1. Cardio Phase 1a Miles Benjamin Daniel Bradbury
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2. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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3. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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4. Muscle Action potential arrives at sarcomere.
Opening of Ca2+ channels.
Influx of calcium ions.
Initiates muscle contraction.
The heart is a muscular pump, and operates pretty much in the same manner.
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5. Troponin Three types of troponin:
Troponin C – calcium binds to cause a conformational change in Troponin I.
Troponin T – binds to tropomyosin, forming a tropomyosin – troponin complex.
Troponin I – inhibtory binds to actin, to hold the tropomyosin – troponin complexes in place.
Troponin is important complex of proteins
Attatched to tropomysosin
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6. Cardiac Contraction Contraction of involuntary striated muscle.
Controlled by Ca2+
Increase in concentration causes contraction
Sliding filament theory
Troponin is comprised of a complex of three proteins. – I T and C
It is attatched to tropomyosin.
When Calcium binds to Troponin C, the whole tropomyosin rolls out the way and allows the actin-myosin bridge to be formed.
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7. So …
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8. The Cardiac Cycle
The cariac cycle is the contolled contraction of all the sarcomeres in the heart – to enable EFFECTIVE pumping of blood to the bodies tissues.
Systole = contraction
Diastole = relaxation and coronary supply.
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9. Atrial Systole Contraction of the left and right atria.
blood pressure in atria increases forcing blood into the ventricles.
begins with the onset of the ‘P’ wave on ECG
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10. Ventricular Systole
Ventricular systole is the contraction of the left and right ventricles.
Blood is forced out of the pulmonary and aortic valves
“Lubb – Dub”
Lubb is the closure of AV valves at beginning of ventricular systole.
Dub is the closure of aortic and pulmonary at end of ventricular systole.
QRS complex
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11. Diastole When do coronary arteries perfuse heart tissue with blood?
In diastole the heart is in an mostly un-contracted state
As pressure drops in ventricles, AV valves open. Blood begins filling chambers again.
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12. CO = SV x HR Leaving the heart Cardiac Output SV = Stroke Volume
HR = Heart Rate
5+ litres a minute
Are ventricles pumping effectively?
Lower heart rate in athletes with big cardiac output.
Very high heart rate in people with MI etc.
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13. Electro Cardiography
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14. Main waves P wave QRS complex T wave
Atrial depolarization, SA node towards the AV node, spreads from the right to left atrium.
QRS complex
 Rapid depolarization of the right and left ventricles. Larger muscle so larger amplitude.
T wave
Repolarisation of the ventricles.
More components such at ST segment, QT interval etc etc. Wikipedia page on ECG very useful – good animations etc.
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15. The whole contraction takes around 0. 8 seconds. (0. 6 – 1
The whole contraction takes around 0.8 seconds. (0.6 – 1.2 seconds) = 60 to 100 bpm.
P wave about 0.08 seconds
PR interval 0.12 – 0.2 seconds
QRS is less than 0.12 seconds
T wave about 0.16 seconds
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16. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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17. Mean Arterial Pressure
Definition
The average arterial blood pressure over the entire cardiac cycle
Formula?
MAP is the term used to describe the average blood pressure in an individual.
It is the most important pressure description you can get because it descirbes the pressure driving blood into the tissues and is averaged over the entire cardiac cycle.
CO = HR x SV x TPR
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18. Physiology Definition Formula? Mean Arterial Pressure (MAP) Total
The average arterial blood pressure over the entire cardiac cycle
Formula?
Mean
Arterial
Pressure
(MAP)
Total
Peripheral
Resistance
(TPR)
Cardiac
Output
(CO)
MAP is the term used to describe the average blood pressure in an individual.
It is the most important pressure description you can get because it descirbes the pressure driving blood into the tissues and is averaged over the entire cardiac cycle.
CO = HR x SV x TPR = x
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19. Cardiac Output Definition Formula?
Volume of blood ejected by each ventricle per minute
Formula?
So in more detail, the cardiac output refers to the volume of blood flowing through systemic (flowing through the body as a whole) or pulmonary (flowing through the lungs) circuit per minute
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20. Physiology Definition Formula? Cardiac Output (CO) Heart Rate (HR)
Volume of blood ejected by each ventricle per minute
Formula?
