Robbins Patho, 10 e.

12 The Heart

Table of Contents
12 The Heart.................................................................1
The Heart..................................................................1
Cardiac Structure and Specializations................1
Overview of Cardiac Pathophysiology................3
Heart Failure.........................................................3
Cardiac Development...........................................3
Congenital Heart Disease.....................................3
Ischemic Heart Disease.........................................3
Arrhythmias..........................................................3
Hypertensive Heart Disease.................................3
Valvular Heart Disease.........................................3
Cardiomyopathies.................................................5
Pericardial Disease...............................................5
Tumors of the Heart.............................................5
Cardiac Transplantation......................................5
Cardiac Devices....................................................5

The Heart Both reflect compensatory changes in response to volume and/or

- remarkably efficient, durable, and reliable pump pressure overloads
- propelling more than 7500 L of blood through the body
each day, and beating more than 40 million times a year Cardiomegaly
- wellspring for tissue oxygenation, nutrition, and waste
- Increased cardiac weight / size (or both)
removal
- From hypertrophy and/or dilation
- 8 wks gestation: heart and vasculature are the first fully
functional organ system Myocardium
- pumping function of the heart occurs through coordinated
Cardiovascular disease
contraction (during systole) and relaxation (during
o including coronary artery disease [CAD], stroke, diastole) of cardiac myocytes (the myocardium)
and peripheral vascular disease
Left ventricular myocytes Right ventricular myocytes
o the number-one cause of worldwide mortality - a spiral circumferential - less structured organization,
orientation generating overall less robust
Cardiac Structure and Specializations
- generate vigorous coordinated contractile forces.
- heart weight varies with body habitus waves of contraction - Contraction is achieved by
- Average weight: - spreading from the cardiac shortening of serial contractile
o 0.4% to 0.5% of body weight apex to the base of the heart elements (sarcomeres) within
o M: 300-360 g parallel myofibrils.
o F: 250-320 g Atrial cardiomyocytes Ventricular myocytes
- Hypertrophy: Increased heart weight or ventricular - have cytoplasmic storage - contain B-type natriuretic
thickness granules peptide
- Dilation: enlarged chamber size - contain atrial natriuretic
peptide
- protein hormones that are released in response to

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increased stretch a. (e.g., vagal stimulation)

- promote arterial vasodilation and stimulate renal salt and 2. extrinsic adrenergic agents
water elimination (natriuresis and diuresis) a. (e.g., circulating adrenaline)
3. hypoxia, and potassium concentration
a. (i.e., hyperkalemia can block signal transmission
Valves
altogether)
- maintain unidirectional blood flow
- Valve function depends on the mobility, pliability, and Components of conduction system
structural integrity of the leaflets of the atrioventricular
valves (tricuspid and mitral) or cusps of the semilunar Sinoatrial (SA) node at the junction of the right
valves (aortic and pulmonary) pacemaker atrial appendage and SVC
Atrioventricular (AV) node located in the right atrium
CARDIAC VALVES along the interatrial septum
Atrioventricular valves Semilunar valves Bundle of His (AV bundle) connecting the right atrium to
Tricuspid Valve Aortic Valve the ventricular septum
Mitral Valve Pulmonary Valve Right and Left bundle branch stimulate their respective
Competence depends on the Function depends on the divisions ventricles via further
proper function of the leaflets, integrity and coordinated arborization into the
tendinous cords, and the movements of the cuspal Purkinje network
attached papillary muscles of attachments. The cells of the cardiac conduction system depolarize spontaneously,
the ventricular wall potentially enabling all of them to function as cardiac pacemakers.
Valvular insufficiency Valvular regurgitation
Left ventricular dilation, a dilation of the aortic root SA node
ruptured cord, or papillary
muscle dysfunction that can - 60 to 100 beats/min
interfere with mitral valve - faster than the other components
closure - it normally sets the pace

If nodal tissues become dysfunctional, other cells in the conduction

- Lined by endothelium system can take over, generating, for example, a junctional escape
rhythm (usually at a much slower rhythm).
Layers of cardiac valves
AV node
1. Fibrosa layer
o dense collagenous layer at the outflow surface - has a gatekeeper function
o connected to the valvular supporting structures - by delaying the transmission of signals from the atria to the
o providing mechanical integrity ventricles, it ensures that atrial contraction precedes
ventricular systole
2. Spongiosa layer
o central core of loose connective tissue Blood Supply
3. Ventrucularis or atrialis layer Cardiac myocytes rely almost exclusively on oxidative
o depending on which chamber it faces phosphorylation for their energy needs.
o layer rich in elastin on the inflow surface
o providing leaflet recoil  High density of mitochondria (20% to 30% of myocyte
volume)
Cardiac valves  Myocardial energy generation also requires a constant
supply of oxygenated blood
 thin enough to be nourished by diffusion from the blood
 normal leaflets and cusps have only scant blood vessels Myocardium is extremely vulnerable to ischemia.
limited to the proximal portion of the valve
 does not express ABO or histocompatibility antigens Nutrients and oxygen are delivered via the coronary arteries with
 cryopreserved valvular tissues can be transplanted with ostia immediately distal to the aortic valve
relative impunity
↓
Conduction System
Initially course along the external surface of the heart (epicardial
Coordinated contraction of the cardiac muscle depends on the
coronary arteries)
initiation and rapid propagation of the cardiac initiation and rapid
propagation of electrical impulses ↓
Frequency of electrical impulses is sensitive to: penetrate the myocardium (intramural arteries)
1. neural inputs ↓

