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Year 1: Cardiovascular > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

The heart exhibits “autorhymicity”. What does this mean?

A

It can beat rhythmically in the absence of external stimuli

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2
Q

where in the heart does excitation normally originate?

A

the SA node (pacemaker)

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3
Q

What are factors which change the heart rate?

A

mainly the autonomic nervous system
-vagus = continuous influence on SA node under resting conditions (dominates when resting, slows heart from 100bpm to normal 70bpm)

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4
Q

bradycardia is

A

60

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5
Q

tachycardia is > __bpm

A

100

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6
Q

Parasympathetic/ Sympathetic tone normally dominates on the heart under resting conditions?

A

parasympathetic (vagal) tone

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7
Q

Parasympathetic/ Sympathetic tone normally dominates on the heart under resting conditions?

A

parasympathetic (vagal) tone
Vagal stimulation slows heart rate and increases AV nodal delay
Neurotransmitter is ACh acting through muscarinic M2
decreases slope of pacemaker potential so it takes longer to depolarise (-ve chronotropic effect)

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8
Q

sympathetic stimulation has +ve/ -ve chronotropic effect?

A

+ve

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9
Q

what is the pacemaker potential?

A

It is part of the action potential of SA node cells. It is the slow, +ve increase in voltage across the cell’s membrane that occurs at the end of one AP and the beginning of the next one.

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10
Q

Which ionic events is the pacemaker potential due to?

A
  • decreased K influx
  • the funny current (influx of Na and K)
  • transient Ca influx (through T-type Ca channels)
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11
Q

what is the “funny current”?

A

a mixed Na-K current that activates upon hyperpolarisation at voltages in the diastolic range (normally from -60/-70mV to -40mV)

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12
Q

T-type Ca channels?

A

low voltage activated Ca channels that open during membrane depolarisation. These channels aid in mediating Ca influx directly by allowing the cytosolic concentration to increase.

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13
Q

T-type Ca channels?

A

low voltage activated Ca channels that open during membrane depolarisation. These channels aid in mediating Ca influx after an action potential or depolarising signal. This increases contraction in cardiac muscle directly by allowing the cytosolic concentration to increase.

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14
Q

Which ionic events are responsible for the rising phase of the action potential (depolarisation) of conducting cardiac cells?

A

-the activation of long-lasting Ca channels (L-type Ca channels)

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15
Q

L-type Ca channels?

A

These are high-voltage activated Ca channels, which are responsible for the excitation-contraction coupling of skeletal, smooth, cardiac muscle, and for aldosterone secretion in endocrine cells of the adrenal cortex. In cardiac myocytes, the L-type Ca channel passes inward Ca current and triggers Ca release from the sarcoplasmic reticulum (leading to contraction)

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16
Q

which ionic events cause the falling phase (repolarisation) of the action potential of conducting cardiac cells?

A
  • inactivation of L-type Ca channels

- activation of K channels, resulting in K efflux

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17
Q

What is the route of the cardiac impulse spread over the heart?

A
  • SA node (through both atria through cell to cell conduction via gap junctions)
  • AV node (cell to cell conduction via gap junctions, there is delay in conduction)
  • Bundle of His
  • Left and right branches
  • Purkinje fibres (allow rapid spread of action potential to ventricles)
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18
Q

What are the ionic events which cause depolarisation in ventricular myocytes?

A

-Na influx (fast - rapidly takes the membrane potential from -90mV to +20mV). This is known as Phase 0 of AP in contractile cardiac muscle cells.

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19
Q

What occurs in phase 1 of the ventricular muscle action potential?

A
  • closure of Na channels

- transient K efflux

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20
Q

What are the ionic events which cause phase 2 (the plateau phase) of ventricular myocyte action potential?

A

-mainly due to influx of Ca through L-type Ca channels
(plateau phase sustained by a balance of inward movement of Ca, and efflux of K)
Plateau phase if a UNIQUE characteristic of contractile muscle cells.

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21
Q

What are the ionic events which cause phase 3 of ventricular myocyte action potential?

