cardiology Flashcards
Define atherosclerosis.
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.
Atherosclerosis: can lead to?
- 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
Give 9 risk factors for atherosclerosis.
Explain for each risk factor the pathophysiological processes that promote the development of atherosclerosis. (see notion)
- Family history.
- Increasing age.
- Smoking.
- Hyperlipidaemia and hypercholesterolaemia (High levels of LDL’s)
- Obesity.
- Diabetes (uncontrolled - hyperglycaemia).
- Hypertension.
- Male Gender
- Lower socioeconomic status
Angina: define
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
Angina: aetiology?
most commonest cause
(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
Angina: risk factors?
- > 6 modifiable risk factors for angina.
- > 3 non-modifiable risk factors
Modifiable:
- Smoking.
- Diabetes.
- High cholesterol (LDL).
- Obesity
- Sedentary lifestyle.
- Hypertension.
Non-modifiable:
- Genetics/Family History
- Increasing Age
- Gender. male bias
Angina: pathophysiology that results from atherosclerosis?
pathophysiology that results from anaemia?
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.
Why are blood vessels unable to compensate for increased myocardial demand in someone with CV disease?
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!
How can angina be reversed?
Resting - reducing myocardial demand.
Angina: presentations?
and how would you describe the chest pain in angina?
- 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.
What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?
Pre-test probability of CAD. It takes into account gender, age and typicality of pain.
Angina: investigations?
- 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).
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?
Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.
Primary prevention vs secondary prevention?
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.
Angina: management?
- Modify risk factors
- Treat underlying conditions
- Pharmacological:
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.
- Beta blockers.
- Nitrates e.g. GTN spray.
- Calcium channel blockers.
- Aspirin.
- Statins.
Angina management: beta blockers
Function
Describe action of beta blockers
give examples
side effects
When might beta blockers be contraindicated?
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*
Angina management: Nitrates:
function?
Describe the action of nitrates.
Side-effects?
- 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
Angina management: statins?
function?
action?
examples?
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
Angina management: Ca2+ channel antagonists/blocker:
function?
action?
give eg
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
Angina management: Aspirin: function? action? side effects? eg?
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
Angina management:
Revascularisation
what is it?
Name 2 types of revascularisation.
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
Give 2 advantages and 1 disadvantage of PCI.
Give 1 advantage and 2 disadvantages of CABG.
pci
- Less invasive.
- Convenient and acceptable.
- High risk of restenosis.
CABG
- Good prognosis after surgery.
- Very invasive.
- Long recovery time.
Why are beta blockers good in chronic heart failure?
They block reflex sympathetic responses which stress the failing heart.
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.)
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
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
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
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
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
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.)
ECG: what would you see on ECG of someone w heart block?
long PR interval and rate is slow
>1 P wave
In which leads must the S wave grow?
From chest leads V1 to V3. It must also disappear in V6.
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
Define sinus rhythm.
Sinus rhythm - a P wave precedes each QRS complex.
ECG of tachycardia?
rate usuallly above 120bpm
P waves may or may not be visible/abnrmal
ECG of atrial fibrillation?
no P wave
QRS complex is usually narrow
ECG of ventricular fibrillation?
no P waves or QRS
completely chaotic and irregular rhythm and rate
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.
Name 4 valvular heart diseases.
- Aortic stenosis.
- Mitral regurgitation.
- Mitral stenosis.
- Aortic regurgitation.
aortic stenosis: aetiology?
- 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
- 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.
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.
Aortic stenosis: 3 symptoms?
- Exertional syncope.
- Angina.
- Exertional dyspnoea.
(^classic triad)
Onset of symptoms is associated with poor prognosis.
think aortic stenosis w any person who has the triad
Aortic stenosis: 3 signs?
- Slow rising carotid pulse and decreased pulse amplitude.
- Soft or absent heart sounds. (second heart sound is less intense)
- Ejection systolic murmur: <> shape.
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
Aortic stenosis: management?
surgical Aortic valve replacement or TAVI(for those who are weaker/other health issues)
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
In what type of valvular heart disease would you hear a ejection systolic murmur?
Aortic stenosis.
Aortic Regurgitation: define
A regurgitant aortic valve means blood leaks back into the LV during diastole due to ineffective aortic cusps.
Aortic Regurgitation: aetiology?
- Bicuspid aortic valve.
- Rheumatic.
- Infective Endocarditis.
4/ Marfan’s and Ehlers-Danlos syndrome - connective tissue disorders
Aortic Regurgitation: pathophysiology?
Pressure and volume overload.
thus
Compensatory mechanisms - LV dilatation, LVH.
Progressive dilation -> HF.
Aortic Regurgitation: symptoms?
patients remain asymptomatic for many yrs before symptoms develop
- Dyspnoea on exertion.
- Angina.
- Syncope
- Palpitations
- Orthopnea.
- Paroxysmal nocturnal dyspnea.
Aortic Regurgitation: 4 signs?
- Wide pulse pressure. (Wide pulse pressure so increased SBP nd decreased DBP)
- Diastolic blowing murmur. at left sternal border
- Systolic ejection murmur.
- Collapsing water hammer pulse (bounding and forceful rapidly increasing and subsequently collapsing)
Aortic Regurgitation: investigations?
CXR and echocardiogram.
Aortic Regurgitation: management?
- IE prophylaxis.
- Vasodilators e.g. ACEi. eg Ramipril will improve stroke volume and reduce regurgitation but only if patient is symptomatic or has hypertension
- Regular echo’s to monitor progression.
- Surgery if symptomatic.
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).
