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Primary Physiology > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

Is cardiac muscle striated muscle? How does its cells microscopic structure compare to skeletal muscle?

A

Yes
Myofibrils identical to skeletal muscle with same banding and mechanism
Same sarcolemma with t tubules at the z lines, sarcoplasmic reticulum surrounds in similar manner.

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2
Q

Differences between cardiac and skeletal muscle cellular layout
What is the functional implication

A

Individual cells are tightly coupled mechanically and electrically by branching and interdigitation of the cells and intercalated discs forming membrane junctions.

Functionally means cardiac contraction is all or nothing

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3
Q

What is the term for a single cell containing several nucli
Is cardiac muscle true one

A

Syncitium
No - though cells all interconnected each cell has a single nucleus and is surrounded by the sarcolemma

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4
Q

AP function of cardiac muscle and difference to skeletal

A

Allows rapid low resistance conduction of AP along length of cells
Easy transmission between cells through intercalated discs

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5
Q

What are intercalated discs

A

Gap junctions - open channels connecting cytoplasm of adjacent cells

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6
Q

How does cardiac muscle mitochondria and capillary supply compare with skeletal muscle?

A

Higher in both

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7
Q

Events in cardiac muscle post initiation of action potential?

A

Calcium ingress through voltage sensitive Ca channels
Raising calcium causes release of Ca from sarcoplasmic reticulum
Ca binds to trop C and results in movement of tropomyosin exposing binding sites on actin
Myosin heads attach and move
Atp binds causing release of head then is hydrolysed to adp and pi resetting the system.
Calcium released and returned to sarcoplasmic reticulum by calcium magnesium ATPase

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8
Q

Types of action potential in cardiac muscle? Tissues associated.

A

Fast response - contractile myocardial cells and conduction system cells
Slow response - SA and AV nodal cells

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9
Q

What is the term for the spontaneous depolarisation of cardiac pacemaker cells

A

Automaticity

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10
Q

Phases of a fast response cardiac action potential (overview )

A

0 - rapid depolarisation
1 - early rapid repolarisation
2 - prolonged plateau
3 - final rapid repolarisation
4 - resting membrane potential

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11
Q

Resting membrane potential of fast response cardiac muscle cells

A

-90mV

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12
Q

How is the cardiac cell fast response negative membrane potential maintained?

A

Retention of anions (such as proteins, sulphites, phosphates) in cell but facilitation of cations to leave (permeable to K which diffuses down concentration gradient to leave cell until equilibrium reached between the concentration gradient and electrostatic attraction then Na/KATPase pumps return K and exchange Na out).

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13
Q

What is the Nernst equation?

A

E = (RT/FZ) x log10 ([Ke]/[Ki])
Membrane potential = (gas constant x absolute temp)/(fariday constant x valency) x log10 (external concentration/internal concentration)
Can be dervived to
E = 62/z x log10 ([Ke]/[Ki])

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14
Q

Given internal concentration of K is 150 and external is 5 what is the membrane potential it exerts over the membrane of a cardiac muscle cell

A

E = 62/1 x log10 (5/150)
= -94

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15
Q

Why is k the main determinant of cardiac muscle cell resting potential?

A

Permiable to k
Not to Na so leakage of this is small making little difference to the potential (around 4mV move +ve)

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16
Q

How is phase 0 initiated in cardiac fast response action potential

A

Resting membrane potential increased by electrical stimulus (less negative)
Reaches threshold potential
Fast sodium channels open and potassium channels close
Rapid influx of Na down concentration gradient and towards electrostatic attraction of intracellular anions
Cell interior reaches membrane potential of +20 and sodium channels close

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17
Q

Mechanism of phase 1 of cardiac fast cell action potential

A

Brief fall in membrane potential from +20 towards 0
Caused by potassium flow out of cell down electrical and chemical gradients
Opening of slow L-type ca channels providing prolonged influx of Ca ions maintaining +ve intracellular charge. Chloride also follows Na back into cell.

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18
Q

Mechanism of stage 2 of cardiac fast action potential

A

Continued influx of Ca through slow l-type ca channels balancing the efflux of potassium, membrane potential maintained around zero or slightly positive.

