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CVS > CVS SEM 2 > Flashcards

CVS SEM 2 Flashcards

1
Q

Above what distance would diffusion be too slow?

A

1mm

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2
Q

How is O2 tranported through the body?

A

Convection

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3
Q

Define convection

A

Mass movement of fluid caused by pressure difference

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4
Q

Where is electrical activity generated in the heart?

A

The SA node

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5
Q

What happens to electrical activity generated in the SAN?

A

Electrical activity spreads out into the atria, via the gap junction, and towards the AV node

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6
Q

Why is conduction delayed at the AVN?

A

To allow for correct filling of the ventricles

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7
Q

What’s the electrical activity conducted through after the AVN?

A

Conduction occurs rapidly through the bundle of His and simultaneously up through Purkinje fibres in the ventricle walls from the apex of the heart, causing ventricular contraction

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8
Q

What does the P wave of an ECG signify?

A

Atrial depolarisation

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9
Q

What does the PR segment of an ECG signify?

A

AV nodal delay

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10
Q

What does the QRS complex of an ECG signify?

A

Ventricular depolarisation (and simultaneous atrial repolarisation)

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11
Q

What does the ST segment of an ECG signify?

A

Time during which the ventricles are contracting and emptying

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12
Q

What does the T wave of an ECG signify?

A

Ventricular repolarisation

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13
Q

What does the TP interval of an ECG signify?

A

The time during which the ventricles are relaxing and filling

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14
Q

What causes heart valves to open or close?

A

Changes in pressure in the chambers

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15
Q

Describe ventricular filling

A

Blood moves from the atria into the ventricles due to greater pressure in the atria causing the tricuspid and mitral valves to open. Filling of the ventricles is aided by atrial systole

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16
Q

Describe isovolumetric contraction

A

Pressure in the ventricles becomes greater than in the atria, causing the tricuspid and mitral valves to close. The ventricles contract and pressure greatly increases

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17
Q

Describe ejection

A

Pressure in the ventricles becomes greater than that in the aorta and pulmonary trunk. The aortic and pulmonary valves open and blood is ejected into the aorta and pulmonary trunk. More blood arrives at the atria

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18
Q

Describe isovolumetric relaxation

A

The pressure becomes greater in the aorta and pulmonary trunk than in the ventricles, so the aortic and pulmonary valves close and the ventricles relax to receive more blood

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19
Q

What proportion of blood is forced out of the ventricles in a normal systole?

A

About 2/3

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20
Q

What’s the end diastolic volume in a healthy person?

A

EDV is around 120ml

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21
Q

What’s the end systolic volume in a healthy person?

A

ESV is around 40ml

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22
Q

What is normal stroke volume in a healthy person?

A

80ml

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23
Q

What’s the equation of stroke volume?

A

EDV- ESV

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24
Q

What’s the ejection fraction?

A

SV/EDV

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25
Q

What is the equation for stroke work?

A

Change in ventricular pressure x change in volume

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26
Q

What part of a ventricular pressure-volume loop curve signifies stroke work?

A

The area under the curve

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27
Q

What causes heart sounds?

A

S1- The closure of the tricuspid and mitral valves at the beginning of ventricular systole
S2- Closure of the aortic and pulmonary valves at the beginning of ventricular diastole

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28
Q

What causes S3 heart sounds?

A

Turbulent blood flow into the ventricles, which is detected just after S2 and is called ‘ventricular gallop’

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29
Q

What is S4?

A

A pathological heart sound caused by forceful atrial contraction against a stiff ventricle at the end of diastole

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30
Q

What is cardiac output?

A

The volume of blood ejection from the heart per minute.

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31
Q

What’s the equation for blood flow?

A

CO= BP/TPR

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32
Q

What is preload of the heart?

A

Stretching of the heart during diastole due to filling pressure

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33
Q

What is contractility?

A

Strength of contraction at a given diastolic loading due to sympathetic nerves and circulating adrenaline increasing Ca2+ concentration

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34
Q

What is after load?

A

The pressure the heart must work against to eject blood in systole

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35
Q

What is systole?

A

The period of ventricular contraction that occurs between the first and second heart sounds, causing the ejection of blood into the aorta and pulmonary trunk

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36
Q

What is diastole?

A

The period of relaxation of heart muscle and simultaneous refilling of the atria

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37
Q

What is energy of contraction?

A

The amount of work required to generate stroke volume, which depends on Starling’s law and contractility

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38
Q

What’s energy of contraction of cardiac muscle proportional to?

A

Muscle fibre length at rest

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39
Q

What is Starling’s law of the heart?

A

Energy of contraction is proportional to the muscle fibre length at rest. Greater stretch of the ventricle in diastole gives greater energy of contraction, so greater SV is achieved in systole

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40
Q

How does increase in EDV affect stroke volume?

A

Increase in EDV increases stroke volume, up to a point at which stroke volume plateaus, and after which SV decreases due to overstretching of the heart from excess filling

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41
Q

What’s responsible for the fall in cardiac output following a drop in blood volume?

A

Preload

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42
Q

What leads to the fall in cardiac output during orthostasis, that causes postural hypertension?

A

Preload

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43
Q

What determines after load?

A

Wall stress- force through the heart wall

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44
Q

What does Laplace’s law involve and what’s the equation?

A 
Laplace's law involved the parameters that determine after load
S= P x r/2w
S- wall stress
P- pressure
r-radius
w- wall thickness
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45
Q

How does increase in pressure affect wall stress?

A

Increase

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46
Q

How does increase in wall thickness affect wall stress?

A

Reduce

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47
Q

How does increase in radius affect wall stress?

A

Increase

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48
Q

Why does small ventricular radius decrease afterload?

A

Small ventricular radius means greater wall curvature, more wall stress directed towards the centre of the chamber and better ejection

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49
Q

How does Laplace’s law oppose Starling’s law at rest?

A

Increasing preload increases chamber radius. This increases after load, opposing ejection of blood from a full chamber.

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50
Q

What happens in a healthy heart regarding Starilng’s law and Laplace’s law?

A

Starling’s law overcomes Laplace’s law to maintain ejection

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51
Q

What is phase 0 of the cardiac cycle?

A

Rapid depolarisation

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52
Q

What is phase 1 of the cardiac cycle?

A

Early repolarisation

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53
Q

What is phase 2 of the cardiac cycle?

A

The plateau phase

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54
Q

What is phase 3 of the cardiac cycle?

A

Rapid repolarisation

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55
Q

What is phase 4 of the cardiac cycle?

A

Resting phase

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56
Q

How does Laplace’s law facilitate ejection during contraction?

A

Ventricular contraction decreases chamber radius. Laplace’s law says this will reduce after load in the emptying chamber. This aids ejection during reduced ventricular ejection in phase 4

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57
Q

How does Laplace’s law contribute to a failing heart?

A

In a failing heart, chambers are often dilated, so radius is increased. Ejection is reduced as there’s greater after load opposing rejection

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58
Q

What does Laplace’s law state?

A

Increased arterial blood pressure leads to increased after load, reducing ejection.

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59
Q

What’s a consequence of chronic high arterial blood pressure?

A

Blood flow to end organs is poor because SV and CO are decreased and after load is increased

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60
Q

Define contractility

A

The strength of contraction at a given resting loading, due to sympathetic nerves and circulating adrenaline increasing Ca2+ concentration

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61
Q

What’s the force of contraction proportional to?

A

The concentration of Ca2+

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62
Q

What’s diastolic Ca2+ concentration?

A

Around 100nM

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63
Q

What is normal systole Ca2+ concentration?

A

Around 1uM

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64
Q

What’s maximum systole Ca2+ concentration?

A

Around 10uM

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65
Q

What causes local Ca2+ influx in myocytes?

A

An action potential upstroke via Na+ ions depolarises T-tubules, opening VGCCs to allow Ca2+ influx

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66
Q

What does Ca2+ bind to on the SR for CICR?

A

Ca2+ binds to ryanodine receptors on the SR to trigger release of stored Ca2+ form the sarcoplasmic reticulum

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67
Q

What does Ca2+ bind to to trigger muscle contraction?

A

Ca2+ binds to troponin C, displacing it from the troponin-tropomyosin complex from myosin binding sites on actin to expose the active sites

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68
Q

How does greater Ca2+ concentration affect contractility?

A

More Ca2+ means more myosin binding sites on actin are exposed, so more cross bridges can form and contractions are stronger.

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69
Q

What does TnT do?

A

TnT binds to tropomyosin

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70
Q

What does TnI do?

A

TnI binds to actin filaments to hold tropomyosin in place

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71
Q

What does TnC do?

A

TnC binds to Ca2+

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72
Q

How does Ca2+ decrease in muscle tissue at the sub cellular level? 5 ways

A

AP downstroke via K+ ions repolarises T-tubules, closing VGCCs and decreasing Ca2+ concentration
No Ca2+ influx means no CICR. Ca2+ is extruded from cells by Na+/Ca2+ exchanger. Ca2+ is uptaken into the SR via Ca2+ ATPase and uptaken in mitochondria

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73
Q

How does decrease in Ca2+ affect muscle contraction?

A

Reduction in Ca2+ concentration means myosin head ATPase activity releases energy. The contraction mechanism is prevented by troponin binding back to tropomyosin and blocking active sites, preventing cross bridge formation.

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74
Q

What is hyperkalaemia?

A

A condition in which external K+ concentration is high (normal concentration is 3.5-5mM)

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75
Q

At what K+ concentration does the heart stop beating and why?

A

7-8mM. The membrane potential depolarises, reducing onset time and inactivating Na+ channels, so aptitude decreases and action potentials are shortened

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76
Q

How does increased H+ concentration affect contraction?

A

H+ competes with Ca2+ for troponin C binding sites, impairing contraction

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77
Q

How does low O2 levels affect contraction?

A

Hypoxia leads to local acidosis, impairing contraction due to raised H+ levels. Hypoxia also affects ion channels, causing depolarised membrane potential and making action potentials smaller, so contraction becomes poor

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78
Q

What’s the name of the effect where contractility increases?

A

Positive inotropic effect

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79
Q

What’s the name of the effect where relaxation increases?

A

Positive iusotropic effect

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80
Q

What’s the name of the effect where heart rate increases?

A

Positive chronotropic effect

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81
Q

What’s the name of the effect where conduction increases?

A

Positive dromotropic effect

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82
Q

How can high resting heart rate cause greater risk of CVD?

A

Higher heart rate means increased myocardial O2 consumption, which reduces coronary circulation perfusion time, which only occurs during diastole. Risk of arrhythmia and coronary artery plaque disruption are increased

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83
Q

How can phase 0 of the cardiac cycle be reduced?

A

Inhibition of VGCCs slows down the upstroke

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84
Q

How can phase 4 be increased?

A

Inhibition of funny channels means Ca2+ channels are activated slower

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85
Q

What are CCBs?

A

Ca2+ channel blockers

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86
Q

How do CCBs work?

A

CCBs sit in the pore of Ca2+ channels and block Ca2+ entry into sino-atrial cells to reduce heart rate

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87
Q

What are the 3 subtypes of CCB?

A

Dihydropyridines (vascular selective)
Diphenylalkylamines (cardiac selective)
Benzothiazepines (vascular + cardiac)

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88
Q

Name a dihydropyridine

A

Amlopdipine

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89
Q

Name a diphenylalkylamine

A

Verapamil

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90
Q

Name a benzothiazepine

A

Diltiazem

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91
Q

What property allows CCBs to be selective to cardiac or vascular Ca2+ channels?

A

Cardiac and vascular Ca2+ channels have slightly different structures

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92
Q

Why can CCBs worsen heart failure and cause heart block?

A

The AV node is needed for atria-ventricle conduction and CCBs have non-selective blocking actions on Ca2+ channels in cardiac myocytes

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93
Q

Name a funny channel blocker

A

Ivabradine

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94
Q

How does ivabradine work to lower heart rate?

A

Ivabradine is a selective inhibitor of funny channels in the SAN. It decreases the If current, reducing pacemaker potential frequency and decreasing the heart rate to reduce myocardial O2 demand

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95
Q

Why are ß1-adrenoreceptor blockers central drugs in treatment of angina?

A

ß-blockers such as atenolol reduce the action of the sympathetic nervous system on the SAN, preventing heart rate from increasing too much

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96
Q

Why shouldn’t ß1-adrenoreceptor blockers be used in combination with CCBs?

A

Together, they can reduce contractility too much and produce too much bradycardia, leading to fatigue

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97
Q

How do Muscarinic receptor blockers work to increase heart rate?

