Hemodynamic Cycle

8/18/2019 Hemodynamic Cycle

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Hemodynamic cycle, heart sounds,

valvular heart disorders

Physiology and Pathophysiology of the heart

Part 1


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Phase 1

Atrial Contraction

RV

LV

LA

PARA

A

RV

LV

LA

PARA

A

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


3/57

Phase 2

Isovolumetric

Contraction

RV

LV

LA

PARA

A

P

P 120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

Phase 2

Isovolumetric

Contraction

RV

LV

LA

PARA

A

P

P

RV

LV

LA

PARA

A

P

P 120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


4/57

Phase 3

Rapid Ejection

RV

LV

LA

PARA

A

120

40

80

0

40

80

120

LV

Vol

(ml)

Press

(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

Phase 3

Rapid Ejection

RV

LV

LA

PARA

A

RV

LV

LA

PARA

A

120

40

80

0

40

80

120

LV

Vol

(ml)

Press

(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

120

40

80

0

40

80

120

LV

Vol

(ml)

Press

(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


5/57

RV

LV

LA

PARA

A

Phase 4

Reduced Ejection

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

RV

LV

LA

PARA

A

Phase 4

Reduced Ejection

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


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RV

LV

LA

PARA

A

Phase 5

Isovolumetric

Relaxation

P P 120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

RV

LV

LA

PARA

A

Phase 5

Isovolumetric

Relaxation

P P 120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


7/57Time (sec)

RV

LV

LA

PARA

A

Phase 6

Rapid Filling

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv

Time (sec)

RV

LV

LA

PARA

A

Phase 6

Rapid Filling

120

40

80

0

40

80

120

LV

Vol

(ml)

Press(mmHg)

1 2 3 4 5 6 7

Phase

0 0.4 0.8

Time (sec)

Heart

Sounds

ECG

LV Press

AorticPressure

LA Press

LVEDV

LVESV

I II IIIIV

a cv


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HR 75/MIN HR 200/MIN Skeletal muscle

Hemodynamic cycle duration 0,80 0,30

Systole 0,27 0,16

Action potential duration 0,25 0,15 0,005

Absolute refraction period 0,20 0,13 0,004

Relative refraction period 0,05 0,02 0,003

Diastole 0,53 0,14


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Heart sounds


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Heart soundsSound Appears during Results from:

S1Isovolumetriccontraction

Caused by the sudden block ofreverse blood flow due to closureof the atrioventricular valves

S2Isovolumetricrelaxation

Caused by the sudden block ofreversing blood flow due to closureof the semilunar valves

S3 Rapid ventricle filling

Physiology (benign) in children,also trained individual andsometimes in pregnancy;protodiastolic gallop, ventriculargallop

Pathology–

failing left ventricle(dilated ventricle)

S4 Atrial systoleLow plasticity of the ventricles (ex.Hypetrophy)presystolic gallop or atrial gallop


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Heart sounds -

murmurs


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Cardiac Output = Heart Rate (HR) x Stroke Volume (SV)

• HR regulation

• SV regulation

Cardiac output


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HR regulation

www.cvphysiology.com


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ANS and regulation of the heart work

Muscarinic M2 rec

activation

SA

AV

Vagal nerveSympathetic system

ACh NE

HR

Inotropy

+

–

+

Adrenergic β1 rec

activation


15/57

β GscAMP

β

GscAMP

NA

NA

Na+ Na+

Na+

Na+

Na+

Na+

Na+ Na+ Na+

Na+

Na+

Na+

Na+

Na+

Na+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca

2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Na+

Na+

Na+

Ca2+


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Sarcoplasmic reticulum

β

β

Gs

Gs

Ca2+ Ca2+

Ca2+ Ca2+

Ca2+

Ca2+ Ca2+

Ca2+ Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+ Ca2+

Ca2+

Ca2+ Ca2+

Ca2+

Ca2+ Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca

2+

Ca2+

Ca2+

Ca2+ Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

NA

NA

cAMP

cAMP


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M

ACh

K+

K+

K+ K+

K+

M

ACh

Gi

Gi

K+

K+ K+

K+

K+

K+

K+

K+

K+

cAMP

Na+

Na+

Na+

Na+

Na+

Ca2+

Na+ Na+

Na+

Na+

Na+ Na+

cAMP

+

+

+

+

+

+

+

+

+

-

-

-

-

-

-

-

-

-

-

-

-

-

--

-

-

-

-

--

+++

+

+

+

++

+

+

+

+K+

K+ K+

K+

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+ Ca2+

Ca

2+


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FRANK-STARLING LAW

Increased afterloadDecreased afterload

preload



20/57

What affects preload?