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19
Q

Mechanism of stage 3 of fast action cardiac action potential

A

Rapid increase in potassium permeability
Transmembrane potential restored to -90
Though potential is back to baseline the ionic gradients are not yet reestablished.

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20
Q

Mechanism of stage 4 of fast cardiac action potential

A

ATPase ion pumps exchange na and k restoring ionic gradients back to resting membrane potential.

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21
Q

How do atrial myocytes differ from ventricular myocytes in their fast action potentials

A

Shorter plateau phase (phase 2) due to much greater early repolarisation current

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22
Q

What controls excitability of cardiac cells?
How can it be influenced?

A

The difference between resting membrane potential and threshold potential (bigger difference means less excitable)
Influenced by various factors including catecholamines, beta blockers, local anaesthetics, electrolyte levels.

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23
Q

What is the refractory period of a fast response cardiac action potential

A

Absolute refractory period - The cell cannot be depolarised again during phase 0,1,2 and early stage 3 regardless of stimulus strength as the sodium and ca channels are inactivated
Relative refractory period - during latter part of stage 3 and early stage 4 a stronger than normal impulse can trigger an early AP

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24
Q

Term for combined absolute and relative refractory period

A

Effective refractory period

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25
Q

What can trigger depolarisation/automaticity outside of the normal pacemaker system

A

Injury can trigger spontaneous depolarisation of normal myocytes

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26
Q

Where are pacemaker cells found in the heart?

A

SA, AV, his-purkinje system,
Latent pacemaker cells in other parts of conduction system that can take over if AV blocked.

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27
Q

Phases of cardiac slow response action potential

A

4 - restoration of ionic gradients
0 - rapid depolarisation
3 - repolarisaiton

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28
Q

During phase 4 of a slow response cardiac action potential what occurs

A

No resting potential!
Depolarise spontaneously because of increased membrane permeability to cations allowing Na and Ca to leak into cell counteracting and overcoming slow loss of K
Membrane potential gradually increases from maximum diastolic potential of -60mV to threshold potential of -40mV

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29
Q

Mechanism of phase 0 of slow response cardiac action potentials
How does it compare to phase 0 of rapid response cardiac cells

A

Rapid depolarisation on reaching threshold potential due to opening of t-type calcium (t for transient) channels and influx of calcium
Slower influx than the rapid sodium influx in rapid response cells so slope of phase 0 less steep, and less overall change due to less negative starting membrane potential.

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30
Q

Mechanism of phase 3 cardiac slow response action potential.

A

Equivalent to phase 3 in rapid response - influx of K causing repolarisation
The phase 1 is absent and phase 2 is very brief so no plateau

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31
Q

Differences between pacemaker and myocardial cell AP

A

Less negative phase 4 membrane potential
Less negative threshold potential
Spontaneous depolarisation of phase 4
Less steep slope in phase 0
Absence of phase 1/2 plateau

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32
Q

What ion channels and current are responsible for the pacemaker potential
What can influence this

A

Leaking sodium channels that open when membrane hyperpolarised
Cause an inward current (If) causing depolarisation

Influenced by autonomic nervous system and various drugs

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33
Q

How can pacemaker discharge rate be altered in myocytes

A

Altering slope of phase 4 (increased slope discharges faster)
Altering threshold potential
Altering hyperpolarisation potential - if membrane reaches more negative value then will take longer to reach threshold

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34
Q

What drugs cause less negative threshold potential in cardiac pacemaker cells

A

Quinidine
Procainamide

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35
Q

What effect does high acetylcholine levels have on cardiac slow response pacemaker discharge rate

A

Hyperpolarisation thus slower to reach threshold potential

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36
Q

Rate of sinoatrial node pacemaker resting rate

A

60-100/min

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37
Q

Location of SA node
Blood supply

A

RA posterior wall close to entry of SVC (just below and lateral)
Branch of RCA

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38
Q

What pathways connect SA to AV node

A

Bachmann, Wenckebach, Thorel (anterior, middle, posterior).

