Part 2 cardiac cycle Flashcards
بسم الله الرحمن الرحيم وبه نستعين
Ventricles act as compression suction pump
comrpeesion in systole high pressure system for djection
Suction in diatsole low pressure system for filling
In each phase of the cycle there is changes on ?
Atrial Pressure Ventruclar voulme venrticular pressure Aortic pressure Heart valves Heart sounds ECG
Atrial systole repesents?
firsth phase of new cycle
third phase of ventricular filling become more imp in increased HR
ATRIAL PRESSURE UN ATRIAL SYSTSOLKE ?
Increased = a Wave in juglar venous pressure cureve
Aortic pressure: is,,,,,,,,,,,,,,,,,,,,,,,, as semilunar valves are
still closed why?
decreased
no blood ejection, while there is
continuous escape of blood to the periphery.
Atrial systole responsible for sounds?
Yes ,4th heart sound not audibe normally
Atrial systole and pwave
p wave before atrial systole by 0,02 seconds the latter last for 0,1 second\
• During ventricular systole there are 3 phases:
- Isovolumetric contraction
- Rapid ejection
- Reduced ejection
• During which both types of valves are closed.
isovlumetric contraction 0,04 seconds
isovlumertic relaxation
And so isometric contarcvtion is responsible for switching of the ventricular
pressure from the low pressure system to the high pressure
system. how ?
contract ismoetrically increasing tension on the walls increasing intraventriculare pressure
Isovoumetric contracio0n and Jugular venous pressure?
increaing atrial pressure due to ?
Bulging of cusps into atira casuing
C wave in jugular venous pressure
Heart sound on isovolumetric contraction ?
First heart sounds shrae by 2 components?
Vlavlar compnent: closed valve
Musclear: contraction of muscles
Q wave and isovoulmetric contraction ?
Q wave begins beofr it 0,02seconds
Rapid ejection phase 0,16 second and jugular venous pressure ?
Pulling the AV Fibrous skeletion down increasing caivty decreasing the pressure
causing X descent in jugular venous pressure
Ventricular pressuer in rapid ejection phase?
the muscles contiume contracting increasing intraventricular pressure
Heart sounds in the rapid ejection phase ?
First one
due to vascular compnent : rush of blood into aorta and pulmonary artery
rapid ejection phase in ECG?
ST segment and begining of T wave
reduced ejection phase ?
0,1 second
Firsth half of t wave and its Top
Protodiastole
0,02 to 0,04 second between the systole and diastole dut to momentum of blood to aorta when momentum is overcome the aortic valve is closed produng second heart sound
Second heart sound in ?
portodiastole
During ventricular diastole there are 4 phases:
- Isovolumetric relaxation.
- Rapid filling .
- Reduced filling.
- Next Atrial systole
Isovolumetric relaxation and jugular venous pressure
increased vr with closed valve inicreasing the pressure casuing V wave
in juglar venous pressure
Ventricular pressure in IVR ?
Decreasd in high rate to reach 0 to be filled by the atrial blood
incisura of aorta occur in —- phase
IVR
IVR
0,06 SECONDS
2ND HEART SOUND
End of T wave and start of TP segment
Rapid filling phase and JVP ?
Decreased pressure due to evacuation
Y descent in JVP
Ventricular pressure: remains very low during this phase
(~ 0 mm Hg).
Rapid filling phase ?
0,1 Second
S3 SOUND
TP isolectric line
diastasis
Blood passes from big veins through atria to
ventricles, without staying in the atria (that is why it is also called?
RED F P
This phase is the longest phase in the cardiac
cycle, and continues for 0.2 sec. or even
more, and is prolonged when the heart rate
decreases.
Reduced filling Phase
In case of tachycardia, the role of atrial systole in ventricular
filling becomes more important ?
and may cause, in this case,
filling up to 50 % of blood
EDV
ESV
EDV=130 Ml after atrial systole
ESV=50 Ml after reduced ejection phase
Stroke volume (SV= EDV- ESV) = ~ 80 ml.
• It is the difference between end diastolic
volume and end systolic volume
There is no a wave in ?
Atrial fibrillation
In case of tricuspid stenosis there is ?
large a wvae
tricupsid insufficienct there is ?
Giant c wave
In case of heart block first degree there is prolongation of ?
pr interval
ac interval
In complete heart block there is
Canon giant a Wave
Pulse is ?
Presure wave not blood voulme wave trasmitted through the vessel due to ejection from LV
4-8 M/SEC IN AORTA AND LARGE ARTERIRES
RACH 16M/S IN SMALL ARTERIES
Arterial pulsations reach to the capillaries, and end at the ?
post capillary
resistance
Anacrotic limb due to ?
rapid ejection phase
Catacrotic limb
Reduced ejection
Diastole
• Dicrotic notch: is a small oscillation on the falling phase of the pulse wave caused by vibrations set up by sudden closure of the aortic valve (In the aorta and in central arteries, the closure of aortic valve causes a larger oscillation known as ..........................).
incisura
Factors affecting pulse pressure velocity?
elasticity
1-age
2-distance
3-atherosclerosis
➢Arterial pulse volume is very high in atherosclerosis and in aortic
regurgitation and may be so much increased to be known as
Collapsing pulse = Corrigan =Water Hammer puls
Arterial pulse volume is decreased in aortic stenosis and in
hemorrhage and may be very small leading to what is known as
thready pulse.
