Circulatory Physiology Flashcards
Distribution of cardiac output at rest
Blood flow is adjusted depending on metabolic need
Blood flow
From higher to lower pressure
Directly proportional to pressure gradient
Inversely proportional to vascular resistance
F=🔺P/R
F = flow rate of blood through a vessel
P = pressure gradient
R = resistance of blood vessels
Pressure change
Driving pressure for systemic flow is created by LV
If blood vessels construct = BP increases
Resistance
Measure of opposition to blood flow
Depends on = blood viscosity (p), vessel length (1), vessel radius(r) (biggest effect)
R = 1xp/r^4
Effect of vessel radius
If vessel radius decreases by a factor of 2, flow would decrease by a factor of 16 Decrease radius (vasoconstrict) = increased resistance, decreased flow Increase radius (vasodilate) = decreases resistance, increased flow Thus vessel vasoconstriction and dilation controls flow
Vascular tree
Consists of = arteries, arterioles, capillaries, venules, veins, lymph vessels
Vasculature
Layers = connective tissue, smooth muscle, endothelium
Arteries
High flow rate/high pressure
Large radius (low resistance)
Pressure reservoir when heart is relaxing
Collagen fibres (tensile strength), elastin fibres (stretch/recoil of walls)
Pulsatile flow
Systolic pressure ~120, Diastolic pressure ~80
Atherosclerosis
Cardiovascular disease
Caused by cholesterol buildup within arteries
Arterioles
Major resistance vessels
Acts to smooth out pulsatile flow
Radius can be adjusted to: distribute cardiac output among organs depending on bodies need, help regulate arterial blood pressure
Only blood supply to _______ remains constant
Brain
Blood supply to other organs alter via arteriole radius
Vasoconstriction
Narrowing of vessel (increased resistance)
Contraction of smooth muscle
Vasodilation
Enlargement of vessel
Relaxation of smooth muscle
Decreased resistance
Increased flow
Factors affecting vascular tone
Local influences = local metabolic changes, histamine release, endothelial factors (nitric oxide, EDRF, endothelin)
Local physical influences = heat or cold, myogenic response to stretch
Arterioles (vasodilation occurs with:)
Decreased oxygen Increased carbon dioxide Increased acid Increased potassium Increased osmolarity Adenosine release Prostaglandin release
Extrinsic control
Sympathetic input
Hormones
Alpha 1 receptors = norepinephrine (vasoconstriction)
Alpha 2 receptors = epinephrine, heart/skeletal muscles (vasodilation)
Capillaries
Thin walled (decrease diffusion distance) Small radius (velocity of blood flow is slow, gas exchange time increases) Extensively branched (increased surface area) Site of gas exchange
Pre-capillary sphincters
Constrict sphincter = closes capillary bed (many capillaries are not open at rest)
Relax sphincter = opens capillary bed
Met arterioles = runs between an arteriole and a venule
Capillary types
Continuous = most common, least permeable, (muscle, lungs, brain, CT) Fenestrated = have pores, (kidneys, small intestine) Sinusoids = large clefts for RBCs, proteins, (liver, bone marrow, spleen)
Capillary bulk flow
Sterling forces that determine fluid flow between tissue and capillary
Capillary blood pressure
Interstitial fluid hydrostatic pressure (Pif)
Plasma colloid osmotic pressure (pi cap)
Interstitial fluid colloid osmotic pressure (pi if)
Capillary blood pressure
Hydrostatic pressure
Encourages fluid flow into tissue
Interstitial fluid hydrostatic pressure
Opposes hydrostatic pressure
Plasma colloid osmotic pressure
Encourages movement of fluid into capillary
Interstitial fluid colloid osmotic pressure
Opposes plasma colloid osmotic pressure
Hydrostatic pressure and osmotic pressure regulate…
Bulk flow
Lymphatic system
Network of open-ended vessels (helps drain fluid from tissues)
Lymph vessels = similar in structure to veins, low pressure, have valves
Functions = return of excess filtered fluid, defence against disease, (lymph nodes = phagocytes), transport of absorbed fat, return of filtered proteins
Edema
Swelling of tissues
Occurs when too much interstitial fluid accumulates
Causes = reduced concentration of plasma proteins, increased permeability of capillary wall, increased venous pressure, blockage of lymph vessels
Venules
Formed when capillary beds unite
Very porous (allows fluids and WBCs into tissues)
Larger venules have one or two layers of smooth muscles
Veins
Return to heart Low pressure Low resistance Larger radius Slow flow Serves as a blood reservoir Capillaries drain into venules (smaller venules merge to form larger vessels)
Venous return
Decreased by = venous compliance
Increased by = driving pressure from cardiac contraction, sympathetically induced venoconstriction, skeletal muscle activity, effect of venous valves, respiratory activity, effect of cardiac suction
Venous valves = prevent backflow
Skeletal pump = pushes blood upward
Varicose veins
Weak valve = allows backflow
Blood stagnates and clots
Blood pressure is determined by
Cardiac output and total peripheral resistance
Mean arteriole pressure = cardiac output x total peripheral resistance
Blood pressure control
Short term = within seconds, baroreceptors, cardiovascular system
Long term = minutes to hours, kidneys
Short term control - baroreceptors
Fast control = cardiovascular
Pressure receptors = send input to cardiovascular centre, output to heart and blood vessels
Response to low blood pressure
Decrease firing of baroreceptors to cardiovascular centre
Triggers = increase in vasoconstriction and venoconstriction, increase contractility so stroke volume increases and heart rate increases
These things increase cardiac output = increases blood pressure
Long term mechanisms: renal regulation
Control blood pressure by altering blood volume
Kidneys = direct renal mechanism, indirect renal (renin-angiotensin) mechanism
Direct renal mechanism
Alters blood volume independently of hormones
Increased blood pressure or blood volume (increased filtration, causes kidneys to eliminate more urine thus reducing blood pressure)
Decreased blood pressure or blood volume causes the kidneys to conserve water and blood pressure rises
Indirect (renin-angiotensin) mechanism
Decreased arteriole blood pressure = release of renin
Renin triggers production of angiotensin ll (potent vasoconstrictor)
Angiotensin ll = aldosterone and ADH secretion (conservation of fluid)
Blood pressure abnormalities
Hypertension and hypotension
Hypertension
Blood pressure above 140/90 mm Hg
Two broad classes = primary hyper tension and secondary hypertension
Primary hypertension
Potential causes = poor kidney function Excessive salt intake or hormones Na+ K+ or Ca++ imbalance (eg- defective Na+/K+ pumps) Abnormalities in arterioles Stress Smoking
Secondary hypertension
Accounts for 10% of hypertension cases
Occurs secondary to another known primary problem
Examples - renal hypertension, endocrine hypertension, neurogenic hypertension
Complication of hypertension
Congestive heart failure Stroke Heart attack Spontaneous hemorrhage Renal failure Retinal damage
Hypotension
Blood pressure below 100/60 mm Hg
Low blood pressure
Occurs when = there is too little blood to fill the vessels, heart is too weak to drive the blood
Orthostatic (postural) hypotension
Transient hypotension condition resulting from insufficient compensatory responses to gravitational shifts in blood when person moves from horizontal to vertical position
Hypotension (circulatory shock)
Occurs when blood pressure falls so low that adequate blood flow to the tissues can no longer be maintained Four main types = Hypovolemic (low volume) shock Cardiogenic (heart produced) shock Vasogenic (vessel produced) shock Neurogenic (nerve produced) shock
