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Acute Coronary Syndrome
Definition
• ACS = a constellation of symptoms resulting from acute myocardial ischemia
• Associated with rupture of an atherosclerotic plaque and partial/complete thrombosis of the infarctrelated artery
• An ACS resulting in myocardial injury (i
...
enzymes) is termed → Myocardial Infarction (MI)
o STEMI = ST elevation/new LBBB + cardiac enzymes
o NSTEMI = non-ST elevation changes + cardiac enzymes
• Unstable angina = non-specific changes but normal cardiac enzymes
Causes
• Common = atherosclerotic plaque rupture → thrombosis → inflammation
...
heart beat)
• Acute Central Chest Pain: usually described as pressure, squeezing, or burning sensation across
precordium
...
in elderly/diabetics)
o Syncope; pulm
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Peak at 24-48h
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o If normal at >6h + ECG normal, risk of MI = 0
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Symptoms of myocardial ischaemia
2
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Pathological Q waves
4
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g
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g
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No CLEAR guidelines
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g
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What is clear is that you need dual anti-platelets + PCI + anti-coagulation
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Prasugrel may be preferred over ticagrelor for PCI
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If clopidogrel has been used, use Bivalirudin
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Anti-coagulants may be combined with GPIIb/IIIa inhibitors
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g
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5 SC (bleed risk and no angiography in 24hrs)
o or…Unfractionated heparin (angiography likely in 24hrs or Cr >265)
▪ LMWH and fondaparinux need dose reduction in renal failure
▪ Unfractionated heparin is better alternative
GRACE Poor prognostic factors
• Risk stratification e
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GRACE score, troponin, dynamic ECGs
•
Age
o If high risk (>3%) → PCI + GP IIb/IIIa inhibitor
•
Heart failure
o If low risk (<3%) → repeat troponin normal → discharge
•
PAD
•

Low sBP

•
Initial creatinine
Chronic ACS Rx (these can be given while PCI is being prepared)
•
 cardiac markers
• ACE-inhibitor + β blocker (± eplenerone if signs of HF)
•
cardiac arrest on admission
• Statin e
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atorvastatin 80mg (c
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20mg in primary prevention)
•
ST segment deviation
• Dual anti-platelet therapy: Aspirin 75mg (lifelong) +
•
Killip class*
o
1: no hf 6% 30dm
• 2nd antiplatelet
o
2: crackles, s3 17%
o ACS (no PCI): + ticagrelor for 12 months
o
3: pulm
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• REVIEW AT 5 WEEKS (SYMPTOMS), THEN AT 3 MONTHS (FASTING LIPIDS)
Complications (DARTH VADER) – see end of document for more details
•
Death: usually from VF
•
Arrhythmia
•
Rupture: septum (VSD → pan-systolic + RVF), papillary muscles (MR → pan-systolic + pulmonary oedema)
•
Tamponade: Beck’s Triad (low BP, JVP, muffled HS) + pulsus paradoxus + Kussmaul sign
•
Heart failure: right-sided = fluid + avoid diuretics; left-sided = diuretics + avoid fluids
•
Valve disease: MR commonest
•
Aneurysm: 4 weeks after MI → persistent ST elevation + LVF + thrombus ( anticoagulate)
•
Dressler’s syndrome: post-MI pericarditis (myocardial neo-antigens formed post-MI)
•
Embolism (mural thrombus)
•
Recurrence

ACS
Aspirin 300mg
2nd antiplatelet
(Prasugrel if PCI, Ticagrelor if not)
Nitrates
Morphine + anti-emetic
STEMI
Oxygen if SaO2 <94%

NSTEMI/UA
Oxygen if SaO2 <90%

Sx < 12hrs
PCI in 120’?
Thrombolysis:
Alteplase
(2nd streptokinase)
Ticagrelor

GRACE >3%

PCI
+ Prasugrel (or Ticagrelor)
+ Bivalirudin OR
+ Heparin ± GPIIa/IIb

Time-limited CI to thrombolysis
•
Non-compressible puncture <24hrs
•
Recent major surgery/trauma <3w
•
GI bleeding 1 month
•
Ischaemic stroke 6 months

PCI
+ Prasugrel (or Ticagrelor)
+ Unfractionated heparin
+ GPIIa/IIIb-inhibitor
(Tirofiban)

