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DONT FORGET SIMPLENURSING.

COM has videos for the EGG, Cardiac enzymes,
meds, an and answers most the objective questions if you get stuck!
 MI - Tropnin - CPK - Myoglobin (one video)
 Cardiac stroke volume 1 of 2
 Cardiac stroke volume 2 of 2
 Cardiac Glycoside (Digoxin)
 CHF Drugs Part 1
 CHF Drugs Part 2
 Stress Test Cardiac
 Acute Coronary Syndrome, Coronary Artery Disease and MI
 CAD vs ACS 1 of 2
 CAD vs ACS 2 of 2
 Post Angio Cath
 4 Drugs Given During an MI Heart Attack (MONA) morphine, Oxygen, Nitro, Asa
 MI drugs & Beta Blockers
 CHF drugs vs. MI (heart attack) 1 of 2
 Heart failure Drugs vs. MI drugs 2 of 2
 Heart Failure vs. MI drugs (Heart failure Beta Blockers focus)
 Heart Failure vs. MI drugs (Calcium Channel blocker focus)
 MI heart attack medications
 Heart Attack MI drugs MONA & Beta blockers
 CHF vs. MI Drugs
 CHF vs. MI Drugs PART 2
 CHF vs. MI drugs BETA Blockers
 CHF vs. MI drugs CALCIUM CHANNEL BLOCKERS
 Post Angio Cath
 Cardiac Assessment: S1 S2 & APETM
 MI (patho, Nursing interventions, drugs, labs)
 Cardiac Glycoside (Digoxin) Positive Inotropic Drug
 Nursing Students CHF drugs (Part 1)
 Nursing Students CHF Drugs (part 2)
 Cardiac Glycoside (Digoxin) Positive Inotropic Drug
 34-rythems.pdf
 EKG intro electrical conduction
 EKG A-fib, AV blocks, V- Tach
 Atrial Fibrillation part 1
 Cardiac Glycoside (Digoxin)
 MI
 Stress Test Cardiac

Cardiovascular Assessment
(Objectives)

Identify important history information in a cardiovascular assessment, including risk factor assessment.

**Chest pain can also indicate: non-cardiac conditions: GERD, anxiety, neuromuscular abnormalities, pleurisy,
PE, hiatal hernia,

*Describe pain (if able) Is it different from other episodes of pain?
What were you doing at the time? Arguing, sleeping, running?
Is pain sharp/dull/radiating/crushing? Pain scale?
Diaphoretic?
Dyspnea – breathing difficulties with rest? Exertion (an EARLY symptom of HF)?
Orthopnea? - Breathlessness while lying flat?
Paroxysmal nocturnal dyspnea – develops when patient lying flat for several hours

Fatigue: Usually described as “bone weary.” If it develops after mild activity, = indicates inadequate Cardiac
output.

Palpitations: unpleasant feeling in chest like heart skipping beats or has extra beats.
Non cardiac reasons for palpitations are: anxiety, stress, fatigue, hyperthyroidism, caffeine, nicotine, alcohol

myocardial and valvular disease/dysfunction Location and extent of heart disease (look at right side. pale. silhouette. Creatine Kinase.2 pounds = 1 liter extra fluid in interstitial space Syncope: brief loss of consciousness. Chest X-ray: looking for size.Troponin. moist skin) ▪Cyanosis ▪Dark-skinned pts w/ cyanosis may appear grayish ▪Central cyanosis = oxygenation of arterial blood in lungs àbluish tinge of mucus membranes of tongue and mouth & conjunctiva ▪Peripheral cyanosis = â blood flow to periphery ▪Skin temperature – ▪ blood flow to skin = temperature Describe the purpose of and the nursing management for the following diagnostic studies. and position of the heart Cardiac Catheterization: Most definitive and most invasive Can confirm suspected heart disease (congenital abnormalities. The catheter is guided to heart by use of fluoroscope.Edema: Sudden weight increase = 2. Results from brief reduction of cardiac output Diagnostic test. and Myoglobin Family history HDH and HDL levels History of cardiovascular health ECG ▪General build ▪Skin color ▪Pallor/cyanotic/pink ▪Moisture (decreased perfusion = cool. Images detect arteries that are narrowed or blocked NURSING MANAGEMENT: . left side or coronary arteries) Table and severe angina unresponsive to medical tx Unstable angina Uncontrolled heart failure Determine best therapeutic option Evaluate side effect of medical treatment Catheter inserted into artery through the groin or brachial area. CAD. Contrast dye is injected image captured and recorded.

Hydration and acetylcysteine post study to reduce risk NPO after midnight or only liquid breakfast if afternoon study Antiseptically prepare site and clip hair Vitals. auscultate lungs and heart pre assessment Assess history of iodine based allergies (shellfish also) Mild sedative admin before procedure If on digitalis or diuretic withheld for procedure Analysis of BNP. Vitals q 15 mins for the first hour and q1hr thereafter. assess urination and adequate fluid intake to make sure pt. dysrhythmia. 5 pound bag of sand on the groin area for 6 hours r/t bleeding risk.Before procedure Pt is admitted to hospital the day of the procedure Fluids may be given before procedure for renal protection (pg 643) Contrast induced renal dysfunction can result from vasoconstriction and direct toxic effect of dye on renal tubules. Report to Dr. hematoma formation. You have to get creative if they need to go to the bathroom. COMPLICATIONS: Right sided catheterization Thrombophlebitis Pulmonary embolism Vagal response (vitals drop) Left sided catheterization Myocardial infarction Stroke Arterial bleeding or thromboembolism Dysrhythmias Happens for each side . Critical rescue box : If s/s of cardiac ischemia chest pain. Can excrete it. or dramatic change in peripheral pulses in affected extremity. Could be acute MI call rapid response team! If neurologic changes Visual disturbance. color and pulses each VS check Contrast medium is an osmotic diuretic. swallowing difficulties. bleeding. slurred speech. they can’t get up!!!! Book slightly dif from Marti Pwpt Some cardiologist allow HOB at 30 degrees Can use vascular closure devices that eliminate need for compression of 5 lb sand. Assess temperature. report immediately could be s/s of stroke. coagulation. extremity weakness. CBC pre and post procedure Post procedure Pt returns to their room lying flat.