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FRANK-STARLING LAW - Contractility

preloadwww.cvphysiology.com

Increased contractility

Decreased contractilty

C t ti l ti


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Anrep effect – wzrost kurczliwości w odpowiedzi na gwałtowny wzrost afterload

Bowditch effect – depends on HR increase

HOMEOMETRIC regulation – depends on contractility

HETEROMETRIC regulation – depends on Frank-Starling mechanism

Contraction regulation


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Clinical index for inotropy evaluation:

Ejection Fraction (EF) = SV/EDV * 100%

dP/dt

Contractility


24/57

Stroke volume regulation



25/57

Case 1

• 62-years old women with history of atrial

fibrillation

• shortness of breath, when she lies down flat in

the supine position,

• nocturia,

• she has run out of digoxin, which she took to

control her heart rate


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Case 1

• bood pressure 90/65 mm Hg,

• irregular heart rate ~ 120/min,

• pulmonary rales,

• increased jugular venous distension,

• peripheral edema of legs


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the primary diagnosis


28/57

the primary diagnosis

atrial fibrillation

congestive heart failure


29/57

Question 1:

What can be a cause of atrial fibrillation in this

patient?


30/57

Answer 1:

• the run out of digoxin


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Question 2:

What is the mechanism of digoxine in the heart?

• the positive inotropic effect

• the negative chrono- dromotropic effect

Why?


32/57

The sodium/potassium pomp inhibition

in cardiomiocytes membrane


33/57

Question 3:

What factors affect stroke volume?


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Answer 3:

• Contractility

• Preload

• Afterload

Which of above factors was changed during atrial

fibrillation?


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Question 4:

How does stimulation of muscarine receptors affect

contractillity?


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Answer 4:

• stimulation of muscarinic receptors decreases

contractility only in atria


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Case 2

• 25-year old pregnant women

• no medication,

• no complications with this pregnancy

• she was admitted to the hospital in active

phase of labor

• she asked for pain relief


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Case 2

• the epidural nerve block has been done

• dizzines

• low blood pressure

• raid heart rate


39/57

Case 2

• intravenous fluid bolus and a small amount

of ephedrine were recommended

• the lack of sympthoms


40/57

Question 1:

Why would epidural analgesia cause these

sympthms?


41/57

Answer 1:

• sympathetic blockade (T10 – L3) resulting in

decreased venous pressure and thus decreased

cardiac output and decreased pheripheral

resistance resulting in hypotension


42/57

Question 2:

How would ephedrine (IV) counter the hypotension?


43/57

Answer 2:

• ephedrine increases 1 stimulation, leading to

contraction of the venous musculature,

increasing VP, and thus CO and pheripheral

resistance

Cardiac Output in relation


44/57

Cardiac Output in relationto venous pressure


45/57

• 62-year old man

• 10-year history of arterial hypertension and dyslipidemia;

• Since couple moths lack tolerance for physical effort (he can’t

climb up to the 2’nd floor) and several times he reported angina

pectoris

• Admitted to a Cardiology Unit after syncope with arising

dyspnoe;

Case 3


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Physical examination:

•HR 123/min

• Heart gallop

•Loud heart murmur in the aortic area

•Blood congestion in pulmonary circulation;


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48/57


49/57

LV

hypetrophy

Calcificatedaortic valve


50/57

Turbulent blood

flow through LVoutflow


51/57

Cli i l ti


52/57

Clinical questions:

1. What should be diagnosed in our patient?

2. Why systolic murmur in the aortic area?

3. Why patient developed heart failure?

4. Why in the echocardiography LV hypertrophy was

observed?

5. Why patient developed symptoms of the ischaemia?

Cli i l ti


53/57

Clinical questions:

1. What should be diagnosed in our patient?

Severe symptomatic aortic stenosis complicated with

acute heart failure.

Cli i l ti


54/57

Clinical questions:

1. Why systolic murmur appeared in the aortic area?

Sytolic aortic murmur appeared when blood was ejected from

LV through narrow aortic valve.

Cli i l ti


55/57

Clinical questions:

1. Why patient developed heart failure?

Blood stasis in LV according to the narrowing of aortic

valve resulted in the volume and pressure overload of the

LV (↑LVEDP) -> and LA.

Increased left atrium pressure decreased venous return from

pulmonary circulation what resulted in pulmonary

congestion.

Cli i l ti


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Clinical questions:

1. Why in the echocardiography LV hypertrophy was

observed?

During development of the aortic stenosis afterload gradually

increased. A rise in afterload increased duration of a isovolumetric

systole.

Cli i l ti


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Clinical questions:

1. Why patient developed symptoms of the ischaemia?

Cardiac muscle hypertrophy -> higher metabolic

demand (higher O2 demand).

Higher afterload -> lower stroke volume

Low SV -> low BP

Low coronary perfusion

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Hemodynamic Cycle