The Cardiovascular System
Pathology
Functions of the
Cardiovascular System
• Delivers vital oxygen and nutrients to cells
• Removes waste products
• Transports hormones
Branches of the
Cardiovascular System
• Systemic
– Carries blood throughout the body to meet the
body’s needs and removes waste products
– Includes arteries, veins, and capillaries
– Works with the lymphatic system
• Pulmonary
– Carries blood to and from the lungs for gas
exchange
Heart
• Pericardium
– Surrounds the heart to provide protection and support
• Myocardium
– Cardiac muscle
• Endocardium
– Inner structures, including the valves
• Four chambers
– Two atria: receiving chambers
– Two ventricles: pumping chambers
• Ventricular walls (esp. left ventricle)—thicker than atrial walls
Blood Flow Through the Heart
(1 of 2)
• Deoxygenated blood from the systemic circulation
enters from the superior vena cava and the inferior
vena cava.
• Blood empties directly into the right atrium.
• From the right atrium, blood travels through the
tricuspid valve to the right ventricle.
• The right ventricle pumps blood through the
pulmonic valve to the pulmonary arteries.
• The pulmonary arteries carry blood to the lungs for
gas exchange.
Blood Flow Through the Heart
(2 of 2)
• Oxygenated blood from the pulmonary circulation
enters from the pulmonary veins.
• Blood empties directly into the left atrium.
• Blood leaves the left atrium through the mitral valve
to the left ventricle.
• The left ventricle then pumps blood through the
aortic valve to the aorta.
• From the aorta, the blood is carried the rest of the
body.
Review of Vascular Structure & Function
• Two systems comprise the vascular system
– Blood vascular system
• Continuous flow system transporting
blood to and from the heart
– Lymphatic vascular system
• Allows for exchange of gases, nutrients,
and metabolic wastes across its walls
Review of Structure and Function
Vascular system:
• The walls of veins and arteries are lined with
epithelial cells.
• Larger arteries are elastic, smaller = muscular
• Stimulation by the sympathetic system results
in vasoconstriction, while the cholinergic
system results in vasodilation
Review of Structure and Function
• Arteries are muscular and have a higher blood
pressure ~120/80 mmHg
• Veins are thin-walled and have a much slower
rate of flow and lower pressure—mean
~30mmHg
• Capillaries: primary site where oxygen and
metabolites are transferred
Review of Lymphatic Structure & Function
• Facilitates centripetal flow of lymph from
tissues towards the heart
• Formed in peripheral tissues and organs from
serum and extracellular fluids
• Similar to blood but does not contain rbc’s or
clotting factors
• Flow is interrupted by lymph nodes
• All vessels converge on into large veins in the
neck and enter the circulatory system
Lymphatic System
• Works to return excess interstitial fluid
(lymph) to the circulation
• Plays a role in immunity
• Includes lymph nodes, the spleen, the thymus,
and the tonsils
Conduction System
• Organizes electrical impulses in the cardiac
cells
• Controls
– Excitability: ability of the cells to respond to
electrical impulses
– Conductivity: ability of the cells to conduct
electrical impulses
– Automaticity: ability to generate an impulse to
contract with no external nerve stimulus
Conduction Pathway
(1 of 2)
• Impulses originate in the sinoatrial (SA) node high in
the right atrium at a rate of 60–100 bpm.
• Impulses travel through the right and left atria,
causing atrial contraction.
• Impulses then travel to the atrioventricular (AV)
node, in the right atrium adjacent to the septum.
– The AV node can initiate impulses if the SA node fails (rate:
40–60 bpm).
Conduction Pathway
(2 of 2)
• Impulses are delayed in the AV node to allow
for complete ventricular filling.
• Impulses then move rapidly through the
bundle of His, right and left bundle branches,
and Purkinje network of fibers, causing
ventricular contraction.
– The ventricles can initiate impulses if the SA and
AV nodes fail (rate: 20–40 bpm, which may be
inadequate).
