Physiology of Circulation Study Guide Flashcards
How does blood flow along a pressure gradient?
Blood flows from high to low pressure against resistance
(always moves DOWN the pressure gradient)
Blood flow
the volume of blood flowing through a vessel, organ, or circulation system in a period of time - remains fairly constant, and relatively equivalent to CO
Blood pressure
the force per unit area exerted on a vessel wall by the contained blood, typically measured in the largest arteries near the heart
- The hydrostatic pressure gradient – the difference in blood pressure within the vascular system – provides the driving force to keep blood moving
Resistance
opposition to flow, the amount of friction that blood encounters
- Most friction is encountered well away from the heart – total peripheral resistance (TPR)
3 sources of resistance
blood viscosity, vessel length, and vessel diameter
source of resistance that is the most important in determining blood flow
Vessel diameter is the most important in determining blood flow because a change in diameter = a change in TPR, the more the resistance increases, the more the blood flow decreases (resistance occurs as a result of the diameter decreasing / vice versa)
How blood pressure differs in arteries, capillaries, and veins
Blood pressure in the arteries is highest, followed by the capillaries, and lastly the veins
In the process of moving from the aorta to the right atrium, where does blood pressure decrease the most?
The arterioles – resistance is highest here
average blood pressure in the right atrium
0mmHg
Systolic blood pressure
blood is expelled into the aorta, the walls are stretched, aortic pressure peaks (average = 120 mmHg)
Diastolic blood pressure
aortic walls recoil, aortic valve closes, and pressure drops (average = 80 mmHg)
Pulse pressure
the difference in systolic and diastolic pressure (Increased SV and contractility can temporarily increase PP, Atherosclerosis chronically increases pulse pressure)
Mean arterial pressure (MAP)
the pressure that propels blood into the tissues – useful tool for determining tissue perfusion
Why is MAP not just SBP averaged with DBP
Because diastole lasts longer than systole, MAP is NOT simply the halfway point between SBP and DBP (both MAP and pulse pressure decrease as you get further from the heart)
Sounds of Korotkoff
heard when taking blood pressure, typically measured in the brachial artery, when a practitioner uses a sphygmomanometer and a stethoscope to listen to them. These sounds detect SBP and DBP
What is it more difficult for blood to make its return trip to the heart via the veins?
The blood flowing through veins has to fight against gravity, and the pressure in veins is much less than arteries
3 functional adaptations for assisting blood to return to the heart via the veins
- Muscular pump (skeletal muscles squeeze veins and propel blood to heart)
- Respiratory pump (breathing causes pressure changes in ventral cavity that propels blood to heart)
- Sympathetic vasoconstriction (during SNS firing veins constrict, venous volume is reduced, and blood goes toward heart)
relationships between CO, TPR, and blood volume
- Blood Pressure (BP) varies directly with CO and TPR
- Anything that increases CO or TPR will increase BP
- Anything that increases HR or SV will increase BP
- Any change that threatens BP homeostasis will be compensated for
Baroreceptors
pressure-sensitive mechanoreceptors that respond to changes in arterial pressure and stretch, whose inputs are integrated into the cardiovascular center of the medulla oblongata. The outputs travel via autonomic fibers to the heart and the vascular smooth muscle
- Ex – rising arterial BP activates baroreceptors in the carotid sinuses, aortic arch, and walls of nearly every large artery of the head and neck. They will then send impulses to the cardiovascular center – cardioinhibitory center is stimulated; vasomotor and cardioacceleratory centers are inhibited
- Orthostatic hypotension is a failure of the baroreceptor reflex
Chemoreceptors
receptors that respond to changes in levels of CO2, H+, and O2 in the blood. They stimulate the cardioacceleratory center to increase CO and the vasomotor center to increase vasoconstriction when: CO2 level rises, pH level falls, O2 level falls. Located close to baroreceptors, the most prominent chemoreceptors are the carotid bodies and the aortic bodies. They also play a role in regulating respiratory rate
Higher brain centers