Cardiac tamponade. return to normal in 10-14 days. pericardial effusion. and Myoglobin Troponin myocardial muscle protein released into blood stream with injury to heart muscle. . Any rise is treated aggressively Can be tested at bedside in ER and results back within 15-20 min.03 ng/ml Rise . ventricular aneurysms. Used if other methods do not create a clear enough picture BLOOD TEST Acute coronary syndrome (AMI) confirmed by abnormally high levels of 3 Cardiac Markers: Troponin. cardiac tumors Transesophageal Echocardiography Uses sound waves to create high-quality moving pictures of the heart and blood vessels.type of pericardial effusion (fluid. clots. pus. left ventricular function.4-6 hours. peak – 10-24 hours. drawn q 8 hrs x 3. valvular disorders. blood.10 ng/ml Cardiac troponin I = <0. Creatine Kinase. Myocardial muscle protein released during injury Not found in healthy persons – ANY rise indicates cardiac necrosis or MI Cardiac troponin T = <0. or gas accumulates in the pericardium) Hypovolemia Pulmonary edema Hematoma or blood loss at insertion site Reaction to contrast medium Risk of MI or stroke ECG (electrocardiography) Recording of the heart's electrical functioning Electrodes placed on 12 sites (hence 12 lead) as opposed to tele in hospital using 6 lead Provided MD with 12 view of heart's electrical activity Echocardiography Non-invasive Checks function of heart muscles under stress Exercise tolerance testing Use of treadmill IV drugs – usually dobutamine (whips the heart muscle) Assess/dx cardiomyopathy.

Any measurement above 15 is considered high C-Reactive Protein (CRP) Most studied marker for inflammation Elevations seen in HTN. vasodilation. drawn q8 hours x 3. peak – 12-24 hours. and skeletal muscle Cardiac specificity determined by 3 isoenzymes activity: CK-MM – found in skeletal muscle CK-BB – found in the brain CK – MB – most specific for MI. greater values indicate MI Found in cardiac and skeletal muscle▪ Earliest marker detected – Rise – 2-3 hours. and does so by diuresis. levels over 100 pg/ml may indicate heart failure Increased urine output. return to normal in 24 hours Clinical usefulness more limited than troponin Homocystine Amino acid produced when proteins break down Elevated levels may be risk factor for CVD The link is controversial but elevated levels may be as big of risk factor as smoking and hyperlipidemia especially in women. and inhibiting the renin-angio Valvular and Inflammatory Cardiac Disorders . Creatine Kinase (CK)-MB Enzyme specific to brain. Rise – 3-8 hours. return to normal 2-3 days. < 1 mg/dL = low risk > 3 mg/Dl = high risk Myoglobin <90mcg/ml normal. myocardium. peak – 6-9 hours. High-risk patients with personal or family history of premature heart disease should be tested for this amino acid Levels in the blood between 4 and 15 micromoles/liter (µmol/L). smoking. decreased blood volume Has opposite effects opposite that of aldosterone. and infection Levels over 3 mg/dL indicate high risk for heart disease CRP levels are helpful in managing statin therapy post MI Brain natriuretic peptide (BNP) Secreted by ventricles of the heart in response to increase blood volume and pressure (stretch receptor in heart) Normal levels = 100 pg/ml. BNP helps reduce the stress on the heart.

Chart 35-6 page 692 Correlate common signs and symptoms with the pathophysiology of following valvular disorders: Mitral stenosis (narrows) page 692 .

dry cough As progresses: hemoptysis (cough up blood) Pulmonary edema. L/T left atrial pressure ↑. pitting edema (late sign) Pulse may be normal.usually has some mitral stenosis with regurgitation when it is rheumatic fever. enlarged liver. rapid. A rumbling apical diastolic murmur may be noted on auscultation (Review) Chart 35-6 Key Features of Mitral Stenosis: Fatigue Dyspnea on exertion Orthopnea (lying down w/SOB) Paroxysmal nocturnal dyspnea (severe SOB and coughing at night. neck vein distention. rupture from ischemic heart disease. or irregularly regular *have an abnormal but predictable rhythm-Like A fib Any new atrial fibrillation means pt may be decompensating Report changes to Dr. left atrium enlarges (L/T=leads to) Pulmonary artery pressure increase Right ventricle hypertrophies Pulmonary congestion and Right -Sided heart failure occur first What it looks like: Mild stenosis is asymptomatic As it worses (valve opening narrows more) Pressure in lungs ↑. become stiff. palpitations. congenital anomalies. apical diastolic murmur (atrium rest/filling up) Mitral regurgitation (leaky) pg 693 Primary cause is degenerative r/t aging. Usually from rheumatic carditis (rheumatic fever) Mitral valve thickens by fibrosis and calcification What happens: Valve leaflets fuse. awakens person sleeping) Hemoptysis (coughing up blood) Hepatomegaly (abnormal enlargement of liver) Neck vein distention Pitting edema Atrial fibrillation Rumbling. dyspnea on exertion. Also Rheumatic fever. Other causes are papillary muscle dysfunction. and infective endocarditis. Affects women more often than men What happens: . Chordae tendineae contract and shorten Valve opening narrows Prevents normal flow from left atrium to left ventricle. orthopnea paroxysmal nocturnal dyspnea (night waking dyspnea).

syncope . Incomplete closure causes backflow of blood into left atrium when left ventricle Contracts. Associated with marfan syndrome and other congenital heart defects. What happens: Mitral valve leaflets enlarge and prolapse into left left atrium during systole What it looks like: Mostly benign. enlarged liver. Afib.can progress to mitral regurgitation in some Most are asymptomatic May report chest pain. Normal HR and B/P Mid systolic click and late systolic murmur heard at apex of heart. Usually no other cardiac abnormality is found. Chest pain usually atypical. CT is the material that holds together many structures in your body including heart valves. and respiratory changes. High pitched systolic murmur at apex with radiation to left axilla heard on auscultation. Symptom free for decades. Fibrotic and calcification changes prevent mitral valve from closing during systole. palpitations.distended neck veins. Chart 35-6 Key Features Mitral Valve Prolapse Atypical chest pain Dizziness. pitting edema. described as sharp and on left side of chest. Later: dyspnea on exertion and orthopnea Assessment may show normal B/P. exercise intolerance. During systole the extra blood that flowed into left atrium moves with normal blood flow into left ventricle. Chart 35-6 Key Features Mitral Regurgitation: Fatigue Dyspnea on exertion Orthopnea Palpitations Atrial fibrillation Neck vein distention Pitting edema High-pitched holosystolic murmur Mitral Valve prolapse Etiology is variable. atypical chest pain. But there is now a larger volume. chronic weakness (think reduced cardiac output) anxiety. Can be hereditary. What it looks like: Progresses slowly. Severe regurgitation exhibits a third heart sound at S3. Symptoms start when left ventricle fails r/t chronic volume overload.fatigue. *intensity of murmur not related to severity of prolapse. Larger volume causes left atrium and ventricle to dilate and hypertrophy. When left ventricle fails. Note Marfan syndrome-rare disorder t/causes connective tissue in body to be weaker than it should be. ● Right sided heart failure .

