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Physiology > Physiology of the Heart > Flashcards

Physiology of the Heart Flashcards

1
Q

List the transportation roles of the heart and circulation

A

Transporting:

  • Vitamins
  • Nutrients
  • Oxygen/CO2
  • Hormones
  • Immunoglobulins
  • RBC/WBCs
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2
Q

Give the thermoregulatory roles of the heart and circulation

A
  • Counter-current exchange mechanism
  • Circulation of the skin
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3
Q

Give the 3 major parts of the circulation

A
  • Heart
  • Systemic circulation
  • Lung circulation
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4
Q

Describe Starling’s effect

A

To increase load, the heart automatically reacts with extra work

without hormonal/neuronal factors

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5
Q

Describe the heart’s work load status during rest

A

The heart is working in the lower range of its total working capacities

This is ensured by parasympathetic predominance

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6
Q

A decrease of parasympathetic activity may cause…

A

An increase in the mechanical performance of the heart

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7
Q

The autonomity of the heart rythmn is due to…

A

Rythmn generators in the SA node

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8
Q

Give the main parameter of cardiac mechanical performance

A

Cardiac output

The volume of blood propelled into the aorta from the left ventricle per unit time

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9
Q

List the layers of the heart

A
  • Endocardium
  • Myocardium
  • Epicardium
  • Pericardium
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10
Q

Give the contractile components of the myocardium

A
  • Heart muscle fibres (working fibres)
    • Stretching enhances their force-generating capability
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11
Q

Give the non-contractile components of the myocardium

A
  • Serially attached elastic elements (SEC)
  • Parallelly attached elastic elements (PEC)
  • Collagen
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12
Q

List the functions of the pericardium

A
  • Fixation: keeps the heart in the mediastinum
  • Protection from infection from other organs
  • Prevents excessive dilation of the heart during hypervolemia
  • Lubricates the heart
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13
Q

Describe fetal circulation in relation to the pulmonary circulation

A
  • Lungs not functioning
    • Blood bypasses lungs → foramen ovale
    • Between L & R atrium
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14
Q

Describe the closing of foramen ovale

A
  1. Pressure in left atrium increases
  2. Flap valve covers foramen ovale
  3. After 1 year, the foramen completely closes
  4. It is then regarded as fossa ovalis
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15
Q
  • What percentage of the population does the foramen ovale not seal?
  • What is the condition called?
A
  • 30%
  • Patent foramen ovale (PFO)
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16
Q

Name the fetal vessel between a. aorta thoracica and a. pulmonalis

A

Ductus botallo

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17
Q

When does ductus botallo close?

A

4 weeks postpartum

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18
Q

List the excitable varieties of cardiac tissue

A
  • Pacemakers
  • Conductive system
  • Working fibres
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19
Q

Purpose of the Aschoff-Tawara (AV) node

A

Delays the atrial signal

So atrial contraction precedes the ventricular contraction

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20
Q

Resting membrane potential (RMP)

A

Diastole:

  • -90mV
  • Spontaneous depolarisation followed by AP
  • RMP doesn’t exist in pacemaker cells
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21
Q

Describe action potential (AP)

A
  1. Stimulation
  2. _Ion channel_s of membrane open
  3. Ion exchange between the two sides
  4. Action potential
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22
Q
A

Pacemaker potentials

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23
Q

Pacemaker cells

A
  • Located: SA / AV node
  • Allow continuous generation of excitation
  • No RMP
  • Repolarisation: Transmembrane potential -55mV
  • Automatic depolarisation follows
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24
Q

This electrical activity is expressed in…

A

Sinoatrial (SA) node

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25
Q

This electrical activity is expressed in…

A

Ventricular muscle

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26
Q

Pacemaker action potential is…

  • Slower/faster

and

  • Lower/higher

…than cardiomyocytes

A
  • Slower
  • Lower
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27
Q

Round pacemaker cells

A

Sites of the generation of excitation

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28
Q

Elongated/slender cells

A

Conduct/synchronise excitation generated in round pacemaker cells

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29
Q

Maximal depolarisation potential (MDP)

