9.2 Cardiac & Pulmonary Pathology
Key Takeaways
After a myocardial infarction, coagulative necrosis and neutrophils appear within 1–3 days, macrophages at 3–7 days (when free-wall rupture risk peaks), granulation tissue at 1–2 weeks and a collagen scar by about 2 months.
Right-sided heart failure causes dependent pitting pedal edema, hepatic congestion and jugular venous distension; left-sided failure causes pulmonary edema and orthopnea.
Infective endocarditis produces painful Osler nodes on finger and toe pads, painless Janeway lesions on palms and soles, and splinter hemorrhages; Staphylococcus aureus causes acute disease and affects the tricuspid valve in people who inject drugs.
Emphysema from smoking is centriacinar and upper-lobe predominant, whereas alpha-1 antitrypsin deficiency causes panacinar, lower-lobe emphysema.
Hypertrophic pulmonary osteoarthropathy (digital clubbing plus symmetric periostitis of the tibia and fibula) is a classic radiographic clue to intrathoracic malignancy, especially lung adenocarcinoma.
9.2 Cardiac & Pulmonary Pathology
Peripheral artery disease and venous thrombosis are covered in 7.3 and 8.1. The outline also lists the cardiovascular and pulmonary systems as separate disorder categories. Many podiatric patients have coronary disease, heart failure or lung disease, and several cardiopulmonary disorders produce signs in the lower extremity.
Ischemic Heart Disease
Atherosclerosis of the coronary arteries (pathogenesis in 8.1) produces a spectrum of disease:
- Stable angina: fixed stenosis (usually 70% or more) causes exertional chest pain relieved by rest or nitroglycerin.
- Acute coronary syndrome: plaque rupture or erosion with thrombosis causes unstable angina, non-ST-elevation MI or ST-elevation MI.
- Sudden cardiac death: most often a ventricular arrhythmia.
Timeline of Myocardial Infarction
| Time after occlusion | Gross and microscopic findings | Main complication risk |
|---|---|---|
| 0–4 hours | No visible change | Arrhythmia |
| 4–24 hours | Early coagulative necrosis, wavy fibers, contraction bands with reperfusion | Arrhythmia, heart failure |
| 1–3 days | Neutrophilic infiltrate | Fibrinous pericarditis |
| 3–7 days | Macrophages remove necrotic debris; the wall is softest | Free-wall rupture, septal rupture, papillary muscle rupture |
| 1–2 weeks | Granulation tissue at the margins | |
| 2 weeks to 2 months | Collagen scar | Ventricular aneurysm, mural thrombus, Dressler syndrome (autoimmune pericarditis weeks later) |
Troponin I or T rises within hours, peaks within about a day and stays elevated for 7–10 days.
Heart Failure
| Feature | Left-sided failure | Right-sided failure |
|---|---|---|
| Usual cause | Ischemic heart disease, hypertension, valvular disease | Most often left-sided failure; also cor pulmonale from lung disease |
| Congestion | Pulmonary: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, crackles | Systemic: dependent pitting pedal edema, jugular venous distension, hepatomegaly ("nutmeg liver") |
| Pathology | "Heart failure cells" (hemosiderin-laden alveolar macrophages) | Centrilobular hepatic congestion |
Heart failure is also classified by ejection fraction. In HFrEF the ejection fraction is 40% or less; in HFpEF it is preserved, with diastolic stiffness. Natriuretic peptides (BNP, NT-proBNP) rise with ventricular wall stretch. Bilateral leg edema has a broad differential: heart failure, nephrotic syndrome, cirrhosis, venous insufficiency, lymphedema and dihydropyridine calcium channel blockers.
Valvular & Myocardial Disease
- Calcific aortic stenosis: age-related dystrophic calcification, accelerated by a bicuspid valve. Classic symptoms are angina, syncope and heart failure. It causes a crescendo-decrescendo systolic murmur radiating to the carotids.
- Mitral regurgitation and mitral valve prolapse: myxomatous degeneration (associated with Marfan syndrome) or papillary muscle dysfunction.
- Rheumatic heart disease: follows group A streptococcal pharyngitis (5.1); chronic disease causes mitral stenosis.
- Cardiomyopathies: dilated (alcohol, doxorubicin, viral myocarditis, genetic); hypertrophic (sarcomere gene mutations, asymmetric septal hypertrophy, sudden death in young athletes); restrictive (amyloidosis, sarcoidosis, hemochromatosis).
