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Physiology > L5-10: Cardiovascular System > Flashcards

L5-10: Cardiovascular System Flashcards

1
Q

What are the main functions of the CVS?

A

Controlled and continuous flow of blood
Homeostasis
Transport of hormones

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2
Q

How does the CVS control homeostasis?

A

Transports nutrients
Transports metabolic products
Distributes heat
Defends
Regulates pH and osmolality

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3
Q

What are the right and left pumps of the heart known as and what pressure do they have?

A

Left: systemic - high pressure
Right: pulmonary - low pressure

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4
Q

Which way does the blood flow?

A

Unidirectional

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5
Q

What volume does each circulation receive when the heart contracts?

A

The same volume

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6
Q

Where do blood vessels emerge from the heart?

A

At the base (top)

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7
Q

Where do the aorta and artery carry blood?

A

Away from the heart

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8
Q

Where do the vena cava and pulmonary veins carry blood?

A

To the heart

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9
Q

How is one-way flow maintained?

A

Using valves

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10
Q

What are the AV valves known as in the left and right sides of the heart?

A

Right - tricuspid
Left - mitral or bicuspid

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11
Q

What are the semilunar valves known as in the left and right sides of the heart?

A

Right - pulmonary
Left - aortic

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12
Q

What is stroke volume?

A

The volume of blood pumped by one ventricle (averages about 75mL at rest)

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13
Q

What is cardiac output and what does it depend on?

A

The total volume of blood pumper per ventricle per minute and it depends on heart rate

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14
Q

What is the equation for cardiac output?

A

Cardia output = stroke volume x heart rate

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15
Q

What is venous return?

A

The amount of blood returning to the heart

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16
Q

What happens to venous return when at steady state?

A

Venous return = cardiac output

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17
Q

What are components of arteries?

A

Allow high pressure as they are highly elastic which is provided for distribution around the body

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18
Q

What are components of arterioles?

A

High resistance vessels, control of blood flow to tissures

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19
Q

What are components of capillaries?

A

Thin walled vessels arranged parallel to allow exchange

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20
Q

What are components of veins?

A

Maintain low pressure, capacitance vessels (ability to stretch easily without change in pressure) one-way valves used for collection and storage

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21
Q

How is blood flow driven?

A

Using a pressure gradient

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22
Q

How is the pressure gradient created?

A

It is seat up by the heart acting as a pump, energy is required to maintain pressure gradient

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23
Q

What is blood flow in vessels proportional to?

A

Pressure gradient (delta P)

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24
Q

What are the units of pressure for the CVS?

A

mm Hg

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25
Q

How does pressure change once blood flows out the heart?

A

Pressure decreases with distance, due to friction, as the blood travels through the vessels

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26
Q

How is pulsatile in large arteries measured?

A

Max systolic (systolic pressure)
Min diastolic (diastolic pressure)

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27
Q

Where does the biggest drop in pressure take place?

A

In the arterioles

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28
Q

How is pulse pressure found?

A

Pulse pressure = SP-DP

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29
Q

What is mean arterial blood pressure?

A

Pressure averaged over time

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30
Q

What is the average systemic pressure?

A

120/80 mm Hg

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31
Q

What is the average pulmonary pressure?

A

25/9 mm Hg

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32
Q

What can blood flow be affected by?

A

Resistance to flow in the vessel

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33
Q

What is the relationship between resistance and blood flow?

A

Inversely proportional

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34
Q

What is Darcy’s law?

A

Flow = delta P/R
delta P - pressure gradient
R - resistance

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35
Q

What parameters are used to determine resistance?

A

R= 8Leta/pi*r^4
R - resistance
L - length blood vessel
r - radius blood vessel
eta - viscosity of blood

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36
Q

How can flow be changed?

A

By changing the radius

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37
Q

What happens when the radius of the blood vessel changes?

A

Resistance decreases and flow increases

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38
Q

What is the difference between blood flow and blood velocity?

A

Flow - volume per minute
Velocity - distance travelled per minute

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39
Q

What does blood velocity depend on?

A

Flow and cross-sectional area of vessel

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40
Q

What is the equation for blood velocity?

A

Velocity = blood flow/ cross-sectional area

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41
Q

How does the velocity increase?

A

By the narrowing of the blood vessel

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42
Q

Is blood velocity highest in the capillaries?