Electrical Activity
(1 of 2)
• Depolarization
– Increase in electrical charge
– Accomplished through cellular ion exchange
– Generates cardiac contraction
• Repolarization
– Cellular recovery
– Ions returning to the cell membrane in
preparation for depolarization
Electrical Activity
(2 of 2)
• Can be read by an electrocardiogram
– P wave: atrial depolarization
– QRS complex: ventricular depolarization
– T wave: ventricular repolarization
• Sinus rhythm
– Electrical activity when impulses originate in the SA node
• Dysrhythmias
– Abnormal electrical activity
– Can result from issues such as myocardial infarctions and
electrolyte imbalances
Conduction Control
• Electrolyte signals
– Sodium, potassium, and calcium
• Medulla monitoring
– Autonomic nervous system, endocrine system,
chemoreceptors, and baroreceptors
• Effects
– Chronotropic: rate of contraction
– Dromotropic: rate of electrical conduction
– Inotropic: strength of contraction
Blood Pressure
• Force that blood exerts on the walls of blood vessels
• Reflects how hard the heart is working
• Represented as a fraction
– Systolic: top number; cardiac work phase
– Diastolic: bottom number; cardiac rest phase
• Normal BP according to AHA: 120/80 mmHg
• Pulse pressure (~40)—difference between the two
numbers
– Reflects force of each contraction
Influences on Blood Pressure
(1 of 2)
• BP = CO × PVR
• Cardiac output (CO)
– CO = SV × HR
– Stroke volume (SV)
– Heart rate (HR)
• Peripheral vascular resistance (PVR)
– Sympathetic nervous system
– Parasympathetic nervous system
– Arterial elasticity
Influences on Blood Pressure
(2 of 2)
• Afterload: pressure needed to eject the blood
– Blood viscosity
– PVR
• Preload: amount of blood returning
– Blood volume
– Venous return
• Hormones
– Antidiuretic hormone
– Renin–angiotensin–aldosterone system
Blood Vessels
(1 of 2)
• Arteries: carry oxygenated blood away from
the heart
• Veins: carry deoxygenated blood back to the
heart
• Capillaries: site of exchange
Blood Vessels
(2 of 2)
• Three layers
– Tunica intima: inner layer
– Tunica media: middle muscular layer
– Tunica adventitia: outer elastic layer
• Exception
– Pulmonary artery: carries deoxygenated blood
away from the heart
– Pulmonary vein: carries oxygenated blood to the
heart
Understanding Cardiovascular
Conditions
• Alterations resulting in decreased cardiac output:
pericarditis, infective endocarditis, myocarditis,
valvular disorders, cardiomyopathy, electrical
alterations, heart failure, and congenital heart
defects
• Alterations resulting in altered tissue perfusion:
aneurysm, dyslipidemia, atherosclerosis, peripheral
vascular disease, coronary artery disease, thrombi
and emboli, varicose veins, lymphedema, and
myocardial infarction
• Alterations resulting in both: hypertension and shock
Major Diseases
• Congenital Heart Disease
• Ischemic Vascular Disease
• Hypertension-related diseases
• Inflammatory Disease
• Metabolic Disease
Congenital Heart Defects
(1 of 3)
• Structural issues present at birth
• Most common type of birth defect
• Examples:
– Septal defect
– Patent ductus arteriosus
– Valve disorders
– Dextro-transposition of great arteries
– Tetralogy of Fallot
Congenital Heart Defects
(2 of 3)
• Risk factors: heredity, genetic disorders (Down’s
syndrome), fetal exposure to tobacco and certain
medications, maternal health status (e.g., diabetes
mellitus, obesity).
• Manifestations
– Can be asymptomatic.
– Symptoms, when present, include heart murmurs,
dyspnea, tachypnea, cyanosis, fatigue, chest pain or
discomfort, difficulty gaining weight.
• Heart failure can develop due to increased cardiac
workload.
