Acute myocardial infarction is defined as myocardial cell death due to prolonged myocardial ischaemia. ^[1]

The slide sequence shows the central mechanism visually: an atherosclerotic plaque develops a disrupted fibrous cap, the exposed plaque contents trigger platelet-rich and fibrin-rich thrombus, coronary flow falls or stops, and the downstream myocardium becomes ischaemic and then necrotic. Complete occlusion is common in STEMI, but the ECG label and the angiographic degree of occlusion are not perfectly interchangeable. ^[1]

Historical context: The lecture quotes older angiographic and mortality cohorts, including very high early mortality and frequent early complete occlusion. These figures explain the development of coronary care and rapid reperfusion systems, but they should not be used as universal contemporary prognostic estimates: outcome varies substantially with pre-hospital delay, reperfusion, infarct size, age and comorbidity. ^[1]

Evolving phase (first 6 hours, up to 12 hours): ^[1]

• Potential for recovery of heart muscle if: (a) improve blood supply → revascularisation, (b) decrease oxygen demand → ↓ heart rate + BP
• The slide describes ionic disturbance in ischaemic muscle as “loss of Ca²⁺ and influx of K⁺”

Convalescence phase: ^[1]

• Infarcted muscles will NOT recover
• Treatment can improve mortality/morbidity by: (a) avoiding remodelling of infarct (thinning of infarct wall + dilation of infarct zone) → aneurysm, VSD rupture, HF; (b) improving collateral circulation

Physiology correction: The slide's ion directions are reversed. Ischaemia causes ATP depletion and membrane-pump failure, intracellular Na⁺ and Ca²⁺ overload, and K⁺ efflux with extracellular K⁺ accumulation. The resulting spatial heterogeneity in conduction and refractoriness promotes re-entry and early ventricular arrhythmia. The evolving phase is the opportunity to salvage myocardium by reperfusion; later care focuses on complications and prevention of adverse remodelling.

Predisposing factors for AMI: ^[1]

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

Why 6 AM to noon? Morning catecholamine surge → ↑ heart rate, ↑ BP, ↑ platelet aggregability, ↑ coronary artery tone. This is also why beta-blockers are protective — they blunt the morning sympathetic surge.

Nature of chest pain in AMI: ^[1]

1. Severe, maybe intolerable
2. Prolonged, usually > 30 minutes
3. Nature: constricting, crushing, compressing, heavy weight
4. Radiation: left arm (ulnar aspect)
5. Other symptoms: SOB, weakness, dizziness, palpitation, nausea, vomiting (Bezold-Jarisch reflex)

The lecture figure further details pain distribution ^[1]:

• Chiefly retrosternal and intense
• Most commonly radiates to the left shoulder and ulnar aspect of the left arm and hand
• May also radiate to: neck, jaw, teeth, back, abdomen, right arm
• Other manifestations: fear, perspiration, weakness, collapse, coma

The Bezold-Jarisch reflex is a vagal reflex triggered by ischaemic stimulation of cardiac C-fibres (especially in inferior MI) → causes bradycardia, hypotension, nausea, and vomiting. This is why inferior MI patients often present with vomiting and sinus bradycardia — don't mistake it for a GI problem! ^[1]

What differentiates MI pain from stable angina pain?

Chest pain descriptors and probability of ischaemia (from lecture figure) ^[1]:

Presentations without classic pain: Older adults, people with diabetes and women may present with dyspnoea, diaphoresis, nausea, syncope or unexplained weakness rather than textbook crushing pain. Do not use any one descriptor to rule ACS in or out. ^[14]

Differential diagnosis: ^[1]

1. Acute pericarditis — aggravated by respiratory movement, sharp, knife-like; radiates to the trapezius ridge (characteristic site of pericardial pain)
2. Pulmonary embolism — haemoptysis
3. Aortic dissection — radiation to back, ripping or tearing sensation

