 The Heart

 The Blood Vessels

 The Blood
 Blood pressure in heart chambers (mm Hg):
LA~10, LV~120, RA~10, RV~25
 Heart rate (at rest, adult): 70+/- 10 bpm
 Stroke volume: ~70 mL/beat
 Cardiac Output (CO): ~5 L/min
 Ejection fraction: ~60%
 Arterial pressure (aorta): 120/80 mm Hg
 Venous pressure (vena cava): 5-7 mm Hg
 Arterial disorders

 Venous disorders
 Atherosclerosis
 Aneurysm
 Arteritis
 Raynaud’s Syndrome
 Thrombotic Disorders
 Atherosclerosis is a form of arteriosclerosis that is
characterized by lipid accumulation and smooth muscle
cell proliferation within the walls of arteries, eventually
resulting in narrowing of the vessel lumen and
impairment in its ability to dilate.

 This narrowing may result in some degree of stasis,

ischemia and tissue hypoxia, and it increases the
likelihood of clot formation (thrombosis) thereby
exacerbating the vessel occlusion and its associated
problems.
 Currently, the leading theory regarding the initiating
event in the development of atherosclerosis is the
response to chronic endothelial cell injury in arteries.

 This chronic damage results in chronic inflammation

which brings about a cascade of events resulting in the
formation of atherosclerotic fatty plaque lesions. Genetic
and environmental factors are also involved in the
development of these lesions.
 Hemodynamic processes: pressure, shear force, turbulent
flow, pulsation, stretching, tortuosity

 Chemical injury: endogenous/exogenous chemicals

 Infectious agents: chlamydia, bacterial toxins, cytomegalic

virus (CMV), mycoplasma….

 Hyperlipidemia: LDL (esp. oxidized form)

 Immune reactions: C’, AgAb reactions

 Injury to arterial endothelium:
 Increased endothelial permeability: macrophage
emigration, platelet activation
 Smooth muscle cell proliferation: emigration to intima
(due to PDGF), macrophage activation
 Macrophages engulf LDL eventually forming fatty streak
(first visible sign of plaque lesion)
 Collagen deposition by smooth muscle cells
 Platelet adhesion to plaque/fibrin deposition
 Plaque growth and protrusion into lumen
 Platelet/fibrin deposition: clot formation…occlusion
 Smoking
 Hypertension
 Glucose intolerance
 High fat diet
 Blood cholesterol: high LDL, low HDL
 Decreased physical activity
 Obesity
 Poor stress management
 Excessive weight fluctuations
 Age

 Gender

 Genetics
 Tissue ischemia/hypoxia resulting in diminished
function and/or pain (e.g. CAD/IHD, angina,
decreased C.O., arrythmia, TIA, claudication)

 Infarction (e.g. myocardial, stroke [CVA])

 Aneurysm

 Thrombosis/embolism
 An aneurysm is a localized arterial dilation due to
a weakness in the arterial wall. If the weak-ness
in the arterial wall becomes sufficient, the vessel
wall may bulge outward creating the aneurysm.

 Aneurysms are most often found in cerebral

arteries and in the thoracic and abdominal aorta.
 Aneurysms may be caused by anything that
undermines the strength of the arterial vessel (or
myocardial) wall. Acquired processes that may
weaken blood vessel walls include: atherosclerotic
plaque lesions, infections, inflammation and physical
trauma.
 Aneurysms may also result from congenital
malformations of blood vessel walls.
 Hypertension may exacerbate any weakness in blood
vessel walls.
 Aneurysms are classified as being true or false
aneurysms.

 In true aneurysms, all three arterial layers are

involved.

 In a false aneurysm, at least one layer is

unaffected. False aneurysms are usually due to
trauma rather than vessel disease.
 Ischemia/hypoxia (dissecting)

 Tissue/organ infarction (dissecting)

 Severe pain

 Hemorrhage due to rupture (slight to massive)

 Thromboangiitis obliterans

 Raynaud’s Disease
 Thromboangitis obliterans (Buerger’s Disease) is a
relatively uncommon inflammatory disease which
affects small and medium-sized arteries of the upper
and lower extremities. This may result in occlusion
of these arteries (i.e. obliterans).

 This inflammation may also result in thrombosis,

fibrosis and formation of scar tissue that may affect
nearby nerve tissue.
 Thromboangiitis obliterans is strongly associated with
cigarette smoking and is more common in populations of
Asian men under the age of 40. Its etiology is unknown
but it is suspected to be some type of auto-immune
response involving chemicals in smoke.

