Learn about the Heart. The lecture includes the anatomy of the heart, physiology, and pathology.

1. The Heart

2. Normal Heart
• Weight
• 250 – 300 g in Females
• 300 – 350 g in Males
• Thickness
• R ventricle – 0.3 -0.5 cm
• L ventricle – 1.3 – 1.5 cm
• Increase in weight or ventricular thickness
HYPERTROPHY
• Increase in chamber size
DILATATION

3. MYOCYTES
1. Cell Membrane
2. Sarcoplasmic Reticulum
3. Contractile Elements
4. Mitochondria
5. Nucleus
5 major components:
Normal Heart

4. Other Histological Features
• Specific atrial granules
• Sites of storage of Atrial Natriuretic Peptide
• Intercalated discs
• Specialized gap junctions
• Specialized excitatory and conducting myocytes
• SA node, AV node, Bundle of His, left and right bundle branches
Normal Heart

5. Blood Supply
• Epicardial coronary arteries
• Left anterior descending
• Left circumflex arteries
• Right coronary arteries
• Intramural arteries
• Blockage of these arteries can cause myocardial ischemia
Normal Heart

6. Valves
•2 semilunar valves
• Aortic and Pulmonary
• Node of Arantius
•2 atrioventricular valves
• Mitral and Tricuspid
• Chordae Tendinae
MICROSTRUCTURE:
Normal Heart

7. Cardiac Dysfunction
5 principal mechanisms
1. Failure of the pump
2. Obstruction to flow
3. Regurgitant flow
4. Disorder of cardiac conduction
5. Disruption of continuity of circulation

8. HEART FAILURE
• Inability of the heart to pump blood at a rate commensurate with the
requirements of metabolizing tissues
• Mechanisms by which cardiovascular system maintains pressure and
perfusion at the presence of excessive hemodynamic burden
• Frank- Starling mechanism
• Myocardial structure changes
• Activation of neurohumoral systems

9. CARDIAC HYPERTROPHY
• Pressure overload
• Cross sectional area of myocytes in expanded
but cell length is not increased
• Concentric hypertrophy
• Volume overload
• Both cell length and width is increased

10. CARDIAC HYPERTROPHY
• Increase in myocyte size causes
• Decreased capillary density
• Increased intercapillary distance
• Deposition of fibrous tissue
FORMING ABNORMAL TISSUE
• Hypertrophy is both adaptive and deleterious

11. CONGESTIVE HEART FAILURE
• Features
• Increase in weight
• Chamber dilatation
• Thin walls
• Microscopic changes of hypertrophy

12. LEFT SIDED HEART FAILURE
• Caused by:
1. Ischemic heart diesease
2. Hypertension
3. Aortic and Mitral Valvular Diseases
4. Non-ischemic myocardial disease

13. LEFT SIDED HEART FAILURE
• Systemic Effects
• Lungs – pulmonary edema
• Kidney – prerenal azotemia
• Brain – hypoxic encephalopathy

14. RIGHT SIDED HEART FAILURE
• Causes
• Left sided heart failure
• Pulmonary hypertension (cor pulmonale)

15. RIGHT SIDED HEART FAILURE
• Effects
• Liver and portal system– congestive hepatomegaly, passive congestion,
centrilobular necrosis, congestive splenomegaly, ascites
• Kidney – peripheral edema, azotemia
• Brain – hypoxia
• Pleural and pericardial effusion
• Subcutaneous tissue – edema (hallmark)

16. FIVE MAJOR FORMS OF HEART
DISEASE
1. Congenital heart disease
2. Ischemic heart disease
3. Hypertensice heart disease
4. Valvular heart disease
5. Nonischemic (primary) myocardial disease

17. Congenital Heart Disease
• Abnormalities of the heart present from birth
• Insult occurs at 3-8 weeks AOG, where cardiovascular structures
would develop
• 3 MAJOR CATEGORIES
• Malformations causing a Left to Right shunt
• Malformations causing a Right to Left shunt
• Malformations causing an obstruction

