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Year 1 Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

Bundle of pacemaker cells

A

Sinoatrial Node

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2
Q

Location of Sinoatrial node

A

Upper right atrium proximal to the entry of Superior Vena Cava

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3
Q

A heart controlled by the SA Node is said to be in…

A

Sinus Rhythm

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4
Q

Only area of the heart where the impulse can pass from the atria to the ventricle

A

Atrioventricular Node

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5
Q

What is the function of the AV node

A

To delay the spread of the impulse between atria and ventricle to allow complete atrial systole

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6
Q

Speed the impulse down the ventricular walls to the apex where the excitation occurs

A

Bundle of His

Purkinje Fibres

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7
Q

Determines the heart rate

A

Reciprocal action of the parasympathetic and sympathetic

nervous system.

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8
Q

Parasympathetic nerve that controls the heart rate

A

X cranial or vagus nerve

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9
Q

What dominates the heart under resting conditions

A

Vagal tone, at rest parasympathetic impulses dominate

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10
Q

Parasympathetic system innovates in the heart

A

SA and AV node

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11
Q

Sympathetic system innovates in the heart

A

SA, AV and Myocardium

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12
Q

On an ECG. P is

A

Atrial depolarization

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13
Q

On an ECG. QRS is

A

Ventricular depolarization, atrial repolarization is masked

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14
Q

On an ECG. T is

A

Ventricular repolarization

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15
Q

On an ECG. P to R is

A

Largely due to AV node delay

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16
Q

On an ECG. S to T is

A

Ventricular systole

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17
Q

On an ECG. T to P is

A

Diastole

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18
Q

What can cause changes to action potentials

A 
Nerves
Hormones
Cardiac disease
pH and electrolyte imbalances
Drugs
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19
Q

Resting Potential of Ventricular cells

A

Around -90mV

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20
Q

Phase 4

A

Outward flux of K+ is dominant
Background leakage of Na+
Na+/K+ ATPase imports K+ exports Na+ regulates membrane potential

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21
Q

In Phase 4 what ion channels are dominant

A

Inward Rectifier K+ channels or Iki

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22
Q

What drug inhibits the Na+/K+ ATPase

A

Digoxin - slightly depolarizes membrane so slows heart rate but increases force of contractiom

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23
Q

Threshold Potential

A

Around -65mV

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24
Q

Maximum Potential reached during Phase 0

A

Around +30mV

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25
Q

Phase 0

A

Rapid opening of voltage gated Na+ channels leads to depolarization
Voltage gated Na+ channels quickly deactivate

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26
Q

In which type of cells is Phase 1 most dominant

A

Cells with a prominent phase 2 such as Purkinje fibres or epicardial cardia muscle

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27
Q

Type of ion channels open in Phase 1

A

Transient Outward K+ channels or Ito

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28
Q

Phase 1

A

Outward K+ flow is dominant repolarization
Rapid opening of Ito channels by voltage gated K+ channels
Na+ Channels closed

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29
Q

Phase 2

A

Due to balance in conductances inward depolarising Ca2+ and outward repolarizing K+ causes a plateau

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30
Q

What is the importance on Phase 2

A

Entry of Ca2+ into the cell acts as a trigger releasing intracellular Ca2+ from sarcoplasmic reticulum triggering contraction

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31
Q

Where is Intracellular Ca2+ stored

A

Sarcoplasmic Reticulum

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32
Q

What type of ion pumps lead to the plateau in Phase 2

A

Long acting Ca2+ or Ica,L

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33
Q

At what voltage are L-type Ca2+ channels activated

A

Around -30mV

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34
Q

Phase 2- Which K+ pumps are active in 4 but decreased?

A

Iki or Inward Rectifier Potassium Channels

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35
Q

Phase 2- Which K+ pumps continue to exert repolarizing effect initially but reduce over time?

A

Ito or Transient Outward Potassium Channels

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36
Q

Phase 2- Which ion pumps are voltage activated and increase over time?

A

Voltage activated delayed rectifier potassium channels- Ik

  1. Iks are slower so open later
  2. Ikr are initial channels
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37
Q

What is the effect of blocking Ica,l or L-type Ca2+ channels?

A

Reduce duration of Phase 2 and the force of contraction

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38
Q

What is the effect of blocking Ik or delayed rectifier potassium channels?

