This document summarizes cardiovascular system regulation presented by Namungu Rickens. It introduces basic principles like blood flow regulation via pressure differences and vascular resistance. The Frank-Starling relationship and cardiovascular control loop are described. Local short-term regulation occurs via endothelial secretions and long-term via angiogenesis. Cardiac reflexes like the baroreceptor reflex and Bezold-Jarisch reflex maintain homeostasis through neural and humoral responses. The document provides an overview of cardiovascular system regulation at both the local and systemic levels.

1. CVS REGULATION
PART 1...
PRESENTER; Namungu Rickens
MMED 1, Thoracic & Cardiovascular surgery(UON)
FACILITATOR: DR MUJAHID F. DIN.
Senior Lecturer, Dept of Medical Physiology & Consultant ENT
Surgeon, AKUHN

2. TO DELIVER AND REMOVE METABOLIC
SUBSTRATES AND WASTES FROM; POINTS
OF ENTRY; TO POINTS OF USE; TO POINTS
OF EXCRETION/ELIMINATION,
RESPECTIVELY.
Why do we need a CVS…

3. FOR HOMEOSTASIS .
TO SUSTAIN METABOLIC TISSUE REQUIREMENTS -
OXYGEN AND NUTRIENTS, AS PER DEMAND AND
WASTE ELIMINATION OF CO2 & OTHER
PRODUCTS OF METABOLISM.
WHY REGULATE?

4. OBJECTIVES
1) Introduction; Basic principles
- Blood flow
- Frank starling relationships
- CVS control loop
1) Agents of CVS regulation;
- Local control of CVS
- Cardiac reflexes.

5. INTRODUCTION; Basic Principles.
Blood flow; quantity of blood passing a given
part of circulation in a given period of time.
 It is controlled according to tissue needs.
 it is determined by;
-pressure difference btn two ends (dP)
-vascular resistance(R)

6. BASIC PRINCIPLES CONT..
• Therefore, to achieve control of blood
flow/perfusion, control of vascular resistance
and pressure is required.
• Pressure is centrally controlled, while Resistance
is controlled both locally and centrally
• (OHMs law anologous)- Flow is directly
proportional to pressure gradient, and inversely
proportional to Resistance.
• F= dP/R

7. Frank Starling Relationship.
• Gives us the length - tension relationship in the
cardiac muscle.
• ‘Energy of contraction is proportional to the
initial length of the cardiac muscle fibre’
• Increases in end-diastolic volume cause an
increase in ventricular fiber length, which
produces an increase in developed tension.
• Explanation. actin/myosin overlap.

8. CONTROL LOOP OF THE CVS.
Negative feedback control
INFLUENCES INFLUENCES
Forcing functions Controlled variable(BP)
CONTROLLER CONTROLLED
VMC PROCESS-CVS
SENSORS

9. AGENTS OF CVS CONTROL

10. AGENTS OF REGULATION
Local CVS
regulation
short term
long term
Systemic BP
Control
Neural control
Humoral control
Renal control

11. LOCAL CONTROL
SHORT TERM-
Endothelial secretions; Endothelins, NO,
prostaglandin and thromboxane.
 Hyperemia; active/reactive, eg coronary circulation
Autoregulation; capacity of vessels to regulate their
own blood flow. This is thought to occur via;
- Myogenic theory, Metabolite theory,Tissue
pressure hypothesis, Tubuloglomerular Feedback
hypothesis(TGF)

12. LOCAL CONTROL Cont.
1. MYOGENIC THEORY
• Refers to intrinsic contractile response of vascular
smooth muscle to stretch .
• The Stretch induces vascular depolarization, leads to
rapid calcium entry from ECF, causing them to contract.
• This is necessary because of the Law of Laplace-
‘tension in the wall of a cylinder(T), is equal to product of
trasmural Pressure(P), and Radius, divided by wall
thickness. T= PR/W, P=T/R
-therefore to maintain a given wall tension as blood
pressure rises, it requires decrease in the radius.