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39
Q

Location of AV node
Blood supply

A

posterior right atrium near interatrial septum near coronary sinus opening
Usually rca

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40
Q

Length of delay at AV node
Purposes

A

0.13seconds
Allows atrial activation prior to ventricular activation

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41
Q

Where do the bundle branches run? What does the left bundle divide into?

A

subendocardially down the septum
Anterior and posterior fascicles

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42
Q

How does action potential and contraction spread through the heart wall
What about repolarisation

A

From the endocardium spreading outwards and apex to base
Repolarisation spreads from outside in.

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43
Q

Factors influencing QRS amplitude

A

Myocardial mass
Cardiac axis
Anatomical orientation of heart
Distance from heart to sensing electrode

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44
Q

Typical QT interval

A

350ms

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45
Q

Bazett’s formula to calculate QTc

A

QTc = QT/square root R-R

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46
Q

When does ventricular contraction end on an ECG

A

End of T wave (end of repolarisation)

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47
Q

What is the u wave on the ecg?

A

Uncertain but maybe slow repolarisation of papillary muscles

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48
Q

What is the cardiac axis of the heart?
What is the rough normal direction

A

The maximum vector of electrical activity produced during ventricular depolarisation
Down and left

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49
Q

How do ECG leads detect a potential difference

A

Either between 2 electrodes or 1 electrode and a common point

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50
Q

What are the groupings of ecg leads (views)

A

Frontal plane leads:
Standard I, II, III
Unipolar limb leads avR, avL, avF

Horizontal plane leads
V1-6

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51
Q

How are the standard limb leads set up and how do they work

A

Record between 2 active electrodes
Record around the sides of Einthovens triangle
Lead I negative right arm, positive left arm
Lead II negative right arm positive left foot
Lead III negative left arm, positive left foot

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52
Q

Characteristics of normal standard limb lead ecg trace

A

Very similar - all positive p, qrs and t waves

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53
Q

Characteristics of the unipolar limb leads

A

Record difference in potential between single limb lead and an indifferent (zero potential) electrode centre of einhovens triangle
Low amplitude signals so need amplification
aVR - upper right unipolar arm electrode to indifferent electrode - usually negative waves
aVL - upper left unipolar arm electrode to indifferent electrode
aVF - left leg unipolar electrode to indifferent electrode

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54
Q

How does the ecg calculate the indifferent electrode for analysis of the unipolar limb leads

A

Combining the activity of the 2 electrodes that are not active (e.g. for aVF left foot as active and combining left and right arm to make indifferent

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55
Q

Locations of the chest electrodes on ecg

A

V1 fourth ics right of sternum
V2 fourth ics left of sternum
V3 halfway between v2 and v4
V4 fifth ics midclavicular line
V5 fifth ics anterior axillary line
V6 fifth ics mid axillary line

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56
Q

Normal anatomical orientation of heart

A

Atria posterior
Ventricles anterior/basal with right ventricle anteriolateral to left

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57
Q

What muscle masses predominate on ecg trace

A

Interventricular septum and left ventricle free wall

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58
Q

Method to calculate heart rate from ECG

A

Interval in seconds between r waves and dividing 60 by that number
Number of r waves in a 6 second trace and x10

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59
Q

Usual paper speed and square sizes on ecg

A

Usually 2.5cm/sec
Thus each large square (5mm) represents 200ms and each small square (1mm) 40ms

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60
Q

Normal range for cardiac axis

A

0 to 90o

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61
Q

Calculation of cardiac axis from ecg (mathematical and why)

A

Lead one reads directly left to right (0o)
Lead aVF reads directly top to bottom (90o)
Determine amplitude of qrs in both (subtract hight of s wave from hint of r wave)
Tan(angle ) = amplitude aVF/amplitude I
Angle = tan-1 amplitude aVF/amplitude I

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62
Q

At what angles do leads I, II, III and aVF run at?

