cardiovascular system, htn, coronary artery disease, heart failure, vascular disorders
DESCRIPTION
Cardiovascular System, HTN, Coronary artery disease, heart failure, Vascular disorders. Zoya Minasyan , RN, MSN- Edu. Blood Flow Through the Heart. Arrows indicate direction of flow . - PowerPoint PPT PresentationTRANSCRIPT
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Cardiovascular System, HTN, Coronary artery disease, heart
failure, Vascular disordersZoya Minasyan, RN, MSN-Edu
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Blood Flow Through the Heart
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 thenpasses 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.
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Cardiac Valves
Anatomic structures of the heart and heart valves.
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Coronary Arteries and Veins
Coronary arteries and veins.
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Location of pain during angina or myocardial infarction.
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Common Sites for Palpating Arteries
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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 minuteCO = SV × HR
Preload◦ Volume of blood in ventricles at the end of diastole
Afterload◦ Peripheral resistance against which the left
ventricle must pump
Mechanical System
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Relationship of Electrocardiogram, Cardiac Cycle, and Heart Sounds
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Chest X-ray
Standard posterior-anterior view.
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Noninvasive studies◦ Magnetic resonance imaging◦ Computed tomography◦ Echocardiogram◦ Nuclear cardiology
Diagnostic Studies of Cardiovascular System
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• 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.
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.
Diagnostic Studies of Cardiovascular System
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Echocardiogram
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.
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Computed Tomography
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◦ Cardiac catheterization and coronary angiography◦ Intracoronary ultrasound◦ Fractional flow reserve◦ Electrophysiology study◦ Blood flow and pressure measurements
Diagnostic Studies of Cardiovascular System
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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.
Diagnostic Studies of Cardiovascular System
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Normal Left Coronary Artery Angiogram
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Normal left coronary artery angiogram.
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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.
Question
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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
Cardiac markers
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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
Gerontologic Consideration
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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
HypertensionDefinition
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Normal <120and <80 Prehypertension 120-139 and 80-
89 Stage one hypertention 140-159 and 90-99 Stage 2 hypertention >or=160 and
>or=100
BP classification
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Factors Influencing Blood Pressure (BP)
Blood Pressure
Cardiac Output
Systemic Vascular
Resistance= ×
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Primary (essential) hypertension ◦ Contributing factors
↑ SNS activity ↑ Sodium-retaining hormones and vasoconstrictors Diabetes mellitus > Ideal body weight ↑ Sodium intake Excessive alcohol intake
Etiology of Hypertension
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Secondary hypertension◦ Contributing factors
Aortic abnormalities Renal disease Endocrine disorders Neurologic disorders Cirrhosis Sleep apnea
Etiology of Hypertension
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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
Risk Factors for Primary Hypertension
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Factors Influencing BP
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 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)
Altered renin-angiotensin mechanism: High plasma renin activity
Endothelial cell dysfunction Water and sodium retention
◦ High sodium intake may activate a number of pressor mechanisms, resulting in water retention.
Pathophysiology of Primary Hypertension
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Target organ diseases occur most frequently in the◦ Heart◦ Brain- Cerebrovascular disease-Stroke◦ Peripheral vasculature ◦ Kidney: Nephrosclerosis◦ Eyes Retinal damage
HypertensionComplications
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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
• Physical activity: Regular physical (aerobic) activity, at least 30 minutes, most days of the week
◦ Avoidance of tobacco products◦ Psychosocial risk factors
Drug therapy: Classifications of drugs used to treat hypertension◦ Diuretics◦ Adrenergic inhibitors◦ Direct vasodilators◦ Angiotensin-converting enzyme inhibitors◦ Angiotensin II receptor blockers◦ Calcium channel blockers
Hypertension: Collaborative Care
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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:
1. Progressive target organ damage.2. The possibility of drug interactions.3. The patient not adhering to therapy.4. The patient’s possible use of recreational drugs.
