Case 3 Blood...quo vadis?
11 important questions on Case 3 Blood...quo vadis?
Tunica externa/adventitial layer
mainly loose collagen fibers that protect and reinforce the vessel and anchor it to surrounding.
Infiltrated with nerve fibers, lymphatic vessels
Contains tiny blood vessels, vasa vasorum, these supply the external tissues of the blood vessel wall
Arterial blood pressure
Systolic pressure: average: 120 mmHg, pressure generated by ventricular contraction
Diastolic pressure: aortic valve closes, no back flow, walls of elastic arteries recoil, average 70-80 mmHg.
Pulse pressure: systolic - diastolic pressure
Capillary blood pressure
Low pressure is desired because, capillaries are fragile, and most of them are extremely permeable.
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Venous blood pressure
3 functional adaptations:
- Muscular pump: skeletal muscles surrounding the veins contract and
relax to push the blood towards the heart.
- Respiratory pump: moves blood up toward the heart as pressure
changes during breathing. Inhale > abdominal pressure increases,
squeezing of local veins, force blood towards heart. Pressure in chest
decreases, thoracic veins expand, speeding blood into right atrium.
- Sympathetic venoconstriction: reduces volume of blood in veins, blood
is pushed towards the heart under sympathetic control.
Goals of short term regulation (neural controls)
all vessels except those supplying the heart and brain constrict, as much
blood as possible to heart and brain)
- Altering blood distribution to respond to demand of various organs.
Role of cardiovascular center, and what are the inputs?
Modified by inputs from:
- Baroreceptors (pressure-sensitive mechanoreceptors)
- Chemoreceptors (respond to changes in blood levels of CO2, H+ and O2)
- Higher brain centers
Baroreceptor reflexes and 3 mechanisms
3 mechanisms:
- Arteriolar vasodilation: Decreased output from the vasomotor center allows
arterioles to dilate. As peripheral resistance falls, so does MAP.
- Venodilation: Decreased output from the vasomotor center allows veins to
dilate, which shifts blood to the venous reservoirs. This decreases venous
return and CO.
- Decreased cardiac output: Impulses to cardiac centers inhibit sympathetic
activity and stimulate parasympathetic activity, reducing heart rate and
contractile force. As CO falls, so does MAP.
Higher brain centers
Hypothalamus also mediates redistribution of blood flow and other CV responses that occur during exercise and change in body temperature.
Hormonal control (short term)
the blood. Both enhance sympathetic response by increasing CO and
promoting vasoconstriction.
- Antidiuretic hormone (ADH): hypothalamus, stimulates kidneys to conserve
water. If BP falls, more ADH is released, helps restore arterial pressure by
causing intense vasoconstriction.
- Atrial natriuretic peptide (ANP): atria of heart, reduction in blood volume
and pressure. It antagonizes aldosterone and make the kidneys excrete
more sodium and water from the body, reduces blood volume.
Direct renal mechanism
When blood volume or pressure rises, filtering of fluid from blood into kidney
tubules speeds up, reabsorption is not fast enough then, more leaves the
body in urine -> blood volume and pressure fall
When blood volume or pressure is low, water is conserved and returned to
the blood and blood pressure rises.
Indirect renal mechanism
- When blood pressure declines -> renin released
- Renin cleaves angiotensinogen (plasma proteins made by liver)
- Converts it into angiotensin I
- Angiotensin converting enzyme (ACE) converts angiotensin I into
angiotensin II
Angiotensin II stabilizes BP and ECF volume in 4 ways:
- stimulates adrenal cortex to secrete aldosterone (reabsorption of sodium,
if more sodium is in the bloodstream, water follows)
- Makes posterior pituitary release ADH (water reabsorption)
- Triggers thirst by activating hypothalamic thirst center. (encourages water
consumption, restoring blood volume and so blood pressure)
- Potential vasoconstrictor (increases BP by increasing peripheral
resistance)
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