A

0
60
120
90

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63
Q

What are left and right axis deviation

A

Left axis <0o
Right axis >90o

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64
Q

What leads are typically used interop for ecg monitoring?
Why

A

sII and V5
II best for p waves
V5 best for monitoring ST changes

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65
Q

In a healthy young person what happens to heart rate with inspiration and expiration
Why

A

Increases on inspiration
Decreases on expiration

Breath in stretch lungs, vagaries stimulation, inhibits cardio inhibitory centre in medulla stimulating SA node

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66
Q

Causes of sinus Bradycardia

A

Young and fit
Sleeping
Beta blockers, anaesthetics, digitalis, limiting calcium channel blockers
Myxodeaema
Uraemia
Glaucoma
Increases icp

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67
Q

Causes of sinus tachycardia

A

Hypovolaemia
Anxiety
Pain
Thyrotoxicosis
Toxaemia
Cardiac failure
Drugs

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68
Q

At what heart rate is ventricular filling impaired?

A

140

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69
Q

Effect of high and low k on ecg (pathology and signs)

A

Hyperkalaemia - less negative resting potential closer to threshold - initially more excitable with risk of vt and vf but then reduction in rapid depolarsiation and loss of plateau giving poor contraction. When rmp comes close to tp heart stops in ventricular diastole.
Short qt, narrow peaked ts, widened qrs, pr prolongation then loss of p waves, then sine wave.

Hypokalaemia - more negative rmp, less excitable heart but increased automaticity
Prolonged pr, flat t wave, u wave, qt prolonged, progressing to twi and st depression

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70
Q

Effect of high and low calcium on ecg

A

Low calcium - flat prolonged st segment and qt interval, risk of pvcs and vt

High calcium - makes tp less negative, decreases conduction velocity and shortens refractory period. In very high concentrations can cause calcium rigor . Produces prolonged pr, wide qrs, short qt, broad t.

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71
Q

Effects of hypomagnesaemia on ecg

A

Promotes cell membrane depolarisation and tachyarrhythmias
Low voltage p waves and qrs complexes, prominent u waves peaked t waves

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72
Q

Effects of hypermagnesaemia on ecg

A

Delayed av conduction, prolonged pr and wide qrs and t wave elevation

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73
Q

Effects of hyponatraemia on ecg

A

Low voltage ecg complexes

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74
Q

How will acidosis and alkalosis effect ecg

A

Produce same ecg changes as hyperkalaemia and hypokalaemia respectively.

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75
Q

How does systemic vascular resistance compare to pulmonary vascular resistance?

A

Roughly 5-7 times greater

76
Q

Where does blood return to right atria from

A

Ivc svc and cardiac circulation

77
Q

When does coronary perfusion of the lv/rv occur

A

Lv mainly during diastole
Rv during both systole and diastole

78
Q

Phases of systole

A

Isovolumetric ventricular contraction
Ventricular ejection

79
Q

Opening pressure of aortic valve
Max pressure in lv usually

A

80mmHg
120mmHg

80
Q

Why does the pressure gradient reverse between the LV and aorta

A

LV pressure falls, aortic pressure maintained by momentum of last bit of ejected blood

81
Q

What is the dicrotic notch on an arterial trace?
What about the following dicrotic wave

A

Closure of aortic valve and isovolumetric relaxation of lv
The wave is caused by elastic recoil of artery against closed aortic valve

82
Q

What is typical end systolic lv volume

A

40-50ml

83
Q

Usual max rv pressure

A

20-24mmHg

84
Q

Significance of a low dicrotic notch on art trace

A

Suggests vasodilation as pressure gradient to close aortic valve occurring later in the cardiac cycle.

85
Q

Stages of diastole

A

Isovolumetric relaxation
Opening of mitral valve
Rapid ventricular filling
Passive ventricular filling (diastasis)
Atrial contraction

86
Q

What is the relative contributions of rapid+passive ventricular filling and atrial contraction to left ventricular end diastolic volume

A

75 and 25% respectively

87
Q

Typical End diastolic lv volume

A

120ml

88
Q

What is the usual gradient between lv and aortic pressures during ejection phase of systole?