Congenital Heart Defects
(3 of 3)
• Diagnosis: history (including mother’s history),
physical examination, fetal ultrasound,
echocardiogram, EKG, chest X-ray
• Treatment: heart catheterization or surgery,
heart transplant, medications (diuretics,
antihypertensives, antidysrhythmics)
Aneurysms
(1 of 4)
• Weakening of an artery
– Common in the abdominal aorta, thoracic aorta,
and cerebral, femoral, and popliteal arteries
• Can rupture: exsanguination
• Risk factors: congenital defect, atherosclerosis,
hypertension, dyslipidemia, diabetes mellitus,
tobacco use, advanced age, trauma, and
infection
Aneurysms
(2 of 4)
• True aneurysms: affect all three vessel layers
– Saccular aneurysm: bulge on the side
– Fusiform aneurysm: affects the entire
circumference
• False aneurysms: do not affect all three layers
of the vessel
– Dissecting aneurysms: occurs in the inner layers
Aneurysms
(3 of 4)
• Manifestations
– Depend on location and size
– May be asymptomatic
– May include pulsating mass, pain, respiratory
difficulty, and neurologic decline
Aneurysms
(4 of 4)
• Diagnosis: physical examination, X-ray,
echocardiogram, computed tomography,
magnetic resonance imaging, and
arteriograph
• Treatment: eliminating or managing cause and
surgery
Dyslipidemia
(1 of 4)
• High levels of lipids in the blood.
• Increases risk for many chronic diseases.
• Lipids come from dietary sources and are
produced by the liver.
• Dietary sources
– Cholesterol: animal products
– Triglycerides: saturated fats
Dyslipidemia
(2 of 4)
• Classified based on density, which is based on
the amount of triglycerides (low density) and
protein (high density)
– Very-low-density lipoproteins
– Low-density lipoproteins—AKA “bad” cholesterol
– High-density lipoproteins—AKA “good”
cholesterol
Dyslipidemia
(3 of 4)
• LDL
– Most serum cholesterol is LDL.
– More invasive.
– To decrease LDL level: lifestyle modification.
• HDL
– Helps remove cholesterol from bloodstream
– To increase HDL level: lifestyle modification
Dyslipidemia
(4 of 4)
• Manifestations: asymptomatic until it
develops into other diseases
• Diagnosis: cholesterol screening and lipid
panels
• Treatment: dietary changes, weight reduction,
routine exercise, tobacco cessation, lipidlowering agents, and complication
management
Pericarditis
(1 of 5)
• Inflammation of the pericardium
• Triggered by viral infection, thoracic trauma,
myocardial infarction, tuberculosis,
malignancy, and autoimmune conditions
• Fluid accumulates in the space between
pericardial sac and heart—pericardial effusion
• Swollen tissue creates friction
Pericarditis
(2 of 5)
• Cardiac tamponade
– Cardiac compression from excessive fluid
accumulation
– Life-threatening
– Manifestations: falling arterial pressures, rising
venous pressures, narrowing pulse pressure, and
muffled heart sounds
– Complications: heart failure, shock, and death
Pericarditis
(3 of 5)
• Constrictive pericarditis
– Loss of elasticity (i.e., thick and fibrous
pericardium)
– Results from chronic inflammation
Pericarditis
(4 of 5)
• Manifestations:
– Pericardial friction rub (grating sound heard when breath is
held)
– Sharp, sudden, severe chest pain that increases with deep
inspiration and decreases when sitting up and leaning
forward
– Dyspnea
– Tachycardia
– Palpitations
– Edema
– Flulike symptoms
Pericarditis
(5 of 5)
• Diagnosis: history, physical examination,
complete blood count, electrocardiogram,
chest X-ray, echocardiogram, computed
tomography, and magnetic resonance imaging
• Treatment: identify and resolve the underlying
cause, nonsteroidal anti-inflammatory drugs,
glucocorticoid agents, analgesics, bed rest,
oxygen therapy, pericardiocentesis, and
pericardectomy
Infective Endocarditis
(1 of 3)
• Formally called bacterial endocarditis.
• Infection of endocardium and heart valves.
• Commonly caused by Streptococcus and
Staphylococcus infections.
• Vegetation forms on internal structures and creates
small thrombi.
• Thrombi can travel to other locations—embolism.
