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Sandra phase 1 > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

What is automaticity

A

The intrinsic ability of the heart to spontaneously depolarise and trigger action potentials that are spread across all of the myocardium to trigger the heart muscle to contract.

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2
Q

2 components of myocardium

A

Nodal cells
Contractile cells

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3
Q

Name the nodal cells

A

SA node
AV node
AV bundle (Bundle of His)
Bundle branches (L&R)
Purkinje fibers

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4
Q

Name the contractile cells

A

Actin
Myosin
Troponin
Tropomyosin
Sarcoplasmic reticulum

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5
Q

Who sets the sinus rhythm and how many bpm

A

SA node. 60-80bpm

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6
Q

Action potential from SA node goes to…. and what happens as a result

A

Bachman’s bundle: Depolarises the LA
Internodal branches: Depolarise RA

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7
Q

The SA bundle sends action potential to the rest of Right atrium via the

A

Internodal pathway

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8
Q

Where does the internodal branch converge?

A

AV node

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9
Q

What is the importance of AV node

A

Acts as a gateway between atria and interventricular septum

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10
Q

What is the importance of AV node delay

A

Want to give time for the atria to contract before the ventricles contract

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11
Q

How is AV node delay created?

A

Has fewer gap junctions than other nodal cells
Have a smaller diameter (slower conduction speed)

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12
Q

Cardiac conduction system

A
  1. SA node
  2. AV node
  3. Bundle of His
  4. L/R Bundle branches
  5. Purkinje fibers
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13
Q

What are intercalated discs?

A

Gap junctions(protons move across the nodal cells to contractile cells) + Desmosomes (connect the actual cardiac cells together).

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14
Q

Nodal cell resting potential

A

-60mV

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15
Q

Contractile cell resting potential

A

-90mV

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16
Q

Stage 0 of the cardiac action potential

A

Rapid upstroke and depolarisation
Voltage gated Na+ channels open-depolarisation

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17
Q

Stage 1 of the cardiac action potential

A

Initial repolarisation
Inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.
Causes initial repolarisation

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18
Q

Stage 2 of the cardiac action potential

A

Plateau
Ca2+ channels open up more slowly than K+ channels. Ca2+ influx through the voltage-gated Ca2+ channels balances K+ efflux (plateau period).
Ca2+ influx triggers Ca2+ release from the sarcoplasmic reticulum and myocyte contraction

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19
Q

Stage 3 of the cardiac action potential

A

Rapid repolarisation
Massive K+ efflux due to opening of voltage-gated slow delayed-rectifier K+ channels and closure of voltage-gated Ca2+ channels- Rapid repolarisation

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20
Q

Stage 4 of the cardiac action potential

A

Resting potential
High K+ permeability through K+ channels
Maintaining resting potential (approx -90mV)
Na+ inflow, K+ outflow

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21
Q

H zone what is it?

A

Distance between thin filaments on the same sarcomere

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22
Q

What consists of one sarcomere

A

Z disc - Z disc

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23
Q

What consists in the thin filament

A

Actin
Troponin
Tropomyosin

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24
Q

How many binding sites does troponin have and what are they?

A

3
Troponin C- Ca
Troponin I-Actin
Troponin T- Tropomyosin

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25
Q

What is the Z disc

A

The functional unit of muscle fibre

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26
Q

What does Titin do?

A

Link thick filament to the Z disc

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27
Q

M line what does it do?

A

Connects titin to thick filamet

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28
Q

What protein connects actin to sarcolemma?

A

Dystrophin

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29
Q

What does Limb lead 1 show activity of?

A

High lateral wall of LV

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30
Q

What does Limb lead 2+3 show activity of?

A

Inferior wall of the heart

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31
Q

What does aVR show activity of?

A

RV + Basal septum

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32
Q

What does aVL show activity of?

A

High lateral wall of LV

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33
Q

What does aVF show activity of?

A

Inferior wall of the heart

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34
Q

Where would you place V1

A

right 4th intercostal space, parasternal space

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35
Q

Where would you place V2

A

Left 4th intercostal space (parasternal line)

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36
Q

Where would you place V3

A

Between V2 + V4

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37
Q

Where would you place V4

A

left 5th intercostal space, mid clavicular line

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38
Q

Where would you place V5

A

Left 5th intercostal space, anterior axillary line

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39
Q

Where would you place V6

A

Left 5th intercostal space, mid axillary line

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40
Q

What is happening to the R wave as you go through V1-V6

A

Getting bigger

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41
Q

What is happening to the S wave as you go through V1-V6

A

Getting smaller

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42
Q

What do V1-V3 tell us about the activity?

