Download Heart

2016.11.03.
Related Learing objectives
• 27. Cardiac muscle: structural and functional
characterization, electromechanical coupling, cardiac
metabolism, regulation of contractile force
• 28. Cardiac cycle. Cardiac work.
• 29. Factors determining the cardiac output. The
Frank-Starling law of the heart.
• 30. Cardiac muscle: cellular electrophysiology.
Electrocardiography (ECG)
• 31. The coronary circulation
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II.
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VI.
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Heart
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2016.11.03.
Size and location
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250-350 g
150 mm x 110 mm – about the size of a fist
located anterior to the vertebral column and posterior to the sternum
Pericardium
Wall of the heart: endothel, myocardium, endocardium
Septum cordis
Heart valves between the chambers - Atrium, ventriculus
Coronary circulation
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A heart valve normally allows blood flow in only one direction through the
heart. The four valves determine the pathway of blood flow through the heart. A
heart valve opens or closes incumbent upon differential blood pressure on each
side.
Heart innervation
Automation
Autonomous nervous system
Vagal nerve (X.)
Th1-4
chonotropic, dromotropic, inotropic,
bathmotropic, lusytropic effects
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2016.11.03.
Cardiac muscle
• is a type of involuntary striated muscle found in the walls and
histological foundation of the heart, specifically the myocardium
• Cardiomyocytes – 1-4 cell nuclei
• Intercalated discs – gap junction – syncytium (AP generates local
circuits)
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VI.
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Heart
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2016.11.03.
Intrinsic conduction system of the heart
Conduction rate in cardiac tissue
tissue
Conduction rate (m/s)
SA node
<0.01
Atrial pathway
1.0-1.2
AV node
0.02-0.05
Bundle of His
1.2-2.0
Purkinje system
2.0-4.0
Ventricular muscle
0.3-1.0
I.
II.
III.
IV.
V.
VI.
SA node discharge most rapidly,
spontaneously (100/min)
Latent pacemakers
AV node – slow conduction rate –
delay (0.1s)
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Heart
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SA- and AV-nodes (nodal tissue)
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Pacemaker potential, discharge
spontaneously
Fluctuating membrane potential
(prepotential)
Fast voltage-dependent sodium channels
are inactive
AP
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Atrial and ventricular fibers + bundle
of His, Purkinje-system
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AP
– RAPID and sharp depolarization
– vd Na+ and Ca2+ (L) channels; K+
channels
– Plateau
– High amplitude
– Fast propagation
SLOW depolarization
If; vd. Ca2+ channels (T and L types); multile K+
channels
Small amplitude
Slowly propagation
Dissection of the cardiac action potential.
Top: The action potential of a cardiac muscle fiber can be broken down into several phases: 0,
depolarization; 1, initial rapid repolarization; 2, plateau phase; 3, late rapid repolarization; 4, baseline.
Bottom: Diagrammatic summary of Na+, Ca2+, and cumulative K+ currents during the action potential.
As is convention, inward currents are downward, and outward currents are upward.
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Left: Anatomical depiction of the human heart with additional focus on areas of the conduction
system.
Right: Typical transmembrane action potentials for the SA and AV nodes, other parts of the conduction system,
and the atrial and ventricular muscles are shown along with the correlation to the extracellularly recorded
electrical activity, that is, the electrocardiogram (ECG). The action potentials and ECG are plotted on the same time
axis but with different zero points on the vertical scale. LAF, left anterior fascicle.
neuron
Striated
muscle
Smooth
muscle
Resting potential (mV)
-80-90
-80-90
-40-60
Myocardial
fiber
-80-90
Time of action potential
0.2-2
1-5
20-300
300
1-4
50
0
10-100
200-3000
300
Na+ influx
Ca++ influx
Na+ and Ca++
influx
somatic
autonomic
autonomic
Delay (ms)
Time of contraction (ms)
Mechanism of action
potential
innervation
Na+ influx
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Skeletal muscle vs cardiac muscle
In the absolute refractory period (ARP), the cardiac myocyte
cannot be excited, whereas in the relative refractory period
(RRP) minimal excitation can occur.