What happens: Aortic leaflets do not close properly during diastole Annulus (valve ring that leaflets attach to) is usually dilated. Narrow pulse pressure when BP measured. syncope upon exertion. Atherosclerosis and degenerative calcification of aortic valve are major causative factors in older adults. Palpitations Atrial tachycardia Ventricular tachycardia Systolic click Aortic Stenosis Most common valve dysfunction Disease of “wear and tear” in aging population Congenital bicuspid or unicuspid aortic valves are primary cause for many Rheumatic aortic stenosis occurs with mitral stenosis following rheumatic fever. obstructs left ventricular outflow during systole Increased resistance to ejection or afterload L/T ventricular hypertrophy Cardiac output becomes fixed and cannot increase to meet the demands of the body with exertion. and eventually hypertrophies. Eventually left ventricle fails. HTN. Pulmonary system becomes congested and Right sided heart failure occurs. blood backs up in left atrium. surgery indicated/urgent! What is looks like: Fixed cardiac output creates dyspnea. angina. When cardiac output falls in later stages marked fatigue. Diamond shaped systolic crescendo decrescendo murmur is usually noted on auscultation Chart 35-6 Key Features Aortic Stenosis Dyspnea on exertion Angina Syncope on exertion Fatigue Orthopnea Paroxysmal nocturnal dyspnea Harsh.. marfan syndrome. congenital anatomic aortic valvular abnormalities. systolic crescendo-decrescendo murmur Aortic regurgitation Usually non rheumatic causes Infective endocarditis. loose or deformed This allows backflow of blood from aorta to left ventricle in diastole. Left ventricle to compensate dilates. debilitation and peripheral cyanosis. What it looks like: . When surface area of valve becomes 1 cm or less. What happens: Aortic valve orifice narrows.

kidneys. decrescendo diastolic murmur Correlate common signs and symptoms with the pathophysiology of following inflammatory or genetic cardiac disorders: Infective endocarditis Pathophys: A microbial infection of the endocardium (innermost layer). It also may cause emboli to be released into the general circulation Portals of entry: Oral cavity (think dental procedures… abscessed teeth. extremities ■ R side? Its going to the lungs bro! ● Petechiae (pinpoint red spots) ○ Look on mucous membranes! Palate. Typically in patients that abuse drugs. Bounding arterial pulse Widened pulse pressure Elevated systolic pressure and diminished diastolic pressure High pitched blowing decrescendo diastolic murmur Chart 35-6 Key Features Aortic Regurgitation Palpitations Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Fatigue Angina Sinus tachycardia Blowing. fatigue ○ Recurrent( 99-103) ● Cardiac murmur (newly developed or change in existing) ○ Really common! May even hear and S3 orS4 murmur. brain. have had valve replacements. crackles upon auscultation ● Evidence of systemic embolization ○ Arterial immobilization is a BIG deal! ■ Fragments of vegetation may just randomly fall off and go into circulation ■ L side of the heart? Travels to spleen. worse when lying on left side Nocturnal angina with diaphoresis. Needs to be on antibiotics a week before procedures). and the skin above the clavicles may have small. ● Most common complication is heart failure ○ Right sided HF Via peripheral edema. flat lesions. ● Fever associated with chills. lesions. malaise (feeling ill or not right). or structural cardiac defects. s/s: Clinical manifestations typically occur within two weeks of bacteremia. red. night sweats. Skin rashes. have a systemic infection. Infections or invasives surgeries. GI. Structural defect side note: Blood flow may go from a high pressure to a low pressure zone eroding a section of endocardium. ● Splinter hemorrhages . Palpitations may be noted with severe disease. SOB. orthopnea. conjunctivae.dyspnea. weight gain and anorexia ○ L sided HF via Fatigue. allows a perfect area for bacteria and deposited vegetation to thrive… more platelets and fibrin will come which allows the area to grow leaving the endocardium and valve to be destroyed. paroxysmal nocturnal dyspnea. Most asymptomatic due to compensatory mechanism of left ventricle When left ventricle failure happens. ect.

shoulder. provide adequate rest periods. administer digoxin if prescribed. HF. radiation therapy. including pulsus paradoxus. acute exacerbations of systemic CT disease ● Chronic pericarditis is the chronic inflammatory causes fibrous thickening of the pericardium. trauma. prevents adequate filling of ventricles therefore constricting the heart causing compression ○ Causes: tuberculosis. signs of ventricular failure in clients with chronic constrictive pericarditis. pulsus alternans. and NSAIDS as prescribed ● Administer oxygen. and cardiomyopathy. postpericardiotomy syndrome. pericardium becomes rigid. chest pain. metastatic cancer ○ Can result in loss of pericardial elasticity or an accumulation of fluid within the sac ● HF or cardiac tamponade may result Assessment: ● Pain in anterior chest that radiates to L side of neck. 16-18 gauge needle into pericardial sac) ● Monitor of signs of cardiac tamponade. Look for rebound tenderness. ■ Pleuritic chest pain dyspnea and cough ● Osler’s nodes (On palms of hand and soles of feet) ● Janeway’s lesions (flat reddened maculae on hands and feet) ● Positive blood cultures Pericarditis ● Acute pericarditis is inflammation or alteration of pericardium (membranous sac enclosing the heart) ○ Most commonly associated with: Infective organisms. dyspnea. coughing. systemic infection. Interventions ● Assist client to a position of comfort: such as sitting up and leaning forward. Rheumatic pericarditis . or back ● Pain is grating and is aggravated by breathing. elevated WBC. stroke or pulmonary emboli ■ Look for confusion. ○ Renal infarction?: Flank pain radiating to groin accompanied with hematuria and/or pyuria (WBC in urine). administer antidysrhythmics. jugular vein distension w/ clear lung sounds. monitor toxicity. reduced concentration. limit activities to avoid overexertion. muffled heart sounds. ● Neurologic changes occur in ⅓ of patients. high-pitched sound) ● Fever and chills. administer antibiotics to treat causative organism. tachycardia. salicylates. narrowed pulse pressure. monitor for complications such as: thrombus. NSAIDs or corticosteroids ● Check results of blood culture to identify causative organism ● Administer antibiotics and digoxin as prescribed with chronic constrictive pericarditis---SURGICAL INCISION may be necessary (pericardiocentesis 8 in. may be relieved by leaning forward ● Auscultation: pericardial friction rub at left lower sternal border (scratchy. ● Administer analgesics. tachycardia. and decreased CO Myocarditis Description ● Acute or chronic inflammation of the myocardium as a result of pericarditis. pericardial friction rub. signs of HF. fatigue and malaise. a-fib common. renal failure. ST segment elevation w/ onset of inflammation. Interventions: ● Assess nature of pain ● Position in high fowler's or upright and leaning forward ● Admin analgesics. gallop rhythm murmur that sounds like fluid passing an obstruction. Others may present with pulmonary issues ■ TIA.○ Look at the distal 3rd of nail beds… presents as black longitudinal lines or small red streaks ● Splenic infarction ○ Sudden abdominal pain maybe radiation to the shoulder. or allergic response Assessment ● Fever. post-myocardial infarction (MI) syndrome. fatigue. aphasia or dysphasia. and swallowing ● Pain is worse when in supine position.

