Week 10 Pathology

Congestive Heart Failure (CHF)

  • Definition – heart is unable to pump blood at a rate to match with the requirements of the metabolising tissues or can only do so with elevated filling pressures.
  • Compensatory mechanisms
    • Frank- Starling mechanism – increase preload–> increased myocardial stretch
    • Hypertrophy
    • Neurohumoural systems – adrenaline to increase HR, contractility and vascular resistance, renin angiotensin pathway, release of atrial naturetic peptide.
  • Causes
    • Hypertension
    • MI
    • Valvular pathology – MR, AR, AS, MS
    • Cardiomyopathy
  • Pathology – infarction, ischaemia, calcification, hypertrophy, interstitial fibrosis
  • Liver pathology – congestion –> nutmeg liver, centrilobular necrosis(central hypoxia), centrilobular fibrosis


Ventricular Hypertrophy.

Adaptive but also potentially deleterious – increased capillary to myocyte ratio, increased fibrosis, increased abnormal proteins.

Pressure overload Volume overload
HTN, Aortic stenosis Post MI, some valvular diseases
Concentric hypertrophy
Increased wall thickness, smaller cavity Increased dilation and cavity size so wall thickness maybe normal


LVF vs. RVF:

IHD, HTN, valvular disease – aortic and mitral Secondary to LVF, cor pulmonale
Pulmonary congestion, poor organ perfusion Minimal pulmonary congestion, significant systemic venous and portal congestion.


Cor pulmonale

  • RHF that is not secondary to LHF
  • Causes
    • Lung parenchyma – COPD, fibrosis, bronchiectasis
    • Pulm vessels – pulm HTN, recurrent PE, arteritis eg Wegners
    • Chest movement – obesity, kyphoscoliosis, Neuromuscular
    • Pulm constriction – hypoxia, metabolic acidosis, chronic sleep apnoea
  • Morphological features
    • Systemic and portal venous congestion
    • RV hypertrophy, L bulging septum, Liver – congestive hepatomegaly, centrilobular necrosis, congestive splenomegaly, effusions, ascites.


Ischemic Heart Disease (IHD)

  • Definition – imbalance between supply and demand of the heart for oxygenated blood.
  • Risk factors- atherosclerosis of coronary arteries, cardiac hypertrophy, shock, hypoxaemia
  • Angina – where ischaemia does not cause myocyte death. Stable, unstable and Prinzmetal angina.
  • MI
    • Pathogenesis –
      • Sudden change in atheromatous plaque eg rupture, fissure, haemorrhage –> platelet adhesion–> vasospasm–> activate coag cascade–> thrombus–> vessel occlusion
      • Vasospasm of coronary blood vessels–> occlusion
  • Timing of injury
    • Reversible – cessation of aerobic metabolism in seconds, decreased ATP production(50% at 10mins 10% of normal at 40mins), lactic acid production, loss of contractility and acute heart failure in 1 minute, ultrastructural changes such as myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling in a few minutes
    • Irreversible – myocyte injury and cell leakage in 20-40mins, initially subendocardial then transmural death, microvascular injury in 1 hour, coagulation necrosis in >2hrs
    • Morphological chages only begin at 4-12hrs. 2wks for scar to start, 2 months for a dense scar.
  • Location
    • Isolated RV – 1-3%
    • LAD – 40-50%
    • RCA – 30-40%
    • LCx -15-20%
  • Complications
    • Ventricular fibrillation, heart block, bradycardia, VT, ectopics
    • Contractile dysfunction
    • Myocardial rupture – wall, septum, papillary muscles- usually 3-7d post.
    • Pericarditis – d2-3 post.
    • Infarct extension or expansion
    • Mural thrombus
    • Ventricular aneurysm
    • Mortality – 30% within 1st yr.
    • Ant transmural – more aneurysm, wall rupture, mural thrombi.
    • Post transmural – more conduction issues.
  • Thrombolysis/PCA
    • Reperfusion is the most effective way to salvage tissue but have some pathologies associated
      • Arrhythmias
      • Myocardial haemorrhage with contraction bands
      • Reperfusion injury
      • Microvascular injury
      • Prolonged ischaemic dysfunction – myocardial stunning


Rheumatic fever

  • follows 10d to 6wks after Group A strep pharyngitis(3%)–> fibrotic valves. Esp mitral stenosis.
  • Manifestations – migratory polyarthritis of large joints, carditis, subcutaneous nodules, erythema marginatum of skin, Syndenham chorea.
    • Vegetations, Aschoff body in myocardium, fibrinous pericarditis.
    • Infective endocarditis.
    • Artificial valves



  • Hypertrophic cardiomyopathy
    • Myocardial hypertrophy with out ventricular dilation, asymetrical septal thickening, impaired diastolic filling and LV outflow obstruction in 25%
    • Cx – heart failure, sudden death, ventricular arrhythmias, AF, mural thrombus, stroke, infective endocarditis




  • Causes
    • Infections – viral, bacterial
    • Immunological – SLE, Rh fever, scleroderma
    • Post MI – Dresslers
    • Neoplastic
    • Drug hypersensitivity
  • Exudate types (Types of Pericarditis)
    • Serous – non infectious
    • Fibrinous
    • Purulent
    • Haemorrhagic
    • Caseous
  • Clinical features
    • Pericardial rub, pain, fever, CCF


Congenital heart disease

  • Left to right shunt – cause cyanosis months to years after birth – ASD, VSD, PDA, AVSD
    • VSD is the commonest congenital heart defect.
  • Right to left shunt – cyanosis early in postnatal life – TF, ToGA, TA, total anomalous pulm venous connection, truncus arteriosus.
  • Teratology of fallot is the commonest cyanotic congenital heart disease.
    • VSD
    • Obstruction to RV outflow
    • Aorta that over-rides the VSD
  • Transposition of great arteries – Aorta from RV and Pulm artery from LV – needs a VSD or patent ductus to survive.
  • Truncus arteriosus – single great artery with VSD – greater pulm circulation risks pulm HTN.
  • Obstructive
    • Coarctation- narrowing of aorta, Males affected twice as much. Females with Turners. Babies with PDA –> cyanosis affecting lwoer half of body from birth. Those without PDA may go unrecognised till adulthood – HTN in UL and weak pulses and lower pressure in lower limbs.