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MBBS - Year 2 > Cardiology - Coronary Artery Disease > Flashcards

Cardiology - Coronary Artery Disease Flashcards

1
Q

What does the L coronary artery divide into

A

Left Anterior Descending artery (LAD)

Circumflex artery

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2
Q

What does the LAD supply

A

The anterior wall and part of left ventricle as well as most of inter ventricular septum

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3
Q

What does the circumflex artery supply

A

Lateral and posterior walls of L ventricle

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4
Q

What does the R coronary artery supply

A

Right atrium and ventricle

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5
Q

Right dominant circulation

A

PDA arises from RCA

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6
Q

What does the Posterior Descending Artery (PDA) supply

A

Inferior wall of L ventricle and part of inter ventricular septum

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7
Q

What % of people have a right dominant circulation

A

70%

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8
Q

Left dominant circulation

A

PDA arises from Circumflex artery

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9
Q

What % of people have a L dominant circulation

A

10%

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10
Q

Co-dominant circulation

A

PDA arises from both RCA and Circumflex artery

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11
Q

What % of people have a co-dominant circulation

A

20%

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12
Q

Where does coronary blood flow occur

A

In diastole

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13
Q

What kind of arteries are coronary Arteries

A

Functional end - do NOT have effective anastomoses

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14
Q

How does the coronary circulation meet the hearts high oxygen requirements

A

Stuctural and functional adaptations

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15
Q

Structal adaptation of coronary circulation

A

Myocardial capillary density is v high

1 capillary per cardiac and skeletal myocyte but cardiac mycoses are smaller –> higher density –> shorter diffusion distance

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16
Q

Functional adaptations of coronary circulation

A

High basal flow and oxygen extraction
Metabolic hyperaemia
Autoregulation

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17
Q

Increase in basal flow during exercise

A

10x body’s avg

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18
Q

Increased oxygen extraction during exercise

A

75% vs 25%

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19
Q

Metabolic hyperaemia during exercise

A

Coronary arteries dilate in proportion to hum work the heart is doing
Caused by release of metabolites that cause vasodilation

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20
Q

Most important autoregulation response of heart

A

Myogenic response - stretch in vessel –> dilation

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21
Q

Cardiac output (CO)

A

Volume of blood ejected by 1 ventricle in 1 minute

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22
Q

Stroke volume (SV)

A

Volume of blood ejected from ventricles in systole

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23
Q

Eqn for CO

A

CO = SV x HR

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24
Q

Where is the majority of the bloods distribution

A

65% are stored in veins - acts as reservoir, can ‘top up’ heart after haemorrhage

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25
Q

Why does the amount of blood in capacitance vessels vary

A

These vessels are thin walled and are easily distended/ collapsed
Supplied by sympathetic nerves that can cause constriction

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26
Q

Main factors determining SV

A

Energy of contraction of vessels
BP in aorta

These oppose ventricular ejection

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27
Q

What is the energy of contraction of vessels regulated by

A

Ventricular filling pressure
Myocardial contractility

When these increase as does energy of contraction

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28
Q

How does change in aortic pressure affect SV

A

Rise in aortic pressure causes SV to fall

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29
Q

What is preload in the heart

A

Amount of stretch of the ventricular muscle fibres just before they contract at the end of distale

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30
Q

What are good makers of preload

A

End Diastolic Volume

End Diastolic pressure

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31
Q

What is Central Venous Pressure

A

Pressure in the vena cava at the entrance to R atrium

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32
Q

What can CVP be used as an estimate of

A

RV End Diastole Pressure ie. RV preload

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33
Q

How does distending the heart affect SV

A

Increases it

Stretching myocytes during diastole increases energy of contraction during systole

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34
Q

What is the energy of contraction proportional to

A

Muscle fibre length at rest

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35
Q

What is CVP governed by

A

Volume of blood in circulation and by how the blood is distributed between central and peripheral veins

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36
Q

What happens when CVP falls

A

RVEDP (preload) is reduced –> RV output is reduced –> less blood flows to L heart –> LV SV is reduced

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37
Q

Factors influencing CVP

A

Gravity (decreases)
Soleal pump (increases)
Vasoconstriction by sympathetic nerves (increased)
Pumping ability of heart

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38
Q

How does the pumping ability of heart affect CVP

A

Faster –> drop in CV if no compensatory mechanisms

Slower (e.g. in heart failure and MI) –> CVP rises

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39
Q

Frank Starling mechanism (Law of the Heart)

A

The greater the preload
The greater the force of contraction
The greater the SV

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40
Q

Why is Starling’s law important

A

Balancing output of RV and LV
Contributes to increased SV during exercise
Causes fall in CO during haemorrhage and ‘shock’
Causes fall in CO during standing –> postural hypotension
Helps restore CO in response to IV fluid

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41
Q

Contractility definition

A

Force of contraction which is independent of initial fibre length

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42
Q

What can reduced contractility lead to

A

Heart failure

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43
Q

Afterload

A

Resistance heart has to overcome to eject its contents

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44
Q

Afterload and SV

A

Increased afterload leads to reduced in SV

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45
Q

‘Pump function curve’