18. Left to Right Shunts
1. Atrial Septal Defect
2. Ventricular Septal Defect
3. Patent Ductus Arteriosus
4. Atrioventricular Septal Defect
Congenital Heart Disease

19. 1. Atrial Septal Defect
• Abnormal opening between the left and right atria
• Types:
• Secundum – deficient or fenestrated oval fossa
• Primun – at adjacent AV valves
• Venosus – near entrance of SVC
Congenital Heart Disease

20. 2. Ventricular Septal Defect
• Incomplete closure of ventricular septum
• Types:
• Membranous – region of membranous septum
• Infundibular – below pulmonary valve
• Muscular – within muscular septum, “swiss chesse”
Congenital Heart Disease

21. 3. Patent Ductus Arteriosus
• 90% isolates
• Harsh – machinery like murmur
• Can cause obstructive pulmonary vascular disease upon reversal of
flow
• With other defects, can be life saving
Congenital Heart Disease

22. 4. Atrioventricular Septal Defect
• Types:
• Partial- primum ASD with cleft
• Complete – AV septal defect
• Hole in the heart
Congenital Heart Disease

23. Right to Left Shunts
1. Tetralogy of Fallot
2. Transposition of Great Arteries
3. Persistent Truncus Arteriosus
4. Tricuspid Atresia
5. Total Anomalous Pulmonary Venous Connection
Congenital Heart Disease

24. 1. Tetralogy of Fallot
• Most common cyanotic congenital heart disease
• 4 features
1. Ventricular Septal Defect
2. Right ventricular output obstruction
3. Aorta overriding VSD
4. Right ventricular hypertrophy
– Boot-shaped heart
Congenital Heart Disease

25. 2. Transposition of the Great Arteries
•Ventriculoarterial discordance
• Right ventricle  Aorta
• Left ventricle  Pulmonary artery
•Separation of systemic and
pulmonic circulation
•Incompatible with life unless a shunt
exists
• VSD – stable shunt
• Patent foramen ovale, PDA – unstable
shunt
Congenital Heart Disease

26. 3. Truncus Arteriosus
• Developmental failure of separation of the embryonic truncus
arteriosus into the aorta and the pulmonary
• Single artery receives blood from both ventricles
• Increased pulmonary blood blow  irreversible pulmonary
hypertension
Congenital Heart Disease

27. 4. Tricuspid Atresia
• Occlusion of tricuspid valve orifice
• Caused by the unequal division of AV canal
• Accompanied by hypoplasia of right ventricle
• Circulation is maintained by ASD or patent foramen ovale
Congenital Heart Disease

28. 5. Total Anomalous Pulmonary
Venous Connection
• No pulmonary vein joins the left atrium
• Primitive systemic venous channels from lung remain patent
• Foramen ovale or ASD allow blood to enter left atrium
• Volume and pressure hypertrophy of right atrium and ventricle
Congenital Heart Disease

29. Obstructive Congenital Anomalies
1. Coarctation of the aorta
2. Pulmonary stenosis and atresia
3. Aortic stenosis and atresia
Congenital Heart Disease

30. 1. Coarctation of the Aorta
• Infantile – tubular hypoplasia
• Adult – discrete infolding
• Coarctation with PDA – poor prognosis
without PDA – asymptomatic except for hypertension in
upper extremities
Congenital Heart Disease

31. 2. Pulmonary stenosis and atresia
• Obstruction at the pulmonary valve, can be isolated, or part of a
complex anomaly
• Usually with right ventricular hypertrophy and post stenotic
dilatation
• When valve is totally atretic, there is a hypoplastic right ventricle
• Mild stenosis may be asymptomatic
Congenital Heart Disease

