Part 1 Flashcards
بسم الله الرحمن الرحيم وبه نستعين
إن الله هو الرزاق ذو القوة المتين
توكلنا علي الحي الذي لايموت
Fucntions of CVS?
1-Homeostsis
2-Temperature Regulation
3-Communication
The ultra important funvtion ? keeping adequate blood perfusion to Capillaries Overall the body
قوانين الانسياب في الدوري؟
الدم دايما بيتجه اتجاه واحد في دائرة مغلقة Fluidity Continuity Circuity Unidirectional
اهمية توصيل الدم بالتوازي للأعضاء؟
نفس مكونات الدم الطازج
الدم المنساب لعضو واحد ممكن تتحكم فيه وحده
أقل مقاومة طرفية
Homeostasis how occure?
Maintain intersistial fluid compnents in reguler portions
By:
Pumping Heart
Conditioning of Blood as it passes throug Other organs as lungs and liver and kideny @@
Communcation Of CVS?
By Endocrinal hormones modulating functions of all body through blood
The heart is dual pump ?
Compression in systole
Suction in diastole
Aorta and big arteries and Windkessel ?
Aorta can act as Pressure store accepting more blood soting the excess pressure and expansion of wall during systole then it recolis during diastole to make the stored pressure flow downstream
Musclar arteries?
Delvring arteries low resistance
Arterioles resistance Function
High rssistance and sphincteric as stopcocks that maintain arterial blood pressure and blood flow to tissues
Main effector on the peripheral resistance and blood pressure
Veins (Capacitance Functions)
Venous retuen also CVS reseroir of blood due to capacitance
Types of flow ?
Intermittent from ventricles into the aorta only pump during systole and stop during diastole
Pulsatile in aorta due to Windkessel phenomenon leading to high systole low diastole
Still pulsatile in capillaries with little difference between systole and diastole
Pulstatily disappear in veins the flow is steady
Seires and parllel
Systemic + pulmonary
the branches to the tissues of organs in parallel as to brain - skeletal muscles - kideny -heart
مميزات التوصيل علي التوازي؟
- HOMEOSTASIS
- Control of An organ blood flow separately
- Decreasing TPR
High pressure sysytem ?
Left ventricle during systole
Aorta big aterires muscular arteries
arterioles
Arterial end of capillary proximal to dividing point
Low pressure system
Venous end of capillaries distal to the divifing point
Venules small veins big veins venea Cavae
Right and Left atrium
Pulmonaru circulation as a whole
right and left ventrivle during diasrole
علاقة عكسية بين السرعة والمساحة الكلية المقطعية
كلما صغر مقطع الوعاء كثرت اعداده بمعني
الاورطي عملاق مفيش منه الا واحد فمسحاة المقطع نسبيا صغيرة ل
ان الشعيرات الدموية صغيرة عدد كبير جدا جدا جدا مساحة المقطع الكلية اكبر من الاورطي
فالسرعة فيها اقل من الاورطي وهذا مايسمح بتبادل الغازات
Artery
Capillary
Vein
Velocity
50cm/s
1mm/s capillary
30cm/s
Distensibility =Capacity
حجم الدم المحمول علي في اي جزء من الدوري في لحظة
Volume change per unit change in pressure
the functional capillary pressure ?
the pressure of the dividing point on mid ot the capillary = 17mm Hg
V=Q/A
Q flow direct proprtional
A inversely
الحمدلله رب العالمين
A-V Ring act as ?
Cardiac Skeletion
electrice insulator
Papillary muscles role?
تنقبض مع انقباض عضلة القلب اثناء السيستول
وتمسك في الصمام وشرفاته تمنع انها تتفتح ناحية الاذين بسبب الضغط العالي جوا البطين
Heart is functional syncitum not true one
Gap junctions
One unit
All or none
Functional synctium ?
Gap junctions electrical synctium
Desmosome mechanical synctium
Cardiac muscles are divided into /
Nodal : pacemaer
junctional : conductive
Musclar contractile tissue
Pericardial inelastic or elastic why?