A

1-2mmHg

89
Q

When is the RA filled during the cardiac cycle

A

Continuous

90
Q

What are LA and RA pressures caused by passive filling?
How do they change in diastole

A

Left 2-5mmHg
Right 0-2 mmHg
Mimic ventricular pressure in diastole as valve open

91
Q

What are the atrial pressure waves?
When do they occur?

A

A - atrial contraction, immediately prior to systole
C - av valve bulging back into atria on contraction of ventricle
V - slow filling of atria against closed av valve causing back pressure to build

92
Q

Why is myocardial relaxation considered an active process
What is the term for this phase? What influences it?

A

Active reuptake of calcium into SR
Lusitrophy
Influenced by increased catecholamine levels allowing heart to relax more quickly

93
Q

What is the effect of incomplete reuptake of calcium into the sarcoplasmic reticulum

A

Diastolic dysfunction.

94
Q

As heart rate increases what part of the cardiac cycle shortens first

A

Diastasis

95
Q

What occurs to ventricular filling when hr reaches 140

A

Impacts on rapid filling phase compromising filling and thus stroke volume

96
Q

What would cause the atrial phase of filing to be of greater importance

A

Myocardial ischaemia
Ventricular hypertrophy

97
Q

What are the functions of chordae tendonae and papillary muscles

A

To prevent excessive bulging of AV valves during systole and pull base of heart towards apex

98
Q

Normal aortic valve area
Mitral

A

2.6 to 3.5cm2
4-6cm2

99
Q

Which valves have higher blood velocity and why

A

Semilunar valves - smaller area

100
Q

What is the effect of severe aortic (70% reduction to 0.8cm2) stenosis on pressure gradient across valve

A

Increases markedly to >50mmHg

101
Q

What contracts first, RA or LA
RV or LV

A

RA
LV

102
Q

Which ventricle starts ejecting blood first

A

Rv - despite later start much lower pressure to overcome

103
Q

What causes the heart sounds

A

Closure of valves causing vibration in ventricular walls and valve leaflets + turbulence in interrupted blood flow

104
Q

Valves causing S1 heart sound

A

AV closure

105
Q

Why would S1 heart sound be split

A

Mitral closes 10-30ms before tricuspid

106
Q

What corresponds to s2 heart sound

A

Closure of SL valves

107
Q

Which SL valve closes first

A

Aortic during inspiration due to increased venous return delaying RV ejection
Simultaneous during expiration

108
Q

Cause of third heart sound
When is it heard

A

Heart failure due to rapid filling of dilated non compliant ventricle
Mid diastole (between s2 and s1

109
Q

Cause of fourth heart sound
When heard

A

Conditions that cause stronger atrial contraction to assist filling ventricles
Immediately before S1

110
Q

Why do you get heart murmurs
.

A

Blood flow usually laminar up to critical velocity
When valve narrowed velocity increases and exceeds critical velocity so turbulent flow and
murmur. When valve incompetent blood leaks backward in turbulent regurgitation

111
Q

Cause of cannon a wave

A

Atrial contraction against closed av valve
Eg in heart block

112
Q

What are the x and y descents on a cvp waveform

A

X - fall in rv pressure when pulmonary valve opens (ventricle moves down decreasing pressure on RA
Y - drop in atrial pressure when av valve opens

113
Q

Factors that would increase cvp

A

Cardiac failure
Volume overload
Pericardial tamponade

114
Q

Factors that would reduce cvp

A

Low inter vascular volume

115
Q

Effect of bradycardia on cvp waveform

A

More distinct waves

116
Q

Effect of tachycardia on cvp waveform

A

Fusion of c and a waves

117
Q

Differentiate av junctional rhythm and complete heart block by appearance of jvp waveform

A

Av junctional gives regular cannon a waves
Chb gives irregular cannon a waves

118
Q

Effect of tricuspid regurgitation on jvp waveform

A

Loss of c wave and x decent - becomes massive cv wave
Prominent v waves

119
Q

What is represented by the area within the loop of a lv volume vs pressure graph

A

Stroke work

120
Q

How would an end diastolic pressure volume relationship vary between a compliant heart and a heart with diastolic dysfunction

A

Compliant heart roughly linear relationship (as volume increases pressure increases gradually and linearly
In diastolic dysfunction the gradient is steeper (same change in volume is a greater change in pressure) and sudden increase in pressure with little volume change past a certain point.