Cardiac
Output
(CO)
Heart
Rate
(HR)
Stroke
Volume
(SV)
So in more detail, the cardiac output refers to the volume of blood flowing through systemic (flowing through the body as a whole) or pulmonary (flowing through the lungs) circuit per minute
CO measure in litres/minute = x
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21. Physiology Definition
Total resistance to flow of blood by all systemic blood vessels
Which level of blood vessel offers the most resistance?
Arterioles offer the most resistance to vascular flow as they can be changed by vasoconstriction or vasodilation
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22. Physiology Controlling TPR Locally Extrinsic
Active hyperaemia  ↑ demand by organ = vasodilation
Flow autoregulation  ↓ supply to organ = vasoconstriction
Extrinsic
Autonomic nervous system
Hormones  whole host of vasodilators/constrictors NO
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23. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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24. Atherosclerosis
Definition - Formation of plaques in the intimal layer of medium to large sized arteries. HARDENING OF THE ARTERIES
A disease of the arteries characterized by the deposition of plaques of fatty material on their inner walls.
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25. Atherosclerosis Pathophysiology
LDL oxidation → macrophages & lymphocytes to absorb oxidised LDL → foam cells. White cells
cannot process oxidised LDLs → inflammation & continuation of cycle. Fatty streak → fibrous plaque → atherosclerotic plaque
high levels of LDL in the blood will begin to accumulate in the arterial wall. It may be that these lipid deposition sets off an inflammatory reaction, and the macrophages are attracted like they would be to any type of inflammation.
The macrophages entering the arterial wall will come into contact with these lipid cores, and will take up the oxidized LDL,becoming foam cells. The macrophages will also be activated by the inflammatory products released by the arterial wall.
The foam cells can die, and they release their products, causing the formation of a pool of lipid. This pool is called a lipid core.
The activated macrophages will release lots of their own products. These include cytokines and growth factors, particularly PDGF.These growth factors lead to proliferation of the smooth muscle layer. It will proliferate towards the lipid pool, and in an attempt to repair and stabilise the lesion, it may form a layer around the pool. The smooth muscle cells change their phenotype from contractile, to repair – they now permanently become repair type cells.
If this process of repair is successful, the plaque will be a stable atherosclerotic plaque and will remain asymptomatic, unless it grows big enough to occlude an artery.
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26. high levels of LDL in the blood will begin to accumulate in the arterial wall. It may be that these lipid deposition sets off an inflammatory reaction, and the macrophages are attracted like they would be to any type of inflammation.
The macrophages entering the arterial wall will come into contact with these lipid cores, and will take up the oxidized LDL,becoming foam cells. The macrophages will also be activated by the inflammatory products released by the arterial wall.
The foam cells can die, and they release their products, causing the formation of a pool of lipid. This pool is called a lipid core.
The activated macrophages will release lots of their own products. These include cytokines and growth factors, particularly PDGF.These growth factors lead to proliferation of the smooth muscle layer. It will proliferate towards the lipid pool, and in an attempt to repair and stabilise the lesion, it may form a layer around the pool. The smooth muscle cells change their phenotype from contractile, to repair – they now permanently become repair type cells.
If this process of repair is successful, the plaque will be a stable atherosclerotic plaque and will remain asymptomatic, unless it grows big enough to occlude an artery.
What’s in the plaque? Lipid Core, fibrous cap, macrophages, smooth muscle cells, t lymphocytes
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27. Atherosclerosis Risk Factors Age FH Obesity Male Smoking
Diabetes Mellitus
Hyperlipidaemia
Hypertension
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28. Outcomes of Atherosclerosis
Angina
Claudication MI
Aneurysm
Claudication =  impairment in walking, or pain, discomfort or tiredness in the legs that occurs during walking and is relieved by rest. Due to ischaemia Angina = Reduced blood flow in coronary arteries
MI – infarction of coronary arteries due to rupture of a plaque
Aneurysm -
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29. Angina Atherosclerosis of coronary arteries Pathophysiology
Increased demand without proportional increase in oxygen supply
Clincal Features
SOB, Nausea, Fatigue, Chest Pain
Stable vs. Unstable
Progressive lumen narrowing
Stenosis of >50%
Reversible tissue ischaemia during effort
Coronary arteries
*stable <5min attacks OE
*unstable >5min attacks(no trigger)
*SOB
*nausea/dizziness
*fatigue
Stable angina is usually due to the heart working too hard for its regular blood supply, and typically goes away after a rest period; the "stable" in the name refers to its predictability---it will come back with the same level of exertion.  Unstable angina may refer to any chest pain that isn't "stable"---pain that a patient is experiencing for the first time, that is getting worse or more frequent, or that is occurring with less exertion or at rest. It is usually considered more serious than stable angina, and should generally be thought of as an emergency. 