 Symptoms include: pain with activity and/or cold

temperature, weak peripheral pulse(s)

 Complications: ulceration, gangrene, amputation

 Raynaud’s Syndrome is characterized as a severe
vaso-constrictive response of the small arteries in the
hands and fingers resulting in ischemia and tissue
hypoxia. This occurs as a result of exposure to stress
or cold temperatures. It is most common in healthy
young women.

 It is an exaggerated central and local vasomotor

response.
 After an episode, the vasoconstriction eases and
the area becomes hyperemic. The person feels
throbbing and burning pain as a result of this.

 The etiology is unknown.

 A thrombotic event is when a platelet/fibrin clot
forms on the inner wall of a blood vessel or of
the heart.

 Clot formation is due to platelet adherence to the

endothelium and sub-endothelial lining, followed
by subsequent activation of clotting proteins
resulting in fibrin deposition.
 Atherosclerosis
 Arteritis
 Phlebitis
 Heart failure/atrial fibrillation
 Prolonged bed rest/immobilization
 Post-op/trauma
 Post-partum
 Neoplasia
 Venous stasis
 Valvular incompetence
 Varicose veins
 Venous insufficiency
 Phlebitis/thrombophlebitis (DVT)
 Hemorrhoids
 Competent venous valves do not allow blood in the
veins to flow retrograde.

 Incompetent venous valves are damaged in some

way and do not close properly, thereby allowing
blood to pool in the area and to flow retrograde.

 If the incompetent valve is superficial, it’s called a

varicose vein. If it’s a deep vein, it’s referred to as
chronic venous insufficiency.
 The basic underlying mechanism in the development
of venous insufficiency is an increase in localized
venous pressure which stretches the valves and may
result in their permanent deformation and
dysfunction.

 This increase in pressure may be due to long periods

of standing over time, pregnancy and obesity. There
is a genetic predisposition in some individuals to
develop varicose veins.
 Hemorrhoids are venous varicosities that result
from dilation of the hemorrhoidal plexus of veins
at the ano-rectal juncture.

 They are caused by prolonged pelvic congestion

which may be caused by multiple pregnancies
and/or excessive straining during defecation over
a long time period.
 Esophageal varices may form in individuals who
have cirrhosis of the liver which is accompanied
by portal vein hypertension. The venous
congestion from this condition results in the
formation of varicosities within the esophageal
veins.

 Rupture of one or more of these varices may lead

to massive upper GI bleeding.
 Phlebitis is inflammation of the inner surface of a vein. This may
be a result of trauma to the vein (e.g. chronic stretching) and/or
from irritation of the endothelium from chemicals or infectious
agents. Right-sided heart failure may contribute to this.
 This inflammation may lead to platelet activation and fibrin
deposition leading to clot formation (thrombus, thrombosis) on the
inner vein surface. This lesion is referred to as thrombo-phlebitis.
Conditions that may activate clot formation include: the post-
operative state, prolonged immobilization, heart failure, obesity and
pregnancy.
 If a portion of the clot breaks away, it’s referred to as an embolus
(plural emboli).
 Shock is characterized by systemic tissue hypo-perfusion due
to either a reduction in cardiac output or a decrease in the
effective circulating blood volume. The end result is severe
tissue hypoxia.
 The four general types of shock are:
- Cardiogenic
- Hypovolemic
- Obstructive
- Distributive
 Shock due to a decrease in cardiac output:
- Myocardial infarction
- Cardiomyopathy
- Congenital heart defects
- Heart valve disease
- Arrythmia
 Shock caused by loss of blood volume:
- Acute hemorrhage
- Severe dehydration
- Excessive use of diuretics
- Severe burns
 Shock due to physical obstruction to blood flow:
- Pulmonary embolism
- Cardiac tamponade
- Tension pneumothorax
- Dissecting aortic aneurysm
 Shock caused by systemic vasodilation:
- Anaphylaxis
- Neurological trauma (brain or spinal cord)
- Sepsis
Cardiac disorders include the following:
-> diseases of the myocardium
-> valve defects
-> conduction system aberrations
-> infectious/inflammatory conditions
-> congenital defects
-> others (tamponade, aneurysm, thrombus)
 Diseases involving the myocardium may be
primary in nature or secondary to some other
disease process.
 Cardiomyopathy is an example of a primary
disease of the myocardium.
 Myocardial infarction is an example of
myocardial disease secondary to another process.
 Cardiomyopathy (CM) is a term used to describe
heart disease resulting from a primary abnormality
of the myocardial cells. There are also secondary or
indirect causes of myocardial dysfunction which
include cardiac ischemia, valve disease, arrythmia’s,
etc.

