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You will be responsible for arteries and veins up to the level of the wrist and ankle, to each organ and to the brain (to and including the circle of Willis). If you begin early and review often, then you will find it is not as daunting as it looks. However, there will be little learning time during the lectures, so it will be up to you to put in the time.
Cardioaccleration center Increases HR (is activated when the pressor area is stimulated)
Baroreceptors (pressuresensitive mechanoreceptors) monitor chronic and acute BP changes; respond to arterial BP changes, stretch, mechanical deformation
Baroreceptors -located in carotid sinus and aortic arch and in the walls of arteries, veins, and right atrium
Body temperature
Hormonal control
Neural control 2 main goals: 1) Maintaining adequate MAP by regulating blood vessel diameter 2) Altering blood distribution to respond to specific demands of various organs Most of neural control operates via: baroreceptors and associated afferent fibres the vasomotor center of the medulla vasomotor fibres innervate vascular smooth muscle, (mainly smooth muscles of the arterioles are controlled)
CO
TPR
Neural Control
Blood flow is tightly coupled to oxygen demand Sympathetic stimuli result in: Vasodilation of blood vessels in the heart and skeletal muscles, thus, increased blood flow to these organs Vasoconstriction of blood vessels in the skin and abdominal organs Vasoconstriction of veins
Most postganglionic sympathetic neurons release norepinephrine (noradrenaline) which combines with -adrenergic receptors on smooth muscle in blood vessel walls, causing vasoconstriction What would this do to blood pressure? Blood vessels of the heart and skeletal muscle contain -adrenergic receptors; sympathetic stimulation of these receptors causes vasodilation This control system ensures that the heart and the active skeletal muscles receive adequate blood flow during stress
Symbols
- vasoconstriction
2 - vasodilation 1- vasoconstiction
The Autonomic Nervous System and Cardiovascular Function Parasympathetic HR strength of atrial contraction (vagal innervation of atria but not ventricles)
Table 19.2
Angiotensinogen
Renin
Thirst
Angiotensin I
ACE*
Angiotensin II
Small changes in plasma osmolality are more effective than small changes in blood pressure and volume in stimulating ADH release
Long-term mechanism:
Renal regulation of Blood Pressure
An increase in blood volume is followed by a rise in BP and stimulates kidneys to eliminate water via: direct mechanism independent of hormones indirect mechanism hormone-dependent
Figure 19.9
Release of ANP
Fluid loss from Crisis stressors: hemorrhage, exercise, trauma, excessive body sweating temperature
Bloodborne Dehydration, chemicals: high hematocrit epinephrine, NE, ADH, angiotensin II; ANP release
Body size
Blood volume
Baroreceptors
Chemoreceptors
Venous return
Stroke volume
Heart rate
Blood viscosity
Cardiac output
Initial stimulus
Physiological response Result
Peripheral resistance
Arterial Pulse Produced when the left ventricle forces blood against the wall of the aorta. The impact creates a pressure wave along the branches of the aorta and the rest of the arterial walls Corresponds to the beating of the heart All arteries have a pulse, but you can palpate a pulse at certain landmarks better than others The radial artery is the most common site to take a pulse - use the middle fingers!!!!
Taking a pulse
Pressure wave due to alternating expansion & recoil of elastic arteries Pressure points (push surface artery against firm tissue, usually radial artery)
sln.fi.edu/biosci2/ monitor/inline/pulse.gif
Fig. 19.11
The Procedure of Taking the Radial Pulse (a) and the Carotid Pulse (b)
Tachycardia - pulse rate > 100 bpm Bradycardia - pulse rate < 60 bpm Pulse rate after severe blood loss, exercise, or eating----WHY? Venous Pulse Only occurs in the largest veins It is a reflected pulse produced by the changes in pressure that accompany atrial contractions
Diastolic BP
The lowest force with which blood pushes against arterial walls as a result of ventricular relaxation Provides information about systemic vascular resistance
Systolic BP
The highest force with which blood pushes against arterial walls as a result of ventricular contraction Systolic pressure reflects the force of ventricular contraction
Measuring BP
Auscultatory method using sphygmomanometer (brachial artery)
Cuff fully inflated (artery fully collapsed no flow) Cuff pressure lowered to < peak systolic pressure (momentary high velocity spurt) record cuff pressure as systolic BP Cuff pressure lowered to < diastolic pressure (continuous flow - sounds disappear) record cuff pressure as diastolic pressure
Measurement of Arterial BP
Blood Pressure mm Hg
Normal BP = 120/80 mm Hg High normal = 130-139/85-89 Mild hypertension (high BP) = 140-159/90-99 Moderate hypertension = 160-179/100-109 Severe hypertension = 180-209/110-119 Very severe (morbid) hypertension = >209/120 Hypotension <90/40 Shock <80/40 Prevalence of hypertension increases with age (4% at 18-20 y, 44% at 50-59y, 65% at 80+ y)
Factors influencing BP
BP is influenced by age, gender, weight, race, stress, nutrition, mood, posture, fitness level, etc..