A

RV

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43
Q

What limb leads tell us about the right ventricle

A

V1-V3
aVR

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44
Q

What does V2-V3 tell us about the activity of?

A

Basal septum

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45
Q

What limb leads tell us about the basal septum

A

V2-V3
aVR

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46
Q

What limb leads tell us about the anterior wall of the heart

A

V2-V4

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47
Q

What does V2-V4 tell us about the activity of?

A

Anterior wall of heart

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48
Q

What does V5-V6 tell us about the activity of?

A

LV

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49
Q

What limb leads tell us about the LV

A

V5-V6
Limb lead 1
aVL

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50
Q

How long should PR interval be?

A

<0.2 secs

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51
Q

How long should QRS wave be?

A

>0.12 secs

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52
Q

What is the Electrocardiogram?

A

NOT a DIRECT RECORD of the changes in membrane potential across individual cardiac muscle cells.

But instead it is a measure of the currents generated in the EXTRACELLULAR FLUID by the changes co-occurring in many cardiac cells

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53
Q

What is a P Wave?

A

Atrial depolarisation - seen in every lead apart from aVR

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54
Q

What is the PR Interval?

A

Time taken for atria to depolarise and electrical activation to get through AV node

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55
Q

What is the QRS complex?

A

Ventricular depolarisation, still called QRS even if Q and/or S are missing depending on what lead you are looking at

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56
Q

What is the ST Segment?

A

Interval between depolarisation & repolarisation

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57
Q

What is the T wave?

A

Ventricular repolarisation

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58
Q

What is Tachycardia?

A

Increased heart rate

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59
Q

What is Bradycardia?

A

Decreased heart rate

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60
Q

What is Dextrocardia?

A

Heart on right side of chest instead of left

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61
Q

What happens to the ST segment in an Acute Anterolateral Myocardial Infarction?

A

ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads

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62
Q

What happens to the ST segment in an Acute Inferior Myocardial infarction?

A

ST segments are raised in inferior (II, III, aVF) leads

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63
Q

Why is atrial repolarisation usually not evident on an ECG?

A

since it occurs at the same time as the QRS complex so is hidden

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64
Q

How does the impulse generate the ECG?

A

Electrical impulses in the heart move in 3 dimensions

  • ECG only measure voltage in 1 dimension
  • If an impulse is towards the electrode it looks big
  • If an impulse is away from the electrode it looks small or even negative
  • The impulse from the atria is smaller since the atria are smaller than the ventricles thus less myocytes
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65
Q

What are the 12 leads on a 12 lead ECG?

A

Standard limb leads (I, II & III)
Augmented leads (aVR, aVL & aVF)
The precordial leads (V1 - V6)

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66
Q

When reading an ECG, what are the times represented by the small squares and the big squares?

A

When reading an ECG, the graph shows changes in voltage over time, each small square across represents 40ms & each big square across represents 0.2s

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67
Q

Are P waves positive?

A

In a normal ECG the p waves are POSITIVE in EVERY LEAD (apart from the aVR)

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68
Q

What is the first phase of the cardiac cycle?

A

Mid-late ventricular diastole

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69
Q

What is the second phase of the cardiac cycle?

A

Isovolumetric contraction

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70
Q

What is the third phase of the cardiac cycle?

A

Mid-late ventricular systole

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71
Q

What is the fourth phase of the cardiac cycle?

A

Isovolumetric relaxation

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72
Q

How does blood flow passively into the ventricles in phase 1 of the cardiac cycle?

A

Atria fills with blood but mitral/tricuspid valve. the myocardium is relaxed as its not contracting and so papillary muscles aren’t anchoring valves through chordae tendinea. Results in valve being slight open and blood go down to ventricles.

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73
Q

What happens during mid-late ventricular diastole

A

Atrial p >Ventricular p
Arterial p > Ventricular p
Mitral + Tricuspid: open
Aortic + Pulmonic: closed
ECG: P wave

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74
Q

What happens during isovolumetric contraction

A

Atrial p < Ventricular p
Arterial p > Ventricular p
Mitral + Tricuspid: close (s1)
Aortic + Pulmonic: closed
ECG: QRS complex

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75
Q

What happens during mid-late ventricular systole

A

Atrial p > Ventricular p
Arterial p < Ventricular p
Mitral + Tricuspid: closed
Aortic + Pulmonic: open
ECG: QRS complex

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76
Q

What happens during isovolumetric relaxation

A

Atrial p < Ventricular p
Arterial p > Ventricular p
Mitral + Tricuspid: closed (s2)
Aortic + Pulmonic: closed
ECG: T wave

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77
Q

What is isovolumetric contraction?

