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

Cardiology - Coronary Artery Disease Flashcards

(348 cards)

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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
Why does the amount of blood in capacitance vessels vary
These vessels are thin walled and are easily distended/ collapsed Supplied by sympathetic nerves that can cause constriction
26
Main factors determining SV
Energy of contraction of vessels BP in aorta These oppose ventricular ejection
27
What is the energy of contraction of vessels regulated by
Ventricular filling pressure Myocardial contractility When these increase as does energy of contraction
28
How does change in aortic pressure affect SV
Rise in aortic pressure causes SV to fall
29
What is preload in the heart
Amount of stretch of the ventricular muscle fibres just before they contract at the end of distale
30
What are good makers of preload
End Diastolic Volume | End Diastolic pressure
31
What is Central Venous Pressure
Pressure in the vena cava at the entrance to R atrium
32
What can CVP be used as an estimate of
RV End Diastole Pressure ie. RV preload
33
How does distending the heart affect SV
Increases it | Stretching myocytes during diastole increases energy of contraction during systole
34
What is the energy of contraction proportional to
Muscle fibre length at rest
35
What is CVP governed by
Volume of blood in circulation and by how the blood is distributed between central and peripheral veins
36
What happens when CVP falls
RVEDP (preload) is reduced --> RV output is reduced --> less blood flows to L heart --> LV SV is reduced
37
Factors influencing CVP
Gravity (decreases) Soleal pump (increases) Vasoconstriction by sympathetic nerves (increased) Pumping ability of heart
38
How does the pumping ability of heart affect CVP
Faster --> drop in CV if no compensatory mechanisms | Slower (e.g. in heart failure and MI) --> CVP rises
39
Frank Starling mechanism (Law of the Heart)
The greater the preload The greater the force of contraction The greater the SV
40
Why is Starling's law important
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
41
Contractility definition
Force of contraction which is independent of initial fibre length
42
What can reduced contractility lead to
Heart failure
43
Afterload
Resistance heart has to overcome to eject its contents
44
Afterload and SV
Increased afterload leads to reduced in SV
45
'Pump function curve'
High arterial pressure (e.g. by giving vasoconstrictor drug) impairs output (lowers SV)
46
What is HR controlled by
Sympathetic and parasympathetic nerves which innervate SAN and AVN
47
How does increase in sympathetic activity affect HR
Increase - tachycardia
48
How does increase in parasympathetic activity affect HR
Bradycardia
49
Demands of CVS during exercise
Increase lung oxygen uptake Increase oxygen transport around body Direct increased oxygen specifically to exercising muscle Stabilisation of BP
50
How is lung oxygen uptake increased during exercise
Increase in RV output
51
How is oxygen transport around body increased during exercise
Decreased LV output
52
How is increased oxygen supply directed specifically to exercising muscle
Increase in oxygen extraction from blood | Decrease in vascular resistance in exercising metabolism
53
How is BP stabilised during exercise
Vasoconstriction in non-exercising tissues | Baroreflex rest
54
Baroreflex reset
Prevents HR from falling | Baroreceptors have an increased threshold
55
How does CO increase during exercise
Increase in SV | Increase in HR
56
How is SV increased in exercise
Increased preload - skeletal muscle pump, peripheral vasoconstriction Increased contractility causing faster ejection and a decrease in end-systolic volume
57
How is HR increased during exercise
Increase in cardiac sympathetic activity | Decrease in vagal parasympathetic activity
58
Maximum HR during exercise
