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Cardiovascular System > Physiology > Flashcards

Physiology Flashcards

Cards 1-48 cover lectures 1-3 and are good intro. 50-63 is cardiac cycle.

1
Q

What word is used to describe the fact that the heart is capable of beating rhythmically in the absence of external stimuli?

A

Autorhythmicity

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2
Q

Where in the heart does the excitation normally originate?

A

In the pacemaker cells in the sino-atrial node/ SA Node

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3
Q

Where is the SAN?

A

SA node is located in the upper right atrium close to where the vena cava enters the right atrium.

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4
Q

In terms of membrane potentials what makes the SA node cells different to most?

A
  • do not have a stable resting membrane
  • exhibit spontaneous pacemaker potential
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5
Q

What is the pacemaker potential?

A

The pacemaker potential is the slow depolarisation of membrane potential to a threshold

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6
Q

What is responsible for the pacemaker potential?

A
  1. Decrease in K+ efflux
  2. Na+ and K+ influx i.e. the funny current
  3. Transient Ca+ Influx (t-type Ca+ channels)
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7
Q

Draw graph for pacemaker action potential.

A
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8
Q

List the 3 parts of pacemaker action potential graph

A
  1. Pacemaker potential
  2. Rising Phase of Action Potential
  3. Falling Phase of Action Potential
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9
Q

Describe rising phase of action potential of SAN and AVN (both physiologically and on a graph)

A

GRAPH

Slope upwards from -40mV to 0mV

Sudden increase in gradient

PHYSIOLOGICALLY

Caused by activation of L-Type Ca2+ channels resulting in Ca2+ influx

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10
Q

Describe the falling phase of action potential (both physiologically and on a graph)

A

GRAPH Downward slope of graph from peak at 0mV to -60mV PHYSIOLOGICALLY caused by -inactivation of L-type Ca2+ channels -activation of K+ channels resulting in K+ efflux

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11
Q

The pacemaker cells in the SAN start excitation in the heart but how does it spread?

A

Spreads cell-to-cell via gap junctions -from SAN through both atria -from SAN to AVN (although there is some internodal pathways) -within ventricles

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12
Q

What is the AVN and where is it located?

A

The atrio-ventricular node is a small bundle of specialised cardiac cells Located at base of right atrium, just above junction between atria and ventricles

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13
Q

List the two v.important points about AVN

A
  1. AVN= only point of electrical contact between atria and ventricles 2. AVN cells are small in diameter:. slow conduction velocity
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14
Q

What is significant about AVN cells diameter?

A

AVN cells have smaller diameter :. slower conduction :. atrial systole can finish before ventricular systole starts i.e. it is responsible for the brief pause between the atria contracting and the ventricles contracting

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15
Q

What is the purpose of Bundle of His and Purkinje fibres?

A

Allows rapid spread of action potential to the ventricles Also insures contraction of ventricles works from the apex up

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16
Q

Draw graph for action potential on atrial and ventricular myocytes

A

Week 1, Lecture 2, Alide 23

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17
Q

Describe what happens in each phase of ventricular muscle action potential

A

PHASE 0:Fast influx of Na+

PHASE 1 : Closure of Na+ channels and Transient K+ efflux

PHASE 2: Mainly Ca2+ influx through L-type Ca2+ channels

PHASE 3: Closure of Ca2+ channels and K+ efflux

PHASE 4: Resting membrane potential at -90mV

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18
Q

What changes the heart rate?

A

The autonomic nervous system

  • Sympathetic stimulation increases heart rate
  • Parasympathetic stimulation decreases heart rate
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19
Q

Which part of the autonomic nervous system controls a healthy heart in resting conditions?