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30. Angina Diagnosis Treatment
ECG (ST depression), exercise tolerance, coronary angiogram
Treatment
Immediate= GTN Spray
Long Term= ????????
Progressive lumen narrowing
Stenosis of >50%
Reversible tissue ischaemia during effort
Coronary arteries
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31. Atherosclerosis – Angina
Diagnosis
ECG (ST depression), exercise tolerance, coronary angiogram
Treatment
Immediate= GTN Spray
Long Term= Statins, Beta Blockers, Antiplatelets: ACE inhibitors, Calcium Channel blockers
Long Term:
Why? gtn Statins: Beta Blockers Antiplatelets: ACE inhibitors: Calcium Channel blockers:
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32. Atherosclerosis – MI Complete blockage of coronary artery
Clinical Features
Severe crushing chest pain, Dyspnoea, Nausea, Sweating, Feeling of terror
Diagnosis
ECG, Bloods, Raised Cardiomyocyte
Treatment
Antiplatelet, BB,Statins, PCI
Blockage due to clots or atherosclerosis
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33. Intermittent Claudication
Ischaemia, usually do to atherosclerosis
Typically presents as elderly person who gets leg pain when walking
After they rest for a few minutes the pain goes away and they can start walking again
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34. Aneurysm Localised, permanent dilation of artery
Can be asymptomatic until it ruptures
Ruptured abdominal aneurysm causes sudden severe abdominal pain – surgical emergency
Aortic dissection – blood between layers of aorta
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35. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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36. Thromboembolism Deep vein thrombosis Pulmonary embolism
A thrombus is a blood clot that forms in a vessel and remains there
Embolism is the lodging of a an embolus into a narrow capillary
Virchow's triad describes the three broad categories of factors that are thought to contribute to thrombosis.
Virchow's Triad
Stasis
Blood Constituents
Vessel Wall
In lungs = pulmonary embolism
In brain = stroke
In legs = DVT
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37. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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38. Shock Symptoms: Rapid, shallow breathing
An acute failure of the CVS to perfuse the tissues
Hypovolaemic – blood loss
Anaphylactic – type I hypersensitivity
Septic – vasodilation caused by bacterial toxins
Cardiogenic – heart failure
Symptoms: Rapid, shallow breathing
Faintness,l ight headness, diziness, reduce level of consciouness. Rapid, weak pulse, Muscle weakness ooliguria Skin: Sweating + pallor cold
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39. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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40. Heart Failure
Where the heart is unable to pump enough blood to satisfy the needs of the metabolising tissues.
Breathlessness, tiredness and fatigue are associated with a cardiac abnormality that reduces cardiac output.
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41. Left Heart Failure Fatigue and weakness Exertional breathlessness
Orthopnoea
paroxysmal nocturnal dyspnoea
Cough / pulmonary oedema – crackles in ;lung bases.
Orthopnea = SOB when lying flat
Think in heart failure where the blood is getting backed up in the venous system.
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42. Right Heart Failure Swollen ankles Fatigue
Raised jugular venous pressure
Abdominal swelling/hepatomegaly
Pitting oedema
Ascites
Could be cor pulmonale – query PE, COPD etc.
Ascites – acculmulation of fluid in the peritoneal space.
Think in heart failure where the blood is getting backed up in the venous system.
Cor pulmonale = right sided heart failure in response to pulmonary hypertension.
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43. Congestive Heart Failure
Both!
Very often a case of right heart failure due to severe left failure.
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44. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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45. Arrhythmias Abnormal electrical activity in the heart. Too fast?
Too slow?
Uncoordinated?
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46. Normal ECG
TIME IN ECG!!!
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47. Bradycardia Slow heart rate (< 60bpm)
Sinus node disease, AV block, MI, beta blockers.
non-cardiac
e.g.raised ICP
hypothermia
hypothyroidism
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48. Bradycardia
AV Block
First degree – delayed conductance, prolongation of PR interval.
Second degree – when one or more impulses fail to reach ventricles.
Mobitz 1: progressive lengthening of PR interval each successive complex until a P wave is not conducted.
Mobitz 2: PR interval constant, QRS complexes dropped intermittently or in fixed ratio to P wave rate.
