Exam 1 Review:  Chapter 19:  Blood Pressure

blood pressure - The force exerted by the blood upon the walls of the arteries; the pressure in the arteries originates in the pumping action of the heart, and pressure waves (the pulse) can be felt at the wrist and at other points where arteries lie near the surface of the body; since the heart can pump blood into the large arteries more quickly than it can be absorbed and released by the tiny arterioles and capillaries, considerable inner pressure always exists in the arteries; the pressure is maintained between beats of the heart by the elastic recoil and smooth muscular contraction in the walls of arteries; the contraction of the heart (systole) causes the blood pressure to rise to its highest point, and relaxation of the heart (diastole) brings the pressure down to its lowest point; blood pressure is strongest in the aorta, where the blood leaves the heart; it diminishes progressively in the smaller blood vessels and reaches its lowest point in the veins; degree of physical activity, stress levels, emotional states, obesity, dietary salt and alcohol intake, endocrine and kidney function, and various disease states affect blood pressure.

vasoconstriction - Any decrease in the diameter of blood vessels due to the contraction of the smooth muscle in the vessel's walls; usually regulated by the autonomic NS and certain hormones.

vasodilation - Any increase in the diameter of blood vessels due to the relaxation of the smooth muscle in the vessel's walls; usually regulated by the autonomic NS and certain hormones.

resistance - The opposition of a tube or vessel to a fluid passing through it; if is directly proportional to the viscosity of the fluid and to the length of the vessel and inversely proportional to the diameter of the tube.

blood viscosity - The physical property of blood which determines its internal resistance to flow; it is related to the amount and quality of the dissolved substances in the blood, e.g., decreased water or increased proteins or increased formed elements (blood cells and platelets) cause a marked increase in blood viscosity.

systemic vascular resistance (SVR) = total peripheral resistance (TPR) - The resistance to blood flow offered by all of the systemic vessels, excluding the pulmonary vessels; although SVR is primarily determined by changes in blood vessel diameters, changes in blood viscosity will also affect SVR. 

SVR can be calculated if cardiac output (CO),  mean arterial pressure (MAP), and central venous pressure (CVP) are known.

SVR = (MAP - CVP) ÷ CO

Because CVP is normally near 0 mmHg, the calculation is often simplified to:

SVR = MAP ÷ CO

sphygmomanometer - An instrument for indirectly measuring blood pressure in the arteries, especially one consisting of a pressure gauge and a rubber cuff that wraps around the upper arm and inflates to constrict the arteries.

systolic blood pressure - The pressure exerted on the walls of the arteries during the contraction phase (systole) of the heart; considered abnormally elevated if consistently over 150 mm Hg; it varies with age, sex, body size and relative health and physical condition.

diastolic blood pressure - The pressure exerted on the walls of the arteries during the relaxation phase (diastole) of the heart; considered abnormally elevated if consistently over 90 mm Hg; it varies with age, sex, body size and relative health and physical condition.


 

List:

 

3. three factors that determine resistance to blood flow. Which of these factors can be regulated?

 

Factors That Determine Resistance to Blood Blow

Which Can Be Regulated?

blood viscosity limited ability to adjust blood viscosity under normal circumstances of health; however, many stresses and disease states can alter blood viscosity and therefore affect vascular resistance
vessel length cannot significantly regulate or alter vessel length
vessel diameter readily regulated by adjusting vascular smooth muscle tone

 

Sketch and Label:

 

3. Sketch and label the negative feedback regulation of blood pressure by the baroreceptor reflex.

 

 
 

Describe:

 

5. the relationship between cardiac output and blood pressure.

 

            Since SVR = (MAP - CVP) ÷ CO which generally reduces to SVR = MAP ÷ CO,

 

            rearranging the equation to solve for mean arterial pressure yields:  MAP = SVR  x  CO.

 

            Therefore, at any given value of SVR (systemic vascular resistance), MAP is directly proportional to CO.

 

            Stated simply, the relationship between cardiac output and blood pressure is direct; as cardiac output increases, blood pressure rises, and vice versa.

 

7. the factors that affect increased cardiac output.