moderate to severe. leading to endocarditis ○ Fever. emboli common ● S/S: dyspnea and fatigue. treatment of hypertension. emergency treatment of acute pulmonary edema Collaborative Management of Arterial Disorders Describe the term PAD AKA Peripheral Artery Disease This is a result of systemic atherosclerosis. complement assay. nonobstructed. HF ● Treatment: symptomatic. Chronic condition where partial or total arterial occlusion decreases perfusion to the extremities. small chamber size. . Enlarged thickened muscle= smaller chamber ● S/S: dyspnea.B blockers. HF R side. sudden death. fibrosed walls cannot expand or contract. vasodilators. dilated chambers. dysrhythmias or heart block. syncope. mild cardiomegaly. cardiomegaly ● Treatment: symptomatic treatment of HF. S4 gallop. The tissue below this occlusion cannot survive. restrictive Dilated Cardiomyopathy ● Fibrosis of myocardium and endocardium. antistreptolysin O titer. control of dysrhythmias. HEART TRANSPLANT Nonobstructed: ● Hypertrophy of walls and septum. conversion of a-fib. ventriculomyotomy or muscle resection with mitral valve replacement. tachycardia. pericardial friction rub. C reactive protein ○ New onset murmur. mural wall thrombi present ● Signs/Symptoms: fatigue. Description: ● A sensitivity response that develops after an infection with group A beta-hemolytic streptococci ● Inflammation is evident in all layers of the heart and results in impaired contractile function of the myocardium. fatigue. and or extreme fatigue ○ Acute electrocardiogram changes indicating pericarditis ● Symptoms of cardiac scarring and cardiac valve disease after acute infection or recurrent infection ● Cardiomegaly ● Development of new murmur or change in existing murmur ● Symptoms of HF Treatment: ● Antibiotics: penicillin or erythromycin ● Managing fever ● Adequate rest ● Teaching patient that antibiotic prophylaxis to prevent infective endocarditis is considered for dental and invasive procedures throughout life Cardiomyopathy Description ● Subacute or chronic disorder of the heart muscle ● Treatment is palliative. not curative and client needs to deal with numerous lifestyle changes and shortened life span ● Different types: dilated. and inflamed endocardium. obstructed. conversion from dysrhythmias. angina. mild to moderate cardiomegaly. S3 and S4 gallops. and elevated serum findings of antideoxyribonuclease B titer. nitrates. ventricular dysrhythmias. leading to valvular damage Common manifestations: ● Symptoms of streptococcal infection. Heart block. and other vasodilators contraindicated with obstructed form Restrictive Cardiomyopathy ● Mimics constrictive pericarditis. systemic or pulmonary emboli. digoxin. weakness. L sided HF. S3 and S4 gallops. precordial pain. sore throat. chambers narrowed. exercise restrictions. emboli ● Treatment: supportive treatment of symptoms. thickening of the pericardium. palpitations.

Risk factors for both are: hypertension. obesity high cholesterol and lipid levels and genetic factors Can be classified as: Inflow disease: Discomfort in lower back. Typically have rest pain as well Outflow disease: Burning. Endothelial injury. Indicates a block below the popliteal artery. assessment findings. internal and external illiac arteries ● Outflow: Femoral. may wake up to leg pain at night ○ Numbness. Mild: discomfort after two blocks.burning toothache-y type of pain . Mild: Discomfort felt after walking 5 blocks. dilated superficial veins and hypercoagulability from cancer and previous VTE 2. pitting edema. Three health problem result in PVD 1. Venous blood flow may be altered by thrombus formation and defective valves a. ● Gradual inflow not as big of a deal as gradual outflow Most common cause is atherosclerosis Compare and contrast etiology. Thrombus formation is associated with bed rest of more than 3 days.popliteal tibial arteries. Tends to affect lower extremities. buttock or thigh. cigarette smoking. hyperlipidemia. ankles and feet and toes. pathophysiology. cramping in calves. Intermittent rest pain Severe: Cannot walk more than ½ block. Some patients have both. Venous insufficiency results from prolonged hypertension and phlebiti . which stretch the veins and damage valves 3. and nursing interventions PVD: Disorders that alter the natural blood flow through arteries and veins of peripheral circulation.● Inflow: Distal ends of aorta and common. diabetes mellitus. A diagnosis of this typically implies an arterial rather than a venous involvement. More of a pain but eases with rest and time Severe: Severe pain after walking less than a block. most over 65. Reduces skeletal muscle activity peripheral arterial disease: Blood getting to extremities Etiology: 10-12 million americans have PAD. relieved by rest Moderate: Discomfort after 2 blocks. Pathophys: Atherosclerosis is the most common cause. ○ Symptoms are reproducible ○ Pain will stop at rest until rest pain occurs (stage 3) ● Rest Pain ○ Pain while resting. cramping or burning occurring with exercise and relieved while at rest. tend to hang their feet for relief and sleep at night Assessment findings: Stages and their clinical manifestations ● Asymptomatic ○ No caludation (to limp) ○ Bruit or aneurysm may be present ○ Decreased or absend pedal pulse ● Claudication ○ Muscle pain. African americans are more affected than any other group.

