AAA- Aneurysm

 Is the weakening in an artery wall that causes a localized are of bulging or dilation.
 The weakening segment of the artery creates an outpouching that is susceptible to
rupture.
 The disrupted wall can cause turbulent blood flow.
 The cerebral arteries and the aorta are the typical sites for aneurysms other sites are
abdominal aortic aneurysms.
Epidemiology
 is found in 5% to 7% persons older than the age of 60 years.
 Rupture of AAA causes 15000 deaths each year.
 Females to males 3-8 fold higher risk.
 Twice prevalent in Caucasians compared to African Americans.
 Elderly white males older than age 80 years with risk factors for heart disease have
highest incidence of AAA.
 Cerebral aneurysms are more common in African Americans than Caucasians.
 2% of strokes are caused by ruptured cerebral aneurysms.
Etiology
 Aneurysms are usually the result of damage to the artery lining from arteriosclerosis.
 May also be caused by degenerative vascular disease, infection, collagen vascular disease
or trauma.
 True aneurysm involves three layers of vessel wall.
 False aneurysm is a hematoma where the clot is actually outside the artery wall.
 Aneurysm shape include fusiform and saccular.
 A fusiform aneurysm occurs when all the layers of blood vessel wall dilate together.
 Saccular aneurysm occurs when there is weakness on only one side of the vessel within a
pouchlike bulge.
 Cerebral aneurysm (berry aneurysm) are commonly small, berrylike outpouchings off the
circle of willis with a subarachnoid space.
 There is properly a genetic predisposition to the development of intracerebral aneurysms,
the existence in some families run as high as 10% approximately 10 times higher than
that found in general population.
 Two gene mutations, fibrillin-1, located on chromosome 15, and myofibril associated
protein 5, located on chromosome 12, cause the faulty structural integrity of the aortic
wall in familial aortic aneurysm.
 Risk for cerebral aneurysm has been observed in carriers of the ADAMTS2. Variant gene
codes for defective structural components in the endothelium of cerebral arteries.

Risk factors
  Atherosclerosis, smoking, HTN (contract force against the walls) are major risk factors
for the formation and rupture of aneurysm.
 Genetic factors
 Connective tissue disorders such as marfan’s syndrome and Ehlers Danlos syndrome
increase risk of aortic aneurysm.
Pathophysiology
 In aneurysm, a region of arterial wall bulges and contain an uneven surface
 The wall becomes weaker as blood flows against it and blood can collect within it.
 During the formation of the aneurysm blood can enter the bulging pouch in the wall
and become stagnant and turbulent.
 The stagnant blood inside the aneurysm can give rise to platelet aggression and result
in thrombus development.
 The thrombi embolizes to other organs, they can lodge in small arterial vessels and
cause ischemia, necrosis or gangrene of other organs.
 Aneurysm are classified by their size, shape and location.