A

They reduce the action of the parasympathetic nervous system on the SAN

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98
Q

Name 3 conditions muscarinic receptor blockers may be used for

A

COPD, IBS and overactive bladder

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99
Q

What’s the name of a drug that increases contractility?

A

An inotropic agent

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100
Q

How is sympathetic control of the SAN regulated to increase heart rate?

A

Noradrenaline acts at ß1-adrenoreceptors on the SAN, activating the Gas system to produce cAMP and increase If channel activity

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101
Q

How is parasympathetic control of the SAN regulated to decrease heart rate?

A

Ach binds to M2 receptors on the SAN, acting at Gai protein to inhibit adenylate cyclase, reduce cAMP production and decrease If channel activity

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102
Q

How do ß1-adrenoreceptor blockers such as atenolol prevent heart rate from increasing too much?

A

They reduce the action of the sympathetic nervous system on the SAN, so they’re central drugs in angina treatment

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103
Q

Why shouldn’t ß1-adrenoreceptor blockers be used in combination with Ca2+ channel blockers?

A

Together, these can reduce contractility too much and produce too much bradycardia, leading to fatigue

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104
Q

What’s a possible side effect of muscarinic receptor blockers?

A

Tachycardia and therefore increased O2 demands on the heart

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105
Q

What is the result of improperly maintained cardiac output in heart failure?

A

End organs are poorly perfused

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106
Q

Name 2 Gs-coupled receptor agonists

A

ß1-adrenoreceptor agonists

PDE inhibitors

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107
Q

What heart condition are ß1-adrenoreceptors used to treat?

A

Acute heart failure

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108
Q

When would glucagon be used instead of ß1-adrenoreceptor agonists?

A

When the person is taking beta blockers, so adrenaline, dobutamine and dopamine would not work

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109
Q

Why aren’t Gs agonists used in chronic heart failure?

A

They’d increase heart rate, myocardial work and O2 demand

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110
Q

Name a PDE inhibitor

A

Amrinone

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111
Q

What does PDE inhibitor stand for?

A

Phosphodiesterase inhibitor

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112
Q

How do PDE inhibitors work?

A

They cause a build up of cAMP, activation of PKA and increase in Ca2+ influx via VGCCs

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113
Q

When are PDE inhibitors used?

A

In severe chronic cases such as when waiting for a heart transplant

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114
Q

How do cardiac glycosides work?

A

They increase contractility by reducing Ca2+ extrusion

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115
Q

How does digoxin, a cardiac glycoside, work to increase contractility?

A

Digoxin inhibits Na+/K+ ATPase, so Na+ concentration builds up. There’s then less extrusion of Ca2+ by the Na+/Ca2+ exchanger (NCX). As a result, there’s more Ca2+ uptake into stores and greater CICR, so greater contraction

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116
Q

What are the 2 problems with Gs-coupled agonist-induced rise in Ca2+?

A

There’s increased need for Ca2+-ATPase to reuptake more Ca2+ into SR stores, so there’s more O2 consumption, which stresses the heart.
Also, Gs pathways increase heart rate, so they’re pro-arrhythmogenic

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117
Q

What is a potential solution to Ca2+ related problems with Gs-coupled agonists?

A

Ca2+ sensitisers

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118
Q

Name 2 Ca2+ sensitisers

A

Levosimedan and Omecamtiv

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119
Q

How does levosimedan work?

A

Levosimedan binds to troponin C to increase the binding of Ca2+ to troponin C

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120
Q

How does omecamtiv work?

A

Omecamtiv increases actin-myosin interactions in absence of rise of Ca2+

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121
Q

Do Ca2+ sensitisers affect Ca2+ levels?

A

No

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122
Q

When are Ca2+ sensitisers used?

A

In decompensated heart failure

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123
Q

Why use ß-blockers in chronic heart failure when you’d expect that we’d need to promote ß-adrenoreceptor activity to increase inotropic effect? (4 points)

A

ß-blockers prevent overworking of a failing heart by slowing heart rate and increasing diastolic time, which increases coronary perfusion.
They prevent overworking of a failing heart by reducing contractility to reduce O2 demand, making the failing heart work more efficiently.
They prevent down-regulation of ß-adrenoreceptors caused by excess compensatory sympathetic nerve activity in heart failure, so more ß-adrenoreceptors are available for contractility.
They also prevent ß-adrenoreceptor-associated arrhythmia.

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124
Q

How do loop diuretics, thiazide diuretics and K+ sparing diuretics work to reduce cardiac output and blood pressure?

A

They cause you the excrete more fluid, reducing blood volume and reducing central venous pressure and stroke volume via Starling’s law

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125
Q

How do ACE inhibitors and ARBs such as ramipril and losartan reduce TPR?

A

They reduce Ang II-induced vasoconstriction

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126
Q

What happens when Ang II-induced aldosterone release is reduced?

A

Blood volume and CO are reduced

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127
Q

What causes cardiac pain in angina?

A

Poor blood flow to the heart, often due to occlusion of the coronary arteries

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128
Q

How can cardiac pain from angina be alleviated?

A

Dilation of the coronary arteries to increase blood flow

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129
Q

What drug is commonly used for angina and how’s it administered?

A

GTN (glyceryl trinitrate) is often administered as a sublingual spray

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130
Q

What is the significance of the CVS being a closed system?

A

What happens in one part of the CVS has a major impact on the rest, so, for example, reducing blood flow to 1 area increases the blood pressure in other areas

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131
Q

What does Darcy’s law involve?

A

The role of pressure energy in blood flow

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132
Q

What’s the equation of Darcy’s law?

A 
Q = (P1-P2)÷R
Q= flow
P1-P2= pressure difference
R= resistance to flow
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133
Q

What does Bernoulli’s law involve?

A

The role of pressure, kinetic and potential energies in blood flow

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134
Q

What’s the equation of Bernoulli’s law?

A

Flow = Pressure + kinetic + potential

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135
Q

What is perfusion and its units?

A

Blood flow per given mass of tissue (ml/min/g)

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136
Q

How is velocity of blood flow calculated?

A

Blood flow divided by the cross-sectional area through which the blood flows (cm/s)

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137
Q

What slows blood flow velocity in arteries?

A

The branching of arteries

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138
Q

Where is blood flow the slowest?

A

In the capillaries

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139
Q

What are the 3 patterns of blood flow?

A

Laminar blood flow- most arteries, arterioles, veins and venules
Turbulent blood flow- ventricles, the aorta and atherosclerotic vessels
Bolus flow in capillaries

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140
Q

What does Reynold’s number describe?

A

What determines change from laminar to turbulent flow

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141
Q

What’s the equation for Reynold’s number?

A 
Re= pVD ÷ u
P= density
V= velocity
D= diameter
u= viscosity
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142
Q

Above what value of Reynold’s number does turbulent blood flow occur?

A

2000

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143
Q

What’s the equation for blood flow?

A

Blood flow = arterial blood pressure ÷ total peripheral resistance

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144
Q

Where is blood pressure the highest?

A

In the aortic trunk

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145
Q

What’s normal systolic and diastolic pressure in the aorta?

A

120mmHg and 80mmHg

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146
Q

Name 4 factors that affect arterial blood pressure

A

Cardiac output
Properties of arteries
Peripheral resistance
Blood viscosity

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147
Q

Where is energy stored during LV ejection?

A

In the stretched elastin in the aorta and arteries

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148
Q

What happens to the stored energy during LV diastole?

A

The energy is returned to the blood as the walls of the aorta and arteries contract, sustaining diastolic blood pressure and blood flow when the heart is relaxed

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149
Q

What is pulse pressure?

A

Systolic pressure - diastolic pressure

Represents the force the heart generates each time it contracts

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150
Q

What’s the equation for pulse pressure?

A

Pulse pressure = stroke volume ÷ compliance

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151
Q

What happens if arterial compliance is decreased?

A

Decreased compliance means stroke volume increases systolic and pulse pressure disproportionately

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152
Q

Why does arterial compliance decrease in old people?

A

Arteries become stiffer via arteriosclerosis

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153
Q

How does decreased arterial compliance affect after load?

A

Decreased arterial compliance increases afterload, so the heart has to work harder

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154
Q

How does pulse pressure change as blood moves away from the aorta?

A

Pulse pressure increases

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155
Q

What is aortic stenosis?

A

Narrowing of the aortic valve, which gives a slower upstroke and indicates poor ejection

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156
Q

What is aortic regurgitation?

A

A leaky aortic valve which gives fast upstroke and poor diastolic runoff, that indicates blood entering the aorta/ventricles during diastole

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157
Q

What’s a normal PR interval?

A

0.12-0.20 seconds

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158
Q

What’s a normal QRS duration?

A

0.6-1.2 seconds

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159
Q

What’s a normal QT interval?

A

> 440ms in men

> 460ms in women

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160
Q

What are the 2 types of arrhythmia?

A

Conduction abnormality arrhythmias and abnormal impulse initiation arrhythmias.

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161
Q

What causes conduction abnormality arrhythmias?

A

Blockages

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162
Q

What causes abnormal impulse initiation arrhythmias?

A

VT or ectopia

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163
Q

What is the result on an ECG if the SAN fails to initiate an impulse?

A

There’s no P wave or QRS complex

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164
Q

What are conduction abnormalities characterised by?

A

A delay or interruption in conduction, which can be due to ischaemic heart disease or valve fibrosis

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165
Q

What is VT?

A

Ventricular tachycardia- a broad complex tachycardia originating in the ventricles

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166
Q

What’s the most common variety of VT?

A

Monomorphic VT

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167
Q

How may VT cause hypertension, collapse and acute heart failure?

A

Ventricular tachycardia may impair cardiac output

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168
Q

What are the 3 basic arrhythmogenic mechanisms responsible for initiating tacharrhythmia?

A

Altered automaticity
Triggered activity where normal action potential suddenly swings positive again, allowing another depolarisation to occur abnormally
Re-entry

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169
Q

What’s characteristic of atrial fibrillation on an ECG?

A

No distinct P waves, and there can also be an atrial saw-tooth pattern

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170
Q

What is SVT?

A

Supraventricular tachycardia- an abnormally fast heart rhythm resulting from improper electrical activity in the upper part of the heart.

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171
Q

What are the 4 main types of SVT?

A

Atrial fibrillation, paroxysmal SVT, atrial flutter and Wolff-Parkinson-White syndrome

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172
Q

What causes the ST depression in ischaemia?

A

Ischaemic myocytes have reduce membrane potentials compared to healthy myocytes. The difference in potential between the ischaemic region and healthy region displaces the ST segment. This is called the ‘injury current’ effect

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173
Q

What does TPR control?

A

Blood flow and blood pressure

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174
Q

What 3 things control TPR?

A

Poiseuille’s law, myogenic response and blood viscosity

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175
Q

What does Poiseuille’s law describe?

A

The parameters that govern TPR

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176
Q

What 3 factors determine TPR?

A

TPR is determined by radius ^4, pressure difference across vessels and length

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177
Q

Do capillaries control TPR?

A

No

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178
Q

Why do arterioles control TPR and not capillaries? 3 reasons

A

Radius of capillaries cannot be altered
There’s less pressure drop across capillaries than arterioles due to less resistance to blood flow
Individual capillaries are short compared to arterioles

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179
Q

What reduces viscosity in capillaries?

A

Bolus flow

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180
Q

What is bolus flow?

A

Where erythrocytes travel singly, separated by segments of plasma

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181
Q

What feature of capillary arrangement means they have a low total resistance?

A

They’re arranged in parallel

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182
Q

How is local blood flow through individual organs/ tissues mainly controlled?

A

Via changes in radius of arterioles supplying the organ/tissue

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183
Q

What’s the name for intrinsic control?

A

Bayliss myogenic effect

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184
Q

How does Bayliss myogenic effect work?

A

Dilation of the micro vessel leads to ion influx (Na+, Ca2+) through stretch-sensitive membrane ion channels and, therefore, to contraction of the vessel smooth muscle cells to decrease radius

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185
Q

What are the 3 factors contributing to blood viscosity?

A

Velocity of blood, vessel diameter and haematocrit level

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186
Q

Describe veins

A

Veins are thin-walled, collapsible, voluminous vessels which contain 2/3 of the body’s blood. They contain smooth muscle innervated by sympathetic nerves, so their radius can be controlled by constriction and relaxation

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187
Q

What happens when smooth muscle in veins is contracted (venoconstriction)?

A

Blood is expelled into central veins. Venous return, CVP and end-diastolic volume are increased, so stroke volume is increased

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188
Q

What’s a typical venous pressure range in the limb veins or the heart?