Arterial pulse volume is very high in
atherosclerosis and in aortic
regurgitation
Arterial pulse volume is decreased in
aortic stenosis and in
hemorrhage
• The four sounds can be recoded in the
phonocardiogram.
First Heart sound
0,16 second
Isovlmetric contraction:
valvular comnent
muscluar compnent
Rapid ejection phase:
Vascular compnent
2nd heart sound
0,12 second shorter than s1
Isovolumetric relaxation
closure of semilunar valves
best heaerd at aortic and pulmonary compnent
splitting durin inspiration best heard at pulmonary compnent
3rd sound?
due to rush of blood from atria to ventricule during rapid filling phase
heard in children ,thin people , Heart failure
4th Heart sound
rush of blood from atria to ventricle during atrial systole
not heared masked by s1
accentuated in mitral and tricuspid stenosis
Murmurs?
Abnormal sounds or noise heard due to turbulent flow due to diseased valves
القاعدة: الصمام المفتوح في المرحلة لازم يكون ضيق و الارتجاع في الاخر
ازاي؟
systolic murmurs
aortic or pulmonary stenosis
av valves regrgiutation insufficiency incompetence
Diastolic murmurs:
av valves stenosis
aortic or pulmonary regrgiutation insufficiency incompetence
•Systolic Time Intervals (STI)
• Simultaneous recording of ,??? allows for measurement of the duration of
systolic time intervals (STI).
carotid pulse wave
ECG
phonocardiogram
Total Electromechanical Systole (QS2):
is the period from the
onset of the QRS complex to the closure of the aortic valve as
determined by the onset of the second heart sound.
beginning of the carotid pressure rise to the dicrotic notch.
left ventricular ejection time LVET
Pre-Ejection Period (PEP):
is the difference between QS2 and LVET.
(PEP = QS2 – LVET). PEP represents the time for the electrical
and mechanical events that precede systolic ejection.
The ratio PEP/ LVET can be used as a measure of left ventricular
function. Normally, this ratio is about 0.35, and is increased
without change in QS2 , in case of
left ventricular dysfunction.
Posture and cop ?
cop decreses by 20% on standing
Exercise and metnalitiy on cop ?
Exercise increase
Mental anxiety and dreaming of stressfyl conditions increasing cop
COP FACTORS?
4P TMH
Posture
physical activity
pregnancy
pathological condition
Temperature
Meals
Hormones
Measutment of COP?
On experimetnal animal :
In anasthetazied animals aorta pulmnarry trunk
In Hear-lung preparation Bell cardiometer
On Man:
Echocardiogarphy
Ficks methold
dye dilution technique
CO= ? FICKS
O2 CONSUMPTION
________________
Artterial-Venous difference O2
COP =SV X HR SO =
(EDV-ESV)X HR
SV affected by?
PRELOAD Afterload contractility: 1-blood supply 2-metabolism '3-intact myocardium
Intrinicsi regulation of cop ?
Homeometric regualtion : Preload and EDV
Heteroetirc regulation : the contractilityt at same ED
Heterometric regulation
Preload phenomenon VR Tranisnet postural changes ,adjustment right and left cop , denervated transplanted heart Fallling heart depend mainly on it
Factora affecting EDV?
VR
COMPLIANCE OF HEART
Atrial contraction
VR incrasieis in /
Skeletal pumping
increasing ciruclating blood
increasing intrathoracic negativity
Recumbency increasing the VR
Homeometric regulation
Afterload phenomenon at same EDV
Extirinsic regulation of COP ?
Physiological acting Exterinsic factors
Symp-ParaSymp -Neuro hormone
Humorally mediated Extirnsic factors
Factors acting on cAMP like glucagon + ino +chrnontropics
Digitalis
myocardial deprssion direct
The most important factor that shifts to left?
is the adreanl stimulation of heart or circulating catecholamines
Cardiac Resereve ?
قدرة القلب علي تعزيز المخرج عشان يرضي طلباته المتزايدة
الفرق بين أقصي و أقل مخرج قلبي
short lived mechanisms of regulation of COP?
MOMENT TO MOMENT
depending on VR
within permissive limit 12 litrs/min
increasing sinus rhtym to 90bpm
increasing sv heterometric then homometric regulation
Short term beyond permissive limit ?
Sympathatic adranal and catecholamins
+chorno tropic increasing HR 180bpm
+ Inotrioic increasing SV esv < 30 ml
الحمدلله رب العالمين