The lecture uses an older version of the Universal Definition. The current thresholds below come from the Fourth Universal Definition; the slide's 3× URL after PCI and 5× URL after CABG are obsolete. ^[13]

Criteria for AMI Type 1 & 2 (ESC): Detection of rise and/or fall of cardiac troponin with at least one value above the 99th percentile URL, together with at least one of: ^[1]

• Symptoms of myocardial ischaemia
• New ischaemic ECG changes
• Development of pathological Q waves
• Imaging evidence of new loss of viable myocardium or new RWMA
• Identification of coronary thrombus (angiography/autopsy)

Biomarkers: ^[1]

1. ↑ 2× CPK (creatinine phosphokinase) — MB isoenzyme; CPK-MM = skeletal muscle (may be confusing if given IM injection)
2. SGOT — raised also in liver disease, pulmonary congestion, skeletal muscle injury
3. LDH — LDH1 = cardiac, RBC; LDH4,5 = liver, skeletal muscle
4. Troponin T or I (preferred in the slide):
   • Not normally present in blood
   • More sensitive and specific than CK-MB/CK
   • Long lasting → diagnosis of MI with delayed presentation (but NOT good for reinfarction)
   • "Stick" test available
5. Myoglobin — first marker to increase in MI, but unspecific and eliminated quickly

Reading the biomarker-kinetics graph: The early, short-lived myoglobin curve and later LDH curve explain historical timing strategies. Modern practice uses assay-specific serial hs-cTn pathways; CPK/CK-MB, SGOT/AST, LDH and myoglobin are not routine substitutes. Exact detection times depend on the assay and the time from symptom onset. ^[14][15]

Why troponin is preferred: hs-cTn has greater sensitivity for myocardial injury and is interpreted with its assay-specific 99th-percentile URL and serial change. Persistent elevation does not make reinfarction impossible to diagnose: if cTn is stable or falling after the index MI, a new rise > 20% supports reinfarction when accompanied by compatible clinical/ECG evidence. ^[13]

The lecture describes the classic sequence of ST elevation, pathological Q-wave formation and T-wave inversion. ^[1]

These are pattern descriptions rather than one-to-one histological labels: ST elevation signals acute epicardial injury in the right context, Q waves may reflect electrically silent infarcted tissue, and T-wave inversion is a non-specific repolarisation abnormality. A new LBBB alone is not diagnostic of acute MI; use symptoms, prior ECGs, serial change and validated criteria for occlusion in LBBB or paced rhythm. ^[13]

ECG evolution of STEMI:

Localisation of MI by ECG leads:

R-side chest leads → RV infarction ^[1]

What the three ECG slides show: ^[1]

• Anterior/anteroseptal STEMI: prominent anterior ST elevation, maximal across V2–V4, localises to the LAD territory.
• Inferior STEMI: ST elevation in II, III and aVF with reciprocal ST depression in I/aVL. Check for RV and posterior extension.
• Right-sided tracing: V3R–V6R mirror the left precordial positions across the right chest; ST elevation in V4R supports RV infarction.

Why RV infarction matters: RV dysfunction can make cardiac output preload-sensitive. Avoid routine nitrates and diuretics in hypotension; give a cautious fluid challenge only if there is no pulmonary congestion, reassess frequently, and prioritise urgent reperfusion. Do not reduce management to “give fluids.”

ECG Pitfalls in Diagnosis of MI (ESC): ^[1]

False positives (mimics of STEMI):

• Benign early repolarisation
• LBBB (use Sgarbossa criteria)
• Pre-excitation (WPW)
• Brugada syndrome
• Peri-/myocarditis (diffuse ST elevation with PR depression)
• Pulmonary embolism
• Subarachnoid haemorrhage
• Metabolic disturbances (e.g., hyperkalaemia)
• Failure to recognise normal limits for J-point displacement
• Lead transposition or modified lead configuration
• Cholecystitis
• Takotsubo cardiomyopathy

False negatives (missed STEMI):

