CARDIO PART III

Determinants of Myocardial Oxygen Supply and Demand

Why is coronary perfusion mostly diastolic?

• During systole, the contracting ventricle compresses its own intramyocardial vessels → flow is squeezed down.

• During diastole, the myocardium relaxes → vessels open → LV coronary perfusion peaks.

• 🔴 Clinical pearl: Tachycardia shortens diastole → less perfusion time and higher demand = double hit.

• This is why rate control matters.

Why does ischemia occur?

• When supply can't meet demand → aerobic ATP production fails → contractility drops + electrical instability.

• If flow returns early → recovery

• if prolonged → necrosis.

Collateral circulation

• Gradual, chronic narrowing → time to grow collateral vessels (alternate routes).

• 🧠 "Slow block builds bridges."

• Limitations

  • varies person-to-person, takes time, and cannot compensate for sudden complete occlusion (that's why ACS/MI happens abruptly).

Pathophysiology and Classification of Angina Pectoris

• Definition and Core Distinction:

  • Angina Pectoris: Chest discomfort resulting from transient myocardial ischemia

  • characterized by cellular hypoxia without myocardial cell death

🧠 "Stable = stairs. Variant = vasospasm at rest. Unstable = unpredictable → emergency."

Why ischemia is reversible but infarction is not:

• ischemia = impaired ATP/function (cells still alive)

• infarction = irreversible cell death with release of intracellular contents (troponin).

1.4 Symptom relief ≠ prevention (THE distinction)

• Symptom-relieving antianginals improve the supply–demand balance → relieve ischemia today.

• They do NOT remove plaque, stop thrombosis, or lower future MI risk.

• 🛡 Risk-reducing therapy

  • statins, antiplatelets

  • ACEi/ARBs

  • lifestyle → targets atherosclerosis + thrombosis → lowers future MI.

• 🧠 "Relievers treat the moment; preventers treat the future."

Acute Coronary Syndrome (ACS) Spectrum and Diagnostics

• Pathophysiological Cascade:

Plaque rupture/erosion → exposes subendothelial collagen + tissue factor → platelet adhesion/activation/aggregation → coagulation cascade → thrombus → ↓ coronary flow → ischemia → possible necrosis.

• Why ACS is an acute thrombotic event, not just gradual plaque growth:

  • Stable angina = fixed, gradual narrowing (demand mismatch).

  • ACS = sudden plaque disruption + thrombus → abrupt flow reduction → acute ischemia at rest.

• 🧠 "Stable = slow clog. ACS = sudden clot."

• The Three Classifications of Acute Coronary Syndrome:

  Feature	Unstable Angina	NSTEMI	STEMI
  Coronary problem	Acute ↓ flow	Acute ischemia → infarct	Complete occlusion / severe ↓ flow
  Myocardial necrosis?	❌ No	✅ Yes (subendocardial)	✅ Yes (transmural)
  Troponin	No acute rise	Elevated	Elevated
  ECG	Normal or no ST elevation	Normal, ST depression, T inversion (no ST elevation)	Persistent ST elevation (or STEMI-equivalent)
  Urgency	Urgent eval	MI care	Reperfusion EMERGENCY

  🧠 ECG trick: "S-T-E-M-I = ST Elevation = Muscle Infarct (full thickness)."

• Why troponin indicates injury, but ECG — not troponin height — distinguishes STEMI vs. NSTEMI:

  • Troponin = marker of myocardial injury (any cause — not the pattern of injury).

  • ECG shows the territory/transmural extent of ischemia → drives the STEMI vs. NSTEMI decision.

• 🧠 "Troponin says if; ECG says where/how bad."

• Why unstable angina needs urgent evaluation despite no necrosis:

  • it's an ACS — plaque is disrupted, thrombus is forming

  • can progress to MI

  • No troponin rise ≠ safe

• Why the "partial vs. complete occlusion" rule isn't absolute

  • a "partial" lesion can behave like a complete one (and vice versa)

  • Treat the patient + ECG + biomarkers, not a rule of thumb

Broad ACS treatment goals

1. Relieve ischemia (anti-ischemic therapy)

2. Limit thrombus propagation (antiplatelets + anticoagulants)

3. Reduce further injury (statins, oxygen only if hypoxemic, beta blockers when stable)

4. Consider revascularization (PCI; fibrinolysis only for eligible STEMI)

Purpose of each:

• Antiplatelets → block platelet aggregation (prevent thrombus growth)

• Anticoagulants → limit clot propagation

• Statins → stabilize plaque, lower long-term atherosclerotic risk

• Anti-ischemic → ↓ demand / improve supply

• PCI → mechanically restore flow

Why fibrinolytics are NOT indicated for UA/NSTEMI

• these are usually partial occlusions

• Lysis adds bleeding risk without proven benefit

• best managed with antiplatelets/anticoagulants + PCI if needed

• 🧠 "Lytics are for complete block (STEMI) only."

Management of Acute Myocardial Infarction and Reperfusion

• Manifestations — typical & atypical

  • Typical: persistent chest pressure/tightness/heaviness at rest, radiating to arm/shoulder/jaw/neck/back; dyspnea, diaphoresis, nausea, dizziness.

  • Atypical: minimal/no chest pain — especially older adults,

  • diabetes; women more often report nausea, dyspnea, fatigue.

• ⚠ Absence of crushing chest pain does NOT exclude MI. 🧠 "No classic pain ≠ no MI."

• Troponin — how to think about it (don't memorize a single cutoff)

  • Troponin = protein in cardiac muscle; leaks when cells are injured.

  • Elevated troponin alone ≠ acute MI

• 🧠 "Trend + story + ECG = diagnosis."

• Consequences of infarction (location + size matter)

  • Necrotic tissue can't contract

    • ↓ contractility → ↓ stroke volume → ↓ cardiac output.

  • ↓ Ejection fraction with significant LV damage.

  • Electrical instability

    • dysrhythmias

  • Ventricular remodeling

    • progressive dysfunction.

• Extensive damage → heart failure or cardiogenic shock.

• 🧠 "Bigger infarct = bigger pump failure."

• Reperfusion Strategies for STEMI:

  • PCI = catheter-based; balloon + stent

    • mechanically restores flow

    • preferred for STEMI when promptly available (goal ~90 min first medical contact; ~120 min if transfer).

  • Fibrinolytics = dissolve fibrin in thrombus

    • option only when timely PCI unavailable and patient eligible; best early; bleeding risk (contraindications matter); target ~30 min of arrival.

  • 🧠 "PCI = plumbing. Lytics = draino. PCI first if you can get it fast."

STEMI treatment categories (why one drug can't do it all)

🧠 "No single med fixes obstruction + clot + demand + cholesterol — treat all four."