GRACE <3%
Ticagrelor
Fondaparinux

2X trop + ECG
normal

β blocker (or CCB)
ACE-inhibitor
Statin 80mg
Aspirin 75mg
2nd antiplatelet

Mnemonic for anti-coagulation rationale:
•
Low risk NO PCI: Fondaparinux (no dynamic control) = 1 anticoagulant = 1 anticoagulant option
•
NSTEMI + PCI: Unfractionated (dynamic control) + GPIIb/IIIa = 1 anticoagulant + 1 anti-platelet = 2 anticoagulant options
•
STEMI + PCI: Bivalirudin OR Heparin-GPIIb/IIIa = 1 DIRECT anticoagulant or 1 anticoagulant + 1 anti-platelet = 3 anticoagulant options

Medication
Aspirin
Clopidogrel
Enoxaparin
Fondaparinux
Bivalirudin
Abciximab, eptifibatide,
tirofiban

Mechanism of action
Antiplatelet - inhibits the production of thromboxane A2
Antiplatelet - inhibits ADP binding to its P2Y12 platelet
receptor
Activates antithrombin III, which in turn potentiates the
inhibition of coagulation factors Xa
Activates antithrombin III, which in turn potentiates the
inhibition of coagulation factors Xa
Reversible direct thrombin inhibitor
Glycoprotein IIb/IIIa receptor antagonists

In patients with indication for anti-coagulant (e
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AF) and anti-platelet (e
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ACS)
Situation

Combination

Rule of thumb

Anti-coagulation trumps anti-platelet

2º prevention of stable CVD

Anti-coagulation only

Post-ACS/PCI

2 anti-platelet + 1 anti-coagulant
→ 1 anti-platelet + 1 anti-coagulant

VTE

Low HAS-BLED = anti-platelet + anti-coagulant
High HAS-BLED = anti-coagulant only

ACS: Management of NSTEMI
NICE produced guidelines in 2013 on the Secondary prevention in primary and secondary care for patients
following a myocardial infarction management of unstable angina and non-ST elevation myocardial infarction
(NSTEMI)
...

All patients should receive
• Aspirin 300mg
• Nitrates or morphine to relieve chest pain if required
• Oxygen if SaO2 < 90% (BTS 2008)
All patients
Aspirin 300mg
Oxygen if <90%
Nitrates, morphine
Ticagrelor/prasugrel (12 months)
Anti-thrombin (fondaparinux if no PCI in 24hrs)

High-risk
Anti-thrombin: unfractionated heparin (PCI <24hrs)
Percutaneous coronary intervention
GPIIb/IIIa-R inhibitors (tirofiban, eptifibatide)

Antithrombin treatment
...
If angiography is likely within 24 hours or a
patients creatinine is > 265 µmol/l unfractionated heparin should be given
...
Prasugrel is
generally favoured if the patient is going to have a percutaneous coronary intervention
...

Coronary angiography should be considered within 96 hours (moderate) or 24hrs of first admission to hospital
to patients who have a predicted 6-month mortality above 3
...
It should also be performed as soon as
possible in patients who are clinically unstable
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0%), and who are scheduled to undergo angiography within 96 hours of hospital admission
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NICE released guidelines on the management of STEMI in 2013
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A practical example may be a patient who presents with a STEMI to a small district general hospital (DGH)
which does not have facilities for PCI
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If the patient's ECG taken 90 minutes after fibrinolysis failed to
show resolution of the ST elevation then they would then require transfer for PCI
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Aspirin 300mg should be given to all patients (unless contraindicated)
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A second antiplatelet is normally given, usually ticagrelor, clopidogrel or
prasurgel (all are antagonists of the P2Y12 adenosine diphosphate receptor)
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Myocardial Infarction: Complications
Mnemonic: DARTH VADER
• Death: usually from VF
• Arrhythmia
• Rupture: septum (VSD → pan-systolic + RVF), papillary muscles
(MR → pan-systolic + pulmonary oedema)
• Tamponade: Beck’s Triad (low BP, JVP, muffled HS) + pulsus
paradoxus + Kussmaul sign
• Heart failure: right-sided = fluid + avoid diuretics; left-sided = diuretics + avoid fluids
• Valve disease: MR commonest
• Aneurysm: 4 weeks after MI → persistent ST elevation + LVF + thrombus ( anticoagulate)
• Dressler’s syndrome: post-MI pericarditis (myocardial neo-antigens formed post-MI)
• Embolism (mural thrombus)
• Recurrence
Death: Cardiac arrest
This most commonly due to patients developing ventricular fibrillation and is the most common cause of
death following a MI
...

