Cardiovascular System, HTN, Coronary artery disease, heart ...

Cardiovascular System, HTN, Coronary artery disease, heart ...

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. 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.

Cardiac Valves Anatomic structures of the heart and heart valves. Coronary Arteries and Veins Coronary arteries and veins. Location of pain during angina or myocardial infarction. Common Sites for Palpating Arteries Common sites for palpating arteries.

6 Mechanical System Systole: Contraction of myocardium Diastole: Relaxation of myocardium Cardiac output: Amount of blood pumped by each ventricle in 1 minute CO = SV HR Preload

Volume of blood in ventricles at the end of diastole Afterload Peripheral resistance against which the left ventricle must pump Relationship of Electrocardiogram, Cardiac Cycle, and Heart Sounds 8 Chest X-ray Standard posterior-anterior view.

Diagnostic Studies of Cardiovascular System Noninvasive studies Magnetic resonance imaging Computed tomography Echocardiogram Nuclear cardiology Diagnostic Studies of Cardiovascular System 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.

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. 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. Diagnostic Studies of Cardiovascular System Invasive studies

Cardiac catheterization and coronary angiography Intracoronary ultrasound Fractional flow reserve Electrophysiology study Blood flow and pressure measurements Diagnostic Studies of Cardiovascular System 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 Normal left coronary artery angiogram.

16 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. 2. 3. 4. Troponin T. Homocysteine.

Creatine kinase-MB. Type b natriuretic peptide. Cardiac markers 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 glutamicoxaloacetic 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 Gerontologic Consideration Age alters the cardiovascular response to physical and emotional stress. Heart valves become thick and stiff. Frequent need for pacemakers Less sensitive to -adrenergic agonist drugs Increase in SBP; decrease or no change in DBP

Hypertension Definition 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 20 BP classification

Normal <120and <80 Prehypertension 120-139 and 8089 Stage one hypertention 140-159 and 90-99 Stage 2 hypertention >or=160 and >or=100 Factors Influencing Blood Pressure (BP) Systemic Blood Cardiac

= Vascular Pressure Output Resistance 22 Etiology of Hypertension 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 Secondary hypertension Contributing factors

Aortic abnormalities Renal disease Endocrine disorders Neurologic disorders Cirrhosis Sleep apnea Risk Factors for Primary Hypertension

Age Alcohol

Cigarette smoking Diabetes mellitus Elevated serum lipids Excess dietary sodium Gender Family history Obesity Ethnicity Sedentary lifestyle Socioeconomic status Stress Factors Influencing BP Hypertension develops when one or more of the BP regulating mechanisms are defective. EDRF, Endothelium-derived relaxing factor.

Pathophysiology of Primary Hypertension Insulin resistance and hyperinsulinemia High insulin concentration stimulates SNS activity and impairs nitric oxidemediated 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. Hypertension Complications Target organ diseases occur most frequently

in the Heart Brain- Cerebrovascular disease-Stroke Peripheral vasculature Kidney: Nephrosclerosis Eyes Retinal damage Hypertension: Collaborative Care 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 Question A patients 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. 2. 3. 4. Progressive target organ damage. The possibility of drug interactions.

The patient not adhering to therapy. The patients possible use of recreational drugs. Hypertensive Crisis 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 Nursing and Collaborative Management Hospitalization IV drug therapy Monitor cardiac and renal function Neurologic checks Determine cause Education to avoid future crises Coronary Artery Disease and Acute Coronary Syndrome

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 Etiology and Pathophysiology 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 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. Coronary Artery Disease :Etiology and Pathophysiology

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 Risk Factors for CAD Modifiable risk factors Elevated serum lipids Hypertension

Tobacco use Physical inactivity Non modifiable risk factors Age Gender Ethnicity Family history Genetic predisposition Risk factors 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/m 2 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 for CAD Health Promotion

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 CAD: Health Promotion 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 Health-promoting behaviors Antiplatelet therapy ASA Clopidogrel (Plavix) Clinical Manifestations of CAD

Chronic Stable Angina 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. Chronic Stable Angina Types of Angina 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 Prinzmetals (variant) angina Occurs at rest usually in response to spasm of major coronary artery