13. LOCAL CONTROL Cont.
2. METABOLITE THEORY
Blood flow and tissue metabolism are tightly coupled in that
any reduction in arterial inflow causes a build up of
vasodilator metabolites in the tissue.
This is either due to decreased washout of vasodilator
metabolites eg CO2, or increase in their production due to
hypoxia.

14. LOCAL CONTROL Cont..
3. TISSUE PRESSURE HYPOTHESIS
An increase in perfusion pressure results in fluid
transfer to extravascular compartment. This results
in compression of capillaries and arterioles causing a
reduction in blood flow.

15. LOCAL CONTROL Cont..
4. TUBULOGLOMERULAR FEEBACK HYPOTHESIS
An increase in arterial presure leads to an increase in
glomerular filtration, and further an increase in solute
and electrolyte concentration at the Macula Densa.
This acts as a stimuli to macula densa, via an unclear
mechanism, to cause vasoconstriction of afferent
arteriole smooth muscles.

16. LOCAL CONTROL Cont..
ENDOTHELIAL SECRETIONS
1. NO (Nitric oxide); vasodilator.
-synthesized from arginine by NO synthase.
-produced by endothelium, diffuses to vascular smooth
muscle, activates soluble guanyl cyclase resulting in
conversion of c-GTP to cGMP, and activation of cGMP
dependent protein kinase (PKG), which has several actions
that cause the blood vessels to relax.

17. LOCAL CONTROL Cont.
2. Endothelins( endothelin 1)
-Endothelin 1, acts via G-protein coupled ETA
receptors to mediate vasoconstriction.
- Plays a role in closure of Ductus Arteriosus at birth.
3. Prostacyclin
- Promotes vasodilatation and inhibits platelet
aggregation.

18. LOCAL CONTROL- CONT.
LONG TERM CVS CONTROL
- Days to months.
- As a result of change in pattern and amount of vasculature.
-via;
1. Angiogenesis- increase in vascularity.
-triggers; hypoxia, growth factors(VEGF,
FGF,PDGF,Angiogenin).
-inhibitors- steroids, angiostatin, endostatin.

19. Long term , local control cont..
2. Development of collateral circulation
3. Vascular remodelling;
Eutropic inward remodelling,
Hypertrophic remodelling,
Outward remodelling,
Outward hypertrophic remodelling

20. CARDIAC REFLEXES
These are fast acting reflex loops between the heart
and the CNS. They contribute to regulation of
cardiac function, and homeostasis.

21. CARDIAC REFLEXES.
Baroreceptor Reflex/Valsalva Maneuver
Chemoreceptor Reflex
BainBridge Reflex
Brain ischemic response/Cushing Reflex
Occulocardiac Reflex
Bezold-Jarisch Reflex
Abdominal compression reflex

22. Cardiac Reflexes cont..
Cardiac/extra-cardiac receptor
Afferent nerve
Sympathetic & Para sympathetic Input processed
in the CNS
Efferent nerve
Heart /Systemic circulation
Particular Reaction

23. Baroreceptor Reflex
- Initiated by stretch receptors, baroreceptors,
present in Carotid sinus, Aortic arch, Walls of RA,
at the entrance of SVC and IVC, Walls of LA at the
entrance of pulmonary vein.
- They are stimulated by distension of the structure
in which they are located.
-Conversely, low pressure has opposite effects,
reflexly causing the pressure to rise back toward
normal.

24. Baroreceptor Reflex cont
Triggering factor( BP )
Stimulates baro receptors in carotid sinus/aortic arch
Afferent nerves, through CN ix,& x
Processing in medullary VMC
Increases parasympathetic tone, inhibition of sympathetic
tone
Decreases HR, Stroke volume and vasodilation

25. Valsalva Maneuvre, example of Baroreceptor reflex
Forced expiration against a closed glottis
increase in Intrathoracic pressure (increase BP initially)
compression of veins( increase CVP)
Decreases VR, CO
BP decrease
Inhibit baroreceptors
Sympathetic stimulation
Increase HR, myocardial contractility

26. V. Maneuvre cont..
When glottis opens
Venous Return ↑
Causes heart to respond by vigorous contraction & ↑BP
Stimulate Barorecptors
Stimulation of para sympathetic system
Decrease in HR/bp To normal