A

No RMP developed after the previous AP reaches -55mV

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30
Q
A
  • K+ channels close
  • Na+ channels open
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31
Q
A
  • Ca2+ channels open
  • Na+ channels close
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32
Q

This electrical pattern is representative of…

A

Pacemaker cells

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33
Q
A
  • Ca2+ channels close
  • K+ channels open
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34
Q
A
  • K+ channels close
  • Na+ channels open
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35
Q
A

Overshoot

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36
Q
A

+15 mV

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37
Q
A

MDP

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38
Q
A

SDD

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39
Q
A

Threshold potential

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40
Q

Maximal diastolic potential; virtual resting potential (MDP)

A
  • Slow Na+ channels open spontaneously
  • Slow depolarisation begins
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41
Q

Spontaneous diastolic depolarisation

A

No RMP until threshold potential

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42
Q

‘Overshoot’

A
  • Ca2+ influx and only slow Na+ channels
  • +5/+15mV (Lower than working fibres)
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43
Q

Repolarisation

A
  • K+ efflux until MDP
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44
Q

What does Ih (hyperpolarisation activated) channel opening trigger?

A

If Threshold of -40mV is reached, the following will open:

  • Type-T, rianodin sensitive calcium channel
  • Type-L DHP sensitive calcium channel
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45
Q

The opening of Type-T and Type-L channels causes…

A
  • Calcium to flow from the EC into the cell
  • Causes a transient Ca-influx
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46
Q

The period from MDP to threshold potential is known as…

A

Spontaneous diastolic depolarisation (SDD)

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47
Q

Depolarisation of the SA node is due to which channels?

A

Long-lasting Ca2+ channels

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48
Q

Why is the membrane potential of the ‘0’ phase so steep?

A
  • There are no fast Na+ channels in the membrane of the round cells
  • Only long lasting Ca-channels determine this phase
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49
Q

What occurs from the point of potassium channels opening?

A
  • Efflux of K+ ions from cell
  • Repolarisation until MDP is reached
  • Activation of Ih channels starts a new cycle
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50
Q

Term given to the frequency of contraction

A

Chronotrop

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51
Q

Term given to the speed of conduction

A

Dromotrop

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52
Q

Term given to the threshold of contraction

A

Bathmotrop

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53
Q

Term given to the force of contraction

A

Inotrop

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54
Q

Vagus escape

A
  • Stimulation of n. vagus
  • Effectiveness of further stimulation disappears
  • Switch from nomotop → heterotop excitation
  • AV node now generates rythmn, not SA node
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55
Q

Which nerve controls heart rate?

A

N. vagus

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56
Q

Describe the stimulation of SA node round cells

A

Sympathetic effect

  • Stimulation of B1-receptor​
  • Same effect triggered by norepinephrine and epinephrine
  • Parasympathetic suppression, enhancing the effect
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57
Q

Describe how stimulation of B1-Rec can cause sympathetic effect

A
  1. Stimulation of G-protein mediated IC cAMP increase
  2. Na+ & K+ channels open
  3. MDP shifts upward, steepness of SDD increases
  4. Threshold reduced
  5. Heart rate increase
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58
Q

Describe parasympathetic effects altering heart rate

A
  1. Acetylcholine stimulates muscarinic acetylcholine receptors on round cells
    1. cAMP decreases
    2. MDP shifted down
    3. SDD slope decreases
    4. Threshold potential elevates
    5. Hyperpolarisation
  2. Heart rate decreases
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59
Q

Describe the metabotropic effect on heart rate

A
  1. Acetylcholine opens metabotropic K+ channels
  2. Further hyperpolarisation
  3. Decreased frequency
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60
Q

Heart conduction in small animals

A
  • Subendocardial conduction
  • Conducting fibres don’t penetrate working muscle deeply
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61
Q

Heart conduction in large animals

A
  • Subepicardial conduction
  • Fibres pass deeply into the ventricle
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62
Q
A

Bachmann’s bundle

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63
Q
A

Left posterior bundle

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64
Q

Signal arriving from the SA node

A

Nomotop excitation

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65
Q

A signal arriving from AV node

A

Heterotop excitation

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66
Q

Anulus fibrosus

A
  • Represents electric resistance
  • Synchronises atrioventric cooperation
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67
Q

How long is the indicated period?

