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Medicine Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

Autorhythmicity

A

The ability of the heart to beat rhythmically in the absence of external stimuli

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2
Q

Where does the excitation normally originate?

A

In the pacemaker cells in the Sino-atrial node

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3
Q

If the heart is controlled by the Sino-atrial node, what rhythm is it in?

A

Sinus rhythm

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4
Q

Where is the Sino-atrial node located?

A

The upper right atrium close to where the superior vena cava enters the right atrium

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5
Q

Spontaneous pacemaker potential

A

The ability of the cells in the sino-atrial node to slowly drift into depolarisation spontaneously

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6
Q

What happens when the threshold by the spontaneous pacemaker potential is reached?

A

An action potential is generated, resulting in the generation of regular spontaneous action potentials in the SA nodal cells

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7
Q

What is the pacemaker potential due to?

A

Decrease in K+ efflux, Na+ influx and the transient Ca++ influx

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8
Q

What is depolarisation caused by?

A

The rising phase is caused by activation of long lasting L-type calcium channels resulting in calcium influx

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9
Q

What is repolarisation caused by?

A

The falling phase of action potential is caused by inactivation of L-type calcium channels and activation of potassium channels resulting in potassium efflux

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10
Q

Describe the spread of cardiac excitation across the heart

A
  • Originates in SA node and crosses atria through mainly cell-to-cell gap communication via junctions
  • Excitation reaches AV node, mainly by the same mode but also some internodal pathways
  • Conduction delayed in AV node, allowing atrial systole to precede ventricular systole
  • Bundle of his and purkinje fibres allow rapid spread of action to ventricles
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11
Q

Gap junctions

A

Low resistant protein channels which allow the impulse to spread quickly through the cardiac cycle

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12
Q

The only point of contact between the atria and the ventricles

A

Atrio-ventricular node

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13
Q

Resting membrane potential of pacemaker cells

A

-60mV

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14
Q

Resting membrane potential of cardiac muscle cells

A

-90mV

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15
Q

What causes the rising phase of action potential in pacemaker cells vs cardiac muscle cells?

A

Pacemaker cells = calcium influx

Cardiac muscle cells = sodium influx

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16
Q

Excited action potential of cardiac muscle cells

A

+20mV

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17
Q

Phases of ventricular muscle action potential

A 
Phase 0 = fast Na+ influx
Phase 1 = closure of Na+ channels and transient K+ efflux
Phase 2 = mainly Ca++ influx
Phase 3 = Ca++ influx and K+ efflux
Phase 4 = resting membrane potential
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18
Q

Plateau phase of action potential

A

When the membrane potential is maintained the near the peak of action potential for a few hundred milliseconds

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19
Q

What is the plateau phase of ventricular muscle action potential mainly due to?

A

Influx of Ca++ through L-type calcium channels

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20
Q

What is the falling phase of ventricular muscle action potential due to?

A

Inactivation of calcium channels and activation of potassium channels resulting in potassium efflux

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21
Q

Main influence of heart rate

A

The autonomic nervous system. Sympathetic stimulation increases heart rate, parasympathetic stimulation decreases heart rate

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22
Q

Which nerve dominates under resting conditions?

A

Vagus nerve - vagal tone

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23
Q

What does vagal tone do under resting conditions?

A

Slows intrinsic heart rate from about 100bpm to about 70bpm

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24
Q

Normal heart rate
Bradycardia
Tachycardia

A 
Normal = 60-100bpm
Bradycardia = <60bpm
Tachycardia = >100bpm
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25
Q

Chronotropic effect

A

Something that changes the heart rate
Positive chronotropic effect = increase heart rate and slope of pacemaker potential increases
Negative chronotropic effect = decrease heart rate and slope of pacemaker potential decreases

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26
Q

Which parts of the heart does the vagus nerve supply?

A

SA node and AV node

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27
Q

Vagus nerve:

  • What does stimulation do?
  • Neurotransmitter
  • Which receptors does the neurotransmitter act through?
  • Inhibitor of neurotransmitter, when it is used and what it does
A
  • Slows heart rate and increase AV nodal delay
  • Acetylcholine
  • Muscarinic 2 receptors
  • Atropine, used in extreme bradycardia to increase heart rate. Causes the cell to hyperpolarise and takes it takes longer to reach the threshold, frequency of action potentials decrease
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28
Q

What part of the heart does the sympathetic nerve supply?

