Cardiovascular System

Blood flow and blood pressure are monitored and ultimately controlled by the brain. Peripheral signals are fed to the brain on a beat to beat basis, so that alterations in blood flow can occur to meet the changing metabolic demands of the body’s tissues.

Blood flow in part, depends on maintaining an appropriate BP. Three main factors influencing BP are:

1. Cardiac Output2. Peripheral Resistance3. Blood Volume

Remember Blood Flow = Pressure Resistance

By rearranging so Pressure is isolated, this becomes

Blood Pressure = Blood Flow X Resistance OR = CO X Peripheral Resistance

Cardiovascular System

Neural Control of Peripheral Resistance aims to:

1. Alter blood distribution in response to specific demands.2. Maintain appropriate MAP by changing vessel diameter.

Neural Control of the cardiovascular system originates in the Cardiac Centresfound in the Medulla.

Cardio -Acceleratory Centre sends Sympathetic Neurones down the spine to between T1 and T5, where they exit to the periphery.

Cardio - Inhibitory Centre originates with the Vagus Nucleus in the medulla and this Parasympathetic Nerve leaves the cranium as the Vagus (X) Nerve.

Vasomotor Centre - is a cluster of sympathetic fibres in the Medulla.- transmits impulses via sympathetic vasomotor fibres from T1 to L2 to blood vessels (arterioles)

Vasoconstriction is caused by increased frequency of impulses (Noradrenaline)Vasodilation is caused by decreased frequency of impulses.

Cardiovascular System

Brainstem contains:

PonsMedulla

In the Medulla are the:

Cardiac Acceleratory CentreCardiac Inhibitory CentreVasomotor Centre

Arterial Blood Pressure Regulationf Arterial Blood Pressure Regulation

Arterial blood pressure is regulated by several interrelated systems with specific functions

EXAMPLE: Hemorrhage

Survival is the first aim of the system. Return ABP immediately to a high enough level (nervous control)

Second, is to return blood volume eventually to is normal level (renal control)

Rapid Control

Baroreceptor

CNS ischemic mechanism

ChemoreceptorsCombine to cause venoconstriction, increasing venous return, increase heart rate and contractility, arteriolar constriction

Intermediate Control Long-Term Control (Renal-body fluid pressure control mechanism -hours to days)

Aldosterone

RAS interaction with aldosterone

Short-Term Regulation ofBlood Pressure

• Baroreceptor reflexes– Change peripheral resistance, heart rate, and stroke

volume in response to changes in blood pressure

• Chemoreceptor reflexes– Sensory receptors sensitive to oxygen, carbon

dioxide, and pH levels of blood

• Central nervous system ischemic response– Results from high carbon dioxide or low pH levels in

medulla and increases peripheral resistance

Local mechanisms affect MAP:

Baroreceptor Reflex Control

The Baroreceptor Reflex

Once signals have entered the medulla secondary signals inhibit the vasoconstrictor center and excite the vagal center. This results in vasodilation of the veins and arterioles throughout the systemic circulation and decreased heart rate and contractility.

Therefore, stimulation of the baroreceptor reflex reduces blood pressure through a decrease in peripheral resistance and a decrease in cardiac output. Low pressure has the opposite effect

Typical Carotid Sinus Reflex on Arterial Pressure Caused by Clamping Both Common Carotids

The Baroreceptor Reflex (ctd.)

Function during changes in body posture

When going from lying down to standing up there is a decrease in stretch of the baroreceptors which respond immediately to increase pressure by removal of

inhibition on the vasoconstrictor center.

Buffering daily variationsin blood pressure BP in a normal dog

BP changes in the same dog several weeks after baroreceptordenervation

Cardiovascular System

Baroreceptors are found in

• Carotid Sinuses (blood going to brain) and• Aortic Arch (systemic blood going to body)

As MAP increases this stretches the receptors and they send a fast train of impulses to the Vasomotor Centre. This results in a decrease in the frequency of impulses from the Vasomotor Centre and arterioles dilate.Final result is vasodilation and decreases MAP.

At the same time impulses are also relayed to the Cardiac Centre where

CIC activity increases (stimulating the Vagus nerve) - decreases HR and SV.

CAC activity decreases (inhibiting Sympathetic nerves) - decreases CO.

Chemoreceptor Reflex Control

Cushing Reaction:

If cerebro-spinal fluid pressure exceeds arterial pressure, arterial blood flow to the brain stops, this then triggers increased blood flow and pressure until blood flow returns to normal.

Intermediate Mechanisms

• Fluid shift– Movement of fluid from interstitial spaces into

capillaries in response to decrease in blood pressure to maintain blood volume

• Stress-relaxation– Adjustment of blood vessel smooth muscle to

respond to change in blood volume

Long-Term Regulation of Blood Pressure

• The Renal-Body Fluid System for Control of Arterial Pressure

• Renin-angiotensin-aldosterone mechanism

• Vasopressin (ADH) mechanism

• Atrial natriuretic mechanism

Role of the Kidneys in Long-term Regulation of Arterial Pressure and Hypertension

The Renal-Body Fluid System for Control of Arterial PressureWhen the body contains too much extracellular fluid, the arterial pressure rises. This increase in pressure causes the kidneys to excrete the excess fluid, until pressure returns to normal (pressure diuresis).

Quantification of pressure diuresis using renal function curvesAs pressure increases urinary volume, there is an equal effect on the urinary output of salt (pressure natriuresis),

I.e. the relationship is similar for sodium excretion

Typical Renal Output Curve Measured in an Isolated Perfused Kidney

General control of MAP:

Renin-Angiotensin-AldosteroneMechanism

Vasopressin (ADH) Mechanism

Long Term MechanismsWhich Lower Blood Volume

• Atrial natriuretic factor– Hormone released from cardiac muscle cells when

atrial blood pressure increases, simulating an increase in urinary production, causing a decrease in blood volume and blood pressure

Comparison of Potency and Kinetics of Different Arterial Pressure Control Mechanisms at Different Time Intervals

After the Onset of a Disturbance to the Arterial Pressure