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Cardiology Year3-K > Chest Pain - ACS > Flashcards

Chest Pain - ACS Flashcards

1
Q

What happens in chest pain? What are the commonest causes?

A 
Serious!
Triage as urgent ! Seen within a few mins.
1st dx- Ischaemic heart disease - middle aged or elderly
MSK
ACS*
Pneumothorax*
Oesophagitis
Pneumonia
PE*
Obscure origin e.g. Precordial notch. 
* potentially rapidly fatal.
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2
Q

What are some less common causes?

A 
Aortic dissection*
Cholecystitis
Herpes zoster
Oesophageal rupture*
Vertebral collapse
Tabes dorsalis (very rare)
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3
Q

What should u include in the history?

A

Characerise pain-
Site (central, crushing, retrosternal bilateral, unilateral)
Severity
Time of onset
Character (stubbing, tight/gripping, dull/aching.
Radiation- arms and neck MI
Precipitate and relieving fx(GTN, exercise, rest)

Assc sx? SOB, N+V? Sweating, cough, haemoptysis, palpitations, dizziness, loss of consciousness.
ECG- require!
Quickly consider:
Contacting cardiologists, if ACs likely, ST elevation.

O/E
ABC-? And resuscitate (O2, venous access, IV analgesia.
Listen to both lungs! Tension pneumothorax? Severe LVF?

Inv-
Depends. ECG + CXR usually required. These may be initially normal in Mi, PE and aortic dissection.
ECG monitor and defibrillator available.

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4
Q

What happens in Angina?

A

Defined as discomfort in the chest, arm, neck.
Brought on by: exertion, cold, emotion.
Coronary artery flow fails to meet myocardium demand (eg exercise-> coronary artery spasm or anemia.
Transient Ishaemia may produce ST depression or inversion which resolves after recovery.

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5
Q

Whats the 1st presentation of angina?

A

A+E as the first IHD PC.
Always consider MI esp pain >10mins even if relieved by GTN.
Normal ECG, baseline cardiac markers and normal exam DO NOT exclude MI.

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6
Q

What happens in atypical chest pain?

A

Sent from A+E home.
Poorly localised cardiac pain w/ MSK features or GI upset.
ACS- chest wall tenderness. Others lie to avoid admission.
Even if 15mins + features of IHD.
Refer unwell pts even if pain resolves

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7
Q

ACS

A

Coronary artery plaque rupture –> variety of ischaemic conditions : ACS
Unstable angina, Non-ST elevation MI (NSTEMI) , ST segment elevation Mi, STEMI.

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8
Q

Unstable Angina and NSTEMI- how do you treat?

A

Unstable Angina: worsening angina or single episode of cresendo angina w/ high risk of infraction.
CF: angina at rest, ⬆️ frequency, ⬆️ duration, and severity + response to GTN.
A+ E: hard to distinguish b/w the two.

  1. Provide 02 on admission :94-98% Sats and attach cardiac monitor.
  2. IV opiate analgesia +- antiemetic
  3. Aspirin 300mg PO and clopidogrel 300mg PO.
  4. Start LMWH e.g. Dalteparin 120units/kg SC every 12 hrs max . Or enoxaparin (1mg/kg SC)
  5. If still pain: GTN IV , systolic BP >90mmHg .
  6. Glycoprotein IIb/IIIa inhibitors( tirofiban) NSTeMI risk.
  7. ⬆️ risk for NSTEMI - atenolol 5mg IV slowly over 5mins, repeat once after 15mins.
  8. Refer for admission, repeatECG, blood troponin testing after 12hrs of pain onset
    TIMI score>3 early revascularisation procedures benefit.
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9
Q

What is the TIMI score?

A

Increasing score predicts mortality or adverse event . Everythin takes 1 point:
Age>65
3+ RFs for CHD, FHx of IHD, HTN, hypercholesterolaemia, DM, smoker
Known coronary artery disease with stenosis >50%
Aspirin use in last 7 days
Rx episode of angina prior to event
Raised troponins or other cardiac markers
ST segment deviation >0.5mm on ECG

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10
Q

Whats variant angina? “Prinzmetal “

A

Angina ssc w/ ST elevation - coronary vasospasm? With or without fixed coronary abnormality- distinuished from acute MI as GTN- pain immediately relieved.

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11
Q

What are some risk factors for IHD?

A

Age, gender (M) , FHx,
Hyperlipidaemia (premature atherosclerosis)
Smoking
HTN
Hyperchromocysteinaemia (homosteine- amino acid - atherogenic amd prothrombic tendenicies- elevated levels due to genetic defects- vitamin cofactors- nutritional deficiencies- folic acid, vitB12, Vit B6.
Atheroma RFs-
Lack of ex, DM, abn glucose, raised fasting glucose.

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12
Q

Whats the secondary prevention of cardiovascular events?