A

SA node, AV node and myocardium

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29
Q

Sympathetic nerve:

  • What does stimulation do?
  • Neurotransmitter
  • Which receptor does the neurotransmitter act through?
  • What does the neurotransmitter do?
A
  • Increases heart rate, decreases AV nodal delay and increases force of contraction
  • Noradrenaline
  • Beta-2-adrenoreceptors
  • Pacemaker potential reaches threshold quicker and the frequency of action potentials increases
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30
Q

Fast response action potential:

  • Where is it present?
  • Phases
  • What is it mediated by?
A
  • Atrial and ventricular muscle cells and purkinje
  • Phase 0 (upstroke), phase 1 (partial rapid depolarisation), phase 2 (plateau), phase 3 (repolarisation), phase 4 (resting potential)
  • Voltage activated sodium channels
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31
Q

Slow response action potential:

  • Where is it present?
  • Phases
  • What is it mediated by?
A
  • Sino-atrial node and atrio-ventricular node
  • Phase 0 (upstroke), phase 3 (repolarisation), phase 4 (resting potential)
  • Mediated by voltage activated calcium channels
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32
Q

Influences on the cardiac action potential:

A
  • Normal, physiological influences e.g. autonomic transmitters and some hormones
  • Cardiac disease
  • pH of blood and electrolyte imbalance
  • Drugs, either intentionally (as treatment), or unintentionally as adverse effects
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33
Q

How does the atrial action potential differ from the ventricular action potential?

A

Phase 2 is not quite a plateau due to an increase in potassium channels

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34
Q

What is striation of the cardiac muscle caused by?

A

Regular arrangement of contractile proteins

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35
Q

What do the desmosomes in the heart do?

A

Provide mechanical adhesion between adjacent cardiac muscle cells. They ensure that the tension developed by one cell is transmitted to the next

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36
Q

Actin, myosin and sarcomeres

A 
Actin = thin filaments
Myosin = thick filaments
Sarcomeres = what actin and myosin are arranged into within each myofibril
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37
Q

Smallest contractile units in the heart

A

Sarcomeres

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38
Q

How is muscle tension produced?

A

Sliding of actin filaments on myosin filaments, shortening the sarcomere and producing force

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39
Q

What does force generation of the sliding filament theory depend on?

A

ATP-dependent interaction between actin and myosin

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40
Q

What is required for sliding filament theory?

A
  • ATP (for both contraction and relaxation)

- Calcium (to switch on cross bridge formation)

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41
Q

Calcium release:

  • Where is it stored and released from?
  • What does release depend on?
A
  • Stored in and released from sarcoplasmic reticulum

- Release depends on presence of extra-cellular calcium

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42
Q

Calcium during diastole

A

Intercellular calcium will be low and not sufficient enough to cause a reaction by binding to troponin

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43
Q

Calcium during systole

A

Calcium influx during the plateau phase of action potential causes calcium release from sarcoplasmic reticulum. Surge allows binding to troponin and contraction can occur

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44
Q

Refractory period

A

Period following an action potential where it is not possible to produce another action potential

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45
Q

Function of the refractory period and how long it lasts

A

Prevents generation of tectonic contraction

Lasts almost as long as contraction lasts

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46
Q

Stroke volume:

  • Definition
  • What is it regulated by?
  • How can it be calculated?
A
  • Volume of blood ejected by each ventricle per heartbeat
  • Regulated by intrinsic and extrinsic mechanisms
  • End diastolic volume - end systolic volume
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47
Q

What determines the stroke volume?

A

Stretch of myocardial fibres

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48
Q

End diastolic volume

A

Volume of blood within each ventricle at the end of diastole

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49
Q

What determines the end diastolic volume?

What does the end diastolic volume determine?

