Cardiology Flashcards
Function of a ECG
representation of the electrical events of the cardiac cycle
Function of the SA node?
dominant pacemaker with an intrinsic rate of 60-100 bpm
Function of the AV node?
backup pacemaker with an intrinsic rate of 40-60 bpm
Another pacemaker besides the two nodes?
ventricular cells - intrinsic rate of 20-45 bpm
Impulse conduction pathway of the heart with ECG phase
Sinoatrial node - AV node (flat between P&Q)- bundle of His - bundle branches - Purkinje fibres (all QRS)
Standard calibration & how to determine pos / neg of wave?
- 25 mm/s or 0.1 mV/mm calibration
- impulses that travel towards the node causes an upright positive deflection, goes away causes a negative deflection
To determine heart rate from ECG graph
300 / # large sq between 2 R waves
If heart rate is irregular
count # QRS complex on the strip, usually a strip is 10 seconds long so multiply number of complexes by 6
What does the P wave represent in the heart cycle?
atrial depolarisation, electrical summation within the atrium
features of the P wave in ECG
normally
<120 ms wide, <0.3 mV tall
<3 s. sq wide, <2.5-3 small sq tall
always positive in lead I, II
always negative in lead aVR
How would atrial enlargement show up on the ECG?
Right AE - tall P wave (P pulmonale)
Left AE - bifid, broad notched P wave (P Mitrale)
What does the PR interval represent in the heart cycle?
= start of P to start of QRS
sinoatrial depol, atrial depol, conduction of AV junction so from A to V (node & bundle of His) (in which there is a delay)
Pathological principles of PR interval
if shorter .. if longer ..
Longer: disorders of the AV node and specialised conduction tissues
Shorter: in younger patients and preexcitation
One cause of short PR interval
Wolff Parkinson White Syndrome - extra conduction pathway causing rapid heartbeat with short PR and slurred QRS
One cause of long PR interval
first degree heart block
What does the QRS complex represent in the heart cycle
= start of Q to end of S
- ventricular depolarisation (& purkinje and bundle branches)
- also when atrial repolarisation occurs
Features of the QRS complex in ECG
normal <120ms
size of complex relates to myocardial mass
predominantly neg S wave in V1, transition to positive R by V6
Pathological principles of QRS complex
if broader .. if smaller .. if taller …
Broad QRS = ventricular conduction delay or bundle branch block
Smaller = obese patient, pericardial effusion, infiltrative cardiac disease
Taller QRS = thin patient, LV hypertrophy (S wave in V1 and R wave in V5/V6 > 35mm)
Features of hypertrophies of the ventricles
- deeper waves (best seen in 1 and 6!)
- S wave in V1 and R wave in V5/V6 > 35mm or R wave is 11-13
- due to hypertension or valvular disease
- diagnose using sokolow & lyon criteria
What does the ST segment represent in the heart cycle
interval between ventricular depolarization and repolarization
Features of a ST segment
flat = isoelectric
so elevated or depressed = pathology but 1mm or more is normal in V1 and V2
Diseases in which ST segment is elevated
Early repolarisation, myocardial ischaemia, inflammation, pericarditis or myocarditis
What does the T wave represent in the heart cycle
ventricular repolarisation
Features of a T wave
normal = asymmetrical, first half having a gradual slope than second
12.5% - 66% of amplitude of R but < 10mm
Abnormal T wave can represent (3)
Nonspecific pathology, but can indicate
- ischaemia or infarction
- myocardial strain (hypertrophy)
- myocardial disease (cardiomyopathy)
What does a QT interval represent in the heart cycle
= start of QRS to end of T
time taken for ventricular depolarisation and repolarisation
Features of QT interval
= 0.35-0.45s corrected for heart rate
Should not be extended to halfway point of two QRS complexes
Causes of QT pathology
- drugs, congenital, electrolyte disturbances
- excessively rapid or low repol can be arrhythmogenic
- long QT or short QT syndromes
What is a U wave?
follows after T wave, small round and symmetrical
origin unknown but more common when HR <65bpm
Features of a U wave (abnormal and normal)
should be <25% of T wave voltage, max 1-2mm
abnormal when prominent or inverted
What is the QRS axis
overall direction of the heart’s electrical activity
Abnormalities of QRS axis may be due to ..
