Physiology of cardiovascular system

1. THE BLOOD VESSELS AND
BLOOD PRESSURE
Dr. Jarah Ibrahim

2. INTRODUCTION
• Blood is transported to all parts of the body through a system of
vessels that brings fresh supplies to cells and removes their
wastes
• All blood pumped by the right side of the heart passes through
the pulmonary circulation to the lungs for O2 pickup and CO2
removal.
• The blood pumped by the left side of the heart into the systemic
circulation is distributed to the systemic organs .

4. • The systemic and pulmonary circulations each consist of a
continuum of different blood vessel types that begins and ends with
the heart, as follows:
• Arteries which carry blood from the heart to the organs, branch into
a “tree” of progressively smaller vessels.
• When a small artery reaches the organ it is supplying, it branches
into numerous arteriol
• Arterioles branch further within the organs into capillaries across
which all exchanges are made with surrounding cells.

5. • Capillary exchange is the entire purpose of the circulatory system
• Capillaries rejoin to form small venules, which further merge to
form small veins that leave the organs.
• The small veins progressively unite to form larger veins that
eventually empty into the heart

7. ARTERIES
1- Serve as rapid passage ways for blood from the heart to the organs
2- Act as a pressure reservoir to provide the driving force for blood
when the heart is relaxing.
• The heart alternately contracts to pump blood into the arteries and
then relaxes to refill from the veins.
• As the heart pumps blood into the arteries during ventricular
systole, a greater volume of blood enters the arteries from the heart
than leaves them to flow into smaller vessels downstream

8. • The highly elastic arteries expand to temporarily hold this excess
volume of ejected blood.
• When the heart relaxes and temporarily stops pumping blood into
the arteries, the stretched arterial walls passively recoil, like an
inflated balloon that is released.
• This recoil pushes the excess blood contained in the arteries into
the vessels downstream, ensuring continued blood flow to the
organs when the heart is relaxing and not pumping blood into the
system

9. ARTERIOLES
• Arterioles are the major resistance vessels in the vascular tree
because their radius is small enough to offer considerable
resistance to flow.
• The radius (and, accordingly, the resistances) of arterioles
supplying individual organs can be adjusted independently to :
(1) variably distribute the cardiac output among the systemic
organs, depending on the body’s momentary needs
(2) help regulate arterial blood pressure

10. CAPILLARIES,
• the sites for exchange of materials between blood and tissue cells
• branch extensively to bring blood within the reach of every cell
• Materials are exchanged across capillary walls mainly by diffusion

11. VEINS
• Their walls are relatively thin and easily distended. Therefore
they can accommodate large volume of blood (capacitance
vessels)

12. BLOOD PRESSURE
• It is the force exerted by the blood against a vessel wall.
Systolic pressure
• The maximum pressure in a vessel during systole of the heart.
• Normal value is less than 120 mmHg in adults.
• Systolic blood pressure of 140 mmHg or more is hypertension.

13. Diastolic pressure
• The minimum pressure in a vessel during diastole of the heart.
• Normal value is less than 80 mmHg in adults.
• Diastolic blood pressure of 90 mmHg or more is hypertension.
Pulse pressure
• The difference between the systolic and the diastolic pressures.
• Normal pulse pressure is less than 60 mmHg.

14. Mean arterial pressure
• The mean pressure during the cardiac cycle.
• It is calculated as follows:
• The mean arterial pressure= The diastolic + 1/3 pulse pressure

15. CONTROL OF THE ARTERIAL BLOOD PRESSURE
• Blood pressure = Cardiac output × Peripheral resistance.
• The blood pressure is controlled by controlling the cardiac output
and the peripheral resistance.
• The cardiac output is controlled by controlling both the heart rate
and the stroke volume
• It determines the systolic pressure (i.e. the increase in COP increases
systolic pressure).