A

High arterial pressure (e.g. by giving vasoconstrictor drug) impairs output (lowers SV)

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46
Q

What is HR controlled by

A

Sympathetic and parasympathetic nerves which innervate SAN and AVN

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47
Q

How does increase in sympathetic activity affect HR

A

Increase - tachycardia

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48
Q

How does increase in parasympathetic activity affect HR

A

Bradycardia

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49
Q

Demands of CVS during exercise

A

Increase lung oxygen uptake
Increase oxygen transport around body
Direct increased oxygen specifically to exercising muscle
Stabilisation of BP

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50
Q

How is lung oxygen uptake increased during exercise

A

Increase in RV output

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51
Q

How is oxygen transport around body increased during exercise

A

Decreased LV output

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52
Q

How is increased oxygen supply directed specifically to exercising muscle

A

Increase in oxygen extraction from blood

Decrease in vascular resistance in exercising metabolism

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53
Q

How is BP stabilised during exercise

A

Vasoconstriction in non-exercising tissues

Baroreflex rest

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54
Q

Baroreflex reset

A

Prevents HR from falling

Baroreceptors have an increased threshold

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55
Q

How does CO increase during exercise

A

Increase in SV

Increase in HR

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56
Q

How is SV increased in exercise

A

Increased preload - skeletal muscle pump, peripheral vasoconstriction
Increased contractility causing faster ejection and a decrease in end-systolic volume

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57
Q

How is HR increased during exercise

A

Increase in cardiac sympathetic activity

Decrease in vagal parasympathetic activity

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58
Q

Maximum HR during exercise

A

220 - age in yrs

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59
Q

Threat of hypotension during exercise

A

BP = CO x SVR

Reduced SVR could cause BP to drop but compensatory vasoconstriction in active tissue attenuates fall

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60
Q

SVR

A

Systemic vascular resistance

Same as TPR

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61
Q

What kind of exercise causes SV to be high at rest

A

Supine

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62
Q

The athletic heart vs non-athletic heart

A

Stronger and hypertrophied
Increased SV
Decreased resting HR
CO can be much higher during exercise

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63
Q

How do heart transplant pts increase CO with exercise

A

Transplanted heart is denervated (no cardiac autonomic nerves)
Circulating catecholamines increase HR and skeletal muscle pump increased preload

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64
Q

What is the cardiac cycle about

A

Heart contraction/ relaxation
Rship between electrical activity and contraction of heart
Changes in volume of blood related to pressure

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65
Q

Essentials for normal cardiac function

A

Intact myocardium and mechanics
Substrate to pump around (blood)
Own fuel supply
Electrical activity

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66
Q

Stages in Systole

A

Atrial contraction
Isovolumic contraction
Rapid ejection
End systole

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67
Q

What is seen in atrial contraction - systole

A

P wave on ECG

1st half from R atrium and 2nd half from L atrium

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68
Q

Isovolumic contraction - systole

A

No change in volume but changes in pressure of blood in atria

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69
Q

Whats seen on ECG during isovolumic contraction - systole

A

Causes QRS complex - depolarisation of ventricles

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70
Q

What’s heard during isovolumic contraction - systole

A

1st heart sound

Mitral valve closes first then tricuspid

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71
Q

Whats seen on ECG during rapid ejection - systole

A

ST segment

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72
Q

End systole - systole

A

Pressure starts to drop

Aortic and pulmonic valves close

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73
Q

What’s seen in ECG during end systole

A

T wave - depolarisation of ventricles

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74
Q

Isovolumic relaxation - diastole

A

Heart is relaxed and the valves are closed

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75
Q

What is heard during isovolumic relaxation - diastole

A

2nd heart sound

Closing of aortic valve then pulmonic

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76
Q

How can the second heart sound be split

A

During expiration - S2 is single
During inspiration can be split into A2 and P2 as inspiration sucks into R heart and R heart takes longer to pump out increased volume

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77
Q

Stages in diastole

A

Isovolumic relaxation
Rapid ventricular filling
Reduced ventricular filling

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78
Q

Rapid ventricular filling - diastole

A

Blood flows passively from ventricles to atria

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79
Q

What may be heard during rapid ventricular filling - diastole

A

3rd heart sound

Could be caused by heart failure - ventricle is too stiff

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80
Q

Clicks during cardiac cycle

A

Ejection click at the end of diastole
Mid systolic click
Opening snap in mitral stenosis at beginning of systole

