Cardiovascular Disorders

HNI 310
Pathology
Kenneth Faulkner, MS, RN,
ANP-BC
Department of Undergraduate Studies

Objectives
By completion of this lecture, students should be able to:
1. Describe the process of atherosclerosis
2. Differentiate stable angina, unstable angina/NSTEMI, and STEMI
3. Describe factors associated with increased risk of aneurysm
4. Describe factors associated with development of DVT
5. Differentiate peripheral arterial disease and venous insufficiency
6. Describe hypertrophic cardiomyopathy and describe how pathology
influences clinical presentation
7. Differentiate the symptoms of heart failure as they relate to cardiac
function
8. Describe difference between systolic and diastolic heart failure
9. Differentiate rheumatic heart disease from endocarditis
10.Describe how different valvular heart diseases present
11.Differentiate cyanotic from non-cyanotic congenital abnormalities and
provide examples of both

Cardiology basics
Review chapter 21 for basic cardiac
anatomy , flow of blood through the
heart, capillary exchange, and
nervous system regulation

Vascular anatomy
3 layers
Tunica intima endothelial cells over connective
tissue
Tunica media smooth muscle thicker in arteries
and arterioles
Tunica adventitia
collagen and
connective tissue

Vascular specifics
Intima controls
Transfer of molecules across vessel wall
Platelet adhesion and clotting
Vascular resistance and blood flow
Hormone regulation
Inflammatory response*
When disturbed, intima stimulates release of cytokines and other
products that induce inflammation

Vascular smooth muscle

Dilates and constricts in response to signals
Produces collagen, elastin, growth factors and cytokines
Repairs blood vessels when damaged

Terminology
Ischemia reduction in blood flow
that doesnt meet needs for oxygen
Infarction necrotic tissue resulting
from prolonged ischemia

Atherosclerosis
Formation of fatty lesions in intimal lining of medium and
large sized blood vessels (aorta, coronary arteries, arteries
of brain, etc.)
Leading cause of death in the U.S.
Risk factors:
Unmodifiable
Increasing age
Genetic predisposition/family history
Male gender

Modifiable
High LDL or low HDL
Smoking*
HTN
DM

Atherosclerosis
Three types of lesions
1. Fatty streak early discoloration of the
intima due to infiltration by
macrophages and lipid
2. Fibrous atheromatous plaque further
invasion of the intima triggers the
inflammatory process
3. Complicated lesion hemorrhage within
the lesion or ulceration of the lesion
leading to thrombosis

Process of Atherosclerosis
1. Endothelial injury due to LDL, HTN, smoking, etc.
Allows entry of lipids
Monocytes and platelets can adhere
Fatty streak begins to form

2. Inflammatory cells migrate into vessel wall

Monocytes enter intima (and become macrophages), release toxic
oxygen species to oxidize LDL, and engulf lipids (esp. LDL)
Oxidized LDL further damages endothelium and allows influx of
platelets and fibrin
Macrophages become foam cells

3. Smooth muscle attempts to repair the damage

Foam cells release growth factors to recruit smooth muscle cells
Smooth muscle proliferates and produces extracellular matrix
(collagen)

Atherosclerosis (cont.)
4. Fibrous atheromatous plaque
Superficial smooth muscle cap and dense extracellular matrix
Macrophages, smooth muscle cells, lymphocytes, fatty debris and
foam cells under fibrous cap
Core may be necrotic, calcified, and unstable
Extends into vessel lumen slowing blood flow and promoting
thrombus formation

5. Complicated lesion
Hemorrhage
Unstable cap can ulcerate and
rupture
Coagulation cascade can be
initiated

. See diagrams on pages

750-751

Stable Angina and Acute coronary

syndrome (ACS)
Coronary blood flow regulated by cardiac oxygen
requirements
Heart extracts 60-80% of oxygen in blood

Oxygen requirements dependent upon metabolic

activity of heart
Increased need = increased flow
Vasodilation to accommodate increased need
Mediated by nitric oxide and other chemicals released by
endothelium

Lack of blood flow causes ischemia

Prolonged ischemia can lead to angina or
infarction

Movie time!
http://
www.youtube.com/watch?v=Gg4nhf
remHo

Acute coronary syndrome

(cont.)
Stable plaque
Obstructs blood flow over time

Unstable plaque
Can rupture due to hemodynamic stress
Exposes lipid core to blood
Stimulates platelet aggregation and thrombus formation

Smooth muscle and foam cells express tissue factor

Tissue factor stimulates extrinsic pathway

Result is an acute vascular occlusion

Acute coronary syndrome

(cont.)
Extent of damage dependent upon location of
occlusion, extent and duration of occlusion,
amount of tissue supplied by the vessel,
metabolic needs of the tissue
Three layers of heart wall
Endocardium endothelial cells
Myocardium cardiac muscle
Epicardium connective tissue

Ischemia can affect all vessels (transmural) or

only some
Area below the endocardium affected first

Acute coronary syndrome

(cont.)
Damage is the result of conversion to anaerobic
metabolism and loss of ATP
Lack of energy to meet demands
Decrease in contractile force within 60 seconds
Glycogen is depleted and mitochondria swell
Damage is irreversible after approximately 40 minutes
If flow is restored before then, changes can be reversed
Gross tissue damage not seen for hours

Failure of the left ventricle (LV) to pump may occur

Ventricular remodeling
Changes in size, shape, and thickness of ventricle to
compensate for infarcted areas (which become thin and
dilated)

Presentation of Stable Angina and

ACS
Stable angina pain associated with exertion, relieved by rest
Constricting, squeezing
Consistently the same intensity and character

Acute coronary syndrome (ACS) may result from SA or may

occur without warning
Unstable angina (USA)/Non-ST elevation myocardial infarction (NSTEMI)

Pain with minimal exertion or at rest

MAY be relieved with nitroglycerin (NTG)
Pain is new onset and may vary in intensity, frequency, and character
Differentiated based on presence of biomarkers

ST-elevation myocardial infarction (STEMI)/heart attack acute onset

or progression from NSTEMI

Substernal pain crushing, suffocating, constricting

Prolonged not relieved by rest or NTG
Radiates to jaw, neck, left arm*
Nausea and vomiting*
Fatigue and weakness*

Heart failure
Reduction in cardiac output due to cardiac abnormality
Affects over 5 million Americans over the age of 20
Preload volume of blood stretching ventricle at end of diastole
It is the volume of blood stretching the heart muscle at the end of diastole and is normally determined by the venous
return to the heart. During any given cardiac cycle, the maximum volume of blood filling the ventricle is present at
the end of diastole. Known as the end-diastolic volume, this volume causes an increase in the length of the
myocardial muscle fibers. Within limits, as end-diastolic volume or preload increases, the stroke volume increases

Venous return

Afterload resistance the ventricle must overcome to eject blood

Systemic vascular resistance and ventricular wall tension
The main components of afterload are the systemic (peripheral) vascular resistance and
ventricular wall tension. When the systemic vascular resistance is elevated, as with
arterial hypertension, an increased left intraventricular pressure must be generated to
first open the aortic valve and then move blood out of the ventricle and into the systemic
circulation.

Contractility the contractile force of the ventricle

Actin and myosin filaments shorten

Heart failure (cont.)

Systolic dysfunction
Decrease in cardiac contractility: EF < 40%
Preload increases, ventricle dilates, increased left
ventricular end diastolic (LVED) pressure
Pulmonary hypertension leading to pulmonary edema
increased preload can also lead to one of the most deleterious consequences of
systolic ventricular dysfunctionaccumulation of blood in the atria and the venous
system (which empties into the atria), causing pulmonary or peripheral edema.

Etiology:
Impaired contractility (ischemic heart disease, CMO)
Volume overload (valve insufficiency)
Pressure overload (HTN, valvular stenosis)

Heart failure (cont.)

Diastolic dysfunction
35-55% of cases
Diastolic ventricular dysfunction is characterized by a normal ejection fraction but impaired diastolic ventricular relaxation,
leading to a decrease in ventricular filling that ultimately causes a decrease in pre- load, stroke volume, and cardiac output

Higher in women, and in obesity, HTN, and DM

Relaxation is abnormal ventricular filling is abnormal
Increased ventricular pressures increased pulmonary vascular congestion
With diastolic dysfunction, blood is unable to move freely into the left ventricle, causing an increase in
intraventricular pressure at any given volume. The elevated pressures are transferred backward from
the left ventricle into the left atrium and pulmonary venous system, causing a decrease in lung
compliance, which increases the work of breathing and evokes symptoms of dyspnea. Cardiac output
is decreased, not because of a reduced ventricular ejection fraction as seen with systolic dysfunction,
but because of a decrease in the volume (preload) available for adequate cardiac output. Inadequate
cardiac out- put during exercise may lead to fatigue of the legs and the accessory muscles of
respiration.

Etiology:
Impaired ability of ventricle to expand (pericardial effusion)
Increased wall thickness and reduced LV chamber size (hypertrophic CMO)
Delayed diastolic relaxation (ischemic heart disease)
Ventricle begins to fill while ventricle is still stiff

Heart failure (cont.)

Right ventricular dysfunction

Right-sided heart failure impairs the ability to move deoxygenated blood from the sys- temic circulation into
the pulmonary circulation.

Symptoms are mainly systemic

Peripheral edema, liver congestion (Right-sided heart failure also produces
congestion of the viscera. As venous distention progresses, blood backs up in the hepatic veins that drain
into the inferior vena cava, and the liver becomes engorged)

, anorexia, elevated JVD.

When the right heart failure occurs in response to chronic pulmonary disease, it is referred to as cor
pulmonale

Left ventricular dysfunction

Symptoms are initially pulmonary and progress to
systemic
Left-sided heart failure impairs the movement of blood from the lowpressure pulmonary circulation into the high-pressure arterial side of
the systemic circulation. With impairment of left heart function, there
is a decrease in cardiac output to the systemic circulation; blood
accumulates in the left ventricle, left atrium, and pulmonary
circulation, which causes an elevation in pulmonary venous pressure

Activity intolerance, cyanosis, hypoxia, orthopnea, paroxysmal

nocturnal dyspnea (PND)

Peripheral arterial disease

Acute arterial occlusion
Sudden blockage of flow through a peripheral
artery
Etiology
Embolus or thrombus most common
Trauma can be a cause

Manifestations
Pain, pallor, pulselessness, paralysis, paresthesia, polar (cold)

Atherosclerotic Occlusive disease

Gradual decrease in blood flow 50% narrowing before onset of
symptoms
Etiology
Atherosclerosis

Manifestations
Claudication extremity pain with use (angina of the extremity)
Weak pulses, cool, atrophy

Aneurysms
Abnormal localized dilation of blood
vessel
Etiology
Weakness in blood vessel wall caused by:

Congenital defect
Trauma
Infection
Atherosclerosis

Aneurysm grows as tension and pressure continues

Can cause pressure on surrounding structures or may rupture

Manifestations depend upon location and size

May be asymptomatic
May complain of stabbing substernal, back, and neck pain
May have dyspnea and cough due to impingement on trachea
Hoarseness due to pressure on laryngeal nerve
Difficulty swallowing due to pressure on esophagus

Aortic dissection
Acute, life threatening event
Hemorrhage into vessel wall with tearing along the length
of the vessel loss of blood is usually not significant
Channel may obstruct blood flow to branch arteries
Ascending aorta most affected (2/3)
Etiology
Weakness of vessel
HTN, connective tissue diseases, surgery increases risk

Epidemiology
Most common in men between 40 and 60

Manifestations
Abrupt, excruciating pain described as tearing or ripping
Blood pressure and pulse unobtainable in one arm due to
obstruction
Syncope, paralysis, hemiplegia may occur

Hypertrophic
cardiomyopathy
Unexplained LV hypertrophy
Associated with thickened ventricular septum, abnormal filling
during diastole, arrhythmias, and LV outflow obstruction
Reduced LV chamber size and poor LV compliance
stroke volume due to abnormal filling
Most common cause of sudden death of athletes

Etiology
Autosomal dominant genetic predisposition
Coding for cardiac muscle proteins is abnormal

Epidemiology
1 in 500 people
Can occur at any time (child adult)

Presentation
Dyspnea, chest pain with exertion, exercise intolerance

Pericarditis
Accumulation of fluid in the
pericardial sac
Etiology
Inflammation
Infection
Trauma

As fluid volume in pericardial sac, pressure on heart

Pressures in right side of heart are lower, so
manifestations typically appear as right sided heart failure
Venous return preload
Tachycardia tries to compensate

Prolonged pressure in pericardium leads to cardiac

tamponade
ventricular filling, stroke volume, cardiac output

Endocarditis
Infection of lining of heart
Etiology
Invasion of heart valves and endocardium by bacteria
Staphylococcus is common bacteria for IV drug abusers and
heart valve patients
Many others can cause infection
Bacteria gets into bloodstream through portal of entry
Endothelial damage, altered hemodynamics, and
bacteremia lead to thrombus formation
Thrombus can be seeded by bacteria
Continued activation results in development and growth of
friable vegetations
Destruction of cardiac tissue

Endocarditis (cont.)
Aortic and Mitral valves most affected
Continue to release bacteria
Destroy valves, cause pericarditis, aneurysm, valve
perforation
Fragments may form emboli and travel to brain, lungs,
periphery
Epidemiology
IV drug abuse
Dental procedure
Intracardiac devices (prosthetic heart valves, pacemakers,
LVADs)
MVP

Manifestations
Fever, murmur, splinter hemorrhages

Treatment antibiotics and surgery

Rheumatic heart disease

Complications of immune response to group A
beta-hemolytic streptococcal throat infection
Development of chronic valvular problems

Etiology - not clearly understood

Believed to be autoimmune reaction following creation
of antibodies against M protein of group A betahemolytic strep
Antibodies cross react with self-antigens in heart and
joints (molecular mimicry)
Aschoff bodies are formed necrotic tissue
surrounded by immune cells
Deformity of valves occurs

Rheumatic heart disease

Manifestations
Arthralgia to severe arthritis affecting joints of
knees and ankles
Mitral and aortic valves most commonly
affected MV stenosis
Vegetations and scarring causing deformities
Subcutaneous nodules over extensor muscles of
wrist, elbow, ankle, knee

Valvular heart disease

Stenosis narrowed vascular lumen
Regurgitation backwards flow
Mitral valve stenosis
narrow mitral valve
Etiology rheumatic fever or congenital
abnormality
Fibrous replacement of valve resulting in stiff,
fused valves
Resistance and left atrium dilates, eventually
causing pulmonary vascular congestion

Valvular heart disease

(cont.)
Mitral valve regurgitation
Valve does not close properly
Etiology rheumatic heart disease, ruptured chordae
tendinae, ruptured papillary muscles, LV dilation
Volume overload in LA and LV resulting in pulmonary vascular
congestion

Mitral valve prolapse (MVP)

floppy valve
Etiology genetic disorder resulting in enlarged, floppy
valves
Fibrotic changes develop on valves
May or may not cause mitral regurgitation

Valvular heart disease

(cont.)

Aortic stenosis

Narrow aortic valve lumen

Etiology Most commonly congenital or calcification

More common in men

Calcific AS is usually slow to develop 60-70 years old
Impaired LV outflow
LV hypertrophies with time to accommodate for resistance
May cause cardiac workload angina, syncope, heart failure

Aortic regurgitation
Incompetent AV allowing backflow from aorta to LV
Etiology rheumatic fever, congenital abnormalities, aortic dilation

Increased pressure to LA and pulmonary vessels causing congestion

LV enlarges over time
Asymptomatic at first
Develops exertional dyspnea, orthopnea

Congenital heart disease

Major changes in heart occur
between 4th and 7th week of gestation
Defects are believed to be combination
of genetic and environmental influences
30% can be attributed to modifiable risk
factors (febrile illness, alcohol
consumption, DM, medications, etc.)
Many carry congenital abnormalities into
adulthood

Congenital heart disease

(cont.)
Pathophysiology
3 major mechanisms
1. Shunting of blood
2. Production of cyanosis
3. Disruption of pulmonary blood flow

Abnormal shunting
. Diversion of blood from one system to another
. Determined by presence of abnormal passageway , pressure
differences, and resistance

Shunting and Cyanosis

. Left to right shunts usually are acyanotic (do not interfere with
oxygenation)
Patent ductus arteriosus, atrial/ventricular septal defects

. Right to left shunts are typically cyanotic (blood is not oxygenated)

Tetralogy of Fallot, transposition of great vessels

Congenital heart disease

(cont.)
Cyanosis
Bluish tint in nail beds and mucous membranes
Occurs when O2 levels fall below 80% in capillaries
Shunting of blood without being oxygenated

Disruption of pulmonary blood flow

Reduction in pulmonary blood flow causes fatigue, dyspnea
Pulmonary stenosis

Increase in pulmonary blood flow stimulates

vasoconstriction of pulmonary artery
Pulmonary hypertension can also occur
Left to right shunts

Congenital heart disease

(cont.)
Patent ductus arteriosus
Normally closed 48 hours after birth due to decrease
in pulmonary artery resistance, muscular contraction,
increased O2 saturation and prostaglandin decline
Blood shunted from high pressure on left side to low
pressure on right side
Murmur and widened pulse pressure are common
Typically not cyanotic
Complications include heart failure, pulmonary
vascular disease, aneurysm, thromboembolism, and
calcification
Corrected by surgical closure

Congenital heart disease

(cont.)
Atrial/Ventricular septal defects
Persistent opening in septum
Atrial: Incidence 1 in 1000, more
frequently in girls

Often asymptomatic
Can develop L to R shunt
Dilation of R heart
Fixed split S2 due to delayed closure of
pulmonic valve
Surgical repair if necessary

Congenital heart disease

(cont.)
Ventricular: Incidence 2.5 in 1000, even
distribution in genders
Symptoms dependent upon size of defect
May be asymptomatic or may develop heart
failure
Can develop L to R shunt
Tachypnea, diaphoresis, failure to thrive
Pulmonary hypertension due to increased
volume
Can develop significant increase in
pulmonary vascular resistance
Surgical repair if necessary

Congenital heart disease

(cont.)
Tetralogy of Fallot
5-7% of all heart defects
Four defects
1. Ventricular septal defect
2. Shifting of aorta to the right
3. Pulmonary outflow obstruction
4. Right ventricular hypertrophy

Deoxygenated blood sent through systemic

circulation cyanosis
Crying, feeding, defecating increase oxygen
requirements and increase cyanotic events
Surgical repair is necessary

Congenital heart disease

(cont.)
Transposition of great vessels
Aorta arises from right ventricle,
pulmonary artery arises from left
ventricle
24 per 100,000, more common in boys
Ventricular septal defect present in 50%
of patients allows blood to mix and
allows infants to survive
Cyanosis is most common symptom
Surgical repair is necessary

Vasculitis

Inflammatory disorders affecting vessel wall

Also involve endothelial and smooth muscle cells
All vessels can be affected
Clinical manifestations
Fever, myalgia, malaise

Causes
Direct vascular injury
Infectious agents
Autoimmune disorders
Secondary to other diseases

Small vessels Wegener gramulomatosis

Medium sized vessels polyarteritis nodosa, Kawasaki disease
Large vessel Giant cell (temporal) arteritis

Chronic venous insufficiency

Failure of unidirectional flow through venous
system
Often due to faulty valves in veins
Blood can flow retrograde
Pooling of blood occurs

Manifestations
Tissue congestion
Edema
Reddened extremities
Brown pigmentation of skin
Impaired tissue nutrition leading to
venous stasis ulcers

Varicose veins
Tortuous, dilated blood vessels in lower
extremities
Develop when blood flow through veins
is occluded
Congenital abnormality
Deep vein thrombosis
Prolonged pressure on abdominal veins
due to pregnancy or tumor causes
venous valves to become inefficient
Prolonged standing leads to increased
venous pressure and vascular
stretching

Deep vein thrombosis (DVT)

Aka Thrombophlebitis
Presence of thrombus and inflammatory process in vessel
Usually occur in lower extremities
Elderly more at risk
Three factors associated with development of DVT (Virchows triad)
1. Venous stasis
Bed rest, immobilization, prolonged travel

2. Hypercoagulable state
Post pregnancy, oral contraceptives, HRT

3. Vascular injury
Trauma

Manifestations
.Initially asymptomatic
.Pain, swelling, muscle tenderness, fever, malaise
.Can dislodge and travel to lung, brain

Hypertensive vascular
disease
SBP 140 mmHg and DBP 90 mmHg
Risk factors:
1.
2.
3.
4.
5.
6.
7.

Genetic predisposition
Age (SBP increases, DBP decreases)
Race (African/Caribbean-Americans)
Insulin resistance
High salt intake
Obesity
Excessive alcohol consumption

Hypertensive vascular disease

(cont.)
Essential hypertension
Elevated BP not due to another condition
Thought to involve
1. Kidneys ability to regulate sodium and water
2. Sympathetic hyperreactivity
3. Renin-angiotensin-aldosterone system dysfunction

Uncontrolled leads to
1. LV hypertrophy
2. Heart failure
3. Atherosclerosis
4. Kidney disease
5. Retinopathy
6. Stroke

Hypertensive vascular disease

(cont.)
Secondary hypertension
Due to another disease process
1. Renal hypertension due to glomerulonephritis,
acute/chronic renal failure, UTI, polycystic kidney disease
Dysfunction of renin-angiotensin-aldosterone system
Decreased flow through kidney results in increase in renin production

2. Adrenocortical hormone dysfunction

Increased aldosterone due to adrenal hyperplasia or excessive
release of glucocorticoids due to Cushings disease
Sodium and water retention

3. Pheochromocytoma
Excessive release of catecholamines from tumor in adrenal medulla

4. Oral contraceptives
Estrogens and synthetic progesterones cause sodium retention

Thank you!
Next week Respiratory disorders!