Transcript Cardiovascular System, HTN, Coronary artery disease, heart failure

Zoya Minasyan, RN, MSN-Edu
Arrows indicate direction of flow.
1, The right atrium receives venous blood from the inferior and superior vena cava and the coronary sinus. The blood then
passes through the tricuspid valve into the right ventricle.
2, With each contraction, the right ventricle pumps blood through the pulmonic valve into the pulmonary artery and to the
lungs.
3, Oxygenated blood flows from the lungs to the left atrium by way of the pulmonary veins.
4, It then passes through the mitral valve and into the left ventricle.
5, As the heart contracts, blood is ejected through the aortic valve into the aorta and thus enters the systemic circulation.
Anatomic structures of the heart and heart valves.
Coronary arteries and veins.
Location of pain during angina or myocardial infarction.
Common sites for palpating arteries.
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Systole: Contraction of myocardium
Diastole: Relaxation of myocardium
Cardiac output: Amount of blood pumped by
each ventricle in 1 minute
CO = SV × HR
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Preload
◦ Volume of blood in ventricles at the end of diastole
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Afterload
◦ Peripheral resistance against which the left ventricle
must pump
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Standard posterior-anterior view.
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Noninvasive studies
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Magnetic resonance imaging
Computed tomography
Echocardiogram
Nuclear cardiology
• MRI.
magnetic resonance imaging can detect and localize areas of
MI in a three-dimensional view and can assist in the final diagnosis
of MI. It is also plays a role in prediction of recovery from MI and in
the diagnosis of congenital heart and aortic disorders.
• Computed
Tomography Angiography (CTA)
• noninvasive scan used to quantify calcium deposits in coronary arteries.
• Electron beam computed tomography (EBCT), also known as ultrafast CT,
uses a scanning electron beam to quantify calcification in the coronary
arteries and heart valves. Currently, EBCT testing is used primarily for risk
assessment in asymptomatic patients and to assess for heart disease in
patients with atypical symptoms potentially due to cardiac causes.
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Echocardiogram. The echocardiogram uses ultrasound waves to
record the movement of the structures of the heart and provides
information about abnormalities of
 valvular structure and motion,
 cardiac chamber size and contents,
 ventricular muscle and septal motion and thickness,
 pericardial sac, and
 ascending aorta.
• Nuclear
Cardiology. One of the most common nuclear imaging
tests is the multigated acquisition (MUGA) or cardiac blood pool
scan. This test provides information on wall motion during systole
and diastole, cardiac valves, and EF.
Apical four-chamber two-dimensional echocardiographic view in a normal patient. LA, Left
atrium; LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle; TV, tricuspid
valve.
Examples of coronary calcification of the left anterior descending coronary artery (large arrow) and
left circumflex artery (small arrow) as seen on electron beam computed tomography.
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Invasive studies
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Cardiac catheterization and coronary angiography
Intracoronary ultrasound
Fractional flow reserve
Electrophysiology study
Blood flow and pressure measurements
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Cardiac Catheterization. It provides information about CAD, coronary spasm, congenital and
valvular heart disease, and ventricular function. Cardiac catheterization is also used to measure
intracardiac pressures and O2 levels, as well as CO and EF.
Intracoronary Ultrasound.(ICUS), also known as intravascular ultrasound (IVUS), is an invasive
procedure performed in the catheterization laboratory in conjunction with coronary
angiography. The 2-D or 3-D ultrasound images provide a cross-sectional view of the arterial
walls of the coronary arteries.
Fractional Flow Reserve.(FFR) is a procedure that is done during a cardiac catheterization. It
involves using a special wire that can measure pressure and flow in the coronary artery.
Electrophysiologic Study.(EPS) is the direct study and manipulation of the electrical activity of
the heart using electrodes placed inside the cardiac chambers. It provides information on SA
node function, AV node conduction, and ventricular conduction.
Blood Flow and Pressure Measurements.
• Peripheral Vessel Blood Flow. Duplex imaging is useful in the diagnosis of occlusive
disease in the peripheral blood vessels and for the diagnosis of thrombophlebitis.
Peripheral vessel blood flow is assessed by injecting contrast media into the appropriate
arteries or veins (arteriography or venography).
• Hemodynamic Monitoring. Bedside hemodynamic monitoring of pressures of the
cardiovascular system is frequently used to assess cardiovascular status and monitor
patient response to interventions. Invasive hemodynamic monitoring using intraarterial
and pulmonary artery catheters can be used to monitor arterial BP, intracardiac pressures,
and CO.
Normal left coronary artery angiogram.
