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Cardiology > Blood pressure and SVR > Flashcards

Blood pressure and SVR Flashcards

1
Q

What is the relationship between pressure and force?

A

Pressure = force/surface areaa

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2
Q

What is density

A

Mass/volume

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3
Q

What is the volume of a cylinder

A

pie x r^2 x height

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4
Q

What are the factors determining BP

A

Cardiac output
Peripheral vascular resistance
Total energy gradient of blood flow composed of
- Elastic energy
- potential energy
- Kinetic energy

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5
Q

Define mean arterial pressure

A

◦ Systolic blood pressure is the maximum arterial pressure
◦ Diastolic blood pressure is the minimum pressure
◦ Mean arterial pressure is the area under the pressure/time curve, divided by the cardiac cycle time

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6
Q

Define systolic BP

A

◦ Systolic blood pressure is the maximum arterial pressure
◦ Diastolic blood pressure is the minimum pressure
◦ Mean arterial pressure is the area under the pressure/time curve, divided by the cardiac cycle time

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7
Q

Define disastolic BP

A

◦ Systolic blood pressure is the maximum arterial pressure
◦ Diastolic blood pressure is the minimum pressure
◦ Mean arterial pressure is the area under the pressure/time curve, divided by the cardiac cycle time

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8
Q

What is the Bernoulli principle and how does it apply to arterial pressure?

A

Energy point A = Energy at point B
When you consider energy = static pressure + potential energy + kinetics energy

Potential energy = density x gravity x height

Kinetic energy = 1/2 density x V^2

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9
Q

What is the equation for kinetic energy in Bernoulli principles>

A

Kinetic energy = 1/2 density x V^2

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10
Q

What is potential energy according to Bernoulli?

A

Potential energy = density x gravity x height

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11
Q

What is static pressure according to Bernoulli

A

The pressure

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12
Q

How do you relate static pressure, kinetic and potential energy?

A

By Bernoulli’s prinicple

Energy = static + potential + kinetic

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13
Q

What are the assumptions of the Bernoulli principle 3

A

Incompressible fluid
Frictionless tube
Rigid tube

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14
Q

What is the elastic energy of circulation

A
  • Pressure generated by energy stored by the stroke volume through proximal arterial distension
    * Pressure generated by constant vascular smooth muscle tone
    * Reflected pressure wavesW
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15
Q

What determines the static pressure in the Bernoulli equation

A
  • Pressure generated by energy stored by the stroke volume through proximal arterial distension
    * Pressure generated by constant vascular smooth muscle tone
    * Reflected pressure waves
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16
Q

What is the purpose of potential energy in the Bernoulli equation when referring to blood pressure?

A

Potential energy due to gravity - difference in BP in different points of the circulatory system

182cm talll person with a MAP of 83 –> 171mmHg at feet and decreases to 39mmHG at the brain

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17
Q

Kinetic energy of blood is determined by? Of what level of importance is this to total energy?

A

1/2 x density x V^2

60cm/s x 70mL of blood will be a minimal value therefore kinetic energy is only 3% of energy at any one time

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18
Q

Drawing a pulse wave demonstrate effect of arterial stretch, augmentin BP, stored elastic energy and MSFP

A
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19
Q

How does compliance of arteries influence diastolic BP - draw a pulse wave to reflect this

A
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20
Q

Draw how aortic vs brachial vs dorsalis pedis BP varies

A
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21
Q

What is systolic BP determined by?

A
  1. Arterial elastance and compliance
  2. SV - in so far as it effects arterial compliance
  3. Total arterial peripheral resistance - 50% of SV is generally managed with stretch of the arteries and 50% displaces blood downstrem, this will determine that fraction
  4. Reflected waves
  5. Minimal from kinetic energy
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22
Q

What impact to reflected waves have on blood pressure? When are they useful? When are they counterproductive?

A

because BV are not infinitely elastic there is reflection of waves e.g. occluding femorals increases SBP by 10mmHg . In healthy ciruclation these waves a slow and augment diastolic BP and coronary filling but in diseased atheromatous circulation they are rapidly reflected contributing to afterload

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23
Q

What is the most important factor to SBP

A

Arterial compliance/elastance

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24
Q

What is the most important factor to diastolic BP

A

Arterial peripheral resistance as it finluences the rate of diastolic run off to peripher circulation

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25
Q

What factors influence diastolic BP

A
  1. Vascular resistance
  2. Arterial elastance and compliance determines how rapidly pressure is changes by as SV is lost –> 2x more prominent in diastole compared to systole
  3. Time constant of peripheral vessels
  4. Stroke volume - minimal relationship
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26
Q

What is equation for time constant?