As QRS = L&R ventricular depolarisation, abnormalities will show
- ventricular hypertrophy
- conduction blocks or infarction
How to determine the QRS axis
By looking at the nature of Lead I and lead aVF, combine and determine, confirm through lead II
(I) (aVF) pos pos normal pos neg LAD neg pos RAD neg neg indeterminate axis
What do arrhythmias show
Ion channels that conduct the action potentials are affected
What affects the amplitude of deflection as shown on the ECG?
mass of myocardium
ventricle has a larger wave than atrium
What affects the width of deflection as shown on the ECG?
speed of conduction
Causes of tachycardia
> 100 bpm
atrial fibrillation, atrial flutter
Causes of bradycardia
< 60 bpm
- conduction tissue fibrosis / wear and tear
- ischaemia
- inflammation / infiltrative disease
- drugs
Causes of diseased ventricular rhythm
caused by cell to cell propagation
Causes of diseased sinus rhythm
- disease of the sinus node
- sinus pause - lack of cardiac output during the time
- AV node / distal conduction problems
How is AV block classified
For every QRS wave, there should be a P wave preceding it (1:1)
Define 1st degree AV block
longer PR interval
still 1:1 P:QRS
Define 2nd degree AV block
2:1
One conduct and one doesnt
Two subtypes, Mobitz I and II
Define Mobitz type I 2nd degree AV block
gradual increase in length of PR intervals until it eventually drops, no conduction to QRS
Define Mobitz type II 2nd degree AV block
- sudden unpredictable loss of AV conduction and loss of QRS
- PR interval randomly seen // alternating with no R
- due to loss of conduction in bundle of His, purkinje fibres
Define 3rd degree AV block
no influence of atria at all on ventricle (complete heart block)
How to identify bundle branch blocks
identify through V1 and V6 M or W pattern - wiLLiam maRRow
Features of left bundle branch block
wilLLiam
- W in V1
- LL - left!!
- M in V6
Features of right bundle branch block
maRRow
- m in V1
- RR - right!
- W in V6
Signs of ischaemia and infarction
- flattening of T wave
- ST segment depression
(STemi and non stemi)
Signs of a full infarction
- SR segment elevation
- Inversion of T
- isoelectric ST, T still inversed
- Q wave - old infarction
Define atherosclerosis
degenerative disease where atherosclerotic plaques form in the intima or L&M arteries. rupture will lead to thrombus formation, partial / complete arterial blockage / heart attack
Cause or risk of atherosclerosis
obesity / age / family history
- systemic hypertension
- smoking
- diabetes m
- elevated serum cholesterol / hyperlipidemia
What triggers the formation of the atherosclerotic plaque (2 physical properties)
- fatty streaks in children to AP
- injuries to endothelium or arterial wall (turbulent flow at bifurcations / neointima formation)
- tissue response of vascular wall to injurious agents
Predecessor of atherosclerotic plaques
fatty streaks - may disappear or progress
What is the fatty streak made of and where is it found
- lipid laden macrophages / T lymphocytes
- intimal linings, in children
Composition of atherosclerotic plaques
- endothelial surface
- fibrous cap
- degenerate material / necrotic core
- (platelet derived) growth factor
- lipid
- inflammatory cells - lymphocytes
- connective tissue
- calcification / damage to local wall
Complications of plaque presence
occlude vessel lumen: restrict blood so angina, chronic narrowing of blood vessel, dissection
Briefly outline the development of plaques
- fatty streaks / injury to endothelium
- Injury to endothelial cells → endothelial dysfunction → signal sent to circulating leukocytes → leukocyte accumulate & migrate into vessel wall → inflammation, with:
- LDL causes endothelial dysfunction → response to injury hypothesis where chemoattractants & neutrophils are released e.g. IL 1, 6, 8 and CRP
What is a fibrous cap
layer of connective tissue full of collagens (strength) and elastin(flexibility) laid by smooth muscle cell that overlies lipid core and necrotic debris
Features of the smooth muscle cell in the atherosclerotic lesion
can move around
Outline how an atherosclerotic plaque may rupture
- fibrous cap has to be resorbed and redeposited for maintenance
- if balance shifts: increased enzyme activity (inflammatory conditions) : chew away the plaque and led blood in to the wall: cap becomes weak and plaque ruptures leading to thrombosis
Other growth mechanism of the plaque
Haemorrhage - results from rupture or leakage of microvessels within
(the other one is platelet drived growth factors)
Presentation of atherosclerosis
- angina - worse in exercise, stress or comorbid
- MI
- chronic congestive heart failure
- sudden death
Complications of plaque rupture
- acute occlusion
- chronic & significant narrowing of blood vessel
- aneurysm
- thrombosis: could impact downstream esp to feet, toes & leg
- dissection
Pharmacological treatments for atherosclerosis
- *canakinumab**: inhibit interleukin-1 (big boss for inflammation):
- *aspirin** !! both as management and prevention
- *clopidogrel**- inhibit platelets
- *statins** - inhibit HMG CoA reductase, reduce cholesterol synthesis
- *PCSK9 inhibitors** if statins don’t work
colchicine:low dose anti inflam
procedural treatment for atherosclerosis
if coronary artery disease:
Percutaneous Coronary Intervention = stenting
- uses drugs such as sirolimus or rapamycin to inhibit regrowth
define aneurysm
if there is a permanent dilatation of the artery TWICE the normal diameter
normal diameter of the aorta?