1. As with skeletal muscle, the action potential in a heart cell will initiate
contraction of that cell.
2. action potential duration is much longer than in skeletal muscles.
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3. the contraction in the heart muscle occurs
during the action potential, as shown in
figure A (while in skeletal muscles the
contraction occurs after the action potential).
4. The refractory period of the cardiac action
potential is much longer
5. Therefore, in the heart, the contraction is
finished before a second action potential can
be generated, as shown in figure B.
6. Thus, the contractions in the heart can not
summate (as they can in skeletal muscles;
temporal summation).
1. In skeletal muscle the resting length is quite close to the optimal length of muscle contraction
2. The passive tension in cardiac muscle rises more steeply than in skeletal muscle
3. The active length -tension curve of cardiac muscle shows that small changes in sarcomere length
produces large changes in tension due to:
a) better overlap between the myofilaments
b) enhanced sensitivity of the myofilaments to Ca → At a longer muscle fibre length more
troponin C molecules are bound to Ca resulting in greater crossbridge cycling.
4. cardiac muscle normally operates only on the ascending limb of the curve
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Regulation of contractile force
1.
2.
Initial sarcomer length – Frank-Starling law of the heart – „heterometric” regulation
SY nervous system – „homometric” regulation (β1)
1.
2.
The increase of extracellular calcium concentration (Caffeine: SR Ca++ release)
Na-K-pump inhibition (cardiac glycosides)
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I.
II.
III.
IV.
V.
VI.
VII.
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Coronary circulation
Heart
Divisions of the cardiac cycle: A) systole and B) diastole. The phases of the cycle are identical in both
halves of the heart. The direction in which the pressure difference favors flow is denoted by an arrow;
note, however, that flow will not actually occur if valve prevents it.
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Stages of the cardiac cycle
DIASTOLE
530 ms
Phases
Time
(ms)
Semilunar
valves
Atrioventricular
valves
pressure
volume
Proto
-diastole
40
Start to close
closed
↓
No
change
Isovolumetric
Relaxation
80
closed
closed
↓
No
change
Rapid
filling
100
closed
opened
No
change
↑
Slow
filling
210
closed
opened
No
change
↑
Atrial
systole
100
closed
opened
small
↑
↑
50
closed
closed
↑
No
change
rapid
ejection
90
opened
closed
small↑
↓
Slow
ejection
130
opened
closed
no
change
↓
Isotonic
relaxation
SYSTOLE
270 ms
Isovolumetric
contraction
ejection
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Volume-pressure curve of the left ventricle
Vena pulse
Right atria l
pressure
Atrial systole
Closure of the
AV valves
Fast ventricular
filling
Upward
movement of
anlus fibrosus –
atrial pressure
increase
10-7. ábra . A jobb pitvari nyomásingadozások és a vena jugularis externa térfogatingadozásai a szívciklus alatt. Little, R. C., Little, W. C.
(1989): Physiology of the Heart and Circulation. 4. kiadás, Year Book Medical Publ. Chicago ILL alapján. A felső (színes) görbén a v.
jugularis externán regisztrált térfogatváltozás (vénapulzus), az alsó (fekete) görbén a jobb pitvar nyomásingadozásai láthatók. A
függőleges szaggatott vonalak jelzik, hogy a vénapulzus később következik be, mint az azt létrehozó pitvari nyomásváltozás
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Heart sounds
Stethoscope
„lub” S1: vibration induced by the sudden
closure of the atrioventricular valves at
the start of the ventricular systole
„dup” S2: shorter, high pitched, closure of
the aortic and pulmonary valves just after
the end of ventricular systole
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Standard two-dimensional, three-dimensional, and Doppler ultrasound to create images
of the heart
Non-invasive
Indications:
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Geometry of the heart
Detection of volume-changes
SV determination
Valves
Echocardiography
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End-diastolic volume (EDV): 110-160 ml
End-systolic vloume (ESV): 40-80 ml
Stoke volume (SV): 70 ml (physical exercise: 140 ml)
Ejection fraction=SV/EDV (0.5-0.7)
Left ventricle:
– Systole: 110 mmHg
diastole: 6-8 mmHg
• Left atrium: 6-8 mmHg
• Right ventricle:
– Systole: 24 mmHg diastole: 0-2 mmHg
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Right atrium: 0-2 mmHg
Heart rate: 70/min (physical exercise: 180)
Cardiac output: 5.5 L/min (Physical exercise: 24 L/min)
cardiac index=CO/body surface area 3,2 l/minxm2
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Heart
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• CO=Heart rate x SV
• SV=EDV-ESV
• Cardiac index:
Cardiac output
CO/body surface area (male, at rest, lying: 3.2 L/m2)
Effect of sympathetic (noradrenergic) and vagal (cholinergic) stimulation on the
membrane potential of the SA node.