Figure 19.12
Local factors causing vasodilation include: Decreases in O2 or nutrient levels Increases in CO2 levels in that area Decrease in pH Increases in adenosine, lactic acid, cAMP, cGMP, K+, heat, inflammatory chemicals and nitric oxide (NO)
Myogenic Controls (Local!): vascular smooth muscle responds to increased stretch with increased tone stretch is resisted vasoconstriction decreased stretch results in vasodilation
Myogenic control
Both physical (myogenic) and chemical (metabolic) factors determine final autoregulatory response in tissues
Dilate Constrict
Figure 19.14
Figure 19.15
http://www.skcc.org/n_im ages/transcytosis.jpg
Diffusion: primary mechanism for dissolved solutes & gases; eg: O2, CO2, glucose follow gradients heat moves via convection down a thermal gradient water-filled pores (Na+. K+, Cl-, glucose) or through bilayer (O2, CO2, urea) pores <1% capillary SA; lipid-soluble substances have 100X more SA
J. Carnegie, UofO
Fluid exchange
~ 20 L of fluid are filtered out of capillaries each day before returning to blood
Fluid exchange
As blood flows through a capillary, the blood hydrostatic pressure (BHP = HP) tends to push fluid out through the capillary pores The blood colloid osmotic pressure (BCOP = OP) tends to pull water from the interstitial fluid into the capillary There is a very small interstitial fluid osmotic pressure (IFOP) that tends to move fluid out of the capillaries into the interstitial fluid NEF = the difference between BHP and BCOP Net filtration pressure (NFP) shows direction of fluid movement
Fluid exchange
The formula for calculating NFP: NFP = [HPC Hpif] [OPC OPif]
Example: when HPC = 35 mmHg at the arterial end of capillary and 17 mmHg at the venous end; OPC=26mmHg and OPif =1 mmHg; unlike HP, OP does not vary from one end of capillary to the other Thus, net osmotic pressure that pulls fluid back to capillary is OPC Opif =
= 26 mmHg 1mmHg = 25 mmHg
NFP = (35 - 0) (26 1) = 10 mmHg The net force at the arterial end = 10 mm Hg forcing plasma out of capillary by a process called filtration The net force at the venous end is equal to (17-0)-(26-1) = -8 mmHg, pulling water back into the capillary by osmosis
As a result of this exchange, a constant flow of interstitial fluid washes over the tissue cells, supplying O2 and nutrients and carrying away CO2 and wastes
Figure 19.17
Paths of Circulation
A. Pulmonary Circuit = the vessels that carry blood from the right ventricle to the lungs, and the vessels that return blood to the right atrium (i) pulmonary trunk (ii) Right and left pulmonary artery (iii) Capillaries in the lungs (iv) Right and left pulmonary veins
B. Systemic Circuit = the vessels that carry blood from the heart to body cells and back to the heart 1. Arterial System 2. Venous System
Coronary arteries originate behind aortic semilunar valve: fill during ventricular diastole
Note the anastomoses between the coronary arteries. This is an interarterial anastomosis which provides collateral circulation to different parts of the myocardium. The fact that the coronary arteries fill during ventricular diastole allows them to overcome the resistance which would be too great during ventricular systole.
Descending aorta
Thoracic aorta
Bronchial artery Pericardial artery Esophageal artery Mediastinal artery Posterior intercostal artery
Abdominal aorta
Celiac artery Phrenic artery Superior mesentric artery Supra renal artery Renal artery Gonadal artery Inferior mesenteric artery Lumbar artery Middle sacral artery Common iliac artery
Fig. 19.4b
Fig 19.5d
Ascending aorta
Arch of aorta
Heart
Venous System
Veins that return blood to the heart after gas, nutrient and waste exchange, usually follow pathways that are parallel to the arteries. Some exceptions: (i) Jugular veins (head) -external jugular (face and scalp) -internal jugular (brain)
(v) Coronary sinus (cardiac veins) (vi) Cardiac veins (caps of the myocardium)
(vii) Hepatic Veins (drain the Hepatic Portal System) (viii) Great Saphenous vein= longest vein in the body, extends from the medial ankle to the external iliac vein (ix) Inferior vena cava (drain from the abdominal & lower limb)
To right atrium
All coronary veins empty into the coronary sinus, which enters the right atrium directly, without going through either the inferior or superior vena cave. This is the only systemic venous drainage which does this. Note the anastomosis of these veins as well
Spleen
Hepatic artery
Large Intestine
Small Intestine