EXAM 2 - CV System 2***** Flashcards
Arteries
DEFINITION: Takes blood away from heart
STRUCTURE: Mostly smooth muscle & elastic tissue
FUNCTIONS:
- High elasticity
- Delivers blood to organs
- Vasoconstriction & Vasodialation
Arterioles
STRUCUTURE: Small blood vessels
FUNCTION:
- Also carry blood (oxygenated) away from heart
- Vessels that constrict when Sympathetic NS activated
Capillaries
STRUCTURE: thinnest & smallest blood vessel
FUNCTION:
- direct contact with tissue cells;
- directly serve cellular needs
- gas/nutrient/waste exchange between blood and ISF
CAPILLARY BED: Interwoven network of capillaries between arterioles & venules
Veins
DEFINITION: Takes blood towards the heart
STRUCTURE: Mostly connective tissue & Collagen fibres
FUNCTION:
- Large lumen (diameter) for low resistance
- Have Valves to prevent backflow
- Blood reservoir
Venules
STRUCTURE: Capillaries unit to form postcapillary venules
- endothelium & a few pericytes
- Very porous
Larger venules have 1-2 layers of smooth muscle cells
What is Blood Flow
Volume of blood flowing through vessel, organ or entire circulation in a given period
- Measured in ml/min
- Equivalent to CO for entire vascular system
What is Blood Pressure
Force per unit area exerted on wall of blood
vessel by blood
– Expressed in mm Hg
– Measured as systemic arterial BP in large arteries near heart
Resistance (peripheral resistance)
(Definition & Factors)
DEFINITION: Measurement of the amount of friction blood encounters with vessel walls.
THREE FACTORS:
- Viscosity
- Blood vessel lengeth
- Blood vessel diameter
How do the resistance factors affect Peripheral Resistance
**THINK GARDEN HOSE EXAMPLE****
VISCOSITY:
- Increased viscosity (blood thickness) = increased resistance
VESSEL LENGTH:
- Increased vessel length = increased resistance
VESSEL DIAMETER:
- Decreased (smaller) vessel diameter = increased resistance
- Has the GREATEST influence on resistance (viscosity & length stay relatively constant)
Relationship between flow, pressure and resistance
Blood Flow (F) = Pressure gradient (∆P) / Resistance (R)
because these things affect flow:
- If pressure gradient INCREASES, Flow INCREASES
- If resistance INCREASES, flow DECREASES
CONTROL OF BLOOD FLOW*
Tissue perfusion + 4 Steps
(A.D.G.U)
Tissue Perfusion: Blood flow through body’s tissues; involved in:
1. Absorption of nutrients (digestive track)
2. Delivery of O2 & nutrients TO, and removal of wastes FROM tissue cells
3. Gas exchange (lungs)
4. Urine formation (kidneys)
Rate of flow is precisely right –> to provide a proper function to that tissue/organ
What is Cardiac Output (CO), and how is it calculated
CO: amount of blood pumped out by each ventricle in 1 minute
CO (mls/min) = SV (mls/beat) x HR (beats/min)
Example:
HR (75 beats/min) × SV (70 ml/beat)
CO (ml/min= 5.25 L/min
What is Stroke Volume, and how to calculate
Stroke Volume: Quantity of blood pumped by left ventricle during each contraction.
Stroke Volume = EDV - ESV
Stroke Volume (SV) 3 x Factors
1.Preload
2. Contractility
3. Afterload
Stroke Volume Factor: PRELOAD
PRELOAD: Degree to which cardiac muscles are stretched before they contract. i.e. amount of blood sitting in ventricle BEFORE it contracts (EDV = same thing as Preload)