A

Ventricular contraction when all valves are closed. This increases ventricular pressure but as the valves are closed the volume remains unchanged.

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78
Q

What produces the first heart sound?

A

Closing of the mitral valve.

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79
Q

What causes the mitral valve to close?

A

When the ventricular pressure is greater than the atrial pressure and the arterial pressure s greater than
and the ventricular pressure.

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80
Q

Describe systole.

A

A wave of depolarisation arrives, and Ca2+ channels open.

LVp>LAp and the mitral valve closes.

LVp rises, isovolumetric contraction,

LVp>aortic p.

The aortic valve opens and ejection begins.

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80
Q

Describe systole.

A

A wave of depolarisation arrives, and Ca2+ channels open.

LVp>LAp and the mitral valve closes.

LVp rises, isovolumetric contraction,

LVp>aortic p.

The aortic valve opens and ejection begins.

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81
Q

What produces the second heart sound?

A

Closing of the aortic valve.

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82
Q

Describe diastole.

A

LVp decreases and there is a phase of reduced ejection.

LVp is less than aortic pressure and the aortic valve closes isovolumetric ventricular relaxation.

LVp is less than LAp and the mitral valve opens - ventricles fill with blood.

Atria contract - atrial booster.

LVp > LAp and mitral valve close.

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83
Q

What is the duration of systole?

A

0.3s.

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84
Q

What is the duration of diastole?

A

0.5s.

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85
Q

What is end systolic volume?

A

The volume of blood remaining in the LV following systole.

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86
Q

Define preload.

A

The volume of blood in the ventricles just before contraction (EDV).

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87
Q

Define afterload.

A

The pressure against which the heart must work to eject blood in systole.

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88
Q

Define contractility.

A

The inherent strength and vigour of the heart’s contraction during systole.

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89
Q

Define elasticity.

A

Myocardial ability to recover it’s original shape after systolic stress.

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90
Q

Define compliance.

A

How easily a chamber of the heart expands when it is filled with blood (C=ΔV/ΔP).

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91
Q

Define diastolic distensibility.

A

The pressure is required to fill the ventricle to the same diastolic volume.

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92
Q

Define resistance.

A

A force that must be overcome to push blood through the circulatory system.

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93
Q

What is the basic principle of Starling’s law of the heart?

A

Increased EDV = increased SV.

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94
Q

Explain Starling’s law.

A

The greater the EDV, the greater the sarcomeres are stretched and the more forceful the contraction.

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95
Q

With relation to Starling’s law, what is the effect of an increased venous return?

A

EDV will increase and so SV increases and so Cardiac output also increases as CO=SVxHR.

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96
Q

Give the equation for stroke volume.

A

SV=EDV-ESV.

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97
Q

Give the equation for cardiac output.

A

CO=SVxHR.

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98
Q

Define cardiac output.

A

The volume of blood each ventricle pumps per unit time.

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99
Q

Give the equation for mean arterial pressure.

A

MAP = DP + 1/3(SP-DP).
(SP - systolic pressure, DP - diastolic pressure).

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100
Q

Give the equation for pulse pressure.

A

PP=SP-DP.

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101
Q

Give the equation for blood pressure.

A

BP=COxTPR.

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102
Q

What is Poiseuille’s equation?

A
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103
Q

What is Ohm’s law?

A

F=ΔP/R.

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104
Q

What are the principal vessels of resistance?

A

Arterioles

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105
Q

What do arterioles respond to?

A

Blood pressure changes. Local, neural and hormonal factors.

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106
Q

Name 2 local factors that result in vasoconstriction

A

Endothelin, internal BP.

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107
Q

Name 5 local factors that result in vasodilation.

A

Hypoxia, NO, K+ (accumulate from AP), CO2, H+, adenosine.

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108
Q

What neural factors result in vasoconstriction?

A

Sympathetic nerves that release noradrenaline.

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109
Q

What neural factors result in vasodilation?

A

Parasympathetic innervation.

110
Q

Name 3 hormonal factors that result in vasoconstriction.

A

Angiotenisn 2, ADH, Adrenaline (binds to alpha-adrenergic receptors in smooth muscle).

111
Q

Name 2 hormonal factors that result in vasodilation.

