Sie sind auf Seite 1von 56

Blood pressure

Physics and physiology


Goal of the
Cardiovascular System:
deliver blood to all
parts of the body
•Does so by using
different types of
tubing, attached to a
pulsatile pump
•Elastic
arteries
•Muscular
arteries
•Arterioles
•Capillaries
•Venuoles
•Veins
•Distribution system
broken up into areas
called vascular beds
•Skin
Why does blood flow through this closed circuit?

•Blood flows down a pressure gradient


•The absolute value of the pressure is not important to flow, but the
difference in pressure (DP or gradient) is important to determining flow.

The resulting pressure is called the driving pressure in the vascular system
Structure of vasculature changes in response to different needs
Vascular system possesses different mechanisms for promoting continuous flow
of blood to the capillaries:
Elastic recoil smooth m. regulation of diameter sphincters
valves
Muscular arteries
Systole and Diastole

The arteries fluctuate between a state of


systole and diastole



In systole, the pressure in the arteries
increases as the heart pumps blood into the
arterial system
As the pressure increases, the elastic walls of

the arteries stretch



This can be felt as a pulse in certain arteries

Systole and Diastole


In diastole, the recoil of the elastic arteries
forces blood out of the arterial system into the
capillaries

The pressure in the arteries falls as blood
leaves the system

Minimum diastolic pressure is typically 70-80
mmHg

Maximum systolic pressure is typically 110-120
mmHg

Blood pressure (BP)

A constant flow of blood is necessary to


transport oxygen to the cells of the body


The arteries maintain an average blood

pressure of around 90 mmHg



This helps push the blood from the arteries
into the capillaries
In the capillaries, oxygen transfers from the

blood to the cells



Put another way
Think of the arterial system as a long balloon that you

are trying to blow up. Unfortunately the balloon has an


hole in the end…


However, as long as the puff going in is equal to the air
leaking out, the balloon remains inflated (BP is
maintained)
Resistance = tendency of the vascular system to oppose flow
•Influenced by: length of the tube (L), radius of the tube (r), and viscosity of
the blood (η )
Poiseuille’sLaw R = Lη /r
4

•In a normal human, length of the system is fixed, so blood viscosity and radius
of the blood vessels have the largest effects on resistance
P1 > P 2
P1 FLOW P2

mm Hg
P = FLOW x R

FLOW = P
R
P
R =
FLOW
L/min
or mm Hg
ml/sec ml/sec

Peripheral Resistance Units (PRU)


Determinants of Blood Pressure
Pressure drop is greatest at the level of the

arterioles.

Velocity of blood is slowest at the capillaries


Turbulence: The higher the velocity of blood


flow, the greater the likelihood of turbulence.


Arterial Elasticity (The Windkessel Effect):


Arterial Elasticity accounts for a smaller pulse


pressure.
Thus, atherosclerosis ------> Larger Pulse

PRELOAD: The diastolic filling pressure, or end-

diastolic volume.

AFTERLOAD: Ventricular systolic pressure, which is


equal to arterial systolic pressure under normal


circumstances.


LAPLACE'S LAW: The stress on the ventricular wall
is proportional to the Ventricular Pressure x
Ventricular Radius, where the size of the ventricle is
determined by stretching, i.e. by ventricular volume.


STARLING'S LAW OF THE HEART: Within limits,
increases in end-diastolic volume result in a
corresponding increase in stroke volume.
BLOOD PRESSURE AND THE
RESPIRATORY CYCLE


INSPIRATION: Systemic blood pressure goes down and
pulmonary blood pressure goes up.

o The Diaphragm moving down has two effects:

It increases the volume of thoracic airspace and so it
decreases intrathoracic pressure.

Also the abdominal space becomes smaller, so it increases
intra-abdominal pressure.

The combination of above two effects results in an increased
pressure gradient for venous return from the

IVC ------> increased venous return ------> More blood to
right atrium and more blood to pulmonary

circulation ------> less respective blood in left heart and less
CO.
BLOOD PRESSURE AND THE
RESPIRATORY CYCLE


Thus overall result is the following:

Lower systemic pressure.

Higher pulmonary pressure.

Larger Blood Volume in pulmonary circulation.

The change in MABP from inspiration normally does
not exceed 10 mm Hg.

EXPIRATION: Has the exact opposite effect.

o Pulmonary pressure decreases.

o Systemic pressure increases.
PRESSURES IN PERIPHERY -vs- AORTA

Mean Arterial Pressure is slightly higher in the


Aorta than in, for example, the radial artery.



But, Pulse Pressure is greater in the periphery,
i.e. the systolic is higher and the diastolic is
lower.
This effect in the periphery is due to

constructive interference of reflected waves.



COMPLIANCE: The degree to which a pressure
change leads to a corresponding change in volume

Compliance = ΔV /ΔP, or the slope of a


pressure-volume curve.

