Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the LAD supply

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the circumflex artery supply

A

Lateral and posterior walls of L ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the R coronary artery supply

A

Right atrium and ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Right dominant circulation

A

PDA arises from RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the Posterior Descending Artery (PDA) supply

A

Inferior wall of L ventricle and part of inter ventricular septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What % of people have a right dominant circulation

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Left dominant circulation

A

PDA arises from Circumflex artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What % of people have a L dominant circulation

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Co-dominant circulation

A

PDA arises from both RCA and Circumflex artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What % of people have a co-dominant circulation

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does coronary blood flow occur

A

In diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What kind of arteries are coronary Arteries

A

Functional end - do NOT have effective anastomoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does the coronary circulation meet the hearts high oxygen requirements

A

Stuctural and functional adaptations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Functional adaptations of coronary circulation

A

High basal flow and oxygen extraction
Metabolic hyperaemia
Autoregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Increase in basal flow during exercise

A

10x body’s avg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Increased oxygen extraction during exercise

A

75% vs 25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most important autoregulation response of heart

A

Myogenic response - stretch in vessel –> dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cardiac output (CO)

A

Volume of blood ejected by 1 ventricle in 1 minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Stroke volume (SV)

A

Volume of blood ejected from ventricles in systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Eqn for CO

A

CO = SV x HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Main factors determining SV

A

Energy of contraction of vessels
BP in aorta

These oppose ventricular ejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does change in aortic pressure affect SV

A

Rise in aortic pressure causes SV to fall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are good makers of preload

A

End Diastolic Volume

End Diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Central Venous Pressure

A

Pressure in the vena cava at the entrance to R atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can CVP be used as an estimate of

A

RV End Diastole Pressure ie. RV preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does distending the heart affect SV

A

Increases it

Stretching myocytes during diastole increases energy of contraction during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the energy of contraction proportional to

A

Muscle fibre length at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Factors influencing CVP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Frank Starling mechanism (Law of the Heart)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Contractility definition

A

Force of contraction which is independent of initial fibre length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What can reduced contractility lead to

A

Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Afterload

A

Resistance heart has to overcome to eject its contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Afterload and SV

A

Increased afterload leads to reduced in SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

‘Pump function curve’

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is HR controlled by

A

Sympathetic and parasympathetic nerves which innervate SAN and AVN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does increase in sympathetic activity affect HR

A

Increase - tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does increase in parasympathetic activity affect HR

A

Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How is lung oxygen uptake increased during exercise

A

Increase in RV output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is oxygen transport around body increased during exercise

A

Decreased LV output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is BP stabilised during exercise

A

Vasoconstriction in non-exercising tissues

Baroreflex rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Baroreflex reset

A

Prevents HR from falling

Baroreceptors have an increased threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does CO increase during exercise

A

Increase in SV

Increase in HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How is HR increased during exercise

A

Increase in cardiac sympathetic activity

Decrease in vagal parasympathetic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Maximum HR during exercise

A

220 - age in yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

SVR

A

Systemic vascular resistance

Same as TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What kind of exercise causes SV to be high at rest

A

Supine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Essentials for normal cardiac function

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Stages in Systole

A

Atrial contraction
Isovolumic contraction
Rapid ejection
End systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Isovolumic contraction - systole

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Whats seen on ECG during isovolumic contraction - systole

A

Causes QRS complex - depolarisation of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What’s heard during isovolumic contraction - systole

A

1st heart sound

Mitral valve closes first then tricuspid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Whats seen on ECG during rapid ejection - systole

A

ST segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

End systole - systole

A

Pressure starts to drop

Aortic and pulmonic valves close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What’s seen in ECG during end systole

A

T wave - depolarisation of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Isovolumic relaxation - diastole

A

Heart is relaxed and the valves are closed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is heard during isovolumic relaxation - diastole

A

2nd heart sound

Closing of aortic valve then pulmonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Stages in diastole

A

Isovolumic relaxation
Rapid ventricular filling
Reduced ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Rapid ventricular filling - diastole

A

Blood flows passively from ventricles to atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Ejection systolic murmur

A

Between S1 and S2 - rises and falls

Aortic stenosis, pulmonary stenosis, aortic or pulmonary flow murmurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Pansystolic murmur

A

Steady murmur between S1 and S2

Mitral regurgitation, tricuspid regurgitation, ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Late systolic murmur

A

Between mid-systolic click and S2

Mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Early diastolic murmur

A

After S2 - falls

Aortic or pulmonary regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Mild diastolic murmur