2cm - but increases with age
classification of aneurysms
true or false
aortic aneurysms classified as abdominal or thoracic
define a true aneurysm
- all layers of arterial wall involved in abnormal dilatation
most commonly 2 aorta (abdominal and thoracic), the 3 legs (iliac, popliteal and femoral arteries)
define a false aneurysm
aka pseudoaneurysm
- only the outer layer = adventitia is involved in collection of blood, often after traumaor a perforating injury
how are aortic aneurysms classified?
abdominal or thoracic
cause & risk of abdominal aortic aneurysms
atherosclerosis (and factors)
male, smoke, HT, COPD, HL, age (>60) !
present of unruptured abdominal aortic aneurysms
- pain in abdomen, back, loin or groin (due to impaired blood flow to lower body)
- pulsatile abdominal swelling - less pronounced!
present of ruptured abdominal aortic aneurysms
- IM/cont abdominal pain - radiate to back, iliac fossa or groin
- pulsatile abdominal swelling
- collapse, hypotension, tachy, profound anemia, death
invest of abdominal aortic aneurysms
- abdominal ultrasound! - assess aorta to degree of 3mm
- CT or MRI angiography
treat of abdominal aortic aneurysms
- monitor small <5.5cm
- treat cause, modify risk (smoke / BP / lipid)
- open surgical or endovascular - stent via femoral or iliac arteries for those <5.5cm
epidem of thoracic abdominal aneurysm
ascending, arch or descending thoracic aorta may become aneurysmal
ascending - Marfan or hypertension
descending or arch - secondary to atherosclerosis and rarely syphilis
risk factors for thoracic abdominal aneurysm
- genetic influence
- hypertension, age, smoking, COPD
- atherosclerosis
- previous aortic aneurysm repair
- bicuspid or unicuspid valves
normal size of mid-descending thoracic aorta
26-28mm
patho of thoracic abdominal aneurysm
inflammation / proteolysis & reduced survival of the smooth muscle cells in aortic wall
once aorta reaches a crucial diameter (6 up 7 down) it loses all distensibility so a rise in BP can trigger dissection or rupture
Present of thoracic abdominal aneurysm
- most are asymptomatic
- pain in chest, neck, upper -mid back, epigastrium
- aortic regurgitation
- fever if infective, symptoms from compression
how would you diagnose thoracic abdominal aneurysm
CT, MI
aortography may be helpful in finding the position
echocardiography for aortic dissection
ultrasound
how would you treat thoracic abdominal aneurysm
Ruptured = immediate surgery Symptomatic = surgery regardless of size;
- regular monitoring by CT or MRI every 6 months
- rigorous BP control using beta blockers e.g. bisoprolol
- smoking cessation and treat cause
how does an aortic dissection form?
blood is forced through a tear in the aortic intima, through the medial layer and flows between the layers of the aorta. Layers are forced apart resulting in dissection
Where would blood in the dissecting aneurysm flow
layers in the aortic media (through the aortic intima)
Classification of aortic dissection
according to timing of diagnosis from the origin of symptoms
- acute less than 2 weeks
- subacute 2-8 weeks
- chronic more than 8 weeks
causes of aortic dissection
- trauma: shearing stress in TA
- inflammatory, degenerative e.g. Marfan’s
- atherosclerotic
- hypertension!!
