Cardiovascular Flashcards
(154 cards)
1
Q
Name 6 things an ECG can identify
A
- Arrhythmias
- Myocardial infarction / ischaemia
- Pericarditis
- Chamber hypertrophy
- Electrolyte disturbances
- Drug toxicity
2
Q
What is the SA node?
A
The dominant pacemaker with an intrinsic rate of 60-100bpm
3
Q
What is the AV node?
A
The backup pacemaker with an intrinsic rate of 40-60bpm
4
Q
What are the ventricular cells?
A
Backup pacemaker cells with an intrinsic rate of 20-45bpm
5
Q
Describe the impulse conduction pathway
A
> Sinoatrial node > AV node > Bundle of His > Bundle branches > Purkinje fibres
6
Q
What is the P wave?
A
Atrial depolarisation - seen in every lead apart from aVR
7
Q
What is the PR interval?
A
Time taken for the atria to depolarise and electrical activation to get through the AV node
8
Q
What is the QRS complex?
A
Ventricular depolarisation
9
Q
What is the ST segment?
A
Interval between depolarisation and repolarisation
10
Q
What is the T wave?
A
Ventricular repolarisation
11
Q
Define dextrocardia
A
Heart on the right side of the chest instead of the left
12
Q
What does an ECG of an acute ANTEROLATERAL myocardial infarction look like?
A
ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads
13
Q
What does an ECG of an acute INFERIOR MI look like?
A
ST segments are raised in inferior leads (II, III, aVF)
14
Q
Why can’t you see atrial repolarisation on an ECG?
A
It happens at the same time as the QRS complex
15
Q
On an ECG, how much should one small box across represent? How much should one large box across represent?How much should one large box vertically represent?
A
ACROSS;
One small box = 0.04s
One large box = 0.5
VERTICALLY;
One large box = 0.5mV
16
Q
Where can you palpate the left ventricle?
A
5th left intercostal space in the mid-clavicular line - responsible for the apex beat
17
Q
Define stroke volume
A
Volume of blood ejected from each ventricle during systole
18
Q
Define cardiac output
A
Volume of blood each ventricle pumps out as a function of time
19
Q
What is the equation for cardiac output?
A
CO (L/min) = Stroke volume (L) x Heart rate (BPM)
20
Q
Define total peripheral resistance
A
Total resistance to flow in systemic blood vessels from beginning of aorta to vena cava
21
Q
Define preload
A
Volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction
22
Q
Define afterload
A
Pressure the left ventricle must overcome to eject blood during contraction
23
Q
Define contractility
A
Force of contraction and the change in fibre length during systole
24
Q
Define elasticity
A
Myocardial ability to recover normal shape after systolic shape
25
Define diastolic dispensibility
The pressure required to fill the ventricle to the same diastolic volume
26
Define compliance
How easily the heart chamber expands when filled with blood
27
What is Starling's law?
Force of contraction is proportional to end diastolic length of cardiac muscle fibre
The more the ventricle fills, the harder it contracts
28
How does standing affect BP?
Standing decreases venous return due to gravity
> cardiac output decreases
> drop in blood pressure
> stimulating baroreceptors to increase blood pressure
29
What is heart sound S1?
Mitral and tricuspid valve closure
30
What is heart sound S3?What does it sound like?
Early diastole during rapid ventricular filling
It is normal in children and pregnant children, but is associated with mitral regurgitation and heart failure
KENTUCKY
31
What is heart sound S4?
"gallop" in late diastole, produced by blood being forced into a stiff hypertrophic ventricle
Associated with left ventricular hypertrophy
TENNESSEE
32
Which coronary arteries are prone to atherosclerosis?
- Circumflex
- Left anterior descending (LAD)
- Right coronary arteries
33
What are the risk factors of atherosclerosis?
- Age
- Tobacco
- High serum cholesterol
- Obesity (more pericardial fat -> increased inflammation)
- Diabetes
- Hypertension
- FHx
34
How are atherosclerosis plaques generally distributed in the body?
- Within peripheral and coronary arteries
| - Focal distribution along artery length
35
Describe the structure of an atherosclerotic plaque
Complex lesion of;
- lipids
- necrotic core
- connective tissue
- fibrous "cap"
36
What will eventually happen to an atherosclerotic plaque?