A

~200 ms

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68
Q

What is shown?

A

Action potential of a working fibre

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69
Q
A

Resting Membrane Potential

-90 mV

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70
Q
A

Depolarisation

  • Na+ influx
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71
Q
A

Overshoot

+25 mV

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72
Q
A

Rapid repolarisation

  • K+ efflux (early)
  • Cl- influx
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73
Q
A

Plateau

  • Ca2+ influx
  • K+ efflux (slow)
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74
Q
A

Rapid repolarisation

  • K+ efflux (late)
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75
Q
A

Late hyperpolarisation

  • K+ efflux (late)
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76
Q

What is the purpose of the plateau phase?

A

Blocks premature AP generation/contraction

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77
Q

Ion flow of working fibres during action potential

A
  1. Depolarisation
  2. Rapid repolarisation
  3. Plateau
  4. Rapid repolarisation
  5. Later hyperpolarisation
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78
Q

The flow of charges across the membrane is dependent on…

A
  • Permeability
  • Electrochemical gradient
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79
Q

Metabotropic channels

A
  • Under the control of hormones + neurotransmitters
  • Conductance properties of these channels altered
    • Change in heart function
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80
Q

Which channels are responsible for action potential?

A

Voltage-dependent Na+ channels

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81
Q

Which channels open in each phase of the AP?

A

Phase 1: Early potassium channels

Phase 2: Slow potassium channels

Phase 3: Late potassium channels

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82
Q

The effect of the overshoot

A
  • Activation of calcium channels
  • Calcium ions enter the cell
  • Repolarisation is elongated
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83
Q

The duration of the plateau phase is:

  • Longer closer to the…
  • Shorter closer to the…
A

Longer closer to the endocardium

Shorter in the epicardium

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84
Q
A

Absolute refractory phase (ARP)

  • AP cannot be initiated
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85
Q
A

Relative refractory phase (RRP)

  • Strong stimulus may initiate AP
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86
Q
A

Supernormal phase (Refractory phase)

  • A slight stimulus may initiate AP
  • AP will be submaximal
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87
Q

Absolute refractory phase

A
  • No stimulus
  • A new action potential is elicited before the plateau
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88
Q

Relative refractory phase

A
  • A stimulus is given after the plateau
  • Before reaching threshold potential
  • Can cause a new AP if strong enough
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89
Q

Supernormal phase

A
  • Between threshold and RMP
  • Slight stimulus: Gives new AP
    • Premature new contraction
    • Can be fatal in the ventricle (fibrillation)
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90
Q

Atrial fibrillation

A
  • Electric stimulation of the atrium (repeated contractions)
  • Ventricle maintains normal circulatory pressure
  • Non-fatal
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91
Q

Ventricular fibrillation

A
  • Normal blood pressure cannot be maintained
    • May drop to ‘0’
  • Systole and diastole disappears (Fatal)
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92
Q

Defibrillation

A

Strong electric current:

  • Desynchronisation stops
  • SA node synchronised again
  • Normal rhythm
  • Nomotop excitation returns
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93
Q

Difference between AP and mechanogram of cardiac muscle

A

Mechanogram is almost parallel to AP

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94
Q

Difference between AP and mechanogram of skeletal muscle

A
  • No plateau phase
  • AP lasts for 1 millisec, compared with 200 millisec of heart
  • Mechanogram develops only after AP has vanished
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95
Q

Electromechanical coupling

A

Connection between electric stimulus and mechanical signal

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96
Q

Which process is shown?

A

Electromechanical coupling

97
Q

1

A

AP spreads onto the cell

98
Q

2

A
  • AP reaches T-tubules
  • Activates L-type Ca2+ channels
99
Q

3

A
  • Conformational changes of L-type channels
  • → T-type channels on SR open
100
Q

4

A
  • Elevating the sarcoplasmic level of Ca2+
  • → Opens Ca2+ dependent channels on SR
101
Q

5

A
  • Elevating sarcoplasmic Ca2+ level
  • Opens Ca2+ dependent channels on cell membrane
102
Q

6

A
  • A huge amount of intracytoplasmic Ca2+ around the sarcomeres
  • Contraction
103
Q

Which process is shown?