A

Avoid RFs,
Aspirin -75mg (inhibit platelet cyclo-oxygenase (TXA2) - clopidogrel 75mg when aspirin CI/ not tolerated.
Statins- lipid lowering- reduce mortality 3.5 -> fibrate
B-blockers (symptomatic relief)
Acute attacks: sublingual glyceryl trinitrate tablet/spray, use b4 exertion.

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13
Q

Whats the tx for worsening or persisting angina?

A

CABG- coronary artery bypass grafting or Angioplasty.

Coronary angioplasty
- cardiac cath- balloon inflated at isolated, promixal, non- calcified atheromatous plaques. ⬇️ risk of acute vessel closure amd restenosis rates . Increase cost tho.

CAGB
L or R internal mammary artery used to bypass stenoses in LAD or RCA. Less commonly- saphenous vein from leg anastomosed w/ proximal aorta and coronary artery distal to obstruction.
90% cases relieves angina. Operative mortality

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14
Q

Complications of cardiac surgery:

A

Coronary angioplasty: 1% death, Acute MI 2%, 2% need for urgent CABG, restenosis in first 6M (30%)

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15
Q

ACS tx?

A

Antiplatelets- aspirin 300mg initially, then 75mg, ⬇️ risk of events and mortality.
Clopidogrel is also given, and to pts with aspirin CI.

High risk pts- also given glycoprotein IIB/IIIa recepor inhibitors- abciximab.

Heparin: LMWH- enoxaparin 1mg/kg 2x daily sc- intereferes with thrombus formation at site of plaque ruprture

Anti- Ischaemia agents: Nitates - GTN sublingual :0.4mg every 5mins for 3 doses, or IV infussion for continuous pain (50mg in 50mL 0.9% saline. To maintain SBP > 90mmHg for 24-48hrs
Recurrent ischaemia- long acting nitrates
B- blockres- oral or OV - metoprolol 5mg I.v over 2mins, repeted every 5mins to max of 15mgs, then 2-15mg by mouth 2x daily.

Plaque stabilisation- statins- atrovastatin 80mg daily + ACE inhibitor - ramipril 2.5-10mg = Long term reduce future events.

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16
Q

Emergency mx of ACS

A

Chest pain suggestive of:
IV access, blood for cardiac markers :FBC, U+Es, glucose, lipids,
ECG- cardiac monitor 12ECg,repeat after 15mins if non dx,
Chew aspirin 300mg + 300mg clopidogrel
Pain relief: GTN, diamorphine 2.5-5mg IV w/ antiemetic (meroclopromide)
⬇️⬇️⬇️⬇️⬇️⬇️
STEMI: persistent ST elevation or new LBBB -> ⬆️⬆️⬆️

Possible NSTEMI/Unstable Angina
Hx, ECG changes- ST depression, T wave inversion, elevated cardiac markers, –> Admit to ICU, bed rest, continious ECG monitoring, intensive med therapy, Risk stratification (TIMI score)
↪️ Modification of RFs

Stable Angina
Early discharge

Non ischaemic chest pain
Cause dependent

17
Q

What happens in an MI?

A

Commonest death in developed
Rupture of atherosclerotic plaque - thrombosis-> occlusion a

CF
Central chest pain similar to angina pain
Occurs at rest, more severe, lasts for hours.
Pain Assc w/ N+V + restlesness,
Pale, sweaty, grey.
20% silent pain , unnoticed or hypotension arrythmias or pilm oedema.
Inv
ECG
Cardiac markers, creatine Kinase, AST + LDH

18
Q

In what populations are silent infractions most common?

A

Elderly,
DM
HTN

19
Q

MI investigations?

A

Mins : STE in 2 or more contiguous leads, >1mm
Patho Q waves- broad >1mm and deep >2mm or >25% 2 wave amplitude. (-ve deflections before QRS) - seen in full- thickness infraction (non-Q wave- subendocardial thickness infraction) - away from lead- > -ve.
⭐️ new LBBB also acute MI

Leads II, III, AVF- Inferior infracts
I,II, AVL- Lateral infracts
V2-V6 Anterior infracts
Posterior infracts- (no posterior leads-> changes in V1-V2 - development of tall initial R waves, STD , talk upright T waves. )

Cardiac markers
Necrotic cardiac muscle releases stuff to circulation:
Troponin T + I - regulatory proteins , highly specific for cardiac muscle damage- within 8hr onset - there is High sensitivity Troponin -6hrs
Perists for several days - bedside

CK- also produced by skeletal muscle damage, brain damage, less specific
CK-MB more for heart- size proportional for infract size.

Asparate aminotransferase - AST + Lactic Dehydrogenase - LDH - rarely used - serum levels high for more than 10days after infraction- measure if patient Presents days after.

Other- CXR, FBC, U+E, blood glucose, lipids (within 12 hrs indicate precipitation levels .

20
Q

MI management

A

Immediate mx
ACS mx
Thrombolytic management- t-PA (tissue type plasminogen activator) - cheapest-> Streptokinase :1.5 million units in 100mL 0.9% sodium Cl sol, over 1hr IV infussion pump.
Metoprolol 5mg slow iv infussion, if systolic HR >100bpm ❌❌ if bradycardia, asthma or HF, or hypotension.

