ECG include:
•
•
•
•
Direction and shape of the P wave and T wave
Duration of the P-R Segment
Relative position of the S-T segment
Presence of a large Q wave.
Mohie-Aldine A.Sherief
Pacemaker and Action Potentials of the Heart
18.13
Mohie-AldineFigure
A.Sherief
Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node generates impulses about 75
times/minute
Atrioventricular (AV) node delays the impulse
approximately 0.1 second
Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)
Mohie-Aldine A.Sherief
Heart sounds (lub-dup) are associated with closing of heart
valves
-S1:(loud sounds,produced by AV valves)
-S2:(loud sounds,produced by semilunar valves )
-S3, S4:(soft sounds,blood flow into ventricles and atrial contraction)
Figure 20–
18b
Mohie-Aldine A.Sherief
Positioning the Stethoscope
To detect sounds of each
valve
Figure 20–
18a
Mohie-Aldine A.Sherief
Coordinating the Pump: Electrical Signal Flow
AP from autorhythmic cells in sinoatrial node (SA)
Spreads via gap junctions down internodal pathways and
across atrial myocardial cells (atrial contraction starts)
Pause –atrioventricular (AV) node delay
AV node to bundles of His, branches & Perkinje fibers
Right and left ventricular contraction from apex upword
Mohie-Aldine A.Sherief
Coordinating the Pump: Electrical Signal Flow
Figure 14-18: Electrical conduction in myocardial cells
Mohie-Aldine A.Sherief
Coordinating the Pump: Electrical Signal Flow
Mohie-Aldine A.Sherief
Age-Related Changes Affecting the Heart
Sclerosis and thickening of valve flaps
Decline in cardiac reserve
Fibrosis of cardiac muscle
Atherosclerosis
Mohie-Aldine A.Sherief
Cardiovascular Changes with Aging
Autonomic N.S.
- vagal tone
- response to
tone
Vascular
-connective tissue
-calcification
Blood pressure
-SBP
Pulmonary
- chest
compliance
- elastic recoil
- VC; TV
Musculoskeletal
- BMD
- muscle mass
- aerobic
enzymes
- body fat
Cardiac
- myocardial demand
- cardiac mass
- systolic time
- diastolic function
- end-diastolic volume
- SV, EF
- Chronotropic changes
Coronary Arteries
- perfusion
Mohie-Aldine A.Sherief
THANK YOU
Mohie-Aldine A.Sherief