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Physiology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the features of cardiac muscle?

A

Single nucleus
Striated
Branched
Intercalated discs
Gap junctions
Activated by pacemaker cells
Longer action potentials

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2
Q

What are the features of skeletal muscle?

A

Multinucleated
Striated
Unidirectional
Motor neurone innervation
Shorter action potential
Possibility of tetany

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3
Q

What are sarcomeres?

A

They are composed of actin and myosin which are aligned in bands and overrated by sarcoplasmic reticulum which forms a highly loaded Ca store

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4
Q

How is depolarisation carried down the membrane

A

Through t-tubules

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5
Q

How does calcium activate contraction?

A

It binds to troponin C and moves the tropomyosin molecule out of the myosin binding site on the actin fibre
Cross bridge cycling can then occur

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6
Q

What is diastole? What is systole?

A

Diastole - relaxation
Systole - contraction

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7
Q

What is preload? What is afterload?

A

Preload - wall tension at the end of diastole
Afterload - wall tension during systole

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8
Q

What doe Inotropic state mean?

A

Contractility of the heart independent of preload or afterload

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9
Q

What is the ejection fraction and how do you work it out?

A

Fraction of end-diastolic volume ejected by each systolic (55-75%)
EF = SV / end diastolic vol

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10
Q

How do you measure CO in humans?

A

Fick’s principle
Dye dilution
Thermodilution
Ultrasound/Doppler flow

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11
Q

What is fick’s principle?

A

The total uptake or release of a substance by the body is the product of the blood flow to the body multiplied by the difference in the content of the substance in the arterial and venous blood going to and returning from the body
VO2 = CO x (CaO2 - CvO2)

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12
Q

What are the pros and cons of ficks law?

A

Good for low COs
Fairly invasive
Tricuspid or pulmonary valve issues
Not very accurate or reliable

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13
Q

What is the dilution principle?

A

Flow of blood can be calculated when a measurable indicator substance is delivered upstream of the right ventricle, mixes with blood in the right ventricle and is remeasured in the pulmonary artery

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14
Q

How is the dilution principle carried out?

A

Dye injected into large vein
Dye passes through heart and lungs
Dye passed into arterial system
Maximal dye conc detected
Dyes starts 2nd pass - recirculation
Extrapolated return to zero (12s)

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15
Q

What are the pros and cons of the dilution principle?

A

Still relatively invasive
Depends on extrapolation of dye decay
Not all blood in right ventricle is ejected (over estimates CO)
Possible reactions to dye
Not useful if CO is low

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16
Q

Explain the use of thermodilution

A

Small volume of chilled saline solution in vein via a catheter in right atrium
Temperature gauge in pulmonary artery
Generates temp vs time curve similar to dilution but returns to zero as temperature equilibrates in 1 cycle

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17
Q

What are the pros and cons of thermodilution?

A

No extrapolation - more accurate
Less like hood of adverse reaction to saline
Invasive
Not suitable for low CO
Not suitable for patients with valve regurgitation

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18
Q

How does Doppler ultrasound work?

A

Two measurements needed:
- total blood viscosity in the left ventricular outflow tract
- estimated aortic cross sectional diameter

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19
Q

What equation is used when using Doppler ultrasound to check CO?

A

CO = pier2 x VTI x HR
VTI = velocity time integral

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20
Q

What are the pros and cons of using Doppler ultrasound?

A

Minimally invasive
Cheap
Relatively accurate
Shape of waveform allows for assessment of preload, contractility and afterload
An experienced operator is needed

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21
Q

What is the frank-starling mechanism?

A

Strength of ventricular contraction increased when the ventricle was stretched prior to contraction

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22
Q

What impact does muscle length have on the ability to contract?

A

The longer the muscle is (the more it’s stretched) the more myosin heads are displaced, further away from actin binding sites - cannot form cross bridges

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23
Q

What is the optimum range of diastolic pressure for the heart?

A

5-20cm/H2O

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24
Q

What influence does venous return have?