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Question
A patient arrives at an urgent care center after experiencing
unrelenting substernal and epigastric pain and pressure for
about 12 hours. The nurse reviews laboratory results with the
understanding that at this point in time, a myocardial
infarction would by indicated by peak levels of:
1. Troponin T.
2. Homocysteine.
3. Creatine kinase-MB.
4. Type b natriuretic peptide.
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Troponin is the biomarker of choice in the diagnosis of
myocardial infarction. Troponin is a myocardial muscle
protein released into the circulation within 1 hr after
injury. Troponin levels peak at 10 to 24 hours.
When Myocardial cells are injured, they release their
content, including enzymes and other proteins, into the
circulation
◦ Enzymes called creatine kinase (CK); lactate dehdrogenaze-(LDH);
and serum aspartate aminotransferase (AST) formally called
glutamic-oxaloacetic transaminase (SGOT)
◦ CK is present in heart ,brain and skeletal muscles
◦ CK-MM primarily in skeletal muscle
◦ CK-BB brain and nervous tissue
◦ Ck-MB specific for myocardial injury;
 It rises in 4-6 after onset, peak in 18-24 hr
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Age alters the cardiovascular response to
physical and emotional stress.
Heart valves become thick and stiff.
Frequent need for pacemakers
Less sensitive to β-adrenergic agonist drugs
Increase in SBP; decrease or no change in DBP
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Persistent elevation of
◦ Systolic blood pressure ≥140 mm Hg
OR
Diastolic blood pressure ≥90 mm Hg
OR
◦ Current use of antihypertensive medication(s)
◦ Table 33-6 page 769
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Normal
<120and <80
Prehypertension
120-139 and 8089
Stage one hypertention 140-159 and 90-99
Stage 2 hypertention
>or=160 and
>or=100
Systemic
Blood
Cardiac
=
× Vascular
Pressure
Output
Resistance
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Primary (essential) hypertension
◦ Contributing factors
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↑ SNS activity
↑ Sodium-retaining hormones and vasoconstrictors
Diabetes mellitus
> Ideal body weight
↑ Sodium intake
Excessive alcohol intake
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Secondary hypertension
◦ Contributing factors
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Aortic abnormalities
Renal disease
Endocrine disorders
Neurologic disorders
Cirrhosis
Sleep apnea
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Age
Alcohol
Cigarette smoking
Diabetes mellitus
Elevated serum lipids
Excess dietary sodium
Gender
Family history
Obesity
Ethnicity
Sedentary lifestyle
Socioeconomic status
Stress
Hypertension develops when one or more of the BP regulating mechanisms are defective.
EDRF, Endothelium-derived relaxing factor.
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Insulin resistance and hyperinsulinemia
◦ High insulin concentration stimulates SNS activity and
impairs nitric oxide–mediated vasodilation
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Stress and increased SNS activity
◦ Produce increased vasoconstriction
◦ ↑ HR
◦ ↑ Renin release(first-vasoconstrictor, second -can cause
the stimulation of aldosterone which causes Na and H2O
retention)
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Altered renin-angiotensin mechanism: High
plasma renin activity
Endothelial cell dysfunction
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Water and sodium retention
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◦ High sodium intake may activate a number of pressor
mechanisms, resulting in water retention.
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Target organ diseases occur most frequently
in the
◦ Heart
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Brain- Cerebrovascular disease-Stroke
Peripheral vasculature
Kidney: Nephrosclerosis
Eyes Retinal damage
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Lifestyle modifications
◦ Weight reduction: Weight loss of 10 kg
(22 lb) may decrease SBP by approx 5 to
20 mm Hg
◦ Dietary sodium reduction: <2300 mg of sodium/day
◦ Moderation of alcohol consumption:
 Men: No more than 2 drinks/day
 Women: No more than 1 drink/day
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Physical activity: Regular physical (aerobic) activity, at least 30 minutes,
most days of the week
◦ Avoidance of tobacco products
◦ Psychosocial risk factors
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Drug therapy: Classifications of drugs used to treat hypertension
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Diuretics
Adrenergic inhibitors
Direct vasodilators
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Calcium channel blockers
Question
A patient’s blood pressure has not responded
consistently to prescribed medications for
hypertension. The first cause of this lack of
responsiveness the nurse should explore is:
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4.
Progressive target organ damage.
The possibility of drug interactions.
The patient not adhering to therapy.
The patient’s possible use of recreational drugs.