A

compliance x resistance = time constant

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27
Q

What is the time constant refering to?

A

Time required to achieve 63% of new steady state after a step change in conditions

Refers to taking the tangent at time 0 when conditions are changed representing the rate of change and determines how long it would take to get to zero if this rate was continued. This ends up representing 0.63

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28
Q

What factors determine time constants?

A

compliance x resistance

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29
Q

Why is time contant relevant to BP

A

Helps explain diastolic BP as explained by peripheral vessels interaction between comlpiance and resistance

HR is a mjor important factor

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30
Q

Draw a pressure volume curve representing a 30 year old vs a 90 year old

A
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31
Q

What are the contributors to elastic energy in the arterial system

A
  • Elastance = resistance to stretch (pressure generated by a change in volume) - capicatance is the reverse
  • Factors contributing to this in circulation
    ◦ Constant pressure - tone in circulation (mean circulatory filling pressure)
    ◦ Distension of proximal arteries - elastic energy produces pressure in proximal vessels as they distend in systole
    ◦ Stored elastic pressure - following rapid ejection some of the energy in the proximal arteries is transmitted back to the blood volume - contributes to diastolic blood pressure
    ◦ Reflected pressure wave - reflects from branch points nad surfaces
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32
Q

Why do we use MAP as the pressure to target? 3

A
  1. Mean pressure in the cardiac cycle should bear the closest relationship to flow, even though flow and resistance are the independent variables
  2. The downstream pressure at target organs is the MAP, as blood flow is no longer pulsatile
  3. Resistant to confounders of measurement - under damping, over damping, NIBP oscillometry measurements, less affected by pulse wave amplification and vessel compliane

Even better it correlates with survival!

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33
Q

What is SVR

A
  • SVR is often calculated from the pressure difference between arterial and venous circulations (flow = pressure/resistance)
34
Q

Why is the concept of SVR using veinous resistance flawed?

A
  • SVR is often calculated from the pressure difference between arterial and venous circulations (flow = pressure/resistance)

However the actual site of pressure difference determining flow is in the small arteries which have a closing pressure due to the surrounding tissue pressure

35
Q

What is the closing pressure of small arteries?

A

the actual site of pressure difference determining flow is in the small arteries (20-200 microm diamtre) which have a closing pressure due to the surrounding tissue pressure

They act as Starling resistors

36
Q

What is true SVRI

A

700-1500 dyanes/sec/cm^5

37
Q

Where does maximal pressure drop occur in the arterial circulation

A

Arterioles 20-200 microm

Pressure drop from 100mmHg to 30mmHg

38
Q

What equation is commonly used in determining vascular resistance

A

Flow = Pressure/resistance

Resistance = pressure/flow

39
Q

What is vascular conductance

A

reciprocal of resistance

40
Q

What equation can be used to describe vascular resistance

A

Hagen Poiseuelle
◦ Factors which affect peripheral vascular resistance are the parameters of the Hagen-Poiseuille equation, which is R = (8 l η) / πr4, where:
‣ l = length of the vessel
‣ η = viscosity of the blood
‣ r = radius of the vessel

41
Q

How does viscocity change in vessel size? What is the effect called?

A

‣ Under condition of low shear stress viscoity increased; whereas blood under high shear stress in small vessles has markedly reduced viscocity i.e. non newtonian fluid (Fahreus Lindquist effect) and becomes non Newtonian in BV below 300 micrometers in diameter - as RBCs sit in the centre and don’t touch the sides and viscocity is decreased at the sides.

42
Q

How is viscocity related to vascular resistance? What factors need to be considered as affecting viscocity 4

A

‣ Under condition of low shear stress viscoity increased; whereas blood under high shear stress in small vessles has markedly reduced viscocity i.e. non newtonian fluid (Fahreus Lindquist effect) and becomes non Newtonian in BV below 300 micrometers in diameter - as RBCs sit in the centre and don’t touch the sides and viscocity is decreased at the sides.

Affected by vessel diamtre, haematocrit, lipid and protein content, temperature

43
Q

What affects viscocity of blood

A
  • Vessel diametre - decreases in small vessels
    * Haematocrit - increases viscocity
    * Lipid and protein content of blood - increase viscoity
    * Temperature - increases at low temperatures
44
Q

What is the most important factor affecting vascular resistance?

A

Vessel radius

45
Q

How would you divide the factors affecting vessel radius?