A

Increased venous return means increased stroke volume
Increased stroke volume means increased CO
Decreased venous return means decreased stroke volume
Which mean decreased CO

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25
Q

What effect does the change in blood volume have on CO

A

Increased blood volume - increased CO
Decreased blood volume - decreased CO

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26
Q

What pumps are present to shift blood around the body?

A

Thoracic pump
Abdominal pump
Muscle pump

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27
Q

What effects to veins have on compliance for the cardiovascular system?

A

When veins contract it lowers compliance and storage and so increases return
When veins are relaxed it increases compliance and storage meaning less return

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28
Q

What is venomotor tone?

A

Inverse of venous compliance
Increases the filling pressure, venous return and CO

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29
Q

What are the regulatory influences on CO?

A

Mechanical
- preload
- afterload

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30
Q

What are the factors influencing CO

A

Changes in total peripheral resistance
- shifts max CO but not mean central filling pressure
LaPlace’s law
- ventricular wall tension is proportional to the pressure times the radius divided by wall thickness for spheres or cylinders

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31
Q

What are the nervous and humoral influences on CO?

A

Chronotropic - enhance cardiac function by increasing heart rate
Inotropic- length independent activation of myocardial contractility

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32
Q

What are the effects of positive inotropes on stroke volume?

A

Increased contraction
Reduced afterload
Adrenaline

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33
Q

What are the effects of negative inotropes on stroke volume?

A

Decreased contractility
Increased afterload
Beta blockers

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34
Q

What can you see when you combine CO and SV curves?

A

The point at which the heart functions when healthy and at rest

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35
Q

What effects do metabolites have on CO?

A

Increase in metabolites
- vasodilation
- reduced TPR and afterload
- Chemoreceptors increase nervous activity

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36
Q

What effect does nervous activity have on CO?

A

Increased nervous activity
- increased sympathetic activity
- increased HR and inotropic effect
- decreased parasympathetic
- increased HR

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37
Q

What effect does muscle pump have on CO?

A

Increased muscle pump
Increased venous return
Increased stroke volume and preload

38
Q

How does pregnancy affect CO?

A

Changes in BP and volume and inotropic changes dues to hormones enhance CO and move steady state operating point up
Higher metabolic needs can be met

39
Q

What happens during cardio genic shock?

A

Impaired pumping ability of the left ventricle
Decreased CO
Decreased BP
Decreased tissue perfusion

40
Q

What happens during hypovolemic shock?

A

Decreased intravascular volume
Decreased venous return
Decreased ventricular filling
Decreased stroke volume
Decreased output
Inadequate tissue perfusion

41
Q

How do you measure ventricular stiffness?

A

EDPVR - end diastolic pressure volume relationship
The slope of EDPVR is the reciprocal of ventricular compliance and this is used

42
Q

What represents the inotropic state of the ventricle?

A

EPSVR - end systolic pressure volume relationship

43
Q

What effect does stiffness of the heart have?

A

The stiffer the heart the more the pressure rises

44
Q

What is isovolumetric contraction?

A

The pressure in the ventricle rises rapidly but the volume does not change
Just before the aortic valve opens

45
Q

What is arterial BP directly related to?

A

Cardiac output
Total peripheral resistance
BP = CO x TPR

46
Q

What does TPR depend on?

A

The contractile state of smooth muscle in the arterioles
Perfusion gradient
Level of vasodilation
Nervous inputs

47
Q

What does stroke volume depend on?

A

Contractile force of the left ventricle and venous return

48
Q

What does venous return depend on?

A

Pressure gradient
Thoracic pump
Abdominal pump
Muscle pump
Venomotor tone
Blood volume

49
Q

What does heart rate depend on?

A

SA node depolarisation rate
AV node conduction rate
Local stretch of right atrium
Nervous input

50
Q

What nervous reflex occurs with the respiratory centre?

A

During inspiration
- respiratory centre signal to the cardiac vagal centre
- vagal tone decreases
- HR increases

51
Q

What nervous reflex happens involving lung volume receptors?

A

During inspiration
- intrathoracic pressure decreases and lung volume receptors activate
- message sent to cardiac vagal centre
- vagal tone decreases
- HR increases

52
Q

What is the bainbridge reflex?