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81
Q

Ejection systolic murmur

A

Between S1 and S2 - rises and falls

Aortic stenosis, pulmonary stenosis, aortic or pulmonary flow murmurs

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82
Q

Pansystolic murmur

A

Steady murmur between S1 and S2

Mitral regurgitation, tricuspid regurgitation, ventricular septal defect

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83
Q

Late systolic murmur

A

Between mid-systolic click and S2

Mitral valve prolapse

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84
Q

Early diastolic murmur

A

After S2 - falls

Aortic or pulmonary regurgitation

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85
Q

Mild diastolic murmur

A

Starts at opening click and continues to S1

Mitral stenosis, tricuspid stenosis, mitral or tricuspid flow murmurs

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86
Q

How is CO, MAP & SVR related

A

CO = MAP/ SVR

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87
Q

What does AF limit during exercise

A

Expected increase in ventricular SV and CO

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88
Q

Cardiac Resynchronisation Therapy

A

Delivers regular signals to pace L ventricle

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89
Q

When do we see the basement membrane

A

In vessels larger than 1mm

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90
Q

What does the endothelium determine

A

When and where the WBC leave circulation

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91
Q

What does the endothelium secrete

A

Paracrine factors for vessel dilation, constriction and growth of adjacent cells

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92
Q

Vasa vasorum

A

“Vessels of the vessels”

Have arterioles, capillaries and venules that branch profusely in the adventitia and the outer media to provide metabolites

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93
Q

When do we see the vasa vasorum

A

Adventitia and outer media in larger vessels too thick to recieve nutrients via diffusion

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94
Q

Adaptations of larger elastic/ conducting arteries

A

Large lumen
Elastic recoil
Several elastic laminae

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95
Q

Function of large lumen in elastic arteries

A

Allows low-resistance conduction of blood and acts as conduits

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96
Q

Function of elastic recoil in large elastic arteries

A

Absorb impulse of cardiac systole

Maintains blood flow in diastole

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97
Q

Function of elastic laminae in large elastic arteries

A

Making blood flux more uniform

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98
Q

Muscular vs conducting arteries

A

Thicker tunica media
Narrower lumen
Thickened elastic lamina
More smooth muscle and less elastin in tunica media

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99
Q

How many layers of circularly arranged smooth muscle are there in arteries

A

3-8 layers in small arteries

1-2 in arterioles

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100
Q

What are arterioles main control points for

A

Regulation of physiological resistance to blood flow

Pressure and velocity sharply reduced –> steady flow vs pulsatile

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101
Q

What is present in large arterioles but absent in terminal arterioles

A

Thin, fenestrated internal elastic lamina

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102
Q

Types of capillaries

A

Continuous capillaries
Fenestrated capillaries
Discontinuous capillaries

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103
Q

Where are continuous capillaries found

A

Muscle
Lungs
CNS

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104
Q

Where are fenestrated capillaries found

A

Endocrine glands, sites of metabolic and fluid absorption

e.g. gallbladder, kidney, and intestinal tract

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105
Q

Where are discontinuous capillaries (sinusoidal capillaries) found

A

Liver
Spleen
Bone marrow

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106
Q

Continuous capillaries

A

Have tight junctions that completely surround endothelium

Intercellular clefts of un-joined membranes; allows passage of fluids

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107
Q

Fenestrated capillaries features

A

Endothelium with fenestrations

Greater permeability to solutes and fluid than other capillaries

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108
Q

Sinusoidal capillaries

A

Highly modifiable, leaky, fenestrated capillaries with larger lumen
Discontinuous basal lamina
Allows larger molecules (proteins and blood cells) to pass between the blood and surrounding tissues

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109
Q

What do post capillary venues participate in

A

Exchanges between the blood and tissues - 1’ site fo WBC leaving

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110
Q

Characteristic feature of venules

A

Large diameter of lumen compared to overall thickness

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111
Q

Where do valves project from

A

Tunica intima

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112
Q

What hormone does the heart release

A

Atrial naturietic factor

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113
Q

3 tunics of heart

A

Internal - endocardium
Middle - myocardium
External - pericardium

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114
Q

Central fibrous skeleton of heart

A

Base of heart valves
Site of origin and insertion of the cardiac muscles
Electrical insulation between atria & ventricles
Separates atria and ventricles

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115
Q

Subendocardial layer of heart

A

Layer of connective tissue connecting endothelial layer to myocardium
Contains veins, nerves, branches of the Purkinje cells

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116
Q

Thickest heart tunic

A

Myocardium

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117
Q

Subepicardial layer

A

External to myocardium

Loose connective tissue containing veins, nerves and nerve ganglia and adipose tissue that surround the heart

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118
Q

What is the epicardium composed of

A

Superficial mesothelial lining supported by connective tissue

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119
Q

Composition of pericardial sac

A

Fibrous outer skeleton attached to diaphragm
Parietal pericardium
Visceral pericardium

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120
Q

What is found in between the layers of the pericardium

A

Small amount of fluid facilitating the heart movements

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121
Q

Cardiac conduction pathway

A 
SAN 
AVN 
Bundle of His 
L and R bundle branches 
Purkinje fibres
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122
Q

