Ischaemic Heart Disease Flashcards
1
Q
What are the characteristic presentations of myocardial ischaemia?
A
- crushing, gripping, heavy pain centrally on chest
- can radiate to neck, shoulder or jaw (classically L sided radiation)
- assoc. w paraesthesia/heaviness in one or both arms
- assoc. w dyspnoea, N&V
- comes on over mins
2
Q
What are the characteristic presentations of aortic dissection?
A
- severe, central chest pain, radiating to back and down arms
- patients may be shocked + have neurological symptoms secondary to loss of blood supply to spinal cord
- may be signs of distal ischemia or absent peripheral pulses
-comes on over secs
3
Q
What are the characteristics of pleural disease?
A
- localised sharp pain, radiates to back and down arms
- assoc, w costo-chondral tenderness
- pain in shoulder tip suggested of diaphragmic pleural irritation
4
Q
What are the characteristics of oesophageal disease?
A
-retrosternal chest pain (difficult to separate from cardiac)
-worse on bending over or lying down
- relieved by antiacids
5
Q
What are the characteristics of MSK disease (eg. costochondritis)?
A
- can be very severe pain, assoc. w local tenderness
- worse w certain movements , often history of trauma or causative event
6
Q
What is IHD?
A
- aka coronary artery disease
- general term for spectrum of disease caused by atheromatous plaque build up in the coronary arteries -> lack of blood supply in heart
- IHD encompasses both stable angina and acute coronary syndrome (ACS)
7
Q
What is the pathology of atheroma formation?
A
- damage to endothelium due to variety of RFs allows entry to LDLs into intima
- LDLs taken up by macrophages in intima,
+ accumulate excessively as they bypass normal receptor mediated uptake, forming a fatty streak - as the macrophages take up more and more lipid, they release free lipid into the intima
- the macrophages also stimulate cytokines -> leads to collagen deposition by inflammatory cells, and the intimal lipid plaque becomes fibrotic
- at this stage it appears raised and yellow -> leads to pressure atrophy of the media and disruption of the elastic lamina
- incr. secretion of collagen forms a dense fibrous cap to the plaque, which is now hard and white
- the endothelium is fragile and can ulcerate, allowing platelet aggregation and acute vessel blockage.
8
Q
What 4 main characteristics inform us if the chest discomfort is secondary to IHD?
A
- LOCATION: retrosternal, anywhere from umbilicus to jaw
- CHARACTER: tightness, pressure
- DURATION: less than 10 mins, not a few secs
- EXACERBATING FACTORS: cold weather, after heavy meal etc., not respiratory or position
9
Q
What are the risk factors of IHD?
A
- age
- gender (higher in men than pre-menopausal women)
- FH (higher rates if first degree relative had IHD before 50)
- smoking (stopping red. risk by 25%)
- diet (high fat, low fresh fruit & veg)
- obesity (worse if primarily abdominal obesity)
- HPT
- Hyperlipidaemia (high serum cholesterol, esp. if high HDLs/TGs)
- DM: DM, IGT + IFG
9
Q
What is stable angina?
A
- episodic pain that occurs when there is increased myocardial demand
- usually upon exercise, in the presence of impaired myocardial perfusion
10
Q
What is stable angina most commonly due to?
A
- low flow in atherosclerotic coronary arteries (patients with angina have stenosis of over 70% in a main coronary artery)
11
Q
What is stable angina pain like?
A
- classical ischaemic pain of the myocardium
- varies from mild ache to severe pain that provokes sweating and fear
12
Q
What provokes stable angina pain?
A
- exercise
- after meals
- in the cold
- if patient is angry or excited
in some at certain levels of exertion
13
Q
How long is stable angina pain and what else can it be assoc. with?
A
- fades quickly over minutes with rest / GTN
- breathlessness
14
Q
Will stable angina always have abnormal findings on exam?
A
no
15
Q
What are the variants of stable angina?
A
-decubitus angina
- variant / prinzmetal angina
16
Q
What is decubitus angina?
A
- angina precipitated by lying down as there is incr. venous return to the heart
- assoc. w LVF
17
Q
What is variant/prinzmetal angina?
A
- occurs without provocation at rest as a result of coronary artery spasm
- there is ST elevation during episode, consider if ST elevation but no troponin rise
18
Q
What are the investigations for angina?