- inherited
- connective tissue disorders
Briefly detail how an aortic dissection forms
- tear in intimal lining of the aorta
- a column of blood under pressure enters the aortic wall, forming a haematoma which separates intima from adventitia
- false lumen is created, extends in either direction: anterograde = to bifurcations, retrograde = to aortic foot
2 most common sites of intimal tears
- within 2-3cm of aortic valve
- distal to the left subclavian artery in the descending aorta
(perhaps also at turbulent flows and bifurcations?)
present - aortic dissection
- sudden onset of severe and central chest pain that radiates to the back and down the arms
- pain often tearing in nature and may be migratory
- hypertension
- pain is maximal from time of onset unlike MI where pain increases in intensity
- potential absence of peripheral pulse
- potential neurological symptoms & shock: loss of blood supply in spinal cord
- potential aortic regurg, coronary ischaem, cardiac tamponade
- distal extension may produce acute kidney failure, acute lower limb ischaem or visceral ischaem
how would you diagnose aortic dissection
- CXR for widened mediastinum
- CT MRI to see clearly (urgent)
treatment for aortic dissection
aim: contain propagating haematoma by reducing arterial pressure and immediate surgical repair
- urgent antihypotensive - IV beta blockers: metoprolol or vasodilators e.g. IV GTN
- analgesia and surgical repair or stent
- long term follow up with CT or MRI
what is peripheral vascular disease
essentially lower limb ischaemia - partial blockage of peripheral vessels by an atherosclerotic plaque / thrombus resulting in insufficient perfusion of the leg
symptoms of mild peripheral ischaemia
- stress induced physiological malfunction
- exercise induced angina
- intermittent claudication: cramping pain induced by exercise and relieved by rest
- pain is distal to site of atheroma due to lactic acid production
- caused by inadequate O2 supply
- limb is usually cold, leg pulses often absent
symptoms of moderate peripheral ischaemia
- ischaemic cardiac failure
- critical limb ischaemia:
- rest pain is typically nocturnal
-
limb is cold, often pulseless
- chronic and most severe becomes peripheral vascular disease
Differential diagnosis of peripheral vascular disease
- osteoarthritis of hip/ knee if knee pain at rest
- peripheral neuropathy if tingling
how would you diagnose peripheral vascular disease
- 1st line color duplex ultrasound
- for severity Ankle Brachial Pressure Index (ABPI):
- 0.5 - 0.9 = intermittend claud
- < 0.5 = critical leg ischaemia
- MR/CT angiograpy to assess extent, location and quality of distal vessels
Exclusion principle
- ESR / CRP for arteritis (= raised)
- FBC to exclude anemia (= raised RBC)
- ECG for cardiac ischaemia
How does an ABPI work?
Ankle Brachial Pressure Index
- compares between the cuff pressure in ant/post tibial arteries vs the brachial artery
- Doppler ultrasound used
Numeral criteria on an ABPI to diagnose leg ischaemia
0.5-0.9 - intermittent claudication
< 0.5 - critical leg ischaemia
What is acute lower limb ischaemia?
sudden decrease in limb perfusion that threatens the viability of the limb
occurs either due to embolic disease or thrombotic disease (or trauma)
Examples of embolic disease
- cardiac thrombus, arrhythmias
- rheumatic fever
- may also occur secondary to aneurysm thrombus or thrombus on athero plaque
Examples of thrombotic disease
- usually forms on a chronic atherosclerotic stenosis in patient w/ prev claudication
- also in normal vessels in individuals who are hypercoagulable bc of maliganancy or thrombophilia defects
- popliteal aneurysms: may thro/embose distally!
Symptoms of thrombotic disease!
6P’s
- Pain
- Pallor
- Perishing cold
- Pulseless
- Paralysis
- Paraesthesia (tingling / prickling, pins & needles)
- the more P’s the more sudden and complete the ischaemia
Treatment of thrombotic disease?
- Risk factor modification
- smoke: bl supp reduce
- treat HP, HL, diabetes, exercise
- antiplatelet - clopidogrel to prevent progression
- depends if acute or critical limb ischaemia, treat accordingly
Treatment for acute limb ischaemia?
- if patient loses use of side of body and fast irregular pulse
- nature is similar to MI
surgical emergency!
requires revascularisation 4-6hrs to save limb
- angioplasty (widens artery with a balloon)
- intra aterial thrombolysis
- surgical removal of embolus if present
Treatment for critical ischaemia?