220 - age in yrs
59
Threat of hypotension during exercise
BP = CO x SVR | Reduced SVR could cause BP to drop but compensatory vasoconstriction in active tissue attenuates fall
60
SVR
Systemic vascular resistance | Same as TPR
61
What kind of exercise causes SV to be high at rest
Supine
62
The athletic heart vs non-athletic heart
Stronger and hypertrophied Increased SV Decreased resting HR CO can be much higher during exercise
63
How do heart transplant pts increase CO with exercise
Transplanted heart is denervated (no cardiac autonomic nerves) Circulating catecholamines increase HR and skeletal muscle pump increased preload
64
What is the cardiac cycle about
Heart contraction/ relaxation Rship between electrical activity and contraction of heart Changes in volume of blood related to pressure
65
Essentials for normal cardiac function
Intact myocardium and mechanics Substrate to pump around (blood) Own fuel supply Electrical activity
66
Stages in Systole
Atrial contraction Isovolumic contraction Rapid ejection End systole
67
What is seen in atrial contraction - systole
P wave on ECG | 1st half from R atrium and 2nd half from L atrium
68
Isovolumic contraction - systole
No change in volume but changes in pressure of blood in atria
69
Whats seen on ECG during isovolumic contraction - systole
Causes QRS complex - depolarisation of ventricles
70
What's heard during isovolumic contraction - systole
1st heart sound | Mitral valve closes first then tricuspid
71
Whats seen on ECG during rapid ejection - systole
ST segment
72
End systole - systole
Pressure starts to drop | Aortic and pulmonic valves close
73
What's seen in ECG during end systole
T wave - depolarisation of ventricles
74
Isovolumic relaxation - diastole
Heart is relaxed and the valves are closed
75
What is heard during isovolumic relaxation - diastole
2nd heart sound | Closing of aortic valve then pulmonic
76
How can the second heart sound be split
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
77
Stages in diastole
Isovolumic relaxation Rapid ventricular filling Reduced ventricular filling
78
Rapid ventricular filling - diastole
Blood flows passively from ventricles to atria
79
What may be heard during rapid ventricular filling - diastole
3rd heart sound | Could be caused by heart failure - ventricle is too stiff
80
Clicks during cardiac cycle
Ejection click at the end of diastole Mid systolic click Opening snap in mitral stenosis at beginning of systole
81
Ejection systolic murmur
Between S1 and S2 - rises and falls Aortic stenosis, pulmonary stenosis, aortic or pulmonary flow murmurs
82
Pansystolic murmur
Steady murmur between S1 and S2 | Mitral regurgitation, tricuspid regurgitation, ventricular septal defect
83
Late systolic murmur
Between mid-systolic click and S2 Mitral valve prolapse
84
Early diastolic murmur
After S2 - falls Aortic or pulmonary regurgitation
85
Mild diastolic murmur
Starts at opening click and continues to S1 Mitral stenosis, tricuspid stenosis, mitral or tricuspid flow murmurs
86
How is CO, MAP & SVR related
CO = MAP/ SVR
87
What does AF limit during exercise
Expected increase in ventricular SV and CO
88
Cardiac Resynchronisation Therapy
Delivers regular signals to pace L ventricle
89
When do we see the basement membrane
In vessels larger than 1mm
90
What does the endothelium determine
When and where the WBC leave circulation
91
What does the endothelium secrete
Paracrine factors for vessel dilation, constriction and growth of adjacent cells
92
Vasa vasorum
"Vessels of the vessels" Have arterioles, capillaries and venules that branch profusely in the adventitia and the outer media to provide metabolites
93
When do we see the vasa vasorum
Adventitia and outer media in larger vessels too thick to recieve nutrients via diffusion
94
Adaptations of larger elastic/ conducting arteries
Large lumen Elastic recoil Several elastic laminae
95
