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HBM1001 > EXAM 2 - CV System 2***** > Flashcards

EXAM 2 - CV System 2***** Flashcards

1
Q

Arteries

A

DEFINITION: Takes blood away from heart

STRUCTURE: Mostly smooth muscle & elastic tissue

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

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2
Q

Arterioles

A

STRUCUTURE: Small blood vessels

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

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3
Q

Capillaries

A

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

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4
Q

Veins

A

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

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5
Q

Venules

A

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

Larger venules have 1-2 layers of smooth muscle cells

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6
Q

What is Blood Flow

A

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

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7
Q

What is Blood Pressure

A

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

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8
Q

Resistance (peripheral resistance)
(Definition & Factors)

A

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

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

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9
Q

How do the resistance factors affect Peripheral Resistance

A

**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)

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10
Q

Relationship between flow, pressure and resistance

A

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

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

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11
Q

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

A

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

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12
Q

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

A

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

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13
Q

What is Stroke Volume, and how to calculate

A

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

Stroke Volume = EDV - ESV

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14
Q

Stroke Volume (SV) 3 x Factors

A

1.Preload
2. Contractility
3. Afterload

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15
Q

Stroke Volume Factor: PRELOAD

A

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

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16
Q

Stroke Volume Factor: CONTRACTILITY

A

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)

17
Q

Stroke Volume Factor: AFTERLOAD

A

AFTERLOAD: Pressure that ventricles must overcome to eject blood

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

18
Q

Regulation of Heart Rate (4 x things)

A
  1. ANS: Sympathetic Division
  2. ANS: Parasympathetic Division
  3. Hormones
  4. Ions
19
Q

Regulation of Heart Rate: Sympathetic Division

A
  • Norepinephrine released
  • Pacemaker (SA node) fires more rapidly
  • HR Increases
    - EDV decreases (decreased filling time)
    - Contractility increases
    - ESV decreases because of increased contractility
20
Q

Regulation of Heart Rate: Parasympathetic Division

A
  • Acetocholine released
  • Hyperpolarises SA node (pacemaker) by opening K+ channels
  • HR slows
21
Q

Regulation of Heart Rate: Hormones and Ions

A

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

Epinephrine & Thyroxine increase heart rate

22
Q

Systolic Pressure

A

Pressure exerted in Aorta during ventricular contraction

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

23
Q

Diastolic Pressure

A

lowest level of aortic pressure when heart is at rest

24
Q

Pulse Pressure & Pulse

A

Pulse pressure: Difference between systolic and diastolic pressure

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

25
Q

Mean Arterial Pressure (MAP)

A

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

26
Q

Factors that regular BP (MAP)

main equation thingy at the start of the session

A
  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)
27
Q

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

A
  1. Neural mechanisms
  2. Vasomotor centre
  3. Reflex Control (Baroreceptors & Chemoreceptors)
  4. Hormonal control
  5. Higher order brain centres
28
Q

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

A
  1. NEURAL MECHANISMS:
    • CV Centre of medulla oblongata
    • Cardioinhibitory & Cardioacceletory centres (inc/dec CO)
  2. VASOMOTOR CENTRE
    • Control vasoconstriction & Vasodilation
  3. HORMONAL CONTROL:
    • regulate BP via changes in resistance OR long-term via blood volume
    • hormones (ADH, Angiotensin I) increase CO and vasoconstriction
  4. HIGHER ORDER BRAIN CENTRES
    • Reflexes that regulate BP –> Medulla
    • Hypothalamus = moderates redistribution of blood during exercise, increase BP during stress
29
Q

BP Short-Term Regulations: 3

A
  1. 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

  1. 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

30
Q

HOMEOSTASIS: BP too high

A

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

31
Q

HOMEOSTASIS: BP too low

A

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

32
Q

Long-term

A

HBM1001 (13 decks)

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