 

 

General Categories of Extrinsic Factors Specific Examples
Autonomic Nervous System Regulation Sympathetic Division:  releases Norepinephrine which increases CO.
Parasympathetic Division:  releases acetyl choline which decreases CO.
Endocrine System Regulation Epinephrine = Adrenalin and Thyroid Hormones (T3 & T4) increase CO
Electrolytes = Ions Changes in Calcium (Ca++) & Potassium (K+) concentrations in plasma and interstitial fluid influence CO.
Body Temperature Hypothermia decreases CO while hyperthermia & fever increase CO.
Demographics Increasing age decreases CO.
Males tend to have higher CO.
Body Size Characteristics Increased body mass or increased blood volume tend to increase blood pressure and therefore may decrease CO.
Lifestyle Regular exercise tends to increase CO; tobacco and alcohol and many types of drug abuse tend to increase blood pressure and therefore decrease CO.
Pathology Stress and many illnesses effect CO; stress and most sressful acute diseases increase Sympathetic Division activity, releasing Norepinephrine, which increases CO.

 
General Categories of Intrinsic Factors Specific Examples
Internal Conduction System Regulation Anything which interferes with or blocks impulse transmission through the internal conduction system decreases CO.
Coronary Circulation Anything which interferes with or blocks coronary circulation decreases CO.  Ischemia and hypoxia are generally involved.
Myocardial Disease or Injury Anything which damages the myocardium decreases CO.  Ischemia and hypoxia may or may not be involved.
Problems with the Pericardium Any increase in pericardial fluid volume, e.g., inflammation, hemorrhage, or development of adhesions (scarring), decreases CO.
 

See illustration below:

 

8. the factors that affect systemic vascular resistance.

 

          blood viscosity -- vessel length (e.g., from obesity) -- vessel diameter (atherosclerotic changes or changes in vascular smooth muscle tone/contraction)

 

          (See illustration above.)

 

9. the input to and output from the cardiovascular center in the regulation of the heart and blood vessels.

 

In brief, sensory information body temperature (thermoreception), on blood levels of oxygen, carbon dioxide, hydrogen ion, and bicarbonate ion (chemoreception), and information on blood pressure (baroreception) are reported to the higher centers within the cerebrum.  Information relating to stress and/or emotional states will also impact these higher centers.  The higher centers then transfer information to the hypothalamus where it is further integrated and coordinated.  The hypothalamus then generates commands which are transferred to the Cardiac Centers and Vasomotor Centers in the Medulla Oblongata.  Parasympathetic commands from the Cardioinhibitory Center will travel to the heart by way of the Vagus Nerve = X (and in the case of the blood vessels, other cranial and spinal (autonomic) nerves) to the heart, releasing acetyl choline, to decrease heart rate.  Sympathetic commands from the Cardioacceleratory Center and Vasomotor Centers will travel to the heart and blood vessels by way of various cranial and spinal (autonomic) nerves to the heart to increase heart rate and cardiac output and to adjust the vasomotor tone in various arterial walls.  Remember that the impact of norepinephrine on arterial smooth muscle will depend on the adrenergic receptor type (alpha and beta subtypes) present in a given artery.  See the diagrams below for the specifics of the routes.

 
Higher Centers Which Influence Autonomic Control of the Heart & Vessels Medullary Centers Which Influence Autonomic Control of the Heart
Parasympathetic Pathway to the Heart (Vagus = X) Sympathetic Pathway to the Heart (upper thoracic segment lateral horns)

 

 
Similar Negative Feedback Control for Chemoreceptors for O2, H+, and CO2 Levels also Contribute to Adjustments in Heart Rate and Blood Pressure.

 

10. the neural regulation of blood pressure.

In brief, sensory information body temperature (thermoreception), on blood levels of oxygen, carbon dioxide, hydrogen ion, and bicarbonate ion (chemoreception), and information on blood pressure (baroreception) are reported to the higher centers within the cerebrum.  Information relating to stress and/or emotional states will also impact these higher centers.  The higher centers then transfer information to the hypothalamus where it is further integrated and coordinated.  The hypothalamus then generates commands which are transferred to the Cardiac Centers and Vasomotor Centers in the Medulla Oblongata.  Parasympathetic commands from the Cardioinhibitory Center will travel to the heart by way of the Vagus Nerve = X (and in the case of the blood vessels, other cranial and spinal (autonomic) nerves) to the heart, releasing acetyl choline, to decrease heart rate.  Sympathetic commands from the Cardioacceleratory Center and Vasomotor Centers will travel to the heart and blood vessels by way of various cranial and spinal (autonomic) nerves to the heart to increase heart rate and cardiac output and to adjust the vasomotor tone in various arterial walls.  Remember that the impact of norepinephrine on arterial smooth muscle will depend on the adrenergic receptor type (alpha and beta subtypes) present in a given artery.  See the diagrams above for the specifics of the routes.