A

NO

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43
Q

Why is blood velocity not highest in capillaries?

A

Because of the parallel arrangement the total cross-sectional area of all the capillaries is taken into account so cross-sectional area is greatest in capillaries

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44
Q

Where is blood velocity lowest?

A

In capillaries for efficient exchange of nutrients and gases from blood to cells

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45
Q

What are the components of cardiac muscle cells?

A

T-tubules
Sarcoplasmic reticulum
Sarcomeres

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46
Q

What is the role of the action potential in cardiac muscle cells?

A

To generate an elevation in cytoplasmic Ca2+ conc

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47
Q

What is the role of elevated cytoplasmic Ca2+ conc in cardiac muscle cells?

A

To generate the contraction response

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48
Q

What is the process of excitation contraction (EC) coupling?

A

Role of action potential is to generate inc in cytoplasmic [Ca2+] which then generates the contraction response

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49
Q

What are the 2 myocytes used to drive the heart?

A

Conducting cells/systems - used for fast spread of electrical activity throughout the heart
Work cells - generate force

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50
Q

Where does the initiation of the heart beat begin?

A

In the Sino Atrial (SA) node in right atrium

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51
Q

What are the 2 ways excitation occurs in the heart?

A

By the specialised ‘conducting fibres’ in atria and ventricles
Cell to cell, via gap junctions

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52
Q

How are work cells stuck together in the heart?

A

Intercalated discs

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53
Q

What do work cells form when stuck together?

A

They form a functional syncytium

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54
Q

What is the electrical pathway in the heart made up of?

A

SA node
Internodal pathways
AV node
Bundle of His
Bundle branches
Purkinje fibres

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55
Q

What is pacemaker potential?

A

The unstable membrane potential SAN cells have

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56
Q

How can the rate of electrical activity be altered in the SAN?

A

By the autonomic nervous system

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57
Q

What happens when the SAN is dysfunctional?

A

Other conducting cells takeover the role with a slower firing rate

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58
Q

What takes place in the slow initial depolarisation phase in the SAN?

A

cations leaks out through nonspecific cation channels causing the membrane to slowly depolarise to threshold

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59
Q

What takes place in the full depolarisation phase in the SAN?

A

At threshold VG Ca2+ channels open and Ca2+ enters the cell causing the membrane to fully depolarise

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60
Q

What takes place in the repolarisation phase in the SAN?

A

Ca2+ channels close and VG K+ channels open, causing K+ outflow and membrane repolarisation

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61
Q

What takes place in the minimum potential phase in the SAN?

A

K+ channels remain open and the membrane hyperpolarises which opens nonspecific cation channels, repeating the cycle

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62
Q

What is the time difference between cardiac and neuronal/skeletal APs?

A

Cardiac potentials are much longer

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63
Q

What is the rapid depolarisation phase in ventricular muscle cells?

A

VG Na+ channels activate and Na+ enters rapidly depolarising the membrane

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64
Q

What takes place in the initial repolarisation phase in ventricular muscle cells?

A

Na+ channels are inactivated and some K+ channels open. K+ leaks out causing small initial repolarisation

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65
Q

What takes in the plateau phase in ventricular muscle cells?

A

Ca2+ channels open and Ca2+ enters as K+ exits prolonging the depolarisation

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66
Q

What is Ca2+ known as in the plateau phase?

A

Trigger Calcium

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67
Q

What takes place in the repolarisation phase in ventricular muscle cells?

A

Na+ and Ca2+ channels close as K+ continues to exit causing repolarisation?

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68
Q

What is the process of trigger calcium entering the muscle cell during the plateau phase?

A

Its known as calcium-induced calcium-release (CICR)

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69
Q

What is the cascade caused by trigger calcium?

A

Ca2+ induce Ca2+ release through ryanodine receptor-channels
Causes Ca2+ spark
Which creates a signal
Ca2+ bind to troponin to initiate contraction
Relaxation occurs when Ca2+ unbinds
Ca2+ is pumped back to SR

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70
Q

What is force of contraction proportional to?

A

Number of active crossbridges

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71
Q

How is the number of active crossbridges determined?

A

By how much calcium is bound to troponin C which is dependent on the amount of CICR

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72
Q

What is one of the factors affecting the force of muscle contraction?

A

Sarcomere length

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73
Q

What does the refractory period outlast?

