Elina_Physiology_Cardiac Cycle And Valvular Heart Disease

Front 1

What is causes causes the valves to open or close.?

Back 1

It is always a pressure difference

Front 2

When is final closure of mitral valve?

Back 2

---t QRS ---t contraction of ventricle ---t rise in ventricular pressure above atrial pressure
---t

Front 3

When is begin isovolumetric
contraction.?

Back 3

Closure of the mitral valve terminates the ventricular filling phase and begins isovolumetric
contraction.

Front 4

What is Isovolumetric contraction?

Back 4

Isovolumetric contraction-no change in ventricular volume, and both valves (mitral,
aortic) closed. Ventricular pressure is increasing, and volume is equivalent to enddiastolic
volume.

Front 5

When is begin the ejection
phase.?

Back 5

Opening of the aortic valve terminates isovolumetric contraction and begins the ejection
phase. Aortic valve opens because pressure in the ventricle slightly exceeds aortic
pressure.

Front 6

What is Ejection Phase-?

Back 6

Ejection Phase-ventricular volume decreases, but most rapidly in early stages.
Ventricular and aortic pressures increase initially but decrease later in phase.

Front 7

When is begin the isovolumetric
relaxation.?

Back 7

Closure of the aortic valve terminates the ejection phase and begins isovolumetric
relaxation. The aortic valve closes because pressure in the ventricle goes below aortic
pressure. Closure of the aortic valve creates the dicrotic notch

Front 8

What is isovolumetric
relaxation.?

Back 8

Isovolumetric relaxation-no change in ventricular volume, and both valves (mitral,
aortic) closed. Ventricular pressure is decreasing, and volume is equivalent to endsystolic
volume.

Front 9

When is begin the filling
phase.?

Back 9

Opening of the mitral valve terminates isovolumetric relaxation and begins the filling
phase. Mitral valve opens because pressure in the ventricle goes below atrial pressure

Front 10

What is the filling
phase.?

Back 10

Filling Phase-the final relaxation of the ventricle occurs after the mitral valve opens
and produces a rapid early filling of the ventricle. This rapid inflow will in some cases
induce the third heart sound. Final increase in ventricular volume is due to atrial contraction,
which is responsible for the fourth heart sound. Atrial contraction normally
is not important in the filling of the ventricle unless heart rate is elevated as occurs
during exercise or in the case of a stiff ventricular chamber

Front 11

What the systolic sounds are due to?

Back 11

The systolic sounds are due to the sudden closure of the heart valves.

Front 12

which the valves of the heart are close first?

Back 12

Normally the valves on
the left side of the heart close first.

Front 13

which the valves of the heart are open first?

Back 13

Valves on the right side open first

Front 14

Systolic sounds S1

Back 14

51: Produced by the closure of the mitral and tricuspid valves. The valves dose with only a
separation of about 0.01 seconds which the human ear can appreciate only as a single sound.
One exception is in the right bundle branch block where an audible split can be detected due
to a delay in the closure of the tricuspid valve.

Front 15

Systolic sounds S2

Back 15

Produced by the closure of the aortic (A2 component) and pulmonic valves (P2 component).
They are heard as a single sound during expiration but during inspiration the increased
output of the right heart will cause a physiological splitting.

Front 16

Systolic sounds S3

Back 16

When it is present, occurs just after the opening of the AV valves during the rapid filling of
the ventricle. It tends to be produced by the rapid expansion of a very compliant ventricle and
is a normal finding in children and young adults. In older adults it occurs with volume overload
and often is a sign of cardiac disease.

Front 17

Systolic sounds S4

Back 17

Coincident with atrial contraction and is produced when the atrium contracts against a stiff
ventricle. Examples include concentric hypertrophy and myocardial infarction.

Front 18

The jugular pulse
is ?

Back 18

The jugular pulse
is generated by changes on the right side of the heart

Front 19

The jugular pulse
a wave?

Back 19

a wave
• Highest deflection of the venous pulse and produced by the contraction of the right
atrium
• Correlates with the PR interval (see figure)
• Is prominent in a stiff ventricle, pulmonic stenosis and insufficiency
• Is absent in atrial fibrillation and other atrial arrhythmias

Front 20

The jugular pulse
c wave?

Back 20

cwave
• Mainly due to the bulging of the tricuspid valve into the atrium (rise in right atrial
pressure)
• Occurs near the beginning of ventricular contraction
• Is often not seen during the recording of the venous pulse

Front 21

The jugular pulse
x descent?

Back 21

xdescent
• Produced by a decreasing atrial pressure during atrial relaxation
• Separated into two segments when the c wave is recorded
• Alteration would occur with atrial fibrillation and tricuspid insufficiency

Front 22

The jugular pulse
v wave?

Back 22

vwave
Produced by the filling of the atrium during ventricular systole when the tricuspid
valve is dosed
Peak corresponds to T wave of the EKGand the opening of the tricuspid valve
• A prominent v wave would occur in tricuspid insufficiency and right heart failure

Front 23

The jugular pulse
y descent?

Back 23

, descent
• Produced by the rapid filling of the right ventricle immediately after the opening of
the tricuspid valve
• A more prominent wave in tricuspid insufficiency and a blunted wave in tricuspid
stenosis.

Front 24

The jugular pulse
when recording to the systemic venous pulse?