VENOUS COMPLIANCE is about twenty times


more than arterial compliance, therefore veins


can hold a larger volume of fluid at lower
pressure.
Arterial Compliance is about 2.5 mL / mm Hg

Venous Compliance is about 60 mL / mm Hg



VASCULAR COMPLIANCE

C =
V
Arteries P250 ml =2.5 ml/mmHg
Ca=
100- 100 mmHg
Sym
Cv= 300 ml = 60 ml/mmHg
Sym 5 mmHg
Cv = 24 x Ca
PRESSURE
(mmHg)

Veins
Sym
Sym
1 2 3 4
VOLUME (L)

• EFFECTS OF COMPLIANCE on Blood Pressure:

Higher Venous Compliance ------> higher capacitance in


veins ------> less venous return ------> lower CVP.



Lower Venous Compliance (sympathetic influence) ------>
lower capacitance veins ------> more venous return via
the one-way valves ------> higher CVP.

Lower Arterial Compliance results in a higher pulse


pressure.

AGE: Arteries in old people have lower compliance. Thus


old people have higher pulse pressures.




EFFECT OF STROKE VOLUME: All other factors
held constant, a high stroke volume results in a
higher pulse pressure, i.e. higher systolic and
lower diastolic but MABP remains constant.

PULSE PRESSURE IS USUALLY DIRECTLY


RELATED TO STROKE VOLUME



EFFECT OF EXERCISE:

Increased CO and Stroke Volume


Compensatory lower vascular resistance (TPR)


MABP doesn't change (within limits).


HIGH SYSTOLIC PRESSURE: Tends to occur


with higher stroke volume.


HIGHER DIASTOLIC PRESSURE:

CORRELATES WITH HIGH TPR.


Factors affecting ABP:



Sex … M > F …due to hormones/ equal at menopause.
■ Age … Elderly > children …due to atherosclerosis.

■ Emotions … due to secretion of adrenaline &


noradrenaline.


Exercise … due to  venous return.
■ Hormones … (e.g. Adrenaline, noradrenaline,

thyroid H).


Gravity …  Lower limbs > upper limbs.
■ Race … Orientals > Westerns … ? dietry factors, or
weather.
■ Sleep …  due to  venous return.
■ Pregnancy … due to  metabolism.
CHANGES IN CARDIOVASCULAR
PERFORMANCE

BY ALTERING THE CARDIAC FUNCTION CURVE


- CHANGING CONTRACTILITY
- CHANGING HEART RATE

BY ALTERING THE VASCULAR FUNCTION CURVE


- CHANGING MEAN CIRCULATORY PRESSURE
Blood Volume
Venous Capacity
- CHANGING TOTAL PERIPHERAL RESISTANCE
Regulation of ABP )

cardiac control centers in medulla
oblongata
1. Cardiacaccelerator 2. Cardiacinhibitory
center center
(V.M.C) (C.I.C)

Sympathetic n. fibers Parasympathetic n. fibers


ü Regulatory mechanisms depend on:
a. Fast acting reflexes:
Concerned by controlling CO (SV, HR), & PR.
b. Long-term mechanism:
Concerned mainly by regulating the blood volume.
Vasoconstriction
Put another way
If your balloon was losing pressure, there are

two actions you can take…


1. put more puff into the balloon (increase CO)


2. let less air out of the balloon by pinching the
end (increase SVR)


A fall in BP triggers vasoconstriction
A fall in BP triggers an increase in cardiac
output
HEART
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


Pressure-Volume Curve


The slope of the curve is compliance.
Pressure is on the X-Axis. Volume is on the Y-

Axis.

If you plot systolic and diastolic pressure, and
look at the corresponding Y-Values, you can
calculate the

following:
The difference on the Y-axis (i.e. the volumes

corresponding to systolic and diastolic


pressures) is stroke volume.
HEART
SYSTOLIC PRESSURE CURVE

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


E D Y HEART
A S LIT
E TI SYSTOLIC PRESSURE CURVE
C R C
IN TRA
O N
C
Isotonic (Ejection) Phase
After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


E D Y HEART
A S LIT
RE TI SYSTOLIC PRESSURE CURVE
C AC
DE TR
O N
C
Isotonic (Ejection) Phase
After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


HEART

G D
IN SE SYSTOLIC PRESSURE CURVE
LL A
FI RE
C
IN

Isotonic (Ejection) Phase


After-load
PRESSURE

Isovolumetric
Phase
Stroke
Volume
DIASTOLIC
Pre-load PRESSURE CURVE

End Systolic Volume End Diastolic Volume


3. Other Vasomotor Reflexes:

 1. Atrial stretch receptor reflex:



 Venous Return  ++ atrial stretch
receptors  reflex vasodilatation &  BP.
 2. Thermoreceptors: (in skin/or
hypothalamus)
• Exposure to heat  vasodilatation.
• Exposure to cold  vasoconstriction.
 3. Pulmonary receptors:

Lung inflation  vasoconstriction.
Regulation of Blood Volume:

■ A long-term regulatory mechanism.


