Cardiology JC012: Sudden Severe Chest Pain: Acute MI And Aortic Dissection Flashcards
ST elevation MI: Pathophysiology and Clinical features
Pathophysiology:
Plaque with fibrous cap
—> Cap rupture
—> Blood clots form around rupture
—> Block coronary artery
—> Death of cardiac tissue
Predisposing factors
1. **Unusual heavy exercise
2. **Emotional stress
3. Progression from unstable angina
4. **Surgical procedures
5. **Infection e.g. pneumonia
6. Circadian periodicity (peak incidence between 0600-1200)
Clinical features:
1. Chest pain
- severe, intolerable
- prolonged > 30 mins
- constricting, crushing, compressing, heavy weight
- radiation to left arm (ulnar aspect) / jaw
- Others
- SOB, weakness, dizziness, palpitations, N+V (Bezold-Jarisch reflex)
Acute Coronary Syndrome (ACS)
ACS: Plaque rupture leading to occlusion of vessels
—> If **complete occlusion —> **ST elevation
ACS: STEMI + NSTEMI
ACS with persistent ST elevation
- **Complete occlusion
- **↑ Troponin
- Medical emergency
ACS without persistent ST elevation
- ***Incomplete occlusion
- ↑/- Troponin
- ST depression / non-ST elevation MI
STEMI have worse 1 month survival but ***similar prognosis overall
Acute MI
Pathology:
- Myocardial cell death ∵ prolonged myocardial ischaemia
Prognosis:
- 40% mortality in first 4 weeks
- 90% of patients with transmural infarct have total occlusion of relevant artery within 4 hours of pain, secondary to plaque fissure
Myocardial response during AMI
Myocardial cells will not die / necrotic immediately after ischaemia —> ***12 hours
- Evolving phase
- first 6 hours from time of pain (up to **12h)
- potential for recovery of heart muscle
—> ↑ Blood supply (via revascularisation)
—> ↓ Oxygen demand (↓ HR + BP)
- infarcted muscles are **acidotic, with Ca loss + K influx —> Arrhythmia - Convalescence phase
- infarcted muscles will not recover
- treatment can still improve mortality / morbidity by
—> Avoid remodelling of infarct (Thinning of infarct wall + **Dilation of infarct zone —> can cause Aneurysm, Ventricular septal rupture, HF)
—> Improve **collateral circulation
Features NOT characteristic of MI
- Pleuritic pain
- sharp pain by respiratory movement / cough - Primary / Sole location in middle / lower abdominal region
- Localised at 1 finger tip, particularly over LV apex
- Pain on movement / palpitation
- Very brief episodes
- Radiate to lower limbs
DDx of life-threatening chest pain
- Acute pericarditis
- aggravated by respiratory movement, sharp pain
- radiate to ***trapezius ridge (characteristic site)
- may have fever - Pulmonary embolism
- haemoptysis - Aortic dissection
- radiate to back
- tearing sensation
***Classification of AMI
Type 1 (most common): Atherothrombotic CAD —> ***Plaque rupture, erosion, fissuring, dissection —> spontaneous MI related to ischaemia
Type 2: **Coronary spasm / **Anaemia / **Hypotension / **CHF —> imbalance of O2 demand and supply —> ischaemia
- unrelated to Atherothrombotic CAD
Type 3: **Sudden cardiac death with symptoms of ischaemia (patient死左)
- **before determination of elevation of cardiac biomarker
- accompanied by new ST elevation / LBBB
or
- verified coronary thrombosis by angiography / autopsy
—> for epidemiological study purpose only
Type 4a: ***PCI associated
Type 4b: Verified stent thrombosis associated
Type 5: ***CABG associated
***Diagnosis of AMI type 1 and 2
Detection of ↑ / ↓ of cardiac biomarkers (***Troponin)
- at least 1 value > 99th percentile of URL
AND
- evidence of ischaemia with >=1 following:
- Symptoms of ischaemia
- ECG changes of new ischaemia (***New ST-T changes / New LBBB)
- Development of ***pathological Q waves (∵ transmural infarct)
- Imaging evidence of new **loss of viable myocardium / new **regional wall motion abnormality
Investigations of STEMI
- Biomarkers
- ECG
- Cardiac imaging
- Echocardiogram
- Angiogram + PTCA
- Nuclear imaging
Biomarkers for AMI
- ↑ 2x CPK (creatinine phosphokinase)
- **MB isoenzyme, CPK MM - skeletal muscle (may be confusing if give imi)
- high sensitivity but NOT specific
- good for detecting **reinfarction - SGOT (i.e. ***AST) (serum glutamic oxaloacetic transaminase)
- ↑ also in liver disease, pulmonary congestion, skeletal muscle injury - LDH
- ***LDH1: cardiac, RBC
- LDH4, 5: liver, skeletal muscle - Troponin T / I
- not normally present —> more sensitive + specific than CK-MB/CK