A
  • Venous return to the heart determines the EDV

- EDV determines the cardiac preload

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50
Q

Cardiac preload

A

How much the heart is loaded with blood before it contracts

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51
Q

What does the Frank-Starling mechanism describe

A

The relationship between venous return, end diastolic volume and stroke volume.
The more the ventricle is filled with blood, the greater the volume of blood ejected

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52
Q

Afterload

A

The resistance into which the heart is pumping

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53
Q

Intrinsic control of stroke volume

A

Nerves and hormone

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54
Q

Inotropic effect

A

Something that changes force of contraction of the heart
Positive inotropic effect - something that increases force of contraction (e.g. stimulation of sympathetic nerves)
Negative inotropic effect - something that decreases force of contraction

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55
Q

Effects of sympathetic stimulation on ventricular contraction

A

Force increases, peak ventricular pressure increases, rate of pressure change during systole increases (reducing the duration of systole)
Peak ventricular pressure rises - contractility of the heart at a given end diastolic volume rises and frank-starling curve shifted to the left

56
Q

Effects of parasympathetic stimulation on ventricular contraction

A

Very little innervation of ventricles by vagus nerve and therefore has little, if any, direct effect on stroke volume

57
Q

Extrinsic control of stroke volume

A

Adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effects. These effects are usually minor compared to the effects of noradrenaline from sympathetic nerves

58
Q

Cardiac output

A

The volume of blood pumped by each ventricle per minute. CO = SV x HR

59
Q

Resting cardiac output in a healthy adult

A

5L per minute

60
Q

Cardiac cycle

A

Refers to all events that occur from beginning of one heartbeat to the beginning of the next

61
Q

At heart rate of 75bpm, what are the times for diastole and systole

A

Diastole = 0.5 sec, Systole = 0.3 sec

62
Q

Events during the cardiac cycle (5)

A 
1 = passive filling
2 = atrial contraction
3 = isovolumetric ventricular contraction
4 = ventricular ejection
5 = isovolumetric ventricular relaxation
63
Q

What happens during passive filling?

A

Pressure in atria and ventricles is close to zero (with atrial pressure being slightly higher), AV valves open due to pressure gradient so venous return flows to ventricles. Same things happen on right side of heart but smaller pressures

64
Q

The ventricles become 80% full by what?

A

Passive filling

65
Q

Pressure in the aorta in passive filling

66
Q

In an ECG, when is atrial contraction?

A

P wave signals depolarisation which causes atria to contract. Contract between P wave and QRS

67
Q

What happens during isovolumetric ventricular contraction?

A

Ventricular pressure rises, and when it exceeds atrial pressure AV valves shut, producing first heart sound. Tension rises around a closed volume - isovolumetric contraction. Ventricular pressure rises steeply

68
Q

What happens during ventricular ejection?

A

Ventricular pressure > aorta/pulmonary pressure, these valves open. Stroke volume is ejected, leaving end systolic volume. Aortic pressure rises, ventricles relax and pressure falls, and when ventricular pressure < aorta/pulmonary pressure, valves shut producing second heart sound

69
Q

What produces the dicrotic notch in the aortic pressure curve?

A

Vibration of pulmonary and aortic valves closing

70
Q

What happens during isovolumetric ventricular relaxation?

A

Closure of semi-lunar valves signals start of isovolumetric relaxation. Ventricle is closed box as AV valve is shut. Tension falls around a closed volume - isovolumetric relaxation. When ventricular pressure < atrial pressure, AV valves open and new cardiac cycle begins

71
Q

Heart sounds - what causes the first and second heart sound?

A

First heart sound - closing of mitral and tricuspid valves

Second heart sound - closing of aortic and pulmonary valves

72
Q

Why does atrial pressure not fall to zero during diastole?

A

When the blood is ejected during systole, the arteries and heart stretch, and these recoil when the heart relaxes preventing pressure from falling to zero

73
Q

What is vasomotor tone caused by?

A

Tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

74
Q

Exceptions to significant parasympathetic innervation of arterial smooth muscles

A

Penis and clitoris

75
Q

What occurs when adrenaline acts on:

  • Alpha receptors?
  • Beta receptors?
A

Alpha - vasoconstriction

Beta - vasodilatation

76
Q

Where are alpha receptors predominantly found?

A

Skin, gut and kidney arterioles

77
Q

Where are beta receptors predominantly found?