- Occlude the vessel lumen > ANGINA
| - Rupture > THROMBUS FORMATION
37
Briefly describe the process of initial atherosclerosis formation
1. Endothelial cell injury causing endothelial dysfunction
2. Chemoattractants released from endothelium which attract leukocytes
3. Leukocytes accumulate and migrate into vessel wall
4. More chemoattractants released from injury site
38
What inflammatory cytokines are found in atherosclerotic plaques?
- IL-1 (MAIN ONE)
- IL-6
- IFN-gamma
39
What are fatty streaks?
- Earliest lesion of atherosclerosis
- Begin forming <10yrs old
- Consist of aggregations of lipid-laden macrophages and T lymphocytes within intimal layer of vessel wall
40
What are intermediate lesions?
Composed of layers of;
- Lipid laden macrophages (foam cells)
- Vascular smooth muscle cells
- T lymphocytes
There is adhesion and aggregation of platelets to vessel wall
41
How does aspirin prevent thrombus formation?
Aspirin inhibits platelet aggregation
42
What is the fibrous cap of advanced atherosclerotic lesions made of?
Extracellular matrix proteins (e.g. collagen and elastin) laid down by smooth muscle cells that overlie the lipid core and necrotic debrisIt may be calcified
43
What makes up an advanced lesion / fibrous plaque?
- Smooth muscle cells
- Macrophages / foam cells
- T lymphocytes
- Red cells
44
Describe plaque rupture
1. Plaque constantly growing and receding
2. Fibrous cap needs to be resorbed and redeposited in order to be maintained
3. If balance shifts (e.g. in favour of inflammatory conditions - increased enzyme activity), then the cap becomes weak and the plaque ruptures
4. Basement membrane, collagen, and necrotic tissue is exposed
5. Haemorrhage of vessel within plaque
6. Thrombus formation and vessel occlusion
45
What is angina?
Chest pain or discomfort as a result of reversible myocardial ischaemia
46
What is usually meant by "reversible myocardial ischaemia"?
Narrowing of one or more of the coronary arteries
47
What are the three types of angina? Explain them
Stable
- Induced by effort, relieved by rest
Unstable
- Angina of recent onset (< 24hrs)
- Deterioration in previously stable angina, with symptoms occurring at rest
Prinzmetal's angina
- Caused by coronary artery spasm (rare)
48
What causes mismatch between coronary blood supply and metabolic demand?
- Atheroma / stenosis of coronary arteries
- Valvular disease
- Aortic stenosis
- Arrhythmia
- Anaemia (thus, less O2 is transported)
49
Why does ischaemia cause pain?
Ischaemic metabolites (e.g. adenosine) stimulate nerve ending and produce pain
50
Is angina more common in men or women?
Men
51
Name 9 risk factors for angina
- Smoking
- Sedentary lifestyle
- Obesity
- Hypertension
- Diabetes mellitus
- Family history
- Genetics
- Age
- Hypercholesterolaemia
52
What are the 4 stages of angina?
1. Initiation
2. Adaptation
3. Clinical stage
4. Pathological stages
53
Describe the initiation stage of atherosclerosis
- Endothelial injury results in lipid accumulation in the intimal layer of the vessel
- Endothelial cells secrete chemoattractants
- Monocytes arrive and proliferate into macrophages in the presence of oxidised LDL
- Macrophages ingest oxidised LDL and turn into foam cells, forming a lipid core in the intimal layer
- Mural thrombus forms and subsequent healing takes place
54
Describe the adaptation stage of atherosclerosis
- Plaque progresses to 50% of lumen size, and vessel can no longer compensate by remodelling
- Drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix
- Progresses to unstable plaque
55
Describe the clinical stage of athersclerosis
- Plaque continues to grow but runs risk of haemorrhage or exposure of tissue HLA-DR (which might stimulate T cell accumulation)
- Drives inflammatory reaction against plaque
56
What is an intimal cell mass?