A

Atrial natriuretic peptide, Adrenaline (binds to beta2 receptors).

112
Q

What is myogenic auto-regulation of blood flow?

A

An intrinsic mechanism in smooth muscle blood vessels. If BP increases the vessel constricts. This is important in regulating blood flow.

113
Q

Myogenic auto-regulation of blood flow: What is the response to an increase in BP?

A

Increased BP will result in vasoconstriction and so blood flow decreases.

114
Q

Myogenic auto-regulation of blood flow: What is the response to a decrease in BP?

A

Decreased BP will result in vasodilation and so blood flow increases.

115
Q

What is hyperaemia?

A

An increased blood flow to tissues.

116
Q

What is the cause of active hyperaemia?

A

When blood flow increases due to an increase in metabolic activity.
- Increased metabolic activity = decreased O2 and increased metabolites = arteriolar dilation = increased blood flow.

117
Q

What is the cause of reactive hyperaemia?

A

When blood flow increases the following occlusion to arterial flow.

118
Q

Describe excitation-contraction coupling.

A
  1. Na+ depolarises membrane.
  2. A small amount of Ca2+ is released from T tubules.
  3. Ca2+ channels in sarcoplasmic reticulum open.
  4. Ca2+ flows into cytosol. Cytosolic Ca2+ conc raised.
  5. Ca2+ binds to troponin C, this pulls tropomyosin and exposes the myosin-binding site on actin.
  6. Cross bridge cycling begins.
  7. After depolarisation, Ca2+ is returned to SR. K+ outflow = repolarisation.
119
Q

What effect does myocardial contraction have on the A-band of a sarcomere?

A

No effect, it stays the same length.

120
Q

What effect does myocardial contraction have on the I-band and H-zone of a sarcomere?

A

They get shorter.

121
Q

Describe actin (thin filament).

A

A globular protein, a single polypeptide. It polymerises with other actin monomers to form a double-stranded helix. Together they form F actin.

122
Q

Describe myosin (thick filament).

A

2 heavy polypeptide chains and 4 light chains. The myosin heads have 2 binding sites; one for actin and one for ATP.

123
Q

Describe tropomyosin.

A

An elongated molecule made of 2 helical peptide chains.

124
Q

What is the function of troponin I?

A

Troponin I, together with tropomyosin, inhibits actin and myosin binding.

125
Q

What is the function of troponin T?

A

Troponin T binds to tropomyosin.

126
Q

What is the function of troponin C?

A

Troponin C has a high affinity for Ca2+. TnC drives away TnI and so allows cross-bridge formation.

127
Q

Name 3 effectors in circulation control.

A
  1. Blood vessels - vasoconstrict/dilate and effect TPR.
  2. The heart - can affect rate or contractility.
  3. Kidneys - regulates blood volume and fluid balance.
128
Q

Where are baroreceptors located?

A

Aortic arch and carotid sinus.

129
Q

What activates baroreceptors?

A

Baroreceptors contain stretch receptors that respond to pressure.

130
Q

Are atrial baroreceptors involved in short-term or long-term regulation of BP?

A

Short-term. (Cardiopulmonary = long-term)

131
Q

Where are central chemoreceptors located?

A

In the medulla oblangata.

132
Q

What do central chemoreceptors respond to?

A

Changes in pH/(H+).
Increased PaCO2 increases H+ and so decreases pH.

Increased PaCO2 results in vasodilation.

133
Q

What is the ligamentum teres a remnant of?

A

The umbilical vein.

134
Q

What is the ligamentum venosus a remnant of?

A

The ductus venosus.

135
Q

What layer of the tri-laminar disc forms the cardiovascular system?

A

The mesoderm.

136
Q

What does the first heart field produce?

A

The left ventricle.

137
Q

What does the second heart field produce?

A

The right ventricle, atria and outflow tracts.

138
Q

What are the 3 stages of heart formation?

A
  1. Formation of the primitive heart tube.
  2. Cardiac looping.
  3. Cardiac septation.
139
Q

Describe what happens in the formation of the primitive heart tube.

A

Two endocardial tubes form (day 19). The tubes fuse together and the heart beats (day 22).

140
Q

Describe what happens in cardiac looping.

A

Nodes secrete nodal, this circulates to the left due to ciliary movement. Nodal causes a cascade of transcription factors that transduce looping.

141
Q

Describe what happens in cardiac septation.

A

Endocardial cushions form. Fuse at mid-line to form atrioventricular septum. The muscular ridge in the floor of the primitive ventricle migrates to endocardial cushions forming the interventricular septum.