A

5-10mmHg

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189
Q

What’s typical central venous pressure?

A

0-5mmHg

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190
Q

What’s typical venous pressure in the feet while standing?

A

90mmHg

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191
Q

Via what 3 mechanisms is blood returned to the heart?

A

Pressure gradient
Thoracic pump
Skeletal muscle pump

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192
Q

Describe the pressure gradient for returning blood to the heart

A

Pressure in the veins/venules is 10-90mmHg. In the IVC, SVC and right atrium, pressure is <5mmHg. Venous return = venous pressure - pressure in the right atrium ÷ venous resistance

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193
Q

Describe the thoracic pump and its role in returning blood to the heart

A

Inhalation causes the thoracic cavity to expand, leading to increased abdominal pressure, forcing blood upwards towards the heart. This increases right ventricular stroke volume, so blood flows faster with inhalation

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194
Q

Describe the skeletal muscle pump and its role in returning blood to the heart

A

Contraction of leg muscles returns blood into the right atrium. Retrograde flow is prevented by venous valves. When in the upright position, high local venous pressures are reduced. This reduces swelling of the feet and ankles. CVP and SV are increased during exercise.

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195
Q

Due to what 3 factors can standing still for a long time lead to fainting?

A

Gravity, heat-induced vasodilation and lack of muscle use

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196
Q

What’s Bernoulli’s theory?

A

Mechanical energy of flow is determined by pressure, kinetic energy and potential energy

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197
Q

Name some symptoms of arrhythmias

A

Palpitations, dizziness, fainting, fatigue, loss of consciousness, cardiac arrest, blood coagulation, stroke or MI

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198
Q

What can cause arrhythmias?

A

Cardiac ischaemia, heart failure, hypertension, coronary vasospasm, heart block or excess sympathetic stimulation

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199
Q

Arrhythmia can be ventricular or supra ventricular. Where would supra ventricular arrhythmia stem from?

A

The SAN, the atria or the AVN

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200
Q

How do arrhythmias affect cardiac output?

A

They lead to incorrect filling and ejection

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201
Q

What are the 2 mechanisms of arrhythmogenesis?

A

Abnormal impulse generation due to automatic rhythms, which leads to increased SAN activity and ectopic activity, causing triggered rhythms called early-after depolarisations (EADs) and delayed-after depolarisations (DADs)
Abnormal conduction due to re-entry of electrical circuits in the heart and a consequential conduction block

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202
Q

What is atrial fibrillation?

A

Quivering atria activity (no distinct P waves). Irregular ventricular contraction

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203
Q

What’s a characteristic of SVT that shows on ECGs?

A

The P wave is ‘buried in’ the T wave

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204
Q

How do EADs work?

A

Altered ion channel activity removes the refractory period and causes depolarisation

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205
Q

How do DADs work?

A

Abnormal levels of Ca2+ in the SR means Ca2+ leaks out into cytosol and stimulates Na+/Ca2+ exchangers, triggering Na+ influx and depolarisation

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206
Q

Name 3 places of possible ectopic pacemaker activity

A

The AVN, the bundle of His, the Purkinje fibres

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207
Q

How can enhanced stimulation of the sympathetic nervous system lead to arrhythmias?

A

The ectopic pacemaker regions can take over

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208
Q

What causes re-entry based arrhythmia?

A

Different parts of the heart having refractory periods of different lengths

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209
Q

What can cause heart block?

A

Fibrosis or ischaemic damage to conducting pathways

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210
Q

What classifies as first degree heart block?

A

When the PR interval is >0.2s

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211
Q

What classifies as second degree heart block?

A

When more than 1 atrial impulse fails to stimulate the ventricles

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212
Q

What classifies as third degree heart block?

A

When the atria and ventricles beat independently of each other.

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213
Q

What’s the goal of treatment of arrhythmias?

A

To restore sinus rhythm and normal conduction and prevent more serious and possibly fatal arrhythmia occurring

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214
Q

What do anti-arrhythmic drugs do?

A

Reduce conduction velocity, alter refractory periods of cardiac action potentials and reduce automaticity

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215
Q

What are class I anti-arrhythmic drugs?

A

Na+ channel blockers (acting in non-nodal tissue)

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216
Q

What are class II anti-arrhythmic drugs?

A

ß-blockers (acting at nodal and non-nodal tissue)

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217
Q

What are class III anti-arrhythmic drugs?

A

K+ channel blockers (acting at non-nodal tissue)

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218
Q

What are class IV anti-arrhythmic drugs?

A

Ca2+ channel blockers (acting at nodal and non-nodal tissue)

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219
Q

How do Class I anti-arrhythmic drugs work?

A

Class I drugs block Na+ channels in non-nodal tissue, such as the atria or ventricles. They block Na+ channels in their inactivated state. They only block Na+ channels in high frequency firing tissue, so the drugs are use-dependent

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220
Q

What property of class I anti-arrhythmic drugs means they don’t affect normal firing?

A

They are fast-dissociating, so they come off the active site in time for the next impulse

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221
Q

What arrhythmias do class I drugs work for?

A

Very fast arrhythmias

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222
Q

How does stimulation of sympathetic nerves and activation of ß1 receptors in the heart cause pro-arrhythmic effects?

A

There’s increased SAN and AVN firing rate, and increase in ventricular excitability by raising Ca2+ concentration

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223
Q

What do ß1 blockers such as atenolol do and when are they used?

A

Atenolol reduces VT after myocardial infarctions caused by increase in sympathetic nerve activity

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224
Q

How do ß blockers reduce SVT?

A

They slow conduction through the AVN, which reduces ventricular firing rate

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225
Q

How do class III drugs work?

A

Class III drugs increase the length of the action potential to increase the refractory period of the heart. They also inhibit K+ ion channels responsible for repolarisation in atria/ventricles. This is to block channels involved in repolarisation to maintain depolarisation. The Na+ channels become inactivated and cannot fire any more APs, preventing arrhythmias

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226
Q

What are class III drugs used for?

A

SVT and VT

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227
Q

How do class IV drugs work?

A

They block L-type VGCCs, which mainly affects the firing of SAN and AVN APs. Reducing Ca2+ channel activity slows down upstrokes and so less pacemaker potentials fire, decreasing heart rate

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228
Q

What 2 phases of the cardiac cycle do class IV drugs act?

A

Phase 0 and phase 2

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229
Q

Adenosine is an unclassified anti-arrhythmic drug. How does it work?

A

Adenosine decreases activity in the SAN and AVN and slows down the heart by activating K+ channels, so it’s used for SVT

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230
Q

Atropine is an unclassified anti-arrhythmic. How does it work?

A

Atropine is a muscarinic antagonist that reduces parasympathetic activity and may be used to treat AV block and treat sinus bradycardia after MI

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231
Q

Digoxin is an unclassified anti-arrhythmic. How does it work?

A

Digoxin has central effects and increases vagus nerve activity, decreasing heart rate and conduction. Digoxin is a Na+/K+ ATPase blocker. It’s used for AF

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232
Q

How can class III drugs end up being pro-arrhythmic?

A

They increase QT duration. Long QT syndrome leads to arrhythmia due to EAD and DAD generation

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233
Q

How can classes I, II and IV potentially be pro-arrhythmic?

A

They may increase the refractory period and reduce conduction time, which potentially can be pro-arrhythmic. Class IV may also reduce contractility.

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234
Q

What creates a need to transport solutes and fluid?

A

Metabolism

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235
Q

What do cell membranes consist of?

A

2 layers of amphipathic phospholipids

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236
Q

What are the 4 passive transport processes?

A

Osmosis, diffusion, convection, electrochemical flux

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237
Q

Where does solute and fluid exchange occur?

A

Capillaries

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238
Q

What are capillaries?

A

1-cell-thick, semi-permeable blood vessels with the smallest diameter

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239
Q

What properties of solutes affect transport?

A

Concentration gradient
Size of the solute
Lipid solubility of the solute

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240
Q

What properties of the membrane affect transport?

A

Membrane thickness/ composition
Aqueous pores in the membrane
Carrier-mediated transport
Active transport mechanisms

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241
Q

What is Fick’s law equation for solute movement?

A 
Js = -DA (∆C÷x)
D= diffusion coefficient of the solute
A= area
∆C÷x = concentration gradient across distance x
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242
Q

What does a negative value for solute movement mean?

A

The solute is moving down a concentration gradient

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243
Q

What are the 3 distinct types of capillaries?

A

Continuous capillaries
Fenestrated capillaries
Discontinuous capillaries

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244
Q

Describe the properties of continuous capillaries

A

They have moderate permeability, tight gaps between neighbouring cells and a constant basement membrane

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245
Q

Describe the properties of fenestrated capillaries

A

They have a high water permeability, fenestrations and modest disruption of the basement membrane

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246
Q

Describe the properties of discontinuous capillaries

A

They have very large fenestration structures, and a disrupted basement membrane

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247
Q

Where would you find continuous capillaries?

A

The blood-brain barrier

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248
Q

Where would you find fenestrated capillaries?

A

High water-turnover tissues such as salivary glands, kidneys and synovial joints

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249
Q

Where would you find discontinuous capillaries?

A

Where movement of cells is required, such as of RBCs in the liver, spleen and bone marrow

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250
Q

What are 3 other structural features of capillary walls that can influence solute transfer?

A

Intercellular cleft
Glycocalyx
Caveola-vesicle

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251
Q

How wide is the intracellular cleft?

A

10-20nm wide

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252
Q

What is the glycocalyx?

A

Negatively charged material that covers the outside of the endothelium and blocks solute permeation and access to transport mechanisms

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253
Q

How can the caveola-vesicle system influence solute transfer?

A

Large structures or proteins can be taken up by endocytosis from the vascular space, carried across and released by exocytosis into interstitial space

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254
Q

What is permeability?

A

The rate of solute transfer by diffusion across unit area of membrane per unit concentration difference

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255
Q

What’s the equation for permeability?

A 
Js= -P Am ∆C
Js= rate of solute transport
P= permeability
Am= surface area of capillary involved in transport
∆C= concentration gradient
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256
Q

What’s glucose concentration in plasma?

A

1g/litre

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257
Q

What’s the total volume of plasma filtrate flowing into tissues per day?

A

8L

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258
Q

What’s the maximum filtration of glucose?

A

8g/day

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259
Q

What percentage of glucose transport does filtration transport account for?

A

2%

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260
Q

How is 98% of glucose transport carried out?

A

Into interstitial space via passive diffusion via GLUT transporters

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261
Q

How does increased blood flow affect solute concentration in capillaries?

A

Increased blood flow increases solute concentration

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262
Q

What does increased blood flow mean in the lungs?

A

Greater solute concentration means a steeper concentration gradient and so more O2/CO2 exchange along capillaries in the lungs

263
Q

How does dilation of arterioles and the resulting increase in number of capillaries perfused affect diffusion?

A

More capillaries perfused increases total surface area for diffusion and shortens diffusion distance, leading to faster diffusion. O2 transport from blood to muscle increases by over 40 times during strenuous exercise

264
Q

What is a thrombus?

A

A solid mass of blood formed within the cardiovascular system, involving the interaction of endothelial cells, platelets and the coagulation cascade, and which impedes blood flow

265
Q

What does arterial thrombosis usually result from?

A

Atheroma rupture

266
Q

What are arterial thrombi like?

A

Platelet-rich, white masses that block downstream arteries

267
Q

What causes venous thrombosis?

A

Stasis or a hyper coagulant state

268
Q

What are venous thrombi like?

A

Platelet-poor and red in colour

269
Q

What are the 4 main components of the clotting process?

A

Endothelium, platelets, coagulation and fibrinolysis

270
Q

What is normal haemostasis?

A

A state of equilibrium between fibrinolytic factors and anticoagulant proteins, and between coagulation factors and platelets

271
Q

What 3 things do platelets do in primary haemostasis?

A

Adhere, activate and aggregate

272
Q

What does secondary haemostasis involve?

A

Coagulation and the conversion of fibrinogen to fibrin

273
Q

How does fibrinolysis occur?

A

A cascade whereby tissue plasminogen activator (tPA) activates plasminogen, converting it to plasmin. Plasmin then breaks down the fibrin into fragments

274
Q

What 3 factors can govern development of a venous thrombus?

A

Changes in normal blood flow
Alterations in the constituents of the blood
Damage to the endothelial layer

275
Q

What 3 things make up Virchow’s triad?