• Prior Q waves and/or persistent ST elevation
• Paced rhythm
• LBBB
• LVH with strain pattern

Cardiac Imaging: ^[1]

1. Echocardiogram:
   • Abnormal wall motions (regional wall motion abnormalities — RWMA)
   • Ventricular function → use of ACEI
   • Complications: VSD, pericardial effusion, ventricular thrombus, RV infarct
2. Angiogram + PTCA (percutaneous transluminal coronary angioplasty)
3. Nuclear imaging (radionuclide perfusion scan)

Reading the image-heavy slides: ^[1]

• The coronary angiogram demonstrates an abrupt, focal severe narrowing/occlusion: contrast outlines the patent vessel and stops or narrows at the culprit lesion.
• On the radionuclide perfusion image, viable perfused myocardium is tracer-avid; a relatively cold defect represents reduced perfusion. This is not the primary test when acute STEMI already mandates reperfusion.

Prior MI criteria on ECG (ESC):* ^[1]

• Pathological Q waves with or without symptoms, in the absence of non-ischaemic causes
• Q wave ≥ 0.03s duration and ≥ 1mm deep in 2 contiguous leads
• Any Q wave in V2–V3 ≥ 0.02s or QS complex in V2 and V3

The slide-era management list includes: ^[1]

1. Bed rest, O₂, morphine; CCU care ± resuscitation
2. Early presentation ( < 12h) → Opening of infarct-related artery:
   • Fibrinolytic therapy
   • Primary PTCA (PCI)
3. Other measures: Anti-platelet agents, Beta-blockers, ACEI/ARB
4. Complications management and rehabilitation

The occlusive coronary thrombus has three components requiring targeted treatment: ^[1]

• Fibrin → Plasminogen activators (tPA, rPA, TNK-tPA, SK)
• Platelets → Antiplatelet therapy (Aspirin + Clopidogrel/Prasugrel/Ticagrelor, or GP IIb/IIIa inhibitors)
• Thrombin → Antithrombin therapy (Heparin, LMWH, Fondaparinux, Bivalirudin)

Lecture indication: ^[1]

• STEMI within 12 hours when timely primary PCI is unavailable and there is no contraindication

Documentation of successful fibrinolysis: ^[1]

1. Clinical: Decrease in pain
2. ECG Criteria: Early resolution of ST elevation at 90 min; preservation of R wave
3. Biochemical: Early peaking of CPK (normal peak 22–24h; successful thrombolysis 11–12h)
4. Imaging: Radionuclide imaging, angiography

Why does CPK peak earlier with successful thrombolysis? When the artery reopens, the restoration of blood flow "washes out" intracellular enzymes from the necrotic zone into the circulation more rapidly → you see an earlier, sharper CPK peak. This is called a washout phenomenon and is actually a reassuring sign. ^[1]

Visual comparison on the paired ECGs: Before streptokinase, there is marked anterior ST elevation; at 90 minutes, the ST elevation has substantially resolved and T-wave inversion/reperfusion change remains. Current failure criteria are < 50% ST-segment resolution at 60–90 minutes, persistent/recurrent pain, or haemodynamic/electrical instability; failed lysis requires immediate rescue PCI. ^[15]

Historical fibrinolytic examples shown in the lecture: ^[1]

1. Non-specific: Streptokinase (1.5 million units in 1 hour)
   • Activates plasminogen to plasmin in the WHOLE circulation → systemic fibrinolysis
   • Plasmin is a potent lytic agent for fibrin
2. Tissue-type plasminogen activator (alteplase)
   • Inactive in absence of fibrin; activated in presence of fibrin → clot-specific
   • Fibrin-specific; requires protocol-directed adjunctive antithrombotic therapy
3. tPA derivatives: TNK-tPA, Lanoteplase, Reteplase

The lecture's alteplase dose and comparative bleeding claim are not safe prescribing guidance. Fibrinolytic choice, dose adjustments, anticoagulation and antiplatelet therapy depend on the agent, age, weight, renal function and local STEMI protocol; all fibrinolytics carry serious bleeding and intracranial-haemorrhage risk. ^[14][15]