• Embolism can create life-threatening complications
like myocardial infarction, stroke, and pulmonary
embolism.
Infective Endocarditis
(2 of 3)
• Microemboli occur as they are dislodged,
resulting in microhemorrhages.
• Risk factors: intravenous drug use, valvular
disorders, prosthetic heart valves, implanted
cardiac devices, rheumatic heart disease,
coarctation of the aorta, congenital heart
defects, and Marfan syndrome.
Infective Endocarditis
(3 of 3)
• Manifestations: flulike symptoms, embolization, heart
murmur, petechiae, splinter hemorrhages under the nails,
hematuria, Osler’s nodes, and edema.
• Diagnosis: history, physical examination, blood cultures,
complete blood count, urinalysis, serum rheumatoid factor,
erythrocyte sedimentation rate, electrocardiogram, and
echocardiogram.
• Treatment: identification of causative agent, long-term agentspecific therapy, bed rest, oxygen therapy, antipyretics,
surgical valve repair, and prosthetic valve replacement.
• If untreated, infective endocarditis is usually fatal.
Myocarditis
(1 of 3)
• Inflammation of the myocardium.
• Uncommon; poorly understood.
• Organisms, blood cells, toxins, and immune
substances invade and damage the muscle.
• Complications: heart failure, cardiomyopathy,
dysrhythmias, and thrombus formation.
Myocarditis
(2 of 3)
• Manifestations
– Patient may be asymptomatic.
– Symptoms, when present, include flulike
symptoms, dyspnea, dysrhythmias, palpitations,
tachycardia, heart murmurs, chest discomfort,
cardiac enlargement, pale and cool extremities,
syncope, decreased urine output, and joint pain
and swelling.
Myocarditis
(3 of 3)
• Diagnosis: history, physical examination, blood
cultures, electrocardiogram, cardiac enzymes,
complete blood counts, erythrocyte sedimentation
rate, chest X-rays, echocardiogram, and myocardium
biopsy
• Treatment: identify and resolve the underlying cause,
antipyretics, anticoagulants, antidysrhythmics,
diuretics, immunosuppressants, bed rest, activity
restriction, and fluid limitation
Valvular Disorders
(1 of 3)
• Disrupt blood flow through the heart
• Stenosis: narrowing
– Less blood can flow through the valve.
– Causes decreased cardiac output, increased
cardiac workload, and hypertrophy.
• Regurgitation: insufficient closure
– Blood flows in both directions through the valve.
– Causes decreased cardiac output, increased
cardiac workload, hypertrophy, and dilation.
Valvular Disorders
(2 of 3)
• Causes: congenital defects, infective
endocarditis, rheumatic fever, myocardial
infarction, cardiomyopathy, and heart failure
• Manifestations:
– Vary depending on valve involved
– Reflect alteration in blood flow through the heart
Valvular Disorders
(3 of 3)
• Diagnosis: history, physical examination, heart
catheterization, chest X-rays, echocardiogram,
electrocardiogram, and magnetic resonance imaging
• Treatment: diuretics, antidysrhythmics, vasodilators,
angiotension-converting enzyme inhibitors, betaadrenergic blockers, anticoagulants, oxygen therapy,
low-sodium diet, surgical valve repair, and prosthetic
valve replacement
Specific Diseases
• Atherosclerosis
– A degenerative condition that gets worse
with age
– The development of plaque in an artery
– The plaques cause decreased blood flow
with the potential to develop thrombi or
emboli
Atherosclerosis
– “scleros” means hardening
– Lipid, calcium, and fibrous deposits in large and
medium sized arteries
– In coronary arteries it is called coronary artery
disease (CAD)
– In brain, cerebrovascular disease/accidents (CVA)
– In the aorta, usually means aneurysms or aortic
calcifications
– In extremities = peripheral vascular disease
Atherosclerosis
• Injury occurs where the blood meets the arterial wall
– Can be due to injury or hypertension
• Results in deposition of platelets and serum lipoproteins