A

the vagus nerve exerts a continuous influence on the SAN

  • vagal tone slows the intrinsic heart rate from 100bpm to produce a normal resting heart rate of 70bpm
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20
Q

Define bradycardia

A

A resting heart rate less than 60 bpm

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21
Q

Define tachycardia

A

A resting heart rate more than 100 bpm

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22
Q

Give a brief description of parasympathetic supply of the heart

A
  • vagus nerve supplies SAN and AVN
  • negative chronotrophic effect by decreasing slope of pacemaker potential :. decreasing freq. of action potential
  • increases the AV nodal delay
  • Of course, neurotransmitter is acetylcholine acting through muscarinic M2 receptors
  • Fun Fact: atropine= competitive inhibitor is acetylcholine :. used in extreme bradycardia
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23
Q

Give a brief description of sympathetic supply of the heart

A

-cardiac sympathetic nerves supply SAN, AVN, AND MYOCARDIUM ~positive chronotrophic effect by increasing slope of pacemaker potential :. pacemaker potential reached quicker :. freq. of action potentials increases ~decreases AV nodal delay Of course, neurotransmitter is noradrenaline acting through Beta1 receptors

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24
Q

What is the purpose of a desmosome?

A

The desmosomes within the intercalated discs provide mechanical adhesion between adjacent cardiac cells -they ensure the tension developed by one cell is transmitted

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25
Q

Describe the structure of a sarcomere.

A

A muscle fibre is made up of myofibrils which are made up of sarcomeres which are made up of actin and myosin filaments

Sarcomeres are covered in a sarcoplasmic reticulum

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26
Q

What is needed for the sliding action of actin and myosin filaments?

A

ATP (for the myosin head)

and Ca (to get tropomyosin & :. tropin complex to twist to reveal part of actin filament that myosin head binds to)

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27
Q

Describe sarcolemma

A

The sarcolemma wraps around the muscle fibre itself.

The sarcoplasmic reticulum surrounds myofibrils.

T-tubules (not very important for you) run through the muscle fibre at regular intervals and are involved in muscle contraction.

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28
Q

Ca2+ is required for muscle contraction but where does it come from?

A

Comes from sarcoplasmic reticulum but NB: the release of Ca2+ from sarcoplasmic reticulum is dependent on presence of extra-cellular Ca2+

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29
Q

When and how does Ca2+ enter the sarcoplasmic reticulum?

A

Remember in the Plateau Phase of Ventricular Muscle Action Potential there is a Ca2+ influx through L-type Ca2+ channels? This is the key!! This Ca2+ is not enough to cause the next contraction but it is the trigger

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30
Q

Define a refractory period

A

A refractory period is a period following an action potential in which it is not possible to produce another action potential

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31
Q

Draw a graph showing the ventricular muscle action potential & tension developed by muscle fibre and draw in the refractory period.

A
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32
Q

What does the refractory period in myocytes do?

A

Prevent heart attacks

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33
Q

Define stroke volume

A

Stroke Volume is the volume of ejected blood by each ventricle per heart beat

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34
Q

Calculate stroke volume

A

SV= End Diastolic Volume- End Systolic Volume

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35
Q

Very simply, how is the stroke volume controlled?

A

Stroke volume is regulated by intrinsic and extrinsic mechanisms.

  • Intrinsic= within the heart muscle itself
  • Extrinsic= Nervous and hormonal control
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36
Q

What do you need to know about end disastolic volume?

A
  1. The EDV determines the diastolic length of myocardial fibres a) changes in Stroke Volume are brought about by changes in diastolic length of myocardial fibres
  2. The EDV determines the Preload (how much blood heart is holding before it contracts)
  3. The EDV is determined by the venous return to the heart
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37
Q

Draw a graph depicting the Frank-Starling curve

A

Week 1, Physiology Lecture 3, Slide 26

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38
Q

State the Frank-Starling Mechanism/Starling’s Law of the Heart

A

Starling’s Law of the Heart states: ‘the more the ventricle is filled with blood during diastole, the greater the volume of ejected blood will be during the resulting systolic contraction’.

I.E. ‘the larger the end diastolic volume, the greater the stroke volume will be’

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39
Q

Define afterload

A

Afterload means the resistance into which the heart is pumping

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40
Q

What can increased afterload lead to?

A
  1. Heart unable to eject full SV, so EDV increases
  2. Force of contraction increases by Frank-Starling mechanism
  3. Eventually ventricular muscle mass increases (ventricular hypertrophy) to overcome resistance
41
Q

Explain, briefly, extrinsic control of stroke volume

A

nerves & hormones

  • ventricular muscle is supplied by sympathetic nerve fibres (neurotransmitter= noradrenaline)
  • stimulation causes increase of force of contraction
  • a positive inotrophic effect
  • NB: stimulation of sympathetic nerves to the heart also causes positive chronotrophic effect
42
Q

What is the effect of sympathetic stimulation on ventricular contraction at an ionic basis?