Examples from the lecture-era contraindication slide: ^[1]

• Any prior intracranial haemorrhage (ICH)
• Known structural cerebrovascular lesion (e.g., AVM)
• Known malignant intracranial neoplasm
• Recent ischaemic stroke
• Suspected aortic dissection
• Active bleeding or bleeding diathesis (excluding menses)
• Significant closed head or facial trauma within 3 months

Relative contraindications: ^[1]

• Chronic severe, poorly controlled hypertension
• Severe uncontrolled hypertension on presentation (SBP > 180 or DBP > 110)
• Prior ischaemic stroke > 3 months
• Traumatic or prolonged ( > 10 min) CPR or major surgery ( < 3 weeks)
• Recent (2–4 weeks) internal bleeding
• Non-compressible vascular punctures
• Prior SK/anistreplase exposure ( > 5 days ago) or allergic reaction
• Pregnancy
• Active peptic ulcer
• Current anticoagulant use (higher INR = higher bleeding risk)

This list is retained to explain the slide, but it is not a complete current checklist and the slide's “acute stroke within 3 hours” exception must not be used. Before fibrinolysis, use the current, agent-specific local STEMI checklist and obtain senior/cardiology input when uncertainty exists. ^[14][15]

Limitations: ^[1]

1. Only 50% of patients receiving fibrinolysis achieve optimal myocardial perfusion
2. 1/3 reocclude by 3 months
3. Delayed presentation and undiagnostic ECGs
4. Fibrinolytic therapy reduced in-hospital mortality by 50% vs placebo (in trials 6–8%; real world 20%)

Actions to address these: Thrombin inhibition, platelet inhibition, + PTCA; treatment in ambulance and A&E; education ^[1]

Primary PCI (direct angioplasty) is preferred over fibrinolysis when: ^[1]

• PCI can be performed within 120 minutes of first medical contact
• PCI achieves TIMI-3 flow in > 90% (vs ~50% with fibrinolysis)
• Lower risk of ICH

Current timing concept: If primary PCI cannot be delivered within 120 minutes of STEMI diagnosis and symptom onset is within 12 hours, give immediate fibrinolysis when eligible and transfer to a PCI centre. The regression line in the lecture's historical 2003 graph shows that PCI's advantage erodes with delay, but it is not an individual-patient bedside cutoff. ^[14][15]

STEMI Reperfusion Pathway (from lecture slide) ^[1]:

Do not wait at the non-PCI hospital to see whether lysis has worked before arranging transfer. Successful lysis is followed by angiography in 2–24 hours; failed lysis requires rescue PCI. ^[15]

Revascularisation indications beyond 12 hours (JACC 2021): ^[1]

• Cardiogenic shock or heart failure → Primary PCI (or CABG if PCI not feasible)
• Ongoing ischaemia, HF, or electrical instability → PCI
• 12–24 hours from symptom onset → PCI may still be considered
• Totally occluded infarct artery > 24h with no symptoms or severe ischaemia → PCI shows no benefit

Emergency CABG is indicated for: ^[1]

• Failed PCI with ongoing ischaemia
• Left main or severe 3-vessel disease found at angiography
• Mechanical complications (VSD, papillary muscle rupture)

Translating the procedure diagrams: ^[1]

• PCI: the slide shows femoral arterial access, a balloon compressing the culprit plaque/thrombus, and a stent scaffolding the lumen open. Contemporary ACS practice prefers radial access when feasible because it reduces bleeding, vascular complications and death. Restored flow does not “cure” atherosclerosis, and antiplatelet therapy is needed to reduce stent thrombosis. ^[14]
• CABG: a conduit is connected beyond an obstructed coronary segment so blood flows around the lesion; the original plaque is not removed.