A

Elimination of calcium signal

104
Q

1

A

After contraction

Na+/Ca2+ antiporter into extracellular space

105
Q

2

A

ATP-dependent Ca2+ transporter into SR

  • IC Ca2+ conc. decreases
  • Relaxation
106
Q

What is the structural unit of electromechanical coupling?

A

Diad

T-tubules and SR are in contact here

107
Q

Steps of action potential

A
  1. L-type Ca2+ channels open (Voltage-gated)
  2. Rianoid Ca2+ channels open
  3. Elevated Ca2+ in the cytoplasm →
  4. Causes Ca2+ dependent channels to open
  5. Intracytoplasmic Ca2+ around sarcomeres increases
  6. Contraction
108
Q

Describe the ion movement during/after contraction

A
  1. ATP-dependent Ca2+ pump drives Ca2+ back into the SR
  2. Na+/Ca2+ antiport pumps Ca2+ back to the EC space
  3. IC Ca2+ conc. drops
  4. Relaxation
109
Q

What is expressed in the figure?

A

Einthoven’s triangle

  • Einthoven 1: Right Arm ⇔ Left Arm
  • Einthoven 2: Right Arm ⇔ Left Leg
  • Einthoven 3: Left arm ⇔ Left Leg
110
Q

Einthoven’s bipolar leads detect…

A

Changes in the dipole, projected onto the body surface

111
Q

ECG measures…

A

The sum of the electrical activity of single myocytes

112
Q

An ECG is a sum of…

A

An EAG and an EVG

113
Q

Name the trace

114
Q

Name the trace

115
Q

Name the trace

116
Q

How long is this period?

A

0.5-0.10 sec

117
Q

How long is this period?

A

0.12-0.20 sec

118
Q
A

0.06-0.10 sec

119
Q

P-wave

A
  • Upward deflection
  • Atrial depolarisation begins
  • SA node already depolarised (undetectable)
120
Q

PQ-segment

A
  • On isoelectric line
  • Total atrial depolarisation
  • AV conduction
121
Q

QRS-complex

A
  • The beginning of ventricular depolarisation
  • Repolarisation of atrium
122
Q

Q-wave

A
  • Downward deflection
  • Stimulus runs through Bundles of His, through the septum, toward the basis of the heart
123
Q

R-wave

A
  • Max ventricular depolarisation
  • Stimulus runs from endocardium to pericardium
  • From the base to the apex
  • Total ventricular mass depolarises
124
Q

S-wave

A
  • Depolarisation of the right ventricle
125
Q

ST-segment

A
  • Isoelectric line on the oscilloscope
  • Ventricles totally depolarised
126
Q

T-wave

A
  • Ventricular repolarisation
  • Upwards deflection → Man + Small animal
  • Downward deflection → Other species
127
Q

TP-segment

A
  • Resting phase
  • The oscilloscope is at isoelectric line
  • Myocytes are positive outside, negative inside
128
Q

ECG is used in the diagnosis of…

A
  • Pathologic electrical events
  • Problems of conducting system
  • Anatomical disturbances
129
Q

What are the types of ECG?

A
  • Unipolar ECG
  • His bundle ECG
  • Oesophagal ECG
  • Vectorcardiography
130
Q

Unipolar ECG

A
  • RA, LA, LL connected to each other
  • Via 0 potential reference point
  • PD between the reference point and the different points measured
131
Q

His bundle ECG

A
  • An electrode placed up to the septum
  • Through a vein catheter
132
Q

Oesophageal ECG

A

An electrode placed through oesophagus close to the heart

SA, AV nodes + conduction system analysed

133
Q

Vector loop

A
  • Provides information on heart function of territories
  • The connection of vectors from the R wave
134
Q

Vectorcardiography

A
  • Anatomical information of the heart
  • Forms the ‘electrical axis of the heart’
  • Peak values of R-leads: produces a vector
135
Q

Echocardiography

A
  • Ultrasound examination
  • A detailed picture of the cardiac anatomy and blood flow
136
Q

Which fibres passively support the filling of the heart?