- **long lasting: good for diagnosis of MI with **delayed presentation (not good for reinfarction)
- “stick” test available
- Elevated: STEMI, NSTEMI, Myocarditis, Acute decompensated HF, Pulmonary embolism
- ***Not-elevated: Pericardial effusion - Myoglobin
- ***first marker to ↑ in MI
- non-specific
- eliminated quickly
***ECG of AMI
Anterior MI:
- ST elevation in ***V2-V6
Inferior MI:
- ST elevation in Lead 2, 3, aVF
- ST depression in **V2-V6 (*reciprocal change of ST elevation in MI)
RV infarction:
- Right side chest leads
- ST elevation in V4R, V5R
Pitfalls:
**False positive
- Benign early repolarisation (in young patients)
- **LBBB
- Pre-excitation (Wolff-Parkinson-White)
- Brugada syndrome
- **Peri/Myocarditis
- **Pulmonary embolism
- Subarachnoid haemorrhage
**False negative
- Prior Q waves / persistent ST elevation
- **Paced rhythm
- ***LBBB
Cardiac imaging for AMI
- Echocardiogram
- ***abnormal wall motions
- ventricular function: determine need for use of ACEI
- assess complications of MI: VSD, PE, ventricular thrombus, RV infarct - Coronary Angiogram + PTCA (Percutaneous transluminal coronary angioplasty)
- Nuclear imaging
- assess **new loss of viable myocardium / **new regional wall motion abnormality with biomarker criteria for MI in absence of non-ischaemic cause
Criteria for Prior MI
Prior MI:
- Q wave in V2, V3 >=0.02s
or
- Q wave >=0.03s and >=0.1 mV deep
or
- QS complex in any two contiguous leads of lead 1, aVL, V6; V4-V6; lead 2, 3, aVF
- Development of ***new pathological Q waves with / without symptoms
- Imaging evidence of region of **loss of viable myocardium
- **thinned, fails to contract
- in absence of non-ischaemic cause - Pathological findings post-mortem of a ***healed / healing MI
***Treatment of MI
Occlusive coronary thrombus treatment
- ***Antiplatelet
- Aspirin + Clopidogrel / Prasugrel / Ticagrelor or GP2b/3a inhibitors (usually not given e.g. Abciximab, Eptifibatide) - Antithrombin
- Heparin
- ***LMWH
- Fondaparinux
- Bivalirudin - ***Plasminogen activators (causes fibrinolysis)
- tPA (Alteplase)
- rPA (Reteplase)
- nPA (Lanoteplase)
- TNK-tPA (Tenecteplase)
- Streptokinase (old days)
***Management of MI
- General measures
- Bed rest
- **O2
- **Morphine
- CCU care +/- resuscitation - Early presentation (**<12h)
- Opening of infarct related artery
- **Fibrinolytic therapy
- Primary PTCA / ***PCI - Antiplatelets / Anticoagulants
- Aspirin
- Heparin
- Warfarin
- Clopidogrel - Other non-thrombolytic therapy
***↓ Myocardial O2 consumption
- β-blockers
- CCB (Diltiazem)
- Nitrates
↓ LV remodeling
- ACEI / ARB
- β-blockers
- Aldosterone receptor antagonist
- Complications management + Rehabilitation
- Secondary prevention: **Aspirin, β-blockers, ACEI / ARB
- Complications: **HF, Arrhythmia, **VSD (esp. anterior / septal wall infarction), **MR, Pericarditis, Frozen shoulder
Fibrinolytic therapy
Used when no equipment for PCI
Indication:
1. AMI: Pain + ST elevation in 2 contiguous chest leads
2. Time of onset of pain **< 12 hours
3. Absence of CI: **bleeding tendency, cardiogenic shock, recent head injury, stroke
Successful fibrinolysis:
1. Decrease pain
- ECG criteria
- early resolution of ST elevation at 90 mins
- preservation of R wave (i.e. without Q wave) - Biochemical evidence
- e.g. early peaking of CPK
- normal peak: 22-24 hours
- successful thrombolysis 11-12 hours - Imaging
- Radionuclide imaging
- Angiography
Types:
1. Streptokinase
- Non-specific
- activation of plasminogen to plasmin in whole circulation
—> plasmin digest fibrin —> FDP (fibrinogen degradation product)
- Tissue type plasminogen activator (tPA) (Alteplase)
- activated when fibrin present —> activates plasminogen —> rapid lysis
- lower bleeding complications (∵ inactive without fibrin)
- administered with ***Heparin - tPA derivatives
- TNK-tPA (Tenecteplase)
- nPA (Lanoteplase)
- rPA (Reteplase)
Contraindications for Fibrinolytics
Absolute CI:
1. **Prior ICH
2. Structural cerebral vascular lesion e.g. **AVM
3. Malignant intracranial neoplasm (primary / metastatic)
4. Ischaemic stroke within 3 months (except acute ischaemic stroke within 3 hours)
5. Suspected aortic dissection
6. ***Active bleeding / bleeding diathesis (exclude menses)
7. Significant closed head / facial trauma within 3 months
Relative CI:
- poorly controlled chronic severe HT
- pregnancy
- active peptic ulcer
etc.