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Subsequently branching into arterioles  octogenarians (and older) also

frequently have deposition of
↓ extracellular amyloid
- Valvular aging changes are major contributors to
forming a rich arborizing vascular network so that each myocyte
significant valvular disease
contacts roughly three capillaries.
- Progressive atherosclerosis + strong aging component:
- Right and left coronary arteries function as end arteries major cause of IHD
o Even though there are is the presence of collateral
circulation
- Blood flow to the myocardium occurs during ventricular
diastole
o after closure of the aortic valve
o when the microcirculation is not compressed by
cardiac contraction
- At rest, diastole comprises approximately two thirds of the
cardiac cycle
- With tachycardia (increased heart rate), the relative
duration of diastole also shortens, thus potentially
compromising cardiac perfusion.

Cardiac Regeneration
Considerable interest in exploring the possibility of replacing
damaged myocardium by inducing cardiac regeneration in vivo or
implanting stem cell–derived cardiac cells

- myocardium of mammals has a very low replicative

potential after fetal and neonatal life
o less than 1% cardiomyocyte turnover per year in
adult humans
- stimulating cardiac regeneration in vivo in humans could
facilitate recovery of myocardial function after a host of
injurious stimuli
o Implanted cells may show some cardiomyocyte
differentiation
o durability of this benefit has been limited,
o they do not contribute significantly to restoration
of contractile force
o failure to successfully integrate these cells into
Overview of Cardiac Pathophysiology
the conduction pathway of the host heart carries
pathophysiologic pathways that result in a “broken” heart distill down
the very real risk of autonomous arrhythmic foci.
to six principal mechanisms:
Effects of Aging on the Heart
Failure to pump Cardiac muscle contracts
Most forms of heart disease become more prevalent with each
weakly
advancing decade
Systolic dysfunction Chambers cannot empty
- size of the left ventricular cavity, particularly in the base- properly
to-apex dimension, is reduced in later life Diastolic dysfunction Myocardium cannot relax
sufficiently to permit
o exacerbated by systemic hypertension
ventricular filling
 as the basal ventricular septum Obstruction to flow Overworked myocardium,
protrudes into the left ventricular which must pump against the
outflow tract (so-called sigmoid obstruction
septum) e.g. calcific aortic valve Lesions that prevent valve
o Elderly heart stenosis opening
 Lesser myocytes (degenerative e.g. systemic hypertension, cause increased ventricular
attrition) aortic coarctation chamber pressures
 Increased connective tissue Regurgitant flow Backward blood flow
Increased volume workload
May overwhelm the pumping
capacity of the affected

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chambers Sudden Cardiac Death

Shunted flow Divert blood inappropriately
Lead to pressure and volume
overloads Hypertensive Heart Disease
Disorders of cardiac Arrhythmias
conduction Uncoordinated cardiac
impulses or blocked conduction Systemic (Left-Sided) Hypertensive Heart Disease
pathways
Rupture of heart or major Loss of circulatory continuity
vessel Lead to massive blood loss,
hypotensive shock, Pulmonary (Right-Sided) Hypertensive Heart Disease (Cor
and death Pulmonale)

- Most cardiovascular disease results from a complex Valvular Heart Disease

interplay of genetics and environmental factors
o can disrupt signaling pathways that control
morphogenesis Calcific Valvular Degeneration
o affect myocyte survival after injury
o affect contractility or electrical conduction in the
Mitral Valve Prolapse (Myxomatous Degeneration of the Mitral
face of biomechanical stressors.
- Congenital heart defects Valve)
o involves an underlying genetic abnormality
modified by environmental factors. Rheumatic Fever and Rheumatic Heart Disease
- Genes that control the development of the heart may also
regulate the response to various forms of injury including
aging. Infective Endocarditis (IE)
- Subtle polymorphisms can significantly affect the risk of
many forms of heart disease, and
- Adult-onset heart disorders have a fundamentally genetic Noninfected Vegetations
basis.
- Cardiovascular genetics provides an important window on Carcinoid Heart Disease
the pathogenesis of heart disease and molecular diagnoses
are increasingly a critical part of its classification.

Heart Failure

Cardiac Hypertrophy: Pathophysiolgy and Progression to Heart

Failure

Cardiac Development

Congenital Heart Disease

Ischemic Heart Disease

Myocardial Infarction

Chronic Ischemic Heart Disease

Arrhythmias

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Complications of Prosthetic Valves

Cardiomyopathies

Dilated Cardiomyopathy

Arrhythmogenic Cardiomyopathy

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy

Myocarditis

Other Causes of Myocardial Disease

Pericardial Disease

Pericardial Effusion and Hemopericardium

Pericarditis

Tumors of the Heart

Primary Cardiac Tumors

Metastatic Neoplasms

Cardiac Transplantation

Cardiac Devices

Ventricular Assist Devices

Electrocardiogram

History

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