- Revascularisation for critical ischaemia
- percutaneous transluminal angioplasty (squash plaque and increase perfusion to reduce ischaemia
- bypass
- amputate if severe
What is intermittent claudication?
Tissue is suffering not dying
- Oxygen debt when doing mild / moderate exercise = build up of lactic acid resulting in pain
- physiological pain is the same as it is in you
What is critical ischaemia? - symptoms and pathology
- severe pain in all toes of the foot relieved by hanging foot over the edge of bed (gravity to perfuse)
- non healing painful ulcer on big toe with no trauma
Tissue is dying! and suffering at rest
- blood supply is inadequate: basal metabolism
- no reserve available for increased demand
- there is resting pain: typically nocturnal
- gangrene / infection risk
Berry aneurysms
- what are they
- where are they mostly found
- normal muscular arterial wall is replaced by fibrous tissue
- points of branching, e.g. circle of willis - A/P communicating artery, middle cerebral artery
Cause of berry aneurysms
- long standing hypertension: damage to wall of blood vessels
- connective tissue disorders: collagen synthesis issues - vessel wall dilated until it pops
- focal area of weakness within the arterial substructure: branching points of circle of willis
Presentation berry aneurysm
- pronounced neurological deficit: recoverable and persistent
Complication berry aneurysm
- subarachnoid haemorrhage risk
- burst = sudden death
Which aneurysm is associated with hypertension and diabetic vascular disease?
Capillary microaneurysm (Carcot Bouchard aneurysm)
Where are capillary microaneurysm mostly found
branches of the middle cerebral artery in hypertension, particularly the lenticulostriate
Complications of capillary microaneurysm
primary hypertensive intracerebral haemorrhage in basal ganglia, cerebellum or brainstem
What are mycotic aneurysms
- weakening of the arterial wall due to bacterial or fungal infection (enter thru bloodstream)
- commonest in cerebral arteries
- bacterial endocarditis = most common underlying infection
Hypertension definition
BP is more than 140/90 mmHg
Stage 1 Hypertension
140/90 to 159/99 mmHg
subsequent ABPM daytime average or HBPM average ranging from 135/85 mmHg to 149/94 mmHg.
Stage 2 Hypertension
160/100 to 179/119 mmHg
subsequent ABPM daytime average or HBPM average 150/95 mmHg or higher.
Stage 3 Hypertension
> 180/120 mmHg
Commonest consequence of hypertension
cardiac failure
atherosclerosis
cerebral haemorrhage
Classification of hypertension
Essential or secondary
Cause of primary hypertension
Multifactorial:
- genetics, excessive sympathetic nervous activity
- high salt intake & abnormal Na/K membrane transport
- abnormal renin-angiotensin -aldosterone system
Cause of secondary hypertension
- *Renal disease**
- chronic kidney disease, esp diabetes
- renal artery stenosis, glomerulonephritis (less common) - negative cycle
- *Endocrine causes**
- adrenal tumors - cortical or medullary
- cushing’s, conn’s
- coarctation of aorta
- drugs: corticosteroids, oral contraceptives
Risk factors for hypertension
- age
- race - more common in blacks
- fam hist
- obese, lack of ex
- smoking, alcohol, diabetes
- salt in diet
- stress
Impact of hypertension on various systems
- vascular
- heart
- nervous
- kidney
- *Vascular**:
- thickening of media of arteries
- accelerate atherosclerosis
- endothelial cell dysfunction
- *Heart**
- increase risk for ischaemic heart disease
- *Nervous**
- intracerebral haemorrhage causing death
- *Kidneys**
- cause/result renal disease
- kidney size reduced, intimal thickening & medial hypertrophy of small vessels
- sclerotic glomeruli increased
What is malignant hypertension
Markedly raised diastolic BP, usually >120 mmHg and progressive renal disease
Quite rare!
Present malignant hypertension
- Diastole > 120mmHg
- Progressive renal disease
- Can occur in previously fit individuals, often black males 30-40’s
- Prominent renal vascular changes
- Acute haemorrhage
- Papilloedema (optic disk swelling caused by increased intercranial pressure)
Consequences of malignant hypertension
- cardiac failure with LV hypertrophy and dilatation
- blurred vision due to papilloedema and retinal hae
- haematuria and renal failure
- severe headache and cerebral haemorrhage
Briefly outline the Renin-Angiotensin-Aldosterone system?