16. • The peripheral resistance is determined by blood viscosity, length
of arteries and radius of arteries as follows:
PR = 8VL/π 𝒓𝟒
• Where :
oV is the blood viscosity
oL is the length of arteries
o r is the radius of blood vessels.
• The peripheral resistance determines the diastolic blood pressure.

17. • Viscosity of the blood depends on:
o The packed cell volume (PCV)
o Plasma proteins especially globulins and fibrinogen
o Body temperature (constant in the physiological conditions)
• Radius of blood vessels is the most important factor in
determining the peripheral resistance
• It is inversely proportional with the peripheral resistance

18. The mechanisms that control the blood pressure
• Mean arterial pressure is constantly monitored by baroreceptors
(pressure sensors) within the circulatory system.
• When deviations from normal are detected, multiple reflex responses
are initiated to return mean arterial pressure to its normal value.
1- Short term mechanisms (act in seconds)
• Cause alterations in cardiac output and total peripheral resistance,
mediated by means of autonomic nervous system influences on the
heart, veins, and arterioles

19. 2- Long-term mechanisms (requiring minutes to days)
• involves adjusting total blood volume by restoring normal salt
and water balance through mechanisms that regulate urine
output and thirst
• The size of the total blood volume, in turn, has a profound effect
on cardiac output and mean arterial pressure
3- Local regulation of blood pressure

20. SHORT TERM MECHANISMS
• Any change in mean arterial pressure triggers an autonomically
mediated baroreceptor reflex that influences the heart and blood
vessels to adjust cardiac output and total peripheral resistance in an
attempt to restore blood pressure to normal.
• The most important receptors involved in the moment-to-moment
regulation of blood pressure, the carotid sinus and aortic arch
baroreceptors
• They are mechanoreceptors stimulated by stretch caused by high
blood pressure.

21. • They constantly provide information about mean arterial
pressure (in form of action potentials).
• They send impulses through the vagus & glossopharyngeal
nerves to cardiovascular control centers in medulla oblongata.
• The cardiovascular control center alters the ratio between
sympathetic and parasympathetic activity to the effector organ
• The efferent pathway is the autonomic nervous system.

22. • If the arterial pressure increase, the carotid sinus and aortic arch
baroreceptors increase the rate of firing.
• The cardiovascular control center responds by decreasing
sympathetic and increasing parasympathetic activity to the
cardiovascular system.
• These decrease heart rate, decrease stroke volume, and produce
arteriolar and venous vasodilation, which in turn lead to a
decrease in cardiac output and a decrease in total peripheral
resistance, with a subsequent fall in blood pressure back toward
normal
• The opposite occurs when there is reduction in B.P

23. • Chemoreceptors
- The peripheral chemoreceptors are found in the carotid body in
carotid bifurcation and aortic body in aortic arch.
- They are stimulated by hypoxia (low O2 in tissues), hypercapnia (high
CO2) and acidosis (high H + ).
These stimuli are associated with hypotension because of the low
tissue perfusion.
- They send excitatory impulses through the vagus and
glossopharyngeal nerves to the respiratory center to increase
respiration.

24. - The impulses also stimulate the vasomotor and the cardiac
centers (due to radiation of impulses in the medulla).
- This increases the blood pressure by increasing sympathetic
discharge from these centers to the heart and blood vessels
causing increased heart rate, higher stroke volume and
vasoconstriction.

25. LONG TERM MECHANISMS
Renin-Angiotensin Aldosterone system
• Renin enzyme is released by the kidney lead to formation of Angiotensin
II through many steps cascade.
• It is stimulated by renal ischemia, hyponatremia & sympathetic
stimulation (all these are associated with hypotension).
• Angiotensin II rapidly elevates the blood pressure by causing
vasoconstriction.
• In addition it has other long term effects include stimulation of
aldosterone, stimulation of ADH and stimulation of the thirst center..