• Results in proliferation of smooth muscle in the walls of the
artery
• Metabolism is altered and cells collect lipids and cholesterol in
the cytoplasm
• Lipid laden smooth muscle cells die and release lipids
• This collects macrophages that secrete tumor necrosis factor
and other cytokines and biological substances
• This results scar tissue being formed or hardening of the
arteries. (atherosclerosis)
• Artheromas: lesions of artherosclerosis
Symptoms, Signs, and Tests
• Occlusive disease
– Symptoms may be that of infarction (usually
sudden) or ischemic atrophy (more gradual)
– Either results in loss of function of the
organ affected
Most Frequent and Serious Problems
• Varicosities
– Permanently dilated venous channels
• Hyperlipidemia:
– High cholesterol, risk factor for atherosclerosis
• Hypertension
– High arterial blood pressure
Symptoms, Signs, and Tests
• Hypertension
– Correlates with atherosclerosis
– Often asymptomatic, but can present with
headaches and dizziness
Thrombosis
• Thrombi formation
– Thrombi are clots that form as a result of cell injury within
the vasculature (can be caused by artherosclerosis)
– Can occlude blood flow to cause ischemia or infarct
– When pieces of a thrombus break off (emboli) and travel
from their original location and get lodged in the lungs
– In extremities = DVT
– In lungs= PE
– In the brain= CVA (stroke)
– In the heart= MI
Symptoms, Signs, and Tests
• Arteriography or angiography are both
procedures that involve injecting radioopaque dye into vessels, and taking X-rays to
see the distribution of blood flow
• Sphygmomanometer
– Non-invasive monitor of blood pressure
Peripheral Vascular Disease
• Atherosclerosis involving arteries that supply blood to
the extremities and major abdominal organs
• Common in elderly, pts with DM, HTN, hyperlipidemia
• In kidneys: results in renal dysfunction and increased
release of renin (hormone produced by the kidneys in
response to ischemia) and results in HTN, leads to
reduced function and can lead to renal failure
• Chronic or acute to intestines leads to GI problems
and can lead to intestinal infarct
• Most often seen in extremities/legs
Specific Diseases
• Genetic/Developmental diseases
• Angiomas
– Hemangiomas: vascularized tumor of the liver
– Lymphangiomas: in the lymphatic system
• Inflammatory/Degenerative disease
– Arteriosclerosis
– Atherosclerosis
Specific Diseases
• Vasculitits
– Inflammation of arteries and veins
– Patients will have pain at the site
• Thrombophlebitis
Organ Failure
• Failure of the cardiovascular system to maintain
adequate blood pressure to organs results in
shock
Heart Failure
(1 of 2)
• Inadequate pumping
• Leads to decreased cardiac output, increased
preload, and increased afterload
• Causes of heart failure: congenital heart
defects, myocardial infarction, heart valve
disease, dysrhythmias, thyroid disease
Heart Failure
(2 of 2)
• Compensatory mechanisms activated.
– Activation of the sympathetic nervous system
– Activation of the renin–angiotensin–aldosterone
system
– Ventricular hypertrophy
• The compensatory mechanisms help at first,
but create a vicious cycle (perpetuate heart
failure).
Types of Heart Failure
(1 of 2)
• Systolic dysfunction
– Decreased contractility
• Diastolic dysfunction
– Decreased filling
• Mixed dysfunction
– Both
Types of Heart Failure
(2 of 2)
Left-sided failure
• Cardiac output falls.
• Blood backs up to the
pulmonary circulation.
• Causes: left ventricular
infarction, hypertension,
and aortic and mitral valve
stenosis.
• Manifestations: pulmonary
congestion, dyspnea, and
activity intolerance.
Right-sided failure
• Blood backs up to the
peripheral circulation.
• Causes: pulmonary disease,
left-sided failure, and
pulmonic and tricuspid
valve stenosis.
• Manifestations: edema and
weight gain.