What does coordinated contraction of the cardiac muscle depend on

A

Propagation of electrical impulses

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123
Q

How are electrical impulses in heart propagated

A

Specialised excitatory and conducting myocytes

These also regulate HR and rhythm

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124
Q

Where is the SA node located

A

Junction of R atrium appendage and superior vena cava

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125
Q

Fibrous skeleton nd heart conduction

A

Ensures impulses aren’t spread randomly so all chambers don’t beat at same time

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126
Q

AVN location

A

In R atrium along atrial septum

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127
Q

Why is the AVN described as a gatekeeper

A

Delays transmission of signals from atria to ventricles

Ensures atrial contraction preceded ventricular contraction

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128
Q

Where is the Bundle of His found

A

From R atrium to summit of ventricular septum

Forms Purkinje network

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129
Q

Where does the lymphatic vascular start

A

Lymphatic capillaries

Closed ended tubules that anastomose to form vessels of steadily increasing size

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130
Q

Where does the lymphatic vascular system terminate

A

Terminate in blood vascular system emptying into large veins near the heart

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131
Q

Arteriosclerosis

A

Hardening of arteries - arterial wall thickening and loss of elasticity

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132
Q

Where does arteriosclerosis occur

A

Occurs in small arteries and arterioles and causes downstream ischaemic injury

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133
Q

Monckeberg medial sclerosis

A

Calcific deposits within walls of muscular arteries

May undergo metaplastic change into bone

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134
Q

How can atherosclerosis cause aneurysm formation

A

Mechanical obstruct blood flow and can weaken underlying media

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135
Q

What happens when atherosclerosis is complicated by occlusive thrombosis

A

Causes sudden death
MI
Stroke
a/c ischaemia of legs and abdominal organs

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136
Q

Major targets of atherosclerosis

A

Large elastic arteries (aorta, carotid and iliac arteries)

Medium sized muscular arteries (coronary and popliteal arteries)

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137
Q

Constitutional risk factors of atherosclerosis

A

Increasing age
Male
Genetic abnormalities
Fhx

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138
Q

Modifiable risk factors

A 
Hyperlipidaemia 
HTN 
DM 
Smoking 
Infl (CRP)
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139
Q

Causes of c/c endothelial injury

A 
Hyperlipidaemia 
HTN 
Smoking 
Homocystinuria 
Haemodynamic factors 
Toxins 
Viruses 
Immune reactions
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140
Q

Haemodynamic factors of atherogenesis

A

Laminar flow in straight regions of arterioles but oscillatory flow in regions where arteries divide/curve sharply

141
Q

Typical atherosclerotic lesion composition

A

Superficial fibrous cap
Cellular area beneath and to the side of the cap (shoulder)
Necrotic core
Neovascularisation

142
Q

What changes are atherosclerotic plaques susceptible to

A

Rupture, ulceration or erosion
Haemorrhage into plaque
Atheroembolism
Aneurysm formation

143
Q

What does atherosclerotic plaque rupture expose blood to

A

Thrombogenic substances and induces thrombosis

144
Q

Why might an atherosclerotic plaque haemorrhage

A

Rupture of overlying fibrous cap or vessels in area of neovascularisation

145
Q

Atheroembolism

A

Atherosclerotic plaque rupture discharges debris into bloodstream, producing micro emboli

146
Q

How can atherosclerotic plaques cause aneurysm formation

A

Pressure or atrophy of underlying media, loss of weakness –> aneurysmal dilatation

147
Q

Morphologic changes seen in MI

A

Ischaemic coagulative necrosis
Infl
Repair

148
Q

MI appearance <12 hrs

A

Not apparent on gross examination

149
Q

MI appearance 12 - 24hrs

A

Infarct can be identified as a red blue area of discolouration

150
Q

MI apperance 24hrs - 10 days

A

Infarct becomes more sharply defined

151
Q

MI appearance 10 - 14 days

A

Infarct is rimmed by hyperaemic zone of vascular granulation tissue

152
Q

MI appearance 2+ wks

A

Injured area replaced by fibrous scar

153
Q

Histological changes 6-12hrs after onset of MI

A

Changes of coagulative necrosis

154
Q

Histological changes 1-3 days after MI

A

A/c infl elicited by the necrotic muscle fibres

155
Q

Histological changes 3 to 7 days after MI

A

Macrophages remove necrotic muscle fibres

156
Q

Histological changes 1-2 wks after MI

A

The damaged zone is replaced in growth of vascularised granulation tissue

157
Q

Histological changes seen 8 wks after MI

A

Well-developed scar tissues

158
Q

Cells of conduction system

A

Pacemaker cells - generally SAN
Specialised conduction system
Myocardial cells

159
Q

Conduction pathway

A

SAN
AVN
His-Purkinje system

160
Q

What is ECG the sum of

A

The action potential of ALL the cardiac cells

We can consider all atrial cells as one group and same for ventricles

161
Q

Where is depolarisation normally initiated

A

Endocardial layer as Purkinje fibres located in subendocardium

162
Q

What direction does repolarisation happen in

A

Epicardium to endocardium

Opposite to depolarisation

163
Q

What types of waves does the ECG record

A

Depolarisation

Repolarisation

164
Q

Basic features of ECG

A

3 waves - P, QRS complex, T

2 intervening isoelectric periods

165
Q

What is the P wave caused by

A

Atrial depolarisation - contraction

166
Q

What is the QRS complex caused by

A

Ventricular depolarisation - contraction

167
Q

What is the T wave caused by

A

Ventricular depolarisation - relaxation

168
Q

What is the PR interval

A

Time from start of P wave to QRS

169
Q

What does the PR interval signify

A

Delay in transmission through AVN - shouldn’t delay <0.2s (3-5 small squares)
Allows time for ventricle filling before depolarisation