27. Chemoreceptor Reflex
-Mediated by two types chemoreceptors
Peripheral ; Carotid bodies /Aortic bodies
Central chemoreceptors; Medulla-respond to H+
-Chemoreceptors are sensitive to the changes in
blood chemistry. Main function is to keep the
alveolar pCO2 at a normal level of 40mmHg and
also maintains arterial pO2,pCO2 and pH.
- Afferent- Sinus nerve of Hering (branch of 9th
cranial nerve) and vagus nerve

28. Chemoreceptor Reflex cont..
-At an arterial pO2 <50mmHg or in condition of
acidosis, the chemoreceptors send their impulses
to chemosensitive area of medulla.
-This area responds by stimulating the respiratory
centers and there by increasing the ventilatory
drive.
- Hypoxia also produces hyperpnea and increased
catecholamine secretion from the adrenal medulla,
both of which produce tachycardia and an
increase in cardiac output.

29. ATRIAL AND PA REFLEXES.
a) Bainbridge Reflex
-Elicited by stretch receptors in the RA wall, and cavo atrial junction.
Increase in Right sided filling pressure
Stimulates stretch receptor (also has Direct action on SAN)
Vagal myelinated afferent fibres
Cardiovascular center of medulla
Inhibit parasympathetic activity
Increase HR
-This reflex helps prevent damming of blood in the veins, atria, and pulmonary
circulation.

30. b) Volume Reflex.
-Stretch of the atria also causes;
- significant reflex dilation of the afferent arterioles in
the kidneys, resulting in increased filtration.
-Signals are also transmitted simultaneously from the
atria to the hypothalamus to decrease secretion of
ADH, resulting in less reabsoption of water from
tubules.
-The stretch also elicits a hormonal effect on the
kidneys—release of ANP—that adds still further to
the excretion of fluid in the urine ,reducing BP
towards normal.

31. CNS ISCHEMIC RESPONSE
-Its an emergency pressure control system that acts
rapidly and powerfully to prevent further decrease in
arterial pressure whenever blood flow to the brain
decreases dangerously close to the lethal level. -Aka,
last ditch stand.
-Due to fall in blood flow ; CO2 , lactic acid accumulates,
VMC is excited.
-Results in massive sympathetic outflow- vasoconstriction
and rise in BP
- Cushing reaction is a special kind of CNS ischemic
response, due to increase in ICP.

32. CARDIAC REFLEXES.
 Baroreceptor Reflex
 Chemoreceptor Reflex
 BainBridge Reflex
 Bezold-Jarisch Reflex
 Valsalva Maneuver
 Cushing Reflex
Occulocardiac Reflex
 Abdominal compression reflex

33. REFERENCES
1)Essentials of pathophysiology concepts of altered health states,
4th edition.
2)Guyton and Hall textbook of physiology, 13th edition
3)Ganongs review of medical physiology, 24th edition.
4)AHA Journal by ‘autoregulation’, by Paul C Johnson
5)Constanzo BRS physiology 5th edition.

34. Thanks.
PART 2...
Systemic bp control......

35. Bezold- Jarisch Reflex.
- It responds to ventricular stimuli ,e.g Coronary ischemia (MI),
Bradykinin, PGI2, Arachidonic acid, Ventricular distension,
Thrombolysis and Revascularization.
- Sensed by the chemoreceptors and mechanoreceptors within the
left ventricular wall by inducing the triad of;
– Hypotension
– Bradycardia
– Coronary artery dilatation
- The activated receptors communicate along unmyelinated vagal
afferent type C fibers. Inhibit medullary vasomotor centre,
increasing the parasympathetic tone

36. Bezold- Jarisch reflex cont..
- Because it invokes bradycardia, the Bezold jarisch
reflex is thought of as a cardioprotective Reflex.
-The reflex has been implicated in physiologic
response to a range of cardiovascular conditions
such as Myocardial ischemia, thrombolysis,or
revascularisation and syncope.
-Bezold Jarisch reflex may be less pronounced in
patients with cardiac hypertrophy or atrial
fibrillation.