Question
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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: ◦ Hypertensive encephalopathy, cerebral hemorrhage ◦ Acute renal failure◦ Myocardial infarction◦ Heart failure with pulmonary edema
Hypertensive Crisis
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Hospitalization◦ IV drug therapy◦ Monitor cardiac and renal function◦ Neurologic checks◦ Determine cause◦ Education to avoid future crises
Hypertensive CrisisNursing and Collaborative Management
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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”
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)
Coronary Artery Disease and Acute Coronary Syndrome
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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 Endothelial lining altered as a result of
inflammation and injury 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
Coronary Artery Disease Etiology and Pathophysiology
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Pathogenesis of Atherosclerosis
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: Fatty streaks
◦ Earliest lesions◦ Characterized by lipid-filled smooth muscle cells◦ Potentially reversible
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
Coronary Artery Disease :Etiology and Pathophysiology
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◦ Modifiable risk factors Elevated serum lipids Hypertension Tobacco use Physical inactivity
◦ Non modifiable risk factors
Age Gender Ethnicity Family history Genetic predisposition
Risk Factors for CAD
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• 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.
Risk factors
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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
Risk Factors for CADHealth Promotion
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•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-linolenic acid, which becomes omega-3 fatty acid in the body.
Risk Factors for CAD: Health Promotion
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Health-promoting behaviors◦ Antiplatelet therapy
ASA Clopidogrel (Plavix)
Risk Factors for CAD: Health Promotion
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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◦ 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.
Clinical Manifestations of CAD Chronic Stable Angina
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Silent ischemia◦ Ischemia that occurs in the absence of any
subjective symptoms ◦ Associated with diabetic neuropathy◦ Confirmed by ECG changes
Nocturnal angina◦ Occurs only at night but not necessarily during
sleep Angina decubitus
◦ Chest pain that occurs only while lying down◦ Relieved by standing or sitting
Chronic Stable Angina Types of Angina
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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 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
Chronic Stable AnginaTypes of Angina
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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
Chronic Stable Angina Nursing and Collaborative Management
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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
Chronic Stable AnginaNursing and Collaborative Management
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Placement of a Coronary Artery 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.
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Pre- and Post- Percutaneous coronary intervention (PCI) With Stent Placement
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
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.
Acute Coronary Syndrome
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Acute Myocardial Infarction
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).
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Full-Thickness MI
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
Clinical Manifestations of ACS Myocardial Infarction
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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
Nausea and vomiting◦ Can result from stimulation of the vomiting center by severe
pain Fever
◦ Systemic manifestation of the inflammatory process caused by cell death
Stimulation of sympathetic nervous system results in ◦ Release of glycogen◦ Diaphoresis◦ Vasoconstriction of peripheral blood vessels◦ Skin: Ashen, clammy, and/or cool to touch
Clinical Manifestations of ACS Myocardial Infarction
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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.
Healing Process Myocardial Infarction
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Heart failure◦ pumping power of the heart diminished
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
Complications of Myocardial Infarction
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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
Complications of Myocardial Infarction
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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
Collaborative CareAcute Coronary Syndrome
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CABG Surgery
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◦ 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
Collaborative CareAcute Coronary Syndrome
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Nursing diagnoses◦ Acute pain◦ Risk for decreased cardiac tissue perfusion◦ Anxiety◦ Activity intolerance
Nursing Management Chronic Stable Angina and Acute Coronary Syndrome
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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
Nursing ManagementChronic Stable Angina
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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.
Nursing ManagementAcute Coronary Syndrome
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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)
Primary risk factors◦ Left ventricular dysfunction (EF 30%) ◦ Ventricular dysrhythmias following MI
Rapid CPR, and early advanced cardiac life support increase survival rates
Sudden Cardiac DeathEtiology and Pathophysiology
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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◦ CAD◦ Advancing age
Contributing risk factors ◦ Hypertension◦ Diabetes◦ Tobacco use◦ Obesity◦ High serum cholesterol
Heart Failure
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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
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
Types of Heart Failure
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Fatigue Dyspnea, orthopnea, paroxysmal nocturnal
dyspnea Persistent, dry cough, unrelieved with
position change or over-the-counter cough suppressants
Tachycardia
Clinical Manifestations: Chronic HF
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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
Collaborative Management Chronic HF
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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
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)
Collaborative Management: Chronic HF
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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.