121
Q

What effects the gradient of an end systolic pressure volume relationship

A

Contractility - steeper in more contractile heart, less steep in lower contractile heart

122
Q

What are the axis of a frank curve,
What does it address?

A

X - initial length
Y - tension
The tension of an individual muscle fibre based on initial length
Tension increases with length, initially linearly, then less effect, before shifting to decreasing tension past a certain point.

123
Q

How can a frank curve be applied to cardiac muscle as a whole
(Starling curve)

A

The principle can be applied to the entire wall, with tension related to end diastolic volume (representing stretch or length) - increased end diastolic volume causes increased stroke volume until a point then reduces

124
Q

What is the frank starling curve

A

Relationship between stroke volume and ventricular end diastolic volume

125
Q

What causes a raised frank starling curve (higher SV for given ventricular end diastolic volume? Lower

A

Higher - increased contractility - positive inotropy eg adrenaline
Lower - decreased contractility - negative inotropy eg acidosis, beta blockers, hypoxia

126
Q

Would a normal ventricle ever enter the decending limb of the frank starling curve
Wh?

A

No
Decreased compliance with increased stretch limiting max length even at very high pressures.

127
Q

Define stroke volume

A

Volume of blood ejected from ventricle in single contraction
EDV - ESV

128
Q

What is stroke index?
Normal value?

A

Stroke volume / body surface area
In a 70kg person 30-65ml/beat/m^2

129
Q

What is ejection fraction

A

Stroke volume as percentage of EDV
ie ((EDV-ESV)/EDV) * 100

130
Q

Gold standard methods for measuring stroke volume

A

Ventriculography
Cardiac Ct
mri
Radionuculotide scans

131
Q

Practical methods of estimating stroke volume

A

Echocardiography (TOE much more accurate)
Thoracic impedance

132
Q

How does thoracic impedance measure stroke volume

A

Measure changes in electrical impedance around neck and lower thorax
Very inconsistent and innacurate

133
Q

What is cardiac index

A

Cardiac output divided by Body surface area

134
Q

Average cardiac output and cardiac index for 70kg person

A

5-6 litres/min
3-3.5 litres/min/m^2

135
Q

Methods of clincially measuring cardiac output

A

Pulmonary artery catheter (swan ganz)
LiDCO
PiCCO
Pulse contour CO vigileo
Oesophageal doppler

136
Q

How does a pulmonary artery catheter measure cardiac output?

A

Thermodilution
Cold saline into RA and change in blood temp measured in pulmonary artery

137
Q

Using a pulmonary artery catheter and thermodilution how is cardiac output calculated

A

Stewart Hamilton equation
Inverse proportionality to area under temperature time curve

138
Q

What is the Steward Hamilton equation

A

Means of calculating cardiac output by thermodilution

CO = vol of injectable (initial blood temp - injectate temp) x constants. / integral of blood temp change

139
Q

Advantages of co monitoring by swan ganz catheter

A

Can keep running pressure measurements
Can measure PA pressures and PACWP too.
Can by used with intraaortic balloon pump
Little systemic heat dissipation
“Gold standard”

140
Q

Disadvantages of swan ganz catheter for CO measurements

A

Invasive
Risk of heart and vessel injury
Catheter can migrate
No obvious outcome benefit
Not continuous

141
Q

Effects on accuracy of pulmonary artery catheter thermodilution CO measurements

A

Shunts
Tricuspid regurgitation
Positive pressure ventilation

142
Q

How does LiDCO work to measure CO

A

Lithium chloride bolus into CVP and then sample arterial blood
Once calibrated with above can use arterial waveform to continuously give CO

143
Q

Advantages of LiDCO in CO monitoring

A

No heat dissipation errors
Can be done with routine central and arterial lines
Continuously monitors

144
Q

Disadvantages of LiDCO in CO monitoring

A

Needs 24hrly calibration
No PA pressures
Can’t be used if IABP in situ
Can’t be used in patients on lithium Tx

