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Physiology > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

why is the cardiovascular system important?

A

1. transport

  • nutrients, gases
  • wastes, hormones

2. temperature regulation

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2
Q

organization of the CV system

A

arteries carry blood away from the heart

arteries become arterioles then capillaries

capillaries is where exchange occurs

capillaries reunite to form venules and then veins

veins carry blood back to the heart

Total blood volume: 4-6 litres

pulmonary circuit - 15% blood volume (between heart and lungs)

systemic circuit - 85% blood volume - arteries 10%; capillaries 5%; veins 70%

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3
Q

heart anatomy

A
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4
Q

myocardial cells

A

contractile - myocardial cells (cardiomyocytes)

nodal and conducting - myocardial cells

skeletal - striated (thin/thick)

  • cylindrical cells
  • mitochondria
  • Ca2+ to contract
  • motor neuron AP

cardiomyocytes - striated (thin/thick)

  • short and narrow, branched cells
  • lots of mitochondria
  • Ca2+ to contract
  • electrically connected
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5
Q

nodal and conducting cells

A

minimal actin and myosin but self-excitable

  • generates action potentials to spread through heart for contraction
  • examples: Sinoatrial Node, Atrioventricular (AV) Node, Purkinje Fibres, Bundle of His
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6
Q

excitable cells

A

depolarization: cell becomes more positive than RMP

repolarization: positive cell returns to RMP

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7
Q

neuron vs nodal cell RMP

A
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8
Q

neuron vs nodal cell action potential

A

nodal cell - Ca2+ in (depolarization); K+ out (repolarization)

takes around 0.8 seconds

-40 mV threshold

no hyperpolarization

pacemaker potential (yellow line)

neuron - Na+ in (depolarization); K+ out (repolarization)

takes around 4 milliseconds

-55 mV threshold

hyperpolarization

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9
Q

SA Nodal Action Potential

A

SA node sends action potentials for each heart beat

threshold = -40 mV

yellow line - pacemaker potential (increase Na+, increase Ca2+, decrease K+)

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10
Q

the conducting system: AP propagation

A
  1. Sinoatrial (SA) node (100 AP/min)
  2. Atrial Muscle
  3. Atrioventricular (AV) node (action potential SLOW here)
  4. Bundle of His
  5. Bundle Branches (L & R)
  6. Purkinje Fibres (action potential FAST here to push out blood)
  7. Ventricular Muscle
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11
Q

Electrocardiogram (ECG)

A

* important: for muscles to contract, you NEED an action potential first

sum of all electrical events in the heart

body fluids conduct electricity well

recorded by surface electrodes

P -> Atrial depolarization

QRS -> Ventricular depolarization

T -> Ventricular repolarization

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12
Q

what can an ECG tell us?

A
  • heart rate
  • heart damage (myocardial infarction)
  • conduction issues
  • rhythm disturbance
  • effects of drugs
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13
Q

heart rate

A

resting ~ 70 beats/min

maximum: 220 - your age in years

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14
Q

parasympathetic innervation: rest & digest (ACh)

A

ACh binding its receptor will:

  1. increase K+ permeability
  2. decrease Na+ permeability
  3. decrease Ca2+ permeability
    - also AV node innervation
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15
Q

sympathetic innervation: fight or flight (NE)

A

NE (norepinephrine) binding it’s receptor will:

  1. increase Na+ permeability
  2. increase Ca2+ permeability
    - also AV node and ventricular muscle innervation
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16
Q

cardiac cycle: heartbeat events

A

things to understand:

  1. blood moves down a pressure gradient
  2. the ECG event occurs before heart muscle contraction or relaxation
  3. when pressure lines cross, something happens to the heart valves (open/close)
  4. systole = contraction, diastole = relaxation
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17
Q

cardiac cycle: heartbeat phases

A

phases:

  1. Atrial Systole
  2. Isovolumetric Ventricular Systole
  3. Ventricular Systole
  4. Isovolumetric Ventricular Diastole
  5. Late Ventricular Diastole
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18
Q

phase 1: Atrial Systole

A

phase 1

ECG: P wave before

pressures: increase pressure in Atrial but higher than ventricular pressure

volume: increase ventricular volume, blood gets pumped from atrial to ventricular (80% of blood is already in the ventricular because AV valve is open)

valves: AV open

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19
Q

phase 2: Isovolumetric Ventricular Systole

A

phase 2

ECG: QRS wave before

pressures: increase in ventricular pressure, exceeds atrial pressure, but lower than aortic pressure

volume: no change

valves: all valves closed

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20
Q

phase 3: ventricular systole

A

phase 3

ECG:

pressures: increase in ventricular pressure, higher than atrial pressure and aortic pressure

volume: decrease in ventricular volume

valves: aortic valve open

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21
Q

phase 4: isovolumetric ventricular diastole

A

phase 4

ECG: T wave before

pressures: decrease in ventricular pressure, drops below aortic pressure, but is higher than atrial pressure

volume: no change

valves: all valves closed

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22
Q

phase 5: late ventricular distole

A

phase 5

ECG: —

pressures: decrease in ventricular pressure, drops below atrial pressure and lower than aortic pressure

volume: increase in ventricular volume, blood enters from atrial to ventricular

valves: AV valve open

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23
Q

repeats again - phase 1: atrial systole

A

phase 1

ECG: P wave before

pressures: increase in Atrial pressure, but higher than ventricular pressure

volume: increase in ventricular volume

valves: AV valve opens

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24
Q

stroke volume

A

during one ventricular systole = stroke volume

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25
Q

cardiac output

A

per minute of ventricular contractions = cardiac output

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26
Q

what controls stroke volume?

A
  1. autonomic nervous system innervation
  2. preload on the heart
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27
Q

autonomic effects on stroke volume

A

parasympathetic: remember, little innervation to cardiac contractile cells

  • acetylcholine is the neurotransmitter released
  • decrease Ca2+ premeability, so decreases strength of contraction and thus decreases stroke volume (minimally)

sympathetic: innervates ventricular cardiomyocytes

  • norepinephrine/epinephrine binds receptors
  • increases Ca2+ permeability, so increasesstrength of contraction and thusstroke volume
28
Q

other heart volumes

A

end diastolic volume (EDV): amount of blood in the ventricle after atrial systole

stroke volume = EDV - ESV

end systolic volume (ESV): amount of blood in the ventricle after ventricular systole

29
Q

what controls stroke volume?

A
  1. autonomic nervous system innervation
  2. preload on the heart
30
Q

changing stroke volume: preload

A

preload: the “load” on the heart prior to contraction

this load is the end diastolic volume (EDV)

the larger the EDV, the more stretch on the ventricles

larger contraction (bigger stroke volume)

31
Q

end diastolic volume and period

A

an increase in EDV = an increase in period

=> increases the stretch of the contractile cells of the ventricles

=> increases the force of contraction of these cells upon systole

=> increases the amount of blood ejected from the heart

=> increases stroke volume

=> increase cardiac output

32
Q

Frank-Starling’s Law

A

Frank-Starling Law states: “a increase in EDV will cause an increase in stroke volume”

33
Q

increase EDV by more venous return

A

during dynamic exercise

  1. muscle pump
  2. sympathetic nervous system
  3. respiratory pump

result = increase SV => increase CO2

34
Q

sympathetic nervous system and venous return

A

remember the SNS affects SA node (HR) and ventricular muscle (SV)

but also innervates blood vessels

  • causes a small constriction of veins
  • increases venous return
  • increases EDV, SV & CO
35
Q

organization of the CV system

A
36
Q

anatomy of a blood vessel

A

tunica externa

  • fibrous connective tissue

tunica media

  • smooth muscle
  • elastic fibres

tunica interna

  • endothelial cells
37
Q

blood vessels: general properties

A

structure and tissue content determines the vessel’s function

38
Q

arteries

A

distribution vessels

structure:

large diameter

thin walls compared to diameter

lots of elastic => easy to distend

blood characteristics:

very high blood pressure

high blood flow

low resistance, small drop in pressure

purpose:

“shock absorbers”

39
Q

arterioles

A

resistance vessels

structure:

small diameter

thick walls compared to diameter

lots of smooth muscle

smooth muscle innervated by SNS

blood characteristics:

large drop in pressure

slower blood velocity

purpose:

controls blood flow (vasoconstriction, vasodilation)

40
Q

relationship: pressure, blood flow & resistance

A
  1. blood flows down a pressure gradient (high to low)
  2. but resistance decreases flow

blood flow = pressure gradient / resistance

41
Q

resistance

A

blood flow = (P1 - P2) x r4

42
Q

blood flow with resistance

A

total blood flow doesn’t change with added resistance to an arteriole

43
Q

capillaries

A

exchange vessels

structure: one endothelial cell thick very thin walls for diffusion

blood characteristics: low blood pressure, small drop in pressure

very low blood velocity

huge total cross-sectional area for diffusion

purpose: exchange of gases, nutrients, etc

44
Q

blood velocity & total cross-sectional area

A

more cross-sectional area = slower flow

slower flow = maximize exchange

45
Q

capillary structure: exchange vessels

A

in skin, muscles, lungs, CNS: Not so permeable

in kidneys, intestines, some other tissues: More permeable

46
Q

exchange by filtration and reabsorption

A

filtration: movement of fluid out of a capillary

reabsorption: movement of fluid into a capillary

Four Starling Forces

  1. capillary hydrostatic pressure (Pc)
  2. interstitial fluid hydrostatic pressure (PIF)
  3. capillary plasma osmotic pressure (Πc)
  4. interstitial fluid osmotic pressure (ΠIF)
47
Q

hydrostatic pressures: Pc & PIF

A

capillary: due to pressure of blood moving through (15 to 35 mmHg)

interstitial fluid: due to pressure of fluid found here (-3 to +6 mmHg)

48
Q

proteins influence exchange

A

movement of fluid due to proteins = osmotic pressures (Π)

49
Q

osmotic pressures: Πc & ΠIF

A
  1. capillary plasma osmotic pressure (Πc)(25 mmHg)
  2. interstitial fluid osmotic pressure (ΠIF)(1-5 mmHg)
50
Q

putting the starling forces together

A
51
Q

net filtration pressure

A

Net filtration pressure = Kf [(PC + πIF) - (πC + PIF)]

(OUT) (IN)

Kf = filtration coefficient (larger = leakier capillary)

positive number = filtration

negative number = reabsorption

52
Q

calculate net filtration pressure

capillary hydrostatic pressure (PC) = 35 mmHg

capillary plasma osmotic pressure (ΠC) = 25 mmHg

interstitial fluid hydrostatic pressure (PIF) = 3 mmHg

interstitial fluid osmotic pressure (ΠIF) = 2 mmHg

A

Net filtration pressure = Kf [(PC + ΠIF) - (ΠC + PIF)]

= 1[(35 + 2) - (25 + 3)]

= 1[(37) - (28)]

= +9 mmHg

53
Q

veins

A

capacitance vessels

structure: valves

large diameter

very thin walls compared to diameter

some elastic fibers and smooth muscle => SNS innervates smooth muscle

blood characteristics: very low blood pressure

medium blood velocity

purpose:“blood reserve”

54
Q

regulating blood flow

A

increase blood supply to active tissues and decrease it to inactive tissues

increase or decrease heat loss from the body by redistributing blood

maintain blood supply to vital organs - heart and brain - at all times

main blood pressure (mean arterial pressure)

55
Q

vasocontrict & vasodilate

A

vasoconstrict (less flow)

vasodilate (more flow)