Aspirin: ^[1]

• ↓ Acute mortality (especially in conjunction with thrombolysis)
• ↓ Reinfarction in long-term follow-up
• Dose: 160–320 mg/day

Clopidogrel / Prasugrel / Ticagrelor — P2Y12 inhibitors for dual antiplatelet therapy (DAPT) ^[1]

Heparin: ^[1]

• SC heparin (5000u Q8H) for DVT prophylaxis — APTT not changed (or LMWH)
• IV heparin (APTT ratio 1.5–2) for preventing embolisation, mural thrombosis
• Adjunct to fibrinolytic therapy (tPA) or patients without lytic therapy

Warfarin: ^[1]

• For established venous thrombosis or embolisation
• Echocardiographic evidence of LV thrombus

These are lecture-era examples, not a universal prescription. DAPT, parenteral anticoagulation and any longer-term oral anticoagulation must be selected for the reperfusion strategy, bleeding risk, age, renal function and competing indication. In current ACS guidance, the default after ACS is 12 months of aspirin plus an oral P2Y12 inhibitor for patients who are not at high bleeding risk, with shorter or modified regimens when bleeding risk or oral-anticoagulant use requires it. ^[14]

Calcium antagonist (diltiazem): The slide cites older non-Q-wave MI studies. It is not routine mortality-reducing post-MI therapy and should be avoided in LV systolic dysfunction or heart failure. ^[1]

Nitrates: Useful for ongoing ischaemic pain, hypertension or pulmonary congestion when blood pressure permits; they have not shown routine infarct-size or mortality benefit. Avoid in hypotension, suspected RV infarction and recent phosphodiesterase-5 inhibitor use. ^[14]

Beta-blockers: Start oral therapy when the patient is haemodynamically stable and there is no acute heart failure, shock risk, severe bradycardia or conduction block. Routine early IV beta-blockade can precipitate shock and is not a default treatment. Long-term benefit is clearest with reduced LVEF or another indication; do not infer “lifelong for everyone” from the historical percentage slides. ^[14]

Beta-blocker: Should be given to all patients with LV dysfunction ^[1] ACEI: Indicated for all patients with LVEF < 40%, DM, HT, renal dysfunction ^[1] ARB: Indicated for patients intolerant to ACEI ^[1] Aldosterone receptor antagonist (e.g., eplerenone, spironolactone): ^[1]

• Patients on ACEI/BB with LVEF < 40% AND HF, without significant renal dysfunction or hyperkalaemia

A. Risk stratification: ^[1]

• Residual ischaemia → exercise test, angiogram
• Electrical instability → 24h ECG for VT or frequent ventricular arrhythmia

B. Secondary prevention: ^[1]

1. Risk factor modulation: exercise, smoking cessation, lipid lowering (aggressive statin therapy reduces mortality; ezetimibe; PCSK9 inhibitor)
2. Beta-blocker (oral), Aspirin, ACEI/ARB
3. Cardiac rehabilitation and prevention: risk factor control, work, exercise, sex, alcohol, travel

ESC 2020 Lipid targets for NSTE-ACS (applies to all ACS): ^[1]

• LDL-C reduction ≥ 50% from baseline AND LDL-C < 1.4 mmol/L
• If not achieved with max statin → add ezetimibe
• If still not achieved → add PCSK9 inhibitor

The LDL-C target above is the lecture's ESC framework. Current US guidance similarly recommends high-intensity statin therapy for all ACS and addition of non-statin therapy when LDL-C remains ≥1.8 mmol/L (70 mg/dL) on maximal statin; use the locally adopted guideline and recheck lipids after treatment changes. ^[14]

AMI Complications: ^[1]

• Heart failure
• Arrhythmias (VF, VT, heart block — especially inferior MI)
• VSD (anterior MI) — new pansystolic murmur, haemodynamic deterioration
• Mitral regurgitation from papillary muscle dysfunction (inferior MI)
• Pericarditis (early: Day 1–3 from transmural necrosis; late: Dressler syndrome at 2–10 weeks, autoimmune)

Pathology: Medial collagen and elastin degeneration ^[1] The slide says blood “violates aortic intimal and adventitial layers”; anatomically, blood enters through an intimal tear and tracks within the media.

