Cardiovascular Physiology: October 25, 2010
Cardiovascular Physiology: October 25, 2010
Cardiovascular Physiology: October 25, 2010
LECTURE 4
October 25, 2010
Cardiac Cycle
Ana-Maria Zagrean MD, PhD
Physiology Department II
azagrean@gmail.com
www.fiziologie.ro
atrial
ventricular
Obs: the A and V do not contract and relax at the same time
Note the valves (blue) which control the one way direction of blood flow;
also, the tendons prevent the AV valves from turning inside-out.
As the animation starts, the atria fill, then contract (atrial systole), pumping blood
via the AV valves into the ventricles. Then the ventricles contract (ventricular
systole), causing the AV valves to shut and the semicircular valves to open,
allowing blood out of the heart.
This is followed by relaxation (diastole) of the ventricles, and the semilunar valves
shut.
The cycles then repeats itself
AS
AD
VS
VD
1.
2.
3.
4.
5.
6.
7.
8.
Phase of the
cardiac cycle
1
1
1
Diastole
Diastole
Diastole
Systole
3
3
Systole
Systole
Diastole
Closing of AV valves
(tricuspid and mitral)
Opening of semilunar
valves (pulmonary and aortic)
Rapid ventricular ejection (fast muscle
shortening)
Decreased ventricular ejection (slower
muscle shortening)
Closing of semilunar
valves (pulmonary and aortic)
Isovolumetric ventricular relaxation (with all
valves closed)
Opening of AV valves
(tricuspid and mitral)
Atrial Systole
- 0,1 sec
- changes in intra-atrial pressure:
0 4 - 6 mm Hg - right atrium
0 7 - 8 mm Hg left atrium
functional significance:
- contributes to, but is not essential for,
ventricular filling
- A = primer pump for the ventricle
- venous pulse: a wave
- causes the 4th heart sound
Isovolumic
contraction Ejection
AoC
120
Volume (ml) Presure (mmHg)
100
80
60
40
20
Aortic pressure
MC
AoO
MO
0
130
Atrial pressure
Ventricular pres.
90
Ventricular volume
50
S1
S2
S3
S4
S1
Electrocardiogram
Phonocardiogram
Atrial Diastole
- 0,7 sec
- changes in diastolic intra-atrial pressure:
- physiological changes: c and v waves
- pathological changes (valves pathology)
Isovolumic
contraction Ejection
AoC
120
Volume (ml) Presure (mmHg)
100
80
60
40
20
Aortic pressure
MC
AoO
MO
0
130
Atrial pressure
Ventricular pres.
90
Ventricular volume
50
S1
S2
S3
S4
S1
Electrocardiogram
Phonocardiogram
Ventriculare systole
- atrio-ventricular delay in impulse conduction
- 0,27 s;
- phases:
1. isovolumic contraction 0,05 s
2. rapid ejection - 0,09 s; 70% emptying
3. reduced/slow ejection - 0,13 s; 30% emptying
Isovolumic Contraction
Ventricular ejection
Isovolumic
contraction Ejection
AoC
120
Volume (ml) Presure (mmHg)
100
80
60
40
20
Aortic pressure
MC
AoO
MO
0
130
Atrial pressure
Ventricular pres.
90
Ventricular volume
50
S1
S2
S3
S4
S1
Electrocardiogram
Phonocardiogram
Ventricular diastole
- 0,53 s
- phases:
- protodiastole 0,04 s
- isovolumic relaxation - 0,08 s
- rapid filling 0,11 s
- slow filling 0,19 s
- atrial systole 0,11 s
Isovolumic Relaxation
Ventricular changes:
-Wall tension increasing
-Apex-to-base shortening
-Circumferential elongation
Ventricular filling
Isovolumic
contraction Ejection
AoC
120
Volume (ml) Presure (mmHg)
100
80
60
40
20
Aortic pressure
MC
AoO
MO
0
130
Atrial pressure
Ventricular pres.
90
Ventricular volume
50
S1
S2
S3
S4
S1
Electrocardiogram
Phonocardiogram
Flow (A) and pressure (B) profiles in the aorta and smaller vessels.
blood to flow backward across the valvular orifice (i.e., regurgitation) as well as
stenotic lesions that narrow the valve opening, forcing the blood to pass through a
narrower space (i.e., stenosis). During certain parts of the cardiac cycle, blood
passing through either regurgitant or stenotic lesions makes characteristic sounds
that are called murmurs.