A
  • inactivation of Ca channels

- activation of K channels (K efflux)

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22
Q

What is phase 4 of the ventricular myocyte action potential?

A

Back to resting membrane potential (-90mV)

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23
Q

What is atropine?

A

competitive inhibitor of ACh - used in extreme bradycardia to speed up heart

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24
Q

What does it mean when something has a “chronotropic”effect?

A

the thing can alter the heart rate

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25
Q

effect of sympathetic stimulation on heart?

A

increases heart rate and decreases AV nodal delay
also increases force of contraction
Neurotransmitter is noradrenaline acting through B1 receptors
increases slope of pacemaker potential

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26
Q

what is an ECG?

A

a record of depolarisation and repolarisation cycle of cardiac muscle obtained from skin surface

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27
Q

What is the P wave?

A

atrial depolarisation

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28
Q

What is the QRS complex?

A

ventricular depolarisation (masks atrial repolarisation)

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29
Q

What is the T wave?

A

ventricular repolarisation

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30
Q

PR interval?

A

AV node delay

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31
Q

ST segment?

A

ventricular systole

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32
Q

TP interval?

A

diastole (whole heart)

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33
Q

cardiac muscle is striated. True/ false?

A

true

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34
Q

what are myofibrils?

A

basic, rod-like unit of a muscle cell. Myofibrils are made of actin and myosin. Within each myofibril, the actin and myosin are arranged into sarcomeres.

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35
Q

What two things are required for muscle contraction?

A

ATP and Ca (Ca needed for crossbridge formation, ATP needed for the crossbridges to get broken down and the muscle to relax

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36
Q

What is required for muscle relaxation?

A

ATP

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37
Q

Why is Ca needed to switch on crossbridge formation?

A

Ca binds to troponin and causes conformational changes so myosin binding sites are exposed, and actin and myosin can interact with each other –> contraction

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38
Q

What is needed to induce the release of Ca from the sarcoplasmic reticulum?

A

Ca
(Ca induced Ca release)
This will increase cytosolic Ca concentration and lead to contraction
(the Ca influx through L-type Ca channels during the ventricular muscle action potential induces release of Ca from sarcoplasmic reticulum, allowing contraction to occur)

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39
Q

How does the ventricular muscle relax again after systole?

A

Ca is re-sequestered into the SR by Ca-ATPase

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40
Q

what is good about the long refractory period (period during which another AP cannot be generate) in the ventricular muscle?

A

This prevents generation of tetanic contraction
(During the plateau phase the Na channels are closed, and during the repolarisation phase, the K channels are open so membrane cannot be depolarised).

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41
Q

What is stroke volume?

A

the volume of blood ejected by each ventricle per heartbeat

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42
Q

What is EDV?

A

End diastolic volume = the volume of blood in a ventricle at the end of diastole (end of filling)

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43
Q

What is ESV?

A

End systolic volume = the volume of blood in a ventricle at the end of systole (beginning of filling)

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44
Q

what effect does increased venous return have on stroke volume?

A

increased venous return leads to increased EDV (increased fibre length), increased preload, leading to greater stroke volume (by the Starling mechanism)

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45
Q

Stretch of cardiac muscle increases the stroke volume. But it can also increase the affinity of troponin for Ca. What effect will this have?

A

It will increase contractiltity

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46
Q

What is afterload?

A

The resistance into which the heart is pumping. This is imposed AFTER the heart has contracted.

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47
Q

Effect of increased afterload?

A

Short term: heart unable to eject at full SV, so EDV increases
Long term: e.g. in untreated hypertension, the ventricular muscle mass increases to overcome the resistance

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48
Q

What are two types of extrinsic control exerted on the stroke volume?

A
  • hormones (adrenaline and noradrenaline from adrenal medulla have inotropic and chronotropic effect. The effect of hormones is less than the neurotransmitters)
  • nerves (noradrenaline, sympathetic increases the FORCE of contraction - it has a +ve inotropic effect, increases force by activation of Ca channels to make greater Ca influx, this reduces the duration of systole, rate of ventricular relaxation increases (due to increased rate of Ca pumping), reduces the duration of diastole)
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49
Q

what does inotropic effect mean?