 There are several distinct types of cardiomyopathy:

dilated CM, hypertrophic CM and restrictive CM.

 In their primary form, they are generally idiopathic

in nature.
 Dilated or congestive cardiomyopathy is characterized by
ventricular dilation (with thin walls) and severely impaired
LV systolic function (EF <25%), leading eventually to heart
failure.

 The pure form of this disorder is idiopathic and has a familial

aspect to it in ~30% of cases. It is more common in men than
in women. Dilated CM makes up ~90% on CM cases.

 Secondary causes include: ischemia, valve disease, drug

toxicity (including alcoholism), hyperthyroidism, infections
and autoimmunity.
 This type of cardiomyopathy is characterized by a thickened
LV myocardium and septum with a decreased LV volume. The
thickened and stiff myocardium inhibits diastolic filling
thereby decreasing cardiac output.

 It is often accompanied by LA dilation and pulmonary venous

hypertension due to poor diastolic relaxation of LV. Myocardial
fibrosis may develop as the disease progresses.

 There are two types: asymmetric septal (idiopathic, inherited as

AD) and hypertensive/valvular (due to aortic stenosis).

 Increased incidence of ventricular arrythmia’s and sudden

death.
 This type of CM is usually caused by abnormal
deposition of some substance (e.g. amyloid proteins,
iron, glycogen) in the myocardial cells resulting in
decreased ventricular compliance and impaired
diastolic filling.

 The combination of poor LV diastolic filling and a

weak systolic contraction results in a decreased
cardiac output.

 This disruption of normal contraction results in

cardiac arrythmia’s and eventual heart failure.
 Virtually all forms of CM eventually result in
heart failure.

 Treatment may be directed toward an underlying

cause and/or may be mainly palliative in nature.

 At this point in time, a heart transplant is the only

possibility for cure.
 Myocardial infarction refers to death of
myocardial cells as a result of severe hypoxia
secondary to coronary artery ischemia.

 In the vast majority of cases, this ischemia is due

to partial or complete occlusion of one or more of
the coronary arteries with atherosclerotic plaque
accompanied by thrombus formation or
vasospasm.
 Sudden death due to arrythmia (~25%)
 Non-fatal arrythmia
 Cardiogenic shock
 CHF
 Ventricular aneurysm
 Mural thrombus formation
 EKG changes

 Signs and symptoms

 Myocardial proteins in blood

 There are two basic types of heart valve defects:
-> valve prolapse
-> valve stenosis

These disorders may be congenital or acquired. They

result in dysfunction because they either cause blood
flow obstruction or regurgitation or some
combination of the two. Also, the damaged valve is
susceptible to infection. The mitral and aortic valves
are most commonly affected.
 Acquired valve prolapse occurs for a number of reasons including:

 Mitral valve:
-> abnormal leaflets (post-infection scarring)
-> abnormal tensors (papillary muscle rupture)
-> abnormal LV (hypertrophy, CM, endocarditis)

Aortic valve:
-> rheumatoid arthritis
-> post-infection scarring
-> endocarditis
-> Marfan syndrome
 Potential causes of acquired valve stenosis:

 Mitral valve:
-> post-inflammatory scarring (rheumatic HD)

 Aortic valve:
-> post-inflammatory scarring (RHD)
-> calcification
 Infectious/inflammatory diseases of the heart
include:
-> infective endocarditis (acute and subacute)

-> myocarditis

-> pericarditis
 Infective endocarditis is a term used to describe
infection of the cardiac valves or the mural
surface of the endocardium.

 The infection often results in the formation of a

bulky mass of thrombotic debris and organisms
which is termed a vegetation.

 Most cases are caused by bacterial infection.

 Current infection in the body

 Intravenous drug use

 Surgical/dental procedures

 Immune suppression
 Acute endocarditis: infection of cardiac valves with
organisms of high virulence such as some strains of
Haemophilus, Pseudomonas and Staphylococcus
aureus.

 These organisms may infect previously normal valves.