Note the reduced slope of the prepotential after vagal stimulation and the increased
spontaneous discharge after sympathetic stimulation.
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PRELOAD
AFTERLOAD
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The degree to which the myocardium is
stretched before it contracts (venous
return)
Resistance against which blood is expelled
(contraction or dilatation)
– Blood volume
– Venous resistance – decrease the
venous reservoires
– Intrathoracic pressure „respiratory
pump”
– Skeletal muscle contraction (muscular
actvity) – „muscle pump”
– Sucktion force of the heart
• Direct flow into the ventricle during
diastolic filling
• Anulus fibrosus moves downward
during systole, thus decreases atrial
pressure
Peripheral
resistance
Starling heart-lung preparation to determine
cardiac output (CO)
CO
meas.
Intact pulmonary circulation
LV-RA connection with a tube
No innervation
Change periheral resistance (afterload)
Change venous return (preload)
Intact coronary circulation
Venous
return
(tank)
Volume
register
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Interactions between the components that regulate cardiac output and arterial
pressure.
Solid arrows indicate increases, and the dashed arrow indicates a decrease.
Frank-Starling law
„Energy of contraction is proportional to the initial
length of the cardiac muscle fiber”
Length – extent of the preload proportional to the
EDV
 Heterometric regulation of cardiac output
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(vs homeometric SY regulaion)
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reason: calcium sensitivity of the contractile
filaments of myocytes depends on the initial
length of the fiber
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„Frank-Starling –law” and volume-pressure loop
10-14. ábra . Consequencies of Increased preload.
10-15. ábra . Consequencies of increased afterload.
The effect of the autonomic nervous system on the
heart
Sympathetic (SY)
Parasympathetic (PSY)
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positive chronotropic (Firing rate)
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negative chronotropic
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Β1 receptor – cAMP – Ica increase
Speeds If
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Positive inotropic (Contraction force) and
lusitropic
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NA- Β1 receptor – cAMP – Ica increase
SR Ca-pump activity increase
Positive dromotropic (conductivity rate)
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Ca++-channel phosphorilation, ICa++-increase
Delay in the AV node is shortened
Negative dromotropic
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ACh – M2 - cAMP level decrease – decreases If
and slows the opening of the Ca++ channels
ACh-sensitive K+-channel (M2) – slope of
prepotential is decreased because of
hyperpolarization
Positive bathmotropic (excitability)
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ACh-sensitive K+-channel (M2) – slope of
prepotential is decreased because of
hyperpolarization
Delay in the AV node is lengthened
Negative bathmotropic
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Hormonal effects on heart
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Thyroid gland (permissive role):
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Insulin, glucagon, growth hormone:
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positiv inotropic and chronotropic effect
Increased number and sensitivity of 1 receptors
positiv inotropic effect
Anatomy
Origin and spread of cardiac excitation
Heart muscle
Mechanical events of the cardiac cycle
Integrated control of cardiac output
ECG
Heart
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ECG - electrocardiogram
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interpretation of the electrical activity of the heart over a period of time, as
detected by electrodes attached to the outer surface of the skin and recorded
by a device external to the body
ECG is used to measure
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the rate and regularity of heartbeats (tachy/bradycardia; arrhythmias)
the size and position of the chambers (hypertrophy, atrophy)
the presence of any damage to the heart (infarction)
the effects of drugs or devices used to regulate the heart, such as a pacemaker
Calibration (speed of recordings, amplitude)
– 25 mm/s (1mm=0.04s); 10 mm=1 mV (1mm=0.1 mV)
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Unipolar vs bipolar electrodes
Limb leads and precordial leads
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Depolarization moving toward an active electrode in a volume
conductor (body) produces a positive deflection, whereas
depolarization moving in the opposite direction produces a negative
deflection.