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Severe increase in BP (>220/140)
Often occurs in patients with a history of HTN
who have failed to comply with medications
or who have been undermedicated
Hypertensive emergency = Evidence of acute
target organ damage:
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Hypertensive encephalopathy, cerebral hemorrhage
Acute renal failure
Myocardial infarction
Heart failure with pulmonary edema
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Hospitalization
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IV drug therapy
Monitor cardiac and renal function
Neurologic checks
Determine cause
Education to avoid future crises
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Atherosclerosis: Type of blood vessel disorder
◦ Begins as soft deposits of fat that harden with age
◦ Referred to as “hardening of arteries”
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Greek words: athere, meaning “fatty mush,” and
skleros, meaning “hard.”
Terms to describe the disease process
 Arteriosclerotic heart disease
 Cardiovascular heart disease
 Coronary artery disease (CAD)
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Atherosclerosis is the major cause of CAD.
◦ Characterized by a focal deposit of cholesterol and
lipid, primarily within the intimal wall of the artery
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Endothelial lining altered as a result of
inflammation and injury
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C-reactive protein (CRP)
◦ Nonspecific marker of inflammation
◦ Increased in many patients with CAD
◦ Chronic exposure to CRP associated with unstable
plaques and oxidation of LDL cholesterol
A, Damaged endothelium.
B, Diagram of fatty streak and lipid core formation.
C, Diagram of fibrous plaque. Raised plaques are visible: some are yellow, others are white.
D, Diagram of complicated lesion: thrombus is red, collagen is blue. Plaque is complicated by
red thrombus deposition.
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Developmental stages:
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Fatty streaks
◦ Earliest lesions
◦ Characterized by lipid-filled smooth muscle cells
◦ Potentially reversible
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Fibrous plaque
◦ Beginning of progressive changes in the arterial wall
◦ Lipoproteins transport cholesterol and other lipids into
the arterial intima.
◦ Fatty streak is covered by collagen, forming a fibrous
plaque that appears grayish or whitish.
◦ Result = Narrowing of vessel lumen
Complicated lesion
◦ Continued inflammation can result in plaque instability,
ulceration, and rupture.
◦ Platelets accumulate and thrombus forms.
◦ Increased narrowing or total occlusion of lumen
◦ Modifiable risk factors
 Elevated serum lipids
 Hypertension
 Tobacco use
 Physical inactivity
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Non modifiable risk factors
 Age
 Gender
 Ethnicity
 Family history
 Genetic predisposition
• Serum
cholesterol level greater than 200 mg/dL (5.2 mmol/L) or a
fasting triglyceride level greater than 150 mg/dL (3.7 mmol/L).
• Hypertension,
which is defined as a BP > 140/90 mm Hg or
>130/80 mm Hg if the patient has diabetes or chronic kidney
disease.
• Tobacco
use. tobacco smoking decreases estrogen levels, placing
premenopausal women at greater risk for CAD. Risk is
proportionate to the number of cigarettes smoked.
• Physical
inactivity
• Obesity
is defined as a body mass index (BMI) of >30 kg/m2 and a
waist circumference ≥40 inches for men and ≥35 inches for
women.
•2
to 4 times greater among persons who have diabetes.
• Specific
psychological risk factors thought to increase risk of CAD.
These include depression, acute and chronic stress, anxiety,
hostility and anger, and lack of social support.
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Health-promoting behaviors
◦ Physical fitness
 30 minutes >5 days/week
 Regular physical activity contributes
to
 Weight reduction
 Reduction of >10% in systolic BP
 In some men more than women,
increase in HDL cholesterol
•Therapeutic
lifestyle changes include
•a decrease in saturated fat and cholesterol and an
increase in complex carbohydrates (e.g., whole
grains, fruit, vegetables).
• Fat intake should be about 30% of calories, with
most coming from monounsaturated fats found in
nuts and oils such as olive or canola oil.
•For
individuals without CAD, the AHA
recommends eating
•fatty fish twice a week because fatty fish such as
salmon and tuna contain two types of omega-3 fatty
acids: Eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA). Patients with CAD are
encouraged to take EPA and DHA supplements with
their diet.
• tofu, other forms of soybean, canola, walnut, and
flaxseed, because these products contain alpha-
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Health-promoting behaviors
◦ Antiplatelet therapy
 ASA
 Clopidogrel (Plavix)
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Etiology and pathophysiology
◦ Reversible (temporary) myocardial ischemia = Angina (chest
pain)
◦ O2 demand > O2 supply
◦ Primary reason for insufficient blood flow is narrowing of
coronary arteries by atherosclerosis.
◦ Referred pain in left shoulder and arm is from transmission
of the pain message to the cardiac nerve roots.
◦ Intermittent chest pain that occurs over a long period with
the same pattern of onset, duration, and intensity of
symptoms
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Pain usually lasts 3 to 5 minutes.
Subsides when the precipitating factor is relieved
Pain at rest is unusual.
ECG reveals ST-segment depression and/or T-wave
inversion.