Limitations of current Fibrinolytic Regimens
- ***Not 100% successful
- only 50% achieved optimal myocardial perfusion
—> Thrombin inhibition (Anticoagulant) + Platelet inhibition (Antiplatelet) needed -
1/3 reocclusion by 3 months
—> PTCA needed (Mechanically open the occluded artery is the best) - Delayed presentation + undiagnostic ECG
—> Treatment in ambulance + A/E
—> Education - Fibrinolytic therapy ↓ in-hospital mortality by 50% compared to placebo (real world only 20%)
***Flowchart of Management
STEMI ***< 12 hours of chest pain onset —>
If hospital have PCI —> PCI
If hospital no PCI
—> **< 3 hours —> Thrombolysis / immediate transfer to hospitals have PCI
—> **>=3 hours —> immediate transfer to hospitals have PCI
Failed thrombolysis
—> Rescue PCI
Successful thrombolysis
—> PCI within up to 24 hours available —> Post-thrombolysis PCI
—> PCI within up to 24 hours unavailable —> Predischarge ischaemia —> Ischaemia-driven PCI
Early intervention is important
Every 10 min delay to PCI
—> 1% reduction in mortality difference
Emergency CABG
Indication:
- Complicated coronary occlusion not amenable by traditional coronary stenting
- Less common now due to advancement in stenting technique
Antiplatelets and Anticoagulants
- Aspirin
- ↓ Acute mortality (in conjunction with Thrombolysis)
- ↓ Reinfarction in long term follow up - Heparin
- SC heparin (prophylaxis against DVT, aPTT not changed)
- IV heparin (prophylaxis against embolisation, mural thrombosis)
- Adjunct to tPA - Warfarin
- Established VT / Embolisation
- Echocardiographic evidence of LV thrombus - Clopidogrel
- 75mg >=14 days
- after PCI / stenting
Other non-thrombolytic therapy: ***↓ Myocardial O2 consumption
-
**β-blockers
- Use β-blockers **without intrinsic sympathomimetic activities e.g. Metoprolol (β-1 selective), Timolol (non-selective)
- IV: ↓ mortality by 15% with 12 hours of infarct
- IV: hypotension, ***carcinogenic shock risk
- Oral: ↓ long term mortality by 25% - Ca blockers
- Diltiazem (non-Q-wave infarct —> ↓ reinfarction, ↑ survival in patients without HF)
- ***NO outcome performance, only ↓ chest comfort - Nitrates
- IV: ↓ infarct size if mean BP > 80mmHg
- Oral: neutral effect
- ***NO outcome performance, only ↓ chest comfort
Other non-thrombolytic therapy: ***↓ LV Remodeling
- ***β-blockers
- ALL patients with LV dysfunction - ***ACEI
- ALL patients with LVEF <40%, DM, HT, Renal dysfunction - ARB
- patients intolerant to ACE-1 - Aldosterone receptor antagonist
- adjunct: patients on ACE-1 / BB + LVEF <40% + HF without significant renal dysfunction / hyperK
Post-MI management
- Risk stratification
- Residual ischaemia: **Exercise test, Angiogram, PCI
- Electrical instability: **24 hr ECG for VT / Ventricular arrhythmia, Anti-arrhythmic, ICD - Secondary prevention
- ***Aspirin, β-blockers, ACEI / ARB
- Risk factor modulation: exercise, smoking, statin (aggressive lipid lowering)
- Cardiac rehabilitation + prevention: exercise, work, sex, alcohol, travel
—> Reduce symptoms (SpC FM)
—> Improve cardiac function
—> Reduce sudden cardiac death
—> Slow down atherosclerosis process
Complications of AMI
- ***HF
- Arrhythmia
- ***VSD (esp. anterior / septal wall infarction)
- ***MR (∵ Papillary muscle dysfunction in inferior wall infarction)
- Pericarditis
- Frozen shoulder
Flowchart summary
Admission:
- Chest pain
Working diagnosis:
- Suspicion of ACS
ECG:
- Persistent ST elevation
- ST/T abnormalities —> Biochemistry test