32. 3. Aortic stenosis and atresia
• 3 major types
1. Valvular- cusps are hypoplastic, dysplastic, or abnormal in number
2. Subaortic stenosis
• Thickened ring ( discrete type)
• Collar (tunnel type)
3. Supravalvular
Congenital Heart Disease

33. Ischemic Heart Disease
• Insufficiency of oxygen with reduced availability of nutrient
substrates and inadequate removal of metabolites
• The clinical manifestations of IHD can be divided into 4
syndromes
1. Myocardial infarction
2. Angina pectoris
3. Chronic heart disease and heart failure
4. Sudden cardiac failure

34. Pathogenesis
• Acute plaque change
• Inflammation
• Coronary thrombosis
• Vasoconstriction
Ischemic Heart Disease

35. Angina Pectoris
• Symptom complex of IHD characterized by paroxysmal and usually
recurrent attacks of discomfort
• Caused by transient myocardial ischemia that falls short of inducing
the cellular necrosis that defines infarction
Ischemic Heart Disease

36. Myocardial Infarction
• Death of cardiac muscle resulting from ischemia
• Types
• Transmural – full thickness
• Subendocardial – 1/3 to ½ of ventricular wall
Ischemic Heart Disease

37. Pathogenesis
Coronary arterial occlusion
1. Sudden change in the morphology of an atheromatous
plaque
2. Platelets undergo adhesion, aggregation, activation, and
release of potent aggregators
3. Vasospasm
4. Activation of extrinsic pathway of coaglation
5. Thromus evolution to completely occlude the lumen of the
coronary vessel
Ischemic Heart Disease

38. Myocardial Infarction
Ischemic Heart Disease

39. Reperfusion• Salvaging of myocardium
Ischemic Heart Disease

40. Myocardial Infarction
Ischemic Heart Disease

41. Clinical Consequences of Myocardial
Infarction
1. Contractile dysfunction
2. Arrythmias
3. Myocardial rupture
4. Pericarditis
5. Right ventricular infarction
6. Infarct extension
7. Infarct expansion
8. Mural thrombus
9. Ventricular aneurysm
10. Papillary muscle dysfunction
11. Progressive late heart failure
Ischemic Heart Disease

42. Chronic Ischemic Heart Disease
•Cardiac findings in patients, who develop
progressive heart failure as a consequence of
ischemic myocardial damage
•Gross
• Cardiomegaly
• Severe stenosisng atherosclerosis
• Discrete gray-white scars
•Microscopically
• Myocardial hypertrophy
• Diffuse subendocardial vacuolization
• Scars of previously healed infarcts
Ischemic Heart Disease

43. Sudden Cardiac Death
• Unexpected death from cardiac causes early after symptom onset or
without onset of symptoms
• Gross
• Marched coronary atherosclerosis and critical stenosis
• Acute plaque disruption
• Healed myocardial infarct
• Subendocardial myocyte vacuolization
Ischemic Heart Disease

44. Hypertensive Heart Disease
• Response of the heart to increased demands induced by systemic
hypertension (left-sided) or pulmonary hypertension (right-sided)

45. Systemic Hypertensive Heart Disease
• Minimal criteria
1. Left ventricular hypertrophy
2. History or pathologic evidence of hypertension
• Gross
- LV wall thickness exceeds 2.0 cm
- Heart weight exceeds 500 gms
• Microscopic
- Increase in transverse diameter of myocytes
- Variation in cell size
- Interstitial fibrosis
Hypertensive Heart Disease

46. Pulmonary Hypertensive Heart
Disease
• Cor pulmonale
• Acute
• Dilatation without hypertrophy
• Caused by: massive pulmonary embolus
• Chronic
• (+) hypertrophy
• Caused by: emphysema, primary pulmonary hypertension
Hypertensive Heart Disease

47. Valvular Heart Disease
• Stenosis – failure to open completely
• Insufficiency – failure to close completely
• Pure- only stenosis or insufficiency
• Mixed – both are present
• Isolated – 1 valve
• Combined – more than 1 valve
• Functional regurgitation- incompetency of valve due to dilatation of
ventricle or artery