Clinical presentation
 Depends on the size, location and integrity.
 Aortic aneurysm tend to develop gradually with 75% undetected until it ruptures
 Rupture may be first sign of AAA.
 Symptoms: abdominal pain, flank, back pain, can put pressure on adjacent organs,
nausea, vomiting, bowel, ureteral compression symptoms.
 If the cerebral aneurysm are large they can put pressure on adjacent tissues such as
cranial nerves.
 Rupture of cerebral aneurysm causes SAH and classic symptom is very serve
headache. SAH are fatal.
 No sound should be heard if the blood flow is smooth
 Large aneurysm causes turbulent blood flow heard as a bruit.
 In thing patients AAA may be detected by palpations of the abdomen
 A pulsatile mass may be found in someone with scaphoid abdomen.
 With rupture circulation to the lower extremities with diminish resulting in cool, pale
extremities with diminished or absent pulse.
 Patients will feel acute pain and go into shook.
Diagnosis
 Ultrasonography is a diagnostic test for detection and follow up of suspected AAA.
 Ultrasound can indicate the size,, location and progression of the AAA.
 Xray only shows a silhouette.
  CT scan provides detailed information on the size and location of an aneruysm but
requires a contrast medium.
Treatment
 Smoking cessation and reduction in the bp and blood volume.
 Periodic follow up is needed to assess progression and susceptibility to rupture.
 AAA are not usually operated on until the aortic diameter exceeds 4.5cm.
 Surgery: endovascular repair with graft and stent placement.
 Cerebral aneurysms, microsurgical and endovascular procedures aim to impede the
blood flow from the cerebral circulation into the aneurysm.
Insert a clip, coil or band around the aneurysm.
The effects of blood composition on arteries
 The endothelial lining of the arteries consists of metabolically active cells that are
influenced by the constituents of the bloodstreams.
 Common constituents of blood include lipids, glucose and free radicals.
Lipids (70mg/dl)
 Lipids are fats that circulate in the bloodstream and make up the cell membranes in the
body.
 Lipids are mainly composed of cholesterol, a fatty steroidal substance that is ingested
from the diet and synthesized by the liver.
 Cholesterol assist the cell membrane:
- Assist in the maintenance of proper membrane permeability.
- Important component in the body’s hormonal systems for the manufacture of bile
acids, steroid hormones and vitamin D.
 Cholesterol is ingested via animal products, such as meat, milk, butter and cheese; it is
insoluble in blood but is carried by proteins to form soluble lipoproteins.
 There are different types of lipoproteins some contain cholesterol and others contain
triglycerides.
 Triglycerides are large lipid molecules acquired through diet and stores as fat tissues.
 Lipoproteins are classified by size and lips content into low density lipoprotein(ldl) and
high density lipoprotein(hdl)
 Hdl( less than 100 mg/dl) is excreted from the body which is why it is considered ‘good’
cholesterol.
 Ldl (70 mg/dl) is deposited on artery walls which is why it is considered ‘bad’
cholesterol. The deposition occurs at areas of endothelial injury where inflammation is
occurring.
 Wbc phagocytose the LDL and form lipid laden macrophages called foam cells; the foam
cells is the preliminary change in the endothelium that leads to larger collections of fat,
inflammatory mediators and platelets called atherosclerotic plaque.
Electrocardiogram
 Is the recording of the electrical activity of the heart that can be measured from certain
points of the body.
 Electrodes can be placed on the skin and an electrical current will project a pattern on a
graph depicting the phases of resting potential, Depolarization, plateau and
repolarization.
 Points designated as P,Q,R,S and T represents different points within the phases of action
potential generated by cardiac muscle.
 P wave= represents SA node and Atrial depolarization.
 QRS= complex represents ventricular depolarization
 T wave represents ventricular repolarization.
 The horizontal axis of the ECG measures time and seconds
 Vertical axis measures amplitude of the impulse in millivolts (mv)
 The ECG records the potential difference in charge between two electrodes as the
depolarization and repolarization waves move through the heart.
 The shape of the tracing is determined by the direction in which the pulse spreads
through the heart in relation to the electrode placement.
 A depolarization wave that moves towards the electrode registers positive or upward
deflection.
 A depolarization wave that moves away from the electrode registers negative or
downward deflection.
 12 leads are recorded for ECG each providing a view of the heart’s electrical forces from
different position on the body.
Dressler’s syndrome
 Dressler syndrome is the hypersensitivity reaction to the tissue necrosis of MI.
 Dressler’s syndrome includes pericarditis pleuritis and pneumonitis and is treated with
anti-inflammatory agents
 Is characterized as the deposition of immune complexes, causing inflammation and fluid
accumulation in the pericardial sac.

Preload
 Heart failure is a clinical condition commonly resulting from a weakened ventricular
muscle that is unable to sufficiently pump blood to meet the needs of the tissue.
 Left ventricular ejection fraction (LVEF) which is percentage of blood out of the left
ventricle with each contraction.
 Preload is the volume of blood in the heart at the end of diastole
 Preload factors affect ventricle output before contraction.
 Preload refers to the volume of blood that enter the right atrium from the venous system.
  Excessive venous return can overload a weakened ventricle resulting in decreased cardiac
output and leading to heart failure.
Afterload
 Can be describes as the amount of resistance that the ventricle must overcome in order to
pump blood out of the heart.
 The greater the pulmonary vascular resistance the greater the afterload against the right
ventricle.
 Heart failure is diagnosed by the
o The contractility and stoke volume decreases

Acute versus chronic heart failure

 Acute heart failure describes the rapid sudden development of heart failure that is often
caused by substantial ventricular muscle injury as in Massive MI.
 Sudden serve shock is often referred to as cardiogenic shock occurs when there is
significant loss of ventricle ability to pump enough blood to maintain optimal blood
pressure within the body occurs also of extensive MI.
 Chronic heart failure is more common disorder, where the heart gradually suffers
weakening over a long period.
Central venous pressure levels
 pressure is an assessment of venous return, blood volume and, indirectly, of
cardiac output.
o “the normal range for central venous pressure is 1 to 5 mm Hg”