A

Endothelial damage or dysfunction
Hypercoagulability
Stasis

276
Q

Name some risk factors for endothelial damage or dysfunction

A

Smoking, hypertension, surgery, catheterisation, trauma

277
Q

Name acquired factors for hypercoagulability

A

Cancer, chemotherapy, OCR/HRT, pregnancy, obesity, HIT

278
Q

Name some hereditary factors for hypercoagulability

A

Factor V Leiden, Prothrombin G20210A, Protein C and S deficiency

279
Q

Name 2 factors that can contribute to stasis of the blood

A

Immobility, polycythaemia

280
Q

Briefly describe primary haemostasis

A

vWF binds to exposed collagen beneath damaged endothelium. Platelets bind to vWF and are activated. They express fibrinogen receptors and bind to fibrinogen, which causes platelet aggregation to form a thrombus

281
Q

Briefly describe secondary haemostasis

A

Factor VIIa binds to tissue factor expressed by sub-endothelial cells, which leads to conversion of prothrombin to thrombin. Thrombin activates 2 cofactors, factor VIIIa and factor Va, which subsequently form calcium-ion-dependent complexes on the surface of platelets with factor Xa and IXa. These complexes greatly increase production of thrombin and factor Xa

282
Q

Describe briefly the process of fibrinolysis

A

Once the clot is no longer needed, fibrin is broken down into smaller components (fragments). This is initiated by tPA, an endogenous fibrinolytic which sits on the surface of endothelial cells and activates plasminogen to plasmin. Plasmin is the enzyme that degrades fibrin

283
Q

What is DIC?

A

Disseminated intravascular coagulation is a condition in which blood clots form throughout the body, blocking small blood vessels. This results from the proteins that control blood clotting becoming overactive

284
Q

What can cause hypercoagulability?

A

Alterations in the constituents of the blood components. Decrease in fibrinolytic factors and anticoagulant proteins and increase in coagulation factors and platelets

285
Q

What feature of veins can increase likelihood of stasis?

A

Valves

286
Q

What’s the annual incidence of DVT in the UK?

A

1 in 1000

287
Q

Is DVT below the knee more dangerous, or DVT above the knee?

A

DVT above the knee is more likely to lead to pulmonary embolism

288
Q

Name symptoms of DVT

A 
Pain and tenderness of veins
Limb swelling
Superficial venous distension
Increased skin temperature
Skin discolouration
289
Q

Name 2 anticoagulants

A

Warfarin and heparin

290
Q

What are ‘clot busters’ used for?

A

Plasminogen activators and streptokinase can break down a clot when a patient has a massive pulmonary embolism

291
Q

Where does fluid exchange occur?

A

At the capillary wall

292
Q

What causes fluid to move across the basement membrane into interstitial space?

A

Hydraulic pressure from blood flow

293
Q

Fluid movement depends on what pressures across the capillary wall?

A

Hydraulic pressure and oncotic pressure

294
Q

What’s the equation of Starling’s principle of fluid exchange?

A 
Jv = Lp A { (Pc-Pi) - sigma(πp-πi) }
Jv= net filtration
Lp= hydraulic conductance of the endothelium
A= wall area
Pc= capillary blood pressure
Pi- interstitial fluid pressure
sigma= reflection coefficient
πp= plasma proteins
πi= interstitial proteins
295
Q

How is effective osmotic pressure calculated?

A

π x potential osmotic pressure

296
Q

What’s the value of sigma for plasma proteins?

A

0.9 (so only 10% get across the capillary wall)

297
Q

What’s a major problem with Starling’s equation?

A

The glycocalyx is not taken into account

298
Q

What are the generic structural components of the glycocalyx?

A

Proteoglycans and glycoproteins

299
Q

With the glycocalyx, plasma proteins don’t move into interstitial space via intercellular gaps, but via what?

A

Via vesicles

300
Q

What’s the revised Starling equation for fluid exchange?

A

Jv = Lp A { (Pc-Pi) - sigma(πp-πg)}

301
Q

What is hypovolaemia?

A

Abnormally low circulating blood volume

302
Q

What function does the lymphatic system play in blood circulation?

A

The lymphatic system returns excess tissue fluid/ solutes back the the cardiovascular system

303
Q

What 3 things determine overall control of extracellular fluid balance?

A

Capillary filtration
Capillary reabsorption
Lymphatic system

304
Q

What does imbalance in filtration, reabsorption, lymphatic function and glycocalyx function lead to?

A

Excess interstitial fluid build-up and oedema

305
Q

Name 3 clinical causes of increased capillary pressure

A

Dependent oedema, DVT and cardiac failure

306
Q

How does DVT lead to increased capillary pressure?

A

There’s a prevention of venous return, so venous pressure is increased and causes a back-up of pressure, leading to increased Pc across capillaries and increased filtration

307
Q

What is nephrotic syndrome?

A

Kidney disease characterised by oedema and loss of protein from plasma into the urine due to increased glomerular permeability

308
Q

Why does the protein loss in nephrosis lead to oedema?

A

Reduced plasma protein concentration causes reduced plasma oncotic pressure (πp), so Pc has a greater influence. Fluid efflux from the capillaries into the interstitial fluid causes oedema

309
Q

What’s filariasis and how does it happen?

A

Filarial worms migrate to the lymphatic system and mate and multiply, then block lymphatic drainage and cause swelling

310
Q

How can inflammation cause oedema?

A

Inflammation increases Lp, the hydraulic conductance of the endothelium, allowing more fluid movement and therefore build-up

311
Q

What are the names of the 3 layers of blood vessels?

A

Tunica intima, tunica media and tunica adventitia

312
Q

What’s the tunica adventitia and its function?

A

The outer collagenous connective tissue layer that provides anchorage, support and sometimes elasticity, as well as carrying nerve supply and blood supply to the vessel

313
Q

What is the tunica media and its function?

A

A smooth muscle layer for support, elasticity and contractility, allaying for physical regurgitation of blood flow and smoothing of blood flow

314
Q

What is the tunica intima and its function?

A

Endothelium over a little dense connective tissue. A selectively permeable barrier to blood that regulates adhesion of leukocytes and platelets, makes mediators controlling vessel tone and makes mediators of inflammation

315
Q

What fibres intercalate between muscle cells in the tunica media?

A

Elastic fibres

316
Q

How is the tunica media different in arteries compared to in veins?

A

It’s much thicker in arteries

317
Q

What are the 3 types of artery?

A

Elastic arteries
Muscular arteries
Arterioles

318
Q

Give examples of elastic arteries

A

The aorta, pulmonary arteries and their largest branches

319
Q

What’s another name for elastic arteries?

A

Conducting arteries

320
Q

What’s the definitive feature of elastic arteries?

A

They have a very thick tunica media with many elastic laminae

321
Q

What is a dissecting aneurysm of the aorta?

A

Where there’s a partial rupture of the arterial wall which allows blood to enter the tunica media. If tunica adventitia also ruptures, this is fatal

322
Q

What’s another name for muscular arteries?

A

Distributing arteries

323
Q

Describe muscular arteries structurally

A

Muscular arteries have prominent internal elastic laminae between the tunica media and tunica intima. They have a thick tunica media with some elastic fibres but no elastic laminae. The adventitia is mainly collagen

324
Q

What is different about the elastic laminae in elastic arteries and muscular arteries?

A

elastic arteries have many elastic laminae in the tunica media, whereas muscular arteries have a single internal and external lamina

325
Q

What classifies as an arteriole?

A

A microscopic artery of <0.3mm in diameter

326
Q

What is the predominant layer in arterioles and why?

A

The tunica media is predominant for contractility against high BP

327
Q

What direction does the smooth muscle in arterioles run?

A

Circularly

328
Q

What are capillaries?

A

Blood vessels specialised for exchange between blood and tissues, made only of endothelium with scattered pericytes

329
Q

What limits exchange and allows regulation in capillaries?

A

The thin layer of endothelial cytoplasm lining the capillary lumen

330
Q

What are sinusoids?

A

Wider fenestrated capillaries found in the liver and spleen, which allow slow blood flow and the highest rate of exchange

331
Q

What’s the function of veins and venules?

A

These vessels are specialised to return low-pressure blood to the heart

332
Q

Describe the histology of veins

A

Venis have relatively thin, flexible walls, often with prominent adventitia. The media is relatively thin, but still controls flow and pressure

333
Q

What may some major veins have in their walls?

A

Longitudinal smooth muscle to assist flow against gravity

334
Q

What do the atria secrete to regulate blood pressure?

A

ANP (atrial natriuretic peptide)

335
Q

When do the atria release atrial natriuretic peptide from granules?

A

When the atria stretch after being filled with blood

336
Q

What does ANP do?

A

ANP increases secretion of water and Na+ into urine, resulting in reduction or buffering of blood pressure

337
Q

What are the 3 layers of the heart?

A

Epicardium, myocardium, endocardium

338
Q

What’s the epicardium?

A

The outer layer of fatty, loose connective tissue with nerves, blood vessels and smooth, lubricated epithelial covering (mesothelium)

339
Q

What’s the myocardium?

A

The middle layer of cardiac muscle, which contracts to give heart beats

340
Q

What’s the endocardium?

A

A thin layer of endothelium and some loose connective tissue

341
Q

What separates the intima and media of blood vessels?

A

A fenestrated internal elastic lamina

342
Q

What separates the media and adventitia of blood vessels?

A

An external elastic lamina

343
Q

What does vascular tone describe?

A

The degree of constriction of a blood vessel relative to maximum dilation

344
Q

What controls vascular tone?

A

The contractile state of vascular smooth muscle cells

345
Q

Do capillaries have vascular tone?

A

No, as they have no VSMCs

346
Q

What regulates vascular tone?

A

Constrictor responses and dilator responses

347
Q

What are intrinsic local controls needed for?

A

Regulating local blood flow to organs/tissues

348
Q

What are extrinsic controls useful for?

A

Regulating TPR to control blood pressure, as blood pressure is the drive for blood flow

349
Q

What are the nervous extrinsic controls?

A

Vasoconstrictors such as noradrenaline and vasodilators such as Ach and NO

350
Q

What are the hormonal extrinsic controls?

A

Vasoconstrictors- adrenaline, angiotensin II and vasopressin, and vasodilators- ANP

351
Q

What’s the most important extrinsic control of circulation?

A

The sympathetic vasoconstrictor system

352
Q

What do the receptors at postsynaptic membranes of sympathetic vasoconstrictor nerves do?

A

a1-adrenoreceptors: contraction
a2-adrenoreceptors: contraction
ß2-adrenoreceptors: relaxation

353
Q

What’s the purpose of a2-adrenoreceptors on the presynaptic membrane?

A

Excess NA in the synaptic cleft binds to presynaptic a2 receptors to trigger negative feedback and uptake NA back into presynaptic vesicles to be stored

354
Q

What’s the effect of Angiotensin I feeding back onto the presynaptic membrane?

A

NA release is increased and RAAS increases sympathetic activity

355
Q

What’s the effect of K+ and adenosine feeding back onto the presynaptic membrane?

A

They reduce the release of NA in a vasodilatory pathway

356
Q

What controls the sympathetic vasoconstrictor nerves?

A

The brainstem RVLM (rostral ventrolateral medulla)- the vasomotor centre

357
Q

What receptors does NA act at on vascular smooth muscle cells?

A

a1-adrenoreceptors

358
Q

What is meant by the fact that sympathetic nerve activity is tonic?

A

Action potential fire at around 1/second

359
Q

What’s the role of sympathetic vasoconstrictor nerves?

A

Produce vascular tone and allow vasodilation and increased blood flow

360
Q

Give an example of when some vessels vasoconstrictor and others vasodilator simultaneously

A

During exercise, sympathetic innervation to the GI tract is increased to decrease blood flow, while sympathetic innervation to the skin is decreased to increase blood flow and cool the skin down

361
Q

How is precapillary vasoconstriction important in hypovolaemia?

A

Precapillary vasoconstriction decreases capillary pressure due to pressure drop, increasing absorption of interstitial fluid into blood plasma to maintain blood volume

362
Q

How do sympathetic vasoconstrictor nerves control venous blood volume?

A

Venoconstriction decreases venous blood volume by increasing venous return as it increases stroke volume via Starling’s law

363
Q

What are the vasoconstrictor hormones acting on VSMCs?

A

Adrenaline, angiotensin II and ADH

364
Q

What is the vasodilator hormone acting at VSMCs?

A

ANP

365
Q

How can VSMC-controlling hormones become pathological?

A

If they’re produced in excess, they can cause excessive vasoconstriction and vascular disease such as hypertension and heart failure

366
Q

When and where is adrenaline released and what receptors does it act on?