170
Q

What is the ST segment

A

Interval between ventricular depolarisation and depolarisation
Flat isoelectric portion between end of S to start of T wave

171
Q

What changes can be seen in ST segment

A

Elevation

Depression

172
Q

What does the QT interval represent

A

Total time for ventricles to depolarise, rest then repolarise

173
Q

Normal P wave height

A

<2.5mm

174
Q

Normal P wave width

A

<0.12s

175
Q

Leads to look at for atrial depolarisation

A

Lead aVR sees depolarisation wave going from it and lead II sees it coming towards it

176
Q

Normal QRS width

A

<0.10 sec wide

177
Q

What leads are QRS Complex usually -ve in

A

aVR
V1
V2

178
Q

Naming QRS complex

A

If 1st deflection is -ve = Q wave
1st +ve defection = R wave
-ve deflection after R wave = S wave

179
Q

What direction is T wave pointing in

A

Same direction as main deflection of QRS

180
Q

Usual shape of T wave

A

Asymmetric (slow upstroke and rapid downstroke) but can also be symmetric

181
Q

T wave in different leads

A

Always -ve in aVR

Usually -ve in V1, sometimes -ve in V2 and rarely -ve in V3

182
Q

Normal range of QT interval

A

0.33 - 0.44sec

183
Q

How many leads does a typical ECG have

A

12

184
Q

What are limb leads

A

Bipolar leads and augmented leads together

185
Q

What plane do the limb leads look at the heart in

A

Frontal (or vertical) plane

186
Q

Overall direction of mean wave of electrical activity in heart

A

R to LV
R –> L
Back –> front

187
Q

In which directions do the limb leads show activity

A

L –> R

Top –> bottom

188
Q

In what direction do chest leads show activity

A

Back to front

189
Q

How are bipolar leads connected

A

In pairs

190
Q

What does lead I look at

A

Impulses travelling horizontally R–> L

191
Q

How do we get standard lead II

A

Connecting R and F

192
Q

How do we get standard lead III

A

Connecting L and F

193
Q

What must happen before unipolar leads can compare to bipolar leads

A

They must be augmented

194
Q

Unipolar leads

A

aVR - connects to R arm
aVL - connects to L arm
aVF - looks at impulses travelling south

195
Q

How many limb lead views are there

A

All 6 - I, II, III, aVR, aVL, aVF

196
Q

When do we see a +ve complex

A

When depolarisation wave travels from -ve to +ve

197
Q

When do we see a -ve complex

A

When the depolarisation wave travels from +ve to -ve

198
Q

Axis in ECG

A

The overall direction of depolarisation in the frontal plane

199
Q

Normal axis

A

If QRS complexes in Lead I and II/aVF are both +ve

200
Q

When is left axis deviation seen

A

If Lead I is mainly +ve but Leads aVF/II are -ve

201
Q

When is R axis deviation seen

A

If Lead I is -ve but Leads aVF/II are +ve

202
Q

Which chest leads look at ventricular septum

A

V1

V2

203
Q

Which chest leads look at anterior walls of heart

A

V3

V4

204
Q

Which chest leads look at lateral wall of heart

A

V5

V6

205
Q

Inferior leads of heart

A

I
II
aVF

206
Q

What artery is seen by inferior leads of heart

A

RCA

207
Q

Septal leads of heart

A

V1

V2

208
Q

What artery is seen by septal leads of heart

A

LAD

209
Q

Anterior leads of heart

A

V3

V4

210
Q

Lateral leads of heart

A

I
aVL
V5
V6

211
Q

What artery is seen by anterior leads of heart

A

LAD

212
Q

What artery is seen by lateral leads of heart

A

Circumflex

213
Q

Which leads show anterolateral aspect of heart

A

I
aVL
V3 - 6

214
Q

Which artery is seen by anterolateral leads of heart

A

LCA

215
Q

Systematic ECG checklist

A 
Basics (name, paper, speed, calibration)
Rate 
Rhythm 
Axis 
Waves (P, QRS, T)
Intervals (PT, ST, QT)
216
Q

Regular ECG paper speed

A

25mm/s

1 small box = 0.04s

217
Q

Regular ECG paper calibration

A

10mm = 1mV

218
Q

Calculating HR from regular ECGs

A

Divide 30 by no. large boxes between 2 successive QRS complexes

219
Q

Calculating HR from rhythm strip

A

Count no. QRS complexes and x6

220
Q

What do ACS’ include

A

STEMI
NSTEMI
Unstable angina

221
Q

What causes CAD

A

Narrowing of coronary arteries due to atherosclerosis (lipid deposition, infl and thrombosis)