including: Angioplasty: ● Assess neurological and cardiovascular status. dusky.) Rarely in calf or ankle ○ Pain relieved by playing in a dependant position ● Necrosis. teach the patient to report these symptoms to the health care provider as soon as possible: ○ Severe headache ○ Change in level of consciousness or cognition (e. ○ May be cyanotic. arch.g. heel. Thickened toenails ○ Dependent Rubor (redness) may occur.Gangrene ○ Ulcers/blackened tissue occurs on toes. pale or mottled skin. ( see chard 36-4 on pg 721… had a nice picture of the different kind of ulcers) Nursing Intervention: ● Non-surgical management: ○ Exercise and positioning: ■ Work toward Collateral circulation (the more you move. encourage them to raise them above heart level ○ Promoting vasodilation ■ Provide warmth to affected extremity. drowsiness. stroke… but NO GRAPEFRUIT! ■ Satins ■ Phosphodiesterase inhibitors ○ Invasive procedure ■ Percutaneous vascular intervention or percutaneous transluminal coronary angioplasty ● Dilated arteries with a balloon catheter ● Usually have stents placed to ensure blood flow ● WATCH FOR BLEEDING ○ Surgery ■ Arterial revascularization Describe and prioritize post-procedure collaborative care for clients who have undergone peripheral vascular procedures. the more your blood moves) Encourage walking every day… ■ Positioning: if edema in legs.forefoot.. wear socks! ■ Avoid cold ■ Hydrate hydrate hydrate ■ Avoid emotional stress. or pallor ○ ANY SIGN of ulcer formation!!! Prevention is key. scaly.○ Typically in the distal portion of extremities (toes. caffeine and nicotine ○ Drug therapy ■ Aspirin ■ Clopidrogel (helps prevents MI. ● Before discharge after carotid stent placement. forefoot and heel ○ Distinctive gangrenous odor is present ● Things to look for: ○ Loss of hair on lower calf/ankle and foot ○ Dry. new-onset confusion) ○ Muscle weakness or motor dysfunction ○ Severe neck pain ○ Neck swelling ○ Hoarseness or difficulty swallowing (due to nerve damage) .

Must stay in bed for 2-6 hours. Chest pain. Assess peripheral pulses as well as skin temp and color with every vital sign check QSEN: Any s/s of cardiac ischemia (chest pain. dyspnea. observe insertion site for any redness/swelling/pain ect. slurred speech. then as often as facility policy. and acute confusion (older adults) typically occur in patients with PE. then every 30 min for the next two. hematoma. temperature. ○ Home health is usually Rx’d in these cases Thrombolytic therapy: ● Observe the affected extremity for improvement in color. leave dressing in place. and pulse every hour for the first 24 hours or according to the postoperative surgical protocol. Home teaching: Limit activity for several days. An ABI of 0. change in peripheral pulses ect) Contact Rapid Response Team to provide prompt intervention. extremity weakness) Monitor urine output and provide sufficient liquids to help promote the excretion of the dye. Assess insertion site for bloody drainage or hematoma formation. Watch for Neuro changes as well! (visual disturbances. bleeding. ● Notify the health care provider or Rapid Response Team immediately if these symptoms occur. dysrhythmia. Monitor vital signs q15 min for first hour. Discuss the following conditions and/or undergoing the following procedures or treatments Aneurysm Definition: . Must be restricted to bed rest and keep catheter site straight. ● Monitor patients for manifestations of new thrombi or emboli.90 in either leg indicates PAD. people with diabetes are known to have a falsely elevated ABI. Describe the nursing management of the client undergoing the following diagnostic procedures: Arteriography: Client recovers in a specialty area. especially pulmonary emboli (PE). swallowing difficulties. Vascular bypass surgery (arterial revascularization): ● Patients should limit activity ○ Usually need temporary help with daily activities by the family or other caregiver. CT Scan Ankle-Brachial Index (ABI): (pg 720) Used to evaluate outflow disease! Derived by dividing the ankle blood pressure by the brachial blood pressure.

peripheral embolization. or rupture Most common cause: ● atherosclerosis or atheromatous plaque that weakens the intimal surface ● Can be described as true: meaning arterial wall is weakened by congenital or acquired problems ● False aneurysms occur as a result of injury or trauma Contributing factors: ● smoking. with a gnawing quality. ultrasound ● Nonsurgical management: ○ Abdominal aneurysm that is smaller than 2 or 3 inches or when surgery is not feasible: ■ Antihypertensive drugs ○ Teach importance of keeping scheduled CT scans appts ○ Review with patient clinical manifestations that need to be promptly reported ○ Avoid lifting and certain activities ○ Endovascular stent ● Surgical management: ○ Endovascular stent placement via an intra aortic catheter ● Watch for complications: bleeding. and abdomen ○ Symptoms of hypovolemic shock: hypotension. decreased or absent peripheral pulses ○ Xray. usually from motor vehicle crashes Classified as: ● Saccular: outpouching from a distinct portion of artery wall ● Fusiform: a diffuse dilation involving the total circumference of the artery Assessment: ● Most patients with abdominal or thoracic aneurysm are asymptomatic ● Abdominal aortic aneurysms: ○ Abdominal. marfan syndrome. is unaffected by movement.● Permanent. flank. embolize. CT. ripping. and may last for hours or days ○ Prominent pulsation in the upper abdomen DO NOT PALPATE ○ Abdominal or femoral bruit ● Thoracic aortic aneurysms: ○ Back pain. hyperlipidemia Other causes: ● Syphilis. blunt trauma. aneurysm rupture. visible mass above the suprasternal notch ● Abdominal or thoracic rupture: ○ Pain: tearing. difficulty swallowing. hoarseness. chronic inflammation. mis-deployment of the stent graft ● Symptomatic lesions or aneurysm greater than 3 inches: SURGICAL REMOVAL! ○ Replaced with a graft ○ Post op care: maintain MAP and assess peripheral pulses ● More postoperative care: ○ Assess vital signs every hour to detect early signs of hypotension from graft leak ○ Assess circulation by checking pulses distal to graft site when checking vitals . diaphoresis. localized dilation of an artery accompanied by weakening of the vessel wall ● Forms when the media. tachycardia. or back pain that is usually steady. Ehlerstion Danlos syndrome (rare genetic disorder). back. stabbing ○ Pain located in chest. faintness. apprehension. hypertension. and decreased mentation ○ N. or middle layer of the artery is weakened producing a stretching effect in the intima (inner layer) and adventitia (the outer layer) ● High BP can enlarge aneurysm ● Can thrombose. SOB. V.