A

The contraction period

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74
Q

How do long refractory periods impact cardiac muscle?

A

By preventing tetnus

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75
Q

What does an ECG record?

A

The electrical activity during each heart beat

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76
Q

What does an ECG record?

A

Both depolarisation and repolarisation of the atrial and ventricular muscle cells

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77
Q

What are the different peaks of an ECG?

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation

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78
Q

What is arhythmias?

A

Abnormal or irregular heart rhythms

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79
Q

What are examples of arrhythmias in impulse propagation?

A

Heart block

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80
Q

What are examples of arrhythmias in impulse initiation?

A

Fibrillation, atrial and ventricular

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81
Q

What do electrical events drive in the heart?

A

Pressure and volume changes within the heart chambers

82
Q

What is the cardiac cycle?

A

A cycle of pressure and volume changes in the heart every time the heart contracts and relaxes

83
Q

What are the 4 phases of the ventricular cycle?

A

-Ventricular filling
-Isovolumetric ventricular contraction
-Ventricular ejection
-Isovolumetric ventricular relaxation

84
Q

When does contraction and relaxation occur?

A

Contraction - systole
Relaxation - diastole

85
Q

What takes place during late diastole?

A

Both sets of chambers are relaxed and ventricles fill passively

86
Q

What takes place during atrial systole?

A

Atrial contraction forces a small amount of blood into ventricles

87
Q

What takes place during isovolumetric ventricular contraction?

A

Pushes AV valves closed but does not create enough pressure to open SL valves.

88
Q

What is the maximum blood volume in ventricles known as?

A

End-diastolic volume (EDV)

89
Q

What takes place during ventricular ejection?

A

Ventricular pressure rises and exceeds pressure in arteries, SL valves open and blood is ejected

90
Q

What takes place during isovolumetric ventricular relaxation?

A

Pressure falls, blood flows back into cusps of SL valves and snaps closed

91
Q

What is minimum blood volume known as?

A

End-systolic volume (ESV)

92
Q

What are the components of heart sounds?

A

They are the closing of heart valves
First- AV valves closing
Second- SL valves closing
Can be detected using a stethoscope

93
Q

What does a phonocardiogram show?

A

Heart sounds - the frequencies which differ for each valve

94
Q

How could functional abnormalities be detected using heart sounds?

A

All 4 heart valves can be listened to individually to detect functional abnormalities

95
Q

What are the different diseases of heart valves?

A

Stenosis
Incompetent

96
Q

What is mean blood arterial pressure?

A

Pressure in artery averaged over time

97
Q

What is the notch that occurs during an aortic/arterial pressure wave?

A

Dichrotic notch

98
Q

Why does the dichrotic notch occur?

A

Backflow of blood rebounds on valve so movement in pressure

99
Q

What happens to aorta during elastic recoil?

A

Pressure increases so diastole aorta stores energy returning to normal size

100
Q

What is normal blood pressure measured as?

A

Systolic pressure/diastolic pressure
120/80 mmHg`

101
Q

What are the sounds known as when blood pressure is being taken?

A

Korotkoff sounds

102
Q

What happens when blood pressure is being taken?

A

Cuff is inflated which cuts off arterial blood flow, no sound is heard
Korotkoff sounds are produced by pulsatile blood flow through compressed artery
Blood flow is silent when artery is no longer compressed

103
Q

What is turbulent and laminar flow?

A

Turbulent - pulsatile blood flow when cuff loosened
Laminar - silent blood flow when artery no longer compressed

104
Q

How is blood pressure maintained?

A

By the heard pumping

105
Q

How is blood flow provided?

A

By providing a pressure gradient in each circulation

106
Q

What is mean arterial blood pressure?

A

Product of the input to the arterial system (CO=SV x HR)
Resistance to flow - total peripheral resistance (sum of vessels resistance)

107
Q

What is the equation for mean arterial blood pressure (MABP)?

A

MABP = CO x TPR

108
Q

What factors regulate cardiac output?

A

Stroke volume
Heart rate

109
Q

What are the typical values for CO, SV and HR at rest?

A

SV = 70mL HR = 70 bpm
CO = 70 x 70 = 4.9L/min

110
Q

What can cardiac output increase to during exercise?

A

20-25 L/min

111
Q

What is the parasympathetic effect on the heart?