Collection of muscle cells and connective tissue without lipids
57
Describe the composition of an atheromatous plaque
- Distorted endothelial surface containing lymphocytes, macrophages, smooth muscle cells, and damaged endothelial cells
- Local necrotic and fatty matter with scattered foam cells
- Evidence of local haemorrhage with iron deposition and calcification
58
Name four complications of plaque rupture
- Acute occlusion due to thrombus
- Chronic narrowing of vessel lumen with healing of the local thrombus
- Aneurysm change
- Embolism of thrombus +/- plaque lipid content
59
What is the clinical presentation of angina?
- Central chest tightness / heaviness
- Provoked by exertion, especially after;
> eating
> cold windy weather
> anger / excitement
- Relieved by rest or GTN spray
- Pain may radiate to arms, neck, jaw, or teeth
- Dyspnoea, nausea, sweatiness, faintness
60
How do you score angina?
1 point = central / tight / radiation
2 points = precipitated by exertion
3 points = relieved by rest / GTN spray
```
1/3 = non-anginal pain
2/3 = atypical pain
3/3 = typical angina
```
61
What are the differential diagnoses for angina?
- Pericarditis / myocarditis
- Pulmonary embolism
- Chest infection
- Dissection of aorta
- GORD
62
Name five methods of diagnosing angina
- 12 lead ECG
- Treadmill test / Exercise ECG
- CT scan calcium scoring
- SPECT / myoview
- Cardiac catheterisation
63
How do you use a 12 lead ECG to diagnose angina?
- Often normal
- May show ST depression
- Flat or inverted T waves
- Look for signs of past MI
64
Describe the treadmill test for diagnosing angina
1. Put an ECG on a patient, then make up run on an incline treadmill (try to induce ischaemia)
2. Monitor how long patient is able to exercise for
If you see ST segment depression, this is diagnostic of late-stage ischaemia
65
What is the problem with the treadmill test / exercise ECG?
Many patients are unable to use it
E.g. can't walk, unfit, young females, bundle branch block
66
Describe the CT scan calcium scoring
CT the heart and if there is atherosclerosis in the arteries, the calcium will light up white
- Significant calcium = angina
67
Describe the SPECT / myoview for diagnosing angina
1. Radio-labelled tracer injected into patient
2. Taken up by coronary arteries
- Lights up = good blood supply
- Doesn't light up = little blood supply
- No light after exercise = myocardial ischaemia diagnosis
68
Name four methods of treating angina
- Modify risk factors
- Treat underlying conditions - Pharmacologically
- Revascularisation
69
How can you modifiy risk factors to improve angina symptoms?
- Stop smoking
- Encourage exercise
- Weight loss
70
Name 5 types of drugs used to treat angina
- Aspirin
- Statins
- Beta-blockers
- GTN spray
- Ca2+ channel antagonists / blockers
71
How does aspirin help treat angina?
- COX inhibitor - reduces prostaglandin synthesis (inc. thromboxane A2) resulting in reduced platelet aggregation
- Reduces angina events
e. g. SALICYLATE
72
What are the side effects of aspirin?
Gastric ulceration
73
How do statins help treat angina?
- HMG-CoA reductase inhibitors - reduces cholesterol produced by liver
- Reduces angina events and LDL-cholesterol
- Anti-atherosclerotic
74
What are the first line anti-anginal medicines?
- Betablockers
| - GTN spray
75
How do beta blockers help treat angina?
- Reduce force of contraction of heart (e.g. BISOPROLOL and ATENOLOL)
- Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway
- B1 activation > Gs > cAMP to ATP > contraction
76
What do beta blockers 'reduce'?
Reduce;
- Heart rate (negatively chonotropic)
- Left ventricle contractility (negatively inotropic)
- Cardiac output
77
What are the side effects of beta blockers?
- Tiredness
- Nightmares
- Bradycardia
- Erectile dysfunction
- Colds hands and feet
78
What are the contraindications for beta blockers?
- Asthma
- Heart failure / block
- Hypotension
- Bradyarrhythmias
79
How does GTN spray help treat angina?
- Venodilator (nitrate)
- Dilates systemic veins, thereby reducing venous return to right heart
- Reduces preload
- Thus reduces work of heart and O2 demand
- Also dilates coronary arteries
80
What are the side effects of GTN spray?
Strong headache immediately after use
81
How do Ca2+ channel antagonists / blockers help treat angina?