A
- exclude other causes of chest pain :
- CXR
- Bloods including FBC, HbA1c, lipids, TFTs, troponin
- resting 12-lead ECG
- may be normal, may show signs of previous infarction
- CT coronary arteries (CTCA)
- NICE recommends this as first line investigation to confirm stable angina diagnosis
- non-invasive with very good neg predictive value, less sensitive than invasive coronary angiography
- alternate diagnosis options may include myocardial perfusion scanning or stress echo
19
Q
What is the management for angina?
A
- inform patients stable has a good prognosis
- manage CV risk factors (lifestyle advice, smoking cessation, manage HTN / diabetes / hyperlipidaemia)
- symptomatic treatment
- secondary prevention (statin/low-dose aspirin)
- refer to cardiology if any doubt over diagnosis, atypical features, or refractory symptoms (certain patients may require interventional management eventually eg. PCT, CABG)
20
Q
What is the symptomatic treatment for angina?
A
- GTN spray PRN + B blocker or rate limiting CCB (1st line)
- Never combine b blocker and CCB can cause asystole
- for refractory disease, long acting nitrate therapy may be added, eg. nicorandil or isosorbide mononitrate
21
Q
What is the prescribing advice for nitrates?
A
- sublingual GTN spray first line for symptom relief
- patients should be advised to sit down, rest and spray once beneath tongue, wait 5 minutes, spray again if still pain
- if still pain at 10 mins, call 999 + open door
- can be used prior to angina provoking activities
22
Q
What do nitrates do?
A
- cause marked venorelaxation, thus reducing pre-load on the heart
- can cause venous pooling on standing, thus can cause postural hypotension and dizziness
- can also affect large muscular arteries, reducing aortic pressure and cardiac afterload, as well as dilating coronary vessels
- decr. pre-load and after-load decr. the o2 requirement of the myocardium + coronary vasodilation leads to incr. o2 delivery
- they also relieve the coronary artery spasm of Prinzmetal angina
23
Q
How do beta-blockers work?
A
- b1 adrenoreceptors found mainly on heart, act to incr. HR and SV
- b2 adrenoreceptors act to cause smooth muscle relaxation in many organs eg. trachea
- in IHD, b1 selective b-blockers are used to reduce cardiac rate and force (red. myocardial o2 consumption) with as little broncho-constrictive effect as possible
- also have an anti-HPNive effect by reducing cardiac output
24
How do CCB work?
- dihydropyridines (amlodipine / nifedipine) or rate limiting agents (verapamil /diltiazem)
- all work to prevent SM contraction, red. afterload and causing coronary vasodilation
-rate-limiting agents also act on cardiac calcium channels in the AVN to control the heart rate, exhibiting class IV anti-arrythmic effects
24
What are the SEs of beta-blockers?
- bronchoconstriction (contraindicated in asthma, caution in COPD)
- cardiac depression/bradycardia (can be critical if combined w other rate limiting agents
- hypoglycaemia (impair the sympathetic warning signs of hypos)
25
What are the SEs of calcium channel blockers?
- flushing and headache (as w all vasodilators)
- ankle swelling and constipation (GI SM inhibition)
26
How does Nicorandil work?
- causes marked vasodilation
- is a combined NO donor and also an activator of ATP-sensitive K-channels on vascular SM cells -> hyperpolarisation
27
What is Acute Coronary Syndrome (ACS) made up of?
- unstable angina (UA)
- Acute myocardial infarction:
-> non-ST-elevation myocardial infarction (NSTEMI)
-> ST-elevation MI (STEMI)
28
What is the pathology of ACS?
- similar to IHD w fissuring/ulceration of atheromatous plaques -> thrombosis within coronary arteries and myocardial ischaemia
- can occur in areas of low-grade stenosis which have not previously caused anginal symptoms
29
What is unstable angina?
crescendo angina
- angina occurring at rest, or sudden increased frequency / severity of existing angina
- no rise in cardiac enzymes (troponin)
- pathology caused by fissuring of plaques, thus there is a risk of subsequent total vessel occlusion and progression to AMI
30
What does a diagnosis of acute MI (STEMI/NSTEMI) need?
requires elevations in serum cardiac troponin levels (i.e. cardiac myocyte death has occurred), with additional categorisation based on the ECG:
- ST elevation / new LBBB = STEMI
- No ST elevation / LBBB = NSTEMI
the area of infarction depends on the artery occluded, and the size of infarction depends on how proximal/ distal the blockage is.