By convention, an upward deflection is written when the active
electrode becomes positive relative to the indifferent electrode, and
a downward deflection is written when the active electrode
becomes negative.
The correlation of the electrical activity of the heart and the ECG recordings
Spread of cardiac excitation
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Limb leads and augmented limb leads
Einthoven
(standard)
Limb leads
Goldberger
(augmented)
Limb leads
Precordial leads
V1
In the fourth intercostal space (between ribs 4 and
5) just to the right of the sternum (breastbone).
V2
In the fourth intercostal space (between ribs 4 and
5) just to the left of the sternum.
V3
Between leads V2 and V4.
V4
In the fifth intercostal space (between ribs 5 and 6)
in the mid-clavicular line.
V5
Horizontally even with V4, in the left anterior
axillary line.
V6
Horizontally even with V4 and V5 in the midaxillary
line.
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Directions of ECG leads in 3 dimensions
Horizontal and frontal plane
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P wave: atrial depolarization; <100ms
PQ (PR) segment: atrial plateau phase
PQ (PR) interval: Atrial depolarization and conduction through AV node; 120-200 ms
QRS duration:80-120 ms; Ventricular depolarization and atrial repolarization
QT interval: Ventricular depolarization plus ventricular repolarization; 320-390 ms
(heart rate)
ST segment: Ventricular plateau phase
T wave: Ventricular repolarization
12 leads routine ECG
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Limb leads (I, II and III)
Augmented limb leads (aVR, aVL, aVF)
Chest (Precordial) leads (V1-V6)
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Clinical relevance of ECG
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The heart's electrical axis (cardiac vector) is the general direction of the ventricular
depolarization wavefront (or mean electrical vector). The QRS axis can be determined by
looking for the limb lead or augmented limb lead with the greatest positive amplitude of
its R wave.
Left: Einthoven's triangle. Perpendiculars dropped from the midpoints of the sides of the equilateral triangle
intersect at the center of electrical activity. RA, right arm; LA, left arm; LL, left leg.
Center: Calculation of mean QRS vector. In each lead, distances equal to the height of the R wave minus the height of
the largest negative deflection in the QRS complex are measured off from the midpoint of the side of the triangle
representing that lead. An arrow drawn from the center of electrical activity to the point of intersection of
perpendiculars extended from the distances measured off on the sides represents the magnitude and direction of
the mean QRS vector.
Right: Reference axes for determining the direction of the vector.
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The normal QRS axis is generally down and to the left, following the anatomical
orientation of the heart within the chest.
An abnormal axis suggests
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a change in the physical shape and orientation of the heart, or
a defect in its conduction system that causes the ventricles to depolarize in an abnormal way.
Normal
−30° to 90°
Normal
Left axis
deviation
−30° to −90°
May indicate left ventricular
hypertrophy, left anterior
fascicular block
Right axis
deviation
+90° to +180°
May indicate right
ventricular hypertrophy, left
posterior fascicular block
EC calcium level 2,5 mmol/L
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Increased: enhanced myocardial contractility, relaxes less during
diastole, heart eventually stops in systole – calcium rigor
Decreased: decreased contraction force
EC kalium level 4 mmol/L
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hyperkalemia: heart stops in diastole(reason: resting membrane
potential decreases=> muscle fiber becomes unexcitable –
decreased poropagation and contraction => heart failure)
hypokalemia: ventricular extrasystole => heart failure
Ional effects on the ECG
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