■ Mainly renal:
 1. Renin-Angiotensin System.
 2. Anti-diuretic hormone (ADH), or
vasopressin.
 3. Low-pressure volume receptors.


1. Renin-Angiotensin System:

 ■ Most important mechanism for Na+ retention


in
 order to maintain the blood volume.

 ■ Any drop of renal blood flow &/or  Na+, will


 stimulate volume receptors found in
juxtaglomerular
 apparatus of the kidneys to secrete Renin
which will
 act on the Angiotensin System leading to
production
 of aldosterone.
•Renin-Angiotensin System:
 renal blood flow &/or  Na+

++ Juxtaglomerular apparatus of kidneys


(considered volume receptors)

Renin
Angiotensin I
Angiotensinogen
Converting
(Lungs)
enzymes

Angiotensin III Angiotensin II


(powerful vasoconstrictor) (powerful vasoconstrictor)
Adrenal
cortex
Corticosterone
Aldosterone
N.B. Aldosterone is the main regulator of Na+retention.
2. Anti-diuretic hormone (ADH), or
vasopressin:
 ■ Hypovolemia & dehydration will stimulate
the
 osmoreceptors in the hypothalamus,
which will lead
 to release of ADH from posterior pituitary
gland.

 ■ ADH will cause water reabsorption at


kidney tubules.
3. Low-pressure volume receptors:

 ■ Atrial natriuritic peptide (ANP) hormone, is


secreted
 from the wall of right atrium to regulate
Na+ excretion
 in order to maintain blood volume.

Substances causing contraction in vascular smooth
muscle

Chemical Physiologic role Source Type


NE (α ) Baroreceptor reflex Sympathetic neurons Neural

Endothelin Paracrine Vascular endothelium Local

Serotonin Platelet aggregation, smooth Neurons, digestive Local, neural


muscle contraction tract, platelets
Substance P Pain, increased capillary Neurons, digestive tract Local, neural
permeability
Vasopressin Increase blood pressure during Posterior pituitary Hormonal
hemorrhage
Angiotensin II Increase blood pressure Plasma hormone Hormonal

Prostacyclin Minimize blood loss from endothelium local


damaged vessels before
coagulation
Substances that mediate vascular smooth muscle
relaxation
Chemical Physiologic role Source Type
Nitric oxide Paracrine mediator Endothelium Local

Atrial natriuretic Reduce blood pressure Atrial myocardium, Hormonal


peptide brain
Vasoactive intestinal Digestive secretion, relax Neurons Neural, hormonal
peptide smooth muscle
Histamine Increase blood flow Mast cells Local, systemic

Epinephrine (β 2) Enhance local blood flow to Adrenal medulla Hormonal


skeletal muscle, heart, liver
Acetylcholine Erection of clitoris, penis Parasympathetic neural
(muscarinic) neurons
Bradykinin Increase blood flow via nitric Multiple tissues Local
oxide
Adenosine Enhance blood flow to match Hypoxic cells local
metabolism
• TOTAL RESERVE: The total stored
capacity the heart has to do extra
stroke work. It is equal to Starling
Reserve + Inotropic Reserve + Heart-
Rate Reserve.
• STARLING RESERVE: The extent to which
we can increase Cardiac Output simple
by increasing filling, at the same
inotropic state.
• INOTROPIC RESERVE
• HEART-RATE RESERVE

• INOTROPIC STATE: It's the contractile
force in the muscle, at any particular
fiber-length. That is the same as the
Ca++ concentration in the
• HEART-RATE AND STROKE VOLUME: Heart
rate extremes lead to lower stroke
volume.
• • Bradycardia: Heart-rate slower than 40,
Cardiac Output goes way down because
the stroke volume can't increase enough
to compensate for the lower heart-rate.
You've reached the maximum of the
heart's inotropic state.
• Tachycardia: Heart-rate faster than 180.
Cardiac Output goes way down because
there is no longer enough time between
beats for sufficient ventricular filling, i.e.
the short diastolic time cuts into the "Fast-
Filling Phase" of diastole.
MEASURING BLOOD PRESSURE
TURBULENT FLOW

Cuff pressure > systolic blood pressure -- No sound .


The first sound is heard at peak systolic pressure .
Sounds are heard while cuff pressure < blood pressur
Sound disappears when cuff pressure < diastolic pres
Blood Pressure Systolic Diastolic
Category mm Hg (upper #) mm Hg (lower #)

Normal less than 120 and less than 80

Prehypertension 120 – 139 or 80 – 89

High Blood Pressure 140 – 159 or 90 – 99


(Hypertension) Stage 1

High Blood Pressure 160 or higher or 100 or higher


(Hypertension) Stage 2

Hypertensive Crisis Higher than 180 or Higher than 110


(Emergency care needed)

"Understanding blood pressure readings". American Heart Association. 11 January 2011. Retrieved 30 March 2011.

Das könnte Ihnen auch gefallen