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Silent ischemia
◦ Ischemia that occurs in the absence of any
subjective symptoms
◦ Associated with diabetic neuropathy
◦ Confirmed by ECG changes
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Nocturnal angina
◦ Occurs only at night but not necessarily during
sleep
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Angina decubitus
◦ Chest pain that occurs only while lying down
◦ Relieved by standing or sitting
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Prinzmetal’s (variant) angina
◦ Occurs at rest usually in response to spasm of major
coronary artery
◦ Seen in patients with a history of migraine headaches and
Raynaud’s phenomenon
◦ Spasm may occur in the absence of CAD.
◦ May occur during REM sleep
◦ May be relieved by moderate exercise or may disappear
spontaneously
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Microvascular angina
◦ May occur in the absence of significant coronary
atherosclerosis or coronary spasm
◦ Pain is related to myocardial ischemia associated with
abnormalities of the coronary microcirculation.
 Coronary microvascular disease
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Drug therapy: Goal: ↓ O2 demand and/or ↑ O2
supply
◦ Short-acting nitrates:
 Sublingual
◦ Long-acting nitrates
 Nitroglycerin (NTG) ointment
 Transdermal controlled-release NTGβ-Adrenergic blockers
◦ Calcium channel blockers
 If β-adrenergic blockers are poorly tolerated,
contraindicated, or do not control angina
 Used to manage Prinzmetal’s angina
◦ Angiotensin-converting enzyme inhibitors
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Diagnostic studies
◦ Health history/physical examination
◦ Laboratory studies
◦ 12-lead ECG
◦ Chest x-ray
◦ Echocardiogram
◦ Exercise stress test
◦ Cardiac catheterization/coronary angiography
 Coronary revascularization: Percutaneous
coronary intervention (PCI)
 Balloon angioplasty
 Stent
Fig. 34-6. Placement of a coronary artery stent. A, The stent is positioned at the site of the lesion.
B, The balloon is inflated, expanding the stent. The balloon is then deflated and removed. C,
The implanted stent is left in place.
Fig. 34-7. A, A thrombotic occlusion of the right coronary artery is noted (arrows). B, Right
coronary artery is opened and blood flow restored following angioplasty and placement of a
4-mm stent.
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When ischemia is prolonged and is not
immediately reversible, acute coronary syndrome
(ACS) develops.
Clinical Manifestations of ACS
◦ Unstable Angina
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Change in usual pattern
New in onset
Occurs at rest
Has a worsening pattern
◦ UA is unpredictable and represents a medical
emergency.
◦ Result of sustained ischemia (>20 minutes), causing
irreversible myocardial cell death (necrosis)
◦ Necrosis of entire thickness of myocardium takes 4 to 6
hours.
Fig. 34-10. Acute myocardial infarction in the postero-lateral wall of the left ventricle. This is
demonstrated by the absence of staining in the areas of necrosis (white arrow). Note the
scarring from a previous anterior wall myocardial infarction (black arrow).
Fig. 34-11. Myocardial infarction involving the full thickness
of the left ventricular wall.
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The degree of altered function depends on the
area of the heart involved and the size of the
infarct.
Contractile function of the heart is disrupted in
areas of myocardial necrosis.
Most MIs involve the left ventricle (LV).
Pain
◦ Total occlusion → Anaerobic metabolism and lactic acid
accumulation → Severe chest pain not relieved by rest,
position change, or nitrate administration
◦ Described as heaviness, constriction, tightness, burning,
pressure, or crushing
◦ Common locations: Substernal, retrosternal, or
epigastric areas; pain may radiate to neck, jaw, arms
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Cardiovascular
◦ Initially, ↑ HR and BP, then ↓ BP (secondary to ↓ in CO)
◦ Crackles, Jugular venous distention
◦ Abnormal heart sounds
 S3 or S4, murmur
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Nausea and vomiting
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Fever
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Stimulation of sympathetic nervous system results in
◦ Can result from stimulation of the vomiting center by
severe pain
◦ Systemic manifestation of the inflammatory process caused
by cell death
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Release of glycogen
Diaphoresis
Vasoconstriction of peripheral blood vessels
Skin: Ashen, clammy, and/or cool to touch
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Within 24 hours, leukocytes infiltrate the area
of death cell.
Enzymes are released from the dead cardiac
cells (important indicators of MI).
Proteolytic enzymes of neutrophils and
macrophages remove all necrotic tissue by
second or third day.
10 to 14 days after MI, scar tissue is still
weak and vulnerable to stress.