A

Adrenaline is released mainly from the adrenal glands due to sympathetic nerve stimulation. It acts on a1-adrenoreceptors on VSMCs

367
Q

How is angiotensin II formed and where does it act?

A

It’s formed from the RAAS and acts on AT1 receptors on VSMCs

368
Q

Name 2 other important vasoconstrictors besides adrenaline and Ang II

A

Endothelin-1 and thromboxane

369
Q

Where’s endothelin-1 released and where does it act?

A

ET1 is released from the endothelium to act on ETA receptors on VSMCs

370
Q

Where’s thromboxane released and where does it act?

A

TXA2 is released from aggregating platelets to act on TP receptors on VSMCs

371
Q

Describe briefly the process of the RAAS system

A

Renin secreted by the kidney acts on angiontensinogen to release angiotensin I. 10-amino-acid Ang I is then cleaved by angiotensin-converting enzyme (ACE) into the octapeptide angiotensin II. As well as causing vasoconstriction, Ang II increases secretion of cortisol and aldosterone by a direct action on the adrenal cortex

372
Q

Stimulation of what receptors causes renin release from granular cells?

A

ß1-receptors

373
Q

Where does ANP act?

A

ANP acts at NP receptors on VSMCs

374
Q

What does ANP stimulate?

A

Increase in the cGMP pathway

375
Q

How does ANP reduce blood pressure?

A

Systemic vasodilation, which opposes the actions of Na, Adr, Ang II, ADH, ET-1 and TXA2

376
Q

What effect does ANP have on renal afferent arterioles?

A

ANP dilates renal afferent arterioles, increasing glomerular filtration rate and Na+ and H2O excretion by the kidney. This decreases blood volume

377
Q

What hormones does ANP decrease release and action of?

A

Aldosterone, renin and ADH, so as to increase glomerular filtration

378
Q

What is a necrotic core made up of?

A

Lipid, cholesterol clefts, fibrin, foam cell remnants and cell debris

379
Q

What are foam cells?

A

A type of macrophage which localise fatty acid deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance

380
Q

What are the 2 types of foam cell?

A

One is considered a modified smooth muscle cell derived from cells of the arterial tunica media. The other is a macrophage of reticuloendothelial origin (probably a blood monocyte)

381
Q

What’s the relationship between foam cells and the necrotic core in an atheromatic plaque?

A

Foam cells surround the necrotic core

382
Q

What type of factors can contribute to atherosclerosis?

A

Angiogenic factors that induce neovascularisation at the base of the plaque

383
Q

What’s the fibrous cap made of?

A

Predominantly made of collagen intertwined with smooth muscle in dynamic equilibrium

384
Q

How does atherosclerosis begin?

A

As an initial lesion which is isolated from cells. A fatty streak can then form from intracellular lipid accumulation.

385
Q

What happens after formation of a fatty streak in the development of atherosclerosis?

A

Intermediate lesions ensue and the next step is an atheroma. Once fibrotic/ calcific layers develop, the atheroma is considered a fibroatheroma, which can have a single, or multiple, lipid cores.

386
Q

Where are the most common sites of plaque build up?

A

The circle of Willis, carotid arteries, coronary arteries, the aorta or iliac arteries

387
Q

Name some major risk factors for atherosclerosis (12 total)

A 
Age
Male sex
Genetics
Hyperlipidaemia
Smoking
Hypertension
Diabetes mellitus
Obesity
Metabolic syndrome
Alcohol
Drugs
Systemic inflammation
388
Q

What’s an important property of LDL?

A

LDL is an inflammatory mediator, so it can induce cytokine production from other cells

389
Q

What’s the initiation stage of the mechanism of plaque development?

A

A mediator such as oxidised LDL or angiotensin II activates endothelial cells to become dysfunctional. When this happens, the endothelial cells begin secreting cytokines and adhesion molecules, which cause circulating monocytes to stick to the adhesion molecules on the surface of the endothelial cells and then penetrate the endothelial layer to move into the intima (diapedesis)

390
Q

What is diapedesis?

A

The passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation

391
Q

What happens in the plaque development process after the monocytes have moved into the intima?

A

The monocytes then differentiate into tissue macrophages and can secrete other cytokines. The macrophage can then incorporate more LDL and uptake LDL to become foam cells. The increased expression of cytokines by the macrophage causes activation of smooth muscle cells within the lining of the media to migrate into the intima when they start to proliferate

392
Q

What can smooth muscle do in the initiation of plaque development after they migrate into the intima?

A

They can shift from a contractile phenotype to a proliferative phenotype (a synthetic phenotype) which synthesises matrix proteins. This change is caused by an alteration in the gene expression of the smooth muscle cells. The cells can then secrete extracellular matrix components such as collagen and elastin as well as proliferating by division. The smooth muscle cells can also become foam cells by up taking LDL

393
Q

What happens when foam cells apoptose?

A

The LDL accumulates to form a lipid core. The collagen secreted by smooth muscle cells begins to form a fibrous plaque in the intima. Calcium can also be secreted from foam cells to be deposited into the intima and to calcify the fibrous plaque

394
Q

What can an atheroma lead to?

A

Occlusive thrombosis (e.g. myocardial infarction), thromboembolism (e.g. ischaemic stroke), peripheral vascular disease (e.g. critical limb ischaemia) or aneurysm due to wall weakness (e.g. aortic aneurysm)

395
Q

What does an infarction involve?

A

Obstruction of blood flow to an organ or region of tissue, causing local tissue death

396
Q

What is an indicator of cardiac necrosis?

A

Elevated cardiac troponins e.g. cTnT

397
Q

What surgical intervention treatment is there for myocardial infarction?

A

Balloon angioplasty, stenting and coronary bypass

398
Q

What are used in therapeutic thrombolysis for myocardial infarction?

A

tPA and a bacterial activator (streptokinase)

399
Q

When are D-dimers generated?

A

When cross-linked fibrin is degraded.

400
Q

When is FDP generated?

A

Fibrin degradation products are generated if non-cross-linked fibrin or fibrinogen is broken down

401
Q

What are possible complications of MI? (5)

A

Acute pump failure, conduction problems (arrhythmia), valve dysfunction, stroke or chronic pump failure

402
Q

What is vascular tone produced by sympathetic vasoconstrictor nerves inhibited by?

A

Parasympathetic vasodilator nerves, sympathetic vasodilator nerves and sensory (nociceptor C fibre) vasodilator nerves

403
Q

Where in the body do parasympathetic nerves innervate blood vessels?

A

In salivary glands, the pancreas and intestinal mucosa, as well as male genitalia

404
Q

What neurotransmitters are released from parasympathetic nerves that innervate blood vessels?

A

Ach/VIP are released in the salivary glands, while only VIP is released in the pancreas and intestinal mucosa

405
Q

Why do the tissues with blood vessels innervated by parasympathetic nerves need high blood flow?

A

To maintain parasympathetic-mediated fluid secretion

406
Q

What do Ach and VIP released from parasympathetic nerves innervating blood vessels do?

A

They act on endothelium to cause release of NO and stimulation of vasodilation to increase blood flow to produce more saliva or digestive enzymes

407
Q

Describe how the parasympathetic innervation to the blood vessels in the male genitalia work

A

They release NO, causing production of cGMP, which leads to vasodilation.

408
Q

How does Sildenafil (viagra) work?

A

Sildenafil enhances the effects of NO by blocking the breakdown of cGMP by phosphodiesterase 5

409
Q

How do sympathetic vasodilator nerves in the skin work?

A

Sudomotor fibres release Ach/VIP for vasodilation associated with sympathetic-mediated sweating.

410
Q

How do sensory vasodilator fibres work?

A

When trauma stimulates nociceptor C fibres, impulses fire towards dorsal root ganglia in the spinal cord to eventually be perceived as pain. Axon collaterals are also stimulated. Either the impulse down the axon collateral will stimulate release of neurotransmitter (Sub P) to cause vasodilation, or to activate mast cells to release their granule content, and histamine will cause vasodilation. The skin ‘flares up’

411
Q

What is shear stress?

A

The tangential force of the flowing blood on the endothelial surface of the blood vessel

412
Q

What does high shear stress promote?

A

High shear stress, as found in laminar flow, promotes endothelial cell survival and quiescence, alignment in the direction of flow, and secretion of substances that promote vasodilation and anticoagulation

413
Q

What detects shear stress and what effect occurs on detection?

A

Shear stress can be detected by receptors on the endothelial surface, and this causes production of nitric oxide because it stimulates endothelium nitric oxide synthase (eNOS). eNOS causes production of nitric oxide via an amino acid called arginine

414
Q

Describe nitric oxide

A

Nitric oxide, made in large concentrations in the endothelial cells, is a very lipophilic, soluble gas which is freely diffusible and stimulates guanylate cyclase (GC) in vascular smooth muscle cells.

415
Q

What does GC do?

A

GC activates cGMP, which activates PKG

416
Q

What controls vascular tone?

A

Tonic sympathetic activity (constriction) and tonic NO release (dilation) in combination. Vascular tone is a balance between the two

417
Q

Where does NO get released in the circulatory system?

A

NO release occurs almost throughout the circulatory system

418
Q

What effect does shear stress have in the kidney?

A

It causes the production of prostacyclin, as specific membrane lipid are converted into prostacyclin by cyclooxygenase (COX). PGI2 is released, which acts on prostanoid receptors on VSMCs, activating the A pathway and causing vasodilation. This is needed to maintain blood flow in renal arterioles and maintain GFR

419
Q

Why shouldn’t you give someone with renal failure COX inhibitors or NSAIDs?

A

Because this process involving prostacyclin is very important to kidneys to keep blood flowing to via renal arteries. A drug that blocks COX decreases PGI2 production, the A pathway and vasodilation, so a drop in renal blood flow can be dangerous

420
Q

Via what 3 things do the G pathway and the A pathway cause vasodilation?

A

1) They increase Ca2+ ATPase activity, increasing uptake of Ca2+ into the SR stores and exclusion of Ca2+ from the cell, keeping Ca2+ concentration low to produce less contraction
2) They increase K+ channel activity, so K+ channels open and K+ moves out of the cell, causing hyperpolarisation and switching off VGCCs. This means less Ca2+ uptake
3) They decrease myosin light-chain kinase activity

421
Q

How does activation of K+ channels lead to vasodilation?

A

Activation of K+ channels in the endothelium means the release of K+ and rise in local external K+ levels. The potassium activates process on the VSMCs to switch on K+ channels and increase Na2+/K+ ATPase activity. These both lead to hyper polarisation of VSMCs, decrease in VGCC activity and Ca2+ entry, therefore contributing to vasodilation

422
Q

Where is the hyper polarisation from K+ channel activation conducted?

A

The hyper polarisation can be conducted from the endothelium to VSMCs via a gap junction (low resistance pathway). This then decreases VGCC activity and Ca2+ entry, causing vasodilation

423
Q

Stimulation of what receptors on VSMCs produces vasodilation in coronary and skeletal muscle arterioles?

A

ß2-adrenoreceptors

424
Q

What does ß2-receptor stimulation increase?

A

PKA activity

425
Q

What 3 changes occur when PKA activity increases?

A

1) Increase in Ca2+ ATPase activity, lowering Ca2+ concentration inside the VSMC
2) Increase in K+ channel activity, leading to hyper polarisation and consequential decrease in VGCC
3) Decreased MLCK activity

426
Q

Besides vascular tone, what are the functions of endothelium?

A 
Production of Ang II
Blood clotting
Inflammatory pathways
Angiogenesis
Atheroma
427
Q

How does endothelium dysfunction affect vascular tone?

A

The effect is profound. NO and PGI2 production is reduced, so vasoconstriction is enhanced. This is why ED is linked to many CVDs

428
Q

What is the defining level to indicate hypotension?

A

Systolic blood pressure below 60 mmHg

429
Q

What’s Darcy’s law?

A

Blood flow= blood pressure ÷ TPR

430
Q

What does vascular tone mean?

A

It describes the degree of constriction of a blood vessel relative to the maximum dilation.

431
Q

What controls vascular tone?

A

Regulation of vascular smooth muscle cells and endothelium

432
Q

How does sepsis lead to no drive for end organ perfusion?

A

Systemic infection causes excessive vasodilation, which decreases TPR and BP

433
Q

Why does anaphylaxis lead to poor end organ perfusion?

A

The hypersensitivity reaction involves systemic vasodilation

434
Q

How does heart failure cause poor end organ perfusion?

