Cardiovascular System, HTN, Coronary artery disease, heart

failure, Vascular disordersZoya 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 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.

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

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Common sites for palpating arteries.

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

Relationship of Electrocardiogram, Cardiac Cycle, and Heart Sounds

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Chest X-ray

Standard posterior-anterior view.

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.

Diagnostic Studies of Cardiovascular System

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.

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.

Diagnostic Studies of Cardiovascular System

Normal Left Coronary Artery Angiogram

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Normal left coronary artery angiogram.

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

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

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

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

20

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

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

Secondary hypertension◦ Contributing factors

Aortic abnormalities Renal disease Endocrine disorders Neurologic disorders Cirrhosis Sleep apnea

Etiology of Hypertension

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

Factors Influencing BP

Hypertension develops when one or more of the BP regulating mechanisms are defective. EDRF, Endothelium-derived relaxing factor.

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

Target organ diseases occur most frequently in the◦ Heart◦ Brain- Cerebrovascular disease-Stroke◦ Peripheral vasculature ◦ Kidney: Nephrosclerosis◦ Eyes Retinal damage

HypertensionComplications

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

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

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

Hospitalization◦ IV drug therapy◦ Monitor cardiac and renal function◦ Neurologic checks◦ Determine cause◦ Education to avoid future crises

Hypertensive CrisisNursing and Collaborative Management

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

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

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.

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

◦ 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

• 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

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

•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)

Risk Factors for CAD: Health Promotion

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

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

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

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

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

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.

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

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.

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

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

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

Complications of Myocardial Infarction

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

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.

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

Nursing diagnoses◦ Acute pain◦ Risk for decreased cardiac tissue perfusion◦ Anxiety◦ Activity intolerance

Nursing Management Chronic Stable Angina and Acute Coronary Syndrome

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

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

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

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

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

Fatigue Dyspnea, orthopnea, paroxysmal nocturnal

dyspnea Persistent, dry cough, unrelieved with

position change or over-the-counter cough suppressants

Tachycardia

Clinical Manifestations: 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.

Collaborative 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 Chronic HF

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

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

Nursing care focuses on ◦ Promoting patient adaptation to the transplant

process◦ Monitoring cardiac function◦ Managing lifestyle changes◦ Providing relevant teaching

Nursing Management Cardiac Transplantation

Take a break

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

Common Sites of Atherosclerotic Lesions

Common anatomic locations of atherosclerotic lesions (shown in yellow) of the abdominal aorta and lower extremities.

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

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

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

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

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

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

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

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

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

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

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

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 short-

term nicotine replacement and support groups.”

Question

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

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

Abdominal Aortic Aneurysm

Angiography demonstrating abdominal aortic aneurysm. Note calcification of the aortic wall (arrows) and extension of the aneurysminto the common iliac arteries.

Causes◦ Degenerative◦ Congenital Familial tendency related to abnormalities

Ehlers-Danlos syndrome and Marfan’s syndrome

◦ Mechanical Penetrating or blunt trauma

Aortic AneurysmsEtiology and Pathophysiology

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

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

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

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

Aortic dissection of the thoracic aorta.

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

Aorta may rupture.◦ Results in death

Hemorrhage may occur in pleural, or abdominal cavities.

Occlusion of arterial supply to vital organs

Aortic DissectionComplications

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

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

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

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

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

Raynaud’s Phenomenon

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

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

Venous Thrombosis

Inferior vena caval interruption technique using Greenfield stainless steel filter to prevent pulmonary embolism.

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

Venous Thrombosis

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