Back 24

ilinilar recordings to the systemic venous pulse are obtained when recording pulmonary capillary
wedge pressure

Front 25

Mechanically Altered States
Aortic insufficiency:

Back 25

Aortic insufficiency: Increased preload, increased stroke volume, increased ventricular systolic
pressure

Front 26

Mechanically Altered States
Heart failure (decreased contractility):

Back 26

Heart failure (decreased contractility): Decreased ventricular systolic pressure, increased preload,
loop shifts to the right

Front 27

Mechanically Altered States Essential hypertension (aortic stenosis):

Back 27

Essential hypertension (aortic stenosis): Increased ventricular systolic pressure, little change in
preload in the early stages

Front 28

Mechanically Altered State sIncreased contractility:

Back 28

Increased contractility: Increased ventricular systolic pressure, decreased preload, increased
ejection fraction, loop shifts to the left

Front 29

Mechanically Altered States Exercise:

Back 29

Exercise: Increased ventricular systolic pressure, increased ejection fraction, no significant
change in preload except in heavy exercise,when it can increase

Front 30

VALWLAR PROBLEMS
Aortic Stenosis

Back 30

• Large loss in pressure moving the blood through the narrow opening.
• Ventricular systolic pressure increases (increased afterload) to overcome the increased
resistance of the aortic valve.
• Pressure overload of the left ventricle leads to a compensatory concentric hypertrophy
which leads to decreased ventricular compliance (diastolic dysfunction) and coronary
perfusion problems and eventually systolic dysfunction.
Prominent a wave of the left atrium as the left ventricle becomes more dependent on
atrial contraction for filling.
• Mean aortic pressure is maintained in the normal range in the early stages of the disorder.
• There is a pressure gradient between the left ventricle and aorta during ejection.
• Systolicmurmur that begins after 51 (rnidsystolic) which is crescendo-decrescendo in
intensity.
• Slow closure of the aortic valve can cause a paradoxical splitting of the second heart
sound (aortic valve closes after the pulmonic)

Front 31

VALWLAR PROBLEMS
Aortic Insufficiency (Regurgitation)

Back 31

The aortic valve does not close properly at the beginning of diastole. As a result, during diastole
there is retrograde flow from the aorta into the ventricle. The amount of blood regurgitatec
into the left ventricle during diastole may be as much as 60-70% of the amount ejected during
systole.
• Acute insufficiency does not allow development of compensatory mechanisms, which
can lead to pulmonary edema and circulatory collapse.
Very large left ventricles are seen in aortic insufficiency. Large increase in LVEDV
(increase preload) but close to normal end diastolic pressures.
Ventricular failure raises pulmonary pressures and causes dyspnea.
Increased preload causes increased stroke volume, which results in increased ventricular
and aortic systolic pressures.
• Retrograde flow from the aorta to the left ventricle produces a low aortic diastolic
pressure.
• There is no true isovolumetric relaxation and a reduced period of isovolumetric contraction.
• Aortic insufficiency is characterized by a large aortic pulse pressure and a low aortic
diastolic pressure.
Dilation of the ventricle produces a compensatory eccentric hypertrophy.
• Diastolic murmur begins at $2 but may also be accompanied by a systolic murmur

Front 32

VALWLAR PROBLEMS
Mitral Stenosis

Back 32

Mitral Stenosis
• A narrow mitral valve impairs emptying of the left atrium (LA) into the left ventricle
(LV) during diastole. This creates a pressure gradient between the atrium and ventricle
during filling.
• Pressure and volume can be dramatically elevated in the left atrium, dilation of the left
atrium over time, which is accelerated with atrial fibrillation.
• Thrombi appear in the enlarged left atrium
• Increased left atrial pressures transmitted to the pulmonary circulation and the right
heart.
• Little change or a decrease in the size of the left ventricle. Systolic function normal.
• Diastolic murmur begins after 52.

Front 33

VALWLAR PROBLEMS
Mitral Insufficiency (Regurgita1ion)

Back 33

Mitral Insufficiency (Regurgita1ion)
• Acute mitral insufficiency can cause a sudden dramatic rise in pulmonary pressures
and pulmonary edema.
Can result from structural abnormalities in the valve itself, papillary muscles, chordae
tendinae, or possibly a structural change in the mitral annulus.
No true isovolumetric contraction. Regurgitation of blood from the left ventricle to
the left atrium throughout ventricular systole.
Atrial volumes and pressures increased but chronic dilation of the atrium prevents a
dramatic rise in atrial pressures.
Ventricular volumes and pressures are increased during diastole, but there is no pressure
gradient between the atrium and ventricle.
• Increased preload but with normal or reduced aftcrload.
• Systolic murmur that begins at 51 (pansystolic).

Front 34

VALWLAR PROBLEMS
Sounds Created by Turbulent Flow
Causes include:

Back 34

Sounds Created by Turbulent Flow
Causes include:
• Stenosis, e.g_, aortic stenosis
• High output, low viscosity, e.g., anemia
• Dilated chamber, e.g., aortic aneurysm
• Reverse flow across a heart valve, e.g., valvular insufficiency
• Shunting of blood, e.g., ventricular septal defect, patent ductus

Front 35

Systolic murmurs

Back 35

-Ejection murmur (Aortic,pulmonic stenosis)

-Pansystolic
(Mitral, tricuspid regurg.
Ventricular septal defect)

-Late systolic
(Mitral valve prolapse)

Front 36

Diastolic murmurs

Back 36

Early: aortic and pulmonic regurg.

Mid-to-late: mitral and tricuspid stenosis