The primary aortic area: 2nd right intercostal space, adjacent to the sternum.
The secondary aortic area: 3rd left intercostal space, adjacent to the sternum
(known as Erb area).
The pulmonary area: 2nd left intercostal space
The tricuspid area: 4th & 5th intercostal spaces, adjacent to the left sternal
border.
The mitral area at the cardiac apex: 5th left intercostal space, on the
medioclavicular line.
the lub
appears at 0.02 0.04 sec after the beginning of the
QRS complex
vibrations are low in pitch and relatively long-lasting
- lasts ~ 0.12-0.15 sec;
frequency ~ 30-100 Hz;
produced, in this order, by : closing of the mitral valve,
closing of the tricuspid valve, opening of the pulmonar
valve, opening of the aortic valve.
the dub
appears in the terminal period of the T wave
lasts 0.08 0.12s
produced, in this order, by: closing of the aortic valve,
closing of the pulmonic valve, opening of the tricuspid
valve, opening of the mitral valve.
heard like a rapid snap because these valves close
rapidly, and the surroundings vibrate for a short period
physiologic splitting that varies with respiration (wider
splitting with inspiration)
Split S2
Normal or physiologic
Inspiration
Expiration
Split S2
Audible expiratory splitting means > 30 msec difference
in the timing of the aortic (A2) and pulmonic (P2)
components of the second heart sound.
Splitting of S2 is best heard over the 2nd left intercostal
space
The normal P2 is often softer than A2 and rarely audible
at apex
Inspiration accentuates the splitting of S2.
Split S2
Normal or physiologic
Inspiration
Expiration
Phonocardiogram
Isovolumic
contraction Ejection
AoC
120
100
80
60
40
20
Aortic pressure
MC
Ao
MO
0
130
Atrial pressure
Ventricular pres.
90
Ventricular volume
50
S1
S2
S3
S4
S1
Electrocardiogram
Phonocardiogram
ISOVOLUMETRIC CONTRACTION
The beginning of systole
Heart:
The atrioventricular (AV) valves close at the beginning of this phase.
Electrically, ventricular systole is defined as the interval between the QRS
complex and the end of the T wave (the Q-T interval).
Mechanically, ventricular systole is defined as the interval between the
closing of the AV valves and the opening of the semilunar valves (aortic
and pulmonary valves).
Pressures & Volume:
The AV valves close when the pressure in the ventricles (red) exceeds the
pressure in the atria (yellow). As the ventricles contract isovolumetrically - their volume does not change (white
white ) -- the pressure inside increases,
approaching the pressure in the aorta and pulmonary arteries (green).
ECG:
The electrical impulse propagates from the AV node through the His
bundle and Purkinje system to allow the ventricles to contract from the
apex of the heart towards the base.
The QRS complex is due to ventricular depolarization, and it marks the
beginning of ventricular systole. It is so large that it masks the underlying
atrial repolarization signal.
Heart sounds:
The first heart sound (S1, "lub") is due to the closing AV valves and
associated blood turbulence.
RAPID EJECTION
Heart:
The semilunar (aortic and pulmonary) valves open at the beginning of
this phase.
REDUCED EJECTION
The end of systole
Heart:
At the end of this phase the semilunar (aortic and pulmonary) valves
close.
Pressures & Volume:
After the peak in ventricular and arterial pressures (red and green),
blood flow out of the ventricles decreases and ventricular volume
decreases more slowly (white
white ).
When the pressure in the ventricles falls below the pressure in the
arteries, blood in the arteries begins to flow back toward the ventricles
and causes the semilunar valves to close. This marks the end of
ventricular systole mechanically.
ECG:
The T wave is due to ventricular repolarization. The end of the T wave
marks the end of ventricular systole electrically.
Heart sounds:
ISOVOLUMETRIC RELAXATION
The beginning of diastole
Heart:
At the beginning of this phase the AV valves are closed.
ECG:
Heart sounds:
A third heart sound (S3) is usually abnormal and is due to rapid
passive ventricular filling.
It occurs in dilated congestive heart failure, myocardial infarction, or
mitral incompetence.
ECG:
Heart sounds: