Hemodynamic Cycle
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Transcript of Hemodynamic Cycle
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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
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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
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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
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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
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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
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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
www.cvphysiology.com
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What affects preload?
www.cvphysiology.com
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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
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Stroke volume regulation
www.cvphysiology.com
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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
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the primary diagnosis
atrial fibrillation
congestive heart failure
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Question 1:
What can be a cause of atrial fibrillation in this
patient?
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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?
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The sodium/potassium pomp inhibition
in cardiomiocytes membrane
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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
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Case 2
• intravenous fluid bolus and a small amount
of ephedrine were recommended
• the lack of sympthoms
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Question 1:
Why would epidural analgesia cause these
sympthms?
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Answer 1:
• sympathetic blockade (T10 – L3) resulting in
decreased venous pressure and thus decreased
cardiac output and decreased pheripheral
resistance resulting in hypotension
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Question 2:
How would ephedrine (IV) counter the hypotension?
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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
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Cardiac Output in relationto venous pressure
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• 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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LV
hypetrophy
Calcificatedaortic valve
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Turbulent blood
flow through LVoutflow
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Cli i l ti
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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
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Clinical questions:
1. What should be diagnosed in our patient?
Severe symptomatic aortic stenosis complicated with
acute heart failure.
Cli i l ti
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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
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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