222
Q

What does CAD incl

A

ACS - STEMI, NSTEMI, UA

C/c angina

223
Q

Calculating risk of CAD

A

QRISK 2/3

224
Q

What layer of the vessels are usually affected by CAD

A

Intima

225
Q

Pathophysiology of stable angina

A

Ischaemia is due to combo of fixed vessel narrowing and abnormal vascular tone

226
Q

What does the effect of a stenosis on blood flow depend on

A

The degree on narrowing of epicardial vessel

The amount of compensatory vasodilation that arterioles can achieve

227
Q

What causes abnormal vascular tone

A

Endothelial dysfunction

228
Q

What can abnormal vascular tone result in

A

Inappropriate vasoconstriction of coronary arteries

Loss of normal antithrombotic properties

229
Q

What happens in coronary stenosis

A

Metabolic hyperaemia can no longer match myocardial perfusion to myocardial oxygen demand in exercise

230
Q

Location of angina

A

Retrosternal, diffuse (not localised)

May involve both sides chest (L>R), arms (L>R), neck, lower jaw, upper abdomen

231
Q

Character of angina pain

A

Pressure, tightness or heavyweight. sometimes ‘burning’

232
Q

Angina pain in the neck

A

‘Choking’ sensation

233
Q

Angina pain in lower jaw

A

‘toothache’ sensation

234
Q

Precipitating factors of angina

A

Provoked by exertion (esp by walking uphill)

More easily provoked after heavy meal/ cold weather

235
Q

Relief of angina

A

Rapid relief (2 mins) w/ GTN

236
Q

Duration of angina attacks

A

Last a few mins (NOT v brief or v prolonged)

237
Q

Stable angina - pathophysiology

A

Lumen narrowed by plaque

Inappropriate vasoconstriction

238
Q

Unstable angina - pathophysiology

A

Plaque rupture
Platelet aggregation
Thrombus formation
Unopposed vasoconstriction

239
Q

Criteria for typical angina

A

All three of:
Constricting discomfort on the front of the chest, or in neck, shoulders, jaw or arms
Precipitated by physical exertion
Relieved by rest or GTN <5mins

240
Q

Criteria for atypical angina

A

2 of:
Constricting discomfort on the front of the chest, or in neck, shoulders, jaw or arms
Precipitated by physical exertion
Relieved by rest or GTN <5mins

241
Q

Cardiac ddx for recurrent chest pain

A

Angina

Pericarditis - sharp pain

242
Q

GI ddx for recurrent chest pain

A

Reflux (GORD)
Peptic ulcer
Oesophageal spasm
Biliary colic

243
Q

MSK ddx for recurrent chest pain

A

Costochondral syndrome

Cervical radiculitis

244
Q

Pulmonary ddx of recurrent chest pain

A

Pneumothroax
PE
Pneumonia

245
Q

1st line tests for suspected angina

A

ECG

246
Q

2nd line tests for suspected angina

A

CT coronary angiogram

247
Q

3rd line test for suspected angina

A

Stress tests

248
Q

Stress tests for angina

A

Exercise ECG
Myocardial Perfusion Imaging
Stress Echocardiograph
Stress MRI

249
Q

Imaging for angina

A

Non invasive - CT coronary angiogram

Invasive - Coronary angiogram

250
Q

1st line ix for suspected angina in those w/ known CAD

A

Stress tests

251
Q

Which region of heart is affected first by ischaemia

A

Subendothelial region as furthest from blood supply

252
Q

Subendothelial injury on ECG

A

ST depression

253
Q

Transmural injury on ECG

A

ST elevation

254
Q

What is a MI

A

Myocardial infarction
Necrosis of myocardial cells caused by occlusion of coronary vessels
Complete and persistent = STEMI
Partial/ intermittent = NSTEMI/UA

255
Q

Possible effects of atherosclerotic plaque rupture

A

Asymptomatic - reabsorption into plaque

Occlusive - infarction

256
Q

Reperfusion therapy for MI

A

PCI within 2 hrs

Fibrinolysis

257
Q

ECG changes in STEMI

A

ST elevation

May also see L BBB

258
Q

ECG appearance in NSTEMI

A

T wave inversion
ST depression
May see pathological Q waves

259
Q

Where is troponin found

A

Skeletal muscle

Cardiac muscle

260
Q

Cardiac spp troponin

A

I and T

261
Q

Measuring troponin

A

Blood test

262
Q

When is the result of troponin levels significant

A

At least one value >99th percentile of the upper reference limit

263
Q

Non-cardiac symptoms that can elevate troponin

A 
Exercise 
Chronic renal failure 
Sepsis 
Myocarditis 
Aortic dissection 
PE
264
Q

If a pt is having ACS symptoms but ECG has no pathological changes and has normal troponin levels, what is the suspected dx

A

Unstable angina

265
Q

When is troponin measured for suspected ACS

A

On admission and couple hrs after

266
Q

Troponin levels after MI

A

Starts to rise at 3-4hrs and returns to baseline at 10-14 days

267
Q

Serum biomarkers in MI

A

CK-MB

Troponin

268
Q

Complications of MI

A

ACT RAPID

Arrhythmias 
Congestive cardiac failure/ cardiogenic shock
Thromboembolism 
Rupture 
Aneurysm 
Pericarditis 
Ischaemia 
Dressler's syndrome/ death
269
Q

