Cardiovascular Patho 1 Ogena

8/14/2019 Cardiovascular Patho 1 Ogena

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Cardiovascula

r System


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Pathophysiologic

Concepts


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Thrombus

A thrombus

a blood clot that can develop

anywhere in the vascular system causing the narrowing of a vessel.

blood flow can be occluded

(reduced or totally blocked)


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Thrombus develop from any injury to the vessel wall

endothelial cell injury draws platelets and other

mediators of inflammation to the area.

substances stimulate clotting and activation of the

coagulation cascade.

formation can occur when blood flow through a vessel

is sluggish,

when blood flow is irregular or erratic

during periods of irregular heartbeat or cardiac arrest


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Thrombus


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Embolus

Embolus

a substance that travels in the

bloodstream from a primary site to a

secondary site becomes trapped in the vessels at the

secondary site

causes blood flow obstruction.

Most emboli are blood clots

(thromboemboli)

usually deep leg veins


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Other sources of emboli fat

released during the break of a long bone

produced in response to any physical trauma, and

amniotic fluid

which may enter maternal circulation during the

intense pressure gradients generated by labor

contractions.

Air and displaced tumor cells also may act as emboli to

obstruct flow.

Embolus


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Aneurysm Aneurysm

is a dilation of the arterial wall caused by a

congenital or developed weakness in the wall.

Weakness in the wall may develop as a result of an

infection, from trauma, or, more commonly, from

lesions produced by atherosclerosis.

Aneurysms may burst with increased pressure,

leading to massive internal hemorrhage.


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Alterations in Capillary Forces

of Filtration or Reabsorption

Occasionally, forces favoring filtration

from the capillary into the interstitial

fluid are greater than forces favoring

reabsorption of fluid into the capillaryfrom the interstitial space.

The result is net filtration.

Net filtration across the capillary

results in interstitial edema.


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Alterations in Capillary Forces of

Filtration or Reabsorption

The opposite occurs when forces favoring

reabsorption of fluid from the interstitial

space into the capillary are greater than

those favoring filtration. This results in net reabsorption, which

leads to increased plasma volume, stroke

volume, and cardiac output.

Blood pressure may be increasedsignificantly.


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Causes of Increased Capillary

Filtration

Causes of increased capillary filtration include

increased capillary pressure

caused by high blood pressure

increased capillary leakage

caused by injury or inflammation. increase in protein concentration in the

interstitial fluid

caused by increased capillary breakdown

decreased lymph flow to the area would

also cause net filtration, leading to edemaand swelling of the interstitial space.


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Causes of Increased

Capillary Filtration

Causes of increased capillary filtration

include

decreased production or increased

loss of plasma proteins

reduce the reabsorption of fluid

back into the capillary.

can occur with liver disease orloss of protein in the urine.


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Causes of Increased

Capillary Reabsorption Causes of increased

reabsorption of fluid from theinterstitial space include

decreased blood pressure inthe capillary due to a decrease in

systemic pressure or

constriction of the arterioleor precapillary sphincter.


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Increased plasma colloid osmotic pressurealso draws fluid back into the capillary.

Plasma colloid osmotic pressure increaseswith dehydration, leading to a return of fluid

from the interstitium to the plasma, whichhelps return plasma volume toward normal.

Finally, increased interstitial fluid pressureincreases reabsorption by opposing furtheraccumulation of fluid.


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Stenosis

Stenosis

a narrowing of any vessel or opening.

stenosis of the heart valves may

occur.

congenital defect or an inflammatory

process (e.g., after rheumatic fever).


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Results of Cardiac Valve

Stenosis

chamber upstream of the stenosispumping more forcefully to expel itsblood through the narrowed orifice.

After years of this extra work,cardiac muscle can hypertrophy(increase in size).

If the chamber cannot pump

forcefully enough to overcome thestenosis, blood flow out of thechamber will be reduced.


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Results of Cardiac Valve

Stenosis

chamber increases its oxygenconsumption and energy demands.

The coronary arteries supplying themuscle may be unable to supply adequate

oxygen to meet this demand. blood may accumulate in the chamber

and stretch its muscle fibers.

If this is significant or prolonged, a

decrease in muscle contractility can result.


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Examples of Cardiac Valve Stenosis

Any cardiac valve

Mitral stenosis

narrowing of the valve between the left atriumand left ventricle.

Aortic stenosis

narrowing of the valve between the leftventricle and the aorta.

Tricuspid stenosis

narrowing of the valve between the rightatrium and the right ventricle.

Pulmonary stenosis narrowing of the valve between the right

ventricle and the pulmonary artery.


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Valve Incompetence

An incompetent valve is one that

does not close completely, allowing

blood to move in both directionsthrough that valve when the heart

contracts (valve regurgitation).

Any of the cardiac valves may be

incompetent.

Each chamber may hypertrophy.


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Cardiac Shunts

a shunt is a connection between thepulmonary vascular system and thesystemic vascular system.

During fetal life, shunts between the right

and left sides of the heart and between theaorta and pulmonary artery are normal.

The direction blood flows through a shuntis determined by resistance to flow in eachdirection.


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Right-to-Left Shunt

the flow of blood from the right side of theheart to the left, or from the pulmonary arteryto the systemic circulation.

After birth, right heart and pulmonary artery

blood is poorly oxygenated. Therefore, a right-to-left shunt delivers poorly oxygenated bloodto the systemic circulation.

called a cyanotic shunt because delivery of

poorly oxygenated blood to the systemiccirculation causes cyanosis (bluish tinge tothe skin).


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Left-to-Right Shunt

the flow of blood from the left side ofthe heart to the right side, or from theaorta to the pulmonary circulation.

Left heart blood is well oxygenated. Blood going to the lungs from the leftside of the heart recirculates to theleft atrium and left ventricle.

Because the blood is well-oxygenated, this shunt is acyanotic.


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Two Types of Cardiac Defects

Congenital

Anatomic>abnormal function

Acquired

Disease process

Infection

Autoimmune response

Environmental factors

Familial tendencies


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Causes of CHD

Chromosomal/genetic = 10%-12% Maternal or environmental = 1%-2%

Maternal drug use Fetal alcohol syndrome50% have CHD

Maternal illness Rubella in 1st 7 wks of pregnancy50%

risk of defects including PDA andpulmonary branch stenosis

CMV, toxoplasmosis, other viral

illnesses>> cardiac defects IDMs = 10% risk of CHD (VSD,

cardiomyopathy, TGA most common) Multifactorial = 85%


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CHD

Incidence: 5-8 per 1000 live births About 2-3 of these are symptomatic in first year

of life Major cause of death in first year of life (after

prematurity)

Most common anomaly is VSD 28% of kids with CHD have another recognized

anomaly (trisomy 21, 13, 18, +++ )


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Older Classifications of CHD

Acyanotic

May become cyanotic

Cyanotic May be pink

May develop CHF


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Newer Classification ofCHD

Hemodynamic characteristics

Increased pulmonary blood

flow

Decreased pulmonary blood

flow

Obstruction of blood flow out

of the heart

Mixed blood flow


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Increased Pulmonary

Blood Flow Defects

Abnormal connection between

two sides of heart

Either the septum or the great

vessels

Increased blood volume on

right side of heart

Increased pulmonary blood flow

Decreased systemic blood flow


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Increased Pulmonary

Blood Flow Defects

Atrial septal defect

Ventricular septal defect

Patent ductus arteriosus


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ATRIAL SEPTAL DEFECT (ASD)

Abnormal opening between the atria

an abnormal opening between the left and

right atria.

foramen ovale fails to close after birth, or

when another opening between the left

and right atria is present due to improper

closure of the wall between the two atria

during gestation.


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PATHOPHYSIOLOGY

Blood flows from left to the

right

Increase flow of oxygenated

blood nto the right side of the

heart


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ASD


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CLINICAL MANIFESTATIONS

Asymptomatic

May develop congestive heart

failure Murmur

Atrial dysrhythmias


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VENTRICULAR SEPTAL

DEFECT (VSD)

Abnormal opening between

right and left ventricle

the most common cardiac

congenital defect

May close spontaneously : 1st

year of life


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VSD


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PATHOPHYSIOLOGY

Blood flow from higher pressure

left ventricle to low pressure

right ventricle

Increased blood volume is

pumped into the lungs

Right ventricular hypertrophy


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Murmur

Congestive heart failure iscommon

C S


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PATENT DUCTUSARTERIOSUS

Failure of the fetal ductus

arteriosus (artery connecting

aorta and pulmonary artery) to

close within the first weeks oflife


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PATHOPHYSIOLOGY

Blood flow from high pressure

aorta to lower pressure pulmonary

artery Increased workload on the left side

of the heart

Hypertrophy


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PDA


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CLINICAL

MANIFESTATIOn

AymptomaticSigns of congestive heart

failure

Machinery-like murmur

Widened pulse pressure


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Obstructive Defects

Coarctation of the aorta

Aortic stenosis

Pulmonic stenosis


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COARCTATION OF THE AORTA

(COA)

Localized narrowing near the

insertion of the ductus

arteriosus,

increased pressure proximal to

the defect


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COA


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CLINICAL MANIFESTATION

High BP and bounding pulses inarms

Weak or absent femoral pulses

Cool lower extremities Low BP in the lower extremities Dizziness Headache

FaintingEpistaxis


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Aortic Stenosis


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Aortic Stenosis

a narrowing in the opening of the valve betweenthe left ventricle and the aorta.

follows rheumatic fever or is a congenitalmalformation.

ventricle must pump more forcefully to expel

blood through the narrow orifice. This causes ventricular hypertrophy and

eventually reduces compliance. As blood backsup in the ventricle, atrial pressure increases and

blood backs up into the pulmonary system andthe right side of the heart.


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Clinical Manifestations

Clinical manifestations may be absent or severe,depending on the level of stenosis.

Pulmonary congestion, with signs of dyspnea andpulmonary hypertension, may occur if blood backs upinto the pulmonary vascular system.

Dizziness and fatigue may occur due to decreasedcardiac output and decreased stroke volume. Heartrate may be elevated via sympathetic stimulation.


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Diagnostic Tools

A systolic heart murmur may

be heard as blood rushes

through the narrow orifice.

Echocardiography may be

used to diagnose abnormal

valve structure and motion.


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Complications

Left ventricular hypertrophy may

develop, leading to congestive

heart failure. Treatment

Treatment for congestive heart

failure may be required.


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Pulmonic Stenosis


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Pulmonic Stenosis

a narrowing of the opening between theright ventricle and the pulmonary valve.

most commonly occurs due to a congenitaldefect.

With a narrow orifice, the right ventriclemust pump more forcefully to expel blood.This can lead to right ventricularhypertrophy, backing up into the right

atrium and causing dilation of the venacava and blood accumulation in thesystemic veins.


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Blood flow into the lungs andleft side of the heart will bereduced if the stenosis is

severe, leading to a decreasein blood pressure. Right heartfailure may develop.

Clinical


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ClinicalManifestations

may be absent or severe depending

on the level of stenosis.

Decreased pulmonary flow causes

poor oxygenation of the blood andfeelings of weakness and fatigue.

Venous distention and swelling of the

ankles and feet are common.


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Diagnostic Tools

Echocardiography may be used to diagnose

abnormal valve structure and motion. Complications

Right heart hypertrophy and subsequent rightheart failure may occur.

Treatment

Treatment for heart failure may be required. Valve replacement or surgical correction of

the stenosis may be attempted.

Decreased Pulmonary


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Decreased PulmonaryBlood Flow Defects

Tetralogy of Fallot

Tricuspid atresia


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Tetralogy of Fallot

The classic form includes

four defects

Ventricular septal defectPulmonic stenosis

Overriding of the aorta

Right ventricular

hypertrophy


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Tetralogy of Fallot


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Tetralogy of Fallot


Infants

Cyanotic at birth

Episodes of cyanosis

and hypoxia called Blue

or tet spells

Crying or after feeding


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Tricuspid Atresia

Tricuspid Atresia


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Tricuspid Atresia

The deformity consists of a

complete lack of formation of the

tricuspid valve with absence of

direct connection between theright atrium and right ventricle.

prevalence of 0.3-3.7% in

patients with congenital heartdisease

Clinical


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ClinicalManifestation

detected in infancy because ofpresenting cyanosis, congestiveheart failure, and growth

retardation. history of poor skin colorationinability to complete a feedingsession, frequent pauses during

feeding, and/or frank anorexia.


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Clinical Manifestation

As a result, the infantdemonstrates poor growthpatterns.

Respiratory difficulties areoften reported as nasalflaring or muscle retractions


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Mixed Defects

Transposition of great

vessels

Total anomalous pulmonaryvenous connection

Hypoplastic heart syndrome

RightLeft

Transposition of


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Transposition ofGreat Vessels

The pumonary artery

arised from the left

ventricle and the aortaexits from the right

ventricle


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Transposition of Great Vessels


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CLINICAL MANIFESTATION

Depend on the type and size of

associated defects

Minimal communication Severely cyanotic and depressed at

birth

Large septal defects Less cyanotic but may have

symptoms of CHF

Totally Anomalous Pulmonary


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Venous Connection

Rare Defect.

Pulmonary veins fail to join L atrium.

Clinical manifestations: Usually

cyanotic early on. Condition rapidly

deteriorates as pulmonaryblood flow

increases and causes CHF.



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Venous Connection


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Hypoplastic Left Heart

L side of heart is underdeveloped.

L ventricle is small and aortic atresia.

Most blood flows across patent foramen

ovale to R atrium..to R ventricle and out thepulmonary artery.

Descending aorta receives blood from the

PDA to supply the systemic circulation. PDAclosure >>rapid deterioration and CHF.

Hypoplastic Left


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Hypoplastic LeftHeart


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As the ductus arteriosus begins to closenormally over the first 24-48 hours of life

Symptoms of cyanosis, tachypnea,respiratory distress, pallor, lethargy,

metabolic acidosis, and oliguria develop. Without intervention to reopen the ductus

arteriosus, death rapidly ensues.


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With a right-to-left shunt,cyanosis, fatigue, and

weakness occur. Knee-to-chest

or squatting behavior may beobserved. Clubbing of the digits

may develop.


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With a left-to-right shunt,pulmonary congestion and

dyspnea may occur. Left heart

failure may develop.

Treatment


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Some defects may be small, require no treatment, or close

spontaneously. Surgical correction of the defect is often required.

Treatment for congestive heart failure may be necessary.

Prostaglandin E is administered to maintain patency of the

ductus arteriosus in preductal coarctation.

Administration of the prostaglandin inhibitor indomethacin will

initiate closure of the ductus in patent ductuctus arteriosus.


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Cardiovascular Patho 1 Ogena

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