Inelastic pervents cardiac dilatation except in pysiological variations
Pericardial effusin severity?
Cauing increased intrapericardial pressure compressing the heart preventing VR and Ventricular Filling cardiac tamponade
Only connection between atria and ventricles?
Bundle of His
Left ventricular aid
contraction of left ventricle increases pressure in the right ventricle
There are intercalated discs \and desmosmones why?
Intercalated discs areas of low resistance allowing movment of action potenial easily between cardiac cells
Desmosomes helds the muscle cells together
Main 4 proteins for contration ?/
Actin
Myosin
Troponin
Tropomyosin
The Dihydropyrdidine recptors where/
DHP in the T tubules which are voltage gated Ca Channels
The ryanodine recetors where?
In terminal cisternae
Are Ca release Channels
Ca induced Ca Relese ?
CICR ?
This is the release of Ca from the ryanodine receptor of termnal cisrterneae of sarcoplasmic reticulum
due to activation of the DHP dihydopyridine receptors by the ECF Ca entered througth the T-tubule
True synctium =
Prtoplasmic contiunity of cells
Heart is functional synctium ?
Due contraction as a one unit
All or none law following : no gradtion of response in increasing stmulus above the threshold
No protoplamic continuity
Electrical and mechanical synctium of the heart?
Electrical : due to prence of the Gap junctions allowing action poteinal to spread easily between the fibers
Desmosmes: Cohesin between fibers when one fiber contreact attract the olther and is tied with it making the heart contract as a one unit as afully mechanical synctium
Energy soueve of Heart?
Good perfusion
Myoglobin
Mitochondira
Aerobic metabolism and osidative phosprulation for ATP
if there is ischemia > infarction due to necrosis
The Hear differ from skeltal muscles?
No motor unit
no nerual activation
autorhytmic activity node > conductive portion > contractile portion ‘
Properties of cardiac muscles?
Excitability
Autorhymicity
Conductivity
Contractility
Exitibility
Ability of cardiac muscle to repond by intiating action potential and this is divied into
Slow and Fast response
Sliw respones and fast
Slow by slow fibers in SAN,AVN
Fast by fast fibers in ventricles atria his bundles
Fast response RMP
Stable RMP DUE TO
EQUAL EFFLUX OF K AND INFLUX OF Na
Peak of action fast potential and magnitude
+30
+120
30–90=120
Depolarziationin fast fibers?
When excitaioon potential reach the fiber it leads to inward of Na by na voltage gated channels abd and with change of potential -90’-70’-65 more oepining of sodiium channels and overshot of the potential by oeping m gates till reach the peak in one millisecond and then h gate closed ..repoenes in mid repolariTion
Explain repolarIzation of fast f
TRIPHASIC
Phase1 is decersing of the potenital; dfue to closure of the h gate of the na channels
and out ward of the K
Phase2 : is the platea stable potential~0 for 200-300 millisecond and this is due to
opeining of T long lasting Ca channnels that neutrrailiz the outward of the K efflux
phase 3 : is the phase or rapid reploarization due to outward of k rapid and enormiysly more than ca influx
=Na-K pump play a vital role in kicking out Na that had enterd durin dep and welcome K That escaped duriung replolarization
=Na-K pump play a vital role in repolarization ?
kicking out Na that had enterd durin dep and welcome K That escaped duriung replolarization
Diastolc deolarization
Also called preotential
pacemaker ptientail;
this is due to imbalane between entery of na and ca and exiting of K
SAN is the most self excitable tissue why?
Due to preptenital is low -50mv slow slope near to the thresoled -45 mv
The unstrable potential in SAN due to >?