A

Poor cardiac output means blood pressure’s low, which means poor end organ perfusion

435
Q

Why do adrenaline have different responses on resistance vessels?

A

Adrenaline has a higher affinity for ß-adrenoreceptors over alpha-adrenoreceptors, while noradrenaline has a higher affinity for alpha-adrenoreceptors. Alpha1-receptors produce contraction, so noradrenaline acts at a1-receptors to cause vasoconstriction. ß2-receptors produce relaxation, so adrenaline causes vasodilation

436
Q

As a general principle, when would you give noradrenaline?

A

To increase blood pressure whilst protecting the heart

437
Q

Asa. general principle, when would you give adrenaline?

A

To increase heart activity and cause a small increase in blood pressure due to vasodilation

438
Q

Why’s noradrenaline given and how does it work?

A

Noradrenaline is given to primarily act at a1-adrenoreceptors on VSMCs to increase TPR and increase blood pressure without having significant effects on the heart (ß1), so it’s cardiac protective- doesn’t make the heart work hard to increase BP and blood flow

439
Q

Why is the cardiac protective nature of NORAD important?

A

It means NORAD can be given to patients with sepsis and severe heart failure

440
Q

Why is adrenaline given and how des it work? Give an example of its use

A

Adrenaline is given in high concentrations to have an action on both ß1-receptors on the heart and alpha1-receptors on VSMCs to raise BP. An example of a use of adrenaline is in an epipen for anaphylaxis

441
Q

What is raised blood pressure a cause of, which reduces important tonic vasodilation processes and causes poor end organ perfusion?

A

Endothelium dysfunction

442
Q

What does hypertension increase? What effect does this increase have?

A

Afterload

Cardiac output becomes poor and the heart must work much harder

443
Q

What do angiotensin II receptor (AT1) antagonists (ARBs) do?

A

They block AT1 receptors to reduce vasoconstriction in heart failure or hypertension

444
Q

Name an ARB

A

Losartan

445
Q

What do angiotensin converting enzyme inhibitors (ACEi’s) do?

A

They reduce Ang II levels for treatment of heart failure and hypertension

446
Q

Name an ACEi

A

Enalapril

447
Q

What do alpha1-adrenoreceptor antagonists do?

A

They are competitive receptor antagonists for treatment of drug-resistant hypertension

448
Q

Name an alpha1-adrenoreceptor antagonist

A

Prazosin

449
Q

What do ETA receptor antagonists do?

A

They block ETA receptors which are unregulated in pulmonary artery hypertension

450
Q

Name an ETA receptor antagonist

A

Bosetan

451
Q

What do vascular selective CCBs do? Name the vascular selective subtype

A

Dihydropyridine subtypes are vascular selective and block influx of Ca2+ to reduce vasoconstriction for hypertension and angina

452
Q

Name a dihydropyridine CCB

A

Amlodipine

453
Q

What do K+ channel openers do?

A

They open K+ channels to cause hyper polarisation, so there’s less VGCC activation and Ca2+ influx, leading to vasodilation to treat angina

454
Q

Name a K+ channel opener

A

Nicorandil

455
Q

How do nitrates work?

A

They are NO donors, causing PKG-mediated vasorelaxation for treatment of angina and pulmonary oedema

456
Q

Name a nitrate

A

GTN spray (glyceryl trinitrate)

457
Q

How doe PDE5 inhibitors work?

A

They decrease cGMP breakdown, allowing PKG-mediated vasodilation to treat erectile dysfunction

458
Q

Name a PDE5 inhibitor

A

Sildenafil (viagra)

459
Q

Why is a D-dimer test done?

A

D-dimer is an indicator of clot formation because it’s a degradation product of cross-linked fibrin

460
Q

Can D-dimer tests be used to ‘rule-out’ DVT?

A

Only in combination with clinical evaluation

461
Q

What is rivaroxaban?

A

A direct FXa inhibitor- an anticoagulant (blood thinner) which reduces the likelihood of blood clots

462
Q

What are primary and secondary prevention of disease?

A

Primary prevention lowers the risk of the disease occurring. Secondary prevention lowers the risk of disease recurring

463
Q

Name the modifiable risk factors for CVD

A 
Smoking
Abnormal lipid profile
Hypertension
Diabetes mellitus
Abdominal obesity
Psychosocial factors like stress
464
Q

What are protective factors for CVD

A

Regular fruit and vegetables in the diet
Exercise
Moderated alcohol consumption

465
Q

What are the non-modifiable risks for CVD?

A

Age
Family history
Ethnicity

466
Q

What’s the individiual response to primary prevention?

A

A clinician tailors care to an individual patient’s needs and risk factors

467
Q

Give an example of a secondary prevention measure for CVD

A

Prescribing statins after a CHD event

468
Q

How much does CVD cost UK healthcare and the UK economy per year?

A

£9 billion for the NHS and @19 billion for the economy

469
Q

What is cardiovascular disease an umbrella term for?

A

CHD, venous thromboembolism, cerebrovascular disease, peripheral arterial disease, rheumatic and congenital heart disease and lymphatic disease

470
Q

How does risk of stroke change after the age of 55?

A

Risk of stroke doubles every decade after the age of 55

471
Q

How is risk of CVD increase if a direct blood relative had a stroke?

A

Risk is increased if a male relative had a stroke before 55 or if a female relative had a stroke before 65

472
Q

How does ethnicity affect risk of CVD?

A

People from Pakistan, Bangladesh, India and Afro-Caribbean countries are more prone to CVD

473
Q

What are 2 special requirements of cutaneous circulation?

A

It must defend the body against the environment.

It’s important to regulation of body temperature

474
Q

How is cutaneous circulation important to temperature regulation?

A

Blood flow delivers heat from the body’s core, and temperature is regulated via radiation, conduction, convection and sweating

475
Q

What temperatures can skin be at for short periods of time without getting damaged?

A

0° to 40°

476
Q

What does skin temperature depend on?

A

Skin blood flow and ambient temperature

477
Q

What’s a special structural feature of cutaneous circulation?

A

Artery-venous anastomoses- direct connections of arterioles to venules that expose blood to regions of high surface area

478
Q

What are arterioles controlled by?

A

Sympathetic vasoconstrictor and sudomotor vasodilator fibres driven by temperature regulation nerves in the hypothalamus

479
Q

What do Sudomotor fibres do as well as vasodilation?

A

They induce sweating to Coll the body down

480
Q

Name 3 special functional features of cutaneous circulation

A

The skin is responsive to ambient and core temperatures
Severe cold causes ‘paradoxical cold vasodilation’ to prevent skin damage.
Core temperature will change the responses of hypothalamic neurones which control sympathetic activity

481
Q

How does increase in ambient temperature trigger response from cutaneous circulation?

A

The higher ambient temperature triggers vasodilation and ventilation, which help heat loss

482
Q

How does decrease in ambient temperature trigger response from cutaneous circulation?

A

The lower ambient temperature causes vasoconstriction and venoconstriction, which helps to conserve heat. Cold-induced vasoconstriction is caused by an abundance of a2-adrenoreceptors on VSMCs in the skin and decrease in the A pathway. a2-receptors bind NA at lower temperatures than a1-receptors

483
Q

What causes paradoxical cold vasodilation?

A

Paralysis of the sympathetic transmission

484
Q

How does detection of increase in core temperature lead to decrease in body temperature?

A

Increase in core temperature stimulates warmth receptors in the anterior hypothalamus, causing sweating (increased sympathetic activity to sweat glands) and vasodilation (increased sympathetic Sudomotor activity to arterioles in extremities)

485
Q

How does baroreflex/RAAS/ADH-stimulated vasoconstriction of skin blood vessels work?

A

Following decreased BP due to haemorrhage, sepsis or acute cardiac failure, blood is directed to more important organs/tissues. Sympathetic vasoconstrictor fibres are stimulated and more adrenaline is secreted from adrenal glands, increasing sympathetic activity. This leads to more Ang II production and vasopressin secretion. All these factors combine to cause vasoconstriction

486
Q

What will the skin of the patient going through response to haemorrhage be like?

A

Pale and cold

487
Q

Why can it be dangerous for the body to warm up too quickly during haemorrhage?

A

If the body warms up too quickly, cutaneous vasoconstriction will be reduced and blood will flow to the skin and not so much to vital organs/ tissues

488
Q

What’s another specialisation of cutaneous circulation?

A

Blushing shows emotion. It involves sympathetic Sudomotor fibres

489
Q

What’s the Lewis triple response to skin injury?

A

Local redness at the site of trauma
Local swelling- inflammatory oedema
Spreading flare- vasodilation spreading out from the site of trauma

490
Q

What’s the point of the vasodilation involved in the Lewis triple response?

A

Vasodilation increases delivery of immune cells and antibodies to the site of damage to deal with invading pathogens

491
Q

How does the C fibre axon reflex mediate the flare in response to trauma?

A

Trauma stimulates nociceptive C fibres, which causes pain sensation, but also sends impulses down axon collaterals, which causes 2 effects. Firstly, substance P is released, and secondly, mast cells degranulate to release histamine. These 2 substances cause vasodilation. They also increase the permeability of capillaries, so there’s more filtration and therefore local swelling

492
Q

What are 3 special problems of cutaneous circulation?

A

Prolonged obstruction of flow by compression
Postural hypertension/ oedema due to gravity
Raynaud’s disease

493
Q

What can prolonged obstruction of flow by compression lead to?

A

Severe tissue necrosis

494
Q

Where are the common places for bed sores?

A

Heels, buttocks and weight-bearing areas

495
Q

How can bed sores be avoided?

A

Shifting position or turning, causing reactive hyperaemia on removal of compression. The skin has high tolerance to ischaemia

496
Q

How does postural hypertension and oedema due to gravity come about?

A

Standing up for long periods in hot weather will decrease CVP (hypotension) and increase capillary permeability, leading to oedema in the fingers or ankles. Symptoms are faintness and tightening of rings on fingers

497
Q

What’s Raynaud’s disease?

A

Sustained vasoconstriction when your hands get really cold, so there’s no paradoxical vasodilation. This leads to localised tissue ischaemia and numbness

498
Q

What are 2 special requirements of pulmonary circulation?

A

Gaseous exchange

Area for metabolic function

499
Q

How’s the pulmonary circulation adapted for gaseous exchange?

A

The lungs receive the entire cardiac output from the right ventricle. A low-pressure system is needed to get all the blood through.

500
Q

Why is the pulmonary circulation an excellent system to produce or remove substances?

A

Because the lungs receive the entire CO from the RV

501
Q

What are the 2 special structural features of pulmonary circulation?

A

Very high capillary density

Very short diffusion distance between capillaries and alveoli

502
Q

What’s the importance of the very short diffusion distance between capillaries and alveoli?

A

The very short diffusion distance allows for rapid diffusion

503
Q

What do the structural features together provide?

A

Huge oxygen diffusion capacity

504
Q

What are the 3 special functional features of pulmonary circulation?

A

Low vascular resistance
Hypoxia pulmonary vasoconstriction
Metabolic functions

505
Q

How does hypoxia pulmonary vasoconstriction work?

A

In systemic circulation, a drop in O2 levels leads to vasodilation, termed metabolic hyperaemia. Hypoxia that’s not in pulmonary circulation causes vasoconstriction. Vasoconstriction prevents blood flow to poorly ventilated regions of the lungs, optimising ventilation:perfusion ratio. Hypoxia does this by increasing excitability and contractility of vascular smooth muscle

506
Q

Why do pulmonary vessels contain ACE?

A

To produce Ang II and remove bradykinin/5-HT/NA

507
Q

What are the 3 special problems with pulmonary circulation?

A

Gravity
Chronic HPV
Pulmonary oedema

508
Q

What problem does gravity pose to pulmonary circulation?

A

In an upright position, the pulmonary arterial pressures at the apex of the lung are low due to gravity. Mean pulmonary artery (MPA) pressure is 15mmHg, while pressure in the apex is 3mmHg and in the base it’s 21mmHg. Poor perfusion at the apex leads to vessel collapse. Therefore, a standing person has slightly impaired blood oxygenation

509
Q

What happens when you’re at high altitude for long periods of time, or you have COPD?

A

You’re hypoxic, leading to vasoconstriction, pulmonary hypertension and right ventricular failure

510
Q

Why is pulmonary oedema a problem?

A

Thinness of capillary-alveoli interactions means there’s potential for stress and leakage due to breakdown those junctions, e.g. in mitral valve stenosis. Increased pressure in the left atrium leads to increased pulmonary capillary pressures, increased filtration and oedema.

511
Q

What are 2 special requirements of skeletal muscle circulation?