Function of large lumen in elastic arteries
Allows low-resistance conduction of blood and acts as conduits
96
Function of elastic recoil in large elastic arteries
Absorb impulse of cardiac systole | Maintains blood flow in diastole
97
Function of elastic laminae in large elastic arteries
Making blood flux more uniform
98
Muscular vs conducting arteries
Thicker tunica media Narrower lumen Thickened elastic lamina More smooth muscle and less elastin in tunica media
99
How many layers of circularly arranged smooth muscle are there in arteries
3-8 layers in small arteries | 1-2 in arterioles
100
What are arterioles main control points for
Regulation of physiological resistance to blood flow | Pressure and velocity sharply reduced --> steady flow vs pulsatile
101
What is present in large arterioles but absent in terminal arterioles
Thin, fenestrated internal elastic lamina
102
Types of capillaries
Continuous capillaries Fenestrated capillaries Discontinuous capillaries
103
Where are continuous capillaries found
Muscle Lungs CNS
104
Where are fenestrated capillaries found
Endocrine glands, sites of metabolic and fluid absorption | e.g. gallbladder, kidney, and intestinal tract
105
Where are discontinuous capillaries (sinusoidal capillaries) found
Liver Spleen Bone marrow
106
Continuous capillaries
Have tight junctions that completely surround endothelium | Intercellular clefts of un-joined membranes; allows passage of fluids
107
Fenestrated capillaries features
Endothelium with fenestrations | Greater permeability to solutes and fluid than other capillaries
108
Sinusoidal capillaries
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
109
What do post capillary venues participate in
Exchanges between the blood and tissues - 1' site fo WBC leaving
110
Characteristic feature of venules
Large diameter of lumen compared to overall thickness
111
Where do valves project from
Tunica intima
112
What hormone does the heart release
Atrial naturietic factor
113
3 tunics of heart
Internal - endocardium Middle - myocardium External - pericardium
114
Central fibrous skeleton of heart
Base of heart valves Site of origin and insertion of the cardiac muscles Electrical insulation between atria & ventricles Separates atria and ventricles
115
Subendocardial layer of heart
Layer of connective tissue connecting endothelial layer to myocardium Contains veins, nerves, branches of the Purkinje cells
116
Thickest heart tunic
Myocardium
117
Subepicardial layer
External to myocardium | Loose connective tissue containing veins, nerves and nerve ganglia and adipose tissue that surround the heart
118
What is the epicardium composed of
Superficial mesothelial lining supported by connective tissue
119
Composition of pericardial sac
Fibrous outer skeleton attached to diaphragm Parietal pericardium Visceral pericardium
120
What is found in between the layers of the pericardium
Small amount of fluid facilitating the heart movements
121
Cardiac conduction pathway
``` SAN AVN Bundle of His L and R bundle branches Purkinje fibres ```
122
What does coordinated contraction of the cardiac muscle depend on
Propagation of electrical impulses
123
How are electrical impulses in heart propagated
Specialised excitatory and conducting myocytes | These also regulate HR and rhythm
124
Where is the SA node located
Junction of R atrium appendage and superior vena cava
125
Fibrous skeleton nd heart conduction
Ensures impulses aren't spread randomly so all chambers don't beat at same time
126
AVN location
In R atrium along atrial septum
127
Why is the AVN described as a gatekeeper
Delays transmission of signals from atria to ventricles | Ensures atrial contraction preceded ventricular contraction
128
Where is the Bundle of His found
From R atrium to summit of ventricular septum | Forms Purkinje network
129
Where does the lymphatic vascular start
Lymphatic capillaries | Closed ended tubules that anastomose to form vessels of steadily increasing size
