01 cardiac pathology

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Normal Heart
• Fist size muscular pump
• Pumps 6000 lit of blood daily
• Perfuses
– tissues with nutrients and
• Facilitates
– removal of waste products.
• Heart diseases
– Have severe physiologic consequences
– Are leading cause of morbidity and mortality
in developed nations
• 750,000 deaths/ year (In US)

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Normal Heart
• Weight
– 250 – 300 gm adult female
– 300 – 350 gm adult male
• Free wall thickness
– R ventricle (RV) 0.3-0.5 cm
– L ventricle (LV) 1.3-1.5 cm
• Cardiomegaly
– Increase in weight or size
• Due to hypertrophy of myocardium
• Due to dilation of chambers.

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Normal Heart
• Chambers
• Valves
• Endocardium
• Myocardium
• Epicardium

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Normal Heart
• 90% of mass of heart is cardiac muscle known as
Myocardium
• Very special inexhaustible muscle
• Composed of muscle cells called cardiac
myocytes.
– Never rest. Contracts ~ once each
second
– Generate contractile force
– Completely dependent on aerobic
metabolism for energy.
»Therefore, very rich in mitochondria

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Cardiac Myocytes
• Have a single nucleus
• Sarcolemma (cell membrane)
• Sarcoplamic reticulum ( Ca reservoir)
• Mitochondria
• Contractile elements:
– k/a myofilaments
• Arranged in bundles k/a myofibrils
• Myofibrils organized in units k/a Sacomeres
• Are separated from adjacent cells by
Intercalated disks.

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Conduction System
• SA node
• AV node
• Bundle of His
• R & L Bundle
Branches
– arborize into
ventricles

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Cardiac Pathology
1. Hypertrophy of ventricles ( hypertensive heart
disease)
2. Heart Failure
3. Pulmonary Hypertensive Heart disease ( Cor
pulmonale)
4. Ischemic Heart diseases
5. Valvular heart disease
6. Cardiomyopathies
7. Pericardial disease
8. Congenital heart disease
9. Tumors of the heart

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Myocardial Hypertrophy
(Ventricular hypertrophy)

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Normal
• Heart can increase its output many folds as
demand requires.
• This is achieved by:
1. increase in the size of the ventricles
• ventricular dilatation  increased force of
contraction Frank Starling law
2. increase in thickness of myofibers
• ventricular hypertrophy  increased force
of contraction.
• Failure of compensatory mechanism  results in
heart failure

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Two important terms
Preload
and
Afterload

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Preload
• Is the amount of blood in the heart during
diastole.
• Dependent on venous return to right side of
heart.
• Increase in preload leads to stretching of
cardiac muscle  increased force of contraction
 increased Stroke volume

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Afterload
• Is the resistance against which the ventricle
must contract when ejecting blood during
systole.

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Ventricular Hypertrophy
• is a compensatory change that the heart
undergoes when subjected to an increased
workload.
– Augments myocyte contractile strength.
• Increased workload can occur in association
with:
1. Systemic hypertension
2. Valvular stenosis
3. Valvular insufficiency etc.
• Ventricular hypertrophy may involve the Left or
Right ventricle.

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Ventricular Hypertrophy
• Left ventricular hypertrophy
– Two types
1. Concentric
2. Eccentric (dilation and hypertrophy)
• Right ventricular hypertrophy
– Two types
1. Concentric
2. Eccentric (dilation and hypertrophy)

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Concentric Ventricular Hypertrophy
• Pathogenesis:
– Due to contraction against an increased
resistance (afterload)
• Produces concentric thickening of ventricular
wall.
• Causes of Concentric LV hypertrophy:
– Essential hypertension (MCC)*
– Aortic stenosis
• Causes of Concentric RV hypertrophy
– Pulmonary hypertension*
– Pulmonary artery stenosis.

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Normal Heart
Concentric
Left ventricular hypertrophy

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Eccentric ventricular hypertrophy
• Pathogenesis:
– Due to volume overload (increased preload)
• Causes dilatation and hypertrophy (eccentric
hypertrophy) of ventricular wall
• Causes of Eccentric LV hypertrophy:
– Mitral valve or aortic valve regurgitation
– L-R shunting of blood (VSD)
• Causes more blood to return to left side of
heart
• Causes of Eccentric RV hypertrophy:
– Tricuspid or pulmonary valve regurgitation

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Hearts, hypertrophied, normal (middle), and dilated

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Consequences of ventricular
hypertrophy
1. Left or right sided heart failure
2. Angina (primarily LVH)
3. S4 heart sound:
– Correlates with atrial contraction in late
diastole
– Caused by blood entering a noncompliant
ventricle

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Congestive Heart failure
• What is Heart failure?
– When heart is unable to eject blood
delivered to it by the venous system.
• Epidemiology:
– MC hospital admission diagnosis in elderly
patients.
• Types of heart failure:
1. Left sided heart failure
2. Right sided heart failure
3. Biventricular heart failure
4. High output heart failure.

