HEART

September 19, 2011

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
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
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)
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.
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
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
Blood supply
 Three major epicardial arteries:
 Left anterior descending (LAD)
 Left circumflex (LCX)
 Right coronary artery (RCA)
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.
Blood supply
 Functionally the right and left
coronary arteries behave as end
arteries
 Collateral circulation – usually with little
blood coursing through them
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)
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
Cardiovascular Dysfunction
 Loss of blood
 Disorders of cardiac conduction
 Obstructed flow
 Regurgitant flow
 Pump failure
 Contractile dysfunction (systolic failure)
 Inadequate filling.
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.
 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
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.)
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.
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.
Cardiac Hypertrophy
 The pattern of hypertrophy reflects the
nature of the stimulus:
 Pressure overloaded ventricles develop
concentric hypertrophy (reduced cavity
diameter)
 Volume overloaded ventricles develop
hypertrophy accompanied by dilation
(increased ventricular diameter).
 Cardiac hypertrophy
constitute a tenuous
balance between adaptive
characteristics and
potentially deleterious
structural and
 Physiologic hypertrophy
induced by regular strenuous
exercise seems to be an
extension of normal growth and
have minimal or no
deleterious effect.
 Congestive heart failure is
characterized by diminished
cardiac output (forward
failure) or damming back of
blood in the venous system
(backward failure)
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.
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.
 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.
Left Sided Heart Failure
 Left ventricle is usually
hypertrophied & often dilated.
 Secondary enlargement of the
atrium is frequently present.
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”
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.
Brain - Left sided heart
failure.

Hypoxic encephalopathy
with irritability, loss of
attention span and
restlessness which may
even progress to stupor
and coma.
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.
 Right sided Heart failure.

 LUNGS – minimal congestion

 LIVER
 slightly increased in size and
weight
 “nutmeg” appearance
Right sided Heart failure.

 KIDNEY – congestion
 BRAIN- hypoxic

encephalopathy
 Subcutaneous edema on

dependent portions of the

body
 In many cases of frank
cardiac decompensation,
the patient presents with
biventricular congestive
heart failure.
TYPES OF HEART DISEASE
 ISCHEMIC HEART DISEASE
 HYPERTENSIVE HEART DISEASE
 VALVULAR HEART DISEASE
 NON-ISCHEMIC MYOCARDIAL DISEASE
 CONGENITAL HEART DISEASE