Download Lecture 12: Blood Pressure

Lecture 12: Blood Pressure
Reading: OpenStax A&P Text Chapter 20
Blood Pressure
Blood pressure is the force of blood pushing on the surface area of the vessel walls. (Pressure is defined as Force/Area and is
measured in units of atmospheres (atm) or millimeters of mercury (mmHg)). Blood pressure is measured in the aorta, which is the site
of highest BP in the body. (Why?)
1. High BP: hypertension (damages blood vessels = CVD)
2. Low BP: hypotension (decreases perfusion = hungry, dirty cells)
3. Changes in BP are normally noticed (by baroreceptors), addressed (by the cardiovascular control center in the medulla
oblongata), and FIXED (by heart and smooth muscle effectors) within 2 heart beats.
Blood vessel anatomy
Remember basic vessel anatomy…
1. Fibrous tissue: structural support
2. Smooth muscle: controls vasoconstriction and vasodilatation
3. Elastic tissue: allow for the storage of force…
4. Endothelium (a type of epithelium that lines body surfaces INSIDE the body): lines the vessels and allows for exchange in
capillaries
5. Types of vessels:
A. Arteries
B. Arterioles
C. Capillaries
D. Venules
E. Veins
Physics of blood flow
1. Pressure- the force exerted by the BLOOD (fluid) on the VESSELS (container)
A. It is usually measured in mmHg. Sometimes it is referred to as hydrostatic pressure, even though this term technically
describes a fluid at REST.
2. Flow- Pressure gradients provide motivation for fluid to flow, and fluids always flow from high pressure to low pressure.
3. Resistance- This the force that RESISTS flow.
A. Resistance is essentially friction.
B. There are several factors that affect resistance: the diameter of the blood vessel, the length of the vessel, and the thickness
(viscosity) of the blood (fluid).
Cardiac muscle contraction
The mechanism of a cardiac muscle contraction is very similar to the skeletal muscle mechanism. Brace yourself-- this process is
describing the ACTUAL contraction itself (not the action potential that generates the contraction!)
1. AP travels down the CELL membrane, and THROUGH gap junctions in the intercalated disks, and then down t-tubules in a
cardiac muscle fiber!
2. Voltage gated Ca2+ channels in the t-tubules OPEN, and Ca2+ from the ECF rushes into the cell.
3. The influx of Ca2+ into the ICF causes Ca2+ channels in the SR to OPEN, releasing the Ca2+ ions inside the SR.
4. Just like in skeletal muscle, Ca2+ binds to troponin, which moves tropomyosin, revealing the myosin binding sites on actin!
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Graded muscle contractions
1. The more Ca2+ in the ICF, the stronger the contraction.
A. This creates GRADED CONTRACTIONS, based on the amount of Ca2+ present in the ICF. More Ca2+ , more crossbridges
are activated.
B. This is UNLIKE skeletal muscle tissue, which does not exhibit graded contractions (assuming sarcomere length and
stimulus frequency are held constant).
2. If a the heart muscle contracts more STRONGLY, this results in increased STROKE VOLUME, which then results in increased
CARDIAC OUTPUT.
3. Substances that increase contraction strength are INOTROPIC substances.
4. There is another mechanism by which contraction strength can be increased...
Frank-Starling Law
1. Cardiac muscle, when stretched by an increased volume of blood, responds with a more forceful contraction. This can be plotted
on a graph and the line is called a Starling curve.
2. Remember that skeletal muscle tissue has an optimal length in which myosin/actin overlap is optimal for generating maximal
TENSION during contraction. The same is true for cardiac muscle.
3. In general, if the heart muscle is STRETCHED (by being filled more fully!), a greater contraction will be generated.
4. In this way, filling the heart more fully results in a bigger contraction and greater stroke volume (and CO).
5. A concept known as VENOUS RETURN can affect stroke volume thanks to Frank-Starling.
A. Increased venous return means MORE blood is flowing into the ventricles from the body (or lungs).
B. If more blood flows in, the ventricles will STRETCH to accommodate this volume load.
C. The stretch moves sarcomeres into a more optimal position, for increased FORCE.
6. This can all be quantified by End Diastolic Volume (EDV). If EDV is bigger, the heart will generate a bigger contraction force.
IF EDV is smaller, a smaller force will be generated.
Preload and afterload
1. Preload is the amount of STRETCHING experienced by the ventricles when at EDV.
A. Because of Frank-Starling, this can be associated with contraction strength.
B. Inotropic substances increase preload.
2. Afterload is the amount of RESISTANCE the heart must overcome to get the blood out of the ventricle.
A. A BIG afterload means the heart has to work harder to get the blood out into the body (or lungs).
B. If the arteries aren’t very elastic, there is more resistance to overcome.
C. All the blood in the rest of the system must also be MOVED...and this is quantified by the afterload as well.
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Factors affecting resistance
Resistance – a force that opposes the flow of blood -- can be manipulated by changing the diameter of blood vessels (primarily
arterioles…why?)
Arteriole diameter is regulated in 2 ways
1. Myogenic autoregulation
A. Vascular smooth muscle cells in some arterioles are essentially stretch receptors.
B. When they stretch, mechanically gated Ca2+ channels in the smooth muscle cell membrane open…causing contraction
C. Contraction decreases diameter, decreasing flow.
2. Paracrines (hormone-like chemicals that are secreted by local cells and act on their neighbors) affect smooth muscle contraction
in the arteriole
A. NO: paracrine involved in relaxation of smooth muscle. This results in increased blood flow...and is the SAME mechanism
that is used by Viagra!
Clinical Blood Pressure
Vocabulary:
1. Systolic pressure: This is the pressure measured in the aorta during ventricular contraction (vent systole!)
2. Diastolic pressure: This is the pressure measured in the aorta during ventricular relaxation (vent diastole)
A. Ventricular diastole results in 0 mmHg in the ventricle…
B. …but diastolic pressure is 80 mmHg b/c the aorta can store a LOT of the force in its elastic walls!
3. Pulse pressure: Systole - diastole
4. Mean Arterial Pressure (MAP) = diastolic pressure + 1/3(pulse pressure) (MAP closer to diastolic pressure b/c diastole lasts 2x
longer than systole)
Taking blood pressure with the sphygmomanometer
1. Palpate brachial artery
2. Position cuff above the brachial artery
3. Pump up cuff (increasing pressure on the brachial artery) while listening to brachial artery…when the pulse disappears, the
cuff’s pressure is GREATER than the pressure of the blood pushing out! (Usually increase 20 mmHg beyond this point)…
4. Slowly release pressure to allow blood back through.
5. Korotkoff (kŏ-rot′kof) sounds begin, marking systolic pressure.
A. Turbulent blood pushes through the vessel!
B. Eventually as the pressure releases, the turbulence ceases…
6. Turbulence ceases…no turbulent sounds (but can you still hear the pulse?) = diastolic pressure
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Lab 12: PhysioEx #5
Questions based on LABORATORY EXERCISE 5 from PhysioEx 9.0 simulation package by Pearson.
Do activities 4-6 (7 is optional)
Pre-lab work
1. Label the following anatomical structures on this model:
A. Aortic semilunar valve
B. Lungs
C. Left ventricle
D. Pulmonary veins
E. Left AV valve
F. Body
2. Define the following terms:
A. EDV
B. ESV
C. CO
D. SV
3. What are the three factors the body can alter to maintain blood pressure homeostasis?
4. Define the following terms:
A. Preload
B. Contractility
C. Afterload
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External Brain 12: Blood Pressure
Study Guide Questions
It would be awesome if you wrote some EB questions for me!
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