A

Cardiac and skeletal muscle arterioles

78
Q

Examples of humoral agents which cause relaxation of arteriolar smooth muscles resulting in vasodilation

A

Histamine, bradykinin, nitric oxide

79
Q

Examples of humoral agents which cause contraction of arteriolar smooth muscles resulting in vasoconstriction

A

Serotonin, thromboxane A2, leukotrienes, endothelin

80
Q

Factors contributing to endothelial damage/dysfunction

A

High blood pressure, high cholesterol, diabetes, smoking

81
Q

Nitric oxide:

  • Where is it produced?
  • Which amino acid is it produced from?
  • How does it act?
A
  • Vascular endothelium
  • L-arganine through enzymatic action of nitric oxide synthase
  • Diffuses from vascular endothelium to adjacent smooth muscle cells where it activates formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation
82
Q

Temperature response to dilation of blood vessels

A 
Cold = vasoconstriction
Warmth = vasodilatation
83
Q

Factors influencing venous return

A

Venomotor tone, skeletal muscle pump, blood volume, respiratory pump

84
Q

Respiratory pump and venous return

A

Increases pressure gradient for venous return and creates a suction effect that moves blood from veins towards the heart

85
Q

Cardiovascular response to exercise

A
  • Sympathetic nerve activity increases
  • HR and SV increase, increasing CO
  • Vasoconstriction to kidneys and gut (via sympathetic vasomotor nerves)
  • In skeletal and cardiac muscle, metabolic hyperaemia overcome vasomotor drive causing vasodilatation
  • Blood flow to skeletal and cardiac muscle increases in proportion to metabolic activity
  • Increase in CO increases systolic BP, metabolic hyperaemia decreases SVR and diastolic BP
86
Q

Chronic cardiovascular responses to regular exercise?

A
  • Reduction in sympathetic tone and noradrenaline levels
  • Increase parasympathetic tone to heart
  • Cardiac remodelling
  • Reduction in plasma renin levels
  • Improved endothelial function
  • Decreased arterial stiffening
87
Q

What are lipids essential for?

A

Membrane biogenesis and membrane integrity

88
Q

Functions of lipids

A

Energy sources, precursors for hormones and signalling molecules

89
Q

How are non-polar lipids transported in the blood?

A

With lipoproteins

90
Q

What do lipoproteins consist of?

A

A hydrophobic core containing esterified cholesterol and triacylglycerols and a hydrophilic coat consisting of amphipathic cholesterol, phospholipids and one or more apoproteins

91
Q

4 major classes of lipoproteins

A

HDL
LDL
Very-low density lipoproteins
Chylomicrons

92
Q

What is the largest class of lipoproteins?

A

Chylomicrons

93
Q

Apoproteins associated with HDL

A

apoA-I and apoA-II

94
Q

Apoprotein associated with LDL

95
Q

Apoprotein associated with very low density lipoproteins

96
Q

Apoprotein associated with chylomicrons

97
Q

Chylomicrons:

  • Where are they formed?
  • What do they do?
A
  • Enterocytes in the intestinal cells
  • Transport dietary triglycerides via the exogenous pathway. Enter lymph nodes and then bloodstream and then deliver triglycerides to organs
98
Q

What do apoB-containing lipoproteins do?

A

Deliver triacylglycerols to muscle for ATP biogenesis and adipocytes for storage

99
Q

VLDL:

  • Where are they formed?
  • What do they do?
A
  • Formed in liver hepatocytes

- Transport triacylglycerols synthesised by liver to other organs via the endogenous pathway

100
Q

Briefly, how are chylomicrons formed?

A

Monoglycerides and free fatty acids diffuse across the apical membrane of the enterocyte and are reassembled inside into a triacylglycerol
Protein synthesis occurs

101
Q

Briefly, how are very low density lipoproteins formed?

A

Assembled in the liver hepatocytes from free fatty acids, then microsomal triglyceride metabolism protein ladipates apoB-100 forming nascent VLDL that coalesces with TAG droplets

102
Q

How are chylomicrons and VLDL particles activated?

A

By the transfer of apoC-II from HDL particles

103
Q

Lipoprotein lipase

A

Lipolytic enzyme associated with endothelium of capillaries in adipose and muscle tissue

104
Q

Describe intravascular metabolism of apoB-containing lipoproteins?

A
  • apoC-II facilitates binding of these to LPL
  • LPL hydrolyses triacylglycerols to free fatty acids and glycerol which enter tissues
  • Chylomicron and VLDL remnants are now ready for clearance from the plasma
105
Q

After metabolism, where to the remnants of chylomicron and VLDL go and what happens to them?

A

They are returned to the liver and are further metabolised by hepatic lipase

106
Q

How are all of chylomicron remnants and 50% of VLDL remnants cleared?