130
Where does the lymphatic vascular system terminate
Terminate in blood vascular system emptying into large veins near the heart
131
Arteriosclerosis
Hardening of arteries - arterial wall thickening and loss of elasticity
132
Where does arteriosclerosis occur
Occurs in small arteries and arterioles and causes downstream ischaemic injury
133
Monckeberg medial sclerosis
Calcific deposits within walls of muscular arteries | May undergo metaplastic change into bone
134
How can atherosclerosis cause aneurysm formation
Mechanical obstruct blood flow and can weaken underlying media
135
What happens when atherosclerosis is complicated by occlusive thrombosis
Causes sudden death MI Stroke a/c ischaemia of legs and abdominal organs
136
Major targets of atherosclerosis
Large elastic arteries (aorta, carotid and iliac arteries) | Medium sized muscular arteries (coronary and popliteal arteries)
137
Constitutional risk factors of atherosclerosis
Increasing age Male Genetic abnormalities Fhx
138
Modifiable risk factors
``` Hyperlipidaemia HTN DM Smoking Infl (CRP) ```
139
Causes of c/c endothelial injury
``` Hyperlipidaemia HTN Smoking Homocystinuria Haemodynamic factors Toxins Viruses Immune reactions ```
140
Haemodynamic factors of atherogenesis
Laminar flow in straight regions of arterioles but oscillatory flow in regions where arteries divide/curve sharply
141
Typical atherosclerotic lesion composition
Superficial fibrous cap Cellular area beneath and to the side of the cap (shoulder) Necrotic core Neovascularisation
142
What changes are atherosclerotic plaques susceptible to
Rupture, ulceration or erosion Haemorrhage into plaque Atheroembolism Aneurysm formation
143
What does atherosclerotic plaque rupture expose blood to
Thrombogenic substances and induces thrombosis
144
Why might an atherosclerotic plaque haemorrhage
Rupture of overlying fibrous cap or vessels in area of neovascularisation
145
Atheroembolism
Atherosclerotic plaque rupture discharges debris into bloodstream, producing micro emboli
146
How can atherosclerotic plaques cause aneurysm formation
Pressure or atrophy of underlying media, loss of weakness --> aneurysmal dilatation
147
Morphologic changes seen in MI
Ischaemic coagulative necrosis Infl Repair
148
MI appearance <12 hrs
Not apparent on gross examination
149
MI appearance 12 - 24hrs
Infarct can be identified as a red blue area of discolouration
150
MI apperance 24hrs - 10 days
Infarct becomes more sharply defined
151
MI appearance 10 - 14 days
Infarct is rimmed by hyperaemic zone of vascular granulation tissue
152
MI appearance 2+ wks
Injured area replaced by fibrous scar
153
Histological changes 6-12hrs after onset of MI
Changes of coagulative necrosis
154
Histological changes 1-3 days after MI
A/c infl elicited by the necrotic muscle fibres
155
Histological changes 3 to 7 days after MI
Macrophages remove necrotic muscle fibres
156
Histological changes 1-2 wks after MI
The damaged zone is replaced in growth of vascularised granulation tissue
157
Histological changes seen 8 wks after MI
Well-developed scar tissues
158
Cells of conduction system
Pacemaker cells - generally SAN Specialised conduction system Myocardial cells
159
Conduction pathway
SAN AVN His-Purkinje system
160
What is ECG the sum of
The action potential of ALL the cardiac cells | We can consider all atrial cells as one group and same for ventricles
161
Where is depolarisation normally initiated
Endocardial layer as Purkinje fibres located in subendocardium
162
What direction does repolarisation happen in
Epicardium to endocardium | Opposite to depolarisation
163
What types of waves does the ECG record
Depolarisation | Repolarisation
164
Basic features of ECG
3 waves - P, QRS complex, T | 2 intervening isoelectric periods
165
What is the P wave caused by
Atrial depolarisation - contraction
166
What is the QRS complex caused by