First principles: The aortic wall has three layers — intima, media, adventitia. In aortic dissection, the intima tears and blood enters the media, separating the intima from the adventitia. This creates a false lumen that can propagate anterograde (down towards the abdomen) or retrograde (back up towards the heart). The false lumen can compress the true lumen, occlude branch vessels, and/or rupture externally. ^[1][8]

Distinguishing aortic pathologies (from lecture diagram) ^[1]:

Causes: ^[1]

• Coexisting hypertension (80%) — this is the single most important risk factor
• Genetic diseases: Marfan syndrome, Familial aortic aneurysm/dissection, Ehlers-Danlos, Loeys-Dietz
• Bicuspid aortic valve
• Trauma

Additional risk factors from supporting sources: ^[8][9]

• Cocaine use (sudden severe hypertension)
• Pregnancy (3rd trimester, hormonal-mediated connective tissue changes)
• Vasculitis (e.g., Takayasu arteritis)
• Iatrogenic (cardiac surgery, catheterisation)

Classification: ^[1]

• Type A: ascending aorta involved (regardless of where the tear originates — can extend into descending)
• Type B: all dissections NOT involving the ascending aorta

Reading the classification diagram: DeBakey I begins in the ascending aorta and extends beyond the arch; II is confined to the ascending aorta; III begins in the descending aorta. Stanford A means any ascending-aortic involvement, while Stanford B means no ascending involvement. The Stanford system therefore drives the urgent management decision more directly. ^[1][16]

Why Type A is an emergency: The ascending aorta is in close proximity to the coronary ostia, aortic valve, pericardium, and brachiocephalic vessels. Retrograde dissection can cause:

• Acute aortic regurgitation → acute heart failure
• Coronary ostial occlusion → AMI
• Pericardial tamponade → cardiac arrest
• Brachiocephalic artery occlusion → stroke ^[1][8]

Symptoms: ^[1]

• Chronic: can be asymptomatic
• Acute: severe pain (MAXIMUM AT ONSET)
  • "Tearing" quality
  • Anterior chest (ascending aorta — Type A)
  • Interscapular, abdomen (descending aorta — Type B)
• Complications: Syncope, CVA, ischaemic limbs, paraplegia, acute AR → CHF

Signs: ^[1]

• BP — high or low (tamponade)
• Pulse deficits
• Complications: AR, CVA

Key discriminator from AMI: In aortic dissection, pain is maximal at onset (sudden, explosive), whereas in AMI, pain typically builds up over minutes. This is a classic exam discriminator. ^[1][5]

Complications by mechanism:

The lecture reports an abnormal CXR in > 80% of cases ^[1]

• Widened mediastinum (> 6 cm at level of carina on PA film; > 8 cm on AP film) ^[10]
• Pleural effusion (especially left-sided — beware: suggests leaking/rupture)
• Irregular aortic contour

CXR image: The film shows a widened superior mediastinum and abnormal aortic contour. These findings raise suspicion but are neither sensitive nor specific enough to confirm dissection; a normal CXR does not exclude acute aortic syndrome. ^[16]

CT aortogram (usually the initial test): ^[1]

• Ability to identify thrombosed false lumens
• Less invasive
• Shows intimal flap separating true and false lumens

On the axial CT image, an intimal flap divides the contrast-opacified aorta into true and false lumens. The false lumen may be larger, opacify differently or be partly thrombosed. Review the entire aorta and branch vessels for extent, rupture and malperfusion. ^[1][16]

TEE (transoesophageal echocardiogram): ^[1]

• Very rapid (~10 minutes each exam)
• Can be done at bedside with minimal risk
• Limited visualisation of distal aorta
• False-positive results are possible

