1. HEART
September 19, 2011

2. NORMAL
 250 to 300 gms. in females
 300 to 350 gms. in males
 right ventricular thickness 0.3 to 0.5 cm.
 left ventricular thickness 1.3 to 1.5 cm.
 Hypertrophy vs. dilatation.
 cardiomegaly

3. MYOCARDIUM
 Composed of branching and anastomosing striated
muscle cells (cardiac myocytes)
 Cardiac myocytes have 5 major components:
 Cell membrane
 Sarcoplasmic reticulum
 Contractile elements
 Mitochondrion
 nucleus

4. Myocardium
 SARCOMERE – functional intracellular contractile
unit of the cardiac muscle.
 Shorter sarcomere have considerable overlap of actin
and myosin with consequent reduction in contractile
forces (Frank-Starling mechanism)
 Cardiac myocytes account for 90% of the volume
of the heart but only 25% of the total cells (other
cells – endothelial cells and connective tissue cells)

5. Myocardium
 Atrial myocytes are generally smaller in
diameter and less structured than ventricular
myocytes.
 Some atrial cells have distinctive electron dense
granules – specific atrial granules.
 Storage site of atrial natriuretic peptides, that can
induce vasodilatation, natriuresis, suppression of
renin-angiotensin-aldosterone axis and fall in
arterial pressure.

6. Myocardium
 Specialized excitatory and conduction myocytes
regulate the heart’s rate/rhythm
 SA Node - Sinoatrial pacemaker
 AV Node
 Bundle of His
 Right and left bundle branches

8. Blood Supply
 Heart generates energy exclusively by the
oxidation of substrates so it relies heavily on
adequate flow of oxygenated blood.
 Epicardial coronary arteries are 5-10 cm. long, 2-4
mm in diameter that run along the external surface
of the heart
 Intramural arteries – penetrate the myocardium

9. Blood supply
 Three major epicardial arteries:
 Left anterior descending (LAD)
 Left circumflex (LCX)
 Right coronary artery (RCA)

10. Blood Supply
 Blood flows during diastole when the
microcirculation is not compressed by the
contraction.
 Anterior descending branch of the left coronary
artery - apex, anterior surface of the left ventricle
and anterior 2/3 of the interventricular septum
 Right coronary artery - right ventricular free wall,
adjacent half of the posterior wall of the left
ventricle & posterior third of interventricular
septum.

12. Blood supply
 Functionally the right and left coronary arteries
behave as end arteries
 Collateral circulation – usually with little blood
coursing through them

13. Valves
 Maintain unidirectional blood flow
 Normally are thin and translucent
 Free margins of AV valves are attached to
chordae tendinae which are attached to papillary
muscles
 Lined by endothelium and composed of a dense
collagenous core (fibrosa) and loose connective
tissue (spongiosa)

15. Effects of Aging
 Brown atrophy - lipofuscin deposits
 Basophilic degeneration - gray blue deposits
(?glucan)
 fewer myocytes, increased collagen and variable
deposits of amyloid.
 Reduced left ventricular cavity
 calcification of mitral annulus

16. Cardiovascular Dysfunction
 Loss of blood
 Disorders of cardiac conduction
 Obstructed flow
 Regurgitant flow
 Pump failure
 Contractile
dysfunction (systolic failure)
 Inadequate filling.

17. Congestive Heart Failure
 Heart unable to maintain an output sufficient for
the metabolic requirements of the body.
 Occurs either because of a decreased myocardial
capacity to contract or because or an inability to fill
the cardiac chambers with blood.
 Most due to systolic dysfunction.

18. Congestive heart failure
 Factors that affect cardiac response to hemodynamic
burden:
 Frank-Starling Mechanism
 Myocardial hypertrophy with or without cardiac chamber
dilation
 Activation of neurohumoral systems
 Release of norepinephrine by adrenergic cardiac nerves
 Activation of renin-angiotensin-aldosterone system
 Release of atrial natriuretic peptide

19. Congestive heart failure
 Most instances are the result of progressive
deterioration of myocardial contractile function
(systolic dysfunction).
 The most frequent causes are hypertension and
IHD
 Diastolic dysfunction – when heart cannot fill
properly (e.g. massive left ventricular hypertrophy,
fibrosis etc.)