Prorenin’s amino acid hinge, cleaved → Renin, through enzymatic cleavage of angiotensinogen → angiotensin I, through Angiotensin-Converting Enzyme (ACE) → Angiotensin II = vasoconstrictor, can induce hypertension
What is ABPM
Ambulatory Blood Pressure Monitor
- 24 hour BP monitoring and to calculate average BP
- takes a measurement every 20 minutes during the day and less (hourly) during the night
- used to confirm HT diagnosis for those with BP in between 140/90 mmHg and 180/120 mmHg
What is HBPM
Home Blood Pressure Monitor
- for patient to bring home and to calculate average BP
- twice a day for 4-7 days
- two reading per sit down, a minute apart
Treatment goal and principles for hypertension
140/90 mmHg (150/90 mmHg in over 80’s) ± 5/5 for average
- rarely is one med enough so stack step by step until goal is reached
- based on if patient has DM and ethnicity & age; varied 1st & 2nd line then 2rd & 4th same
1st & 2nd line treatment for
- patient with Type 2 DM
- Under 55 & No Type 2 DM
- ACE inhibitor or Angiotensin Receptor Blocker
2. Repeat (1) + CCB or thiazide like diuretic
Treatment steps for
- patient over 55, no DM
- Black African / African Caribbean origin any age
- CCB
2. Repeat (1) + ACE inhibitor or thiazide like diuretic
If 1st and 2nd line treatment fails for hypertension, next step would be …
- ACEi or ARB with CCB and diuretic
(mind connecting words!) - If resistant hypertension: confirm through A/HBPM, check postural hypertension and discuss adherence.
Add:
• low-dose spironolactone if blood potassium level is ≤4.5 mmol/l
• alpha-blocker or beta-blocker if blood potassium level is >4.5 mmol/l
Seek expert help if 4 drugs and still uncontrolled BP
Examples of ACE inhibitors
Ramipril or Enalapril
Side effect cough!
Main side effect of ACEi / Ramipril
cough (15%)
if ACEi contraindicated or not tolerated, another choice as first line
Angiotensin Receptor Blocker (ARBi)
Example of ARBi
Cadesartan or Losartan
Example of Calcium Channel Blocker
Nifedipine or Amlodipine
Side effect oedema!
Main side effect of CCB / amlodipine
oedema
Example of diuretics
Bendroflumethiazide: thiazide (distal tube, less potent)
Furosemide: loop of henle diuretic, more potent
Indapamide:
Example of beta blockers
bisoprolol or metoprolol
consider in young people esp if intolerant to ACEi or ARB
What is the white coat effect?
a discrepancy of more than 20/10 mmHg between clinic and A/HBPM measurements. in 15-30% of people. tackle: use A/HBPM
Where does the first heart sound come from?
- mitral and tricuspid valve closure
Where does the second heart sound come from
- aortic and pulmonary valve closure
When would there be a 3rd heart sound and what is it associated with?
- early diastole during rapid ventricular filling
- normal in children and pregnant women
- associated with mitral regurg and heart failure
When would there be a 4th heart sound and what is it associated with?
- ‘gallop’, in late diastole
- produced by blood being forced into a stiff hypertrophic ventricle
- associated with left ventricular hypertrophy
What is angina?
chest pain or discomfort as a result of reversible myocardial ischaemia
Pathophysio angina
narrowing of one or more of coronary arteries due to
- atheroma / stenosis of coronary arteries thereby impairing blood flow
- valvular disease
aortic stenosis
arrhythmia
anaemia = thus less O2 transported
or ischaemic metabolites including adenosine stimulating nerve endings and producing pain
risk factors for angina
- smoking
- obesity and umbrella: HP, DM, sedentary lifestyle, hypercholesterolaemia
- age, family history, genetics
Types of angina
- Stable angina: induced by effort and relieved by rest
- Unstable (crescendo) angina: angina or recent onset (less than 24 hours) / deterioration in previously stable angina & symptoms ar rest / angina with increasing freq & severity even at rest or minimal exertion = acute coronary syndrome!
- Prinzmetal’s angina: caused by coronary artery spasm (rare)
Presentation angina
- central chest tightness or heaviness
- provoked on exertion? after meal / cold windy weather / anger / excitement
- relieved by rest? or GTN spray?
- radiation of pain to arms? neck? jaw or teeth?