Third degree – No conductance from atria to ventricles. Complete dissociation of P Waves and QRS complexes. Rate / min
Impaired conductance between atria and ventricles.
Ventricles have to pace themselves rather than SAN.
Caused by ischaemia, infarction, fibrosis or drugs
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49. Tachycardia Sinus tachycardia. Rate > 100/min Causes Exercise
Thyrotoxicosis
Catecholamine stimulation (emotion)
Fever
Anaemia
Cardiac failure
Hypovolaemia
Caused by Idiopathic Acute MI, Congenital,Post cardiac surgery, Deposition diseases (amycoid, sarcoid), Infections (e.g. Lyme disease, chronic brucellosis), Drug toxicity (e.g. Digoxin, Beta Blockers, Verapamil)
Too fast bro? Not a big stroke volume innit.
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50. Supra Ventricular Tachycardia
Symptoms include palpitations - sudden onset
sudden offset or gradually tails away
few seconds to hours/days
Precipitating factors
Tea, coffee, tobacco, alcohol, exercise,
emotional upset
Rate /min
P-waves may or may not be present
Caused by Idiopathic Acute MI, Congenital,Post cardiac surgery, Deposition diseases (amycoid, sarcoid), Infections (e.g. Lyme disease, chronic brucellosis), Drug toxicity (e.g. Digoxin, Beta Blockers, Verapamil)
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51. Atrial Fibrilation Irregularly irregular rhythm
Atrium discharge at very high rates /min
Ventricular rate slower and irregular
Irregularly irregular – all over the shop
AF can cause coagulation problems eg formation of clots that cause PE or CVA
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52. Atrial Fibrilation
Causes: Cardiac - Idiopathic - Rheumatic heart disease - Ischaemic heart disease - Cardiomyopathy - WPW syndrome Non-cardiac - Alcohol - Carcinoma of bronchus - Pneumonia - PE Treatments include aspirin/warfarin (for anticoag) and then drugs to alter rate (beta blockers). Pacemakers, implantable defibs?
Irregularly irregular – all over the shop
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53. Atrial Flutter Macro re-entry circuit within right atrium
On ECG there is a saw tooth pattern
atrial rate 300/min
ventricular rate commonly 150/min
Treatment
anticoagulants as for AF
Drugs
rate control difficult
DC cardioversion
ablation
Caused by Idiopathic Acute MI, Congenital,Post cardiac surgery, Deposition diseases (amycoid, sarcoid), Infections (e.g. Lyme disease, chronic brucellosis), Drug toxicity (e.g. Digoxin, Beta Blockers, Verapamil)
Ablation – destroy areas of defective heart causing the problem.
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54. Ventricular Tachycardia
Broad and complex
Can well tolerated.
Risk factor for hypotension.
Wide QRS with shift to left.
Deep S wave.
Treat with drugs (lidocaine) and DC cardioversion.
Implantable defib?
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55. Ventricular Fibrilation
Uncoordinated contraction of ventricles.
Quiver rather than contract.
Usually lead to cardiac arrest > cardiogenic shock.
Treatement
Immediate life support
999
Defibrilation
PCI
Usually as the result of an MI.
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56. Outline Physiology Pathology Clinical Problems
Mechanical activity of heart
Regulation of Mean Arterial Pressure (MAP)
Pathology
Atherosclerosis
Thromboembolism
Shock
Heart Failure
Arrhythmias
Clinical Problems
Chest Pain
Leg Pain
Murmurs
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57. Leg Pain 74 year old man Diabetes Mellitus and Hypertension
Heavy Smoker
Sharp pain in his calves when walking
Has to stop walking to relieve pain
Intermittent claudicatoin
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58. Intermittent Claudication
Characterised by cramp-like pain in the legs on exercise
Muscles deprived of oxygen → lactate production → pain
Occurs after a certain distance and settles on rest after a certain time
Caused by atherosclerosis of one or more of the arteries supplying the lower limb
Same risk factors as for MI
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59. Chest Pain
A 61 year old man presents complaining of increasing SOB on exertion and tiredness. Previous MI 9 weeks ago. You diagnose heart failure. What is the pathophysiological definition of ‘heart failure’? (4) How does left heart failure lead to pulmonary oedema? (6) 3 reasons why people with heart failure experience a progressive decline in cardiac function (3x2) Another symptom for left ventricular failure besides shortness of breath and fatigue? (2)
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60. Murmur
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