A

When something can modify the force or speed of contraction of muscles

50
Q

Why does vagal stimulation not affect the force of contraction (has no inotropic effect)?

A

There is very little innervation of the ventricles by the vagus - so vagus only influences rate, not force, of contraction

51
Q

define cardiac output

A

The volume of blood pumped by each ventricle per minute.

CO = SV x HR

52
Q

Cardiac cycle: Passive filling

A
  • pressure in atria and ventricles is close to 0

- AV valves open so venous return fills ventricles to 80%

53
Q

Cardiac cycle: Atrial contraction

A
  • the P wave is atrial depolarisation
  • atria contract between P and QRS complex
  • atrial contraction completes the EDV in ventricles (130ml)
54
Q

Cardiac cycle: Isovolumetric Contraction

A
  • ventricular contraction starts after the QRS complex
  • ventricular pressure rises, then AV valves shut (LUB)
  • aortic valve still shut - no blood can enter/ leave ventricle
  • pressure rises steeply
55
Q

Cardiac cycle: Ventricular ejection

A
  • when ventricular pressure exceed aortic/ pulmonary
  • aortic/ pulmonary valves open
  • SV ejected, leaving behind ESV
  • SV = EDV - ESV = 136-65 = 70ml
  • aortic pressure rises
56
Q

Cardiac cycle: isovolumetric ventricular relaxation

A
  • the T wave is ventricular repolarisation
  • ventricles relax and ventricular pressure starts to fall
  • when falls below aortic/ pulmonary pressure: the valves shut: DUB
  • valve vibration produces the dicrotic notch in the aortic pressure curve
  • when ventricular pressure falls below atrial - AV valves open, and a new cardiac cycle begins
57
Q

What causes S1?

A

closure of mitral and tricuspid valves (LUB)

S1 is the beginning of SYSTOLE

58
Q

What causes S2?

A

closure of the aortic and pulmonary valves (DUB)

S2 is the beginning of DIASTOLE

59
Q

What are the additional heart sounds?

A
  • S3

- S4

60
Q

how does arterial pressure not fall to 0mmHg during diastole?

A

because the arteries have elastic properties: allowing them to recoil during diastole and push blood forward. Aortic valve stops blood from flowing back into ventricle.

61
Q

Jugular Venous pulse

A

This occurs after RA pressure waves (it’s an indirect measurement of central venous pressure)

62
Q

define blood pressure

A

the outwards hydrostatic pressure exerted by the blood on blood vessel walls

63
Q

is laminar flow audible?

A

no

64
Q

is turbulent flow audible?

A

yes

65
Q

what drives blood round the systemic circulation from the aorta to the RA?

A

the pressure gradient
(equal to MAP - CVP)
But since CVP is almost 0, the driving force is mainly MAP

66
Q

define MAP

A

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

67
Q

how can MAP be calculated?

A

MAP = ((2 diastolic pressure) + systolic pressure) / 3

OR

MAP = DBP + 1/3rd pulse pressure

68
Q

Why must MAP be regulated within narrow ranges?

A

to ensure high enough pressure to perfuse internal organs, but not too high as to stain the heart or damage blood vessels

69
Q

define cardiac output

A

the volume of blood pumped by each ventricle per minute

70
Q

how can MAP be calculated?

A 
MAP = CO x TPR
MAP = SV x HR x TPR
71
Q

what is TPR

A

the sum of resistance of all peripheral vasculature in the systemic circulation

72
Q

what is responsible for the short term control of BP?

A

baroreceptors (aortic arch and carotid sinus)
These respond to pressure changes and alter the activity of cardiac vagal, cardiac sympathetic, and sympathetic vasoconstrictor nerve fibre activity.
Baroreceptors are important in prevention of postural hypotension

73
Q

what is postural hypotension?