- Primary arterodilators
- Dilates systemic arteries, resulting in BP drop
- Thus reduces after load on the heart
- Thus less energy required to produce same cardiac output
e. g. VERAPAMIL
82
When do you perform revascularisation to treat angina?
- When medical fails
| - High risk angina
83
What two methods are there of revascularising a patient to improve symptoms of angina?
- Percutaneous coronary intervention (PCI)
| - Coronary artery bypass graft (CABG)
84
Describe percutaneous coronary intervention
- Dilating coronary atheromatous obstructions by inflating balloon within it
- Expands plaque = makes artery bigger
85
What are the pros and cons of PCIs?
Pro;
- Less invasive
- Convenient
- Short recovery
- Repeatable
Cons;
- Risk of stent thrombosis
- Not good for complex disease
86
Describe coronary artery bypass graft
Left internal mammary artery (LIMA) used to bypass proximal stenosis in LAD coronary artery
87
What are the pros and cons of CABG?
Pros;
- Good prognosis
- Deals with complex disease
Cons;
- Invasive
- Risk of stroke or bleeding
- One time treatment
- Long recovery
88
What is 'acute coronary syndrome'?
An umbrella term that includes;
- ST-elevation myocardial infarction (STEMI)
- Unstable (crescendo) angina (UA)
- Non-ST elevation myocardial infarction (NSTEMI)
89
What is an ST-elevation myocardial infarction (STEMI)?
Complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
It causes full thickness damage of heart muscle
90
How can you diagnose a STEMI?
ECG
- Tall T waves
- ST elevation
- Subsequent pathological Q wave
May present as new left bundle branch block (LBBB) on ECG
91
What is a non-ST-elevation myocardial infarction (NSTEMI)?
Complete occlusion of a MINOR, or partial occlusion of a major, coronary artery previously affected by atherosclerosis
Causes partial thickness damage of heart muscle
92
How do you diagnose an NSTEMI?
- Retrospective diagnosis made after troponin results (and sometimes other)
- No ST elevation or Q wave
- Will see ST depression and / or T wave inversion
93
What is the difference between a UA and NSTEMI?
In an NSTEMI, there is an occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatine kinase-MB
In UA, there is an occluding thrombus that leads to myocardial ischaemia
94
Link myocardial infarction to myocardial ischaemia
Cardiac myocytes dying due to myocardial ischaemia
95
How many types of MI are there?
5
96
Describe MI type 1
Spontaneous MI with ischaemia due to a primary coronary event
e.g. plaque erosion / rupture, fissuring, or dissection
97
Describe MI type 2
MI secondary to ischaemia, due to increased O2 demand or decreased supply, such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
98
Describe MI type 3, 4 and 5
MI due to;
Type 3 = sudden cardiac death
Type 4 = PCI
Type 5 = CABG
99
Describe the epidemiology of STEMI in the UK
- 5/1000 deaths per annum
| - Worse prognosis in elderly and those with left ventricular failure
100
What are the risk factors for a heart attack?
- Age
- Male
- FHx of IHD
- Hx of premature CHD
- Premature menopause
- Smoking
- Hypertension
- Diabetes mellitus
- Hyperlipidaemia
- Obesity & sedentary lifestyle
101
Describe the pathophysiology of a myocardial infarction
- Rupture / erosion of fibrous cap of a coronary artery plaque
- Leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction, and distal thrombus embolism
- Resulting in prolonged complete arterial occlusion within 15-30mins
102
Describe the pathophysiology of a STEMI (specifically with regards to the Q wave)
Sub-endocardial myocardium is initially affected but, with continued ischaemia, the infarct zone extends through the sub-epicardial myocardium, producing a transmural Q wave MI
103
What is the progression from fatty streak to cardiac event?
```
> Fatty streak
> Fibrotic plaque
> Atherosclerotic plaque
> Plaque rupture / fissure
> Thrombosis
> MI / Ischaemia stroke / critical leg ischaemia, sudden CVS death
```
104
What is the difference between the thrombi in unstable angina and myocardial infarction?
```
UA = partial occlusion by thrombus
MI = total occlusion by thrombus
```
105
What is the clinical presentation of an ACS?