A

activation of Ca2+ channels :. greater influx of Ca2+

  • effect is cAMP mediated -increased rate of Ca2+ pumping (rate of ventricular relaxation increases)
43
Q

Draw a graph of the effect of sympathetic stimulation on ventricular contraction.

A

Week 1, Physiology Lecture 3, Slide 34

  • peak ventricular pressure rises
  • rate of pressure change during systole increases
  • reduces duration of systole
  • rate of ventricular relaxation increases
  • reduces duration of diastole
44
Q

What happens to stroke volume on sympathetic stimulation?

A

Frank-Starling curve shifted to the left

45
Q

What effect does heart failure have on the Frank-Starling curve?

A

Shifts to the right -heart failure causes negative inotrophic effect

46
Q

What effects can vagal stimulation have on heart?

A

Vagal stimulation has major influence on rate, not force of contraction!!!!

47
Q

Hormones are also involved in the extrinsic control of the heart. Discuss.

A

Adrenaline & noradrenaline released from adrenal medulla have inotrophic & chronotrophic effect

  • NB: Release of hormones usually happens in association with symapthetic stimulation but DO NOT get this confused with sympathetic system release neurotransmitter
48
Q

Define cardiac output

A

Cardiac output is described as the volume of blood pumped by each ventricle per minute.

CO= SV x HR

:. if we can regulate stroke volume & heart rate we regulate the cardiac output!

49
Q

What must you remember about valve sounds?

A

They make a noise when they shut; not when they open!

50
Q

Define cardiac cycle

A

The orderly depolarisation/repolarisation sequence triggers a recurring cardiac cycle of atrial and ventricular contractions and relaxations

51
Q

Define diastole

A

The heart ventricles are relaxed and fill with blood.

It takes double the time systole takes.

52
Q

Define systole

A

The heart ventricles contract and pump blood into the aorta and pulmonary artery.

53
Q

What valves are open during systole?

A

Atrio-ventricular valves are closed

  • a.k.a mitral (LHS) and tricuspid (RHS)

Aortic and Pulmonary valves are open.

54
Q

What valves are open during diastole?

A

Atrio-ventricular valves are open

  • a.k.a. mitral (LHS) and tricuspid (RHS)

Aortic and Pulmonary valves are closed.

55
Q

List the events (in order) of the cardiac cycle

A
  1. Passive Filling
  2. Atrial Contraction
  3. Isovolumetric Contraction
  4. Ventricular Ejection
  5. Isovolumetric Ventricular Relaxation
56
Q

Discuss the passive filling step of the cardiac cycle

A
  • pressure in atria and ventricles close to zero
  • AV valves open so venous return flows into the ventricles
  • aortic pressure is 80mmHg and aortic valves is closed
  • ventricles become 80% full by passive filling
  • similar events happen in the right side of the heart, but the pressures (right ventricular & pulmonary artery) are much lower
57
Q

Describe the atrial contraction part of that mental graph

A
  • the P-wave in the ECG signal atrial depolarisation
  • the atria contracts between the P-Wave and the QRS
  • Atrial contraction complete the End Diastolic Volume (~130ml in resting normal adult) the end diastolic pressure is few mmHg
58
Q

Describe the isovolumetric ventricular contraction phase of that God-awful hopefully you’ll learn to love it graph

A
  • ventricular contraction starts after the QRS (which signals ventricular depolarisation) in the ECG
  • ventricular pressure rises
  • when ventricular pressure exceeds atrial pressure the AV valves shit
  • LUB sound
  • aortic valve remains shut
  • Isovolumetric Contraction (rise in tension around a closed volume)
  • Ventricular pressure rises very steeply
59
Q

Describe the Ventricular Ejection stage of the graph that looks as complicated as Ross & Rachel’s relationship (#goals)