142
Q

What does the sinus venosus form?

A

The coronary sinus and RA.

143
Q

What does the primitive atrium form?

A

RA and LA.

144
Q

What does the primitive ventricle form?

A

Forms most of LV.

145
Q

What does the bulbus cordis form?

A

Part of the ventricles.

146
Q

What does the truncus arteriosus form?

A

The aorta and pulmonary trunk.

147
Q

What do the 1st and 2nd aortic arches form?

A

Minor vessels in the head.

148
Q

What does the 3rd aortic arch form?

A

The common carotid arteries.

149
Q

What does the left and right 4th aortic arch form?

A

Left - aorta. Right - Right subclavian artery.

150
Q

What does the 5th aortic arch form?

A

There is no 5th arch!

151
Q

What does the left and right 6th aortic arch form?

A

Left - left pulmonary artery and ductus arteriosus. Right - right pulmonary artery.

152
Q

What does the 7th segmental aortic arch form?

A

Left and right subclavian arteries.

153
Q

What does the dorsal aortae form?

A

Left dorsal aortae - descending aorta. Right dorsal aortae - part of right subclavian artery.

154
Q

What are chronotropic effects?

A

Those that change the heart rate. Positive chronotropic = increased heart rate.

155
Q

What are inotropic effects?

A

Those that alter the force of muscular contractions.

156
Q

What affect does parasympathetic stimulation have on heart rate?

A

Decreases heart rate (-ve chronotropic). Cardiac output therefore decreases with parasympathetic stimulation. (CO=HRxSV).

157
Q

What affect does sympathetic stimulation have on force of contraction?

A

Increases force (+ve inotropic).

158
Q

What pump maintains the negative resting potential of a membrane?

A

Na+/K+ pump.

159
Q

What is the purpose of the Nernst equation?

A

It is used to determine a membranes potential.

160
Q

Give the Nernst equation.

A

E = 60log(conc outside/conc inside)

161
Q

What membrane channels are responsible for the plateau period in the cardiac AP?

A

Voltage gated Ca2+ ‘slow’ channels.

162
Q

Briefly describe the cardiac action potential in 5 steps

A
  1. Na+ channels open; influx of Na+ into cell; depolarisation.
  2. When the Na+ channels close, a small number of K+ leave the cell resulting in partial repolarisation.
  3. Ca2+ channels open and there is Ca2+ inflow. K+ channels are also open and there is K+ outflow. This results in the plateau period.
  4. Ca2+ channels close and K+ channels remain open. K+ leaves the cell resulting in repolarisation.
  5. Maintaining the resting potential (approx -90mV). Na+ inflow, K+ outflow.
163
Q

Where is the SAN located?

A

In the RA under the crista terminalis.

164
Q

Briefly describe the electrical conduction pathway in the heart.

A
  1. The SAN generates an electrical impulse.
  2. This generates a wave of contraction in the atria.
  3. Impulse reaches AVN.
  4. There is a brief delay to ensure the atria have fully emptied.
  5. The impulse then rapidly spreads down the Bundle of His and Purkinje fibres.
  6. The purkinje fibres then trigger coordinated ventricular contraction.
165
Q

Why is there rapid conduction in the bundle of his and purkinje fibres?

A
  1. The fibres have a large diameter.
  2. There is high permeability at gap junctions.
166
Q

What is the function of the refractory period?

A
  1. It prevents excessively frequent contractions.
  2. It allows time for the atria to fill.
167
Q

What does the P wave on an ECG represent?

A

Atrial depolarisation. Duration is less than 0.12s.

168
Q

What does the QRS complex on an ECG represent?

A

Ventricular depolarisation. Duration is 0.08-0.1s.

169
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation.

170
Q

What might an elevated ST segment be associated with?

A

Myocardial infarction.

171
Q

ECG: where would you place lead 1?

A

Right arm (-ve) to left arm (+ve).

172
Q

ECG: where would you place lead 2?

A

Right arm (-ve) to left leg (+ve).

173
Q

ECG: where would you place lead 3?

A

Left arm (-ve) to left leg (+ve).

174
Q

What is Einthoven’s triangle?

A

An imaginary formation of the 3 limb leads in a triangle shape.

175
Q

ECG: where would you place lead aVR?

A

Left arm and left leg (-ve) to right arm (+ve).

176
Q

ECG: where would you place lead aVF?

A

Right arm and left arm (-ve) to left leg (+ve).