A

Parasympathetic nerves (vagus)
Acetylcholine
Activation of muscarinic ACh receptors (g-protein coupled)
Decreases heart rate

112
Q

What is the sympathetic effect on the heart?

A

Sympathetic nerves
Noradrenaline
Activates beta1-adrenergic receptors (inc cAMP)
Increasing heart rate and contractility

113
Q

What happens to pacemaker potential when heart rate increases?

A

-Steeper slope of pacemaker potential
-rmp is less negative
-Threshold reached quicker
-Tachycardia

114
Q

What happens to pacemaker potential when heart rate decreases?

A

-Less steep slow
-More negative rmp
-Longer to reach threshold
-Bradycardia

115
Q

What are changes in heart rate known as?

A

Chronotropic effects

116
Q

What are the 2 different mechanisms of force of contraction?

A

Intrinsic and extrinsic

117
Q

What are intrinsic mechanisms of force of contraction?

A

Known as Frank-Starling mechanism
Increase in VR so increase EDV stretching cardiac muscle
Increase in force so SV increases

118
Q

What is the force of contraction proportional to?

A

The initial muscle fibre length in diastole
(initial = just before contraction occurs)

119
Q

What happens to force and stretch according to Starling’s law of the heart?

A

Increases so shifts right

120
Q

What is the basis for Starling’s law?

A

Increase stretch increases sensitivity of contractile proteins to Ca2+
Intracellular Ca2+ required to generate 50% max tension is lower when muscle fibre is first stretched (increase in actin and myosin interaction)

121
Q

What is the importance of Starling effects on the heart?

A

Helps match output of right and left sides of heart
Enables heart to adapt its pumping capacity when either venous return or arterial blood pressure change

122
Q

What is an example of importance of output in right and left sides of the heart matching?

A

If difference was sustained more would go to lungs than rest of the body every contraction
Pulmonary blood volume would rincrease
Cause serious oedema in lungs ‘drown’
Interstitial fluid would flow into lungs

123
Q

What are the extrinsic mechanisms for force of contraction?

A

-Increase in sympathetic activity
enhance contractility, Nadr + Adr bind to beta1 adrenergic receptors

124
Q

What is the result of extrinsic mechanisms for force of contraction?

A

Enhanced stroke volume
Smaller ESV at end of contraction
Positive inotropic (contractility) effect

125
Q

What are the effects of noradrenaline from extrinsic mechanisms of force of contraction?

A

Produces an upward shift in ventricular function curve

126
Q

What are changes in rate of muscle relaxation known as?

A

Lusitropic effects

127
Q

How do catecholamines increase contractility? (phospholamban pathway + duration)

A

Adr/NAdr bind to B1 receptors on myocardial contractile cell activating cAMP 2nd messenger phosphorylating phospholamban increases Ca2+ ATPase activity in SR Ca2+ removed from cytosol faster Ca-troponin binding shorter shorter duration of contaction

128
Q

How do catecholamines increase contractility? (phospholamban pathway + force)

A

Adr/NAdr bind to B1 receptors on myocardial contractile cell activating cAMP 2nd messenger phosphorylating phospholamban increases Ca2+ ATPase activity of SR increasing Ca2+ stores in SR increaseing Ca2+ release so more forceful contraction

129
Q

How do catecholamines increase contractility? (VG Ca2+ pathway)

A

Adr/NAdr bind to B1 receptors on myocardial contractile cell activating cAMP 2nd messenger phosphorylating VG Ca2+ channels increasing open time so more Ca2+ from ECF (more trigger Ca2+) so more forceful contraction

130
Q

What has to be maintained when CO changes?

A

Venous return

131
Q

How is venous return maintained?

A

Venous:arterial pressure difference
Venous valves - prevent backflow and skeletal muscle contraction
Venomotor tome - veins have smooth muscle recieve sympathetic supply
Respiration - inspiration aids venous return

132
Q

What do arterioles control?

A

Total peripheral resistance (TPR)

133
Q

What do arterioles have a good supply of?

A

Vascular smooth muscle

134
Q

What is tissue vessel tone?

A

The smooth muscle cells surrounding arterioles normally partially contracted

135
Q

How is the tissue vessel tone regulated?

A

By affecting the radius of the vessel hence resistance and thus blood flow

136
Q

What is the major role of aterioles?

