CONTIUNE REGULATION OF ABP Flashcards
why some people may go faintaing while shaving ?
That is because carotid sinus syndrome!
the carotid sinus is hyper senstive to any pressure
and this leads to inhibitoin of VMC stimulation OF sympathatic vasodilator system lower BP – FAINTING BECAUSE OF BRAIN ISCHEMIA !
Describe the Cadiopulmonary high pressure type A baroreceptor
it is stimulated as resonse to -atrial systole -ventricular systole -pulmonary hypertension and affects cic and vmc like baroreceptors -Reflex VD -bradycardia -decreased contractility
What is Bainbridge reflex ?
it is a reflex out of low pressure atrial type B baroreceptor causing reflex tachycardia
may be due to direct stimulation of SAN
LOW PRESSURE TYPE B ATRIAL AND PULMONARY BARORECEPTOR , what is their stimulus?
Increased blood volume venous returem
GR/ low pressure barorecptors type b act an intermediate term regulation of abp
that is because their reflex VD in response to the increase in blood volume and venous return and thus causing increasing the capillary filtration pressure
GR/low pressure receptors has a mixed type regulation ?
Long term regulation because of the VD of the afferent arterioles glomerular
intermediate term regulation because of VD of arterioles causing increased capillary filtartion rate
The attempts of low pressure type B baroreceptors in lowering blood volume ?
Bainbridge reflex casusing tachycardia by direct stimuation of SAN
Intemediate regulation by VD of vessels increasing blood capillary filtration to tissue
long term regulation causing VD of afferent glomerulat aretrioles
decrasing ADH كده يزود ادرار البول
Increaseing ANP يخرج الصوديوم لوحده؟. لا أبدا !
اشرح مختصرا عن المستقبلات الكيميائية الطرفية
Peripheral cheomreceptor
Carotid bodies and aortic bodies
the are stimulated by hypoxia hypercapnea and acidosis
when the MAP fall down below 80mm Hg it is stimulated in respone to hypoxia becasue of decrease of the physically dissolved o2 not chmically bounded
this leads to stimulation of of of ! Vasomotor center !
increasing VR HR TPR and adrenal gland sympathathic outflow causing incresing of the MAP
Peripheral chemoreceptores afferent and centres ?
afferent - buffer nerves
centres medulary cardiovascular centers
Illustrate Bezold-jarisch reflex .
it is reflex depending on the chemoreceptor found in the coronary vessels and stimulated by the pharamacological injection of some drugs like : veratidine and serotoinine and also
Mycardial ischemic heart the dead tissue secretes substances causing its stimulations
and thus causing —- severe hypotension and bradycardia
MAP decrasing to 50 or below refers to ?
brain enters a severe state of ischemia
CNS ischemic reflex describe ?
when map decrases to 50 or below this causes decrasring of blood flow tho the brain and especially the vmc
this cause hypoxia hypercapneia and acidosis and these factors are strong in stimulation VMC causing VC of blood vessels for 5-7 minutes incresaing ABP
Cushing reflex mean ?
this is a reflex to the increase in the Intra cranial pressure causing pressure on the vessels and decrasing blood flow to brain and vasomotor center casuing hypoxia hypercapnia and acidosis this leads to stimulation of the VMC and vc of blood vessels and increase ABP and bradycardia due to baroreceptor stimulation or cic stim
brain has no Vasoconstriction
no autononic supply to its vessel they are almost entirely controlled by local mechanisms
Short term regulation hormonal effect ?
Neurohormonal reg
أدبر الليل
AdPR
Adrenalmedullary hormones epinephrine and norepinephrine
Posteior putiutary – ADH Vasopressin
Renin Angiotensin system within 20 minutes
GR/ the COP decreases in norepinephrine release inspite of its cardiac acceleration activity ?
That is because the bradycardia resultus from stimulation of the baroreceptors because of the increase in the ABP because of its effect of vasoconstrivtion by the a receptors !
the brady cardia resulted has the upper hand over the cardiac acceleration by b1 receptors ! so COP DECRASES
GR/ SP and DP increases in case of norepinhorine release ?
this is because it action on the a1 receptor causing vc effect
Epinehrine role ?
AFFECT
a1 vasoconstrrction
b2222 Vasodilation 222overcoming the effect of the a1 vd of skeletal msucles and liver vessels decrasing the tpr and dp and increasing the pp
b111 on the heart + chrono and ino and dromo tropic this cause increase SV HR COP AND arterial blood pressure exceeding the slow stimulation of baroreceptor that cannot lower blood pressure because b1 has the upper hand
in normal dose b mask a
in high dose a mask b
the dose is detrminant of action of epinephrine ?
in normal dose b mask a
in high dose a mask b
despite the action of epinephrine on a1 receptor it causes decrese in DP ???
a1 vasoconstrrction
B22222222 Vasodilation overcoming the effect of the a1 vd of skeletal msucles and liver vessels decrasing the tpr and dp and increasing the pp
ADH HORMONE STIMULUS ?