Ventricular depolarisation - contraction
167
What is the T wave caused by
Ventricular depolarisation - relaxation
168
What is the PR interval
Time from start of P wave to QRS
169
What does the PR interval signify
Delay in transmission through AVN - shouldn't delay <0.2s (3-5 small squares) Allows time for ventricle filling before depolarisation
170
What is the ST segment
Interval between ventricular depolarisation and depolarisation Flat isoelectric portion between end of S to start of T wave
171
What changes can be seen in ST segment
Elevation | Depression
172
What does the QT interval represent
Total time for ventricles to depolarise, rest then repolarise
173
Normal P wave height
<2.5mm
174
Normal P wave width
<0.12s
175
Leads to look at for atrial depolarisation
Lead aVR sees depolarisation wave going from it and lead II sees it coming towards it
176
Normal QRS width
<0.10 sec wide
177
What leads are QRS Complex usually -ve in
aVR V1 V2
178
Naming QRS complex
If 1st deflection is -ve = Q wave 1st +ve defection = R wave -ve deflection after R wave = S wave
179
What direction is T wave pointing in
Same direction as main deflection of QRS
180
Usual shape of T wave
Asymmetric (slow upstroke and rapid downstroke) but can also be symmetric
181
T wave in different leads
Always -ve in aVR | Usually -ve in V1, sometimes -ve in V2 and rarely -ve in V3
182
Normal range of QT interval
0.33 - 0.44sec
183
How many leads does a typical ECG have
12
184
What are limb leads
Bipolar leads and augmented leads together
185
What plane do the limb leads look at the heart in
Frontal (or vertical) plane
186
Overall direction of mean wave of electrical activity in heart
R to LV R --> L Back --> front
187
In which directions do the limb leads show activity
L --> R | Top --> bottom
188
In what direction do chest leads show activity
Back to front
189
How are bipolar leads connected
In pairs
190
What does lead I look at
Impulses travelling horizontally R--> L
191
How do we get standard lead II
Connecting R and F
192
How do we get standard lead III
Connecting L and F
193
What must happen before unipolar leads can compare to bipolar leads
They must be augmented
194
Unipolar leads
aVR - connects to R arm aVL - connects to L arm aVF - looks at impulses travelling south
195
How many limb lead views are there
All 6 - I, II, III, aVR, aVL, aVF
196
When do we see a +ve complex
When depolarisation wave travels from -ve to +ve
197
When do we see a -ve complex
When the depolarisation wave travels from +ve to -ve
198
Axis in ECG
The overall direction of depolarisation in the frontal plane
199
Normal axis
If QRS complexes in Lead I and II/aVF are both +ve
200
When is left axis deviation seen
If Lead I is mainly +ve but Leads aVF/II are -ve
201
When is R axis deviation seen
If Lead I is -ve but Leads aVF/II are +ve
202
Which chest leads look at ventricular septum
V1 | V2
203
Which chest leads look at anterior walls of heart
V3 | V4
204
Which chest leads look at lateral wall of heart
V5 | V6
205
Inferior leads of heart
I II aVF
206
What artery is seen by inferior leads of heart
RCA
207
Septal leads of heart
V1 | V2
208
What artery is seen by septal leads of heart
LAD
209
Anterior leads of heart
V3 | V4
210
Lateral leads of heart
I aVL V5 V6
211
What artery is seen by anterior leads of heart
LAD
212
What artery is seen by lateral leads of heart
Circumflex
213
Which leads show anterolateral aspect of heart
I aVL V3 - 6
214
Which artery is seen by anterolateral leads of heart
LCA
215
Systematic ECG checklist
``` Basics (name, paper, speed, calibration) Rate Rhythm Axis Waves (P, QRS, T) Intervals (PT, ST, QT) ```
216
Regular ECG paper speed
25mm/s | 1 small box = 0.04s
217
Regular ECG paper calibration
10mm = 1mV
218
Calculating HR from regular ECGs
Divide 30 by no. large boxes between 2 successive QRS complexes
219
Calculating HR from rhythm strip
Count no. QRS complexes and x6
220
What do ACS' include