 These infections may progress very rapidly without a

major inflammatory response. They have a high
mortality rate (15-25%).
 Subacute endocarditis: Slowly developing
infection of previously abnormal valves by
organisms of lower virulence such as certain strains
of alpha-hemolytic strep, Staphylococcus and
Candida. These infections progress more slowly and
may be associated with chronic inflammation.

 Predisposing factors include: RHD, valve prolapse,

calcified/stenotic valves and prothetic valves.
 Autopsy findings in both acute and subacute are very
similar: large, bulky vegetations composed of
bacteria and thrombi on the valve(s) and endocardial
wall.

 These lesions may lead to emboli formation and

erosion/perforation of the valve cusp. The valves
tend to become fibrotic and calcified. In acute
endocarditis, the myocardium may erode and
abscess.
 Myocarditis is a disorder in which there is
inflammation and necrosis of the myocardium.

 Myocarditis has many causative agents

including:
bacteria, viruses, protozoa, fungi, rickettsia,
helminthes, auto-immune disease and several
physical agents (Box 18-3 in text).
 In the U.S., and other developed nations, the most
common causative agents are viruses. The viral
myocarditis may cause direct myocardial toxicity
and/or it may induce a autoimmune response against
the heart.

 In South America, Chagas disease (Trypanosoma

cruzi) is the major causative agent. Myocarditis is
responsible for most cases of cardiac-related deaths
in areas where this trypanosome is endemic.
 Acute myocarditis is characterized by an enlarged
heart (dilation of chambers) which may, in some
individuals, progress to cardiomyopathy.

 The heart muscle is flabby with diffuse necrotic

lesions. It is edematous and inflamed with
infiltration with white cells. The endocardium
usually shows no pathological changes.

 Treatment is directed at underlying cause and is

otherwise supportive.
 Pericarditis refers to inflammation of the
pericardium. It may be acute or chronic in nature.

 Pericarditis may result from an infectious agent,

an auto-immune process or a number of other
cardiac/non-cardiac conditions (See Table 18-9).
 Pericarditis may result in cardiac tamponade if the
fluid accumulation is substantial. This will compress
the heart and interfere with function.

 Acute pericarditis may cause sticking and rubbing

of the pericardial layers. This may result in back pain
and esophogeal pain/discomfort.

 Chronic pericarditis may lead to pericardial sac

degeneration and heart adhesion to chest structures
possibly impeding cardiac contraction.
 Congenital heart defects are as a result of abnormal
embryological development of some structure(s) of
the heart. Their incidence is ~0.8% of live births.

 The more common defects involve abnormal

development of:
- the atrial septum
- the ventricular septum
- the main outflow tract (aorta/PA)
- the valves
 The vast majority of heart defects are idiopathic
however some may be attributed to genetic
and/or environmental influences. Rubella
infection of the mother during the first trimester
is a known risk factor. Others include: hypoxia,
ionizing radiation, poor nutrition and heavy
alcohol usage.
 Ventricular septal defect (VSD
 Atrial septal defect (ASD)
 Patent ductus arteriosis (PDA)
 Pulmonic stenosis
 Coarctation of aorta
 Tetralogy of Fallot
 Transposition of great arteries
 Truncus arteriosis
 Most common (31%)
 Effect depends on size
 Shunt left-to-right
 RV hypertrophy
 Pulmonary hypertension
 Acyanotic
 Loud systolic murmur
 If severe, right-sided
heart failure
 ~10% of defects
 Small – asymptomatic
 Acyanotic l-r shunt
 May cause pulmonary
hypertension and RV
hypertrophy
 May progress to right
failure, cyanosis
 ~10% of defects
 Tend to close by
themselves
 L-r shunt - acyanotic
 Possible pulmonary
hypertension, RV
hypertrophy and
respiratory failure.
 Reversal of shunt -
cyanosis
 ~7% of defects
 Males affected: 4:1 ??
 Most common near DA
 May not be detected if mild
 If severe, diminished blood
flow distal and high
pressure in upper body
 May lead to CHF,
hemorrhagic stroke of
aortic rupture
 ~6% of defects
 Enlarged heart
 Cyanotic
 Four defects
- VSD
- RV hypertrophy
- Pulmonic stenosis
- Aortic override
 ~4% of defects
 Cyanotic
 PDA aids in survival
early
 Surgery early
 ~2% of defects
 Non-separation of PA
and aorta
 Receives blood from LV
and RV
 Cyanotic
 RV hypertrophy and
pulmonary hypertension
 Heart/pulmonary failure