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Heart failure
◦ pumping power of the heart diminished
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Cardiogenic shock
◦ Occurs when inadequate oxygen and nutrients are supplied to the
tissues because of severe LV failure
Papillary muscle dysfunction
◦ Causes mitral valve regurgitation
Ventricular aneurysm
◦ Results when the infarcted myocardial wall becomes thinned and
bulges out during contraction
Dysrhythmias
◦ Most common complication
◦ Present in 80% of MI patients
◦ Most common cause of death in the prehospital period
◦ Life-threatening dysrhythmias seen most often with anterior MI,
heart failure, or shock
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Acute pericarditis
◦ An inflammation of visceral and/or parietal
pericardium
◦ May result in cardiac compression, ↓ LV filling and
emptying, heart failure
◦ Pericardial friction rub may be heard on
auscultation.
◦ Chest pain different from MI pain
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Coronary surgical revascularization
◦ Coronary artery bypass graft (CABG) surgery
 Requires sternotomy and cardiopulmonary bypass
(CPB)
 Uses arteries and veins for grafts
◦ Minimally invasive direct coronary artery bypass
(MIDCAB)
 Alternative to traditional CABG
Distal end of the left internal mammary artery is grafted below the area of blockage in the
left anterior descending artery. Proximal end of the saphenous vein is grafted to the aorta and the distal
end is grafted below the area of blockage in the right coronary artery.
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Drug therapy
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IV nitroglycerin
Morphine sulfate
β-Adrenergic blockers
Angiotensin-converting enzyme inhibitors
Antidysrhythmia drugs
Cholesterol-lowering drugs
Stool softeners
Nutritional therapy
◦ Initially NPO
◦ Progress to
 Low salt
 Low saturated fat
 Low cholesterol
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Nursing diagnoses
◦ Acute pain
◦ Risk for decreased cardiac tissue perfusion
◦ Anxiety
◦ Activity intolerance
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Acute interventions for anginal attack
Administration of supplemental oxygen
Assess vital signs, pulse oximetry.
12-lead ECG
Prompt pain relief first with a nitrate followed by an
opioid analgesic, if needed
◦ Auscultation of heart sounds
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Acute intervention
 Pain: Nitroglycerin, morphine, oxygen
 Continuous monitoring
 ECG
 VS, pulse oximetry
 Heart and lung sounds
 Rest and comfort
 Balance rest and activity.
 Begin cardiac rehabilitation.
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Abrupt disruption in cardiac function, resulting
in loss of CO and cerebral blood flow
Death usually within 1 hour of onset of acute
symptoms (e.g., angina, palpitations)
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Primary risk factors
◦ Left ventricular dysfunction (EF 30%)
◦ Ventricular dysrhythmias following MI
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Rapid CPR, and early advanced cardiac life
support increase survival rates
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An abnormal condition involving impaired cardiac
pumping/filling
Heart is unable to produce an adequate cardiac
output (CO) to meet metabolic needs.
Primary risk factors
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Contributing risk factors
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◦ CAD
◦ Advancing age
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Hypertension
Diabetes
Tobacco use
Obesity
High serum cholesterol
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Left-sided HF (most common) from left
ventricular dysfunction (e.g., MI hypertension,
CAD, cardiomyopathy)
◦ Backup of blood into the left atrium and pulmonary veins
 Pulmonary congestion
 Edema
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Right-sided HF from left-sided HF, right
ventricular MI
◦ Backup of blood into the right atrium and venous
systemic circulation
 Jugular venous distention
 Hepatomegaly, splenomegaly
 Vascular congestion of GI tract
 Peripheral edema
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Fatigue
Dyspnea, orthopnea, paroxysmal nocturnal
dyspnea
Persistent, dry cough, unrelieved with
position change or over-the-counter cough
suppressants
Tachycardia
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Oxygen administration
Physical and emotional rest
Nonpharmacologic therapies
◦ Cardiac resynchronization therapy (CRT) or
biventricular pacing
◦ Cardiac transplantation
◦ Intraaortic balloon pump (IABP) therapy
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Therapeutic goals for drug therapy
◦ Identification of type of HF and causes
◦ Correction of sodium and water retention and volume overload
◦ Reduction of cardiac workload
◦ Improvement of myocardial contractility
◦ Control of precipitating and complicating factors
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Drug therapy
◦ Diuretics
 Thiazide ,Loop, Spironolactone ACE inhibitors , Angiotensin II receptor
blockers , Aldosterone antagonists, Nitrates , -Adrenergic blockers
Positive inotropic agents
 Digitalis, Calcium sensitizers, BiDil (combination drug containing
isosorbide dinitrate and hydralazine)
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Nutritional therapy
◦ Diet and weight reduction: Individualize
recommendations and consider cultural background
◦ Recommend Dietary Approaches to Stop Hypertension
(DASH) diet.
