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
cardiac output
**per minute** of ventricular contractions = **cardiac output**
26
what controls stroke volume?
1. autonomic nervous system innervation 2. preload on the heart
27
autonomic effects on stroke volume
**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 **increase****s**strength of contraction and thus**stroke volume**
28
other heart volumes
**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
what controls stroke volume?
1. autonomic nervous system innervation 2. preload on the heart
30
changing stroke volume: preload
**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
end diastolic volume and period
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
Frank-Starling's Law
Frank-Starling Law states: "a increase in EDV will cause an increase in stroke volume"
33
increase EDV by more venous return
during dynamic exercise 1. muscle pump 2. sympathetic nervous system 3. respiratory pump result = increase SV =\> increase CO2
34
sympathetic nervous system and venous return
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
organization of the CV system
36
anatomy of a blood vessel
**tunica externa** - fibrous connective tissue **tunica media** - smooth muscle - elastic fibres **tunica interna** - endothelial cells
37
blood vessels: general properties
structure and tissue content determines the vessel's function
38
arteries
distribution vessels **structure:** large diameter thin walls compared to diameter lots of elastic =\> easy to distend **blood characteristic****s:** very high blood pressure high blood flow low resistance, small drop in pressure **purpose:** "shock absorbers"
39
arterioles
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
relationship: pressure, blood flow & resistance
1. blood flows down a **pressure gradient** (high to low) 2. but **resistance** decreases flow blood flow = pressure gradient / resistance
41
resistance
**blood flow = (P1 - P2) x r4**
42
blood flow with resistance
total blood flow doesn't change with added resistance to an arteriole
43
capillaries
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
blood velocity & total cross-sectional area
more cross-sectional area = slower flow slower flow = maximize exchange
45
capillary structure: exchange vessels
in skin, muscles, lungs, CNS: **Not so permeable** in kidneys, intestines, some other tissues: **More permeable**
46
exchange by filtration and reabsorption
**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
hydrostatic pressures: Pc & PIF
**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
proteins influence exchange
movement of fluid due to proteins = osmotic pressures (Π)
49
osmotic pressures: Πc & ΠIF
1. capillary plasma osmotic pressure (Πc)(25 mmHg) 2. interstitial fluid osmotic pressure (ΠIF)(1-5 mmHg)
50
putting the starling forces together
51
net filtration pressure
Net filtration pressure = Kf [(PC + πIF) - (πC + PIF)] (OUT) (IN) Kf = filtration coefficient (larger = leakier capillary) positive number = filtration negative number = reabsorption
52
calculate net filtration pressure ## Footnote 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
Net filtration pressure = Kf [(PC + ΠIF) - (ΠC + PIF)] = 1[(35 + 2) - (25 + 3)] = 1[(37) - (28)] = +9 mmHg
53
veins
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
regulating blood flow
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
vasocontrict & vasodilate
vasoconstrict (less flow) vasodilate (more flow)
56
mechanisms used to regulate blood flow
1. local (intrinsic) tissue environment (temp, gases, pressure) 2. humoral (extrinsic) substances in blood 3. neural (extrinsic) nervous system
57
local (intrinsic)
tissue environment (temp, gases, pressure) autoregulatory mechanisms **1. Myogenic theory** muscle stretch **2. Metabolic theory** metabolic needs
58
myogenic theory
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
metabolic theory
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
hyperventilation
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
humoral (extrinsic)
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
neural (extrinsic)
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
cardiac output and blood pressure
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
adjusting Mean Arterial Pressure (MAP): Baroreceptor Reflex
**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
baroreceptors
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
what happens when MAP is too high?
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)