A
  • when ventricular pressure exceeds aorta/pulmonary artery pressure aortic/pulmonary valves open -silent event
  • Stroke Volume is ejected leaving the End Systolic Volume -SV= EDV - ESV -aortic pressure rises
  • T-Wave in the ECG signals ventricular repolaristion
  • ventricles relax and ventricular pressure starts to fall
  • ventricular pressure falls below aortic/pulmonary pressure: aortic/pulmonary valves shut
  • Dub sound
  • Dicrotic notch in aortic pressure curve produced by valve vibration
60
Q

Describe the part of that leaves you more confused and terrified than the meaning of life that depicts Isovolumetric Ventricular Relaxation

A
  • closure of aortic/and pulmonary valves signals the start of the isovolumetric ventricular relaxation
  • ventricle is again a closed box, as the AV valve is shut
  • the tension falls around a closed volume: ‘isovolumetric relaxation’
  • when ventricular pressure falls below atrial pressure, AV valves open and a new cycle starts
61
Q

What does JVP stand for?

A

Jugular Venous Pressure

62
Q

When is JVP useful in clinical skills?

A

It is an effective indirect measurement of right atrial pressure

63
Q

Can you see the JVP in a healthy person?

A

NO but if the right atria is working too hard (e.g. in a normal person) you’ll start to see it

64
Q

What is blood pressure?

A

Blood pressure is the ‘outwards hydrostatic pressure exerted by the blood on the blood vessel walls’.

65
Q

What is systolic blood pressure?

A

Systolic blood pressure ‘is the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts’ Should not normally reach or exceed 140mmHg under resting conditions

66
Q

What is diastolic blood pressure?

A

Diastolic blood pressure is ‘the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes’ Should not normally exceed 90mmHg under resting conditions

67
Q

What is pulse pressure?

A

Pulse pressure is the difference between the systolic and diastolic blood pressures

68
Q

What is mean arterial blood pressure?

A

MAP is ‘the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart’

69
Q

What is hypertension?

A

Hypertension is a clinical blood pressure of 140/90 mmHg or higher and daytime average of 135/85 or higher

70
Q

How can you estimate MAP?

A

Use a cuff sphygmomanometer and a stethoscope to find systolic and diastolic pressure Use the following equation: MAP= [(diastolic pressure x2) + systolic pressure] / 3

71
Q

What is the range of normal MAP?

A

70-105 mmHg

72
Q

Why is it important that MAP is regulated within a narrow range?

A
  1. Pressure is HIGH ENOUGH to perfuse internal organs including the brain, heart, and kidneys 2. Pressure is NOT TOO HIGH to damage the blood vessels or place an extra strain on the heart
73
Q

What is the relationship between MAP and: cardiac output, systemic vascular resistance, stroke volume, heart rate

A

-MAP= CO x SVR -CO= SV x HR

74
Q

What are the main resistance vessels?

A

Arterioles Week 1, Physiology Lecture 06, Slide 12.

75
Q

What are baroreceptors?

A

Baroreceptors are mechanoreceptors (this term is from Google not notes so don’t worry too much) in the carotid sinus and the aortic arch. T

hey sense changes in MAP by responding to tension changes in artery wall.

Sends signals to the medulla.

  • carotid: via IXth CN
  • aortic: via Xth CN
76
Q

Why are baroreceptors so important?

A

The baroreceptor reflex is important in moment-to-moment regulation of arterial blood pressure e.g. everyday we lie down and then stand up but without Baroreceptors every time we stand up we’d pass out

77
Q

What happens to the MAP and what is the baroreceptor reflex in a normal person who stands up after lying down?

A
  1. Venous return to heart decreases (gravity)
  2. MAP decreases
  3. Reduces firing rate of baroreceptors
  4. Vagal tone to heart decreases & sympathetic tone to heart increases (increases HR & SV)
  5. Sympathetic constrictor tone increases (particularly in arteries I think) –> increases SVR
  6. Sympathetic constrictor tone to the veins increases the venous return and SV RESULT: HR, SV, SVR increases –> rapid correction of fall in MAP
78
Q

What role do baroreceptors play in the long-term control of MAP?

A

They don’t! -Baroreceptors re-set and only fire again if there’s an acute change in MAP above the new higher steady state -LT control of MAP is mainly in control of blood volume

79
Q

What is used to control MAP in the long-term?