◦ Sodium is usually restricted to 2.5 g per day.
◦ Fluid restriction not generally required
◦ Daily weights are important
 Same time, same clothing each day
◦ Weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb
(2.3 kg) gain over a week should be reported to health
care provider.
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Acute intervention
◦ Salt must be restricted.
◦ Energy must be conserved.
◦ Support systems are essential to the success of the entire treatment plan.
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Implementation: Patient education
◦ Medications (lifelong)
◦ Taking pulse rate
◦ Know when drugs (e.g., digitalis, -adrenergic
blockers) should be withheld and reported to health
care provider.
◦ Home BP monitoring
◦ Signs of hypokalemia and hyperkalemia if taking diuretics that deplete or
spare potassium
◦ Instruct patient in energy-conserving and energy-efficient behaviors.
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Treatment of choice for patients with refractory
end-stage HF, inoperable CAD, and
cardiomyopathy
Goal of the transplant evaluation process is to
identify patients who would most benefit from a
new heart.
Transplant candidates are placed on a list.
◦ Stable patients wait at home and receive ongoing
medical care.
◦ Unstable patients may require hospitalization for more
intensive therapy.
◦ Overall waiting period for a heart is long; many patients
die during this time.
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Bridge to transplantation devices
Surgery involves removing the recipient’s heart,
except for the posterior right and left atrial walls
and their venous connections.
Recipient’s heart is replaced with the donor
heart.
Donor sinoatrial (SA) node is preserved so that a
sinus rhythm may be achieved postoperatively.
Immunosuppressive therapy usually begins in the
operating room.
Infection is the primary complication, followed
by acute rejection, in the first year after
transplantation.
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Nursing care focuses on
◦ Promoting patient adaptation to the transplant
process
◦ Monitoring cardiac function
◦ Managing lifestyle changes
◦ Providing relevant teaching
Take a break
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Involves progressive narrowing and degeneration
of arteries of neck, abdomen, and extremities
Atherosclerosis is the leading cause in majority
of cases.
Typically appears at ages 60s to 80s
Largely undiagnosed
Risk factors
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Cigarette smoking
Hyperlipidemia
Hypertension
Diabetes mellitus
Common anatomic locations of atherosclerotic lesions
(shown in yellow) of the abdominal aorta and lower extremities.
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Classic symptom of PAD—intermittent
claudication
◦ Ischemic muscle ache or pain that is precipitated by
a constant level of exercise
◦ Resolves within 10 minutes or less with rest
intermittent claudication (muscle pain (ache, cramp,
numbness or sense of fatigue),classically in the calf
muscle, which occurs during exercise and is
relieved by a short period of rest)
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Paresthesia
◦ Numbness or tingling in the toes or feet
◦ Produces loss of pressure and deep pain sensations
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Injuries often go unnoticed by patient
Thin, shiny, and taut skin
Loss of hair on the lower legs
Diminished or absent pedal, popliteal, or
femoral pulses
Pallor of foot with leg elevation
Pain at rest
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Occurs in the forefoot or toes
Aggravated by limb elevation
Occurs from insufficient blood flow
Occurs more often at night
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Atrophy of the skin and underlying muscles
Delayed healing
Wound infection
Tissue necrosis
Arterial ulcers
Non healing arterial ulcers and gangrene are
most serious complications.
May result in amputation if blood flow is not
adequately restored, or if severe infection
occurs
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Smoking cessation, including use of nicotine
products
Aggressive treatment of hyperlipidemia
BP maintained <140/90
Glycosylated hemoglobin <7.0% for diabetics
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ACE inhibitors
◦ Ramipril (Altace)
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cardiovascular morbidity
mortality
peripheral blood flow
ABI
walking distance
Drugs prescribed for treatment of intermittent claudication
◦ Pentoxifylline (Trental)
 ↑ erythrocyte flexibility
 ↓ blood viscosity
◦ Cilostazol (Pletal)
 ↑ vasodilation
 ↑ walking distance
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Antiplatelet agents
◦ Aspirin(81-325 mg)
◦ Clopidogrel (Plavix)
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Exercise Therapy
◦ Exercise improves oxygen extraction in the legs
and skeletal metabolism.
 Walking is the most effective exercise
 30 to 60 minutes daily
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Nutritional Therapy
◦ BMI < 25 kg/m2
◦ Waist circumference <40 inches for men and <35
inches for women
◦ Dietary cholesterol <200 mg/day
◦ Decreased intake of saturated fat
◦ Sodium <2 g/day
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Revascularization via surgery
Protect from trauma
Reduce vasospasm
Prevent/control infection
Maximize arterial perfusion
Hyperbaric oxygen therapy
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Indications
◦ Intermittent claudication symptoms become
incapacitating.