What can rupture after an MI

A

Ventricular wall
Septum
Papillary muscle

270
Q

Main late complications of MI

A

Heart failure

Arrhythmia

271
Q

Why does coronary stenosis usually cause angina only during exercise/stress

A

Resistance in series adds up
In stenosed coronary arteries, dilation and arteriogenesis still isn’t enough to meet oxygen demand so ischamenic pain ensues

272
Q

How does coronary stenosis of 70% affect blood flow

A

Blood flow isn’t compromised at rest or exercise

273
Q

What is coronary stenosis of 70-80% associated with

A

Decreased blood flow on exercise on exercise but not at rest

274
Q

What is coronary stenosis of >80% associated with

A

Compromise of blood flow both at rest and exertion

275
Q

What condns affect myocardial oxygen supply

A

Coronary stenosis
Anaemia
Lung problems

276
Q

Factors affecting myocardial demand

A 
Tachycardia 
Pre-load
Afterload 
Muscle mass (e.g. hypertrophy/ infarction)
Muscle contractility
277
Q

Optimum medical therapy for angina

A

2 anti-anginal drugs

278
Q

1st line drugs for angina

A

Beta blockers - aim for resting HR to 50-60 bpm

279
Q

2nd line drugs for angina

A

Long-acting oral nitrates e.g. isosorbide mononitrate added onto BB

280
Q

3rd line treatments for angina

A

Ca-channel blockers

Consider angioplasty

281
Q

What procedure should be considered if angina is not controlled

A

Revascularisation

282
Q

Ix for stable angina

A 
Exercise stress tests 
MIBI 
CTCA
Stress MRI 
Dobutamine stress Echo 
Coronary angio
Bloods
283
Q

Usual approach for coronary angiography

A

Radial artery

284
Q

Indications for PCI - stable angina

A

Limiting symptoms despite 2 anti-anginals
1,2,3 vessel or LMS disease
Less complex disease (SYNTAX score <22)

285
Q

Best graft for CABG

A

Internal mammary/thoracic artery

286
Q

Indications for CABG

A

Left Main Stem disease (>50% stenosis)
Proximal 3 vessel disease
Complex disease (high risk score)

287
Q

Asociated symptoms in MI

A 
SOB 
Leg swelling (heart failure)
Hypotensive symptoms - paleness, clamminess etc
Feeling of impending doom 
Emesis
288
Q

Who have silent MI’s

A

Diabetics - usually present with atypical chest pain

289
Q

Bloods for suspected ACS

A 
FBC (anaemia)
U&Es (prior to ACEi and other meds)
LFTs (statins)
Thyroid function tests
Lipid profile 
Hba1c and fasting glucose (DM)
290
Q

What may be seen on CXR after ACS

A

Pulmonary oedema

Widened mediastinum

291
Q

How is pulmonary oedema treated

A

Oxygen

IV loop diuretic e.g. furosemide

292
Q

Why do MI pts have follow up ECGs after px

A

Assess functional damage

293
Q

Why may ACS pts have a CT angio

A

Asess for CAD

294
Q

When is thrombolysis done for ACS

A

If PCI is unavailable within 2 hrs (risk of bleeding)

ECG done 60-90 mins after

295
Q

A/c NSTEMI therapeutics

A

BATMAN

Beta-blockers
Aspirin 300mg stat
Ticagrelor 180mg stat (Clopi 300mg if high bleeding risk)
Morphine titrated to control pain
Anti-coag - fondaparinux or heparin if bleeding risk
Nitrate - to relieve spasm

Give oxygen if stats dropping

296
Q

GRACE score to assess for PCI

A

6/12 risk of death or repeat MI after NSTEMI

<5% low risk
5 - 10% medium risk
> 10% high risk

If they are medium/ high risk they’re considered for early PCI to treat underlying CAD

297
Q

Dressler’s syndrome

A

Post-myocardial infarction syndrome
Usually occurs 2-3 wks after an MI
Caused by localised immune repose and cause pericarditis

298
Q

2’ prevention after MI - medical mx

A

Aspirin 75mg OD
Another anti platelet (e.g. clop or prasugrel for up to 12/12)
Atorvastatin 80mg OD
ACEi (e.g. ramipril)
Aldosterone antagonist for those with clinical heart failure (eplerenone)
BB

299
Q

2’ prevention after MI - lifestyle

A 
Stop smoking 
Reduce alcohol 
Mediterranean diet 
Cardiac rehab 
Optimise treatment of other medical condn e.g. DM, HTN
300
Q

ECG for suspected posterior MI

A

Use posterior chest wall leads V7 - V9

301
Q

ECG for suspected right MI

A

Use right sided leads - move V4 to opposite side

302
Q

Where is the mediastinum found

A

Middle part of thoracic cavity

Between pleural spaces

303
Q

What is found anteriorly to mediastinum

A

Manubrium

Body of sternum

304
Q

What is found posteriorly to mediastinum

A

Vertebral column (T1 -T12)