A

results from the failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position

74
Q

what do baroreceptors do when there is sustained hypertension?

A

they “re-set” to the higher BP, so only fire again is there is an acute MAP rise

75
Q

which three mechanisms are used in the long-term regulation of MAP?

A
  • Renin-Angiotensin-Aldosterone System (RAAS)
  • Atrial Natriuretic Peptide (ANP)
  • Antidiuretic Hormone (ADH)
76
Q

what proportion of body weight is made up of ECF?

A

1/3rd

77
Q

What two components make up ECF?

A
  • plamsa

- interstitial fluid (tissue fluid)

78
Q

What are the main two factors which affect ECF volume?

A
  • water excess or deficit

- Na excess or deficit

79
Q

Where is renin released from , and what cells produce it?

A

Renin is released from the kidneys, produced by granular cells

80
Q

What hormone stimulates the formation of angiotensin I in the blood, from angiotensinogen (produced by the liver)?

A

renin

81
Q

what converts angiotensin I to angiotensin II?

A

ACE (angiotensin converting enzyme)

82
Q

What produces ACE?

A

the pulmonary vascular endothelium (lungs are a large surface area over which conversion can occur)

83
Q

Which hormone stimulates the release of aldosterone from the adrenal cortex?

A

angiotensin II

84
Q

What is the effect of aldosterone?

A

it acts on the kidneys to increase Na and water retention - to increase plasma volume

85
Q

What are the effects of angiotensin II?

A
  • stimulate release of aldosterone from adrenal cortex
  • causes systemic vasoconstriction (increases TPR)
  • also stimulates thirst and ADH release (contributing to increasing plasma volume)
86
Q

what stimulates the release of renin?

A
  • renal artery hypotension caused by systemic hypotension
  • stimulation of renal sympathetic nerves
  • decreased Na in renal tubular fluid (sensed by macula densa - specialised cells of kidney tubules)
87
Q

Where is atrial natriuretic peptide (ANP) produced and stored?

A

-produced and stored by atrial muscle cells (atrial myocytes)

88
Q

What causes the release of ANP?

A

-released in response to atrial distension (hypervolaemic states)

89
Q

What are the effects of ANP?

A
  • reduced blood volume and BP
  • acts as a vasodilator (decreases BP)
  • decreases renin release (acts as a counter to RAAS)
90
Q

Where is ADH produced and stored?

A

Produced from a hormone precursor synthesised by the hypothalamus, stored in posterior pituitary

91
Q

What stimulates secretion of ADH?

A
  • reduced ECF volume (hypovolaemia)

- increased ECF osmolarity (main stimulus)

92
Q

What is the normal osmolarity of ECF?

A

about 280milli-osmoles/ L

93
Q

What monitors plasma osmolality?

A

osmoreceptors close to the hypothalamus. Increased osmolality will stimulate the release of ADH

94
Q

What are the effects of ADH?

A
  • increases reabsorption of water (concentrates urine)
  • increases ECF and plasma volume, and hence CO and BP
  • vasoconstricts blood vessels - increasing TPR and BP (effect is small in normal people, but becomes important in hypovolaemic shock)
95
Q

what happens to resistance to flow if blood viscosity increases?

A

resistance increases

96
Q

what happens to resistance to flow if length of blood vessels increases?

A

resistance increases

97
Q

what happened to resistance to flow is radius of vessel increases?

A

resistance decreases

98
Q

What is the main control of resistance to blood flow?

A

changes in the arteriole radius of vascular smooth muscle

99
Q

sympathetic nerves supply vascular smooth muscles. What neurotransmitter acts here?

A

noradrenaline, on a-adrenoceptors
Vessels are partially restricted at rest - this is called vasomotor tone - and results from tonic discharge of sympathetic nerves, resulting in continuous noradrenaline release

100
Q

There is no parasympathetic innervation of vessel smooth muscle. True/ False?

A

True - dilation/ constriction depends on decrease/ increase of sympathetic discharge

101
Q

what does adrenaline cause when acting on a receptors?

