CV lecture notes Flashcards
1
Q
risk factors for atherosclerosis?
A
age, smoking, high serum cholesterol, obesity, diabetes, hypertension, family history
2
Q
why is obesity a risk factor for atherosclerosis?
A
fat holds onto inflammatory cells
3
Q
why is diabetes a risk factor for atherosclerosis?
A
hypo/hyperglycaemia affects endothelium function
4
Q
What is the main danger of atherosclerotic plaques?
A
Can rupture, leading to thrombus formation.
Can occlude, leading to ischaemia/infarction
5
Q
Distribution of atherosclerotic plaques?
What are haemodynamic factors that affect plaque distribution?
A
Focal distribution along artery length.
Peripheral and coronary arteries.
Changes in flow such as bifurcations lead to wall thickness changes - neointima
6
Q
Components of atherosclerotic plaques?
A
Complex lesion of:
- lipid
- necrotic core
- connective tissue
- fibrous cap of smooth muscle
7
Q
what is the significance of the fibrous capsule that covers an atherosclerotic plaque?
A
The thicker it is, the less likely the plaque is to rupture.
8
Q
how does the ‘response to injury’ hypothesis explain plaque formation?
A
injury to endothelial cell walls leads to endothelial dysfunction.
This signals to circulating leukocytes which accumulate and migrate to endothelial wall.
Inflammation ensues.
9
Q
how is adhesion of leukocytes in plaque formation mediated?
A
chemoattractants on endothelial cell surface send signals to leukocytes. Selectins mediate slow rolling and capture of leukocytes.
Integrins and chemoattractants located in the tissue mediate firm adhesion and transmigration - entice leukocytes in.
10
Q
what are the 5 stages in the progression of atherosclerosis?
A
- Fatty streaks: present from about 10yr of age
- Intermediate lesions: foam cells, smooth muscle cells, t-lymphocytes…
- Fibrous plaques/advances lesions: foam cells, smooth muscle cells, t-lymphocytes, macrophages, covered by dense fibrous cap of collagen and elastin.
- Plaque rupture: fibrous cap resorbed and redeposited. Balance shifts in favour of inflammatory conditions, weakening cap and plaque ruptures. BM collagen and necrotic tissue is exposed, haemorrhage of vessels.
- Plaque erosion: collagen triggers thrombosis, small early lesions
11
Q
what are ‘foam cells’ present in plaques?
A
lipid laden macrophages
12
Q
From what stage in atherosclerosis do plaques impede blood flow and are prone to rupture?
what do plaques consist of at this point?
A
Stage 3: fibrous plaques/advanced lesions
Consist of foam cells, smooth muscle cells, t-lymphocytes, macrophages, covered by dense fibrous cap of collagen and elastin.
13
Q
what is meant by syncope?
A
episodes of loss of consciousness
14
Q
what are the 3 pacemakers of the heart, and how many bpm do they fire at?
A
SAN - main pacemaker of the heart: 60-100bpm
AVN: back up, 40-60bpm
Ventricular cells: back-up, 20-45bpm
15
Q
WHat will an electrical impulse that travels towards the electrode show up as on an ecg?
A
upright, positive deflection
16
Q
What is the route of conduction of the impulse once generated in the SAN ?
A
To AVN (slows down impulse, allowing atrial contraction). Then to bundle of his --> bundle branches on either side --> purkinje fibres
17
Q
PQRST in ECG
What do the letters represent?
A
P = atrial depolarisation QRS = ventricular depolarisation T = ventricular repolarisation
18
Q
What are the 12 ECG leads?
A
12 leads
3 standard limb
3 augmented limb leads
6 precordial leads (v1-v5)
19
Q
what constitutes a complicated plaque?
A
calcification, mural thrombus, ulcerated, occluding, vulnerable (thin fibrous cap)
20
Q
what does ‘immunogenic’ mean in context of an atherosclerotic plaque?
A
Incited inflammatory response, which may contribute to its growth.
21
Q
what are the patterns that myocardiac infarction can take and associated ecg trace?
A
subendocardial - (NSTEMI) partial infarction of muscle wall, ST depression
transmural infarction - (STEMI) total infarction of muscle wall, ST elevation
Progression of acute coronary syndrome will go from unstable angina -> NSTEMI -> STEMI
22
Q
what are methods for reperfusion of ischaemic myocardium?
A
- coronary artery bypass grafts
- stenting (PCI) * method of choice*
- Percutaneous transluminal coronary angioplasty (PTCA) balloon tipped catheter, balloon inflated and deflated
thrombolytic enzymes
23
Q
what is a cardiac aneurysm?
A
dilation of myocardial wall
24
Q
how can lung disease lead to heart failure?
A
Pulmonary hypertension leads to RV hypertrophy and dilatation
25
what is infective endocarditis?
why does it have high mortality?
infection of the endocardium (inner lining of heart chambers and heart valves), leads to valve distortion and disruption and infected thromboemboli.
30-40% mortality. Hard to spot and treat. Symptoms are generalised and non-specific, such as fever, anorexia, anaemia.
26
what is myocarditis?
inflammation of the myocardium. Usually viral causes, lymphocytic following upper respiratory tract infection.
27
3 types of cardiomyopathy (disease of the heart muscle where it becomes enlarged/thick/rigid)
1. Dilated cardiomyopathy (DCM). Big, dilated heart, non-specific. Secondary dilated cardiomyopathy can be caused by alcohol/cocaine/pregnancy.
2. Hypertrophic cardiomyopathy. Compensatory asymmetrical hypertrophy in response to dysfunction. Accounts for 5-10% sudden deaths in young adults.
3. Arrythmogenic - dilated RV, fat, tissue, inflammatory cells
28
What is the commonest vascular disease and how may it present?
Giant cell arteritis.
Focal, chronic and granulatomous inflammation of temporal arteries which may affect the opthalmic arteries leading to sudden blindness.
Headaches, joint pain, facial pain, fever, and difficulties with vision, and sometimes permanent visual loss in one or both eyes.
29
Common examples of vascular disease?
Hypertensive vascular disease: usually idiopathic, 20-30% population >140/90mmHg
Giant cell arteritis
Abdominal aortic aneurysm
Berry aneurysm (commonly in branching points of circle of Willis)
Varicose veins
30
When is an abdominal aortic aneurysm considered at risk of rupture and operated on?
When it reaches >5-6cm diameter
31
what is angina?
a symptom which occurs as a result of restricted coronary blood flow, almost exclusively secondary to atherosclerosis
32
WHY does angina occur?
Mismatch between oxygen demand and oxygen supply to the heart:
- impairment of blood flow by proximal arterial stenosis affects supply
- increased distal resistance (eg LV hypertrophy) increasing demand
- reduced oxygen carrying capacity in the blood eg in anaemia
33
on ECG paper, horizontally what does one small box represent? What about one large box?
One small box = 0.04s/40ms
| • One large box = 0.20s
34
on ECG paper, vertically what does one large box represent?
• One large box = 0.5mV
35
where is the left ventricle palpated?
5th left intercostal space and mid-clavicular line
36
how is blood flow through the CV system determined?
how does epicardial disease affect this flow? Why does this lead to exertional angina?
```
By resistance (known as 'tone') of microvasculature and epicardial arteries. Poiseuille's law - 4th power of radius - pressure and flow vs vessel size, so small change will have a large impact.
Epicardial disease: increased resistance in epicardial vessels, so microvascular vessels dilate to compensate. This does not cause problems at rest, but during exercise unable to increase flow sufficiently.
```
37
non-modifiable vs modifiable risk factors for cardiovascular disease
non-modifiable:
gender, family history, personal history, age
modifiable:
smoking, diabetes, hypertension, sedentary lifestyle, stress, hypercholesterolaemic
38
3 presenting symptoms of stable angina: how are these used to categorise the angina?
1. Heavy, central, tight chest pain radiating to L arm, jaw and neck
2. Precipitated by exertion
3. Relieved by rest/GTN spray
If an individual has 1 of these = non-anginal pain, 2/3 = atypical pain, 3/3 = typical angina
39
what are common differential diagnoses of angina?
```
Pericarditis/myocarditis
Pulmonary embolism/pleurisy/pneumonia
GORD
MSK problems - such as costochondritis
Anxiety/panic disorders
```
40
What are anatomical vs physiological diagnostic investigations for angina?
Anatomical: CT angiography, invasive angiography. Is there narrowing?
Physiological: exercise stress treadmill, stress echo, perfusion MRI, SPECT
41
what is angina?
chest pain/discomfort due to reversible myocardial ischaemia - usually narrowing of 1/more coronary arteries. Exacerbated by exertion, relieved by rest. Can be stable or unstable.
42
how is 12 lead ECG used in angina diagnosis?
Often normal
May show ST depression
Flat/inverted T wave
Look for signs of past MI
43
How is the treadmill test/exercise ECG used in angina diagnosis? Why is this not always an appropriate test?
Try to induce ischaemia by getting pt to run uphill on a treadmill while attached to an ecg.
ST segment depression = late-stage ischaemia
Unsuitable: unpleasant experience, not suitable if very unfit/unable to walk
44
How is CT angiogram used in diagnosis of angina?
If artherosclerosis in arteries, the calcium will light up white. Significant calcium would indicate angina.
45
how is SPECT/myoview used in diagnosis of angina?
Radio-labelled tracer is taken up by metabolising tissues - heart - via coronary arteries. Tests perfusion under stress and at rest - no light after exercise indicates myocardial ischaemia
46
what does primary prevention of angina involve?
Risk factor modification (diet, smoking, exercise, hbp. cholesterol, diabetes) to decrease risk of coronary artery disease.
10 r risk of an event is calculated using scoring.
47
What does secondary prevention of angina involve?
1. lifestyle changes
2. Pharmacological: to reduce CV events and symptoms
3. Interventional to reduce risk and symptoms (eg revascularisation - PCI/CABG)
48
What are first line pharmacological treatments for angina?
Beta blockers antagonise sympathetic nervous activation: they decrease HR and decrease contractility to reduce the work and O2 demand.
Nitrates (eg GTN) act as venodilators, reducing preload o heart therefore reducing heart work and O2 demand
49
What are side effects and contraindications of beta blockers?
side effects: tiredness, nightmares, bradycardia, cold hands and feet, erectile dysfunction
Contraindications: asthma, heart failure, bradyarrhythmias, hypotension
50
Aside from beta blockers and GTN (first line antianginals), what other medications can be used and how do they have their positive/protective effect?
- Calcium channel agonists: act as arterodilators, reducing afterload, therefore heart work and O2 demand of heart
- Aspirin: antiplatelet effect to avoid thrombosis, to reduce events. COX inhibitor (thromboxane A2, needed for platelet aggregation, not synthesised)
- Statins: anti-atherosclerotic. Reduce events and LDL cholesterol.
51
When and why may revascularisation techniques be used in individuals with angina?
what are 2 techniques?
Done when medication fails or high risk disease identified.
Aim to restore patent coronary artery and increase flow reserve.
PCI or CABG may be used
52
Describe PCI
pros? cons?
Balloon and stent inserted on catheter via shoulder/groin (I think). Inflate balloon and remove, leaving stent keeping the artery patent.
Pros: less invasive, convenient, short recovery.
Cons: risk stent thrombosis and restenosis, not good for complex disease.
53
Describe CABG
| pros? cons?
Left internal mammary artery used to bypass proximal stenosis in LAD
Pros: good prognosis, delas with complex disease
Cons: invasive, risk stroke/bleeding, a 1 time treatment. Need to stay in hospital - long recovery. Not appropriate for the frail/comorbid.
54
what is meant by acute coronary syndrome?
Umbrella term covering a spectrum of acute cardiac conditions ranging from unstable angina (least severe) through NSTEMI and finally STEMI.
55
what is STEMI?
ST elevation myocardial infarction. Complete occlusion of coronary artery leading to transmural infarction (full thickness damage of heart muscle). PCI treatment of choice.
56
Describe the acute management of MI:
- dial 999 if angina that is not relieved by GTN presents, quick to hospital
- paramedics carry out ecg, if ST elevation present contact primary PCI centre for transfer
- take aspirin 300mg immediately
- pain relief to relieve distress and reduce metabolic demands: MONA - morphine, oxygen(if low), nitrates, aspirin
- in hospital, close clinical monitoring: symptoms, BP, HR, O2, pain
- bloods for FBC, troponin, renal function&electrolytes, glucose, lipids, clotting, CRP...
- ecg monitoring
- reperfusion: PCI asap
57
describe the troponin test - how are levels used to confirm/exclude MI?
Test troponin 6hrs after pain. If not elevated, no MI. If there is a rise, test again after 3hrs. A significant rise + other diagnostic factors = MI confirmed.
58
what is an NSTEMI?
Retrospective diagnosis made after troponin/other investigation results.
Complete occlusion of a minor, or partial occlusion of a major coronary artery previously affected by atherosclerosis, resulting in subendocardial (partial thickness) damage to the heart muscle.
No ST elevation/ST depression, T wave inversion seen on ECG
59
Why is clinical diagnosis of DVT unreliable?
Symptoms (pain, swelling) and signs (tender, warm, discolouration) are non specific.
60
As a general rule, where in the body are DVTs more vs less dangerous?
Above the knee = dangerous, below = not dangerous
61
A positive result for d-dimer blood test does not confirm diagnosis of a DVT. What test must be used?
Ultrasound compression test on proximal veins. Veins are pressed closed, which should stop blood flow. If this does not happen = thrombus.
Sites: popliteal fossa, groin, half way up thigh
62
Treatment for DVT
- address underlying cause eg thrombophilia/malignancy
- DOAC
- heparin for 5 days, warfarin for 3-6mo
- compression stockings
- consider provocation: eg immobility due to a hospital stay- if it was a provoked DVT, it is less likely to reoccur
63
Risk factors for DVT
- surgery, immobility, leg fracture
- oestrogen oral contraceptive pill, HRT, pregnancy
- long haul flights (rare)
- inherited thrombophilia
64
Why does pregnancy increase risk of DVT, especially in third trimester?
Blood becomes hypercoagulant to allow separation from the placenta.
Baby presses on blood vessels.
65
Prevention of DVT
mechanical: hydration and early mobilisation, compression stockings, foot pumps
chemical: heparin
66
What is the of pulmonary embolism?
| Treatment?
Haemodynamically significant, leading to hypotension, severe dyspnoea, right heart strain/failure
Treatment: embolectomy/thrombolysis - mechanical or chemical. As for DVT, heparin, warfarin, DOAC, treat underlying cause.
67
Common presentation of a pulmonary embolism
Symptoms: chest painDVT symptoms, risk factors. Signs: tachycardia, tachypnoea, pleural rib
The presenting symptoms of chest pain and SOB mean that there are many differential diagnoses - eg MSK pain, infection, malignancy, pneumothorax
68
what is the most useful investigation in the diagnosis of a pulmonary embolism?
CT pulmonary angiogram (CTPA)spiral CT with contrast allows visualisation of major segmental thrombus.
(can also measure V/Q mismatch, D-dimer, ECG amd blood gases but these are not diagnostic)
69
What type of resp failure will the blood gases of an individual with pulmonary embolism show?
Type 1
| Both O2 and CO2 decreased
70
why is thrombosis more common in venous circulation?
Blood is low pressure so clots form more easily.
71
Compare thrombosis in arterial vs vebous circulation
arterial - high pressure, platelet rich 'white' thrombus
venous - low pressure, fibrin rich: 'red' thrombus
More common in venous due to low pressure
72
what 2 systems in the body aim to increase the blood pressure, and therefore are important in treating hypertension?
What are the key agents that have the effect in both systems
RAAS: angiotensin 2
| and sympathetic nervous system: noradrenaline
73
How does angiotensin 2 contribute to high blood pressure?
- vascular growth: hypertrophy, hyperplasia
- salt retention: aldosterone, Na+ reabsorption
- acts as a potent vasoconstrictor, increasing peripheral resistance
- stimulates noradrenaline production
74
How sympathetic stimulation - noradrenaline release - contribute to hypertension?
Binds to α- and β-adrenergic receptors in the blood vessels, causing vasoconstriction = increased peripheral resistance = which increases blood pressure.
Also increases CO.
75
Which drugs are used in the management of hypertension, and which 2 systems do they act on?
```
Act on RAAS and sympathetic NS
ACE inhibitors
Angiotensin 2 receptor blockers (ARB)
Calcium channel blockers
Beta blockers
Diuretics
```
76
ACE inhibitors:
- nomenclature
- use in?
- action
- main adverse affects
'-pril' eg ramipril
- use in: hypertension, HF, diabetic nephropathy
- action: prevent formation of angiotension 2 by inhibiting ACE enzyme
- main adverse affects: lack of angiotensin 2 -> hypotension, acute renal failure, hyperkalaemia (due to lack aldosterone). ACE is also used to convert bradykinin to inactive peptides, and its inhibition can lead to kinin build up --> dry cough, rash, anaphylactoid reactions
77
Angiotensin 2 Receptors Blockers:
- nomenclature
- use in?
- action
- main adverse affects
'-sartan' eg cardesartan, valsartan
- use in: hypertension, HF, diabetic nephropathy (when contraindications for ACE-i)
- action: prevent angiotensin II from binding to angiotensin II receptors on the muscles surrounding blood vessels. As a result, blood vessels enlarge (dilate) and blood pressure is reduced.
- main adverse affects: symptomatic hypotension, hyperkalaemia, renal dysfunction, rash, angio oedema.
Contra-indicated in pregnancy.
78
Calcium Channel Blockers
- nomenclature
- use in?
- action
- main adverse affects
'-pine' Groups: dihydropines (amlodipine), phenylalkylamines (verapamil), benzothiazepines (diltiazem)
- use in: hypertension, IHD - angine, arrhythmia
- action: act on L-type calcium channels. Different groups have peripheral/more direct effects on the heart. Negatively chronotrophic, peripheral vasodilation, negative inotropism
- main adverse affects: flushinf, headache, oedema, palpitations, bradycardia, AV block. Specifically verapamil: worsening of cardiac failure, constipation.
79
beta adrenoreceptor blockers
- nomenclature
- use in?
- action
- main adverse affects
'-olol' eg bisopralol, pranopralol, atenolol
- use in: IHD - angine, HF, arrhythmia, hypertenson
- action: block effects o nadrenaline. Can be selective/non selective or both
- main adverse affects: fatigue, headache, nightmares, bradycardia, hypotension, cold peripheries, erectile dysfunction. Worsening of asthma, COPD, HF, PVD
80
diuretics
- use in?
- action
- main adverse affects
- use in: hypertension, heart failure
- action: act on nephrons, increase the amount of water and salt expelled from the body as urine. Groups: a)Thiazides act on distal tubule. b) Loop diuretcs act on loop of Henle (more powerful). c) Potassium sparing. d) Aldosterone antagonists
- main adverse affects: hypovolaemia, hypotension, low serum K+/Na+/Mg/Ca
Erectile dysfunction
Raised uric acid
Impaired glucose tolerance
81
What is cardiac / heart failure?
Also known as congestive heart failure
Heart cant meet demands.
Can be diastolic - impaired filling or systolic (impaired pumping). This leads to blood backed up in lungs --> congestion.
Can be acute/chronic.
Describes a complex grouping of symptoms&signs that suggest impaired efficiency of heart.
82
What is meant by the ejection fraction and when is it used?
The stroke volume as a percentage of the total volume in the heart. Therefore it is a measure of how well the heart is pumping.
Used to diagnose systolic heart failure: <40% indicates systolic HF
83
What would the ejection fraction be like in systolic heart failure and why?
Pumping is impaired.
reduced stroke volume compared to total vol
EJ<40% is systolic HF
84
What would the ejection fraction be like in diastolic heart failure and why?
Filling is impaired, meaning reduced total volume (reduced preload). This means stroke volume is also low, explained by Frank-Starling mechanism. EJ will therefore by normal as both values are low.
85
3 causes of left sided heart failure
1. Most common: Ischaemic heart disease caused by plaque in CA --> damaged myocardium
2. Long term hypertension --> increased arterial pressure, increased pressure in systemic circulation. This makes it harder for the heart to pump, leading to hypertrophy of myocytes to compensate. These larger cells need more O2, and also squeeze the CAs. --> weaker contraction
3. Dilated cardiomyopathy
86
What basic investigations (non-diagnostic) are used when an individual first presents with angina?
- 12 lead ECG: cannot exclude IHD, but may provide clues
- Echocardiogram: cannot exclude, but may provide signs of previous infarcts/alternative diagnoses and checks LV function.
- pre-test probability: charts gender, age and typicality of pain. If low<15%, individual is safe and no further investigation is needed. 20-25% = non-invasive diagnostic required, and >85% = CHD
87
What are anatomical vs physiological diagnostic tests used in an individual presenting with angina to diagnose IHD?
- Anatomical