**FRANK-STARLING LAW: Relationship between Preload & SV Increased Preload = Increased SV
**VENOUS RETURN: Amount of blood returning to the heart.
TO SUMMARISE:
- Increased Venous Return = Frank Starling Law (increased EDV/preload –> Increased SV) = Increased CO
- Inc. Venous return = Inc. EDV = Inc. SV = Inc. CO
Stroke Volume Factor: CONTRACTILITY
CONTRACTILITY: Contractile strength of heart/at given muscle length (separate/independent of muscle stretch and EDV)
*Increased Contractility = Decreased ESV (as more blood is pushed out of ventricle, meaning volume decreases)
*Decreased Contractility = Increased ESV (as less blood is pushed out of ventricle, meaning volume increases)
Stroke Volume Factor: AFTERLOAD
AFTERLOAD: Pressure that ventricles must overcome to eject blood
Increased afterload (i.e. increased pressure that ventricles must overcome) = decreased
Regulation of Heart Rate (4 x things)
- ANS: Sympathetic Division
- ANS: Parasympathetic Division
- Hormones
- Ions
Regulation of Heart Rate: Sympathetic Division
- Norepinephrine released
- Pacemaker (SA node) fires more rapidly
- HR Increases
- EDV decreases (decreased filling time)
- Contractility increases
- ESV decreases because of increased contractility
Regulation of Heart Rate: Parasympathetic Division
- Acetocholine released
- Hyperpolarises SA node (pacemaker) by opening K+ channels
- HR slows
Regulation of Heart Rate: Hormones and Ions
ICF & ECF ion concentrations (Na+, Ca2+, K+) must be maintained)
Epinephrine & Thyroxine increase heart rate
Systolic Pressure
Pressure exerted in Aorta during ventricular contraction
(left ventricle pumps blood into aorta, imparting kinetic energy)
Diastolic Pressure
lowest level of aortic pressure when heart is at rest
Pulse Pressure & Pulse
Pulse pressure: Difference between systolic and diastolic pressure
Pulse: throbbing of arteries due to difference in pulse pressures, which can be felt under skin
Mean Arterial Pressure (MAP)
MAP: Pressure that propels blood to tissues
MAP = Diastolic pressure + 1/3 of pulse pressure
EXAMPLE: BP is 120/80
- Diastolic pressure = 80 mm Hg
- Pulse pressure = 40 mm Hg
MAP = 80 + (1/3)x40
= 80 + 13
= 93 mm Hg
Factors that regular BP (MAP)
main equation thingy at the start of the session
- Cardiac Output (CO) (SV x HR)
- Resistance (PR)
- Blood Volume
MAP factors = SV x HR x PR
Anything increasing these = increases MAP/BP
- SV = mainly affected by venous return/preload/EDV
- PR = mainly affected by vessel diameter
- HR = maintained by medullary centers’ (ANS)
BP Factors (SV + HR = PR) can be effected by these SHORT-TERM regulations:
- Neural mechanisms
- Vasomotor centre
- Reflex Control (Baroreceptors & Chemoreceptors)
- Hormonal control
- Higher order brain centres
BP Short-Term Regulations: 1,2,4,5
- NEURAL MECHANISMS:
- CV Centre of medulla oblongata
- Cardioinhibitory & Cardioacceletory centres (inc/dec CO)
- VASOMOTOR CENTRE
- Control vasoconstriction & Vasodilation
- HORMONAL CONTROL:
- regulate BP via changes in resistance OR long-term via blood volume
- hormones (ADH, Angiotensin I) increase CO and vasoconstriction
- HIGHER ORDER BRAIN CENTRES
- Reflexes that regulate BP –> Medulla
- Hypothalamus = moderates redistribution of blood during exercise, increase BP during stress
BP Short-Term Regulations: 3
- REFLEXES - BARORECEPTORS
Location: Carotid sinuses, aortic arch, walls of large arteries
Function: Detect pressure changes (relay BP changes to ANS)
If MAP is high:
- Baroreceptors increase input to vasomotor Centre
- inhibits vasomotor & cardioacceleratory centres
- stimulates cardioinhibitory Centre
- decrease cardio output (CO)
- Cause peripheral vasodilation
Result = decreased blood pressure
- REFLEXES - CHEMORECEPTORS
Location: Aortic arch & large arteries (almost same as above)
FUNCTION: Detects increases in CO2, or drop in pH or O2
If MAP low:
- can increase BP by signaling cardioacceleratory center to increase CO
- Signaling vasomotor center to increase
vasoconstriction
HOMEOSTASIS: BP too high
STIMULUS: BP too high
RECEPTOR: Baroreceptors in carotid sinuses and aortic arch are stimulated
CONTROL CENTRE: Increased Impulses from baroreceptors STIMULATE the C.I centre (and INHIBIT C.A. centre) and inhibit vasomotor centre
EFFECTOR (2): Decreased Sympathetic impulses to heart = lower HR, lower Contractility, lower CO. Decreased vasomotor centre = vasodilation (lower Resistance)
RESPONSE: lower CO and lower R return BP to normal
HOMEOSTASIS: BP too low
STIMULUS: BP too low
RECEPTOR: Baroreceptors in carotid sinuses and aortic arch are inhibited
CONTROL CENTRE: Impulses from baroreceptors STIMULATE the C.A centre (and INHIBIT C.I. centre) and stimulate vasomotor centre
EFFECTOR (2): Increased Sympathetic impulses to heart = higher HR, higher Contractility, higher CO. Increased vasomotor centre = vasoconstriction (higher Resistance)
RESPONSE: higher CO and higher R return BP to normal
Long-term