A

Increase duration of phase 2

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39
Q

Phase 3

A

Outward K+ current exceeds Ca2+ entry so repolarization occurs

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40
Q

Why does hyperpolarization occur in Phase 3

A

L-type Ca2+ channels have inactivated whilst

,Ikr initially the Iks and then Iki dominates in late phase 3, K+ channels have opened

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41
Q

Difference in atrial Cardiac muscle to ventricle in terms of AP

A

Phase 2 is much less evident as an additional K+ channel causes final hyperpolarization to occur faster

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42
Q

What additional K+ channel causes hyperpolarization to cur faster in Atrial cells

A

Ultrarapid delayed rectifier potassium channel or Ikur

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43
Q

Phase 0 AV and SA nodes

A

Activation of voltage gated L-type Ca2+ but no rapid Na2+ so slower depolarization

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44
Q

What 3 time and voltage dependent conductances occur in Phase 4 in AV and SA nodes

A

Outward flow of K+ is reduced , IK is reduced so repolarising factor is reduced
Inward ICa,L effect gradually increases driving membrane potential up until reaches threshold- Phase 0
End of phase 3 HCN channels activated Na+ influx into cell during depolarization

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45
Q

What is special about HCN Channels

A

They are activated by hyperpolarization

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46
Q

What do HCN channels do?

A

Upon activation they trigger a funny current or If, which conducts Na+ into the cell and increase membrane potential slightly

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47
Q

HCN during sympathetic stimulation

A

Channels activate more readily as sensitive to cAMP as a result the slope of the pacemaker potential is increased increasing heart rate

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48
Q

HCN during parasympathetic stimulation

A

Block the HCN channels prohibiting Na+ influx so slope of pacemaker potential is increased reducing heart rate

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49
Q

Selective blocker of HCN

A

Ivabradine,
Used in angina not first line
Reduces heart rate so reduces O2 consumption as a result less toxic build up of waste products alleviating the symptoms

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50
Q

Sympathetic Neurotransmitter

A

Noradrenaline and adrenaline

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51
Q

What receptor does the sympathetic system activate

A

B1 adrenoreceptors in nodal and myocardial cells

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52
Q

Effect of activating sympathetic receptor

A

Gs coupled protein is activated and the alpha subunit stimulates adenyl cyclase to increase intracellular cons of cAMP

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53
Q

What does adenyl cyclase do

A

Increases conversion of ATP to cAMP

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54
Q

What does cAMP

A

Acts as a secondary messenger activating several processes in the cell

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55
Q

Sympathetic effect on heart

A 
Increased If and ICa,L- reduces threshold value and increases slope of pacemaker potential
Increases contraction
Increases Stroke volume 
Increases Conduction velocity in AV node
Automacity increases 
Reduces duration of systole
Increases rate or reactivation
Cardiac hypertrophy over long time
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56
Q

Why under sympathetic influence is the contraction and stroke volume increased?

A

As increased ICa,L more Ca2+ is taken in during phase 2 as a result increased sensitisation of proteins to Ca2+

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57
Q

Why under sympathetic influence is the period of systole reduced?

A

More Ca2+ is taken in so reaches threshold for Ca2+ needed to trigger contraction faster

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58
Q

Why under sympathetic influence is the reactivation period faster?

A

As increased Na+/K+ ATPase so membrane potential is restored faster

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59
Q

Chronotropic effect

A

Those that change the heart rate

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60
Q

Dromotropic effect

A

Changes rate of conductance in AV node

61
Q

Automacity

A

Tendency for non nodal cell to develop spontaneous activity

62
Q

Lucitropic

A

Changes rate of Diastole

63
Q

Parasympathetic Neurotransmitter

A

Acetylcholine

64
Q

Parasympathetic Receptor

A

M2 muscarinic receptors

65
Q

Effect of activating Parasympathetic Receptor

A

Gi coupled protein receptor
Alpha subunit inhibits adenyl cyclase
Beta/Gamma dimer opens specific K+ channels
Causes hyperpolarization

66
Q

What specific K+ channels are activated by Beta/Gamma subunit

A

G protein inward rectifiers or GIRKs

67
Q

Parasympathetic effect

A

Increases threshold reduced pacemaker potential
Reduced If and ICa,L
Reduced atrial contractility
Decreased AV conduction as hyperpolarized

68
Q

Why is contractility in parasympathetic innovation only on atria?

A

As no parasympathetic innovation of ventricles

69
Q

Negative Effect of parasympathetic innovation

A

May trigger atrial fibrillation or tachycardia as impulse is unable to pass into ventricle

70
Q

What channels on the Sarcoplasmic Reticulum are activated by extrinsic Ca2+ entering the cytoplasm?

A

Ryanodine type 2 channels

71
Q

How does Ca2+ cause contraction?