A

To match local blood flow to metabolic need

137
Q

What happens when metabolic need increases?

A

Vessel tone decreases as smooth muscle relaxes and radius increases so resistance to flow decreases and blood flow increases so more oxygen and nutrients

138
Q

What is the process known as when metabolic need increases?

A

Vasodilation

139
Q

How is blood flow through individual vessels determined?

A

By resistance

140
Q

What is resistance controlled by?

A

By vascular smooth msucle surrounding arterioles

141
Q

What are the 3 major physiological mechanisms that regulate arteriolar radius?

A

Local control
Hormonal control
Neural control

142
Q

How do the mechanisms regulate arteriolar radius?

A

By affecting the contractile state of the surrounding vascular smooth muscle

143
Q

What is autoregulation of tissue blood flow?

A

Flow stays constant with increasing pressure
Intrinsic activity of smooth muscle (myogenic response)
Safety mechansim to prevent damage to delicate blood vessels

144
Q

How is blood flow autoregulated tissue?

A

Stretch promotes Ca2+ influx into cells causing smooth muscle to contract

145
Q

What is metabolic control of tissue blood flow?

A

-Metabolism-derived vasodilators (muscle works harder)
Increase CO2
Increase H+ (lactate)
Increase temperature
Decrease oxygen
Increase adenosine
Increase K+

146
Q

What does metabolic control override?

A

Autoregulation

147
Q

What is hormonal control of blood flow?

A

Vasodilators:
Histamine (allergies)
Kinins (e.g. bradykinin- sweating)
Adrenaline (B2-adrenergic receptors)
Vasoconstrictors:
Angiotensin II (renal hormone)
Vasopressin (ADH renal)
Adrenaline (a1-adrenergic receptors)

148
Q

What is neural control of blood flow? (sympathetic)

A

Sympathetic vasoconstrictor fibre - release NAdr
Most widespread
Bind a1-adrenergic receptors - vasoconstriction
2nd messenger IP3 so Ca2+ release so contract

149
Q

What is neural control of blood flow? (parasympathetic)

A

Parasympathetic vasodilator fibres
Cholinergic cause No generation which relaxes VSM
Found in salivary glands, external genitalia and GI tract

150
Q

What does NO production cause?

A

Binding of NO to guanylyl cylase stimulating cGMP which relaxes smooth muscle

151
Q

What is angina?

A

A symptom of ischaemic heart disease related to reduced blood flow in the heart. Characterised by attacks of chest pains

152
Q

How is angina treated and how does it help the symptom?

A

Sodium nitroprusside or organic nitrates
NO relaxes smooth muscle reducing resistance improving coronary blood flow, reduces MABP reduces work of heart so reduces the symptom of angina

153
Q

How does CO change during vigorous exercise?

A

Skeletal muscle receives 88% of CO in comparison to 21% at rest

154
Q

Why does CO change during vigorous exercise?

A

To meet O2 demands

155
Q

What is the equation for MABP?

A

MABP= CO x total peripheral resistance

156
Q

How does MABP change in vigorous exercise?

A

It doesn’t rise very much because of the large drop in total peripheral resistance despite the marked increase in CO

157
Q

Why does blood pressure need to be maintained?

A

To ensure a constant supply of blood to brain and heart

158
Q

What are the 2 main control mechanisms to regulate MABP?

A

Short term (fast)
Long term (slow - kidney and blood vol)

159
Q

What are the 3 main ways of regulating MABP?

A

Blood pressure
Control mechanism (short and long term)
Cortico-hypothalamic influences

160
Q

What is the reflex arc that responds to changes in MABP?

A

Baroreceptors
CV control centre
ANS

161
Q

What does the ANS change when changes in MABP are detected?

A

Heart rate
Stroke volume
Vessel radius

162
Q

What do baroreceptors detect?

A

Changes in MABP

163
Q

What 3 control mechanisms change blood pressure?

A

Heart rate
Stroke volume
Vessel radius

164
Q

Where is the cardiovascular control centre located?

A

At the medulla

165
Q

Where are the nerve endings of baroreceptors located?

A

Adventitia layer of arteries

165
Q

Where are baroreceptors located?

A

In the aortic arch and carotid sinuses

166
Q

What do afferents do in baroreceptors?

A

Send information about MABP to CV control centre in brainstem (medulla)

167
Q

What are the afferents in the aortic arch and carotid sinus?