145
Q

How does PiCCO work to measure CO

A

Cold saline into CVP line
Thermistor detects in a femoral a line
Once calibrated continuous art line analysis for CO

146
Q

Advantages of PiCCO for CO monitoring

A

Continuous
Can use art line for blood sampling as well

147
Q

Disadvantages of PiCCO for CO monitoring

A

Errors due to heat dissipation
Arterial line has to be femoral

148
Q

How does pulse contour CO vigileo work to measure CO

A

Analysis of waveform on art line and use of demographic data to estimate

149
Q

What are the advantages of pulse contour CO vigileo

A

Uses standard art line
No calibration needed

150
Q

What are disadvantages of pulse contour CO vigileo

A

Uses extrapolation from patient demographic data
Depends on a line trace quality
No use if IABP in situ

151
Q

How does Doppler measure CO

A

Oesophageal or sternal notch probe
Uses Doppler signal of blood flow in aorta and patient demographics to calculate Co

152
Q

Advantages of Doppler to calculate CO

A

Does not require vascular access
Does not require calibration

153
Q

Disadvantages of Doppler in Co monitoring

A

Consistency depends on trace
Cannot be used with IABP

154
Q

What is Ficks principle? How can it be applied to cardiac output monitoring?
Issues

A

The amount of substance taken up by an organ (or body) per time is equal to arterial concentration minus the venous concentration multiplied by the blood flow.

By applying Ficks principle to oxygen concentration at a steady state cardiac output can be derived by VO2/(CaO2 -CvO2)
Oxygen uptake in the lungs over 1 min / (arterial oxygen content - venous oxygen content)

Issues are with accurate monitoring and maintaining steady state.

155
Q

How does a Doppler measure cardiac output

A

Measures velocity of blood flow through aorta, heart rate, cross sectional area, velocity-time integral and a constant to calculate output

156
Q

Main factors that determine stroke volume?

A

Preload
After load
Contractility

157
Q

What is the definition of preload?
How can it be practically conceptualised and measured?

A

Presystolic length of cardiac muscle fibres
Practically considered the filling pressures of the ventricles and end diastolic volume
Practically approximated with CVP or PCWP

158
Q

What factors effect preload?

A

Blood volume
Body position
Intrathrocaic and intrapericardial pressures
Venous tone and compliance
Pumping action of skeletal muscle
Ventricular compliance
Synchronous atrial contribution to ventricular filling

159
Q

How is the conceptual preload measured practically

A

Can’t measure EDV so measure end diastolic pressure - this has a linear relationship to volume at normal pressures in a normal heart (edpvr) but increases as filling pressures increase or compliance fails.
Right EDP is measured with right atrial pressure or CVP
Left EDP is measured with PCWP or pulmonary starts diastolic pressure

160
Q

What are the limitations of using CVP / PCWP to approximate end diastolic volume to approximate preload?!?

A

Ventricular compliance may not be normal (e.g. low compliance needs higher pressure for same volume)
Av valve may be abnormal (e.g. MS needing higher pressure for same volume)
Positive interthoracic pressure can transmit through to pulmonary artery catheter increasing mean PCWP (e.g. interference from PEEP)
Placement of pulmonary artery catheter in dependant part of lung could add hydrostatic pressure to PCWP signal
High pulmonary vascular resistance can lead to higher pulmonary artery diastolic pressures (e.g. pulmonary hypertension)

161
Q

Definition of afterload
Practical concept, practical measure

A

Ventricular wall stress developed during systole
Practically considered as interventricular pressure developed during systole using SVR/PVR and MAP/MPAP as practical measures

162
Q

Factors affecting afterload

A

Systemic/pulmonary vascular resistance
Factors stimulating or depressing cardiac contraction
Intrathoracic pressure or intrapericardial pressure
Preload
Ventricular wall thickness

163
Q

Which law links ventricular wall thinkness to afterload
What is it

A

Laplaces law

Pressure = (2 x wall thickness x tension) / radius

164
Q

How does a normal ventricle respond to afterload?
What occurs in case of a sudden increase - what is the effect termed?