◦ Pain at rest
◦ Ulceration or gangrene severe enough to threaten
viability of the limb
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Percutaneous transluminal balloon angioplasty
◦ Involves the insertion of a catheter through the femoral
artery
◦ Catheter contains a cylindrical balloon.
◦ Balloon is inflated dilating the vessel by cracking the
confining atherosclerotic intimal shell.
◦ Stent is placed.
A peripheral artery bypass operation with autogenous vein or synthetic graft material
to bypass blood around the lesion
A, Femoral-popliteal bypass graft around an occluded superficial femoral artery.
B, Femoral-posterior tibial bypass graft around occluded superficial femoral, popliteal, and
proximal tibial arteries.
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Acute intervention
◦ Frequently monitor after surgery.
 Skin color and temperature
 Capillary refill
 Presence of peripheral pulses distal to
the operative site
◦ Sensation and movement of extremity
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Continued circulatory assessment
Monitor for potential complications.
Knee-flexed positions should be avoided except for
exercise.
Turn and position frequently
Sitting for long period of time should be discouragedincrease risk for DVT
If edema-elevate the legs above the hearth level
Elastic bandages or elastic stockings are used to help
control edema
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Ambulatory and home care
Management of risk factors
Importance of meticulous foot care
Importance of gradual physical activity after surgery
Daily inspection of the feet
Comfortable shoes with rounded toes and soft
insoles
◦ Shoes lightly laced
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Question
A patient with peripheral vascular disease has
marked peripheral neuropathy. An appropriate
nursing diagnosis for the patient is:
1. Risk for injury related to decreased sensation.
2. Impaired skin integrity related to decreased
peripheral circulation.
3. Ineffective peripheral tissue perfusion related to
decreased arterial blood flow.
4. Activity intolerance related to imbalance between
oxygen supply and demand.
Question
When teaching a patient with peripheral arterial
disease, the nurse determines that further teaching
is needed when the patient says,
1. “I should not use heating pads to warm my feet.”
2. “I will examine my feet every day for any sores or
red areas.”
3. “I should cut back on my walks if they cause pain
in my legs.”
4. “I think I can quit smoking with the use of shortterm nicotine replacement and support groups.”
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Largest artery
Responsible for supplying oxygenated blood
to essentially all vital organs
Most common vascular problems of aorta
◦ Aneurysms
◦ Aorto iliac occlusive disease
◦ Aortic dissection
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Outpouchings or dilations of the arterial wall
Common problems involving aorta
Occur in men more often than in women
Incidence ↑ with age
Abdominal aortic aneurysms (AAA)
◦ Occur in 18% of men and 5% of women over 60
◦ Most occur below renal arteries.
Angiography demonstrating abdominal aortic aneurysm.
Note calcification of the aortic wall (arrows) and extension of the aneurysm
into the common iliac arteries.
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Causes
◦ Degenerative
◦ Congenital
 Familial tendency related to
abnormalities
 Ehlers-Danlos syndrome and
Marfan’s syndrome
◦ Mechanical
 Penetrating or blunt trauma
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Rupture—serious complication related to untreated
aneurysm
◦ Rupture into retroperitoneal space
 Bleeding may be tamponaded (stopping a
hemorrhage achieved by applying an absorbent
dressing directly onto a wound, creating a
blockage, or by applying direct pressure with a
hand )by surrounding structures, thus
preventing exsanguination and death.
 Severe pain
◦ May/may not have back/flank ecchymosis
◦ Rupture into thoracic or abdominal cavity
 Massive hemorrhage
 Most do not survive long enough to get to
the hospital
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Goal—prevent aneurysm from rupturing
Early detection/treatment
Once detected
◦ Studies done to determine size and location
◦ If carotid and/or coronary artery obstruction
present, may need to correct before repair
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Small aneurysm (<4 cm)
◦ Conservative therapy used
 Risk factor modification
 ↓ blood pressure
 Ultrasound, MRI, CT scan monitoring annually
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5.5 cm is threshold for repair
◦ Intervention at >5 cm in women with AAA
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Note quality and character of peripheral
pulses and neurologic status.
Mark/document pedal pulse sites and any
skin lesions on lower extremities before
surgery.
Monitor for indications of rupture.
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Diaphoresis
Paleness
Weakness
Tachycardia
Hypotension
Abdominal, back, groin, or peri-umbilical pain
Changes in level of consciousness
Pulsating abdominal mass
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Often misnamed “dissecting aneurysm”
Not a type of aneurysm
Result of a false lumen through which blood
flows
Classified by location and duration of onset
Due to degeneration of the elastic fibers in the
medial layer
◦ Tear in intimal lining allows blood to “track” between
intima and media.