177
Q

ECG: where would you place lead aVL?

A

Right arm and left leg (-ve) to left arm (+ve).

178
Q

What are the average systolic and diastolic pressures for the pulmonary circulation?

A

25 and 10 mmHg.

179
Q

What are the average systolic and diastolic pressures for the systemic circulation?

A

120 and 80 mmHg.

180
Q

Why might someone with liver injury experience prolonged bleeding time?

A

Because the liver produces clotting factors.

181
Q

What is exposed if you damage the endothelium of a vessel?

A

Underlying connective tissue and collagen.

182
Q

What is the role of vWF?

A

vWF binds to collagen and platelets bind to vWF.

183
Q

What happens in platelet activation?

A

The change shape: smooth to spiculated. This increases their surface area. New platelets adhere to old ones = platelet aggregation. This forms a platelet plug.

184
Q

What do activated platelets synthesise?

A

Thromboxane A2.
ADP
Serotonin

185
Q

What is the function of Thromboxane A2 (TXA2)?

A

It leads to further platelet aggregation.
Binds to receptors of smooth muscle-muscle contracts increases muscular spasm

186
Q

What are the platelet receptors for fibrinogen?

A

glycoprotein IIb/IIIa. Fibrinogen forms ‘bridges’ between platelets.

187
Q

What does an undamaged endothelium release in order to prevent platelet activation in undamaged areas?

A

Prostacyclin (inhibits platelet aggregation) and NO (inhibits platelet adhesion).

188
Q

What are platelets made from? and where are they made?

A

In the bone marrow from megakaryocytes.

189
Q

In haemostasis what is prothrombin converted into?

A

Thrombin.

190
Q

Give 3 functions of Thrombin.

A
  1. Converts fibrinogen into fibrin.
  2. Activates factor XIII into XIIIa.
  3. Has a positive feedback effect resulting in further thrombin production.
191
Q

What is the essential component of a blood clot?

A

Fibrin.

192
Q

Briefly describe the Fibrinolytic system.

A

Plasminogen is converted into plasmin. Plasmin cuts the fibrin at various places leading to the formation of fragments.

193
Q

What is the purpose of the fibrinolytic system?

A

It acts to prevent blood clots from growing and becoming problematic.

194
Q

Does blood flow to the heart occur during diastole or systole?

A

Diastole.

195
Q

What does the left coronary artery divide into?

A

The left anterior descending, and the circumflex.

196
Q

Why is the O2 saturation in coronary venous blood very low?

A

O2 extraction by the heart muscle is very high.

197
Q

What surface of the heart does the right coronary artery supply?

A

The inferior surface (underside) of the heart.

198
Q

What is released upon cell activation and contains a high concentration of a molecule that acts as an agonist at the platelet P2Y12 receptor?

A

Platelet dense granules.

199
Q

What valve prevents high pressures developing in the jugular veins during ventricular systole?

A

Tricuspid valve.

200
Q

What is the normal duration for the PR interval?

A

0.12-0.2 seconds.

201
Q

What ECG lead yields complexes that are normally inverted compared to the anterior and inferior leads?

A

Lead aVR.

202
Q

Is there a point in the cardiac cycle when both atrial and ventricular diastole occur together?

A

Yes: when the ventricles are relaxing and the atria are filling (before atrial contraction).

203
Q

Why does an increase in LVEDV signify heart failure?

A

Heart failure is the inability to pump blood out of the heart. There is blood remaining at the end of systole. The blood therefore accumulates and so LVEDV increases.

204
Q

Which pressure is most likely to increase in left-sided heart failure?

A

LV EDP.

205
Q

Which pressure is most likely to decrease in left-sided heart failure?

A

Mean aortic pressure.
(Less blood is being pumped into the aorta).

206
Q

What is stenosis?

A

Narrowing.

207
Q

Which pressure is most likely to increase in mitral valve stenosis?

A

Left atrial end-systolic pressure.

208
Q

What does it mean if a heart valve is incompetent?

A

It is regurgitant.

209
Q

Which pressure is most likely to increase when the aortic valve is incompetent?

A

Left ventricular end-diastolic pressure.

210
Q

Pulmonary oedema is a sign of what?

A

Left heart failure.

211
Q

What can severe pulmonary hypertension cause?

A

Right heart failure.
The heart has to pump harder to get blood into the pulmonary circulation due to an increased afterload.

212
Q

Shortness of breath, severe peripheral oedema and ascites after a heart attack can indicate what?

A

Biventricular failure.