A

Serially and Parallelly attached elastic fibres

(SEC/PEC)

137
Q

Give the function of the elastic elements of myocardium

A
  • Passive store of energy while stretched
  • Can be utilised as surplus energy for the next contraction
138
Q

When is SEC stretched?

139
Q

When is PEC stretched?

A

During diastole

140
Q

What is the function of collagen in the myocardium?

A
  • Prevention of overexpansion and rupture
  • Resistant during the maximal filling of the heart
141
Q

Cardiac muscle

A
  • Striated → sarcomeres
  • Shorter than skeletal muscle
  • More mitochondria
  • Less extensive SR
  • Often binucleate and polyploid
  • Continued division after actin/myosin synthesis
142
Q

What are the types of heart contraction?

A
  • Isotonic
  • Isometric
  • Auxotonic
  • Preload
  • Afterload
143
Q

Isometric contraction

A
  • 1st phase
  • Weight stretches SEC elements only
  • Weight doesn’t move yet
  • Stretch present, but no shortening
144
Q

Isotonic contraction

A
  • 2nd phase
  • Stretch with SEC increases
  • Weight begins to move
  • Shortening occurs
  • Stretching force remains
145
Q

What is expressed in the figure?

A

The normal working range of a single working fibre

  • Cardiac muscle shows max tension only at an increased sarcomere length
146
Q
A

Skeletal muscle (Optimum sarcomeric length)

  • Cross bridges in the right place
  • All Ca2+ binding sites saturated
147
Q
A

Cardiac muscle (optimal sarcomeric length)

  • All bridges in correct place
  • Not enough Ca2+
  • Therefore, only a few binding sites are saturated
148
Q
A

Cardiac muscle (Upper-edge of optimal sarcomeric length)

  • Cross bridges in the right place
  • Ca2+ binding sites are saturated
  • This is due to the increased length
149
Q

The degree of contraction of cardiac muscles is dependent on…

A

The length of sarcomeres

150
Q

Compare skeletal and cardiac muscle: At very short sarcomeric lengths

A
  • Both perform less
  • Optimum actin/myosin constellation is distorted
151
Q

Compare skeletal and cardiac muscle: At very large sarcomeric lengths

A
  • Performance is small in both
  • Few/no myosin heads have actin binding sites
152
Q

Compare skeletal and cardiac muscle: between 1.9-2.5 sarcomeric lengths

A
  • An optimal opposition to binding sites and myosin heads occurs
  • Cardiac muscle: Maximal performance requires pre-stretch
153
Q

Give the ‘law of the heart’ (Starling)

A
  • Increased stretch results in increased contraction
  • Irrespective to the innervation of the heart
  • (Like a sling-shot)
154
Q

EDV

A

End-diastolic volume

At the end of diastole, ventricles are maximally filled

155
Q

ESV

A

End-systolic volume

When ventricles are maximally emptied, there is still some blood remaining in them

156
Q

SV

A

Stroke Volume

  • Volume passing through the aorta in each cycle
  • EDV-ESV
157
Q

The formula for Cardiac output

A

(EDV-ESV) x Freq. = CO = SV x Freq.

158
Q

What is shown?

A

Starling’s heart-lung preparation

159
Q

Describe starling’s heart-lung preparation

A
  • Heart can adapt to increased load due to mechanical reasons
  • Also observed in an isolated heart (No nerves/hormones)
  • Arterial side represented by peripheral resistance
  • Venous side represented by a reservoir
160
Q

What was involved in Starling’s two experiments?

A

Experiment 1: Increasing venous return

Experiment 2: Increasing peripheral resistance

Volume fractions were measured for both

161
Q

Describe the effects of increasing venous return

A
  • Immediate EDV increase
  • Delayed ESV increase
  • SV + CO increase

Increased load generates increased contraction

162
Q

Describe the effects of increased peripheral resistance

A
  • Immediate increase in residual volume (ESV↑; SV↓)
  • Delayed ESV and EDV increase proportionally
  • SV increases to the same level

SV and CO will be set as it was before

163
Q

Describe the effects of lying down on the circulation

A
  1. More blood enters ventricle
  2. Dilation
  3. Increased performance
164
Q

Heteromeric autoregulation

A
  1. Increased blood leaving the right compartment
  2. Dilation and stretching of the left side
  3. Starling mechanism activated
  4. Automatic compensation between left and right compartments
165
Q

Heterometry

A

Small differences occurring in the volume of blood appearing the left and right sides of the heart

166
Q

Blood volume passing through the left and right side of the heart should be…

167
Q

Heterometry can be adjusted by…

A

Starling effectt

168
Q

Which two ways can CO be measured?