Arrhythmias
Tachyarrhythmias: Ventricular fibrillation, as mentioned above, is the most common cause of death following
a MI
...

• NB: low K+ and Mg+, hypoxia, and acidosis all predispose to arrhythmias and should be corrected
• Sinus tachycardia: Can  myocardial O2 demand, treat causes (pain, hypoxia, sepsis, etc
...
Otherwise, medical therapy as per p130
• Frequent PVCs (premature ventricular complexes) and non-sustained VT (≥3 consecutive PVCS
>100bpm and lasting <30s) are common after acute MI and are associated with increased risk of
sudden death
...
) Treat with synchronized DC shock (if no
pulse, treat as per advanced life support algorithm, see p894, fig A3)
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Consider ablation +/or ICD
• Ventricular fibrillation: 80% occurs within 12h
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Bradyarrhythmias: AV block is more common following inferior MI that infarcts nodal tissue
• Sinus bradycardia: inferior MIs may suffer atropine-unresponsive bradycardia due to infarction of
nodal tissue

•
•
•
•
•

1st-degree AV block: Most commonly seen in inferior MI
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Mobitz type II block: high risk of developing sudden complete AV block; should be paced
Complete AV block: Usually resolves within a few days
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Features: acute heart failure associated with a pan-systolic murmur, JVP
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Urgent surgical correction is
needed
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Acute mitral regurgitation
More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary
muscle
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Patients are treated with vasodilator therapy but
often require emergency surgical repair
...
Patients present with acute heart
failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
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Tamponade
Due to left ventricular free wall rupture
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Diagnosis: echo
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Heart failure
Acute (Right ventricular failure): Presents with low cardiac output and JVP
...
g
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Inotropes are required in some cases
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Loop diuretics such as furosemide will
decrease fluid overload
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ncbi
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nih
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e
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We don’t care about peripheral oedema, we care about systemic perfusion!
o However, when RV failure occurs in the setting of increased RV afterload, volume loading can
result in displacement of the interventricular septum toward the LV and impaired LV diastolic
filling
...
In this setting, intravascular volume may need to be
decreased
...
We want to reduce this with diuretics

Valvular Disease
Mitral regurgitation commonest
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Presentation: pulmonary oedema
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Cardiogenic shock
If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may
decrease to the point that the patient develops cardiogenic shock
...
Other causes of
cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed
below
...

Aneurysm: Left ventricular
This occurs late (4–6wks post-MI)
...
This is typically associated with persistent ST elevation and left ventricular failure
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Patients are therefore anticoagulated
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10% of patients)
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Dressler's syndrome tends to occur around 2-6 weeks following a MI
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Fever, pleuritic pain, pericardial effusion and a raised ESR
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Embolism
May arise from LV mural thrombus
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Coronary Artery Bypass Graft (CABG)
CABG is performed in left main stem disease; multi-vessel disease; multiple severe stenoses; patients unsuitable for angioplasty; failed angioplasty; refractory angina
...

• Triple-vessel disease involving proximal part of LAD
Indications for CABG—to relieve symptoms:
• Angina unresponsive to drugs
• Unstable angina (sometimes)
• If angioplasty is unsuccessful
NB: when CABG and PCI (e
...
angioplasty) are both clinically valid options, NICE recommends that the
availability of new stent technology should push the decision towards PCI
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Comparison with PCI
• Longer recovery time and length of inpatient stay
• Similar early procedural mortality rates and 5-year survival rates
• More complete long-term relief of angina in patients, and less repeated revascularization
Procedure
• The heart is usually stopped and blood pumped artificially by a cardiac bypass machine
• Minimally invasive thoracotomies not requiring this are well described,21 but RCT are few
• The patient’s own saphenous vein or internal mammary artery is used as the graft
• Several grafts may be placed
...

• Internal mammary artery grafts last longer (but may cause chest-wall numbness)
• On-pump or off-pump: Seems to make little difference
After CABG:
• If angina persists or recurs (from poor graft run-off, distal disease, new atheroma, or graft occlusion)
restart antianginal drugs, and consider angioplasty
• Ensure optimal management of hypertension, diabetes, and hyperlipidaemia, and that smoking is
addressed
• Continue aspirin 75mg OD indefinitely; consider clopidogrel if aspirin contraindicated
• Mood, sex, and intellectual problems are common early
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o Drive at 1 month: no need to tell DVLA if non-HGV licences, p158
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