A

Binds to Troponin C and shifts tropomyosin out of actin cleft
Cross bridge forms between actin and myosin resulting in contraction

72
Q

How is Ca 2+ removed from cytoplasm to allow relaxation

A

Na+/Ca2+ exchanger removes Ca2+ from cell

Ca2+ ATPase activates which pumps Ca2+ into sarcoplasmic reticulum

73
Q

How does relaxation of muscles occur?

A

When sarcoplasm concentration of Ca2+ is reduced enough Ca2+ dissociates from troponin c which breaks the cross bridge between actin and myosin

74
Q

Is cardiac muscle striated?

A

Yes as light and dark filaments are lined up

75
Q

What ensures the cardiac cells are mechanically joined

A

Desmosomes, ensure that tension created is transmitted

76
Q

What allows the electrical current to pass between cells?

A

Gap Junctions

77
Q

What is the contractile unit of a cardiac myocyte?

A

Myofibril

78
Q

What is the thin light filament?

A

Actin

79
Q

What is the thick dark filament?

A

Myosin

80
Q

What is the functional unit in a myofibril?

A

Sarcomere

81
Q

What type of reaction is the contraction of cardiac muscle?

A

ATP dependent, Ca2+ is also required

82
Q

Why is the refectory period so long in cardiac muscle?

A

As the Na+ channels are closed and the K+ channels are open so depolarization is unable to occur

83
Q

What does the refractory period in cardiac muscle prevent ?

A

Tetanic Contraction, continuous contraction, allowing diastole to occur.

84
Q

What is cardiac preload

A

How much the muscle is stretched

85
Q

What brings about changes in the stroke volume?

A

Changes in diastolic length of myocardial fibres

86
Q

What brings about changes in the diastolic length of fibres?

A

End diastolic volume

87
Q

What directly effects the end diastolic volume?

A

The volume of venous return

88
Q

Starling law of the heart

A

The more the ventricle is filled (EDV) the greater the volume of blood ejected during systole

89
Q

What does stretching cardiac muscle do?

A

Pushes the contraction cardiac muscle to optimum
Increases troponins affinity for Ca2+
Achieved by increasing venous return

90
Q

Afterload

A

Pressure heart pumps into

91
Q

Effect of increased after load

A

Ventricle can’t pump out full stroke volume
Increases the EDV
As a result of frank starlings mechanics of the heart, contraction rises to overcome

92
Q

What can chronic high after load or hypertension lead to?

A

Hypertrophy of the myocardium

93
Q

When do heart sounds occur

A

Upon the closing of the heart valves

94
Q

What is the mitral valve?

A

This is the left atrioventricular valve

95
Q

First Heart Sound

A

Lub formed when the Atrioventricular and Mitral valves close, S1

96
Q

Second heart sound

A

Dub formed when aortic and pulmonary valves close, S2

97
Q

Five stages of the cardiac cycle

A 
Passive filling
Atrial Contraction
Isovolumetric ventricular contraction
Ventricular Ejection
Isovolumetric Ventricular relaxation
98
Q

Difference in cardiac and smooth muscle

A

No troponin in smooth muscle, calcium binds to calmodulin instead

99
Q

Whats does the calmodulin Ca2+ complex do?

A

It activates myosin light chain kinase which phosphorylates the light myosin chain causing contraction

100
Q

How does smooth muscle relax

A

cGMP protein kinase G activates a myosin light chain phosphatase
The MLCP de-phosphorylates the myosin light chain causing relaxation

101
Q

What is the target of most drugs

A

cGMP is pharmacologically synthesised

102
Q

What to endothelial cells react to?

A

Histamine, Bradykinin, ADP, 5-HT

103
Q

What does the activation of receptors by vasodilation substances trigger

A

Influx of Ca2+ init the cell, calmodulin complexes form which activates eNOS enzymes.

104
Q

What do activated eNOs enzymes do

A

Synthesise NO from L-arginine

105
Q

Action of NO

A

Diffuses directly into the smooth muscle cell where it activates guanylate cyclase

106
Q

Guanylate cyclase

A

Converts GTP into cGMP- required for smooth muscle relaxation

107
Q

Protein Kinase for contraction

A

Protein Kinase A

108
Q

Protein Kinase for relaxation

A

Protein Kinase G

109
Q

Protein Kinase G

A

Increase Ca2+ ATPase and new Ca2 + membrane ATPase increasing removal of Ca2+ from cytoplasm
K+ channels open hyperpolarising cell membrane

110
Q

Where is the main site of systemic vascular resistance?

A

Arterioles

111
Q

What is resistance related to

A

Directly proportional to viscosity and length of blood vessel
Indirectly proportional to radius of blood vessel to the power of 4

112
Q

Is there parasympathetic innervation to vascular smooth muscle?