STEMI NSTEMI Unstable angina
221
What causes CAD
Narrowing of coronary arteries due to atherosclerosis (lipid deposition, infl and thrombosis)
222
What does CAD incl
ACS - STEMI, NSTEMI, UA | C/c angina
223
Calculating risk of CAD
QRISK 2/3
224
What layer of the vessels are usually affected by CAD
Intima
225
Pathophysiology of stable angina
Ischaemia is due to combo of fixed vessel narrowing and abnormal vascular tone
226
What does the effect of a stenosis on blood flow depend on
The degree on narrowing of epicardial vessel | The amount of compensatory vasodilation that arterioles can achieve
227
What causes abnormal vascular tone
Endothelial dysfunction
228
What can abnormal vascular tone result in
Inappropriate vasoconstriction of coronary arteries | Loss of normal antithrombotic properties
229
What happens in coronary stenosis
Metabolic hyperaemia can no longer match myocardial perfusion to myocardial oxygen demand in exercise
230
Location of angina
Retrosternal, diffuse (not localised) | May involve both sides chest (L>R), arms (L>R), neck, lower jaw, upper abdomen
231
Character of angina pain
Pressure, tightness or heavyweight. sometimes 'burning'
232
Angina pain in the neck
'Choking' sensation
233
Angina pain in lower jaw
'toothache' sensation
234
Precipitating factors of angina
Provoked by exertion (esp by walking uphill) | More easily provoked after heavy meal/ cold weather
235
Relief of angina
Rapid relief (2 mins) w/ GTN
236
Duration of angina attacks
Last a few mins (NOT v brief or v prolonged)
237
Stable angina - pathophysiology
Lumen narrowed by plaque | Inappropriate vasoconstriction
238
Unstable angina - pathophysiology
Plaque rupture Platelet aggregation Thrombus formation Unopposed vasoconstriction
239
Criteria for typical angina
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
Criteria for atypical angina
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
Cardiac ddx for recurrent chest pain
Angina | Pericarditis - sharp pain
242
GI ddx for recurrent chest pain
Reflux (GORD) Peptic ulcer Oesophageal spasm Biliary colic
243
MSK ddx for recurrent chest pain
Costochondral syndrome | Cervical radiculitis
244
Pulmonary ddx of recurrent chest pain
Pneumothroax PE Pneumonia
245
1st line tests for suspected angina
ECG
246
2nd line tests for suspected angina
CT coronary angiogram
247
3rd line test for suspected angina
Stress tests
248
Stress tests for angina
Exercise ECG Myocardial Perfusion Imaging Stress Echocardiograph Stress MRI
249
Imaging for angina
Non invasive - CT coronary angiogram | Invasive - Coronary angiogram
250
1st line ix for suspected angina in those w/ known CAD
Stress tests
251
Which region of heart is affected first by ischaemia
Subendothelial region as furthest from blood supply
252
Subendothelial injury on ECG
ST depression
253
Transmural injury on ECG
ST elevation
254
What is a MI
Myocardial infarction Necrosis of myocardial cells caused by occlusion of coronary vessels Complete and persistent = STEMI Partial/ intermittent = NSTEMI/UA
255
Possible effects of atherosclerotic plaque rupture
Asymptomatic - reabsorption into plaque | Occlusive - infarction
256
Reperfusion therapy for MI
PCI within 2 hrs | Fibrinolysis
257
ECG changes in STEMI
ST elevation | May also see L BBB
258
ECG appearance in NSTEMI
T wave inversion ST depression May see pathological Q waves
259
Where is troponin found
Skeletal muscle | Cardiac muscle
260
Cardiac spp troponin
I and T
261
Measuring troponin
Blood test
262
When is the result of troponin levels significant
At least one value >99th percentile of the upper reference limit
263
Non-cardiac symptoms that can elevate troponin
``` Exercise Chronic renal failure Sepsis Myocarditis Aortic dissection PE ```
264
If a pt is having ACS symptoms but ECG has no pathological changes and has normal troponin levels, what is the suspected dx
Unstable angina
265
When is troponin measured for suspected ACS