Accumulation of positive charges in fiber during repoloariztion
this is due to influx of Na during late part of repolariztion
and enerry of ca throug tranisnt tyupe ca channels
dedcline of K efflux and these leads to pacemaker potential and
high phase 4 slope reaching thresold easily
Deplolariztiopn of slow fibers?
precede by preotential
slow 100 millisecond
by L type Ca channels
Refractoriness
عدم قابلية العضلة علي الاستجابة لمؤثر جديد لان السالبية داخلها مش عالية كفاية
Absliute referaztory peroid
الفترة مفيس استجابة لأي مؤثر مهما كانت قوته بسبب غلق بوابات الصويوم
أطول من فترة العصلات الملساء بسبب البلاتو
أهمية
ARP?
والله هي مهمة جدا عشان ميحصلش انقباضات متتابعة للعصلة القثلبية
Tetanization
وبالتالي يبقي في وقت القلب يملي في الدياستول ويفضي السيستول
RRP ?
الفترة دي ممكن يحصل استثارة لالياف العضلة ليبه
عشان بعض بوابات الاتش اتفتحت قدام الصوديوم فيعرف يعدي بس ..!
لازم
SupraThrsold stimuluis
ERP
Effective referactory period dueing which pr[agated action potential cannot be aroused but local one can !
ERP =ARP+ FIRST 0 MV OF THE RRP
FROM -50 TO -60 MV FINSHIES
Singgincane of ERP ?
1- ARP Prolongation
more time for filling avoding tetanization
2-Cardioverson 2000-3000 V
Supra normal stimulus
In late phase 3 and in phase 4 and in this phase purkinje fibers can respond to SubThreshold timulus
eliciting a Propagating AP
SLOW Fibers has a uineuq characterisitic of reploatriztion mention ?>
Post reploariztion refractoriness ?
RRP extends in phase 3 late and some of phase 4 even after all fibers are repolarized
imp ?
Perserving 180-200 bbpm as the highstef rate thaty can AVN cxonducrt even thers is an extra systole of million beats
Intirincsic factors affecting the contraction?
Preload
afterload
Frequey of timulaitom
contractility
Prload ?
the tension on the wall of the myocardium beofre contraction
=intial length
direct proprtion to EDV
Starling Law ?
Increase in lenth of muscler is acopmmaniued by increase in the force of contraction (within limnits )
why exceeding L max decreasec contractility ?
Because of pulling actin filament away from the myosin decresing the attachgments
LmaX ?
The maximum lenth of sacromere that casue maxiumum developed tension=2,2microns
After load ?
المقاومة اللبي بيقابلها البطين وهو بيضخ الدم
تعتمد علي aortic impedence
تزيد لو في ضغط زيادة او صمام ضيق او polycyhtemia
isometric increase tension without shortening
Isotoneic The tension is enough to carry the load
تأثير afterload الزيادة علي القلب
اول حاجة انه بيزود المقاومة اللي بيقابلها القلب
developed tension : increases
shotreining : decreases till there is now contraction no shortening only Isometric
Velocity of contarctio relations ?
Inversely with the afteroload
direct with preload
Vmax
The maximum velocity of contraction that occrs at 0 Load
so it is indepdnent on Preload
so it is index of contractility
increasd by + inotropes
Why increasing frequency of stimulation increases the contractility?
increasing action potentials increasing enetery of ca from ecf increasing store in Sarcoploaxic reticllum increasing release of Ca from Sarcoplasmic reticuclum during contrraction increasing contractility
Why Contraticilit lof Left vent decreas by stimulation of vagus althoug it is not supllying it?
عشان العصب الحائر بيثبط العقدة الجيب اذينية و يقلل الضربات القلبية
وده يقلل الانقباضية عشان عكس مووضوع الكالسيوم اللي شرحناه
Stair case phenomenon?
Treppe phenoenon or Bodwitch phenomenon ?
step wise incresing in fore of contraction due to
repeated rapid stimulation
مش بيدي فرصة للكالسيوم في الساركوبلازم انه يدخل الشبكة الساركوبلازمية
Stair case phenomenon?
Treppe phenoenon or Bodwitch phenomenon ?
step wise incresing in fore of contraction due to
repeated rapid stimulation
مش بيدي فرصة للكالسيوم في الساركوبلازم انه يدخل الشبكة الساركوبلازمية
Contractility inotrope state?