56
Q

mechanisms used to regulate blood flow

A
  1. local (intrinsic) tissue environment (temp, gases, pressure)
  2. humoral (extrinsic) substances in blood
  3. neural (extrinsic) nervous system
57
Q

local (intrinsic)

A

tissue environment (temp, gases, pressure)

autoregulatory mechanisms

1. Myogenic theory muscle stretch

2. Metabolic theory metabolic needs

58
Q

myogenic theory

A

sudden increase in blood pressure Blood Flow = (P1 - P2) x r4

=> stretches walls of arterioles

=> smooth muscle in arteriole walls contract (reflex)

=> vasoconstriction

=> decreases blood flow and pressure after contraction

*this protects the capillaries and maintains normal blood flow

59
Q

metabolic theory

A

change metabolism, change metabolites and tissue conditions

  • increase in CO2
  • decrease in O2
  • increase in [H+] (increase in acidity = lower pH)
  • adenosine from adenosine triphosphate (ATP) breakdown
  • temperature

these conditions causes arterioles to vasodilate to increase flow = vasodilator metabolites

60
Q

hyperventilation

A

breathing very quickly means there is less carbon dioxide in blood and reduces blood flow

decrease in CO2

increase in pH

vasoconstriction and less blood flow

61
Q

humoral (extrinsic)

A

substances in blood

Vasoconstrictors

  1. Epinephrine
    - an amine, released upon SNS activation
    - binds to alpha adrenergic receptors, increase blood pressure on most blood vessels
  2. Angiotensin II
    - a peptide hormone
    - made during low blood pressure
  3. Antidiurtic Hormone (ADH)
    - a peptide hormone
    - released during low blood pressure

Vasodilators

  1. Epinephrine
    - an amine, released upon SNS activation
    - binds to beta2 adrenergic receptors, decrease blood pressure in skeletal muscle & heart
  2. Atrial natriuretic peptide
    - a peptide hormone
    - released during high blood pressure
  3. Kinins and Histamine
    - inflammatory mediators
    - binds to smooth muscle receptors
62
Q

neural (extrinsic)

A

nervous system

Autonomic Nervous System

1. sympathetic nervous system

  • innervates SA & AV node, ventricular muscle
  • innervates smooth muscle in veins (venous return => increases EDV)
  • innervates smooth muscle in arterioles

2. parasympathetic nervous system

  • innervates SA & AV node
  • no blood vessel innervation
  • but indirect effects because no SNS activation
63
Q

cardiac output and blood pressure

A

clinically: Mean Arterial Pressure = diastolic pressure + 1/3 (systolic - diastolic pressure)

recap: Blood Flow = pressure/ resistance

cardiac output (CO) = mean arterial pressure (MAP) / total peripheral resistance (TPR)

rearrange: MAP = CO x TPR

CO = HR x SV

64
Q

adjusting Mean Arterial Pressure (MAP): Baroreceptor Reflex

A

Negative Feedback Loop

SET POINT (Mean Arterial Pressure)

=> CONTROL CENTRE (CV centre in medulla)

=> EFFECTOR activate SNS or PSNS (Heart and blood vessels)

=> CONTROLLED VARIABLE (Mean Arterial Pressure)

=> SENSORS (Baroreceptors (mechanoreceptors))

=> back to CONTROL CENTRE (Action Potential)

65
Q

baroreceptors

A

located in walls of aortic arch, carotid sinuses

are stretch sensitive sensors = mechanoreceptors

monitor blood pressure

send action potential back to CV centre in medulla of brainstem

66
Q

what happens when MAP is too high?

A

stretches aorta and carotid sinuses and activates baroreceptors

=> action potential sent to CV centre

=> CV centre compares signals to set point

=> shuts off SNS and activates PSNS

=> decrease Cardiac Output (decrease Heart Rate and Stroke Volume) and causes vasodilation (decrease Total Peripheral Resistance)

=> decreases Mean Arterial Pressure (MAP)

Physiology (20 decks)

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