Heart Failure
(1 of 2)
• May be acute or chronic
• Manifestations
– Depend on type
– Fluctuate in severity
– Appear as compensatory mechanisms fail
– Include indications of systemic and pulmonary
fluid congestion
• Grading of severity: I–IV
Heart Failure
(2 of 2)
• Diagnosis: history, physical examination, chest X-ray,
arterial blood gases, echocardiogram,
electrocardiogram, and brain natriuretic peptide
• Treatment
– Identify and manage underlying cause
– Includes lifestyle modification, angiotensin-converting
enzyme inhibitors, diuretics, beta-adrenergic blockers,
calcium channel blockers, biventricular pacemaker, intraaortic balloon pump, and heart transplant
Cardiac Amyloidosis
• disorder caused by deposits of an abnormal protein
(amyloid) in the heart tissue
• occurs when amyloid deposits take the place of normal
heart muscle.
• most typical type of restrictive cardiomyopathy.
• may affect the way electrical signals move through the
heart (conduction system).
• abnormal heartbeats (arrhythmias) and faulty heart
signals (heart block).
• can be inherited.
• can also develop as the result of another disease such as
a type of bone and blood cancer, or as the result of
another medical problem causing inflammation
Shock
• Decreased blood volume or circulatory
stagnation resulting in inadequate tissue and
organ perfusion
Stages of Shock
• Compensatory
– Sympathetic nervous system and renin–angiotensin–
aldosterone system are activated.
• Progressive
– Compensatory mechanisms fail.
– Tissues become hypoxic, cells switch to anaerobic
metabolism, lactic acid builds up, and metabolic acidosis
develops.
• Irreversible
– Organ damage occurs.
Types of Shock
(1 of 2)
• Distributive shock
– Neurogenic shock
• Loss of vascular sympathetic tone and autonomic
function lead to massive vasodilatation.
– Septic shock
• Bacterial endotoxins activate an immune reaction.
– Anaphylactic shock
• Excessive allergic reaction
Types of Shock
(2 of 2)
• Cardiogenic shock
– Left ventricle cannot maintain adequate cardiac
output.
• Hypovolemic shock
– Venous return reduces because of external blood
volume losses.
Shock
(1 of 2)
• Manifestations
– Vary depending on type
– Include thirst, tachycardia, restlessness, irritability,
tachypnea progressing to Cheyne-Stokes respiration, cool
and pale skin, hypotension, cyanosis, and decreasing
urinary output
• Complications: acute respiratory distress syndrome,
renal failure, disseminated intravascular coagulation,
cerebral hypoxia, and death
Shock
(2 of 2)
• Diagnosis: complete blood counts, cultures,
coagulation studies, cardiac biomarkers,
arterial blood gases, chest X-ray,
hemodynamic monitoring, electrocardiogram,
and echocardiogram
• Treatment: identification and treatment of
underlying cause, maintaining respiratory
status, cardiac monitoring, and rapid fluid
replacement
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Review of Structure and Function
• The heart is divided into the systemic (left)
and pulmonary (right) systems
– The pulmonary system has low vascular
resistance, thus the right side is less
muscular
– Each side has an atrium and a ventricle,
separated by valves
http://www.youtube.com/watch?v=SvAVu-7E2gA
Review of Structure and Function
• Cardiac muscle is highly dependent on a large
oxygen supply, supplied by the right and left
coronary arteries
• The flow of electricity through the heart is
what produces contraction
Review of Structure and Function
• The Sinoatrial (SA) node is the pacemaker for
the heart
• The SA node then sends the signal to the
Atrioventricular (AV) node, and finally down
the Bundle of His to stimulate the ventricles to
contract
Most Frequent and Serious Problems
• Atherosclerosis is the most common cause of
death in the United States
– Leads to cardiac dysfunction by interrupting
the delivery of oxygen to the muscle
– This can cause myocardial infarction (heart
attack) or arrhythmias (abnormal heart
beats)
Most Frequent and Serious Problems
• Angina pectoris and congestive heart failure
(CHF) are the major causes of disability from
heart dysfunction
• Angina: narrowed blood flow leads to ischemia of
the myocardium,
– Marked by chest pain
– Can be chronic or acute
– Treated with nitroglycerin to dilate blood vessels
– As atherosclerosis progresses, nitro becomes less
effective
– Can eventually lead to infarction
Symptoms, Signs, and Tests
• Congestive heart failure
– As fluid backs up, it can flood the alveoli,
causing decreased gas exchange and