A

Exercise

Controlling arterial pressure

512
Q

Why can vasodilation and vasoconstriction of skeletal muscle circulation have profound effects on blood pressure?

A

Skeletal muscle makes up 40% of body mass, so vascular resistance is a major contributor to TPR

513
Q

What’s the special structural feature of skeletal muscle circulation?

A

Capillary density differs in different muscles

514
Q

How does capillary density between muscles?

A

Postural muscles such as soles are always active, so they have a higher capillary density than phasic muscles such as forearm muscles or gastrocnemius. Endurance training increases capillary growth at a rate proportional to numbers of mitochondria per fibre

515
Q

What are 4 special functional features of skeletal muscle circulation?

A

High vascular tone
Metabolic vasodilation
High expression of ß2-adrenoreceptors on VSM
O2 extraction

516
Q

Why is vascular tone of skeletal muscle circulation high?

A

This reduces blood flow at rest, enabling significant vasodilation to occur during exercise to increase blood flow. Also, it reduces blood flow to capillaries at rest, switching them off. During vasodilation, capillary recruitment further increases blood flow and increases surface area for gaseous exchange

517
Q

How does metabolic vasodilation relate exercise intensity to increased blood flow?

A

Metabolic products- K+, adenosine, PO4 3-, and H2O2- produce vasodilation

518
Q

What’s the importance of having lots of ß2-adrenoeceptors on VSM?

A

Stimulation of ß2-adrenoreceptors by adrenaline leads to vasodilation, increasing blood flow to the skeletal muscle that we’re using for exercise. Importantly, this has a huge effect on TPR. TPR is reduced so we don’t produce high blood pressure during exercise, which would impede function of the heart

519
Q

How does O2 extraction change during exercise?

A

O2 extraction is increased from 25-30% to 80-90% during high intensity exercise due to increased blood flow, increased area for exchange (capillary recruitment), reduced distance for exchange and muscle cells using lots more O2

520
Q

What are 3 special problems with skeletal muscle circulation?

A

Mechanical interference
Increased capillary pressure during exercise
Leg arteries are a major area for atheroma

521
Q

What is the problem of mechanical interference for skeletal muscle circulation?

A

When muscles contract, blood flow in intra-muscular vessels is reduced. This is OK when you’re doing rhythmic exercise, however, in sustained contraction (carrying something), the reduced blood flow means poor O2 supply, anaerobic respiration, build-up of lactic acid and muscle fatigue. The body tries to force blood through the contracted muscle by increasing blood pressure

522
Q

What’s the problem with increased capillary pressure during exercise?

A

Increased capillary pressure leads to increased filtration of plasma into muscles and oedema. Plasma volume is reduced by around 10% during exercise

523
Q

What causes heart failure?

A

The inability of the heart to supply sufficient blood flow to meet the body’s needs

524
Q

What’s class I of the NYHA functional classification of heart failure?

A

No limitations. Ordinary physical activity does not cause fatigue, breathlessness or palpitation.

525
Q

What’s class II heart failure?

A

Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in mild fatigue, palpitation, breathlessness or angina pectoris

526
Q

What’s class III heart failure?

A

Marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary physical activity will lead to symptoms

527
Q

What is class IV heart failure?

A

Inability to carry on any physical activity without discomfort. Symptoms of congestive cardiac failure are present, even at rest. With any physical activity increased discomfort is experienced

528
Q

What’s the prevalence of heart failure and how does this change in those above 65 years of age?

A

Prevalence is about 1-2%, although it rises to 6-10% in people over 65

529
Q

What are 5 compensatory mechanisms for heart failure?

A 
Ventricular dilation
Inccreased myocardial contractility
Myocardial hypertrophy
Sympathetic stimulation
Renin-angiotensin-aldosterone system
530
Q

What’s the Frank-Starling law and how is it affected in heart failure?

A

Increased ventricular filling of the ventricle results in increased force of contraction. In heart failure, this mechanism fails, as the ventricle is over-stretched, reducing ability to cross-link actin and myosin filaments

531
Q

What deleterious effect does continuous sympathetic activation give?

A

The continuous sympathetic activation leads to ß-adrenergic down regulation and desensitisation, so there’s less inotropic response

532
Q

What negative results can increased heart rate have as a compensatory mechanism to heart failure?

A

Increased heart rate leads to increased metabolic demands and myocardial cell death

533
Q

What’s the deleterious effect of increased preload in heart failure?

A

Increased preload beyond the limits of Starling’s law means pressure is transmitted to pulmonary vasculature, leading to pulmonary oedema

534
Q

What deleterious effect does increased TPR have as a compensatory mechanism during heart failure?

A

Increased TPR means higher afterload leading to decreased stroke volume and carried output

535
Q

What’s bad about continuous neurohumoral activation as a compensatory mechanism for heart failure?

A

Chronically elevated angiotensin-II and aldosterone triggers production of cytokines, which stimulate macrophages and stimulate fibroblasts, resulting in myocardial remodelling, which leads to loss of contractility

536
Q

What’s the points of ventricular dilation in heart failure?

A

The ventricle dilates to maintain SV.

537
Q

What happens when ventricular dilation becomes exhausted?

A

When this compensatory mechanism is exhausted, the pressure in the stretched ventricle steadily increases, resulting in restriction to filling and increased venous pressures

538
Q

What do beta blockers do?

A

They decrease blood pressure (after load) decrease heart rate and decrease contractility

539
Q

What detects decrease in perfusion pressure?

A

Baroreceptors in the carotid sinus and aortic arch

540
Q

What does central and peripheral chemoreflex activation induce?

A

Adrenaline, noradrenaline and vasopressin release. This results in increased heart rate and contractility plus peripheral vasoconstriction

541
Q

What effect do ACEi’s and ARBs have on the heart?

A

They lead to decreased SVR (after load) and decrease in venous pressure (preload) by decreased Na+ and H2O retention.Myocyte damage occurs via myocyte fibrosis and eccentric ventricular hypertrophy

542
Q

What are 3 clinical signs of heart failure?

A 
Peripheral oedema (right heart failure)
Pulmonary oedema (left heart failure)
Congestive cardiac failure (left and secondary right ventricular failure)
543
Q

What are 5 mechanical causes of pump failure?

A 
Impaired ventricular function`
Pressure overload of the ventricle
Inflow obstruction of the ventricle
Valvular disease
Volume overload of the ventricle
544
Q

What conditions cause impaired ventricular function?

A

Myocardial infarction or cardiomyopathy

545
Q

What conditions cause pressure overload of the ventricle?

A

Systemic or pulmonary hypertension

546
Q

What conditions cause inflow obstruction to the ventricle?

A

Restrictive cardiomyopathy, diastolic heart failure or mitral stenosis

547
Q

What conditions cause valvular disease?

A

Aortic, mitral or tricuspid stenosis/ regurgitation

548
Q

What conditions cause volume overload of the ventricle?

A

Ventricular and atrial septal defects

549
Q

What are clinical signs of right ventricular failure?

A

Increased JVP, oedema and right>left pleural effusion

550
Q

What is the clinical sign for left ventricular failure?

A

Pulmonary oedema

551
Q

What are the symptoms of pulmonary oedema from left ventricular failure?

A

Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
Renal dysfunction from low perfusion pressure and high venous pressure
Iron deficiency
Gout
Cardiac cachexia and skeletal muscle wasting

552
Q

What’s the most common cause of left ventricular failure?

A

CAD

553
Q

What’s a biomarker of heart failure?

A

NTproBNP

554
Q

What’s the pitfall with NTproBNP tests?

A

They aren’t specific and NTproBNP is often mildly raised in other conditions like atrial fibrillation and hypertension. If elevated and heart failure is suspected, an echo must be requested

555
Q

What are the treatment options for heart failure?

A 
Biventricular pacing
Cardiac resynchronisation therapy
Heart transplant
Left ventricular assist devices
Palliative care
556
Q

What’s the requirement of coronary circulation?

A

It needs a high basal supply of O2 (20x that of resting skeletal muscle)

557
Q

What’s the importance of high capillary density in cardiac muscle?

A

It provides a large surface area for O2 transfer and reduces diffusion distance to the myocytes and so O2 transport is much faster

558
Q

What allows/ causes a lot of resting vasodilation in coronary vessels?

A

High blood flow is facilitated by sparse sympathetic-mediated vasoconstriction and high NO release

559
Q

What makes further increase in coronary blood flow during increased demand possible?

A

Metabolic hyperaemia and the abundance of ß2-adrenoreceptors to which adrenaline can bind

560
Q

What level is O2 extraction at in cardiac muscle during normal activity?

A

75%

561
Q

How can O2 demands be met during increased demand?

A

Blood flow must be increased. Myocardium metabolism generates metabolites to produce vasodilation and increase blood flow- metabolic hyperaemia

562
Q

When does coronary blood flow occur?

A

During diastole

563
Q

Why does decreased perfusion produce major problems in coronary arteries?

A

Coronary arteries are functional end-arteries

564
Q

What can cause sudden obstruction of coronary blood flow?

A

Acute thrombosis or acute coronary syndrome (ACS)

565
Q

What can cause slow obstruction of coronary blood flow?

A

Atheroma causing narrowing of lumens, which produces angina

566
Q

What 3 mechanical factors reduce coronary flow during diastole?

A

Shortening diastole e.g. high heart rate
Increased ventricular end-diastolic pressure e.g. volume-overload heart failure
Reduced diastolic arterial pressure e.g. hypotension/aortic regurgitation

567
Q

Why can’t coronary blood flow be diverted to ischaemic areas?

A

There are low numbers of cross-branching collateral vessels (artery-arterial anastomoses)

568
Q

What does total occlusion of the left anterior descending artery lead to?

A

A large ischaemic area and myocardial infarction. Ischaemic tissue causes acidosis and pain due to stimulation of C-fibres, impaired contractility, sympathetic activation, arrhythmias and necrosis

569
Q

What is angina pectoris?

A

Strangulation of the chest- A painful, crushing sensation in the chest which radiates to the neck, arms and jaw and is associated with shortness of breath and dizziness.

570
Q

What are the 3 forms of angina?

A

Stable, variant and unstable

571
Q

What causes angina?

A

Ischaemia from O2 and nutrient demands of cardiac tissue not being met, due to partial occlusion of coronary arteries

572
Q

What might be the reason for the increased demand?

A

Increased heart rate, increased left ventricular contractility or increased wall stress

573
Q

What triggers increase in demand for O2 or nutrients?

A

Exercise, hypertension and left ventricular dilation

574
Q

How does resistance in healthy coronary arteries work at rest and during exercise?

A

In healthy individuals, resistance in series adds together in coronary arteries. In exercise, metabolic vasodilation of arterioles reduces total resistance. Blood flow is increased to meet increased O2 demands

575
Q

What happens to resistance in coronary arteries of someone with stable angina?

A

Individuals with stenosis in large coronary arteries have increased resistance. Metabolic hyperaemia occurs at rest, so blood flow meets needs. However, during exercise, arterioles further dilate to reduce resistance, but total resistance is still too high due to the dominance of stenosis. O2 demands cannot be met, so angina develops

576
Q

How can stable angina be treated?

A

It can be relieved with GTN spray or other nitrates

577
Q

How does stable angina affect an ECG?

A

Stable angina causes ST depression due to the ischaemia

578
Q

What’s variant angina and what causes it?

A

Variant angina is uncommon and caused by vasospasm, which can occur at rest and is often not linked to coronary artery occlusion. Excessive responses to vasoconstrictors leads to endothelium dysfunction (less NO produced)

579
Q

What 3 drugs can be used for management of angina?

A

ß-blockers, CCBs and nitrates

580
Q

What can minimise risk of angina?

A

Lifestyle changes, aspirin and statins

581
Q

What is acute coronary syndrome?

A

A spectrum of potentially life-threatening conditions which are classed as medical emergencies

582
Q

Can acute coronary syndrome be relieved by GTN spray?

A

No

583
Q

What is done to investigate ACS?

A

An ECG and troponin T and I measurements

584
Q

What causes a depressed ST segment and a STEMI in terms of ischaemia and depolarisation?

A

In healthy tissue, the ventricles are uniformly depolarised, so no current is detected on the ECG during the ST segment, and the line is isoelectric. In partial/less severe occlusions of coronary arteries, a small area of ischaemia which does not depolarise leads to injury current and depression of the ST segment on an ECG. In total/severe occlusion of a coronary artery, there’s full wall thickness ischaemia which does not depolarise leading to injury current and elevation of the ST segment

585
Q

What are the pharmacological therapies for ACS?