A

By receptor-mediated endocytosis into hepatocytes

107
Q

What is clearance of LDL particles dependent on?

A

The LDL receptor expressed by the liver and other tissues

108
Q

Functions of released cholesterol

A
  • Inhibits HMC-CoA reductase (rate limiting enzyme in de novo cholesterol synthesis)
  • Down regulated LDL receptor expression
  • May be stored as cholesterol ester or used as a precursor for bile salt synthesis
109
Q

First step in the disease progression of atherosclerosis

A

Uptake of LDL from blood into the intima of the artery, where the LDL is oxidised to atherogenic oxidised LDL

110
Q

How are fatty streaks formed in the disease progression of atherosclerosis?

A

Uptake of oxidised LDL by macrophages using scavenger receptors converts them to cholesterol-laden foam cells that form a fatty streak

111
Q

Key role of HDL

A

Removes excess cholesterol from cells by transporting it in the plasma to the liver, where it is eliminated from the body

112
Q

Special adaptations of coronary circulation (3)

A

High capillary density, high basal blood flow, high oxygen extraction under resting conditions

113
Q

When the coronary circulation requires extra oxygen, how is it supplied?

A

By increasing coronary blood flow

114
Q

Intrinsic mechanisms that control coronary blood flow (3)

A

Decreased PO2 causes vasodilatation of the coronary arterioles, metabolic hyperaemia matches flow to demand, adenosine from ATP is a potent vasodilator

115
Q

In extrinsic mechanism of coronary blood flow, what is vasoconstriction overridden by?

A

Metabolic hyperaemia as a result of increased heart rate and stroke volume

116
Q

When does peak left coronary flow occur?

A

During diastole

117
Q

Which arteries supply the brain?

A

Internal carotids and vertebral arteries

118
Q

How long after ischaemia does loss of consciousness and irreversible cell damage occur?

A

Loss of consciousness - a few seconds

Irreversible cell damage - without 3 minutes

119
Q

Circle of Willis formation

A

Basilar and carotid arteries anastomose to form Circle of Willis

120
Q

What arises from the Circle of Willis?

A

Major cerebral arteries

121
Q

Why is the Circle of Willis clinically useful?

A

Cerebral perfusion should be maintained even if one cerebral artery gets obstructed

122
Q

What does autoregulation of cerebral blood flow do?

A

Guards against change in cerebral blood flow if MAP changes within a range (60-100mmHg)

123
Q

When will autoregulation of cerebral blood flow fail?

A

If MABP falls below 60mmHg or rises above 100mmHg

124
Q

What can MABP below 50mmHg result in if not quickly corrected?

A

Confusion, fainting and brain damage

125
Q

Contents of the skull

A

Brain - 80%, blood - 12%, cerebrospinal fluid - 8%

126
Q

Calculation for cerebral perfusion pressure

A

Cerebral perfusion pressure = MAP - intracranial pressure

127
Q

What are cerebral capillaries highly permeable to?

A

Oxygen and carbon dioxide

128
Q

How does glucose cross the blood brain barrier?

A

By facilitated diffusion

129
Q

What is the blood brain barrier exceptionally impermeable to?

A

Hydrophilic substances such as ions, catecholamines, proteins etc.

130
Q

Why is it helpful that the blood brain barrier is exceptionally impermeable to hydrophilic substances?

A

Helps protect brain neurones from fluctuating levels of ions in the blood

131
Q

Pulmonary artery blood pressure

A

20-25/6-12mmHg

132
Q

Pulmonary capillary pressure vs systemic capillary pressure

A

Pulmonary - 8-11mmHg

Systemic 17-25mmHg

133
Q

Special adaptions of pulmonary circulation

A
  • Pulmonary capillary pressure low compared to systemic
  • Absorptive forces exceed filtration forces, protecting against oedema
  • Hypoxia causes vasoconstriction of pulmonary arterioles, opposite to hypoxia on systemic arterioles as it helps divert blood from poorly ventilated areas of the lung
134
Q

Skeletal muscle blood flow increase during exercise

A

Local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity, circulating adrenaline causes vasodilatation, CO increases during exercise (increasing skeletal muscle blood flow by many folds)

135
Q

The skeletal muscle pump

A

Large veins lie in between skeletal muscles and the contraction of these muscles aids venous return

Medicine Cardiovascular (24 decks)

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