Seen in patients with a history of migraine headaches and Raynauds 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 Angina Nursing and Collaborative Management Drug therapy: Goal: O2 demand and/or O2 supply Short-acting nitrates: Sublingual Long-acting nitrates Nitroglycerin (NTG) ointment Transdermal controlled-release NTG-Adrenergic blockers Calcium channel blockers If -adrenergic blockers are poorly tolerated, contraindicated,

or do not control angina Used to manage Prinzmetals angina Angiotensin-converting enzyme inhibitors Chronic Stable Angina Nursing and Collaborative Management 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 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. 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. Acute Coronary Syndrome 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 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). Full-Thickness MI Fig. 34-11. Myocardial infarction involving the full thickness of the left ventricular wall. Clinical Manifestations of ACS Myocardial Infarction

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 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 53

Healing Process Myocardial Infarction 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. Complications of Myocardial Infarction

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

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 Collaborative Care Acute Coronary Syndrome 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 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. Collaborative Care Acute Coronary Syndrome

Drug therapy IV nitroglycerin Morphine sulfate -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 Nursing Management Chronic Stable Angina and Acute Coronary Syndrome Nursing diagnoses Acute pain Risk for decreased cardiac tissue perfusion Anxiety Activity intolerance

Nursing Management Chronic Stable Angina 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 Management Acute Coronary Syndrome

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. Sudden Cardiac Death Etiology and Pathophysiology

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 Heart Failure 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 Types of Heart Failure 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

Clinical Manifestations: Chronic HF Fatigue Dyspnea, orthopnea, paroxysmal nocturnal dyspnea Persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants Tachycardia Collaborative Management Chronic HF 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 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

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. Nursing Management Chronic HF

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 Cardiac Transplantation Treatment of choice for patients with refractory endstage 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 Bridge to transplantation devices Surgery involves removing the recipients heart, except for the posterior right and left atrial walls and their venous connections. Recipients 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 Nursing care focuses on Promoting patient adaptation to the transplant process Monitoring cardiac function

Managing lifestyle changes Providing relevant teaching Take a break Peripheral Artery Disease of the Lower Extremities 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 Common Sites of Atherosclerotic Lesions Common anatomic locations of atherosclerotic lesions (shown in yellow) of the abdominal aorta and lower extremities. Clinical Manifestations Classic symptom of PADintermittent 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 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 Complications 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 Collaborative Care Risk Factor Modification Smoking cessation, including use of nicotine products Aggressive treatment of hyperlipidemia

BP maintained <140/90 Glycosylated hemoglobin <7.0% for diabetics Collaborative Care: Drug Therapy 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 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 Care of Leg With Critical Limb Ischemia Revascularization via surgery Protect from trauma Reduce vasospasm

Prevent/control infection Maximize arterial perfusion Hyperbaric oxygen therapy Collaborative Care Interventional Radiologic Procedures 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 : Surgical Therapy 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.

Nursing Management: Nursing Implementation 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 discouragedincrease 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 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 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. Disorders of the Aorta 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 Aortic Aneurysms Definition 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. Abdominal Aortic Aneurysm Angiography demonstrating abdominal aortic aneurysm. Note calcification of the aortic wall (arrows) and extension of the aneurysm into the common iliac arteries. Aortic Aneurysms Etiology and Pathophysiology Causes Degenerative

Congenital Familial tendency related to abnormalities Ehlers-Danlos syndrome and Marfans syndrome Mechanical Penetrating or blunt trauma Aortic Aneurysm Complications Ruptureserious 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 Aneurysm: Collaborative Care Goalprevent 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 :Nursing Management: Assessment 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 Dissection

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 Aortic dissection of the thoracic aorta. Aortic Dissection Clinical Manifestations 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 Dissection Complications Aorta may rupture.

Results in death Hemorrhage may occur in pleural, or abdominal cavities. Occlusion of arterial supply to vital organs Aortic Dissection: Collaborative Care 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 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: 1. 2. 3. 4. Hypothermia. A wound infection. Bleeding from the graft site. An embolization or graft occlusion. Acute Arterial Ischemic disorder 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. Thromboangitis Obliterans: Burgers

disease 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 meds Pain meds

Raynauds Phenomenon 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) Raynauds Phenomenon

Venous Disorders DVT is a disorder involving a thrombus in a deep vein. Thrombi may detach and result in emboli, PE. Three important factors(called Virchows 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 DVT:

Collaborative care Early mobilization-bed rest, elevation of the extremity and anticoagulation meds Antiembolitic stockings(TED hose) to prevent venous dilationmeasure 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 Thrombosis Inferior vena caval interruption technique using Greenfield stainless steel filter to prevent pulmonary embolism. Venous Thrombosis

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 meds and treat the inflammation Venous Thrombosis Venous Disorders

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

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