A
  • Fick’s principle
  • Stewart’s principle
169
Q

Fick’s principle

A

More widely used method

CO:

  • O2 taken up by the lung per unit time = O2 taken up by tissues
  • CO = Total O2 uptake / arterio-venous O2 difference
170
Q

Stewart’s principle

A
  • Inject IV Evans-blue
  • Sample collection + analysis
  • Plot curve and extrapolation
  • Area under the extrapolated cure = CO
171
Q

Ventricular compliance

A

Dilating capacity

172
Q

Ventricular compliance is an important parameter for assessing…

A

Adaptability of the heart

(Dilating ability of ventricles)

173
Q

Value of EDV ventricular pressure

174
Q

EDV ventricular pressure can be extrapolated to give an EDV value of…

175
Q

Describe the increase of EDVP

A
  • Proportional increase of EDV(+SV)
  • Until 25 mmHg
  • (collagen fibres prevent further dilation)
176
Q

Describe ventricular compliance in elderly animals

A
  • Compliance curve is shifted to the right
  • Two-fold EDVP is needed to achieve the normal EDV level
177
Q

Describe the cause of ventricular compliance in elderly animals

A
  • Increased rigidity of elastic fibre
  • Aging of muscle cells
178
Q

The formula for total work of the heart

A

Wt = Wouter + Winner

  • Wouter = Mechanical*
  • Winner = Heat production*
179
Q

Wouter =

A

SV x ΔP

ΔP = (arterial average pressure)

180
Q

Burning 1L oxygen produces…

A

20kJ energy

181
Q

Give the efficiency of the heart

A

10-20% efficiency

182
Q

Kinetic component of outer mechanical work amounts for…% of total work

183
Q

The formula to calculate the performance of the heart

A

P = Work/time = CO

184
Q

What does the Rushmer diagram analyse

A
  • Analyses outer/mechanical work of the heart
  • as a function of volume and pressure of LV
185
Q
A

Rushmer Diagram

186
Q
A
  • Mitral Valves close
  • Isovolumetric contraction
187
Q
A
  • Aortic valves open
  • Ejection phase
188
Q
A
  • Semilunar valves close
  • Isovolumetric relaxation
189
Q
A
  • Mitral valves open
  • Filling
190
Q

Law of Laplace in a pathological context

A

Increased ventricular volume → increased oxygen consumption → Reduced cardiac efficiency

Wall tension maintained only by increased O2 consumption

191
Q

Increased ventricular volume causes…

A

An increase in the energy required by the heart muscle

192
Q

Law of Laplace

A

Constant pressure (P)

within a sphere of increasing radius (r)

can only be maintained by an increase in wall tension (T)

193
Q

Factors influencing cardiac output can be investigated by analysing…

A

The formula used for calculating CO

194
Q

Factors of EDV affecting cardiac output

A
  • Ventricular filling time
  • Ventricular compliance
  • Central venous pressure
195
Q

Factors of ESV affecting cardiac output

A
  • Arterial pressure
  • Contractility
    • Increases by sympathetic
    • Decreases by sympathetic
196
Q

Factors of frequency affecting cardiac output

A
  • Sympathetic effects
  • Parasympathetic effect
197
Q

Contractility

A

The performance of the heart at a given preload and afterload

198
Q

Contractility is characterised by…

A
  • Isometric tension
  • The speed of contraction
199
Q

Clinically, what is the best estimate of contractility?