A

Hormones act as effectors in LT maintenance of MAP

80
Q

What are the hormones used in control of MAP?

A
  1. The Renin-Angiotensin-Aldosterone System- RAAS
  2. Natriuretic Peptides- NPs
  3. Antidiuretic Hormone (Arginine Vasopressin)- ADH
81
Q

How can blood volume affect MAP?

A
  • Total Body Fluid= Intracellular Fluid (2/3) + Extracellular Fluid (1/3)
  • Extracellular Fluid= Plasma Volume + Interstitial Fluid Volume
  • If plasma falls mechanisms occur that shift fluid from interstitial compartment to plasma compartment
  • PV & :. steady state blood volume& MAP are kept controlled if ECFV is controlled
82
Q

What are the two main factors that affect extracellular fluid volume?

A
  1. Water (excess or deficit) 2. Na ions (excess or deficit)
83
Q

How are water and Na ions controlled?

A

HORMONES!

Hormones act as effectors to regulate the extracellular fluid volume (including plasma volume)

  • by regulating the water and salt balance in our bodies.
  • Healthy people stay in a stable water and salt balance, where water input=water output
84
Q

What is aldosterone?

A

Aldosterone is a steroid hormone that acts on kidneys to increase Na and water retention and :. increase plasma volume

85
Q

What is the rate limiting step for RAAS?

A

Renin Secretion -renin is secreted from juxtaglomerular apparatus in the kidneys

86
Q

Which mechanisms stimulate renin release?

A
  1. Renal artery hypotension
    • caused by systemic hypotension
  2. Stimulation of renal sympathetic nerves
  3. Decreased Na in renal tubular fluid; sense by macula densa
87
Q

What are the two types of natriuretic peptides?

A
  • Atrial Natriuretic Peptide
  • Brain-type Natriuretic Peptide
88
Q

Where is ADH synthesised and stored?

A

ADH is synthesised in hypothalamus and stored in the posterior pituitary

89
Q

What causes ADH to be released?

A
  1. Reduced extracellular fluid volume
  2. Increased extracellular fluid osmolality
90
Q

Do you know the mechanisms of the 3 hormones that control MAP in the long-term?

A

There’s a Word Document on them in Week 1; Physiology. Check!

91
Q

Name and state the location of the respiratoyr centres; indicate briefly what their function is thought to be

A

The neural control centre of respiratory is found in 2/3 parts of the brainstem and the spinal cord.

If the section above the medulla is sectioned; fairly normal ventilation is maintained

BUT if the section below the medulla is sectioned ventilation ceases

therefore MEDULLA IS MAJOR RHYTHM GENERATOR

92
Q

What generates the breathing rhythm?

A

It is generally believed that the breathing rhythm is generated by a network of neurons called the Pre-Botzinger complex.

  • display pacemaker activity
  • located near the upper end of medullary respiratory centre
93
Q

What causes inspiration?

A
  1. Rhythm generated by Pre-Botzinger complex
  2. Excites dorsal respiratory group neurones
  3. Fires in bursts
  4. Firing leads to contraction of inspiratory muscles- inspiration
  5. When firing stops, passive expiration

Police Don’t Fight Caucasian Elite

94
Q

At which vertebrae do the pre-ganglionic nerves responsible for diaphragm contraction exit?

A

C3, C4 and C5

C3, 4 and 5 keep the diaphragm alive!

95
Q

Why does active expiration occur e.g. during hyperventilation?

A
  1. Increased firing of dorsal neurones excites a second group: ventral respiratory group neurones
  2. This excites internal intercostals, abdominals etc
  3. Forceful Expiration is successfully brought about

In normal quiet breathing, ventral neurones do not activate expiratory muscles.

96
Q

What is significant about neurones in the pons?

A

‘pneumotaxic centre’

Stimulation terminates inspiration

PC stimulated when dorsal respiratory neurones fire

Inspiration inhibited

Without PC, breathing is prolonged inspiratory gasps with brief expiration- APNEUSIS

97
Q

What can the ‘apneustic centre’ do?

A

Impulses from neurones in the ‘apneustic centre’ excite inspiratory area of medulla to prolong inspiration.

98
Q
A

Cardiovascular System (3 decks)

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