Infarction: Pathophysiology, Classification, and Clinical Consequences
Infarction is necrosis of tissue due to prolonged ischemia (inadequate blood supply). It results from arterial occlusion (thrombosis, embolism), venous obstruction, or hypoperfusion (shock).
Pathophysiologic Sequence
- Blood flow interruption → O₂/nutrient deprivation.
- Switch to anaerobic glycolysis → ATP depletion → failure of Na⁺/K⁺-ATPase → cellular edema.
- Calcium influx → enzyme activation (proteases, lipases, endonucleases).
- Mitochondrial permeability transition → cytochrome c release → apoptosis/necrosis.
- Inflammatory response: neutrophil infiltration, cytokine release, phagocytosis of debris.
- Healing: Granulation tissue → fibrosis (scar) — except CNS (gliosis) and myocardium (fibrous scar, no regeneration).
Classification by Organ
| Infarct Type | Vessel / Territory | Key Features |
|---|---|---|
| Myocardial Infarction (MI) | Coronary artery | STEMI (transmural) vs. NSTEMI (subendocardial); troponin ↑; ECG changes |
| Cerebral Infarction (Ischemic Stroke) | Internal carotid / vertebral / circle of Willis branches | Territorial (MCA, ACA, PCA) or lacunar; NIHSS; thrombolysis/thrombectomy window |
| Pulmonary Infarction | Pulmonary artery branch (PE) | Hemorrhagic, pleural-based wedge; pleuritic pain, hemoptysis |
| Renal Infarction | Renal artery / segmental | Flank pain, hematuria, AKI; often from cardiac embolus |
| Splenic Infarction | Splenic artery | LUQ pain, fever; sickle cell, emboli, vasculitis |
| Mesenteric / Bowel Infarction | SMA, IMA, SMV | Pain out of proportion, lactic acidosis; surgical emergency |
| Limb Infarction | Peripheral artery / embolus | Pain, pallor, pulseless, paresthesia, paralysis (6 P's) |