قدرة العضلة انها تولد قوة انقباض عند طول معين
physiological mechanisms that can modify the contraction force?
1-preload
2-Contractility
علام تعتمد اساسا قوة الانقباض
علي الكالسيوم كل العوامل اللي بتزود الكالسيوم جوا الخلية بتزود الانقباض والعكس ياعمر
Extirinsic factors affecting contractility?
Nervous
Neurohormonal
ECF IONS
DRUG
Sympathatic stimulation and contraction >?
بيزود الكالسوم جوا الخلية بطريقيتن؟
اولا يفتح SLOW CA CHANNELS L -type
ثانيا أنه بيزود عدد جهود الحركة اللي بتوصل للالياف العضلية
نتيجة الاقنين اللي فوق ؟
بيزود كمية الكالسيوم المخزنة في الشبكة الساركوبلازمية
طبعا كمان عشان بيحفز تسريع الراحة عشان
ca atpase pump stimlulated by sumpathatic increases ca stores in Sacroplasmi reticulum
الباراسمبثاوي هو هدام عمل السمبثاوي عكسه بالظبط في الثلاث أشياء دول
Hyper calacemia and heart?
Hyper kalemia and Heart
+ inotropic and can stop heart during ( Systole) if infused rapidly
- inotrope and can stope heart during (Diastole )
Drugs and heart contractility?
Ca entery blockers decreasing contractility
Digitalis spoil Na/K Pump so Na/Ca exchanger work Ca enters + inotrope
used in Heart failure
Contractility increased by?
Preload and intial lengnth ?
Ca entery
Auto-rhythmicity?
قدرة القلب علي توليد ضرباته المتكررة المنتظمة بدون تحفيز خارجي
charavteristics of san AP?
Slope near thresold
low amplitude
repolarization is fast
high repetitive discharge
Sympathatic stimulation and AP of SAN?
Incresing Na inward and csauing increased diastole deoplariztion and slope near thresold
Increasing Ca influx due to increased cAMP L-Ca cahnnels rapid upstroke as phase 0
Decerasing K efflux increasing the speed of Phase 0 and increasing disaolic deplariztaion
Vagal stimulation عكسه بالظبط
symp and para symp from cardiac pleuxs affect?
COMMON : SAN AVN CORONARIES
Symp only : muscle fibers of atria and venrticles
Sympathatic arise from ?
Cevial and upper thoracic ganglia 3rd and 4th
conduction of SAN
0,05 m/sec
atria conduction
0,1 second
by intetarial pathways
and slow conductig atrial fibers
to AVN
AVN COMPNENTS
A-N slowest maximal delay
N slowest conduction
N-H slow respone TTX NO EFFECT1
AVN characteristics?
AVC Delay between atria and ventricles 100-150 msecond
AVN Block refeactriness - 180-200BPM
Decresae retorgrade conduction prevention of ventricular ectopic vocus from affecting SAN
MAXIMUM CONDUCTION VELOCITY IN ? = ?
Purkinje fibers
4-5 m/second
CICR amount depends on ?
Amount of ecf calcium tiggering the release
amouint of calcium stored in SR
Ca secret?
Ca binds troponin casuing movment of tropomyosin away from the actin binding sites
Not all Tropinin ca site are satured so increasing Ca increase satureation and Acting binding sites availability and then contraciontws
ca affect the ?
FORCE
DURATION Of contraction
increased reate of realasxation by why ?
sympathatic why cpmenstion of short dureation of diastole by more frequent diastoles
sympatahtic and Relaxation of heart muscle?
induce cAMP and increasing the Ca ATPase ability so decersing Ca in sarcoplasm
Diastolic dysfunction occur in ischemia ?
no atp no relaxation no ca atpase
مفيش داياستول يظل في حالة انقباض غير قادر علي الانبساط
Contraction reach its peak at ?
Last 1/3 of the plateua