difficulty swallowing and/or hoarseness ● Community based care: ○ Compliance to CT schedule! ○ Control BP ○ If surgery was performed: ■ Avoid lifting heavy objects 6-12 weeks post op ■ Be aware in activities that involve pulling. but can also occur in abdominal aorta and other arteries ● CIRCULATION IS IMPAIRED THIS IS AN EMERGENCY SITUATION When it can occur: ● More prevalent in 50s and 60s ● Men are more commonly effective than woman Assessment/symptoms: ● Pain: sharp. for example. nausea. straining ■ Avoid certain hobbies such as: tennis. ○ Cardiac tamponade situations: pt will become rapidly hypotensive. horseback riding. tearing. MRI. stabbing: tends to move from point of origin ○ May feel pain in anterior chest. cool to cold extremities below graft. strokes ● Confirming diagnosis: ○ Chest xray. golf ■ Defer from driving car for several weeks ■ Pain management ■ Wound care instructions Aortic Dissection ● Thought to be a sudden tear in the aortic intima. faintness. jaw. neck. back. decreased urinary output ○ Assess renal function and spinal cord when abdominal aneurysm b/c of clamping aorta during repair ○ Instruct patient with thoracic aneurysm repair to report back pain. vomiting. CT. aortic regurgitation (musical murmur). pushing. SOB. or teeth ● Diaphoresis. Altered LOC. ripping. abdominal distention. opening the way for blood to enter the wall Causes/Location ● Degeneration of the aortic media may be primary cause: with hypertension being a contributing factor ● Often associated with CT disorders. apprehension ● BP elevated unless cardiac tamponade or rupture has occurred. throat.9% sodium chloride and give medications ○ Indwelling urinary catheter ○ IV morphine sulfate and IV beta blocker ■ If not effective give nicardipine hydrochloride or other antihypertensive may be used ○ Proximal dissection: surgical treatment ■ Typically require cardiopulmonary bypass (removes the intimal tear and sutures the edges of dissected aorta.○ Report signs of leak or occlusion immediately: pulse changes. Marfan’s syndrome ● Ascending aorta and descending thoracic aortic more common areas. and these other things can also occur: decrease in peripheral pulses. severe pain. aortic angiography ○ MRI is not test of choice b/c it's time consuming ○ If pt cannot be moved from bed: transthoracic echocardiography or transesophageal echocardiography ● Interventions: ○ Elimination of pain and reduction of systolic BP to 100 to 120mm Hg ○ 2 large bore catheters to infuse 0. paraparesis. ○ Uncomplicated Distal dissection: continued medical treatment ○ Long term medical treatment: ■ Systolic BP must be maintained or at/below 130 to 140 mm Hg ■ Beta blockers and Calcium channel antagonists are prescribed to help maintain goal once pt is stabilized . white or blue extremities or flanks.

such as blood in the urine or stool. Warfilone]). ecchymosis.<< Geana :) Anticoagulants are the drugs of choice for actual DVT and for patients at risk for DVT. protamine sulfate for heparin. • When administering subcutaneous heparin. nosebleeds. Collaborative Management of Venous Disorders Describe nursing interventions used to help prevent venous thromboembolism (VTE). for example.. including hematuria. • Have antidotes available as needed (e. • Teach the patient going home while taking an anticoagulant to: Use only an electric razor Take precautions to avoid injury. petechiae. . where accidents commonly occur Report signs and symptoms of bleeding. • Monitor activated partial thromboplastin time (aPTT) for patients receiving unfractionated heparin. • Apply prolonged pressure over venipuncture sites and injection sites. do not use tools such as hammers or saws.g. or altered mental status Take the prescribed dosage of drug at the precise time that it was prescribed to be taken Not stop taking the drug abruptly. frank or occult blood in the stool. The Patient Receiving Anticoagulant Therapy • Carefully check the dosage of anticoagulant to be administered. even if the pharmacy prepared the drug. apply pressure over the site and do not massage. • Monitor the patient for signs and symptoms of bleeding. Monitor prothrombin time (PT)/ international normalized ratio (INR) for patients receiving warfarin or low–molecular-weight heparin (LMWH). which could indicate abdominal bleeding). vitamin K for warfarin [Coumadin. ecchymosis. • Monitor vital signs frequently for decreased blood pressure and increased pulse (indicating possible internal bleeding). the physician usually tapers the anticoagulant gradually Describe the nurse's role in monitoring clients who are receiving anticoagulants. altered mental status (indicating possible cranial bleeding). NOTIFY DOC IF > 70 SEC. or pain (especially abdominal pain.

thrombus formation. Pathophys: Prolonged venous hypertension eventually causes the veins to stretch and damages the valves. such as sequential compression devices (SCDs) • Venous plexus foot pump • Anticoagulant therapy Determine the collaborative management for a client with the following conditions: (what is it. or hypercoagulability ● May include all 3 elements. venous stasis ulcers swelling and cellulitis. thickening the vein wall and possibly leading to an embolization Venous insufficiency: Etiology: Typically due to a valvular dysfunction. engorged veins ● Edema ● Reddish/brown discoloration of the legs (stasis dermatitis) ● Stasis ulcer formation ○ Typically occur over the malleolus and more medially of the ankle ○ Typically chronic. obesity. Can lead to a back up of blood and further the venous hypertension. It typically occurs from prolonged venous hypertension. what do you do about it?) Venous thrombosis: ● A blood clot believed to result from an endothelial injury. hard to heal Nursing Intervention: Decrease edema and promote venous return! ● Ted hose! SCDs! (Una boot if ulcer is present) ● Talk with wound care and dietician to help heal if ulcer is present . • Patient education • Leg exercises • Early ambulation • Adequate hydration • Graduated compression stockings • Intermittent pneumatic compression. • Avoid oral contraceptives. Assessment: Some things you may see are…. Things that are risk factors include: ● People who stand or sit for long times. those who have chronic thrombophlebitis. or just one ● Often associated with inflammatory process ○ When a thrombus develops. • Exercise legs during long periods of bedrest or sitting. ● Varicose veins. and decreased tissue perfusion. venous stasis.. inflammation occurs around the clot. • Drink adequate fluids to avoid dehydration. Results in edema.