A

Starts at opening click and continues to S1

Mitral stenosis, tricuspid stenosis, mitral or tricuspid flow murmurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How is CO, MAP & SVR related

A

CO = MAP/ SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What does AF limit during exercise

A

Expected increase in ventricular SV and CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Cardiac Resynchronisation Therapy

A

Delivers regular signals to pace L ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

When do we see the basement membrane

A

In vessels larger than 1mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What does the endothelium determine

A

When and where the WBC leave circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What does the endothelium secrete

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

When do we see the vasa vasorum

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Adaptations of larger elastic/ conducting arteries

A

Large lumen
Elastic recoil
Several elastic laminae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Function of large lumen in elastic arteries

A

Allows low-resistance conduction of blood and acts as conduits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Function of elastic recoil in large elastic arteries

A

Absorb impulse of cardiac systole

Maintains blood flow in diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Function of elastic laminae in large elastic arteries

A

Making blood flux more uniform

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Muscular vs conducting arteries

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is present in large arterioles but absent in terminal arterioles

A

Thin, fenestrated internal elastic lamina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Types of capillaries

A

Continuous capillaries
Fenestrated capillaries
Discontinuous capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Where are continuous capillaries found

A

Muscle
Lungs
CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Where are fenestrated capillaries found

A

Endocrine glands, sites of metabolic and fluid absorption

e.g. gallbladder, kidney, and intestinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Where are discontinuous capillaries (sinusoidal capillaries) found

A

Liver
Spleen
Bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Continuous capillaries

A

Have tight junctions that completely surround endothelium

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Fenestrated capillaries features

A

Endothelium with fenestrations

Greater permeability to solutes and fluid than other capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What do post capillary venues participate in

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Characteristic feature of venules

A

Large diameter of lumen compared to overall thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Where do valves project from

A

Tunica intima

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What hormone does the heart release

A

Atrial naturietic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

3 tunics of heart

A

Internal - endocardium
Middle - myocardium
External - pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Subendocardial layer of heart

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Thickest heart tunic

A

Myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Subepicardial layer

A

External to myocardium

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the epicardium composed of

A

Superficial mesothelial lining supported by connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Composition of pericardial sac

A

Fibrous outer skeleton attached to diaphragm
Parietal pericardium
Visceral pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is found in between the layers of the pericardium

A

Small amount of fluid facilitating the heart movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Cardiac conduction pathway

A 
SAN 
AVN 
Bundle of His 
L and R bundle branches 
Purkinje fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What does coordinated contraction of the cardiac muscle depend on

A

Propagation of electrical impulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How are electrical impulses in heart propagated

A

Specialised excitatory and conducting myocytes

These also regulate HR and rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Where is the SA node located

A

Junction of R atrium appendage and superior vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Fibrous skeleton nd heart conduction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

AVN location

A

In R atrium along atrial septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Where is the Bundle of His found

A

From R atrium to summit of ventricular septum

Forms Purkinje network

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Where does the lymphatic vascular start

A

Lymphatic capillaries

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Where does the lymphatic vascular system terminate

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Arteriosclerosis

A

Hardening of arteries - arterial wall thickening and loss of elasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Where does arteriosclerosis occur

A

Occurs in small arteries and arterioles and causes downstream ischaemic injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Monckeberg medial sclerosis

A

Calcific deposits within walls of muscular arteries

May undergo metaplastic change into bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

How can atherosclerosis cause aneurysm formation

A

Mechanical obstruct blood flow and can weaken underlying media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Major targets of atherosclerosis

A

Large elastic arteries (aorta, carotid and iliac arteries)

Medium sized muscular arteries (coronary and popliteal arteries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Constitutional risk factors of atherosclerosis

A

Increasing age
Male
Genetic abnormalities
Fhx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Modifiable risk factors

A 
Hyperlipidaemia 
HTN 
DM 
Smoking 
Infl (CRP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Causes of c/c endothelial injury

A 
Hyperlipidaemia 
HTN 
Smoking 
Homocystinuria 
Haemodynamic factors 
Toxins 
Viruses 
Immune reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

174
Q

Normal P wave width

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

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

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

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

203
Q

Which chest leads look at anterior walls of heart

204
Q

Which chest leads look at lateral wall of heart

205
Q

Inferior leads of heart

206
Q

What artery is seen by inferior leads of heart

207
Q

Septal leads of heart

208
Q

What artery is seen by septal leads of heart

209
Q

Anterior leads of heart

210
Q

Lateral leads of heart

A

I
aVL
V5
V6

211
Q

What artery is seen by anterior leads of heart

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

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

224
Q

What layer of the vessels are usually affected by CAD

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

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

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

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

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions