cardiology Flashcards
(142 cards)
1
Q
Define atherosclerosis.
A
A hardened plaque in the intima of an artery. It is an inflammatory process.
Inflammatory process characterised by hardened plaques in the intima of a vessel wall. (vessel walls such as large (aorta) and medium-sized arteries (coronary arteriees
inflammatory process. w build-up of lipids and macrophages and smooth muscle cells in the intima of large and medium sized arteries.
2
Q
Atherosclerosis: can lead to?
A
- Carotid atheroma - emboli causing transient ischaemic attacks and cerebral infarcts
- MI, cardiac failure
- Aortic aneurysms
- Gangrene
- Peripheral vascular disease - can affect any vessel outside of heart
3
Q
Give 9 risk factors for atherosclerosis.
Explain for each risk factor the pathophysiological processes that promote the development of atherosclerosis. (see notion)
A
- Family history.
- Increasing age.
- Smoking.
- Hyperlipidaemia and hypercholesterolaemia (High levels of LDL’s)
- Obesity.
- Diabetes (uncontrolled - hyperglycaemia).
- Hypertension.
- Male Gender
- Lower socioeconomic status
4
Q
Angina: define
A
Angina is a type of IHD. It is a symptom of O2 supply/demand mismatch to the heart experienced on exertion.
Angina is chest pain or discomfort as a result of reversible myocardial ischaemia.
This usually implies narrowing of one or more of the coronary arteries.
Tends to be exacerbated by exertion and relieved by rest
5
Q
Angina: aetiology?
most commonest cause
A
(most commonest cause)
= Narrowing (stenosis) of the coronary arteries due to atherosclerosis.
- Narrowed coronary artery = impairment of blood flow e.g. atherosclerosis.
- Increased distal resistance = LV hypertrophy.
- Reduced O2 carrying capacity e.g. anaemia.
- Coronary artery spasm.
- Thrombosis.
- Valvular Disease
6
Q
Angina: risk factors?
- > 6 modifiable risk factors for angina.
- > 3 non-modifiable risk factors
A
Modifiable:
- Smoking.
- Diabetes.
- High cholesterol (LDL).
- Obesity
- Sedentary lifestyle.
- Hypertension.
Non-modifiable:
- Genetics/Family History
- Increasing Age
- Gender. male bias
7
Q
Angina: pathophysiology that results from atherosclerosis?
pathophysiology that results from anaemia?
A
On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.
On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.
8
Q
Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?
A
In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When this person exercises, the microvascular resistance can’t drop anymore and flow can’t increase to meet metabolic demand = angina!
9
Q
How can angina be reversed?
A
Resting - reducing myocardial demand.
10
Q
Angina: presentations?
and how would you describe the chest pain in angina?
A
- Crushing central chest pain.
- The pain is relieved with rest or using a GTN spray.
- The pain is provoked by physical exertion.( especially after meal or in the cold windy weather or by anger or excitement)
- The pain might radiate to the arms, neck or jaw.
- Breathlessness.
chest pain = Crushing central chest pain. Heavy and tight. The patient will often make a fist shape to describe the pain.
11
Q
What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?
A
Pre-test probability of CAD. It takes into account gender, age and typicality of pain.
12
Q
Angina: investigations?
A
- ECG - usually normal, there are no markers of angina.
- —> - Often normal
- May show ST depression
- Flat or inverted T waves
- Look for signs of past MI - Echocardiography.
- CT angiography - has a high NPV and is good at excluding the disease.
- Exercise tolerance test - induces ischaemia.
- —> - Monitor how long patient is able to exercise for
- If you see ST segment depression then this is a sign of late-stage ischaemia
- Many patients unsuitable e.g. can’t walk, very unfit, young females and bundle branch block - Invasive angiogram - tells you FFR (pressure gradient across stenosis).
13
Q
A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?
A
Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.
14
Q
Primary prevention vs secondary prevention?
A
Primary =
- Risk factor modification.
- Low dose aspirin.
secondary =
- Risk factor modification.
- Pharmacological therapies for symptom relief and to reduce the risk of CV events.
- Interventional therapies e.g. PCI.
15
Q
Angina: management?
A
- Modify risk factors
- Treat underlying conditions
- Pharmacological:
16
Q
Angina management: pharmacological management:
Name 3 symptom relieving pharmacological therapies that might be used in someone with angina.
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.
A
- Beta blockers.
- Nitrates e.g. GTN spray.
- Calcium channel blockers.
- Aspirin.
- Statins.
17
Q
Angina management: beta blockers
Function
Describe action of beta blockers
give examples
side effects
When might beta blockers be contraindicated?
A
aka 1st line antianginal
function =
= symptom relief.
action =
Reduce force of contraction of heart
Act on B1 receptors in the heart as part of the adrenergic sympathetic pathway
B1 activation → Gs → cAMP to ATP → contraction
also -» Reduces:
- Heart rate (negatively chronotropic)
- Left ventricle contractility (negatively inotropic)
- Cardiac output
/Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic. Myocardial work is reduced and so is myocardial demand = symptom relief.
- E.g. Bisoprolol and atenolol
Side effects; 1. tiredness, 2. bradycardia, 3. erectile dysfunction 4. cold hands and feet (cold peripheries) and nightmares
They might be contraindicated in someone with asthma or in someone who is bradycardic. - DO NOT GIVE in *asthma, heart failure/heart block, hypotension and bradyarrhythmias/who is bradycardic*
18
Q
Angina management: Nitrates:
function?
Describe the action of nitrates.
Side-effects?
A
- Glyceryl Trinitrate (GTN) spray 1st line antianginal:
function = symptom relief
action =
Nitrate that is a venodilator
= Dilates systemic veins thereby reducing venous return to right heart
-> Reduces preload
-> Thus reduces work of heart and O2 demand
-> Also dilates coronary arteries
Venodilators -> reduced venous return -> reduced pre-load -> reduced myocardial work and myocardial demand.
Side effect:
profuse headache immediately after use
19
Q
Angina management: statins?
function?
action?
examples?
A
to improve prognosis in someone w angina or someone at risk of angina
They reduce the amount of LDL in the blood.
eg
- HMG-CoA reductase inhibitors reduces cholesterol produced by liver
- Reduce events and LDL-cholesterol
- Anti-atherosclerotic
20
Q
Angina management: Ca2+ channel antagonists/blocker:
function?
action?
give eg
A
symptom relief
action = Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.
Primary arterodilators
- Dilates systemic arteries resulting in BP drop
- Thus reduces afterload on the heart
- Thus less energy required to produce same cardiac output
- Thus less work on heart and O2 demand
- E.g. verapamil
21
Q
Angina management: Aspirin: function? action? side effects? eg?
A
to improve prognosis in someone w angina or someone at risk of angina
action =
Aspirin irreversibly inhibits COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.
Antiplatelet effect (inhibits platelet aggregation) in coronary arteries thereby avoiding platelet thrombosis
- To reduce events
side effects
Caution: Gastric ulcers!
E.g.
- salicylate
- COX inhibitor reduces prostaglandin synthesis including thromboxane A2 resulting in reduced platelet aggregation
22
Q
Angina management:
Revascularisation
what is it?
Name 2 types of revascularisation.
A
Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.
To restore patent coronary artery and increase flow reserve
Done when medication fails (most) or when high risk disease is identified
- PCI.
Dilating coronary atheromatous obstructions by inflating balloon within it - CABG.
Left Internal Mammary Artery (LIMA) used to bypass proximal stenosis (narrowing) in Left Anterior Descending (LAD) coronary artery
23
Q
Give 2 advantages and 1 disadvantage of PCI.
Give 1 advantage and 2 disadvantages of CABG.
A
pci
- Less invasive.
- Convenient and acceptable.
- High risk of restenosis.
CABG
- Good prognosis after surgery.
- Very invasive.
- Long recovery time.
24
Q
Why are beta blockers good in chronic heart failure?
A
They block reflex sympathetic responses which stress the failing heart.
25
Atherosclerosis: treatment?
major limitation of this treatment?
PCI - percutaneous coronary intervention
major limitation of PCI = Restenosis can be avoided following PCI by Drug eluting stents: (anti-proliferative and drugs that inhibit healing.)
26
ECG: what area of the heart do each of the leads show?
```
I = lateral
II = inferior
III = inferior
```
```
aVR = right
avL = lateral
aVF = inferior
```
V1 / V2 = septum
V3 / V4 = anterior wall
V5 / V6 = lateral wall
27
how to put chest leads on?
| and the limb leads?
```
RIDE YOUR GREEN BIKE
right arm = red
left arm arm = yellow
left leg = green
right leg = black
```
28
on ECG, what type of deflection would you get if you have negative electrons moving towards a negative electrode?
what would you get for depolarisation towards a negative electrode?
what would you get for depolarisation away from the + electrode?
```
positive deflection
(repolarisation)
```
depolarisation - getting positive towards a positive electrode so + deflection
negative deflection
ALSO negative charge moving towards a positive electrode = negative deflection
29
ECG: width and length of large and small box?
large box:
width: 5mm = 0.20s (200ms)
length = 5mm = 0.5mV
25 small boxes in large box
small box
width= 1mm = 0.04s (40ms)
height = 1mm = 0.1mV
30
ECG: how long should the PR interval be?
how long should the QT interval be?
<0.2s or 5 small boxes (120 - 200ms.)
male = <430 ms (0.35 - 0.45s.)
female = < 460 ms
<10-11 small boxes
31
ECG: how long should the PR interval be?
how long should the QT interval be?
How long should the QRS complex be?
<0.2s or 5 small boxes (120 - 200ms.)
male = <430 ms (0.35 - 0.45s.)
female = < 460 ms
<10-11 small boxes
<0.12s or <3 small boxes (Less than 110 ms.)
32
ECG: what would you see on ECG of someone w heart block?
long PR interval and rate is slow
| >1 P wave
33
In which leads must the S wave grow?
From chest leads V1 to V3. It must also disappear in V6.
34
Interpreting ECGs: what rule do you have to follow?
```
RRPWQST
RATE
RHYTHM
P WAVE
WIDTH
Q WAVE
ST SEGMENT
T WAVE
look at goodnotes for mroe info
```
35
Define sinus rhythm.
Sinus rhythm - a P wave precedes each QRS complex.
36
ECG of tachycardia?
rate usuallly above 120bpm
| P waves may or may not be visible/abnrmal
37
ECG of atrial fibrillation?
no P wave
| QRS complex is usually narrow
38
ECG of ventricular fibrillation?
no P waves or QRS
| completely chaotic and irregular rhythm and rate
39
aortic stenosis: define
Narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue
- **Normal aortic valve area** is **3-4cm2**
- **Symptoms** occur when **valve area** is **1/4th** of **normal**
A disease where the aortic orifice is restricted and so the LV can't eject blood properly in systole = pressure overload.
40
Name 4 valvular heart diseases.
1. Aortic stenosis.
2. Mitral regurgitation.
3. Mitral stenosis.
4. Aortic regurgitation.
41
aortic stenosis: aetiology?
1. Congenital bicuspid valve. (valve has 2 leaflets instead of 3 due to genetic disease this is the most common congenital heart disease) resulting in stenosis
2. Acquired e.g. age related degenerative calcification (CAVD) (calcification of the aortic valve resulting in stenosis, most commonly seen in elderly)
and rheumatic heart disease.
42
Aortic stenosis: pathophysiology?
Aortic orifice is restricted e.g. by calcific deposits
a pressure gradient between the LV and the aorta
LV function is initially maintained due to compensatory hypertrophy
also thus = ischaemia of LV myocardium
Overtime this becomes exhausted = LV failure.
43
Aortic stenosis: 3 symptoms?
1. Exertional syncope.
2. Angina.
3. Exertional dyspnoea.
(^classic triad)
Onset of symptoms is associated with poor prognosis.
think aortic stenosis w any person who has the triad
44
Aortic stenosis: 3 signs?
1. Slow rising carotid pulse and decreased pulse amplitude.
2. Soft or absent heart sounds. (second heart sound is less intense)
3. Ejection systolic murmur: <> shape.
45
Aortic stenosis: investigations?
ECG - can show LV hypertrophy
Cardiac catheterisation (fed through femoral artery or radial artery until it reaches aortic valve) - allows visuals of aortic valve
Gold standard = transthoracic ECG
46
Aortic stenosis: management?
surgical Aortic valve replacement or TAVI(for those who are weaker/other health issues)
47
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
48
In what type of valvular heart disease would you hear a ejection systolic murmur?
Aortic stenosis.
49
Aortic Regurgitation: define
A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
50
Aortic Regurgitation: aetiology?
1. Bicuspid aortic valve.
2. Rheumatic.
3. Infective Endocarditis.
4/ Marfan’s and Ehlers-Danlos syndrome - connective tissue disorders
51
Aortic Regurgitation: pathophysiology?
Pressure and volume overload.
thus
Compensatory mechanisms - LV dilatation, LVH.
Progressive dilation -> HF.
52
Aortic Regurgitation: symptoms?
patients remain asymptomatic for many yrs before symptoms develop
1. Dyspnoea on exertion.
3. Angina.
4. Syncope
5. Palpitations
6. Orthopnea.
7. Paroxysmal nocturnal dyspnea.
53
Aortic Regurgitation: 4 signs?
1. Wide pulse pressure. (Wide pulse pressure so increased SBP nd decreased DBP)
2. Diastolic blowing murmur. at left sternal border
3. Systolic ejection murmur.
4. Collapsing water hammer pulse (bounding and forceful rapidly increasing and subsequently collapsing)
54
Aortic Regurgitation: investigations?
CXR and echocardiogram.
55
Aortic Regurgitation: management?
1. IE prophylaxis.
2. Vasodilators e.g. ACEi. eg Ramipril will improve stroke volume and reduce regurgitation but only if patient is symptomatic or has hypertension
3. Regular echo's to monitor progression.
3. Surgery if symptomatic.
56
Mitral Stenosis: pathophysiology?
also Why does mitral stenosis cause AF?
Why does mitral stenosis lead to a raised JVP?
obstruction of blood flow from la to lv in diastole
so LA dilation and la hypertrophy leads to ->
1. AF
2. Blood clots (bc ineffective pumping = blood to stagnate/not flow as well = clots)
3. Low C.O. Bc low diastolic filling of LV and thus low end-diastolic volume = low Stroke volume = low C.O/
4. pulmonary congestion bc increase in left atrial pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary oedema → (reactive) pulmonary hypertension to counter this -> backward heart failure and RV hypertrophy
(Consequently pulmonary venous, pulmonary arterial and right heart pressures also increase)
Pulmonary venous hypertension causes RHF symptoms.
b . There is increased LA pressure. This stretches the myocytes in the atria and irritates pacemaker cells -> AF.
c Pulmonary congestion -> pulmonary hypertension causes a raised JVP.
The presence of this continuous column of blood means that changes in right atrial pressure are reflected in the IJV (e.g. raised right atrial pressure results in distension of the IJV).
57
Mitral Stenosis: define?
Obstruction to LV inflow that prevents proper filling during diastole.
58
Mitral Stenosis: aetiology?
1. Rheumatic heart disease.
2. IE.
3. Calcification.
59
Why might someone with mitral stenosis be breathless? Use Starling's law in your explanation.
Mitral stenosis means ventricles don't fill completely -> reduced End Diastolic Vol -> reduced SV -> reduced CO and so breathlessness.
```
SV = edv - esv
CO = SV x HR
```
Starlings law: the force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched.
60
Mitral Stenosis: symptoms?
1. Dyspnoea
2. Haemoptysis
3. RHF symptoms: (due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling)
61
Mitral Stenosis: signs?
1. 'a' wave in jugular venous pulsations.
2. Signs of RHF.
3. Pink patches on cheeks due to vasoconstriction.
4. Low pitched diastolic murmur. - mid-diastolic murmur (rumble)
5. Loud opening 1st heart sound snap.
62
Mitral Stenosis: investigations?
1. ECG.
2. CXR.
3. Echocardiogram - gold standard.
63
Mitral stenosis: management?
If in AF
-> control heart rate by e.g. beta blockers/Ca Channel Blockers.
If in AF -> Anticoagulants to prevent anticoagulation
Balloon valvuloplasty or valve replacement.
IE prophylaxis.
64
Mitral Regurgitation: define
Backflow of blood from the left ventricle to the left atrium during systole
65
Mitral Regurgitation: aetiology?
1. Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse)
Perhaps due to MI!!
2. Ischaemic mitral regurgitation.
3. Rheumatic heart disease.
4. IE.
5. Age related calcification
66
Mitral Regurgitation: Pathophysiology???
LV volume overload! Compensatory mechanisms: LA enlargement and LVH and increased contractility. Progressive LV volume overload -> dilatation and progressive HF.
67
Mitral Regurgitation: symptoms>?
1. Dyspnoea on exertion.
2. HF. So (due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling)
68
Mitral Regurgitation: signs?
1. Pansystolic murmur (always there).
2. Soft 1st heart sound.
3. 3rd heart sound.
In chronic MR the intensity of the murmur correlates with disease severity.
69
Mitral Regurgitation: investigations?
1. ECG.
2. CXR.
3. Echocardiogram: estimates LA/LV size and function.
70
Mitral Regurgitation: management?
Rate control for AF e.g. beta blockers.
Anticoagulation for AF.
Diuretics for fluid overload.
IE prophylaxis.
If symptomatic = surgery.
71
Dressler’s Syndrome: define.
What coronary event might Dressler's syndrome develop after?
Myocardial injury stimulates formation of autoantibodies against the heart. Cardiac tamponade may occur. Dressler's is a secondary form of pericarditis.
Can develop 2-10 weeks after an MI.
72
Dressler’s syndrome: symptoms?
1. Fever.
2. Chest pain.
3. Pericardial rub.
Occurs 2-10 week after MI.
73
Pericarditis: aetiology?
1. Viral (common) e.g. enteroviruses.
2. Bacterial e.g. mycobacterium tuberculosis.
3. Autoimmune e.g. RA, sjögren syndrome.
4. Neoplastic.
5. Metabolic e.g. uraemia.
6. Traumatic and iatrogenic.
7. 80-90% are idiopathic. Eg PCI or radiation
74
Pericarditis: define?
Pathophysiology?
An inflammatory pericardial syndrome with or without effusion.
Jj
75
Pericarditis: 6 symptoms?
What is the triad?
Why would they have hiccups?
1. ECG.
2. CXR.
3. Bloods.
4. Echocardiogram. Chest pain,
pericardial friction rub,
and serial ECG changes
(And pericardial effusion)
**Triad = chest pain, pericardial friction rub and serial ECG changes**
1. Chest pain!
- **Chest pain:**
- Severe
- Sharp & pleuritic (without constricting crushing character of ischaemic pain)
- Rapid onset
- **Worse on inspiration or lying flat relieved by sitting forward**
- Left anterior chest or epigastrium
- **Radiates to arm, more specifically the *trapezius* ridge (has co- innervation with the phrenic nerve) - *whereas a STEMI would be arms, jaw & teeth***
2. Dyspnoea.
3. Cough.
4. Hiccups due to phrenic involvement .
5. Skin rash.
6. Fever
- **Fever and lymphocytosis (increase in lymphocytes) if due to virus or bacteria**
- **Signs of RHF *so raised JVP*, peripheral oedema**
Because of irritation to the phrenic nerve.
76
Pericarditis: investigations? (4)
What would the ECG look like?
1. ECG.
2. CXR.
3. Bloods.
4. Echocardiogram.
1. PR depression seen in most leads.
2. 'Saddle shaped' concave ST elevation.
77
What is the major differential diagnosis of acute pericarditis?
MI - it is important to rule this out ASAP!
78
Pericarditis: management?
1. Patients are advised to avoid strenuous activity until symptom resolution.
2. NSAID or aspirin - high doses. bc they inhibit COX see pic below and PPI to inhibit peptic ulcer formation bc this is a side effect of NSAIDs
3. Colchicine (anti-inflammatory).
79
Why does chronic pericardial effusion rarely cause tamponade?
The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.
80
IE: define?
infection of heart valves or other endocardial lined structure within the heart.
81
IE: investigations?
Name the criteria that is used in the diagnosis of infective endocarditis.
1. Blood cultures are essential for diagnosis.
2. Echocardiogram shows endocardial involvement e.g. TTE or TOE.
3. Bloods - raised ESR/CRP.
4. ECG.
Duke's criteria.
82
Give 2 major points in the Duke's criteria that if present can confirm a diagnosis of IE.
1. Positive blood culture with typical IE microorganism.
| 2. Positive echo showing endocardial involvement.
83
Name 4 types of IE.
1. Left sided native IE.
2. Left sided prosthetic IE.
3. Right sided IE (rarely prosthetic).
4. Device related IE e.g. pacemakers, defibrillators.
84
Which type of IE is more likely to spread systemically?
Left sided IE - these are more likely to cause thrombo-emboli.
(Right side IE could spread to the lungs).
85
IE: risk factors?
1. Having a regurgitant or prosthetic valve.
2. If infectious material is introduced into the blood stream or during surgery.
3. Hx of IE
4. congenital HD
86
IE: aetiology?
- Staphylococcus aureus (IVDU, diabetes and surgery) *most common cause*
- Pseudomonas aeruginosa
- Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic and optochin resistant (*Strep. mutans, strep, sanguis, strep. milleri & strep. oralis)*
- strep bovis
- enterococci
- coxiella burnetti
87
IE: symptoms?
FROM JANE
FEVERS
Roth spots (Roth spots retinal haemorrhages with white or clear centres seen on fundoscopy)
osler nodes(tender nodules in the digits)
murmur (heart murmur)
janeway lesions
anaemia
nail bed haemorrhages (splinter haemmorhages)
emboli
88
IE: management?
1. Antibiotic treatment (which one is decided on organism ascertained from cultures) for 4-6 weeks
---> If staphylococcus then use Vancomycin
----> & Rifampicin (if MRSA)
---> If not staphylococcus then use penicillin ideally Benzylpenicillin & Gentamycin (doesn’t work on own since cannot get through bacterial cell wall)
2. Operate if not cured w ab
- In term of **prevention** recommend **GOOD ORAL HEALTH** and **inform** patients
of **symptoms** that may indicate **infective endocarditis**
89
IE: epidemiology?
```
IV drug users,
immunocompromised patients,
people with prosthetic valves,
aortic/mitral valve disease, p
poor dental hygiene,
pacemakers,
IV cannula
```
90
ACS: common cause?
uncommon causes?
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.
1. Coronary vasospasm.
2. Drug abuse.
3. Coronary artery dissection.
91
MI: complications? (7)
1. Heart failure.
2. Rupture of infarcted ventricle.
3. Rupture of interventricular septum.
4. Mitral regurgitation.
5. Arrhythmias.
6. Heart block.
7. Pericarditis.
92
MI: signs/symptoms?
1. Unremitting and usually severe central cardiac chest pain.
a. Pain occurs at rest.
b. pain may radiate to left arm, jaw, neck
3. Sweating
4. Breathlessness.
5. Nausea/vomiting.
6. 1/3 occur in bed at night.
7. - Distress and anxiety
- Pale, clammy and marked sweating
- Significant hypotension (low BP)
- Bradycardia or tachycardia
93
ECGs of someone with NSTEMI / STEMI / UA?
The ECG from someone with NSTEMI may be normal or might show T wave inversion and ST depression.
---> Will produce a pathological Q wave some time after MI so also known as Q-wave infarction
STEMI
- ST elevation
- Tall T waves
- L bundle branch block (LBBB)
- Will produce a pathological Q wave some time after MI so also known as Q-wave infarction
94
What would the serum troponin level be like in someone with unstable angina?
Normal.
95
A raised troponin is not specific for ACS. In what other conditions might you see a raised troponin?
1. Gram negative sepsis.
2. Pulmonary embolism.
3. Myocarditis.
4. Heart failure.
5. Arrhythmias.
96
STEMI vs NSTEMI: Pathophysiology?
STEMI
- zone of necrosis extends across the whole thickness of wall - **transmural infarct = STEMI**
```
NSTEMI
endocardium (farthest away from artery) = subendocardial infarct = NSTEMI
```
97
STEMI vs NSTEMI: Investigations?
STEMI
ECG:
---- ST elevation
- Tall T waves
- L bundle branch block (LBBB) William 1 and 6
- Will produce a **pathological Q wave** some time after MI so also known as Q-wave infarction
FBC:-
increased Troponin I or T or increased CK-MB
3. Coronary angiography.
4. Cardiac monitoring for arrhythmias.
NSTEMI
- FBC
troponin results - abnormal
- ECG
ST depression and T wave inversion
Will produce a pathological Q wave some time after MI so also known as Q-wave infarction
- NO ST SEGMENT ELEVATION
98
STEMI vs NSTEMI:
1st line management?
treatments for stemi and nstemi
INITIAL MANAGEMENT = MONAC
M = MORPHINE (IV OPIODS)
O = OXYGEN
N = NITRATES
**A = ASPIRIN 300 MG stat**
C = CLOPIDOGREL (a p2y12 inhibitor)
NSTEMI and STEMI
- -->> 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
- If not possible then give patient fibrinolysis and then transfer to PCI centre after infusion
--->>CABG
--->>Fibrinolysis -** enhance the **breakdown** of **occlusive thromboses** by the **activation** of **plasminogen** to form **plasmin**
AND ALSO RISK FACTOR MODIFICATION
- Stop smoking
- Lose weight and exercise daily
- Healthy diet
- Treat hypertension & diabetes
- Low fat diet with statins
99
STEMI and NSTEMI:
| secondary prevention?
**acab**
- **A**CE inhibitors
- **Clopidogrel** (to prevent clots forming)
- **A**spirin (to rpevent clots forming)
and **A**torvastatin
- **B**eta-blockers
and warfarin if large mi
100
where are each of the heart sounds heard?
aortic valve = RHS 2ND intercostal space
pulmonary valve = LHS 2nd intercostal space
mitral valve = LHS 5th intercostal space
tricuspid valve = LHS 4TH intercostal space
101
In what diseases are ACE inhibitors clinically indicated?
1. Hypertension.
2. Heart failure.
3. Diabetic nephropathy.
102
Heart Failure: aetiology?
most common cause?
(describe the 4 causes u need to know in detail)
Ischaemic heart disease (IHD) - MAIN CAUSE
Cardiomyopathy (disease of heart muscles, where the walls have become thickened, stiff or stretched)
- Cor pulmonale
- Hypertensive
- Valvular heart disease e.g. aortic stenosis, aortic and mitral regurgitation
- Alcohol excess
- Any factor that increases myocardial work e.g. obesity.
anaemia, arrhythmias, hyperthyroidism, pregnancy and
103
Heart Failure: risk factors?
Why are men more commonly effected by heart failure than women?
- 65 and older
- African descent
- Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
- Obesity
- People who have had an MI
Women have 'protective hormones' meaning they are less at risk of developing heart failure.
104
Heart Failure: Classification of Heart Failure?
- Systolic versus diastolic failure:
1. Systolic failure: the ability of the heart to pump blood around the body is impaired.
2. Diastolic failure: the heart is pumping blood effectively but is relaxing and filling abnormally.
this means that blood backs up into the lungs which is why HF aka congestive HF bc of congestion (build up)
Acute vs chronic
* *Acute:**
- Often used exclusively to mean new onset or decompensation of chromic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension
**Chronic:**
- Develops slowly
- Venous congestion is common but arterial pressure is well maintained until very late
105
HF: investigations in order?
1. ECG. - Shows underlying causes; ischaemia, left ventricular hypertrophy in hypertension or arrhythmia
2. CXR - might show cardiac enlargement.
3. FBC - Natriuretic peptide levels - raised indicate heart failure.
4. If both ECG and BNP abnormal then go to echocardiogram
106
HF: management?
ABAL
acei, beta, aldos, loop diure
Vasodilator therapy
---->>>>(ACEi, beta blockers) via the neurohumoral blockade (RAAS-SNS).
- --->>> diuretics
- --->>> digoxin
- ---->>> inotropes
107
Give 4 signs you might see on a CXR taken from someone with heart failure.
1. Pleural effusion.
2. Dilated pulmonary arteries.
3. Kerley B lines.
4. Bat's wings.
5. Cardiomegaly.
ABCDE
108
HF: symptoms?
three cardinal symptoms?
Give 3 signs of left heart failure.
and give explanations to some symptoms
Three cardinal symptoms are; shortness of breath, fatigue & ankle swelling
- Dyspnoea especially when lying flat (orthopnoea due to pul oedema)
- Cold peripheries
- Raised jugular venous pressure (JVP)
- Murmurs and displaced apex beat
- Cyanosis
- Hypotension
- Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output
- Tachycardia due to activation of sympathetic system
- Third & fourth heart sounds
- Ascites
- Bi-basal crackles
RHS Filure:
- Ascites
Raised JVP
LHS Failure:
1. Pulmonary crackles.
2. Added heart sounds (3rd and 4th) and murmurs.
3. Displaced apex beat.
4. Tachycardia.
109
HF: pathophysiology
| in particular compensatory mechanisms?
see goodnotes/notion
110
Cor Pulmonale: define?
pathophysiology?
RV hypertrophy due to pul htn
there is a
lung disorder eg COPD, pul embolism, interstitial lung disease, CF, pul htn
THUS harder to oxygenate blood bc of HYPOXIA
THUS HYPOXIC VASOCONSTRICTION occurs (so baso when alveolis don’t ahve enough oxygen, the capillaries vasoconstricts and blood is redirected away from that bad alveoli)
BUT if there’s loads of alveli like this = LEADS TO increased resistance in lungs and PULMONARY HYPERTENSION (pa > 25mmHg)
THUS inc RV afterload then RV dysfunction and failure
111
Cor Pulmonale: symptoms ?
Often patients with early cor pulmonale are ***asymptomatic***.
- The main presenting complaint is **shortness of breath**.
- Peripheral oedema
- Syncope (dizziness)
- Chest pain
112
AAA: define?
| and aetiology?
Weakening of vessel wall (artery) followed by dilation due to increased wall stress
aetiology:
- high bp
- weak vessel wall
- ischaemia in walls
- myoctic
- IE
113
AAA: risk factors?
- smoking!
- male,
age,
atehrosclerosis
FHx
connective tissue disorders
114
AAA: symptoms and signs in asymptomatic vs symptomatic pt?
Asymptomatic, **lower back/abdominal (left flank) pain**, bruit on auscultation
Ruptured AAA: **severe tearing abdominal pain** with **radiation** to back, flank, groin, painful pulsatile mass, hypovolemic shock, syncope, nausea, vomiting
SIGNS: Hypotension, pulsating mass with heartbeat if in abdo
115
AAA: management in symptomatic aneurysm vs asymptomatic aneurysm?
**Symptomatic** aneurysm require **repair**,
**asymptomatic** aneurysms require **watchful waiting** and repair when exceed **5.5cm** in men and **5cm** in women
**Ruptured** aneurysm requires **urgent** **repair** (EVAR – **Endovascular aneurysmal repair**)
(non surgical candidate = palliative care and analgesia)
116
Aortic Disssection: define?
Tear in the intimal layer of the aorta which leads to a collection of blood between the intima and medial layers creating a false lumen
117
Aortic Disssection: aetiology?
**Chronic HTN**
could be from either *stress* or *increased blood vol (eg in pregnancy*) or *blood vessel coarctation (the narrowing of a vessel)*
**weakened aortic wall**
could be from connective tissue disorders like *marfan’s syndrome or E-H syndrome*
**Aneursyms can cause aortic dissections and vice versa**
118
Aortic Disssection: pathophysiology?
**Tear** in the **intimal** layer → the high pa blood then passes through the media propagating distally or proximally → Blood tunnelled **between intima and media** -> **false lumen**.
As the dissection propagates, flow through the false lumen can o**cclude flow through branches of the aort**a, including the coronary, brachiocephalic, intercostal, visceral and renal, or iliac vessels -> *Ischemia of supplied regions*
119
Aortic Disssection: symptoms and signs?
```
Hypotension,
**asymmetrical blood pressure,**
**pulse deficit (**in downstream artery),
heart/renal failure,
diastolic murmur (crescendo pattern),
hypertension
```
Syncope and
**Sudden and severe tearing pain in chest** r*adiating to back*
120
Aortic Dissection: investigations? (3)
gold standard?
others u can do?
ECG (ST depression usually)
Echo
CXR (widened aorta or mediastinum)
CT Scanning (gold standard)
others:
Transoesophageal Ultrasound - can see false and true lumen
CT angiography or MR angiography
121
aortic dissection: management?
**Fluid resuscitation, inotropes, noradrenaline**, oxygen
**Opioid analgesia**
Surgical intervention (**Endovascular stent-graft repair**)
**Antihypertensives** following surgery and recovery
122
Tetralogy of Fallot: 4 features?
1. Overriding aorta
2. RV Hypertrophy
3. Ventricular Septal Defect
4. Pulmonary Stenosis
123
Tetralogy of Fallot: Pathophysiology?
1. Overriding aorta which results in
2. Pulmonary Stenosis - this creates a high pressure in RV than LV so
2. RV Hypertrophy
3. And bc of this Ventricular Septal Defect
It means that blue blood will travel into LV and get into systemic circulation - causing pt to be blue
meaning babies can be born blue
124
Tetralogy of Fallot: Signs and symptoms?
1. Cyanosed/blue
2. Exertion all dysponoea
3. Systolic Ejection Murmurs
4. CXR: boot shaped heart
5. Low birth weight and growth
6. Delayed puberty
125
Tetralogy of Fallot: management?
Risks throughout life?
Full surgical treatment during first two years of life due to the progressive cardiac debility and cerebral thrombosis risk
Often get pulmonary valve regurgitation in adulthood and require redo surgery
Small sudden death risk
Ongoing endocarditis risk
126
Ventricular Septal Defect (VSD): Define.
| Pathophysiology of small vs large defects?
Shunt between right and left ventricles
Small defects:
This means blood can travel from LV (bc at a higher pa) into RV. Baso a left-right shunt
Large defects:
Large volumes of blood will flow into RV from LV and pul htn will develop
And eventually, eisenmenger’s syndrome can develop
RV pa > LV pa
Means blood will flow into LV - blue blood will get into systemic circulation and pt will be cyanosed
127
VSD (ventricular septal defect): clinical manifestations?
Large defects:
1. Eisenmenger’s syndrome can develop and = cyanosed pt
2. Small breathless skinny baby
3. Increased resp rate
4. Tachycardia
5. CXR: big heart
6. Murmurs - vary in intensity
Small defects:
1. Dyspnoea
2. CXR: normal heart size
3. Normal heart rate
4. Large systolic murmur
5. Well grown
6. Thrill (buzzing sensation)
128
VSD: management?
1. Medical initially since many defects will spontaneously close
2. Surgical closure
(If small then no intervention is required)
(If moderately sized lesion; furosemide, ACE inhibitor e.g. ramipril and digoxin may suffice)
129
ASD: define and Pathophysiology?
Small heart defects vs large heart defects?
Abnormal connection between both atrias
LA pa > RA pa so blood flow/shunts left->right
Thus = increased pulmonary flow
Thus RV dilation and RV hypertrophy
Pulmonary htn so eisenmenger’s syndrome can occur
Small heart defects: - small increase in flow
No right heart dilatation
No symptoms
```
Large heart defects:
Significant increased flow through the right heart and lungs in childhood
- Right heart dilatation
- SOB On Exertion
- increased chest infections
```
130
ASD: symptoms and signs?
- dyspnoea
- exercise intolerance
- pul flow murmur!!!!!!!
- fixed split second heart sounddd!!! (Bc of delay of pul valve closing)
CXR:
- big pul arteries
- big heart
ECG:
- RBBB due to RV dilatation
Echo:
Hypertrophy and dilation of rhs
131
Patent Ductus arteriosus (PDA):
| Define and Pathophysiology?
Persistent connection between aorta and left proximal branch of pulmonary artery
In foetus - pul vascular resistance is high SO
pul artery pa > aorta pa
And within few hours of birth - due to low pulmonary bp - ductus arteriosus usually closes up
When it doesn’t - aorta pa > pul artery pa - then pul htn increases a lot - and eisenmenger syndrome can occur (when pul pa> aorta and blood starts to flow right to left and blue blood gets into systemic circulation)
And leads to RHS HF bc of RV hypertrophy
132
PDA: signs and symptoms?
- continuous machinery murmurs
- bounding pulse
- if large then large heart and breathlessness
- eisenmenger’s syndrome with cyanosis
(Extra)
- tachycardia
- ECG: left atrial abnormality and LV hypertrophy
133
PDA: management?
Can be closed surgically or percutaneously
Venous approach may require an AV loop
Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure
134
CoA: define and Pathophysiology?
And epidemiology?
Excessive sclerosing (scarring) that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
A narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus
This results in stronger perfusion to upper body compared to lower body
—-> bc a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body,
(Resultant decreased renal perfusion leads to systemic hypertension that persists even after surgical correction)
Men>women
135
CoA: symptoms and signs?
- htn - right arm htn
- also htn in upper limbs
- discrepancy blood pressure in upper and lower body - radial pulse is stronger than femoral pulse (there is a delay in femoral pulse)
- bruits (buzzes) over the scapulae and back from collateral vessels
- CXR: dilated aorta at site of coarctation
- murmur
- ECG: LV hypertrophy
136
CoA: management?
— surgery
— Balloon dilatation (preferred for re-coarctation) and stenting
— BUT Risk of aneurysm formation at the site of repair
137
Rheumatic Fever: define
Systemic infection from Lancefield Group A β-haemolytic streptococcus infection
138
Rheumatic Fever: Complications?
- Valvular Diseases - mitral regurgitation and mitral stenosis and aortic stenosis and aortic regurgitation
- IE bc They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis
139
Rheumatic Fever: symptoms and signs? (Main)
Erythema marginatum (red rash with raised edges and clear centre on trunk, thighs, or arms), !!!!
Fever
Arthritis (painful and tender joints)
Chorea (jerky movements)
140
Rheumatic Fever: Pathophysiology?
- an antibody (baso you’ve developed immunity against strep infection) - this ab cross reacts with valve tissue (so cardiac myocytes or valvular glycoproteins))
Results in localised inflammation and subsequent scarring aka PERMANANT DAMAGE
141
Shock: define
Describe/Define the 5 types:
When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.
Cardiogenic = due to heart problems/sudden inability of heart to pump SUFFICIENT blood to body
Neurogenic = due to problems w nervous system
Anaphylactic = due to severe reaction to allergen / Sudden onset of life-threatening airway and/or breathing and/or circulation problems after exposure to a trigger
Haemorrhagic/Hypovolemic = due to fluid loss/too little blood vol
Septic = due to infection / Toxins (endotoxins) in blood (normally bacterial infection) causes blood vessels to vasodilate and leak
142
Shock: Hypovolemic/Haemorrhagic shock aetiology?
Due to fluid loss or blood loss
Eg dehydration or haemorrhage
1. Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
2. Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