brown pigmentation from extravasated RBCs and pain ● Diagnosed by: simple ultrasonography or duplex ultrasonography ● ELASTIC EXERCISE ELEVATION ○ Avoid high impact exercises ● Different procedures/options: ○ Sclerotherapy: HCP injects a chemical to sclerose the vein. edema.● Elevate lower extremities. Venous pressure increases and valves become incompetent. feeling of fullness in the legs. performed on small or a limited number of varicosities ○ Laser treatment: uses heat and close main vessel that is contributing to the problem ○ Radiofrequency ablation: heating the vein from the inside and shrinking the vein. Surgical intervention entails ligation and stripping the affected veins with the patient under general anesthesia Arteriosclerosis and Hypertension Discuss the role of diet therapy. Phlebitis ● Vein inflammation ● Associated with invasive procedures such as IV therapy ● Can also predispose patient to thrombosis Varicose veins ● Definition: distended. and pruritus ■ As a result: venous stasis ulcers. Weight reduction. lifestyle. and drug therapy in the management of clients with atherosclerosis. protruding veins that appear darkened and tortuous ● Vein walls weaken and dilate. Long term emotional support… will most likely have this for rest of their life. pregant women are also at risk. What is atherosclerosis? *type of arteriosclerosis (thickening or hardening of arterial wall assoc w/ aging) Involves formation of plaque w/in arterial wall Leading risk factor for cardiovascular disease Thought to occur from blood vessel: damage causes inflammation Diet therapy Lifestyle . but they are common in adults older than 30 yrs whose occupations require prolonged standing activity. inquire family history ● Telangiectasias aka spider veins: are dilated intradermal veins less than 1 to 3 mm in diameter that are visible on skin surface ○ Most patients are not bothered by these ○ Most do not develop the severe varicose vein disease ● More advanced disease: ○ Venous distension. Incompetent valves enhance vessel dilation and veins become tortuous and distended ● Can occur in anyone.

Essential(primary) is the most common and is not caused by a preexisting condition. patients whose blood pressures are above these goals should be treated with drug therapy Stabilizing mechanisms exist in the body to exert an overall regulation of systemic arterial pressure and to prevent circulatory collapse. ▪For people over 60: ▪Below 150/90 ▪For people younger than 60: ▪Below 140/90 ▪According to Joint National Committee 8 (JNC 8) guidelines. Drug therapy Describe the differences between essential and secondary hypertension. • Vascular autoregulation: keeps perfusion of tissues in the body relatively constant. Sodium retention inhibits fluid loss. Hypertension is also classified into two categories based on the cause. (Iggy. an enzyme that acts on angiotensinogen (a plasma protein substrate) to split off angiotensin I. oral contraceptives) Cushing's disease Glucocorticoids Coarctation of the aorta Mineralocorticoids0 Brain tumors Sympathomimetics Encephalitis Identify normal values for arterial blood pressure and discuss physiological mechanisms that regulate blood pressure. • The renin-angiotensin-aldosterone system: The kidney produces renin. or magnesium intake Excessive and continuous stress Secondary Hypertension is caused by a preexisting health condition. • Regulation of body fluid volume: If there is an excess of sodium and/or water in a person's body. Family history of hypertension Excessive sodium and caffeine intake African-American ethnicity Overweight/obesity Hyperlipidemia Physical inactivity Smoking Excessive alcohol intake Older than 60 years or postmenopausal Low potassium.g. If the kidneys are functioning adequately. Four control systems play a major role in maintaining blood pressure: • The arterial baroreceptor system: Monitors the level of arterial pressure and counteracts a rise in arterial pressure through vagally mediated cardiac slowing and vasodilation with decreased sympathetic tone. a rise in systemic arterial pressure produces diuresis (excessive voiding) and a fall in pressure. the blood pressure rises through complex physiologic mechanisms that change the venous return to the heart. Angiotensin II has strong vasoconstrictor action on blood vessels and is the controlling mechanism for aldosterone release. which is converted by an enzyme in the lung to form angiotensin II. Kidney disease Pregnancy Primary aldosteronism Drugs: Pheochromocytoma Estrogen (e. appears to be important in causing hypertension. thus increasing blood volume and subsequent blood pressure. Aldosterone then works on the collecting tubules in the kidneys to reabsorb sodium. .. producing a rise in cardiac output. 710) Identify cultural considerations that impact care for clients with hypertension. calcium.

women have a much higher percentage of the disease (Go et al. Efforts to raise awareness of hypertension through education within African-American communities. Be able to recognize those meds that have the intended purpose of controlling hypertension. lung crackles) Safe and Effective Care Environment 1. Identify risk factors for vascular problems. making them much more likely to die from strokes. a. 2013). 2013). and kidney disease (Go et al. heart disease. Obesity/Overweight h. After age 54 years. stroke. are meds used in the control of hypertension. 2. a. including the importance of receiving treatment and controlling blood pressure. Many of the medication listed above under the heading of Heart Failure. Teach patients about lifestyle modifications to prevent vascular problems (Pretty much common sense). Heart Failure Compare and contrast the clinical findings for a patient with right-sided heart failure with a patient with left-sided heart failure. chronic pulmonary diseases. Sedentary lifestyle g. weight gain. high BP. have been somewhat successful.. anorexia) Left sided heart failure (fatigue. connective tissue diseases. 2013). Geographic differences still exist (Go et al. Nutrition/Diet .. women have a slightly higher percentage of hypertension than men. Prioritize care for patients with hypertension. bleeding disorders. heart disease. Hyperlipidemia d.. HTN c. and thrombophlebitis. The prevalence of hypertension in African Americans in the United States is among the highest in the world and is constantly increasing. Collaborate with interdisciplinary healthcare team members when providing care for patients with perfusion and clotting problems. but genetics and environmental factors may play a role. The exact reasons for these differences are not known. shortness of breath. High cholesterol e. anemia. they develop high BP earlier in life. When compared with Euro-Americans. Right sided heart failure (edema. The causes for these differences are not known. From 45 to 54 years. Smoking b. Hx of diabetes mellitus. 2. renal disease. Health Promotion and Maintenance 1. A higher percentage of men than women have hypertension until age 45 years. Familial pre-disposition f.