213
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity, this can cause abdominal swelling.

214
Q

How long is the PR interval on an ECG?

A

0.12-0.2 seconds.

215
Q

What does the PR interval represent?

A

The slow conduction between the AVN and the His-Purkinje system.

216
Q

Diastole: what is diastasis?

A

When LVp = LAp. Net movement of blood is zero. This is the time between ventricular suction and atrial contraction

217
Q

What branch does the right coronary artery give off as it reaches the inferior border of the heart?

A

The right marginal branch.

218
Q

What artery does the RCA anastomose with on the diaphragmatic surface of the heart?

A

The circumflex artery.

219
Q

What does the LAD anastomose with on the diaphragmatic surface of the heart?

A

The posterior inter-ventricular branch of the RCA.

220
Q

Where is the coronary sinus found?

A

Between the LA and LV - left atrio-ventricular sulcus.

221
Q

What does the coronary sinus drain into?

A

The RA.

222
Q

What artery arises from the RCA in 90% of hearts, the circumflex in 30% and in 20% arises from both the RCA and circumflex?

A

The posterior interventricular branch.

223
Q

What equation explains why small changes in the diameter of a blood vessel have a great effect on the resistance to flow of a fluid through that vessel?

A

Poiseuille’s equation. Q=r^4.

224
Q

Describe the arterial baroreceptor reflex in response to an increase in blood pressure.

A
  • Increased parasympathetic outflow to the heart means contractility and heart rate are reduced and so cardiac output is reduced: CO=HRxSV.
  • Decreased sympathetic outflow to the arterioles results in vasodilation and so TPR is reduced.
  • BP=COxTPR and so blood pressure is lowered.
225
Q

Describe the arterial baroreceptor reflex in response to a decrease in blood pressure.

A
  • Increased sympathetic outflow to the heart means contractility and heart rate are increased and so cardiac output is increased: CO=HRxSV.
  • Increased sympathetic outflow to the arterioles results in vasoconstriction and so TPR is increased.
  • BP=COxTPR and so blood pressure is increased.
226
Q

What phase of the cardiac action potential coincides with diastole?

A

Phase 4.

227
Q

What part of the ECG does the plateau phase of the cardiac action potential coincide with?

A

QT interval.

228
Q

Give 4 factors that affect the gating of ion channels.

A

Voltage, drugs, hormones, temperature.

229
Q

What is Virchow’s triad?

A

It describes 3 categories thought to contribute to thrombosis.

230
Q

What are the 3 categories of Virchow’s triad?

A
  1. Stasis of blood flow.
  2. Endothelial injury.
  3. Increased coagulation ability.
231
Q

Define ischaemia.

A

A decrease in blood flow to a tissue.

232
Q

Define infarction.

A

No blood flow to a tissue - tissue death.

233
Q

Explain the formation of fluid exudate in inflammation.

A

Chemical mediators cause vasodilation of vessels and an increase in permeability.

234
Q

What are the roles of lymphatics in acute inflammation?

A

Lymphatics drain exudate and carry antigens.

235
Q

What happens in phase 4 of the cardiac action potential?

A

Pacemaker potential - Na+ inflow and slowing of K+ outflow. Slow depolarisation begins = innate contractility.

236
Q

Where is Ca2+ released from in excitation contraction coupling?

A

The T tubules and the sarcoplasmic reticulum.

237
Q

What is the resting potential of the SA node?

A

-55 to -60 mV.

238
Q

How do central chemoreceptors respond to an increase in PaCO2?

A

Vasoconstriction.

239
Q

Why do central chemoreceptors stimulate vasoconstriction in response to an increase in PaCO2?

A

They act to counter the affect of CO2 as a vasodilator and so maintain blood flow to tissues.

240
Q

What reaction does adenyl cyclase catalyse?

A

The conversion of ATP into cAMP.

241
Q

How do muscarinic M2 receptors cause a decrease in cAMP?

A

They inhibit adenyl cyclase.

242
Q

What 2 channels are closed during the refractory period in a cardiac action potential?

A

Fast Na+ and Ca2+ channels.

243
Q

What surface of the heart does the RCA supply?

A

Inferior.

244
Q

Describe parasympathetic cardiac stimulation and its effects?

A
  • Fibers are transmitted via the vagus nerve (CN10)
  • Controlled by acetylcholine which bind to muscarinic receptors
  • Decreases heart rate (negatively chronotropic)
  • Decreases force of contraction (negatively inotropic)
  • Decreases cardiac output (by up to 50%)
  • Decreased parasympathetic stimulation will result in an increased heart rate
245
Q

Describe sympathetic cardiac stimulation and its effects?