shortness of breath
– Physical exam identifies jugular venous
distension, crackles in the lungs, and
dullness to percussion over lung fields
Most Frequent and Serious Problems:
complications of an infarct
• Ventricular rupture: softened necrotic membrane
may rupture due to HTN
– Blood fills the pericardial sac, compressing the heart
• Cardiac Tamponade: compression of the heart by
blood in the pericardial cavity
– Occurs 5-7 days later and is usually lethal
• Ventricular aneurysm: infarct in the LV will scar
and can form an aneurysm
Most Frequent and Serious Problems
• Cor pulmonale: enlargement of RV in response
to pulmonary HTN
– Results in heart failure
• Sudden cardiac death
• Endocardial mural thrombus:
– Endocardium overlying infarcted myocardium can
be damages and disrupted
– Blood in the ventricle coagulates in contact with
necrotic tissue and forms a thrombus on the wall
of the ventricle
– Interfere with blood flow and weaken the hearts
contraction
– Can become an emboli and move to other organs
Symptoms, Signs, and Tests
• Myocardial infarcts
– Patients can present with chest pain that
radiates to the left shoulder, arm, neck, or
jaw
– Women will present with atypical
symptoms
– Diagnosed with electrocardiography (ECG)
and laboratory exams
Symptoms, Signs, and Tests
• Congestive heart failure
– Caused by progressive and chronic ischemia
– Hypoperfusion of the myocardium leading to pump
failure
– May be asymptomatic or have chronic angina
– Secondary thrombosis is common
– Diagnosed through physical exam, chest x-ray, ECG,
echocardiogram, and laboratory exams
• The ultimate test is cardiac catheterization
Specific Diseases
• Genetic/Developmental Diseases
– Bicuspid aortic valve
• Instead of three cusps, only two or
present, this allows for the valve to
become scarred
Specific Diseases
• Genetic/Developmental Diseases
– Atrial and Ventricular Septal Defects
(ASD/VSD)
• VSD is more serious due to the larger
pressures present in the ventricles
• The heart must pump the same blood
more than once, which can potentially
lead to heart failure
Specific Diseases
• Tetralogy of Fallot
– A cyanotic disease, actually caused by four
defects
• Pulmonary stenosis
• Right ventricular hypertrophy
• Overriding aorta—both ventricles empty
into it
• VSD
Specific Diseases
• Contraction of the Aorta
– Narrowing of the thoracic aorta
– Can result in left ventricular hypertrophy
and heart failure
Specific Diseases
• Hypertrophic Cardiomyopathy
– Caused by a genetic mutation that affects
the proteins that promote contraction
– The interventricular septum becomes so
large it affects ventricular filling, thus
decreasing stroke volume
Specific Diseases
• Inflammatory/Degenerative Diseases
– The major cause of morbidity and mortality
in the United States
Specific Diseases
• Coronary Artery Atherosclerosis
– In some patients, plaque formation is
gradual, which allows for collateral blood
vessel formation
– However, in some patients, a single larger
plaque in a strategic location may prove
fatal
Specific Diseases
• Coronary Artery Atherosclerosis
– If coronary artery insufficiency does occur,
the end result could be arrhythmias or
infarcts
– One symptom of coronary insufficiency is
angina pectoris, which becomes worrisome
when the patient begins having unstable
angina—or chest pain at rest
Specific Diseases
• Coronary Artery Atherosclerosis Treatment
– Angioplasty
• A catheter with a balloon on the tip is inserted
to the area of narrowing, then it is inflated,
compressing the plaque out of the way
• A stent can be placed to maintain patency
• Coronary artery bypass graft (CABG)—open
heart surgery, uses segments of other veins to
bypass blockages
Specific Diseases
• Aneurysms
– Weakening of the heart or vessels, leads to
impaired ventricular function
• Rheumatic heart disease
– Can occur following streptococcal
infections, resulting in myocarditis or
valvulitis
Specific Diseases
• Infective Endocarditis
– Caused by an organism living on a heart
valve, producing an inflammatory response
• Hypertensive heart disease
– Causes an increased workload for the heart,
which can lead to hypertrophy and
eventually failure
Specific Diseases
• Cor Pulmonale
– Pulmonary hypertension caused by chronic
lung disease leads to an increased workload
on the right heart and eventually failure
Cardiac Sarcoidosis
• rare disease in which clusters of white blood cells, called
granulomas, form in the tissue of the heart.