A

Stretch receptors in the junction of the right atrium and vena cava/luminary being and left atrium respond to changes in volume
Fibres in the vagus nerve signal to the medulla
Inhibition of the vagus outflow to SA node - increases HR

53
Q

What is baroreceptor reflex?

A

Sense stretch of blood vessel wall via activation of TRPC5 channels
Activate with each heart beat
Signal via vagal and glossopharyngeal afferents
To the medullary cardiac and vasomotor areas
Make changes appropriate to keep BP within normal range

54
Q

What innervation follows the baroreceptor reflex?

A

Increased BP decreases sympathetic outflow
-blood vessel constriction
Increased BP increases parasympathetic (vagal) outflow
- decreased HR
-blood vessel dilation
Decreased BP decreases parasympathetic outflow
- increased HR
- vasoconstriction

55
Q

Describe the diagram that describes nervous reflexes with breathing pattern

A

Inspiration
Respiratory centre (medulla)
Change in intrathroacic pressure (-)
- changes lung volume
- cardiac vagal centres (medulla)
Changes in venous return (-)
- bainbridge reflex
- cardiacs vagal centre (medulla)
Change in arterial pressure (+)
- barorecpetor reflex
- cardiac vagal centre (medulla)
Heart rate

56
Q

Describe what happens to the baroreceptor reflex with a decreases in BP

A

Decreased BP
Each heart beat activates much less afferent nervous signals
Low level of signally recognised by RVLM
Decreases vagus but increases sympathetic outflow
Increases heart rate
Increases contractility
Increases vasomotor tone

57
Q

What happens to the baroreceptor reflex when there’s an increase in BP?

A

Increased BP
Each heart beat activates many more afferent nervous signals
Higher levels of signals recognised by RVLM
Increased vagus but decreased sympathetic outflow
Decreased heart rate
Decreased contractility
Decreased vasomotor tone

58
Q

What effect does BP have ADH releases?

A

Normal or increased BP inhibits supraoptic and paraventricular dependent release of ADH
Less water reabsorption

59
Q

Describe the relationship between renin and blood pressure

A

Juxtaglomerular cells are sensitive to BP via TRPV4
Increased afferent arteriole pressure activates TRPV4
Ca2+ influx inhibits adenylate Cyclades V
Decreases in cAMP production reduces renin release from JG cells
Reduced afferent arteriole pressure reduces the activation of TRPV4
Increases renin release

60
Q

When is atrial natriuretic peptide released?

A

Released by atrial myocytes in response to atrial distension

61
Q

What does atrial natriuretic peptide do?

A

Systemic vasodilation
Improve GFR
improve filtration fraction
Inhibit renin release
Decreases circulating angio ll and aldosterone
Natriuresis and diuresis
Decreased blood volume, atrial pressure, central venous pressure and cardiac output

62
Q

What is hypopnea?

A

Excessively shallow/rapid breathing

63
Q

What is bradycardia?

A

Abnormally low resting HR

64
Q

What is tachycardia?

A

Abnormally high resting HR

65
Q

What is the bezold jarisch reflex?

A

Pressure receptors in the left ventricle wall and trabeculae sense underfilling
Activate C fibre afferent nerves
Trigger paradoxical bradycardia
Decreased contractility
Decreased atrial hypotension
After prolonged standing certain chemicals (capsaicin) may contribute to post infarct pathology

66
Q

What is cushings reflex?

A

Cerebral ischaemic reflex
Compressive ischeamia of CNS
Increased BP
Initial tachycardia followed by bradycardia
Followed by irregular breathing
Increased pressure on brain stem

67
Q

What is the chemoreceptor reflex?

A

Carotid bodies (peripheral receptors)
Sense decreased pO2, pH, increased pCO2
Signals to NTS and RVLM
Increased sympathetic outflow
Vasoconstriction
Decreased vagal nerve outflow
Increased HR, CO, BP
Increased blood flow to lungs
Increased respiratory rate

68
Q

What is the basal a manoeuvre?