What about on B receptors?

A
  • a: vasoconstriction (a receptors predominant in skin, gut, kidney arterioles)
  • B: vasodilatation (B receptors predominant in cardiac and skeletal muscle)
102
Q

What can override extrinsic control mechanisms of vascular smooth muscle control?

A

INTRINSIC factors (chemical/ physical)

103
Q

Name some intrinsic factors which can vasodilate and cause metabolic hyperaemia?

A 
Local metabolites:
-decreased local PO2
-increased local CO2
-increased local H conc
-increased ECF K conc
-increased osmolality of ECF
-adenosine release (from ATP)
Local humoral agents:
-histamine
-bradykinin
-NO (nitric oxide - released continuously by endothelium of arteries and arterioles)
104
Q

NO?

A
  • produced continuously by vascular endothelium (from L-arginine through enzyme NOS - nitric oxide synthase)
  • short life (seconds)
  • shear stress on endothelium (result of increased flow) causes release of Ca and subsequent activation of NOS
  • production can be receptor stimulated
  • NO diffuses into adjacent smooth muscle cells where it activates cGMP - which is a second messenger for signalling relaxation
105
Q

Name some humoral agents which cause vascular constriction?

A
  • serotonin
  • thromboxane A2
  • leukotrienes
  • endothelin
106
Q

effect of temperature of vascular smooth muscle?

A
  • cold - constriction

- warm - dilate

107
Q

what is the myogenic response to stretch?

A

-MAP increases: vessels constrict
-MAP decreases: vessels dilate
(important in brain and kidney)

108
Q

Name some factor increasing venous return?

A

-increased venomotor tone
-increased blood volume
-increases skeletal muscle pump
increased atrial pressure
-increased respiratory pump
All of these lead to increased EDV and stroke volume

109
Q

increased veno/ vaso -motor tone increases venous return, SV and MAP?

A

veno

110
Q

increased veno/ vaso -motor tone increases TPR and MAP?

A

vaso

111
Q

what is shock?

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

112
Q

what two things does adequate tissue perfusion depend on?

A
  • adequate BP

- adequate cardiac output

113
Q

how does hypovolaemic shock come about?

A

loss of blood volume (leads to decreased venous return… decreased CO and decreased BP)

114
Q

how does cardiogenic shock come about?

A

inadequate circulation of blood due to primary failure of the ventricles (decreased contractility - leading to decreased stroke volume, decreased CO and decreased BP)

115
Q

how obstructive shock come about?

A

This arises from physical obstruction of the great vessels of the heart (has a lot in common with cardiogenic shock)
e.g. from PE, tension pneumothorax, cardiac tamponade (increased intrathoracic pressure decreases venous return, decreasing CO and BP)

116
Q

how does neurogenic shock come about?

A

this is a type of distributive shock.
Neurogenic shock is caused by loss of vascular tone - which is normally supported by the sympathetic nervous system due to spinal cord injury. There is loss of sympathetic tone, leading to massive dilatation of all vessels, decreased venous return and TPR, decreased CO and BP

117
Q

how does vasoactive shock come about?

A

This is combined distributive and hypovolaemic shock.
Can occur in septic shock: when there is release of vasoactive mediators (these result in increased capillary permeability - so volume is lost, and increased dilatation). There is decreased venous return and decreased TPR, decreased CO and BP

118
Q

outline for shock treatment

A

-ABCDE approach
-high flow O2
volume replacement
-inotropes for cardiogenic shock
-immediate chest drain for tension pneumothorax
-adrenaline for anaphylactic shock
-vasopressors for septic shock

119
Q

causes of hypovolaemic shock?

A

haemorrhage (trauma, surgery, GI haemorrhage)

vomiting, diarrhoea, excessive sweating

120
Q

how much blood can be lost before compensatory mechanisms can no longer maintain BP?

A

30%

121
Q

when lots of blood has been lost, what is the body’s way of compensating in the long term?

A

increasing production of RBCs

Year 1: Cardiovascular (16 decks)

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