- Unstable angina
- New onset angina
- Acute central chest pain
- Sweating
- Nausea
- Vomiting
- Dyspnoea
- Fatigue
- Shortness of breath
- Palpitations
- Distress and anxiety
- Pallor
- Tachycardia OR bradycardia
- Hypotension
- Reduced heart sound S4
- May be signs of heart failure
- Peripheral oedema
106
What are the differential diagnoses for ACS?
- Angina
- Pericarditis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
- Oesophageal reflux/spasm
107
Name 2 ways of diagnosing an MI
- 12 lead ECG
| - Biochemical markers
108
Describe how you can use an ECG to diagnose a NSTEMI
- ECG may be normal, should use biochemical markers for certain diagnosis
- ST depression
- T wave inversion
109
Describe how you can use an ECG to diagnose a STEMI
- Persistent ST elevation
- Hyperacute T waves
- Possible LBBB
- May see pathological Q waves and T wave inversion a few days after an MI
110
Which biochemical markers can you use to diagnose an MI?
- Troponin T & I
- CK-MB
- Myoglobin
- CXR
111
How can you use troponin (T & I) to diagnose a heart attack?
- Sensitive and specific markers of myocardial necrosis
- Serum levels increase within 3-12 hours from the onset of chest pain, and peak at 24-48 hours
- Fall back to normal over 5-14 days
- Act as a prognostic indicator to determine mortality risk and define which patients may benefit from aggressive medical therapy and early coronary revascularisation
112
How can you use CK-MB to diagnose a heart attack?
- Marker for myocyte death, but has low accuracy since it can be present in serum of normal individuals and in patients with significant skeletal muscle damage
- Can be used to determine re-infarction as levels drop back to normal after 36-72 hours
113
How can you use myoglobin to diagnose an MI?
Becomes elevated very early in MI but the test has poor specificity since myoglobin is present in skeletal muscle
114
How can a CXR help identify an MI?
Look for cardiomegaly, pulmonary oedema, or a widened mediastinum (aortic rupture)
115
What are the various methods of treating an MI?
- Pain relief
- Anti-emetic
- Oxygen
- Anti-platelets
- Beta blockers
- Statins
- ACE inhibitors
- Coronary revascularisation
- Risk factor modification
116
What do you use for pain relief following an MI?
- GTN spray
- MORPHINE!
Remember: MONA (M = morphine)
117
What oxygen saturation should you aim for in a normal patient?
94-98%
118
What oxygen saturation should you aim for in a patient with COPD?
88-92%
119
Why do you give anti-platelet medication to someone who has just had an ACS?
- Atheromatous plaque rupture results in platelets being exposed to ADP / thromboxane A2 / adrenaline / thrombin / collagen tissue factor
- This results in platelet activation / aggregation via IIb/IIIa glycoproteins binding to fibrinogen
- Then thrombin is able to enzymatically convert fibrinogen to fibrin resulting in the formation of a fibrin mesh over platelet plug, and the formation of a thrombotic clot
- Anti-platelet drugs help prevent this
120
What anti-platelet drugs can you give to someone who has just had an ACS?
- Aspirin (oral)
- P2Y12 inhibitors (oral)
- Glycoprotein IIb/IIIa antagonists (IV)
121
What is the mechanism of action of aspirin?
COX-1 inhibitor - blocks formation of thromboxane A2, thus prevents platelet aggregation
122
What is the mechanism of action of P2Y12 inhibitors?
Inhibits ADP-dependent activation of IIb/IIIa glycoproteins, thereby preventing amplification response of platelet aggregation
e.g. CLOPIDOGREL, PRASUGREL, TICAGRELOR
123
When should you use P2Y12 inhibitors?
- Allergic to aspirin
| - Alongside aspirin as a dual anti-platelet therapy
124
What are the side effects P2Y12 inhibitors?
- Neutropenia
- Thrombocytopenia
- Increased risk of bleeding
125
What are the contraindications of P2Y12 inhibitor use?
If a CABG is planned
126
When do you use glycoprotein IIb/IIIa antagonists to treat an ACS?
Used (in combination with aspirin and oral P2Y12 inhibitors) in patients with ACS undergoing percutaneous coronary intervention
127
What are the side effects of glycoprotein IIa/IIb antagonists?