A

Very little only penis and clitoris have significant

113
Q

What does increasing the sympathetic discharge do?

A

increases vasomotor tone increasing constriction

114
Q

Adrenalines affect of Alpha receptors

A

Found on kidney gut skin etc causes vasoconstriction

115
Q

Adrenalines affect on B2 receptors

A

In cardiac skeletal muscle etc causes vasodilation

116
Q

What other hormones cause Vasoconstriction?

A

Angiotensin II and antidiuretic hormone- intermediate control

117
Q

Intrinsic control

A

Matching blood flow to metabolic demands, overrides extrinsic nerves and hormones

118
Q

What kind of output is the sympathetic nerves

A

Thoracolumbar

119
Q

Where do sympathetic nerves synapse?

A

At ganglion outside the spinal column but not on the organs

120
Q

What are the post synaptic nerves that innervate the heart called and to which vertebrae do they correspond to?

A

Cardiopulmonary Splachnic nerves T1 to T5 and lower cervical

121
Q

What is the cardio plexus

A

Located posterior to aorta on superior heart border, where the sympathetic fibres mingle with parasympathetic and visceral afferent nerves

122
Q

What is sympathetic ganglion neurotransmitter?

A

Acetylcholine

123
Q

What is the sympathetic neurotransmitter to the organ?

A

Noradrenaline

124
Q

What is the parasympathetic neurotransmitter for both the ganglion and the organ?

A

Acetylcholine

125
Q

What is the difference between post synaptic nerves in the sympathetic and parasympathetic system?

A

The parasympathetic nerves are much shorter as the ganglion is located on the surface of the organ itself

126
Q

Viscerent afferent reflex

A

Baroreceptros relayed via Vagus nerve

127
Q

Viscerent Afferent Pain

A

Relayed by sypathetic system

128
Q

What percentage of O2 does the coronary circulation absorb under resting conditions?

A

75%

129
Q

Intrinsic control of coronary circulation

A

Decreased pO2 causes vasodilation, metabolic hyperaemia matches flow to demand
Adenosine a by-product of ATP breakdown is a vasodilator

130
Q

Extrinsic control- functional sympatholysis

A

Despite sympathetic innervation upon sympathetic vasomotor increase, arterioles dilate due to intrinsic override

131
Q

What is the effect of increasing the heart rate on coronary blood flow?

A

As the coronary arteries fill on diastole if you shorten diastole blood flow decreases

132
Q

Function of the circle of willis

A

Means if one of the larger arteries are blocked due to anastomoses brain will still be supplied with oxygenated blood- if a branch of it is blocked small area it supplies is deprived

133
Q

What vessels supply the brain?

A

Right and left internal carotid arteries

Vertebral arteries form the basilar artery

134
Q

How long can grey matter survive without O2 before damage

A

3 minutes

135
Q

What are the two types of stroke?

A

Haemorrhage- vessel burst and bleeds into the brain

Emboli- Vessel is blocked off

136
Q

Within what range is the coronary BP autoregulated?

A

60-100mmHg MAP

137
Q

Does sympathetic stimulation or baroreceptor reflex have any effect on the coronary BP

A

Very little sympathetic and no baroreceptor

138
Q

MABP rise in coronary causes?

A

Vasoconstriction to limit blood flow

139
Q

MABP falls in coronary causes?

A

Vasodilation to increase blood flow

140
Q

Affect of a MABP of less than 50mmHg?

A

Confusion fainting brain damage

141
Q

What does a decrease in pCO2 trigger?

A

Vasoconstriction, hence hyperventilation causes you to faint

142
Q

What other way is the blood flow affected in the brain?

A

For unknown reasons active areas of the brain have increased blood flow

143
Q

How do you work out the cerebral perfusion pressure CPP?

A

CPP=MAP- ICP

ICP is inter cranial pressure usually 8-13mmHg

144
Q

What can cause an increased ICP and in turn reduce perfusion to the brain?

A

Head trauma bleeding brain swelling etc

Brain tumour

145
Q

What is the blood brain barrier?

A

Formed by the cappiliaries in the brain that have very tight intercellular junctions

146
Q

What is the Blood brain barrier permeable to?

A

CO2 O2, Glucose is transported across by facilitated diffusion

147
Q

What is the blood brain barrier impermeable to?

A

H+ ions catelchoamines proteins, this protects brain from the effect of fluctuating levels in the blood

148
Q

What is the pulmonary pressure?

A

10% of systemic pressure

149
Q

What is the reason for allow pulmonary pressure?

A

So the absorptive forces exceed filtration to prevent build up of oedema

Year 1 Cardiology (17 decks)

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