modify arterial pressure via relays to the brain stem – like fight or flight response, redistribution of blood flow by the hypothalamus
- Reflexes regulating blood pressure are integrated into the medulla oblongata of the brain stem – the cerebral cortex and hypothalamus are not involved in routing regulation of BP
Cardiovascular center
- cardioacceleratory center – sympathetic
- Cardioinhibitory center – parasympathetic
- Vasomotor center: transmits impulses along sympathetic efferent fibers called vasomotor fibers, which exit the spinal cord and innervate the smooth muscle of the blood vessels – mainly arterioles
- Increased sympathetic activity will cause vasoconstriction and raise BP, decreased sympathetic activity will decrease vasodilation and lower BP
Vasomotor tone
arterioles are almost always moderately constricted resulting in a baseline vasomotor tone
Epinephrine/Norepinephrine
released in response to stress, enhance sympathetic response by increasing CO and promoting vasoconstriction
Angiotensin II
Renin (generates angiotensin II) is released by the kidneys when blood pressure or volume are lowk, promotes intense vasoconstriction to rapidly increase blood pressure, stimulates release of ADH and Aldosterone, which both participate in longer term BP regulation
Atrial Natriuretic Peptide (ANP)
produced by the atria of the heart to reduce blood volume and pressure, antagonizes aldosterone, promotes vasodilation, stimulates excretion of sodium and water
Antidiuretic Hormone (ADH)
also called vasopressin, produced by the hypothalamus, stimulates the kidneys to conserve water and widespread vasoconstriction
neural methods of short term regulation of blood pressure
baroreceptors, chemoreceptors, brain’s cardiovascular centers, vasomotor tone, effects of higher brain centers
hormonal methods of short term regulation of blood pressure
Epinephrine, norepinephrine, renin, angiotensin II, ADH, aldosterone, and ANP.
long term regulation of blood pressure
renal mechanisms (direct and indirect)
Direct renal mechanism
when BV or BP rise, fluid is filtered from the bloodstream to the kidneys more rapidly -> increased urine -> decreased BV and BP (opposite also occurs)
Indirect renal mechanism
when BP declines, kidneys release enzyme renin into blood, renin splits the plasma protein angiotensinogen to make angiotensin I, angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) , ACE is found in the capillary endothelium of various body tissues – especially the lungs
The 4 actions of Angiotensin II
- Stimulates the adrenal cortex to secrete aldosterone
- Stimulates the pituitary gland to secrete ADH
- Triggers the sensation of thirst
- Vasoconstriction to increase TPR
Hypertension (HTN)
chronically elevated blood pressure – SBP > 130 mmHg, DBP > 80 mmHg, strains heart and damages the blood vessels
Hypotension
blood pressure < 90/60 mmHg, usually harmless / healthy
Can be a sign of serious underlying condition:
- Addison’s disease
- Hypothyroidism
- Severe malnutrition
Primary hypertension
hypertension without a specific cause, environmental factors that contribute to it are:
- Heredity, diet, obesity, age, diabetes mellitus, stress, and smoking
- Can be controlled with improved diet, exercise, -stopping smoking, managing stress, and taking anti HTN meds
- HTN meds include diuretic, beta blockers, calcium channel blockers, ACE inhibitors, and angiotensin II receptor blockers
Secondary Hypertension
less common, has identifiable cause –
- Obstructed renal arteries
- Kidney disease
- Endocrine disorders – hyperthyroidism or cushing’s disease
dangers of prolonged hypertension
major cause of heart failure, vascular disease, renal failure, and CVA
dangers of prolonged hypotension
Circulatory shock – blood vessels are filled inadequately; blood cannot circulate normally – body tissues are not adequately perfused
3 types of circulatory shock
Hypovolemic Shock
Vascular Shock
Cardiogenic Shock
Hypovolemic Shock
blood volume is too low
- Results from large scale blood or fluid loss
- HR will increase in response to a dramatic drop in blood volume
- Intense vasoconstriction will shift blood out of reservoirs
- Treatment: replace fluid volume ASAP
Vascular Shock
blood volume is normal; poor circulation because of extreme vasodilation and lost TPR
- Anaphylactic: lost vasomotor tone in response to an allergic reaction
- Neurogenic: failure of the autonomic nervous system
- Septic: severe systemic bacterial infection
Cardiogenic Shock
pump failure
- Results from extensive myocardial damage – an inefficient heart