Framingham criteria for diagnosing congestive heart failure

 Major criteria
- Paroxysmal nocturnal dyspnea
- Jugular vein distension
- Auscultation of s3 heart sound
- Increased cvp (greater than 16cm h20)
 Minor criteria
- Bilateral extremity edema
- Nighttime cough
- Dyspnea on exertion
- Hepatomegaly
- Pleural effusion
- Reduced pulmonary vital
- Tachycardia (120 beats/ min or greater)
At least one of the major criteria and two of the minor criteria should be present from
Framingham criteria for diagnosis of heart failure.
Anatomy and function of cardiac calves
 Mitral and tricuspid valves are located between the atria and ventricles.
 Attached to myocardium via support structures called chordae tendineae and papillary
muscles.
First and second heart sound
 the first heart sound (s1) and the second heart sound (s2) are vibrations transmitted
through the chest wall that are caused by the closure of the heart valves.
 Referred to as sounding audibly as “lub-dub”
 Closure of the mitral and tricuspid valve is s1
 Closure of the aortic and pulmonic valve is s2
 During systole, as ventricle contacts, the mitral and tricuspid valves closes creating s1.
 During diastole as the ventricle fill with blood from the atria the aortic and pulmonic
valve close creating s2
 Deep inspiration is referred to as an audible a2 and p2 a split s2
 A2 refers to aortic closure.
 P2 refers to pulmonic valve closure.
The third heart sound
 The vibration of blood as it flows from the atria into the ventricles.
 S3 gallop om older adults decreased ventricular muscle elasticity (heart failure)
Fourth heart sound
 Atrial contraction may be auscultated as a fourth heart sound.
 Occurs when the left atrium contracts against a noncompliant, stiff left ventricle
 Associated with hypertension causes left ventricular hypertrophy that creates stuff left
ventricle.
Heart murmurs
 Are sounds transmitted through the chest wall heard with a stethoscope caused by
turbulent blood flow through the heart or great vessels.
 Caused by heart valves deformity, valve dysfunction or defects in the heart wall.
Two types of heart murmurs
 Two type of heart murmurs are pathological and physiological
 Physiological heart murmurs sometimes called innocent or functional heart murmurs are
heard in states of high blood flow within the heart.
 Causes : anxiety, stress, fever, anemia, overactive thyroid and pregnancy.
 They are faint intermittent occur small area of the chest and usually do not cause
symptoms.
  Pathological heart murmurs are sounds caused by abnormalities of the heart that include
valvular deformities, valvular dysfunction and heart wall defects.
 Shortness of breath, dizziness, chest pains or palpations

Heart sounds in hypertrophic cardiomyopathy

 is a disease in which the heart muscle becomes abnormally thick (hypertrophied).
The thickened heart muscle can make it harder for the heart to pump blood.
 Interventricular septum is disproportionately enlarged, the left ventricle is
eccentrically hypertrophied and the anterior mitral leaflet opens against the enlarged
septum, creating an obstructed outflow of blood from the ventricle into the aorta.
 Signs and symptoms are commonly asymptomatic, atrial fibrillation, premature
ventricular contractions, ventricular tachycardia, ventricular fibrillation can occur
 Chest pain and fatigue
Findings
 Harsh diamond shaped systolic murmur; begins after s1 at the lower left sternal border
and apnex.
 Ejection of blood flow is usually impeded until late in systole; therefore the murmur
occurs after s1.
 If atrial fibrillation is present, irregular pulse, palpations, dyspnea on exertion, dizziness
can occur.
Diagnosis
 Echocardiogram shows an enlarged interventricular septum, left ventricular hypertrophy.
 A 48 hour holter ECG needed to check for ventricular dysrhythmias.
 MRI or CT scan
Treatment
 Surgical reduction of the interventricular septum
 Nonsurgical injectable alcohol
 Implantable cardioverter defibrillator
 Medications for angina or heat failure, beta blockers, calcium antagonist.
Greenfield filter
 Also known as an IVC filter, is often inserted to block clots from travelling up from
the lower extremity to the pulmonary circulation.
 These filter are inserted with the use of abdominal ultrasonography.
 Surgical removal of a thrombus also called thrombectomy, may be used if other
treatments prove effective
 It can prevent a DVT from becoming a PE.
 Varicose veins
 Clinical examination of the legs in the standing position reveals the regions of
varicose veins
 The duplex ultrasound which highlights the major superficial vein in the leg of the
great saphenous vein has become the most useful tool for diagnosing.
 Causes of varicose veins are:
- High pressure within the superficial veins that weaken venous valves.
- High pressure is known to occur in prolonged standing, sitting, pregnancy and
obesity.
- Higher in women than men
- Women found to be obese, have lower levels of physical activity and have systolic
blood pressure
- Sitting or standing for 8 hours
- Pregnancy
- Men: high smoking rate, lower levels of physical activities.
a. Diagnostic test for collateral blood flow: Venography