A

AA - carotid depressor
CS - Hering’s/ IX glossopharyngeal

168
Q

What are the properties of baroreceptors?

A

Respond to changes in stretch of the artery due to changes in BP

169
Q

What happens when stretch in arteries is increased?

A

Due to an increase in blood pressure it causes receptors to fire more action potentials

170
Q

What are the minimum and maximum responses of baroreceptors?

A

~40mmHg and ~160mmHg

171
Q

What do baroreceptors respond best too?

A

Pulsatile pressure changes

172
Q

What do baroreceptors respond to?

A

Pulsatile pressure changes
Maintained changes in pressure (change set-point)

173
Q

Where do the action potentials travel when pressure changes?

A

Via afferent nerves to the CV control centre

174
Q

What response do APs have to a decrease in MABP?

A

Decreased firing rate

175
Q

What happens to vagal tone and sympathetic stimulation when MABP decreases?

A

Decrease vagal tone
Increase sympathetic stimulation to heart and blood vessels

176
Q

What happens overall when arterial blood pressure drops?

A

Increase in heart rate and contractility
Constriction of arterioles (increase TPR)
Veins constrict (increase CVP)
Increase adrenaline

177
Q

How is blood redistributed when lying down to standing occurs?

A

Blood travels from intrathoracic vessels to veins of lower limbs
Venous return decreases, SV decreases
CO falls
MABP falls, can cause dizziness

178
Q

What does the reflex activation of baroreceptors produce?

A

Reflex tachycardia
Positive inotropic effects
Vasoconstriction in skeletal, GI and renal beds
MABP restored

179
Q

What is postural hypotension?

A

Decrease in systolic BP of 20mmHg/ more after 1 min of standing compared to supine values

180
Q

How does blood volume impact BP?

A

It is a physical determinant
Decrease blood vol decreases BP

181
Q

How is blood pressure changed quickly?

A

Via the baroreceptor reflex

182
Q

How is blood pressure changed slowly?

A

Via kidney and thirst response

183
Q

What is involved in long-term regulation of blood volume?

A

Arterial pressure receptors
Renal responses (control fluid excretion/absorption)

184
Q

What is ANP?

A

Atrial natriuretic peptide

185
Q

What is the function of ANP?

A

To increase Na+ and water excretion from kidney

186
Q

How does renin work?

A

Angiotensin- aldosterone system (RAAS)

187
Q

What is the function of renin?

A

To promote Na+ and water re-absorption into body

188
Q

What is ADH?

A

Vasopressin

189
Q

What is the function of ADH?

A

To promote water uptake into body

190
Q

What is the response to decrease in blood volume?

A

Decrease BP
Vol receptors in atria, carotid and aortic baroreceptors
Kidneys- conserve H2O
Behaviour- thirst, increase ECF and ICF
CVS- increase CO and vasoconstriction

191
Q

What are examples when there is a decrease in blood volume?

A

Haemorrhage
Vomiting and diarrhoea
Severe burns
Diabetes
Excessive use of diuretics

192
Q

What is the response to an increase in blood volume?

A

Increase BP
Kidneys- excretion of more fluid in urine
CVS- decrease CO and vasodilation

193
Q

What are examples when there is an increase in blood volume?

A

Diet - excessive salt intake
Too much aldosterone
Genetic disease (i.e. Liddle syndrome)

194
Q

What are portico-hypothalamic influences?

A

Adaptive responses (higher centres)
e.g. playing dead, fight or flight, feeding, diving, thermo-regulatory, sexual

195
Q

How does emotional response to e.g. needles cause stress/fear leading to fainting?

A

Decrease sympathetic supply to skeletal muscle, relaxes smooth muscle in arterioles so decrease in TPR
Increase in parasympathetic output to heart so decrease in HR
Rapid decrease in BP and flow to brain so loss of consciousness

196
Q

What is vasovagal syncope?

A

Fainting due to emotional stress

197
Q

What is feeding behaviour?

A

Increase BP
Increase intestinal motility
Increased intestinal blood supply
Decreased blood supply to muscles

198
Q

What is defence behaviour?

A

Increases BP
Decreased intestinal motility
Decreased intestinal blood supply
Increased supply to muscles

199
Q
A
200
Q
A

Physiology (6 decks)

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