A

Increases intrathoracic pressure
1)Onset
2)Decreased venous return
3)Relaxation
4)Decreases BP

69
Q

What happens during the valsava manoeuvre?

A

Onset
- increased intrathoracic pressure
- increases BP
- increases vagal outflow
- decreased HR
- bainbridge reflex also decreases HR
Decreased venous return
- decreased EF
- decreased vagal activity
- Increased sympathetic, increased HR and TPR
-Cushing reflex
- HR roses then falls
Relaxation
- decreased intrathoracic pressure
- increased venous return
- rebound HR
Decreased BP
- barorecptors off
- increased TPR and VR
- increased EF
- increased BP
-eventually normal BP and HR

70
Q

Why is the inside of cells negative?

A

Selectively permeable membrane
Channels move 3 Na+ out for every 2 K+ in
Also negative proteins and acids are trapped inside the cell

71
Q

What is the Nernst equation!

A

Ex = (RT/zF) ln(Xout/Xin)
Ex - equilibrium potential
R - ideal gas constant
Z - charge of ion X
F - faradays constant

72
Q

What RT is used for the Nernst equation at different temperatures?

A

At 37 Celsius - 62
At 21 Celsius - 58

73
Q

What is the Goldman Hodgkin equilibrium equation?

A

RMP = (RT/F) ln(Xout/Xin)

74
Q

What prevents summation happening in cardiac muscle?

A

Long AP
Long refractory period
Relaxation is complete before a new AP is generated

75
Q

What are the five stages of AP in the ventricles?

A

Upstroke
Early depolarisation
Plateau
Late repolarisation
Resting

76
Q

What happens during the upstroke of ventricular APs?

A

Fast Na+ channels open
Rapid depolarisation
Short lived
Ca2+ channels also start activating

77
Q

What happens during early repolarisation in ventricular APs?

A

Voltage activated K+ channels open
K moves out
Short lived as coupled to closure of Na+ channels

78
Q

What happens during the plateau of ventricular APs?

A

Small number of Na+ channels remain open
Ca2+ remain open, little activity though
Only Kv7.1 channels to oppose Na and Ca dependent depolarisation

79
Q

What happens during late repolarisation in Ventricular APs?

A

All Na channels closed
Ca channels closed
hERG channels activate
Hyperpolarisation

80
Q

What happens during the testing stage of ventricular APs?

A

Kir remain active
Keeps cell hyperpolarised
Small leaks of Ca and Na into the cell bring the resting membrane potential back

81
Q

How are AP spread through cardiac muscle?

A

Through gap junctions

82
Q

What happens during SA node electrical activity?

A

Threshold for L type Ca2+ channels is reached
Channels open depolarisation occurs
K+ channels open and repolarisation happens
Slow depolarisation due to If
Hyperpolarised activated HCN channels
T type Ca2+ channels open and continue slow depolarisation

83
Q

What happens to APs in ischaemic heart tissue?

A

Significant disruption of normal signals and loss of co-ordinated electrical signals and contraction
Think it is equals ventricular fibrillation

84
Q

Describe what happens during the P QRS T graph of electrical activity

A

P/R - depolarisation travelling toward electrode (+ve deflection)
Q/S - depolarisation travelling away from an electrode (-ve deflection)
Repolarisation travelling toward an electrode (-ve deflection)
T - repolarisation travelling away from an electrode (+ve deflection)

85
Q

What is primary AV block?

A

PR interval is abnormally long

86
Q

What is secondary AV bloc?

A

Occasional QRS complexes missing after P waves

87
Q

What is tertiary AV block?

A

Total heart block
P waves and QRS complexes not sequential

88
Q

What is atrial fibrillation?

A

A re-entrant arrhythmia sustained by circuits propagating in remodelled atrial tissue

89
Q

What is ventricular fibrillation?

A

Alterations in ion channel function or expression can disrupt the morphology of the AP waveform
Ultimately leads to abnormal propagation of the hearts electrical impulse and arrhythmia

90
Q

What is the RVLM?

A

A region of the ventral brain stem that is responsible for both resting levels and reflex regulation of sympathetic outflow

Physiology (9 decks)

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