1- changes in the osmolarity direct proprtional
2 decreased atrial volume causing decrased action of low pressure type b atrial receptor
mention actions of the ADH OR VASOPRESSIN
- Kidney Water retention at DCT and CT through V2 .
- bvs Vasoconstriction of blood pressure high dose V1 .
Site of release and site of formation of ADH ?
1- PSOTEIROR PITUITARY
2- HYPOTHALAMUS
Why renin is released in case of hyponatremia ?
that is because it turnis angiotensingogen from liver into ang 1 then converted into ang 2 that
1- induce release of ADH stimulating water perservastion
2- INCREASING Alodsterone responsible for salt and water retention pharma ?!
Sympathahtic and b1 receptors can raise VC HOW ?
Becuase it works on b1 on juxta glmerular appartus which will release renin converting angen to ang1 then it will be converted to ang 2 the most potenet vasoconstrictior in the body
Renin angiotensisn system decribe it and how many type of regulation it shares in ?
It depend on the angiotensiongen a2 glubulin released from the liver which will be activated by reinin release to ANG1
RENIN RELEASE DEPENDS ON :
1- LOW RENAL PERFUSION BECAUSE
A- RENAL ISCHEMIA B- DECREASE IN ARTERIAL BLOOD PRESSURE
2-HYPONATREMIA
SYMPATHATIC STIMUALTION WORKING ON THE B1 ON JGA
then ang1 will converted by the mean of ACE into ANG2
WHICH IS
- THE MOST POTENT VASOCONSTRICOR ON THE BODY
-INCREASING ALDOSTERONE TO SALT AND WATER RETENTION
-INCREASE ADH
-THIRST SENSASTION TO INCREASE BLOOD VOLUME THUS INCREASING BP
GREAT GREAT MY GREAT STAR !
INTERMEDIATE TERM REGULATION MECHANISM ?
- STRESS AND ANTI STRESS MECH
- CAPILLARY FLUID SHIFT
SHOW THE MECHANISM OF STRESS METHOD REGULATION ?
INCREASING THE ABP increaseing the vasucluar capacity by opening of the artriole veins and capillarires decresaing the bp
anti stress
لما يقل الضغط يقل فتح الاوعية الدموية وتقل السعة الوعائية بتاعتها وعلي كده يزيد ضغط الدم علي الجدران مسخرة ؟ مش مفهومة ولا ايه ؟
Show Capilllary fluid shift
s
simply it is when there is increase in abp increasing the filtration at the capillary and decreasing the reabsorption at the venous side and this will decresing the plasma volume and decresing the abp
وبكل بساطة لو قل الضعط الدموي هيقل الفلترة عند الشعيرات الدموية و هيزيد اعادة الامتصاص عند الجانب الوريدي وده بكل بساطة هيزود حجم البلازما مؤديا الي زيادة الضغط الدموي ؟!
GR/the long term regulation may depends on the kideny ?
لانه بزيادة ضغط الدم هيزداد الامداد الدموي للكلية وهيزداد الفلترة الكلوية وهيزداد اخراج الصوديوم وفي ظهره الماء مؤديا لنقص حجم البلازما ونقص الرجوع الوريدي ونقص المخرج القلبي ونقص الضغط الدموي
والعكس صحيح فلو كان الضغط قليل لقل الامداد الدموي للكلية و قل الفقلترة الكلوية وقلت اخراج الماء والصوديوم و يزداد حجم البلازما والرجوع الدموي واملخرج القلي و في الاخر زيادة الضغط الدموي يا عمر !
long term regulation may depends on hormones ? true or false why ?
yes can depend on slow reacting hormones like ?
1- the ADH
يقلل التبول ويزود حجم الدم يطلع عند انخقاط ضغط الدم
2-ANP بيطلع من الاذين يزود خروج الماء والصويدوم يعمل توسيع للاوعية يعمل مضاد للرنين وهو كمان بيقلل الضغط
3-CORTISOL ALODSTERONE ACTION ! يزود الضعط تركيز الماء والملح
4-ALODSTERNE تركيز الماء والملح يزود الضغط
5-RENIN ANGIOTENSIN SYSTEM !
في انخفاض ضغط الدم
Classify the excitatory and inhibitory factor on the VMC
A-Excitatory alram emotion musclar excercis mild moderate pain
B-inhibitory grief emotion severe pain
lung over inflation
muscular excercise has to ways to excite VMC
1- CEREBRAL CORTEX VIA HYPOTHALAMUS
2- AFFERENTS VIA RETICULAR FORMATION
Is there any direct stimulation for the VMC?
YES OF COURESE ESPECIALLY BY hypercapnia and hypoxia and acidosis
this lead to vc and inc in arterial blood pressure like in cushing reflex increasing ICP
which is stronger the diret or indirect stim of VMC
Direct stimulation is much more stronger than the indirect Stimulation
Baroreceptors work only in increasr BP ?
DEFINTELY FALSE !
ALL TIME