A
  • Sympathetic postganglionic fibers innervate the entire heart
  • Controlled by adrenaline & noradrenaline

• Increases heart rate (positively chronotropic)
• Increases force of contraction (positively inotropic)
• Increases cardiac output (by up to 200%)
• Decreased sympathetic stimulation will result in decreased heart rate & force of
contraction and a decrease in cardiac output by up to 30%

246
Q

Define Total Peripheral Resistance?

A

The total resistance to flow in systemic blood vessels
from beginning of aorta to vena cava - arterioles provide the most resistance

247
Q

Define Intrinsic Autoregulation?

A

when the arterioles either vasoconstrict or vasodilate in response to changes in resistance seemingly automatically - with the aim of maintaining constant blood flow

248
Q

What is the sarcoplasmic reticulum?

A

membrane network that surrounds the contractile proteins. Releases Ca2+ when Ca2+ binds to it ryanodine receptor

249
Q

What is the difference between skeletal muscle contraction and cardiac muscle contraction?

A

Contraction lasts LONGER than in skeletal muscle - up to 15 times longer in duration; this is due to the slow calcium channels

250
Q

What are the three heart sounds?

A
  • One is a soft, low pitched lub, associated with the closure of the atrioventricular valves
  • The second is, a louder dub is associated with the closure of the aortic & pulmonary valves

• The third is the sounds of blood rushing into the left ventricle

251
Q

What ions affect heart rate and how?

A

increase Ca- chronotropic
decrease Ca-inotropic
Increase Potassium - inotropic

252
Q

How to peripheral chemoreceptors affect heart rate?

A

Increase

253
Q

What do chemoreceptors respond to?

A

decrease pH, decrease pO2, increase pCO2

254
Q

How do you increase venous return

A
  • muscle milking
  • respiratory pump
  • venoconstriction
255
Q

What three things affect stroke volume

A

Afterload
preload
contractility

256
Q

What does preload depend on?

A

EDV
Filling time
Starlings Law

257
Q

What does contractility depend on?

A

Hormones (T3+T4, Glucagon)

SNS

Drugs

Ions

258
Q

How does EDV affect preload?

A

Increases preload

259
Q

What drugs stimulate contractility

A

Digitalis
Dopamine

260
Q

What drugs inhibit contractility

A

Beta-blocker
Calcium channel blocker

261
Q

What affects afterload

A

Aortic valve dysfunction
Plaque occlusion
Hypertension

262
Q

Explain the Atrial Bainbridge Reflex

A

Positive effect on heart rate
increase venous return –> increase in stretch–> + CA centre–> Sa node–> Increase HR

263
Q

Where does the highest velocity of blood flow take place

A

Aorta

264
Q

Where does the lowest velocity of blood flow take place?

A

Capillaries

265
Q

What does the slow flow of blood allow?

A

Good capillary exchange

266
Q

What vessel network has the highest cross-sectional area

A

Capillaries

267
Q

What vessel network has lowest cross-sectional area

A

aorta

268
Q

Where does oxygenation occur during foetal circulation

A

Placenta

269
Q

Adaptation for foetal circulation

A

Umbilical veins and arteries

Ductus venosus

Foramen ovale

Ductus arteriosus

270
Q

Foetal circulation

A

Placenta →

The umbilical vein carries oxygenated blood to the liver. Once it reaches the liver it dumps blood into the portal vein. The portal vein goes to every lobule of the liver and becomes deoxygenated. Deoxygenated blood enters the hepatic vein which drains into the IVC. Before it joins the IVC the ductus venous which is branching off of the umbilical vein bypasses the liver and goes to the IVC. The deoxygenated blood and oxygenated blood is mixed when entering IVC.

Due to hypoxic vasoconstriction, the right side of the heart is greater than the left and blood flow from the right atrium → left atrium via foramen ovale.

Blood from the aorta goes to the pulmonary artery via ductus arteriosus.

The aorta pumps blood to the rest of the body. Splits and goes to the right and left common iliac artery → internal/external iliac artery → gives rise to the umbilical artery and goes back to the placenta

271
Q

What keeps the ductus arteriosus open

A

Prostaglandin

272
Q

dromotropic

lusitropic

A

dromotropic: conduction through AV node
lusitropic: increases relaxation of the myocardium during diastole

Sandra phase 1 (16 decks)

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