- dyspnoea, nausea, sweatiness and faintness
Angina scoring
Out of 3
- Central, tight, radiation to arms, jaw & neck
- precipitated by exertion
- relieved by rest or GTN spray
Out of 3
3/3 = typical angina
2/3 = atypical pain
1/3 = non-anginal pain
How would you diagnose angina
ECG
- often normal
- ST depression, flat or inverted T
- look for signs of past MI
Treadmill / exercise ECG
- trying to induce ischaemia
- ST depression is late-stage ischaemia
- bundle branch block not suitable
CT scan calcium scoring
- if atherosclerosis in the arteries then the calcium will light up white, if significant calcium then = angina
Catheterisation
SPECT / myoview = radio-labelled tracer injected into patient, take (light) up where good blood supply
- no light after exercise = myocardial ischaemia
How would you diagnose angina
ECG
- often normal
- ST depression, flat or inverted T
- look for signs of past MI
Treadmill / exercise ECG
- trying to induce ischaemia
- ST depression is late-stage ischaemia
- bundle branch block not suitable
CT scan calcium scoring
- if atherosclerosis in the arteries then the calcium will light up white, if significant calcium then = angina
Catheterisation
SPECT / myoview = radio-labelled tracer injected into patient, take (light) up where good blood supply
- no light after exercise = myocardial ischaemia
A treatment plan for angina
- Treat active attacks PLUS anti-anginal drug PLUS drug for secondary prevention of cardiovascular disease
- modify risk factors through lifestyle changes
- treat underlying conditions
1st line pharmacological PREVENTION for angina (2)
First line
Beta Blockers
- act on B1 receptors in the heart & reduce force of contraction of heart (heart rate, LV contractility, cardiac output)
→ bisoprolol & atenolol
- SE tiredness, nightmares, brady, erectile dysfunc & cold hands and feet
- CONTRAINDICATED asthma, heart failure/block, hypotension & bradyarrhythmias
Calcium Channel Blockers
- arterodilators: dilates systemic arteries resulting in BP drop, thus reduces
1) afterload on heart
2) energy required for same cardiac output
3) work on heart and O2 demand
→ verapamil
- CONTRAINDICATED BETA BLOCKER, AF, HEART BLOCK AND FAILURE, patient with MI history, LV dysfunc
1st line pharmacological TREATMENT for angina (1)
Glyceryl Trinitrate (GTN) spray
- used for active attacks
- venodilator: dilates systemic veins thereby reducing venous return to right heart, also dilates coronary arteries
- reduces preload thus work of heart and O2 demand
- SE profuse headache immediately after use
Differences between verapamil and amlodipine
both CCBs
Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.
Amlodipine = dihydropyridines (DHP)
- potent vasodilators
- act mainly on vascular smooth muscle, relaxes them and dilates arteries
- more dilating less depressing
Verapamil = non-DHP
- acts mainly on the heart
- potent myocardial depressants (inotropic)
- depress cardiac contractility
- depress conduction rate through SA node and slow AV node: useful for SVT, AF
- more depressing less dilating
Inotropic - meaning
modifying the force or speed of contraction of muscles
2nd line for pharmacological PREVENTION of angina
a long-acting nitrate
- GTN is short acting
- Isosorbide mono/dinitrate dose
or
ivabradine [CI resting HR <70 bpm, preg, cardiac his] or
nicorandil or
[CI hypo, G6PD deficient, pulmonary oedema, heart failure (no cardiac MI! good to go]
ranolazine [CI renal or hepatic impairment]
Supplementary drugs for PREVENTION of cardiac events (for angina)
Aspirin
- antiplatelet in coronary arteries (COX inhibitor: reduces prostaglandin synthesis) thereby reduces platelet thrombosis
→ salicylate
Statins
- HMG-CoA reductase inhibitor - reduces cholesterol production by liver
- reduce events and LDL cholesterol
- anti-atherosclerotic
Revascularising procedures for angina
= to restore patient coronary artery and increase flow reserve
= if medical fails or high risk disease identified
Percutaneous Coronary Intervention
- dilating coronary atheromatous obstruction by inflating balloon with stent
- expanding plaque = make artery bigger
- less invasive, convinient, short recovery and repeatable
- risk of stent thrombosis, not good for complex disease
Coronary Arter Bypass Graft (CABG)
- Left Internal Mammary Atery used to bypass proximal stenosis (narrowing) in LAD artery
- good prognosis, deals with complex disease
- invasive, risk of stroke or bleeding, long recovery & one time