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Left sided heart failure (LHF)
• Forward failure:
– Left side of heart cannot eject blood into the
aorta.
– Pathophysiology:
• Blood builds up behind the failed left heart:
• Increase in left ventricular volume /
pressure 
• Increase in left atrial pressure 
• Increase in pulmonary venous pressure 
• Hydrostatic pressure overrides pulmonary
capillary oncotic pressure 
• Pulmonary edema results**

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1. Mechanism: Decreased ventricular contraction
– Causes:
• Myocardial infarction***
• Myocardial fibrosis, myocarditis,
cardiomyopathy.
2. Mechanism: Noncompliant ventricle ( restricted
filling)
– Causes:
• Concentric LVH***
• Infiltration of muscle by amyloid, iron or
glycogen ( e.g. Pompe’s disease)

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3. Mechanism: Increased workload
– Causes
• Increased afterload (resistance)
– Systemic hypertension
• Increased preload (volume)
– Mitral regurgitation

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• Gross and microscopic findings:
– Lungs are congested and exude a frothy pink
transudate (edema)
– Alveolar macrophages contain hemosiderin (
heart failure cells)

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Normal Lung
Pulmonary edema Heart failure cells

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• Clinical findings: Symptoms outnumber signs
– Dyspnea:
• Difficulty breathing
• Patient cannot take a full inspiration
– Pulmonary edema:
• Due to increased pulmonary venous
hydrostatic pressure
• Bibasilar inspiratory crackels
• Chest radiographs show congestion in upper
lobes and alveolar infiltrates

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– Left sided S3 heart sound
• Caused by blood entering a volume
overloaded left ventricle
• Intensity of the heart sound increases with
expiration
• First cardiac finding* in LHF.
– Mitral valve regurgitation:
• Caused by stretching of the valve ring
• Pansystolic murmur at apex
• Increases in intensity during expiration

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• Paroxysmal nocturnal dyspnea:
– Choking sensation at night due to increased
venous return to the failed left side of heart
– Blood backs up in lungs producing pulmonary
edema
– Relived by standing or placing a pillow under
the head (pillow orthopnea)
• These maneuvers increase the effect of
gravity on reducing venous return to the
heart.

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• Cough:
– Sputum rusty colored
– Due to alveolar macophages
phagocytosing RBCs (“heart failure”
cells)

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• Chest X ray in heart failure:
– Prominent congestion of blood in the upper
lobes
– Perihilar congestion : Batwing configuration
– Kerley’s B lines: represent septal edema at
the costophrenic angle.
– Patchy interstitial and alveolar infiltrates
– Pleural effusion

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Congestive Heart Failure
Batwing Pattern

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Right sided heart failure
• Backward failure:
– Right side of the heart cannot pump blood
from the venous system to the lungs.
• Pathophysiology:
– Blood accumulates behind failed right heart:
– ↑ in right ventricular volume/ pressure 
– ↑ in right atrial pressure 
– ↑ in jugular venous pressure 
– Increase in venous hydrostatic pressure 
– Hepatomegaly, dependent pitting edema +
ascites

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• Pathogenesis:
– Decreased contraction ( right ventricular
infarction)
– Noncompliant right ventricle (e.g. RVH)
– Increased afterload (left sided heart failure,
MCC)
– Increased preload (e.g. tricuspid valve
regurgitation)

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• Clinical findings:
– Signs outnumber symptoms
– Prominence of jugular veins
• Due to increased venous hydrostatic
pressure
– Right sided S3 heart sound :
• due to volume overload in the right ventricle
• Increases in intensity with inspiration
– Tricuspid valve regurgitation
• Caused by stretching of valve ring

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• Painful hepatomegaly:
– Passive liver congestion due to backup of blood
into the central veins (Nutmeg liver)
• Dependent pitting edema and ascites
– Due to an increase in venous hydrostatic
pressure

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High-output heart failure
• A form of heart failure in which CO is increased
compared with values for the normal resting
state.
• Pathogenesis:
– Increase in stroke volume
• Hyperthyroidism, increased blood volume
– Decrease in blood viscosity
• Severe anemia
– Vasodilation of peripheral resistance arterioles
• Increases venous return to the heart
– Causes of vasodilation:
»Thiamine deficiency, early phase of
endotoxic shock

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High-output heart failure
• Pathogenesis:
– Arteriovenous fistula:
• AV communications bypasses the
microcirculation
• Increases venous return to the heart
• Causes of AV fistulas:
– Trauma from knife wound (MCC)
– Surgical shunt for dialysis
– Pagets disease of bone: AV fistulas
develop in the bone

01 cardiac pathology

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01 cardiac pathology