Insulin infusion if admission blood glucose >11 mmol/L- aim 7-10mmol/L
Treat complic.
Persistent pain- GTN infussion - consider angiography- possible angioplasty?

Uncomplicated infraction
Repeat ECG, cardiac markers, U+Es after 48hrs
Sec prevention therapy- start- aspirin, statin, metoprolol, ACEI, modification CAD
Transfer to medical ward, mobilise after 24-48hrs if pain free
Discharge after 6days, submaximal exercise ECG prior to discharge.
Consider angiograpgy if ECG changes persist or chest pain in early stages.

Refer to rehab nurse, no driving 1M, special ass for public service or heavy goods transport liscence .
Return to work 2 M.

DM- mortality ⬆️ due to higher rate of HF. (High metabolic changes during Mi- thats we we give insulin inffusion-2hrs) +if on admission gluc >11.

21
Q

What are the risks of steprokinase?

A

Anti- streptokinase Abs- risk of allergic rctn and reduces effect of thrombolysis.
Thrombolysis-

22
Q

If thrombolysis CI?

A

Rescue recanalization
Primary (direct) angioplasty - therapeutic if experienced and rapid access to catheterizationn- or received thrombolysis and still not reperfused (ongoing chest pain +

23
Q

Complications of an MI

A

HF
Rupture of ventricle free wall- fatal
Mitral Regurg
Ruprture of interventricylar septum
Heart block
Arrythmias
Thromboembolism- prolonged bed rest (persistent AF, anticoagulated w/ warfarin to achieve INr 2-3.
Pericarditis-> sharp chest pain and pericardial rub. - NSAIDS, until spont. Resolution 1-2 d later. Late pericarditis (2-12w after, w/ fever + pericardial effusion (Dresslers syndrome)-rare - corticosteroids.
Dresslers syndrome *+Ventricular aneurysm * may develop months after MI.

24
Q

Infective endocarditis- what happens?

A

Infx of endocardium or vascular endothelium
Fulminating or acute infx - usually subacute bacterial endocarditis SBE.
Infx occurs on:
Valves- that have congenital or aquired defect, usually LHS. RH endocarditis more usualy in iV deug users.
On normal valves w/ vurilent organism like strep pneumoniae or staph aureus.
Prosthetic valves - early infx or bactereamia late.
Oftwn need replacement.
In assc w/ VSD or PDA.

Patho- mass of fibrin, platelets, infctv organisms, at edges of valve.
Staph aureus, enterococci, strep viridans.

25
Q

DUKE Criteria for infective endocarditis

A

Major:
+ve cultures for infc endocarditis.
Typical microorganism from 2 separate cultures: strep viridans, strep Bovis,
HACEK group: Haemophilus group, actinobacillus actinomycetmcomitans, cardiobacterium hominis, Eikenella corrodens, Kingella kingae.
CAP- staph aureus, enterococci.

Persistent +ve blood cultures- maybe recovered once.

Single +ve culture for Coxiella burnetii or antiphase IgG >1:800.

Evidence for endocardial involvement:
TTE( transthoracic echo for TEE- thanseosophageal echo- in prosthetic valves) oscillating intracardiac mass on valve or supporing structures.
Abscess
New dehiscence of valve

Minor:
Predisposition- prosthetic valve, IV drugs
Fevere 38
Vascular phenomena
Immunological phenomena
Microbiological evidence- +ve cultures but not major criteria

26
Q

Whats angina?

A

Chest pain arising from heart, as a result of myocardial ishaemia.

27
Q

What fx might exacerbate angina?

A

Cold,
Excitment,
Angry

28
Q

What are some different varieties of angina?

A

Decubitus- on lying down

Nocturnal: at 🌙✨, wakes up pts.

Variant- Prinzmental- coronary artery spasm, so occurs w/o provocation, and at rest.

Unstable angina: can b/c severe very quickly, occurs at rest or is of recent onsent

29
Q

How would you investigate Angina?

A
  1. Resting ECG- N b/w attacks-> ST depression or T wave flattering or inversion during attack.
  2. Exercise ECG- +ve in 75% of severe CAD - N one does not exclude dx.
  3. Pts who cannot exercise- ECHO .or pharmacological stress testing by image perfusion.
  4. Coronary angiography (usually for anatomy b4 coronary artery angioplasty or surgery.
30
Q

What signs indicate severe CAD?

A

ST depression >1mm at low workload within 6mins of starting the Bruce protocol

OR

Paradoxical fall in BP with exercise.

31
Q

How do you manage angina?

A

2o prevention: smoking stop, HTn control, BMI ⬇️, regular exercise, glycaemic control in DM.
+ aspirin, statins, B-blockers: ⬇️ the risk.

Cardiology Year3-K (8 decks)

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