Increases risk of MAJOR bleeding
128
Give some examples of glycoprotein IIb/IIa antagonists
- ABCIXIMAB
- TIROGIBAN
- EPTIFBATIDE
129
What beta blockers should you give to a patient who has just had an ACS?
ATENOLOL or METOPROLOL (IV then oral)
130
What are the side effects and contraindications of beta blocker use?
Avoid with asthma, heart failure, hypotension, and bradyarryhthmias
131
Which statins do you give to a patient to treat a recent ACS?
HMG-CoA reductase inhibitors (e.g. SIMVASTATIN, PRAVASTATIN, ATORVASTIN)
132
Which ACE inhibitors do you give a patient to treat a recent ACS?
RAMPIRPIL, LISONOPRIL
133
What must you do if you prescribe ACE inhibitors?
Monitor renal function
134
What is the clinical presentation for an AMI?
- Chest pain > 20mins
- Severe central ongoing pain
- Pain radiating to left arm, jaw or neck
- Does not usually respond to GTN spray
- Pain = substernal pressure, squeezing, aching, burning, sharp
- Sweating
- Nausea
- Vomiting
- Dyspnoea
- Fatigue
- Palpitations
- Breathlessness
- Distress / anxiety
- Pale, clammy
- Significant hypotension
- Brady/tachycardia
135
What are the differential diagnoses for acute myocardial infarction?
- Stable / unstable angina
- NSTEMI
- Pneumonia
- Pneumothorax
- Oesophageal spasm
- GORD
- Acute gastritis
- Pancreatitis
- MSK chest pain
136
In a STEMI with infarction of the anterior border of the heart, what will you see on an ECG?
ST elevation in V1-V3
137
In a STEMI with infarction of the inferior border of the heart, what will you see on an ECG?
ST elevation in II, III, aVF
138
In a STEMI with infarction of the lateral border of the heart, what will you see on an ECG?
Change in I, aVL, V5-V6
139
In an MI with infarction of the posterior border of the heart, what will you see on an ECG?
- ST depression in V1-V3
- Dominant R wave
- ST elevation in V5-V6
140
In a STEMI with infarction of subendocardium of the heart, what will you see on an ECG?
Changes anywhere on ECG
141
Describe the evolution of a STEMI ECG
First few minutes;
- T wave becomes tall, pointed, and upright
- ST elevation
First few hours;
- T waves invert
- R wave voltage decreases
- Q waves develop
Few days later;
- ST segment returns to normal
Weeks / months;
- T wave may return upright
- Q wave remains
142
Describe the biochemical changes following a heart attack
- Trop I & T increase
| - Myoglobin increases
143
What is the pre-hospital treatment for an MI?
- Aspirin 300mg chewable
- GTN (sublingual)
- Morphine
144
What is the hospital treatment for an MI?
- IV morphine
- Oxygen (if sats <90% or SOB)
- Beta-blocker (ATENOLOL)
- P2Y12 inhibitor (CLOPIDOGREL)
145
Who is offered a PCI?
Presented to all patients who present with an acute STEMI who can be transferred to a primary PCI centre WITHIN 120 MINUTES of first medical contact
146
What happens if a patient cannot get a PCI?
Fibrinolysis, and then transfer to PCI after infusion
147
What are the complications of myocardial infarction?
- Sudden death
- Arrhythmias
- Persistent pain
- Heart failure
- Mitral incompetence
- Pericarditis
- Cardiac rupture
- Ventricular aneurysm
148
What tends to cause sudden death after an MI?
Ventricular fibrillation a few hours after MI
149
What causes persistent pain after an MI?
Progressive myocardial necrosis
150
What is heart failure?
When cardiac output is insufficient to meet body's metabolic demands
151
What causes mitral incompetence following an MI?
Myocardial scarring preventing valve closure
152
What causes pericarditis following an MI?
Due to transmural infarct resulting in inflammation of pericardium
153
What causes cardiac rupture after an MI?
Early rupture - result of shearing between mobile and immobile myocardium
Late rupture - due to weakening of wall following muscle necrosis and acute inflammation
154
What causes ventricular aneurysm after a heart attack?
Stretching of newly formed collagenous scar tissue