26. • Aldosterone Acts on the distal convoluted tubules and collecting
ducts in kidney causing reabsorption of sodium and secretion of
potassium. Water follows sodium to the intravascular space.
• This increases blood volume & therefore the blood pressure

27. Hormonal vasoconstriction
1- anti diuretic hormone (ADH)
• Release from the posterior pituitary gland is stimulated by hypotension.
• It elevate blood pressure by:
- acts on receptors in the blood vessels causing vasoconstriction.
- Acts on receptors in the kidney causing reabsorption of water to the
intravascular space (increases blood volume )

28. 2- Catecholamines
• Adrenaline and noradrenaline are released in response to
hypotension (which is a form of stress).
• They act on receptors in blood vessels causing vasoconstriction.
This elevates the blood pressure.

29. LOCAL REGULATION
• Aim of Local regulation of blood pressure:
o To maintain adequate perfusion and therefore adequate supply of O2
and nutrients to the tissues.
o To adjust the perfusion to tissues according to their needs; which vary
from time to time according to variation in activities.
• Local regulation occurs by the following:
1- Autoregulation:
• It is the intrinsic capacity of tissues to regulate their own blood flow.
• Found in many tissues like skeletal muscles, cardiac muscle, and brain

30. 2- Substances secreted by the endothelium:
A- Prostacyclin: -
• Cause vasodilatation & inhibits platelet aggregation
B- Nitric oxide (NO): -
• It is the endothelial derived relaxation factor (EDRF).
• It is an important vasodilator in many organs; however, it has
many other functions in other organs

31. HEART FAILURE
• It is failure of the heart to meet the metabolic demands of tissues.
• Causes include:
Severe anemia, severe hypertension, arrhythmia, myocardial infarction,
valvular disease and thyrotoxicosis.
• Heart failure can be classified as:
o Left sided HF (LHF): failure of the left side of the heart
o Right sided HF (RHF): failure of the right side of the heart
o Congestive HF (CHF): failure of the left & right sides of the heart

32. PHYSIOLOGICAL MECHANISMS IN HEART
FAILURE
• All the mechanisms in heart failure are stimulated by
hypotension and tissue hypoxia.
• These include activation of the renin-angiotensin-aldosteone
system because of the low blood supply to the kidney.
• This results in retention of sodium and water and therefore
contributes to edema formation.

33. • When the left ventricle fails to eject blood (LHF), blood
accumulates in the lung causing pulmonary edema
• When the right ventricle fails (RHF), blood accumulates in the
venous side causing raised JVP, hepatomegaly, ascites and lower
limb edema.
• When the two ventricles fail (CHF), blood accumulates in the lung
and the venous side; therefore, all symptoms and signs of LHF
and RHF are found in CHF

34. SHOCK
• When blood pressure falls so low that adequate blood flow to the
tissues can no longer be maintained, the condition known as shock
occurs
• Types
1. Hypovolemic shock (due to decreased blood volume)
2. Distributive or low resistance shock (due to vasodilatation)
3. Cardiogenic shock (due to cardiac lesion causing low COP)
4. Obstructive shock (due to obstruction of blood flow in the chest)

35. • Symptoms
• o Irritability (due to low blood supply to the brain)
• o Thirst (due to hypovolemia)
• o Palpitation (due to increased contractility of the heart for
compensation)

36. • Signs (Not in all types of shock)
o Pallor and cold clammy skin (due to vasoconstriction)
o Sweating (due to sympathetic activation)
o Tachycardia (due to sympathetic activation)
o Hypotension (due to hypovolemia, vasodilatation, cardiac lesion …)
o Low urine output (due to low renal blood flow and high release of
ADH)
o Hyperventilation (due to chemoreceptor stimulation by hypoxia or
acidosis)

37. Complications of shock
• Failure to treat shock leads to refractory or irreversible state.
Here a positive feedback mechanism is initiated (low COP= low
blood pressure= low venous return= low COP= low blood
pressure and so on) which leads eventually to death