A

Increases its performance to maintain stroke volume
Sudden afterload increase would cause fall in stroke volume with subsequent increased EDV which causes increased stroke volume - the Anrep effect

165
Q

What measures can be used to determine afterload

A

Arterial pressure - used as a proxy for ventricular pressure
SVR / PVR
Systemic vascular impedance

166
Q

Limitation of using arterial pressure to infer ventricular pressure

A

Inaccurate if significant gradient across av

167
Q

How is SVR calculated

A

MAP-CVP/CO * 80 dynes.sec.cm-5

168
Q

Normal range for SVR
Normal range for PVR

A

900-1400 dynes.sec.cm-5
90-150 dynes.sec.cm-5

169
Q

Why is SVR a poor indicator of afterload

A

Only one component of it.
If the ventricle is contracting poorly afterload will be low no matter how high SVR

170
Q

Formula for pulmonary vascular resistance

A

MPAP-PCWP/CO * 80 dyne.sec.cm-5

171
Q

Components of systemic vascular impedance

A

SVR
Reactive component - compliance/elasticity of the wall - high elasticity gives higher afterload

172
Q

Which wall would have a higher afterload - a thin or thick walled ventricle

A

Thin - higher stress for given systolic pressure

173
Q

Definition of contractility
Practical concept

A

Systolic myocardial work done for given preload / afterload
Ejection fraction for given cvp/map

174
Q

Factors effecting contractility

A

Increased with
Calcium levels
Sympathetic stimulation
Parasympathetic inhibition
Inotropy and digoxin

Decreased with
Opposite of above
Hypoxia and acidosis
Myocardial ischaemia and infarction.

175
Q

Formulae for stroke work of the ventricle
How can it be normalised for body size

A

SW = stroke volume x (MAP - filling pressure)
Convert to stroke volume work index (calculated for BSA)

176
Q

What is the intrinsic rate of a denervated heart
Why different to physiological resting heart rate

A

110
Dominant parasympathetic tone

177
Q

What is the sympathetic stimulation that influences heart rate

A

Circulating catacholaminies
Cardiovascular reflexes via cardio accelerator nerves (T1-5)

178
Q

Where are the centres responsible for cardiovascular rate control

A

Sympathetic and parasympathetic nuclei of the medulla

179
Q

What is the parasympathetic supply to the heart, where does it originate and insert?

A

Dorsal motor nucleus of the vagus and nucleus ambiguus in medulla
Right and left vagus nerve
Right vagus to SA node, left to AV node

180
Q

Physiological effect of vagal stimulation to the heart

A

Decreased slope of phase 4 and increased hyperpolarisation slowing heart rate

181
Q

Sympathetic stimulation to the heart
Origin and insertion

A

T1-5 sympathetic chain
Stellate ganglion to all parts of heart (esp ventricular muscle)
Right side covers SA node and left AV node

182
Q

Physiological effect of sympathetic stimulation to the heart

A

Increase slope of phase 4 increasing heart rate

183
Q

Other than direct stimulation of the heart how else do the sympathetic and parasympathetic nerves influence heart rate

A

Inhibit one and other through direct interconnections

184
Q

What cardiovascular reflexes influence heart rate?

A

Lung volume stretch - increase in lung volume increases heart rate
Chemoreceptor reflex - vagal stimulation slowing heart rate, offset by stimulation of resp centres
Bambridge reflex - stretch of atrial stretch receptors causes increased heart rate
Baroreceptor reflex - stretch of baroreceptors causes decreased heart rate

185
Q

What is the effect of heart rate on cardiac output

A

Increases up to 140bpm
After 140-150bpm significant reduction in filing time overall reduces output

186
Q

What occurs to contractility with increasing heart rate
Effect name
Why

A

Increases
Bowditch effect
Less diastolic time for reuptake of calcium so more available for contration

187
Q

At what decreasing heart rate will cardiac output begin to be effected (ie. When stroke volume increases can’t overcompensate for rate)

A

40

Primary Physiology (15 decks)

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