◦ May occlude major branches of aorta
 Cutting off blood supply to brain,
abdominal organs, kidneys, spinal
cord, and extremities
Aortic dissection of the thoracic aorta.
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Pain characterized as
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Cardiac tamponade
◦ Sudden, severe pain in anterior part of chest, or intrascapular
pain radiating down spine to abdomen or legs
◦ Described as “sharp” and “worst ever”
◦ May mimic that of MI
◦ Severe, life-threatening complication
◦ Occurs when blood escapes from dissection into pericardial sac
◦ Clinical manifestations include
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Hypotension
Narrowed pulse pressure
Distended neck veins
Muffled heart sounds
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Aorta may rupture.
◦ Results in death
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Hemorrhage may occur in pleural, or
abdominal cavities.
Occlusion of arterial supply to vital organs
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Initial goal
◦ ↓ BP and myocardial contractility to diminish pulsatile
forces within aorta
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Drug therapy
Surgical therapy
◦ Emergency surgery for acute ascending aortic dissection
◦ When drug therapy is ineffective or when complications
of aortic dissection are present
◦ Surgery is delayed to allow edema to decrease and to
permit clotting of blood.
◦ Surgery involves resection of aortic segment and
replacement with synthetic graft material
Question
Following an aortic aneurysm repair, the patient
suddenly develops severe pain in the right lower
extremity. The right pedal pulse is decreased, and
the right foot is cool and pale. The nurse suspects:
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Hypothermia.
A wound infection.
Bleeding from the graft site.
An embolization or graft occlusion.
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Clinical manifestations: 6 Ps
◦ Pain, pallor, pulslessness, parasthesia,, paralysis,
poikilothermia( adaptation to environmental
temperature)
◦ Foot drop from nerve damage
◦ Anticoagulation therapy-IV heparin
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Etiology and pathophysiology
◦ Sudden interruption in the blood supply to tissue,
an organ, or an extremity that, if left untreated, can
result tissue death
◦ It can be cause by embolism, thrombosis of
preexisting atherosclerotic artery, or trauma.
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Non atherosclerotic, recurrent inflamatory
vaso-occlusive disorder of small and medium
sized arteries, veins, and nerves of the upper
and lower extremities
Starts with ischemia of the small, distal
arteries and veins, progressing to more
proximal arteries
Treatment
◦ smoking cessation
◦ Antiplatelet med’s
◦ Pain med’s
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Vasospastic disorder of small arteries,
involving the fingers and toes. Pt describes
coldness and numbness followed by
throbbing aching pain, tingling.
Typists, pianists; those using vibrating
equipment, exposure to heavy metals-lead;
exposure to cold; coffee, alcohol; stress,
anxiety; vasoconstrictors.
Characterized by vasospasm- color changes
of the fingers, toes, ears and nose(white, blue
than red)
 DVT is a disorder involving a thrombus in a
deep vein. Thrombi may detach and result in
emboli, PE.
◦ Three important factors(called Virchow’s triad) are
venous stasis, damage to endothelium, hyper
coagulation of the blood.
◦ Venous stasis occurs when valves are dysfunctional
or muscles are inactive.
◦ Endothelial damage occurs when external pressure,
venpuncture for IV therapy..
◦ hyper coagulation of the blood- when hematologic
disorders, cancer, brain, GI
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DVT: Collaborative care
Early mobilization-bed rest, elevation of the extremity and
anticoagulation med’s
Antiembolitic stockings(TED hose) to prevent venous
dilation-measure the size, stocking are rolled down, no
compression devices when pt has active DVT due to risk of PE.
Drug Therapy-Vit K antagonists- Warfarin(cumadin),
heparin; tissue plasminogen activator tpa (Alteplase)
Surgical therapy- Greenfield filter device inserted into veins
Inferior vena caval interruption technique using Greenfield
stainless steel filter to prevent pulmonary embolism.
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Superficial Thrombo phlebities- palpable,
cordlike, tender to the touch, reddened and
warm.
◦ Cause by vein trauma by IV therapy, infection at IV
catheter site
◦ Collaborative care- elevate the extremity to
promote venous return ant to decrease edema;
remove IV catheter, give pain med’s and treat the
inflammation
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Chronic venous insufficiency and venous leg
ulcers: Valves are damaged, pooling of blood
in the legs and swelling
Varicose veins: superficial veins in the lower
extremities become dilated.
◦ Risk factors-congenital, obesity, pregnancy,
increasing age
◦ Most common symptoms- pain after prolonged
standing which is relived by walking or elevating
limbs; nocturnal leg cramps in the calf may occur