A
  1. Local
    - Myogenic
    - Humeral
    - Metabolic
    - Flow
    - Local control factors
  2. Systemic
    - Drugs
    - SNS/PSNS
    - Temperature
    - Chemo and baroreceptors
46
Q

What is the primary regulator of PVR

A

Baroreflex control

47
Q

Where is the primary site of peripheral vascular resistance? What capacity does this have to change? How quickly

A

◦ Arterioles with a radius <100 micrometres are muscular structures - their capacity for change in diametre can be up to 100% (i.e. complete occlusion) and can perform so rapidly i.e. 15 seconds

48
Q

What systemic factors regulate PVR

A

‣ Arterial baroreflex control (increased BP leads to a decrease in SVR) - the primary control
‣ Peripheral and central chemoreceptors (hypoxia leads to increased SVR and cardiac output e.g. hypertension in OSA)
‣ Pulmonary baroreceptors (hypoxia leads to increased SVR) - in the pulmonary arteries, stimulated by stretech and subsequently increase sympathetic acitivty causing higher peripheral vascular smooth muscle tone and increased cardiac output
‣ Hormones (eg. vasopressin and angiotensin)
‣ Temperature (hypothermia leads to increased SVR)

49
Q

How does myogenic autoregilation work

A

‣ Intrinsic myogenic regulation (in response to stretch) - increased pressure streches vascular smooth muscle - smooth muscle depolarises in response (mechanosensitive ion channel ? nobody knows) –> opens voltage gated calcium channels –> vasoconstriction via myosin light chain phorphorylation

50
Q

How does flow associated regulation work

A

‣ Flow- or shear-associated regulation (in response to increased local flow) - proximal vasodilation in response to distal vasodilation
* Local vasodilation in small distal arterioles result in increased flow to an rea
* Larger proximal arteriole experience an increase in flow producing increased shear stress on the wall sof the proximal arteriole
* Shear stress results in vasodilatory mediators from endothelium; Bernoulli principle states pressure drops in this circumstance
* Sluggish reflex taknig 30-40 seconds
‣ Conducted vasomotor responses from neighbouring vascular sites - electrotonic propogation of signals from smooth muscle cells

51
Q

Why is the Hagen Poiseuelle equation a flawed model of discussion PVR 4

A
  1. Blood is non Newtonian
  2. The vessels are distensable, and not always cylindrical, and length is difficult to measure
  3. Models constant flow and the flow is pulsatile
  4. Only works with laminar flow
52
Q

Using a diagram explain how resistance is related to blood flow

A
53
Q

What is a Wood unit

A

These describe the ratio of a driving pressure of 1 mmHg to a resultant flow of 1 L /min. These units are in mmHg⋅min⋅mL-1 and are still in use by the AHA

54
Q

What is the conversion factor for 1 wood unit to Dynes.s.cm-5

A

one wood unit = 80 dynes/s/cm^5

55
Q

What is normal pulse pressure variation

A

40mmHg

56
Q

What influences normal pulse pressure

A

◦ During systole, the height of the systolic peak is dependent on
‣ Arterial elastance and compliance (major influence)
‣ Stroke volume, insofar as it affects elastance and compliance
‣ Total arterial peripheral resistance
◦ During diastole, the depth of the diastolic trough is determined by:
‣ Total arterial peripheral resistance (major influence)
‣ Arterial elastance and compliance
‣ Time constant of the peripheral vessels (and therefore heart rate)

57
Q

What are the primary determinants of systolic BP

A

◦ During systole, the height of the systolic peak is dependent on
‣ Arterial elastance and compliance (major influence)
‣ Stroke volume, insofar as it affects elastance and compliance
‣ Total arterial peripheral resistance
◦ During diastole, the depth of the diastolic trough is determined by:
‣ Total arterial peripheral resistance (major influence)
‣ Arterial elastance and compliance
‣ Time constant of the peripheral vessels (and therefore heart rate)

58
Q

What are the primary determinants of diastolic BP

A

◦ During systole, the height of the systolic peak is dependent on
‣ Arterial elastance and compliance (major influence)
‣ Stroke volume, insofar as it affects elastance and compliance
‣ Total arterial peripheral resistance
◦ During diastole, the depth of the diastolic trough is determined by:
‣ Total arterial peripheral resistance (major influence)
‣ Arterial elastance and compliance
‣ Time constant of the peripheral vessels (and therefore heart rate)

59
Q

So what is the main determinants of pulse pressure

A

Stroke volume
Arterial compliance

Pulse pressure = stroke volume / compliance

60
Q

What is pulse pressure variability

A

Pulse pressure change over time

61
Q

Why does pulse pressure have any variation normally?