On admission and couple hrs after
266
Troponin levels after MI
Starts to rise at 3-4hrs and returns to baseline at 10-14 days
267
Serum biomarkers in MI
CK-MB | Troponin
268
Complications of MI
ACT RAPID ``` Arrhythmias Congestive cardiac failure/ cardiogenic shock Thromboembolism Rupture Aneurysm Pericarditis Ischaemia Dressler's syndrome/ death ```
269
What can rupture after an MI
Ventricular wall Septum Papillary muscle
270
Main late complications of MI
Heart failure | Arrhythmia
271
Why does coronary stenosis usually cause angina only during exercise/stress
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
How does coronary stenosis of 70% affect blood flow
Blood flow isn't compromised at rest or exercise
273
What is coronary stenosis of 70-80% associated with
Decreased blood flow on exercise on exercise but not at rest
274
What is coronary stenosis of >80% associated with
Compromise of blood flow both at rest and exertion
275
What condns affect myocardial oxygen supply
Coronary stenosis Anaemia Lung problems
276
Factors affecting myocardial demand
``` Tachycardia Pre-load Afterload Muscle mass (e.g. hypertrophy/ infarction) Muscle contractility ```
277
Optimum medical therapy for angina
2 anti-anginal drugs
278
1st line drugs for angina
Beta blockers - aim for resting HR to 50-60 bpm
279
2nd line drugs for angina
Long-acting oral nitrates e.g. isosorbide mononitrate added onto BB
280
3rd line treatments for angina
Ca-channel blockers | Consider angioplasty
281
What procedure should be considered if angina is not controlled
Revascularisation
282
Ix for stable angina
``` Exercise stress tests MIBI CTCA Stress MRI Dobutamine stress Echo Coronary angio Bloods ```
283
Usual approach for coronary angiography
Radial artery
284
Indications for PCI - stable angina
Limiting symptoms despite 2 anti-anginals 1,2,3 vessel or LMS disease Less complex disease (SYNTAX score <22)
285
Best graft for CABG
Internal mammary/thoracic artery
286
Indications for CABG
Left Main Stem disease (>50% stenosis) Proximal 3 vessel disease Complex disease (high risk score)
287
Asociated symptoms in MI
``` SOB Leg swelling (heart failure) Hypotensive symptoms - paleness, clamminess etc Feeling of impending doom Emesis ```
288
Who have silent MI's
Diabetics - usually present with atypical chest pain
289
Bloods for suspected ACS
``` FBC (anaemia) U&Es (prior to ACEi and other meds) LFTs (statins) Thyroid function tests Lipid profile Hba1c and fasting glucose (DM) ```
290
What may be seen on CXR after ACS
Pulmonary oedema | Widened mediastinum
291
How is pulmonary oedema treated
Oxygen | IV loop diuretic e.g. furosemide
292
Why do MI pts have follow up ECGs after px
Assess functional damage
293
Why may ACS pts have a CT angio
Asess for CAD
294
When is thrombolysis done for ACS
If PCI is unavailable within 2 hrs (risk of bleeding) | ECG done 60-90 mins after
295
A/c NSTEMI therapeutics
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
GRACE score to assess for PCI
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
Dressler's syndrome
Post-myocardial infarction syndrome Usually occurs 2-3 wks after an MI Caused by localised immune repose and cause pericarditis
298
2' prevention after MI - medical mx
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
2' prevention after MI - lifestyle
``` Stop smoking Reduce alcohol Mediterranean diet Cardiac rehab Optimise treatment of other medical condn e.g. DM, HTN ```
300
ECG for suspected posterior MI
Use posterior chest wall leads V7 - V9
301
ECG for suspected right MI
Use right sided leads - move V4 to opposite side
302
Where is the mediastinum found
Middle part of thoracic cavity | Between pleural spaces
303
What is found anteriorly to mediastinum
Manubrium | Body of sternum
304
What is found posteriorly to mediastinum
Vertebral column (T1 -T12)
305
What is found laterally to mediastinum
Parietal pleura
306