31
What does the right coronary artery supply, what MI does blockage cause?
- supplies RA, RV, posterior septum
- blockage gives posterior/inferior MI: leads II, III, aVF
- also supplies AVN in 80% and SAN in 60%
32
What does the left coronary artery split into, what MI does blockage cause?
- splits into circumflex and left anterior descending artery
- blockage gives massive antero-lateral MI : leads I, aVL, V1-V6
33
What does the circumflex artery supply, what MI does blockage cause?
- mainly supplies LA & LV
- blockage gives lateral MI: leads I, aVL, V5/6
34
What does the L anterior desc. artery supply, what MI does blockage cause?
- mainly supplies LV and anterior septum
- blockage gives antero-septal MI: leads V1-V4
35
What are ACS symptoms?
* severe crushing, gripping or heavy chest pain lasting >20 mins (not relived by 3x GTN sprays at 5-min intervals
* radiates to L arm, neck and jaw
* assoc. with dyspnoea, nausea, and sweating, with distress and feeling of impending death
36
What is a silent infarct?
* ACS presenting without chest pain
* particulary in elderly or diabetics, who can present later w variety of symptoms
37
What are signs of ACS O/E?
| can be variable
* sympathetic activation: tachycardia, HTN, pallor, sweatiness
* vagal stimulation: bradycardia, vomiting
* myocardial impairment: hypotension, narrow pulse pressure , raised JVP, basal crepitations
* tissue damage: low grade pyrexia
38
What are some cardiac causes of chest pain?
* coronary artery spasm
* pericarditis/myocarditis
* aortic dissection
39
What are some non-cardiac causes of chest pain?
* PE
* pneumothorax
* oesophageal disease
* mediastinitis
* costochondritis
* trauma
40
What are intial investigations for ACS?
* ECG: essential in all patients presenting w. chest pain, repeated every 15 mins whilst in pain or continuous monitoring in ACS due to high chance of arrythmias developing.
* Bloods:
-> FBC & U&E
-> cardiac enzymes (tropinin I in NUH, to confirm infarction of myocardium)
----> troponin levels rise within 3 hours of onset of symptoms, peak at around 24-48 hours, can be detectable for around 10 days (although variable by assay type)
* CXR: assess for evidence of pulmonary oedema, widened mediastinum in aortic dissection
## Footnote
if diagnosis is still in doubt, transthoarcic echocardiography can confirm presence of regional wall motion abnormalities (reflect areas of infarcted myocardium), or help detect alternative diagnoses
41
What are the ST changes in a non-reperfusion?
5 minutes after event
* tall, pointed T-waves
30 minutes after event
* ST elevation
2+ hours after
* T wave inversion
* q waves develop
days after
* ST segment returns to normal
weeks after
* T wave may return to normal
* Q wave returns
## Footnote
cardiac chest pain w new onset LBBB can be assumed as a STEMI, as further interpretation of the ECG is not possible
42
STEMI generally correlates with a ... thickness myocardial infarct, whereas NSTEMI is a ... thickness
* full
* partial
43
Q waves in NSTEMI?
ST?
unstable angina ST?
* no Q waves develop in an NSTEMI
* may be ST depression, T-wave inversion or other non-specific changes
* in unstable angina, there may be ischaemic ST depression in the leads affected, but there will be no troponin rise (i.e. no infarction)
44
MI leads to the replacement of the infarct area with collagenous scar, occuring in a predictable time course:
* 0-12 hrs: infarct not visible, loss of oxidative enzymes
* 12-24 hrs: infarct pale and blotchy, with intercellular oedema
* 24-72 hrs: infarcted area excites acute inflammatory response, with dead area soft and yellow with neutrophilic infiltration
* 3-10 days: organisation of infarcted area by vascular granulation tissue
* 10 days: several months: collagen deposition, infarct replaced by collagenous scar
45
What is the early management of ACS?
* A-E resuscitation (oxygen only required if SpO2 <94%, baseline bloods incl. troponin and clotting)
* 300mg aspirin
* IV morphine
* GTN spray / IV nitrates (unless hypotensive)
* if there is ST elevation on ECG, immediate referral to cardiology for PCI