• Any part of the heart can be affected, though these cell
clusters most often form in the heart muscle where they
can interfere with the heart’s electrical system
(conduction defects) and cause irregular heartbeats
(arrhythmias).
• can also result in heart failure.
• The disease tends to affect younger people, generally
between 25 and 45 years old.
• Most people diagnosed with cardiac sarcoidosis also
have granulomas in other organs of the body, most
commonly in the lungs (pulmonary sarcoidosis).
Specific Diseases
• Cardiomyopathy
– Disease intrinsic to the cardiac muscle
• Dilated
• Hypertrophic
• Restrictive
Specific Diseases
• Atrial Fibrillation
– The atria quiver rather than contract
– This allow for blood to pool, potentially
developing clots
– This also does not allow for complete
ventricular filling, which can result in
decreased cardiac output
Organ Failure
• Cardiogenic Shock
– Perfusion of tissues is inadequate to meet
the metabolic demand of those tissues
– In the case of cardiogenic shock, it is the
result of inadequate contractility
Coronary Artery Disease
• Athersclerosis of the coronary arteries
presents in many forms, all leading to
myocardial ischemia
• Myocardial Ischemia:
– Decrease in blood flow to the cardiac muscle leads
to decreased oxygen supply
– Leads to damage to heart muscle
– Reduced ability of the heart to function efficiently
– May cause arrythmias
– May lead to infarction or serious disease
Myocardial Ischemia
• May result from slow narrowing of arteries or
sudden occlusion
• Extent of ischemia depends on
– Anatomic location
– Extent of occlusion
– Presence or changes in other diseases
(hyperthyroidism, hypertension, diabetes, etc)
– Extent of athersclerosis in other coronary arteries
– Speed at which ischemia develops
Myocardial Ischemia
• Causes:
– Athersclerosis (plaque)
– Nonocclusive Thrombus
– Occlusive Thrombus
• Clinical presentation
– 10-25% occlusion: asymptomatic or angina
– 50-70%: angina or congestive heart failure
– 70-100%: congestive heart failure or infarction
Complication of Infarction
• Ventricular Rupture:
– Weakened myocardium may rupture, blood fills the
pericardial sac and compresses the heart
• Cardiac Tamponade:
– Compression of the heart by blood in the pericardial
cavity (5-7days post MI); lethal
• Ventricular aneurysm:
– Due to massive infarct, scarring
• Endocardial mural Thrombus
– Endocardium overlying infarct is disrupted and causes
blood to cooagulate
– Can become emboli, contributed to CHF
Myocardial Infarction
• Hibernation:
– refers to adaptive reduction of myocardial
contractile function in response to reduction of
myocardial blood flow.
• Stunning
– Prolonged and fully reversible dysfunction of the
ischemic heart that persists despite the
normalization of blood flow.
Organ Failure
• Congestive Heart Failure
– The heart is unable to pump the blood that
is returned to it, resulting in the blood
backing up into the pulmonary system
Electrocardiograms
• is a test that measures the electrical activity of the heartbeat.
• an electrical impulse (or “wave”) travels through the heart.
• The current causes the muscle to squeeze and pump blood
from the heart.
• A normal heartbeat on ECG will show the timing of the top
and lower chambers.
• “P wave” The right and left atria make the first wave
• a flat line: the electrical impulse goes to the bottom ventricles
• “QRS complex“: the right and left ventricles make the next
wave
• “T wave” represents electrical recovery or return to a resting
state for the ventricles.
Electrocardiograms
Normal Sinus Rhythm
Arrhythmia's