A

Morphine for pain, anti-platelets such as aspirin and clopidogrel, anti-thrombin such as heparins and NOACs, and log-term therapy from ß-blockers, CCBs and ACEi’s

586
Q

What treatment may be appropriate for an individual at moderate-high risk, with persistent symptoms and occlusions showing on angiography?

A

A coronary artery bypass graft (CABG) is given if 3 or more main coronary arteries are diseased, or the main left coronary artery is occluded and the occlusion position isn’t appropriate for PCI. If 1 or 2 arteries are diseased, the patient can have percutaneous coronary intervention

587
Q

Compare PCIs and CABGs

A

PCIs involve a less invasive procedure, but restenosis can occur. Restenosis can occur with CABG too, but it’s less common with the mammary artery

588
Q

Describe the process of a PCI

A

A balloon catheter is inflated in the area of the blockage to increase luminal diameter.

589
Q

What vein is used to bypass the part of the functional end artery that’s been occluded in a CABG?

A

The saphenous vein

590
Q

How is a STEMI investigated?

A

ECG and troponins T and I measured

591
Q

What are the pharmacological therapies for STEMI?

A

Morphine, aspirin, heparins, streptokinase, tissue plasminogen activators

592
Q

What do thrombolytics do?

A

They cause fibrinolysis to breakdown the fibrin clot and increase the reperfusion zone

593
Q

What’s the preferred treatment of a STEMI?

A

Revascularisation within 2 hours of onset.

594
Q

What are the life-threatening complications that can occur with revascularisation?

A

Cardiac failure from intraaortic balloon artificially increasing BP, rupture of the ventricular septum (leading to blood leakage between the ventricles), and arrhythmia

595
Q

What’s a pressor response?

A

An excitatory input from stimulation of arterial chemoreceptors or muscle metaboreceptors, which switches on reflexes to increase CO/BP/TPR

596
Q

What is a depressor response?

A

An inhibitory input from stimulation of arterial baroreceptors, switching off reflexes, to decrease CO/TPR/BP

597
Q

What do baroreceptors measure?

A

Blood pressure, but also blood flow indirectly

598
Q

Where are baroreceptors found?

A

The walls of the carotid sinus and the aortic arch

599
Q

At what point do action potentials fire most from baroreceptors?

A

Directly as the pressure changes, action potential fire the most, before they drop to an adapted frequency. With decrease in pressure, there’s an initial period without action potentials, before a slower, adapted frequency of Ads firing picks up

600
Q

What happens in the face of continued high or low pressure?

A

The threshold for baroreceptor activation changes

601
Q

What happens to the baroreceptors in someone with hypertension?

A

They are less activated because the threshold becomes much greater, so blood pressure isn’t as well regulated

602
Q

What happens when baroreceptors are loaded?

A

A depressor reflex reduces blood pressure. The vagus nerve is stimulated, increasing parasympathetic response. Heart rate is slowed and vasodilation decreases TPR and therefore blood pressure

603
Q

What happens when baroreceptors are unloaded ?

A

A pressor reflex maintains blood pressure/blood flow to vital organs. Increased sympathetic activity and decreased vagus activity leads to increased heart rate and force of contraction, so CO is increased. Arteriolar constriction means greater TPR. Venous constriction increases CVP, SV and CO via Starling’s law

604
Q

How does Ang II secretion lead to increase in blood volume?

A

Ang II stimulates aldosterone secretion, so there’s Na+/H2O reabsorption in the kidneys, which leads to more water reabsorption into the blood

605
Q

Where are veno-arterial mechanoreceptors found?

A

In the great veins entering the right atrium and in the walls of the right atrium

606
Q

What happens when veno-atrial mechanoreceptors are stimulated?

A

Signals are sent to the brain about central venous rpessure and filling of the heart in diastole

607
Q

What do ventricular mechanoreceptors tell the brain?

A

Whether the heart is over-distended or not

608
Q

What fibres tell the brain about referred pain?

A

Sympathetic afferents (nociceptors)

609
Q

Describe nociceptive sympathetic afferents and the basis of referred pain

A

These are chemo-sensitive ventricular afferent fibres that are stimulated by K+, H+ (lactate) and bradykinin (during ischaemia). The fibres converge onto the same neruones in the spinal cord as somatic afferents, which is the basis of referred pain

610
Q

Describe veno-atrial mechanoreceptors

A

These receptors are stimulated by an increase in cardiac filling/ CVP. The initial pressor reflex increases sympathetic response and causes tachycardia.

611
Q

What is the Bainbridge effect?

A

Reflex tachycardia due to rapid infusion of volume into the venous system (vena-atrial stretch receptors and pacemaker distension)

612
Q

What happens in longer-term depressor reflex?

A

Increased diuresis and decreased blood volume. This happens in a feedback loop in response to changes in ADH, ANP and RAAS

613
Q

What do ventricular mechaonreceptors do?

A

They sense over-distension of ventricles and this triggers a depressor reflex

614
Q

Where are arterial chemoreceptors found?

A

In the carotid boy and aortic bodies (similar areas to baroreceptors)

615
Q

What stimulates arterial chemoreceptors?

A

Low O2, high CO2, H+ and K+

616
Q

What do arterial chemoreceptors regulate?

A

Ventilation and cardiac reflexes (during asphyxia, shock and haemorrhage)

617
Q

What do muscle metaboreceptors respond to?

A

Increases in metabolites such as ATP, K+, lactate and adenosine

618
Q

Where are muscle metaboreceptors found?

A

In skeletal muscle

619
Q

What response do muscle metaboreceptors trigger?

A

A pressor response. Sympathetic activity is increased, causing tachycardia and increased arterial/venous constriction. This leads to increased cardiac output/BP

620
Q

When are muscle metaboreceptors important?

A

In isometric exercise, where joint angle and muscle length do not change. They aid maintenance of blood perfusion to contracted muscle. These muscles undergo metabolic hyperaemia, allowing blood to flow to the contracted tissue

621
Q

How are sensory receptor signals coordinated in the brain?

A

There are lots of different inputs into the NTS, which then sends inputs either to the nucleus ambiguous or into the caudal and rostral ventrolateral medulla. This is the basis for controlling cardiovascular reflexes

622
Q

What is there between the caudal and rostral ventrolateral medulla?

A

There’s an inhibitory pathway in the thermostat area which is really important for how the baroreceptors and arterial chemoreceptors work

623
Q

Where does stimulatory input to baroreceptors send excitatory information?

A

To the caudal ventrolateral medulla

624
Q

What happens when excitatory information is sent to the caudal ventrolateral medulla?

A

This excites an inhibitory pathway, which inhibits the rostral ventrolateral medulla and switches off sympathetic outflow to the heart and blood vessels to cause a depressor response

625
Q

What happens when there’s stimulatory input to arterial chemoreceptors or muscle work receptors?

A

Inhibitory input is sent to the caudal ventrolateral medulla. This switches on the rostral ventrolateral medulla and sympathetic nerves to generate a pressor response

626
Q

What happens when baroreceptors are stimulated?

A

An excitatory neurone in the nucleus tracts solitarius is stimulated, which switches on the vagus nerve in the nucleus ambiguous and information is sent to the heart via vagal parasympathetic fibres to cause a depressor effect and reduction in heart rate

627
Q

Describe the inhibitory link between respiration and the vagus nerve

A

Every time you breathe in, vagus activity switches off. During a long period of inspiration, heart rate goes up, and vice versa. This is to get more blood flow to transport the added oxygen through the body. This is called sinus tachycardia

628
Q

What happens in syncope with regards to the vagus nerve?

A

The limbic system sends huge amounts of information to the vagus nerve, causing vagal bradycardia. This is a vaso-vagal attack. The bradycardia results in decreased cerebral blood flow and reduced oxygen delivery due to sudden decrease in arterial blood pressure

629
Q

What effect would not having CVS reflexes have?

A

Without CVS reflexes, there’d be less control and blood pressure would be higher. CVS reflexes stabilise blood pressure

630
Q

How does orthostasis affect the CVS?

A

On standing up, the CVS changes accordingly to the effect of gravity. At first, blood pressure falls (postural hypotension), however it quickly recovers due to homeostatic mechanisms. 3 smaller changes are increased heart rate, contractility and TPR

631
Q

What’s Bernoulli’s law?

A

Blood flow= pressure energy + potential energy + kinetic energy

632
Q

Why does gravity induce high blood pressures in the venous system?

A

Pressure is higher towards the bottom of the veins, so they become distended

633
Q

How does orthostasis cause hypotension?

A

Decreased CVP leads to decreased EDP, leading to decreased SV and CO, and so decreased BP

634
Q

What does poor perfusion of the brain lead to?

A

Dizziness and fainting

635
Q

What factors worsen postural hypertension?

A

Drugs that reduce sympathetic activity or block vascular tone, varicose veins (impaired venous return), lack of skeletal muscle activity due to paralysis or forced activity, reduced circulating blood volume, increased core temperature (peripheral vasodilation, less blood volume available)

636
Q

Why is postural hypertension a serious issue in the elderly?

A

It leads to them having falls

637
Q

How does microgravity affect the CVS?

A

Standing and lying down is the same, so there’s less need for ANS, RAAS, ADH and ANP systems to control blood pressure.

638
Q

How is blood redistributed in the chest region in microgravity?

A

Initially, preload/EDP is increased, as is atrial/ ventricular volume. This is sensed by baroreceptors/ cardiac receptors. The sympathetic NS doesn’t need to work because there’s no gravitational pressures on blood flow. Decreased sympathetic NS actions, RAAS system and ADH release are the result of blood pressure being even throughout the body

639
Q

Why is diuresis a symptom of microgravity?

A

More blood is going to the heart because there’s greater stroke volume and cardiac output, so there’s more blood supply to the kidneys and glomerular fltration rate must increase.

640
Q

How does diuresis from microgravity affect the CVS?

A

The diuresis causes reduction in blood volume by 20%. In the long-term, blood volume is decreased; there’s reduced stress on the heart, meaning the heart can suffer hypotrophy; and there’ll be a general drop in BP, as less blood pressure is needed to drive circulation

641
Q

What happens to the CVS on return from microgravity to gravity?

A

Severe postural hypotension will become apparent due to a hypotrophy of cardiac muscle, for which the baroreceptor reflex cannot compensate

642
Q

What happens to the CVS when you exercise?

A

When you exercise, your heart must increase lung O2 uptake and increase O2 transport around the body, particularly to selective tissues e.g. exercising muscle. To prevent excessive afterload on the heart, BP must be controlled in the face of huge CO increase

643
Q

How much does O2 uptake by pulmonary circulation increase during strenuous exercise?

A

13.5x

644
Q

Via what 3 smaller changes does O2 uptake increase by 13.5x?

A

Heart rate can triple, stroke volume can increase by 1.5x, and arteriovenous O2 difference can triple to give a greater concentration gradient in the lungs

645
Q

How is cardiac output increased during exercise?

A

Stroke volume increases to a maximum value, giving a plateau phase on Starling’s curve

646
Q

Describe exercise-induced tachycardia

A

Heart rate increases before exercise begins. On initiation of exercise, muscle mechanoreceptors provide fast feedback to the brain to increase heart rate. Vagal tone decreases and sympathetic activity increases

647
Q

Describe exercise-induced stroke volume increase

A

Increased end-diastolic volume results in increased venous return/CVP through vasoconstriction. Increased contractility due to sympathetic activation of ß1-adrenoreceptors causes faster ejection of blood. End-systolic volume is decreased

648
Q

What does vasodilation of arterioles in active muscle allows?

A

Vasodilation of arterioles in active muscle allows for more oxygen supply to myocardium and the skin during moderate exercise. There’s metabolic vasodilation from increased K+/H+ and there’s ß2-mediated vasodilation via circulating adrenaline

649
Q

Why is blood pressure only mildly affected when CO increases by 4.5x?

A

Because skeletal muscle arterioles vasodilator and so TPR decreases to prevent excessive afterload on the heart

650
Q

What are the 3 types of exercise?

A

Static. dynamic and resistive

651
Q

What’s resistive exercise?

A

Where static and dynamic exercise are combine and there’s a high load, such as in weightlifting

652
Q

Which form of exercise increases blood pressure more?

A

Static exercise increases BP more than dynamic exercise

653
Q

Describe the sensory fibres in skeletal muscle

A

The sensory fibres have a small diameter. They’re chemosensitive- stimulated by K+, H+ and lactate, which increase in concentration in exercising muscle tissue

CVS (2 decks)

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