EXAM 2 - CV System 2*****

Question 1

Arteries

Answer 1

DEFINITION: Takes blood away from heart

STRUCTURE: Mostly smooth muscle & elastic tissue

FUNCTIONS:
- High elasticity
- Delivers blood to organs
- Vasoconstriction & Vasodialation

Question 2

Arterioles

Answer 2

STRUCUTURE: Small blood vessels

FUNCTION:
- Also carry blood (oxygenated) away from heart
- Vessels that constrict when Sympathetic NS activated

Question 3

Capillaries

Answer 3

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

Question 4

Veins

Answer 4

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

Question 5

Venules

Answer 5

STRUCTURE: Capillaries unit to form postcapillary venules
- endothelium & a few pericytes
- Very porous

Larger venules have 1-2 layers of smooth muscle cells

Question 6

What is Blood Flow

Answer 6

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

Question 7

What is Blood Pressure

Answer 7

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

Question 8

Resistance (peripheral resistance)
(Definition & Factors)

Answer 8

DEFINITION: Measurement of the amount of friction blood encounters with vessel walls.

THREE FACTORS:
- Viscosity
- Blood vessel lengeth
- Blood vessel diameter

Question 9

How do the resistance factors affect Peripheral Resistance

Answer 9

**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)

Question 10

Relationship between flow, pressure and resistance

Answer 10

Blood Flow (F) = Pressure gradient (∆P) / Resistance (R)

because these things affect flow:
- If pressure gradient INCREASES, Flow INCREASES
- If resistance INCREASES, flow DECREASES

Question 11

CONTROL OF BLOOD FLOW*
Tissue perfusion + 4 Steps
(A.D.G.U)

Answer 11

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

Question 12

What is Cardiac Output (CO), and how is it calculated

Answer 12

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

Question 13

What is Stroke Volume, and how to calculate

Answer 13

Stroke Volume: Quantity of blood pumped by left ventricle during each contraction.

Stroke Volume = EDV - ESV

Question 14

Stroke Volume (SV) 3 x Factors

Answer 14

1.Preload
2. Contractility
3. Afterload

Question 15

Stroke Volume Factor: PRELOAD

Answer 15

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

Question 16

Stroke Volume Factor: CONTRACTILITY

Answer 16

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)

Question 17

Stroke Volume Factor: AFTERLOAD

Answer 17

AFTERLOAD: Pressure that ventricles must overcome to eject blood

Increased afterload (i.e. increased pressure that ventricles must overcome) = decreased

Question 18

Regulation of Heart Rate (4 x things)

Answer 18

1. ANS: Sympathetic Division
2. ANS: Parasympathetic Division
3. Hormones
4. Ions

Question 19

Regulation of Heart Rate: Sympathetic Division

Answer 19

• Norepinephrine released
• Pacemaker (SA node) fires more rapidly
• HR Increases
  - EDV decreases (decreased filling time)
  - Contractility increases
  - ESV decreases because of increased contractility

Question 20

Regulation of Heart Rate: Parasympathetic Division

Answer 20

• Acetocholine released
• Hyperpolarises SA node (pacemaker) by opening K+ channels
• HR slows

Question 21

Regulation of Heart Rate: Hormones and Ions

Answer 21

ICF & ECF ion concentrations (Na+, Ca2+, K+) must be maintained)

Epinephrine & Thyroxine increase heart rate

Question 22

Systolic Pressure

Answer 22

Pressure exerted in Aorta during ventricular contraction

(left ventricle pumps blood into aorta, imparting kinetic energy)

Question 23

Diastolic Pressure

Answer 23

lowest level of aortic pressure when heart is at rest

Question 24

Pulse Pressure & Pulse

Answer 24

Pulse pressure: Difference between systolic and diastolic pressure

Pulse: throbbing of arteries due to difference in pulse pressures, which can be felt under skin

Question 25

Mean Arterial Pressure (MAP)

Answer 25

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

Question 26

Factors that regular BP (MAP) main equation thingy at the start of the session

Answer 26

1. Cardiac Output (CO) (SV x HR) 2. Resistance (PR) 3. Blood Volume MAP factors = SV x HR x PR Anything increasing these = increases MAP/BP 1. SV = mainly affected by venous return/preload/EDV 2. PR = mainly affected by vessel diameter 3. HR = maintained by medullary centers' (ANS)

Question 27

BP Factors (SV + HR = PR) can be effected by these SHORT-TERM regulations:

Answer 27

1. Neural mechanisms 2. Vasomotor centre 3. Reflex Control (Baroreceptors & Chemoreceptors) 4. Hormonal control 5. Higher order brain centres

Question 28

BP Short-Term Regulations: 1,2,4,5

Answer 28

1. NEURAL MECHANISMS: - CV Centre of medulla oblongata - Cardioinhibitory & Cardioacceletory centres (inc/dec CO) 2. VASOMOTOR CENTRE - Control vasoconstriction & Vasodilation 4. HORMONAL CONTROL: - regulate BP via changes in resistance OR long-term via blood volume - hormones (ADH, Angiotensin I) increase CO and vasoconstriction 5. HIGHER ORDER BRAIN CENTRES - Reflexes that regulate BP --> Medulla - Hypothalamus = moderates redistribution of blood during exercise, increase BP during stress

Question 29

BP Short-Term Regulations: 3

Answer 29

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 3. 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

Question 30

HOMEOSTASIS: BP too high

Answer 30

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

Question 31

HOMEOSTASIS: BP too low

Answer 31

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

Question 32

Long-term