48. Calcific Aortic Stenosis
• Most common of all valvular abnormalities
• Acquired aortic stenosis is the consequence of calcification due to
‘wear and tear’
• Incidence increases with the rising average age of the population
• Hallmark – heaped up calcified masses within the aortic cusps that
ultimately protrude through the outflow surfaces into the sinuses of
Valsalva, preventing the opening of the cusps
Valvular Heart Disease

49. Calcific Stenosis of Congenitally
Bicuspid Aortic Valve
• Bicuspid aortic valves are neither stenotic nor symptomatic at birth
or throughout early life
• However, they are predisposed to progressive degenerative
calcification, similar to that of calcific aortic stenosis.
Valvular Heart Disease

50. Mitral Annular Calcification
• Calcific deposits can develop in the fibrous ring of the mitral valve
• Seen as irregular, stony hard and occasionally ulcerated nodules that
lie behind the leaflets
Valvular Heart Disease

51. Myxomatous Degeneration of the
Mitral Valve (MVP)
• One or more mitral leaflets are “floppy” and prolapse/balloon back
to left atrium during systole
Valvular Heart Disease

52. Myxomatous Degeneration of the
Mitral Valve (MVP)
• Morphology
• Gross – the affected leaflets are often enlarged,
redundant, thick and rubbery. Tendinous cords are
elongated, thinned, and occasionally ruptured
• Histological- there is attenuation of the fibrosa layer of
the valve, thickening of the spongiosa layer with
deposition of mucoid/ myxomatous material
• 4 serious complications
1. Infective Endocarditis
2. Mitral Insufficiency
3. Stroke or other systemic infarct
4. Arrythmias
Valvular Heart Disease

53. Rheumatic Fever and RHD
• Acute Rheumatic Fever
• Aschoff bodies
• Anitschow – pathognomic for RF, ‘caterpillar cells’
• Pancarditis
• Mac Callun plaques
Valvular Heart Disease

54. Rheumatic Fever and RHD
• Chronic RHD
Organization of acute inflammation to subsequent fibrosis
• Cardinal Anatomic Changes
1. leaflet thickening
2. commisural fusion and shortening
3. thickening and fusion of the tendinous cords
Aschoff bodies are replaced by a fibrous scar
Valvular Heart Disease

55. Infective Endocarditis
•Colonization or invasion of the heart valves or mural
endocardium by a microbe, leading to the
formation of bulky, friable vegetations
•Acute endocarditis – decribes a destructive
infection, frequently of a previously normal heart
valve with a highly virulent organism which leads to
death within days or weeks
•Subacute endocarditis – with organisms or low
virulence in a previously abnormal heart. The
disease may aappear insidiously or pursue a
protracted course of weeks to months
Valvular Heart Disease

56. Non-infected Vegetation
NBTE –Nonbacterial Thrombotic Endocarditis- characterized by the
deposition of fibrin, platelets, and other blood components on the
leaflets of cardiac valves. Does not contain microorganisms
Libman-Sacks Disease – mitral and tricuspid valvulitis with small sterile
vegetations seen in SLE
Valvular Heart Disease

57. Carcinoid Heart Disease
• The cardiac manifestation if the systemic syndrome caused by
carcinoid tumors
• Involves the endocardium and valves of the right heart
• Morphology – fibrous intimal thickenings in the inside surfaces of the
cardiac chambers and valvular leaflets

58. Cardiomyopaties
• Heart disease resulting from a primary abnormality in the
myocardium
• Types
1. Dilated Cardiomyopathy
2. Hypertrophic Cardiomyopathy
3. Restrictive Cardiomyopathy