A

Ejection fraction

200
Q

Give the sympathetic effects of CO frequency

A
  • Artificial increase
    • Duration of diastole
    • therefore CO decreased
  • Natural increase
    1. Reduced systolic time
    2. Reduced diastolic time
    3. CO increases
201
Q

Which system controls the:

  • Chronotrop
  • Dromotrop
  • Bathmotrop
  • Inotrop
A

Sympathetic nervous system

202
Q

An increase in heart rate does not guarantee an increase in…

A

Cardiac output

203
Q

Why doesn’t CO increase with artificial heart rate increase?

A
  • The heart rate increased at the expense of diastole
  • The dilation of ventricles, therefore, doesn’t increase
  • SV therefore increased
204
Q

Sympathetic stimulation increases…

A
  • Heart rate
  • Velocity of contraction
  • Maximal isometric contraction force
205
Q

Why does natural heart rate increase cause larger cardiac output?

A
  1. Sympathetic stimulation
  2. The velocity of contraction increases
  3. Duration of systole decreases
  4. Stroke volume maintained
  5. CO increases
206
Q

What occurs because systole and diastole don’t separate fully in time?

A
  • A fraction of blood can enter the ventricles
  • During ventricular diastole
207
Q

Prior to systole, which muscular motions occur in the heart?

A
  • Twisting of the heart
  • Shift of the heart towards the base and back to the apex
208
Q
209
Q
A

Isovolumetric contraction

210
Q
A

Auxotonic contraction

211
Q
A

Fast ejection

212
Q
A

Slow ejection

213
Q
A

Isovolumetric relaxation

214
Q
A

Fast filling

215
Q
A

Isotonic relaxation

216
Q
A

Reduced filling

217
Q
A

Atrial systole

218
Q
A

Aortic pressure

219
Q
A

Atrial pressure

220
Q
A

Ventricular pressure

221
Q
A

Ventricular volume

223
Q
A

Heart sounds

224
Q

Analysis of ECG and pressure values can show…

A
  • Bloodflow of the heart
  • Role of the valves
225
Q

Atrial contraction

A

Phase 1

  • Begins after P-wave
  • Pressure increase in lumen
  • Blood passes into ventricles through cuspidal valves
  • Ventrical muscles relaxed
  • Aortic BP decreases
226
Q

Isovolumetric phase

A

Phase 2

  • Begins with QRS complex
  • Increased ventricular wall tension
  • Increased pressure
  • AV valves closed
  • Ventricular pressure increases until aortic pressure is reached
227
Q

Rapid ejection

A

Phase 3

  • Semilunar valves open
  • Cuspidal valves closed
  • Blood passes into aorta + pulmonary trunk
  • Increased aortic pressure
228
Q

Reduced ejection

A

Phase 4

  • Semilunar valves open
  • Cuspidal valves remain open
  • Blood passes into aorta + pulmonary trunk
  • Increased aortic pressure
229
Q

Isovolumetric relaxation

A

Phase 5

  • All valves are closed
  • No blood flow
230
Q

Rapid filling

A

Phase 6

  • Semilunar valves closed
  • Cuspidal valves open
  • Low ventricular pressure
  • Ventrical filling
  • Major volume of blood flows into ventricles in this phase
231
Q

Reduced filling

A

Phase 7

  • Cuspidal valves open
  • Semilunar valves closed
  • Ventricular muscles cells relaxed
  • Passive flow into ventricles
  • Aortic pressure drops
232
Q

What generates heart sounds?

A

The closing of valves

233
Q

Ist heart sounds

A

Systolic - closure of cuspid valves

  1. The vibration of contracted muscle
  2. Turbulence due to cuspid closure
  3. Turbulence due to fast ejection
234
Q

IInd heart sounds

A

Diastolic - Closure of semilunar valves

  1. Aoric valve closes
  2. Pulmonary valve closes
  3. Intrathoracic pressure drops
  4. Delayed closure of pulmonary semilunar valves
235
Q

3rd heart sounds

A

Arabic label

Rapid filling of ventricle

236
Q

4th heart sounds

A
  • Turbulent flow
  • Caused by atrial contraction
237
Q

Murmurs are caused by…

A

Stenosis

(distorted heart sounds)

238
Q

Ejection fraction

A

Volumetric fraction of fluid ejected from a chamber with each contraction

Physiology (18 decks)

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