What is found superior to mediastinum
Superior thoracic aperture
307
What is found inferior to mediastinum
Internal thoracic aperture
308
Superior mediastinum
Above level of thoracic plane (sternal angle)
309
Inferior mediastinum
Below level of thoracic plane (sternal angle)
310
What can inferior mediastinum be divided into
Anterior Middle Posterior
311
What level is the thoracic plane found at
Level of 2nd rib anteriorly and 4th thoracic vertebrae posteriorly
312
Structures found in superior mediastinum
``` Trachea Oesophagus Arch of aorta (+ branches) Superior vena cava Vagus nerves Phrenic nerves L recurrent pharyngeal nerve ```
313
Structures found in anterior mediastinum
Thymus
314
Structures found in middle mediastinum
``` Heart Pericardium Phrenic nerves Ascending aorta Pulmonary trunk ```
315
Structures found in posterior mediastinum
``` Oesophagus Sympathetic chain Azygous vein Thoracic duct Descending duct Vagus nerve ```
316
What does the carotid sheath contain
Common carotid artery Internal jugular vein Vagus nerve
317
Recurrent laryngeal nerve
Wraps around subclavian artery | Innervates intrinsic muscles of larynx - motor
318
What do phrenic nerves innervate
Diaphragm Mediastinum Mediastinum floor
319
Which vessels are found in inferior mediastinum
Internal thoracic vessels
320
What is the heart encased in
Pericardial sac
321
Pericardial sac layers
Outer, fibrous layer | Serous pericardium layers
322
What are the serous layers of the pericardium
Parietal pericardium | Visceral pericardium
323
What does outer, fibrous layer of pericardium do
Helps keep heart in place in case of pneumothorax
324
What does outer, fibrous layer of heart attach to
Great vessel superiorly and central tendon of diaphragm inferiorly
325
What does the serous pericardium layers secrete
Little amount of serous fluid so heart is able to move around
326
Where are phrenic nerves found
L and R of heart
327
Where do phrenic nerves branch from spinal cord
C3, C4 & C5
328
What do phrenic nerves innervate
Hemi diaphragm
329
Where do coronary arteries originate from
Root of aorta - aortic sinus
330
How many aortic sinuses are there
3 but only L and R sinuses are origin of coronary arteries
331
Where does the RCA come from
R sinus
332
Where does the RCA pass
Laterally between atria-ventricular groove - coronary sulcus
333
Branches of RCA
Sino-atrial nodal artery Diagonal branches R marginal artery Posterior interventricular branch (posterior descending artery)
334
Where does the R marginal artery travel
Lateral margin of L ventricle to apex
335
Branches of LCA
``` Anterior interventricular (anterior descending artery) Circumflex artery ```
336
What does the LAD supply
Mainly L ventricle
337
What does heart drain into
Coronary sinus
338
Myocardial bridge
Myocardium covering of LCA - can only see branches
339
When do you give furosemide for STEMI
When presenting with symptoms of acute heart failure
340
What ix could be useful in pts presenting w/ chest pain
Nuclear med - imaging spread of radioactive material
341
When is angiography not as useful
Pts with AF, tachycardia or build up of Ca
342
Features of UA
Cardiac chest pain (at rest) Abnormal/ normal ECG Normal troponin
343
Features of NSTEMI
Cardiac chest pain Abnormal/ normal ECG (no ST-elevation, repolarisation abnormalities) Raised troponin
344
Can you dx a STEMI if the pt has no ST elevation
Yes, if new LBBB is present
345
STEMI algorithm
ROMANCE ``` Reassure Oxygen - sats >94% Morphine 10mg (+ antiemetic) Aspirin 300mg stat Nitrates - GTN prn Clopidogrel 300mg/ Ticagelor 180mg stat Enoxaprin 2.5mg ```
346
Driving after ACS
If the pt had an angioplasty, banned for a week | If no angioplasty, banned for 1/12
347
Initial ACS mx
MONA Morphine (anti-emetic) Oxygen if needed Nitrates Aspirin 300mg stat
348
Mx of Dressler's syndrome
High dose aspirin

MBBS - Year 2 (20 decks)

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