Collaborative Management Chronic HF
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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.
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.
Nursing Management Chronic HF
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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.
Nursing Management Cardiac Transplantation
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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.
Nursing Management Cardiac 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
Nursing Management Cardiac Transplantation
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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
◦ Cigarette smoking◦ Hyperlipidemia◦ Hypertension◦ Diabetes mellitus
Peripheral Artery Disease of the Lower Extremities
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Common Sites of Atherosclerotic Lesions
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)
Clinical Manifestations
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Paresthesia◦ Numbness or tingling in the toes or feet◦ Produces loss of pressure and deep pain sensations
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
◦ Occurs in the forefoot or toes◦ Aggravated by limb elevation◦ Occurs from insufficient blood flow◦ Occurs more often at night
Clinical Manifestations
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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
Complications
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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
Collaborative Care Risk Factor Modification
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ACE inhibitors◦ Ramipril (Altace)
↓ 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
Antiplatelet agents◦ Aspirin(81-325 mg)◦ Clopidogrel (Plavix)
Collaborative Care: Drug Therapy
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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
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
Collaborative Care
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Revascularization via surgery Protect from trauma Reduce vasospasm Prevent/control infection Maximize arterial perfusion Hyperbaric oxygen therapy
Collaborative Care Care of Leg With Critical Limb Ischemia
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Indications◦ Intermittent claudication symptoms become
incapacitating. ◦ Pain at rest◦ Ulceration or gangrene severe enough to threaten
viability of the limb 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.
Collaborative Care Interventional Radiologic Procedures
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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.
Collaborative Care : Surgical Therapy
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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 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 discouraged-
increase risk for DVT◦ If edema-elevate the legs above the hearth level◦ Elastic bandages or elastic stockings are used to help control
edema
Nursing Management: Nursing Implementation
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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
Nursing ManagementNursing Implementation
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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
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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 short-
term nicotine replacement and support groups.”
Question
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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
Disorders of the Aorta
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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.
Aortic AneurysmsDefinition
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Abdominal Aortic Aneurysm
Angiography demonstrating abdominal aortic aneurysm. Note calcification of the aortic wall (arrows) and extension of the aneurysminto 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
Aortic AneurysmsEtiology and Pathophysiology
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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
Aortic AneurysmComplications
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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 Small aneurysm (<4 cm)
◦ Conservative therapy used Risk factor modification ↓ blood pressure Ultrasound, MRI, CT scan monitoring annually
5.5 cm is threshold for repair◦ Intervention at >5 cm in women with AAA
Aortic Aneurysm: Collaborative Care
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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.◦ Diaphoresis◦ Paleness◦ Weakness◦ Tachycardia◦ Hypotension◦ Abdominal, back, groin, or peri-umbilical pain◦ Changes in level of consciousness◦ Pulsating abdominal mass
Aortic Aneurysm :Nursing Management:Assessment
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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
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Aortic Dissection
Aortic dissection of the thoracic aorta.
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Pain characterized as ◦ 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
Cardiac tamponade◦ Severe, life-threatening complication◦ Occurs when blood escapes from dissection into pericardial sac◦ Clinical manifestations include
Hypotension Narrowed pulse pressure Distended neck veins Muffled heart sounds
Aortic DissectionClinical Manifestations
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Aorta may rupture.◦ Results in death
Hemorrhage may occur in pleural, or abdominal cavities.
Occlusion of arterial supply to vital organs
Aortic DissectionComplications
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Initial goal ◦ ↓ BP and myocardial contractility to diminish pulsatile
forces within aorta 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
Aortic Dissection: Collaborative Care
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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:
1. Hypothermia. 2. A wound infection.3. Bleeding from the graft site.4. An embolization or graft occlusion.
Question
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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
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.
Acute Arterial Ischemic disorder
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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
Thromboangitis Obliterans: Burgers disease
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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)
Raynaud’s Phenomenon
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Raynaud’s Phenomenon
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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
Venous Disorders
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DVT: Collaborative careEarly 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
Venous Disorders
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Venous Thrombosis
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
Venous Thrombosis
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Venous Thrombosis
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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
Venous Disorders