59. 1. Dilated Cardiomyopathy
•Characterized by progressive cardiac dilatation and
contractile (systolic) dysunction, usually with
concomitant hypertrophy
•The heart is usually heavy, often weighing two to
three times normal, large and flabby, with dilatation
of all chambers
•Mural thrombi are common
•Histologically, muscle cells are hypertrophied with
enlarged nuclei, but many are attenuated,
stretched, and irregular. Endocardial fibrosis of
variable degree is present
Cardiomyopathies

60. 2. Hypertrophic Cardiomyopathy
• Characterized by myocardial hypertrophy, abnormal diastolic filling
and in 1/3 of cases, intermittent ventricular outflow obstruction.
• Massive myocardial hypertrophy without ventricular dilatation.
• On cross section, the ventricular cavity loses it’s round-to-ovoid
shape, and is compressed into a ‘banana-like’ configuration
Cardiomyopathies

61. 3. Restrictive Cardiomyopathy
• Characterized by a primary decrease in ventricular compliance,
resulting in impaired ventricular filling during diastole
• Ventricles are approximately normal size or slightly enlarged, the
cavities are not dilated, and the myocardium is firm.
Cardiomyopathies

62. Myocarditis
• Inflammatory process of the myocardium which result in injury to
the cardiac myocytes
• Types of myocarditis
1. Lymphocytic myocarditis
2. Hypersensitivity myocarditis
3. Giant cell myocarditis
4. Myocarditis of Chagas disease

63. Pericardial Disease
•Pleural effusion and hemopericardium
Normal 30-50 ml, thin, clear, straw-like fluid
•Hemopericardium – blood
•Pericardial effusion – fluid of variable composition
•Purulent pericarditis – pus
•Slow accumulation – enlargement of cardiac
shadow
•Rapid accumulation – cardiac tamponade

64. Pericarditis
• Acute
1. Serous – caused by non infectious inflammation
- surface with scan number of PMN’s, lymphocutes
and monocytes
2. Fibrinous and serofibrinous – most frequent
- serous fluid and fibrinous exudates
fibrinous – surface is dry, with fine granular
roughening
serofibrinous – more and thicker fluid which is
yellow and cloudy
* pericardial friction rub

65. Pericarditis
c. Purulent or suppurative pericarditis
- direct extension
- seeding
- lymphatic
- direct introduction
Morphology
exudate – thin to creamy pus
surface – redenned, granular and coated with the exudate
Organization produces CONSTRICTIVE PERICARDITIS

66. Pericarditis
d. Hemorrhagic
Most common cause – malignant neoplasm
e. Caseous pericarditis
Causes – Tuberculosis, Fungal Infection

67. Chronic / Healed Pericarditis
A. Adhesive mediastinopericarditis
Pericardial sac is obliterated and adherence to external aspect of
parietal layer to surrounding structure
B. Constrictive pericarditis
Pericardial space is obliterated
Plaster mold

68. Tumors of the Heart
Most of the primary tumors are rate, metastasis are more common
Primary cardiac tumors:
1. Myxoma
2. Lipoma
3. Papillary fibroelastoma
4. Rhabdomyoma

69. Myxoma
• Most common primary tumor
• Gross
• Commonly single
• Mostly on fossa ovalis of atria
• Size – 4 cm to 10 cm
• May be sessile or pedunculated
• Microscopic
• Stellate/globular myxoma
• Etc.
Tumors

70. Lipoma
• Excessive fat accumulations
• May occur in the subendocardium, subepicardium or within the
myocardium
Tumors

71. Papillary fibroelastoma
• Located on valves
• Distinctive cluster of hair like projections up to 1 cm in diameter
• Histological features:
• Covered by endothelium
• Myxoid connective tissue with MPS matrix
• Elastic fibers
Tumors

72. Rhabdomyoma
• Most frequent primary tumor of infants and children
• Gross
• Small , gray- white
• Microscopic
• Mixed population of cells
• Large, rounded or polygonal cells containing numerous glycogen laden
vacuoles
• SPIDER CELL
Tumors

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