20. Cardiac Hypertrophy
 Normal myocytes = 15 µm in diameter.
 Hyperplasia cannot occur in an adult heart.
 Pattern of hypertrophy reflects the stimulus:
 concentric hypertrophy in pressure over-loaded
ventricles ex. HPN or aortic stenosis.
 Eccentric hypertrophy in volume over-loaded
ventricles ex. mitral regurgitation.

21. Cardiac Hypertrophy
 In many cases heart failure is preceded by cardiac
hypertrophy
 There is an increase in the rate of protein synthesis,
the amount of protein in each cell, the size of the
myocyte, the number of sarcomeres and
mitochondria – consequently the total mass and size
of the heart.

22. Cardiac Hypertrophy
 The pattern of hypertrophy reflects the nature of
the stimulus:
 Pressureoverloaded ventricles develop concentric
hypertrophy (reduced cavity diameter)
 Volume overloaded ventricles develop hypertrophy
accompanied by dilation (increased ventricular
diameter).

25. Cardiac hypertrophy constitute a
tenuous balance between adaptive
characteristics and potentially
deleterious structural and

26. Physiologic hypertrophy induced
by regular strenuous exercise seems to
be an extension of normal growth and
have minimal or no deleterious effect.

27. Congestive heart failure is
characterized by diminished cardiac
output (forward failure) or damming
back of blood in the venous system
(backward failure)

28. Congestive heart failure
Morphologic changes of CHF are
distant from the heart and are
produced by the hypoxic and
congestive effects of the failing
circulation.

29. Congestive heart failure
Left-sided and right-sided failure
can occur independently but failure of
one side cannot exist for long without
eventually straining the other –
producing global heart failure.

30. Left Sided Heart Failure
 Most often caused by:
1. Ischemic heart disease
2. Hypertension
3. Aortic and mitral valvular diseases
4. Non-ischemic Myocardial diseases.

31. Left Sided Heart Failure
 Left ventricle is usually hypertrophied & often
dilated.
 Secondary enlargement of the atrium is
frequently present.

32. Lungs - Left sided heart failure.
 Pulmonary congestion and edema
 Lung changes include:
1. Perivascular and interstitial transudate
2. Progressive edematous widening of alveolar septa.
3. Accumulation of edema fluid in alveolar spaces.
 “heart-failure cells”

34. Kidney - Left sided heart failure.
 Reduction in renal perfusion which activate renin-
angiotensin-aldosterone system inducing retention
of salt and water with consequent expansion of the
interstitial fluid and blood volume.
 Acute tubular necrosis.
 Pre-renal azotemia.

35. Brain - Left sided heart failure.
Hypoxic encephalopathy with
irritability, loss of attention span and
restlessness which may even
progress to stupor and coma.

36. Right sided Heart failure.
 Usually a consequence of left sided
heart failure.
 Pure right sided heart failure occurs in
Cor pulmonale i.e.. Right ventricular
pressure overload induced by intrinsic
diseases of the lung or pulmonary
vasculature.

37. Right sided Heart failure.
 LUNGS – minimal congestion
 LIVER
 slightly
increased in size and weight
 “nutmeg” appearance

38. Right sided Heart failure.
 KIDNEY – congestion
 BRAIN- hypoxic encephalopathy
 Subcutaneous edema on dependent
portions of the body

42. In many cases of frank cardiac
decompensation, the patient
presents with biventricular
congestive heart failure.

43. TYPES OF HEART DISEASE
 ISCHEMIC HEART DISEASE
 HYPERTENSIVE HEART DISEASE
 VALVULAR HEART DISEASE
 NON-ISCHEMIC MYOCARDIAL DISEASE
 CONGENITAL HEART DISEASE