On the TEE image, a mobile intimal flap separates the true and false lumens; Doppler can demonstrate differential flow or a re-entry jet. This makes TEE valuable at the bedside in an unstable patient and intraoperatively. ^[16]

MRI: ^[1]

• Identifies intimal flaps, great vessel anatomy, type A & B, degree of AI
• Time consuming ( > 30 min) → unsuitable for unstable patients
• Patient needs to be disconnected from monitoring devices, IV pumps
• Useful for serial follow-up of chronic dissections

Practical hierarchy: CT is recommended for initial imaging in suspected acute aortic syndrome because it is rapid, widely available and defines branch-vessel anatomy. TEE and MRI are reasonable alternatives selected according to haemodynamic stability, contraindications, availability and local expertise. The lecture's “almost 100%” test-performance statements should not be treated as universal. ^[16]

The lecture quotes mortality approaching 1% per hour in the first 48 hours and survival exceeding 90% with prompt care. ^[1] Death in aortic dissection results from progression of dissection → vascular compromise or rupture ^[1]

These figures are historical teaching estimates, not promises for an individual patient. Contemporary outcome depends on anatomy, rupture, tamponade, malperfusion, comorbidity and time to definitive treatment. ^[16]

1. Immediate anti-impulse therapy in an ICU setting: ^[16]

• Arterial-line monitoring; target SBP < 120 mmHg or the lowest pressure that maintains end-organ perfusion, and heart rate 60–80/min
• IV beta-blocker first; add an IV vasodilator only if blood pressure remains high after rate control
• Analgesia to blunt the sympathetic response

2. Definitive treatment: ^[16]

• Acute Type A dissection → immediate surgical consultation and repair
• Uncomplicated acute Type B → initial medical therapy
• Complicated Type B (rupture, malperfusion/branch occlusion, extension, progressive enlargement, intractable pain or uncontrolled hypertension) → intervention; TEVAR is preferred over open repair when anatomy is suitable

Why beta-blockers FIRST before nitroprusside? Nitroprusside is a pure arteriolar vasodilator that reduces afterload. But by reducing afterload, it causes reflex tachycardia and increases the rate of aortic pressure rise (dp/dt), which can propagate the dissection. Beta-blockers reduce both heart rate and dp/dt, so they must be given FIRST to blunt this reflex before adding nitroprusside. ^[1][12]

Why is the target conditional? Lower pressure reduces aortic-wall shear, but cerebral, renal and coronary perfusion must be maintained; this is why the target is “< 120 mmHg or the lowest pressure that preserves perfusion,” not simply “drive SBP to 100.” ^[16]

The lecture provides a systematic triage algorithm for acute chest pain ^[1]:

“Two negative troponins = low-risk unstable angina” is an obsolete shortcut. Use an assay-specific hs-cTn 0/1-hour or 0/2-hour pathway, serial ECGs and clinical risk assessment; a negative biomarker result alone neither excludes all ACS nor determines disposition. ^[14][15]

The lecture slide uses an older risk-stratified timing table. Current principles are: ^[14][15]

Key pharmacological principles:

• Antiplatelet: Aspirin + P2Y12 inhibitor (Clopidogrel / Prasugrel / Ticagrelor)
• Anticoagulant: LMWH or fondaparinux
• Anti-ischaemic: Beta-blocker, nitrate
• Risk stratification: GRACE score

1. ECG — stat, repeat serially
2. Cardiac biomarkers — hs-cTn at presentation and at the assay-specific serial interval (commonly 1 or 2 hours)
3. CXR — widened mediastinum (dissection), pulmonary oedema (HF), pneumothorax
4. Bloods — CBC, RFT, LFT, lipid profile, glucose, coagulation profile
5. If dissection suspected → urgent CT aortogram
6. Echocardiogram — RWMA, LV function, complications (VSD, MR, pericardial effusion, LV thrombus)
7. Coronary angiography → if STEMI (for primary PCI) or high-risk NSTEMI