A

Respiratory pulse pressure variation due to intrathroacic pressure changes on preload and afterload

62
Q

Describe how spontaneous breathing affecting pulse pressure

A

‣ In spontaneous breathing - decreased intrathroacic pressure during inspiration increases pressure gradient increasing venous return –> increases LV stroke volume after pulmonary transit time of 2-3 seconds (during expiration) and increased SBP occurs during expiration. During expiration preload decreases and stroke volume decreases which is then seen in inspiration as a decrease in stroke volume

63
Q

Describe how pulse pressure variation is affected by positive pressure ventilation

A

‣ In positive pressure ventilation - increased intrathoracic pressure decreases venous pressure gradient driving venous return and SBP decreases later - during inspiration the reverse

64
Q

What is normal pulse pressure variation

A

<12%

65
Q

When considering pulse pressure variation what subdivisions are important to talk about

A
  1. Determinants - systolic BP determinants, diastolic BP determinants
  2. Normal values - 40mmHg
  3. Equation = SV/complaince
  4. Normal scenarios
    a) respiratory
    b) exercise and stress
    c) HR
    d) Stroke volume
  5. Abnormal scenarios
    - Shock
    - Wide and narrowed pulse ressure states
  6. Measurement
66
Q

What happens to blood pressure and pulse pressure in exercise?

A

‣ Increased sympathetic activity increases the stroke volume (contractility and cardiac output) and therrefore the systolic blood pressure - this increases the pulse pressure. Diastolic BP may even fall as decrease in peripheral vascular resistance with Beta 2 activation in muscle

67
Q

What effect does compliance have on pulse pressure variation

A

‣ As arterial compliance decreases, systolic pressure increases and diastolic pressure drops because of the steeper pressure-volume curve. DBP drops more than SBP rises (steeper pressure volume curve)

68
Q

What effect does heart rate have on pulse pressure variation

A

‣ With a slower heart rate, the diastolic pressure decline occurs over a longer time period, and is therefore deeper, and the diastolic filling is longer, resulting in a higher stroke volume and higher systolic pressure

69
Q

Pulse pressure vs site of measurement

A

‣ Distal pulse pressure amplification due to constructive interference of reflected waves increases the systolic and decreases the diastolic pressure in distal arteries

70
Q

Why might a pulse pressur be narrowed

A
  • Reduce stroke volume - cardiogenic shock, heart failure, aortic stenosis, cardiac tamponade, higher afterload
    * Increased arterial compliance - AV fistula
71
Q

Why might a pulse pressure be widened

A
  • Increased stroke volume
    ◦ Sepsis - early
    ◦ Beri Beri
    ◦ Thyrotoxicosis
    ◦ Anaphylaxis
    * Decreased arterial compliance
    ◦ Age related
    ◦ Atherosclerosis and PVD - icnreased distal pulse amplification
    ◦ Aortic aneurysm - failure of windkessel effect
    * Structural cardiac
    ◦ aortic regurgitation
72
Q

Pulse pressure variation in shock - how do you become more volume sensitive? How does cardiac tamponade affect pulse pressure

A

‣ In hypovolemia the pressure gradient for venous return becomes more sensitive to changes in intrathoracic pressure - decreased MSFP and RA pressure mean changes within the normal respiratory cycle may affect venous return
‣ In cardiac tamponade, changes in preload exaggerate the normal inspiratory drop in blood pressure through interventricular interdependence - inspiration increases RV filling and leftward bulge of septum decreasing LV stroke volume and exaggerates the normal inspiratory drop in BP known as pulsus paradoxus

73
Q

What is the lower limit of oxygen supply at peripheral tissues called

A

Pasteur point

74
Q

What is a valsalva manouvre and how is it performed clinicaly

A

Forced expiration against a closed airway

Mercury colum to produce a pressure of 40-50mmHg and hold it for 15 seconds

Rise in intrathoracic, intra-abdominla and CSF pressures

75
Q

What is the effect of Valsalva on CVP

A

rise by 7mmHg for each 10mmHg rise in mouth rpessure

76
Q

Describe phase 1 of Valsalva

A

Increased intrathoracic pressure is transmitted to aorta with a small rise in BP and brief fall in HR

Blood forced out of pulmonary circulation temporarily increasing SV

77
Q

Phase 2 of Valsalva

A

Raised intrathoracic pressure decreases venous return to the right heart and decreased cardiac output and BP

Fall in BP sensed by barorecpetors with reflex increased SNS< increased HR and peripheral vasoconstriction with restoration of BP

78
Q

Phase 3 of valsalva

A

Fall in intrathoracic presure witha loss of transmitted pressure to the aoerta

Re-expansion of pulmonary vessels and fall in storve volume

Transient fall in BP and rise in HR

79
Q

Phase 4 of Valsalva

A

Venous return and normal cardiac output restored

BV remain constricted so an overshoot of BP

Sensed by baroreceptors leading to reflex bradycardia

Relaxation of PVR restored BP

80
Q
A

Cardiology (9 decks)

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