305
Q

What is found laterally to mediastinum

A

Parietal pleura

306
Q

What is found superior to mediastinum

A

Superior thoracic aperture

307
Q

What is found inferior to mediastinum

A

Internal thoracic aperture

308
Q

Superior mediastinum

A

Above level of thoracic plane (sternal angle)

309
Q

Inferior mediastinum

A

Below level of thoracic plane (sternal angle)

310
Q

What can inferior mediastinum be divided into

A

Anterior
Middle
Posterior

311
Q

What level is the thoracic plane found at

A

Level of 2nd rib anteriorly and 4th thoracic vertebrae posteriorly

312
Q

Structures found in superior mediastinum

A 
Trachea 
Oesophagus 
Arch of aorta (+ branches)
Superior vena cava 
Vagus nerves 
Phrenic nerves 
L recurrent pharyngeal nerve
313
Q

Structures found in anterior mediastinum

A

Thymus

314
Q

Structures found in middle mediastinum

A 
Heart 
Pericardium 
Phrenic nerves 
Ascending aorta 
Pulmonary trunk
315
Q

Structures found in posterior mediastinum

A 
Oesophagus 
Sympathetic chain
Azygous vein 
Thoracic duct 
Descending duct 
Vagus nerve
316
Q

What does the carotid sheath contain

A

Common carotid artery
Internal jugular vein
Vagus nerve

317
Q

Recurrent laryngeal nerve

A

Wraps around subclavian artery

Innervates intrinsic muscles of larynx - motor

318
Q

What do phrenic nerves innervate

A

Diaphragm
Mediastinum
Mediastinum floor

319
Q

Which vessels are found in inferior mediastinum

A

Internal thoracic vessels

320
Q

What is the heart encased in

A

Pericardial sac

321
Q

Pericardial sac layers

A

Outer, fibrous layer

Serous pericardium layers

322
Q

What are the serous layers of the pericardium

A

Parietal pericardium

Visceral pericardium

323
Q

What does outer, fibrous layer of pericardium do

A

Helps keep heart in place in case of pneumothorax

324
Q

What does outer, fibrous layer of heart attach to

A

Great vessel superiorly and central tendon of diaphragm inferiorly

325
Q

What does the serous pericardium layers secrete

A

Little amount of serous fluid so heart is able to move around

326
Q

Where are phrenic nerves found

A

L and R of heart

327
Q

Where do phrenic nerves branch from spinal cord

A

C3, C4 & C5

328
Q

What do phrenic nerves innervate

A

Hemi diaphragm

329
Q

Where do coronary arteries originate from

A

Root of aorta - aortic sinus

330
Q

How many aortic sinuses are there

A

3 but only L and R sinuses are origin of coronary arteries

331
Q

Where does the RCA come from

A

R sinus

332
Q

Where does the RCA pass

A

Laterally between atria-ventricular groove - coronary sulcus

333
Q

Branches of RCA

A

Sino-atrial nodal artery
Diagonal branches
R marginal artery
Posterior interventricular branch (posterior descending artery)

334
Q

Where does the R marginal artery travel

A

Lateral margin of L ventricle to apex

335
Q

Branches of LCA

A 
Anterior interventricular (anterior descending artery) 
Circumflex artery
336
Q

What does the LAD supply

A

Mainly L ventricle

337
Q

What does heart drain into

A

Coronary sinus

338
Q

Myocardial bridge

A

Myocardium covering of LCA - can only see branches

339
Q

When do you give furosemide for STEMI

A

When presenting with symptoms of acute heart failure

340
Q

What ix could be useful in pts presenting w/ chest pain

A

Nuclear med - imaging spread of radioactive material

341
Q

When is angiography not as useful

A

Pts with AF, tachycardia or build up of Ca

342
Q

Features of UA

A

Cardiac chest pain (at rest)
Abnormal/ normal ECG
Normal troponin

343
Q

Features of NSTEMI

A

Cardiac chest pain
Abnormal/ normal ECG (no ST-elevation, repolarisation abnormalities)
Raised troponin

344
Q

Can you dx a STEMI if the pt has no ST elevation

A

Yes, if new LBBB is present

345
Q

STEMI algorithm

A

ROMANCE

Reassure 
Oxygen - sats >94%
Morphine 10mg (+ antiemetic)
Aspirin 300mg stat 
Nitrates - GTN prn
Clopidogrel 300mg/ Ticagelor 180mg stat
Enoxaprin 2.5mg
346
Q

Driving after ACS

A

If the pt had an angioplasty, banned for a week

If no angioplasty, banned for 1/12

347
Q

Initial ACS mx

A

MONA

Morphine (anti-emetic)
Oxygen if needed
Nitrates
Aspirin 300mg stat

348
Q

Mx of Dressler’s syndrome

A

High dose aspirin

MBBS - Year 2 (20 decks)

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