- Normal / Undetermined ECG —> Biochemistry test
Biochemistry:
- Troponin: Positive / Negative (need x2)
Risk stratification:
- Troponin +ve: High risk
- Troponin -ve: Low risk
Diagnosis:
- STEMI
- NSTEMI
- Unstable angina
Treatment:
- STEMI —> Reperfusion (∵ complete occlusion)
- NSTEMI / Unstable angina —> Invasive / Non-invasive
Aortic dissection
Pathology:
- Tunica ***Media collagen + elastin degeneration
Pathophysiology:
- Blood violates aortic **intimal and **adventitial layers
—> ***False lumen created
—> Dissection may extend proximally / distally / both
Causes:
- **Coexisting HT (80%)
- Genetic: **Marfan, Familial aortic aneurysms / dissection, ***Ehlers-Danlos, Loeys-Dietz aneurysm syndrome
- Biscuspid aortic valve
- Trauma
Aortic dissection vs Aortic aneurysm
True aneurysm:
- dilated aorta
- 3 layers all intact
False aneurysm:
- ruptured intima / media
- still enclosed by adventitia
Dissection:
- dissection into medial layer
S/S, Complications of Aortic dissection
Symptoms:
- Chronic: can be asymptomatic
- Acute: severe pain (maximum at onset)
—> Tearing
—> Anterior chest (ascending aorta)
—> Interscapular, Abdomen (descending aorta)
Signs:
- BP: High (Tamponade if dissection involve pericardium) / Low
- ***Pulse deficits (Pulse not reaching periphery) (Radio-radial delay, measure 2 arm BP (SpC Medicine))
- Complications
Complications:
- **Syncope
- CVA (i.e. stroke)
- **Acute AR (∵ dilation of aortic root) —> CHF
- **Ischaemic limb
- Paraplegia
- **Renal, Intestinal failure
Classification of Aortic dissection
Stanford:
- Type A (life-threatening): Ascending aorta
—> Can involve Coronary artery, Aortic valve, Dissect into pericardium
—> **Acute MI , **Acute AR, ***Acute pericardial effusion
- Type B: All parts except Ascending aorta
—> can be medically managed, surgery might not be needed
DeBakey:
- I: Stanford A
- II: Stanford A
- III: Stanford B
Investigations
- CXR
- widening of mediastinum - ***CT thorax (preferred over MRI)
- quicker
- ~100% specificity / sensitivity
- ability to identify thrombosed false lumen
- less invasive - MRI
- ~100% specificity / sensitivity
- identify intimal flaps, great vessel anatomy, Type A vs B, degree of aortic insufficiency
- useful test for serial FU of patients with chronic dissections
- unsuitable for confused / claustrophobic patients
- unsuitable for pacing wire
- CI in some life supporting equipment
- time-consuming
- need to be disconnected from monitoring devices, IV pumps - Transthoracic (TTE) + Transesophageal Echocardiogram (TEE)
- suitable for patients with renal failure (unsuitable for contrast injection)
- >95% sensitivity / specificity
- very rapid
- done at bedside with minimal risk
- limited visualisation of distal aorta
- false positive possible
Prognosis of Aortic dissection
Not good overall
- mortality rates approach 1% per hour within 1st 48 hours (i.e. 50% mortality if not treated within 2 days)
- survival >90% with prompt diagnosis / management
Death:
- Progression of dissection»_space; Vascular compromise / rupture
Management of Aortic dissection
- Haemodynamic stabilisation
- Control BP (SBP: 100-120)
—> **Labetalol
—> **Nitroprusside (may ↑ dP/dt, ***pretreated with β-blockers)
- Surgical drainage (Tamponade) - Resection + Graft (definitive)
- Acute Type A dissection
- Distal usually ***not require surgery unless: Involve distal organ, rupture, retrograde dissection, Marfan, concomitant aneurysm
- Stent graft (newer treatment)