Infective Endocarditis
| Feature | Acute | Subacute |
|---|---|---|
| Typical organism | Staphylococcus aureus | Viridans streptococci, enterococci |
| Valve | Normal valves; tricuspid in people who inject drugs | Previously damaged valves |
Vegetations embolize and trigger immune-complex phenomena:
- Osler nodes: painful nodules on finger and toe pads
- Janeway lesions: painless hemorrhagic macules on the palms and soles
- Splinter hemorrhages in the nail beds, plus Roth spots and glomerulonephritis
Diagnosis rests on blood cultures and echocardiography. Septic emboli can cause digital infarcts or a cold foot.
Pulmonary Pathology
Obstructive Diseases (FEV1/FVC reduced)
- Asthma: Th2-driven eosinophilic airway inflammation, smooth muscle hypertrophy and mucus plugs containing Curschmann spirals and Charcot-Leyden crystals.
- Emphysema: destruction of alveolar walls. Smoking causes centriacinar, upper-lobe emphysema; alpha-1 antitrypsin deficiency causes panacinar, lower-lobe emphysema (and possibly liver disease).
- Chronic bronchitis: productive cough for at least 3 months in each of 2 consecutive years; the Reid index (gland-to-wall thickness) is increased.
- Bronchiectasis: permanent airway dilation (cystic fibrosis, Kartagener syndrome).
Restrictive Diseases (total lung capacity reduced)
- Idiopathic pulmonary fibrosis: honeycomb fibrosis in older adults.
- Pneumoconioses: asbestosis (lower lobes, pleural plaques, mesothelioma) and silicosis (upper lobes; increased TB risk).
- Sarcoidosis: noncaseating granulomas, bilateral hilar adenopathy, hypercalcemia, and erythema nodosum with ankle arthritis (Löfgren syndrome).
- ARDS: diffuse alveolar damage with hyaline membranes; triggers include sepsis, trauma and fat embolism (7.3).
Infection and Embolism
- Community-acquired pneumonia: lobar consolidation from Streptococcus pneumoniae, atypical pneumonia from Mycoplasma, and aspiration into dependent segments, usually of the right lung.
- Tuberculosis: Ghon complex and cavitary reactivation (5.5).
- Pulmonary embolism: most arise from proximal leg deep vein thrombosis. Postoperative immobilization after foot and ankle surgery, casting and non-weight-bearing are recognized risk factors. Presentations range from pleuritic pain and tachycardia to sudden death from a saddle embolus.
Lung Cancer
| Type | Location and features | Paraneoplastic and extrathoracic clues |
|---|---|---|
| Adenocarcinoma | Peripheral; most common type overall and in nonsmokers; EGFR, ALK and KRAS mutations | Hypertrophic pulmonary osteoarthropathy, Trousseau migratory thrombophlebitis |
| Squamous cell carcinoma | Central; smoking-related; cavitation | PTHrP-mediated hypercalcemia |
| Small cell carcinoma | Central; strongly smoking-related | SIADH, ectopic ACTH, Lambert-Eaton syndrome (proximal leg weakness) |
| Superior sulcus (Pancoast) tumor | Lung apex | Horner syndrome, brachial plexus pain |
Tip
Hypertrophic pulmonary osteoarthropathy combines digital clubbing (toes as well as fingers), symmetric painful periosteal new bone along the tibia and fibula and joint effusions. Finding it on foot and ankle radiographs should prompt a chest evaluation.
Five days after a large anterior myocardial infarction, a patient suddenly develops hypotension, jugular venous distension and muffled heart sounds. Which pathologic stage explains why this complication occurs at this time?
Neutrophils within the first 24 hours release proteases that liquefy the myocardium
Collagen scar formation weakens the wall into a thin ventricular aneurysm
Macrophages clear necrotic myocytes before granulation tissue forms, so the wall is weakest
Contraction band necrosis from reperfusion injury makes the infarcted wall rigid and prone to cracking
A patient who injects drugs has fever, a new systolic murmur that increases with inspiration, and painful erythematous nodules on several toe pads. What is the most likely diagnosis?
Acute Staphylococcus aureus endocarditis of the tricuspid valve with Osler nodes
Nonbacterial thrombotic endocarditis from mucin-producing adenocarcinoma
Subacute viridans streptococcal endocarditis of a damaged mitral valve
Libman-Sacks endocarditis from systemic lupus erythematosus
Ankle radiographs of a 64-year-old former smoker with painful legs show bilateral, symmetric periosteal new bone along the distal tibial and fibular diaphyses, and the toes are clubbed. Which next evaluation is most appropriate?
Serum uric acid and joint aspiration for tophaceous gout of the ankle
Bone biopsy for Ewing sarcoma
Venous duplex ultrasound for chronic venous insufficiency
Chest imaging for an intrathoracic cancer such as lung adenocarcinoma
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