Desirable LDL= <130 mg/dL for healthy. Smoking cessation d. fruits. Elevated cholesterol levels are confirmed by HDL and LDL measurements (LDL=bad. Atherosclerosis i. sugar sweetened beverages. whole grains. Arteriosclerosis i. b. poultry. Secondary hypertension is caused by specific disease states and drugs 5. impaired leukocytic response to wounds. Stress importance of taking as prescribed. Educate patient on sticking to drug adherence. Explain the inflammation process that is associated with the development of arteriosclerosis and atherosclerosis. Elevated levels are considered a marker for other lipoproteins. forming a fibrous plaque. a. women should be below 135mg/dL. The fibrous plaque is often elevated and protrudes into the vessel lumen. Plaques are either stable or unstable. a.b. and nuts. other existing illnesses. side effects. resulting in ischemia. severity of blood pressure elevation. Lifestyle changes: restrict sodium intake in the diet. Garlic and CoQ10. <70mg/dL for older adults diagnosed with CVD or who are diabetic. After the vessel becomes inflamed. Consume low fat dairy products. Total serum cholesterol levels should be below 200mg/dL. Unstable plaques are prone to rupture and are often clinically silent until they rupture. Document a teaching plan for patients receiving drug therapy for hypertension. use alcohol sparingly (no more than 1 drink/day). Drug therapy: individualized for each patient with consideration given to culture. nontropical (canola) vegetable oils. although discuss with provider before starting any herbal remedy with other medications c. a fatty streak appears on the intimal surface (inner lining) of the artery. 2. a. High levels of both indicate risk for atherosclerosis. cost of drugs. Desirable HDL= >45mg/dL for men and >55mg/dL. Elevated lipids including cholesterol and triglycerides. HDL=good). and follow up. Discuss the role of nutrition therapy in the management of patients with arteriosclerosis a. and drug interactions for antihypertensives. Interpret essential laboratory data related to risk for atherosclerosis. reduce percent of calories from trans fat 4. Activity/Exercise c. Provide oral and written info about the indications. partially or completely obstructing blood flow through the artery. collagen migrates over the fatty streak. fish. Decrease alcohol consumption Physiological Integrity 1. and increased susceptibility to wound infection. Triglycerides may be elevated with atherosclerosis and is emerging lipid risk factor. legumes. reduce weight if overweight or obese. b. 6. Through the process of cellular proliferation. Higher intake of veggies. Many patients require more than 2 drugs a day to control HTN. Best therapy is blood pressure med and diuretic. age. exercise 3 to 4 days a week for 40 minutes each time. use relaxation techniques to decrease stress. Develop an evidence-based plan of care for a patient with essential hypertension. times for administration. suggest metabolic syndrome (increases risk for coronary heart disease) 3. red meats. >160mg/dL=hypertriglyceridemia in men. dosage. Limit intake of sweets. a. avoid tobacco/caffine b. Describe the differences between essential and secondary hypertension. even when asymptomatic b. Reduced local tissue circulation. Urge to report unpleasant side effects . Essential hypertension is the most common type and is not caused a pre existing health problem. Aim for dietary pattern that includes 5%-6% of calories from saturated fat. a.

previous documented DVT b. round. Instep/foot pain=obstruction below popliteal artery. assess for ulcers (small. Inflow obstruction involve distal end of aorta and common/internal/external iliac arteries. Identify when venous thromboembolism (VTE) and complications of VTE occur. Extreme: extremity is cold. c. e. intermittent or continuous warm soaks to the area. Some patients have both arterial and venous. cramping muscle discomfort and pain occurs. endothelial injury. Gently palpate. statis of blood flow. Preventative measures are best bet. Elevate. rest pain c. SCDs. casting of an extremity. severe: pain after ½ block. Outflow involves femoral. Monitor BP at home (obtain an ambulatory blood pressure monitoring (ABPM) device). described as toothache severe enough to wake patient up at night) d. phlebothrombosis (thrombus w/ no inflammation). muscle atrophy. with punched out appearance. paralysis. dopplers. well defined borders. distances get shorter and shorter. severe= 40-50 difference. usually develop on great toe. darkened. buttocks or thighs. (DO NOT MASSAGE). drug therapy . and tibial arteries and below superficial femoral artery. Associated with PE. divide ankle pressure by brachial (ABI<0. thickened toe nails. A diagnosis of PVD implies arterial disease rather than venous involvement. such as excessive fatigue. Intermittent claudication: Can walk certain distances then burning. feel for induration (hardening) along blood vessel for warmth/edema. Discomfort in lower back. moderate: pain in 1-2 blocks. Burning/cramping in calves. Eventually pain happens at rest (numbness/burning sensation. feet. intermittent rest pain. DVT. major surgery w/ GA within last 3 months.90 in either leg is diagnostic of PAD. Classic signs: calf/groin tenderness. calf swelling of greater than 3cm larger when compared to other leg. MRA used to assess blood flow. Compare common assessment findings present in patients with peripheral arterial and peripheral venous disease. Mild: painful after walking 5 blocks. Result of systemic atherosclerosis. hypercoagulability (Virchow’s triad) f. cough. monitor weight on scale c. bedridden for more than 3 days. Outflow: ankle brachial index (ABI). dilated superficial veins in one leg. popliteal. ankles. Observe for loss of hair on lower calf/ankle/foot. sexual dysfunction. ambulation. Plan evidence-based nursing interventions to help prevent VTE. a. moderate: pain after 2 blocks. rubor (redness) when extremity is lowered. Symptoms: SOB. localized tenderness along deep venous system. pain/sudden onset of swelling of leg. patients with diabetes known to have falsely elevated ABI) 8. a. chest pain. acute confusion (older patients) 9. a. Active cancer. Combination of rest and drug therapy. swelling of entire leg. dry/scaly/dusky/pale/mottled skin. pain in calf on dorsiflexion of foot (although unreliable. Complications: thrombophlebitis (thrombus w/ inflammation). Some patients asymptomatic. pitting edema in one leg. b. rest pain. and toes. BP readings are usually higher in thigh than arm (readings lower than brachial show presence of PAD) inflow: mild=difference of 10-30 mm HG pressure than brachial. Mild: walk 2 blocks before painful enough to stop. Instruct on dietary and lifestyle changes 7. returns after walking again. Homans’ sign). cyanotic. pallor if elevated. Pain stops after rest. redness may be present d. Palpate pulses (posterior tibial pulse best one). severe: painful after walking < 1 block. compression stockings.

Ulcerations/gangrene occur on digits. Raynaud’s: painful vasoaspasms in extremities especially digits. Safety b. or inferior vena cava filtration (umbrella placed in femoral that traps blood clots that could travel to lungs. Are they smooth and rounded.12 second? 2. Do they all look similar on the strip you are reading? PR interval = (Time required for the impulse to travel through AV node – atrial depolarization…thru wbundle of His. . Pericarditis. or are the inverted. but still allows the flow of blood). possible autoimmune (associated with many rheumatic diseases such as lupus) b. 4. STEMI ST depression can indicate MI. Tall-T’s . and upright. Surgical removal is rare and only happens if occlusion is bad and cannot/will not respond to drug therapy. Cause unknown. Compare assessment findings associated with Raynaud's phenomenon and Buerger's disease. Are PR intervals greater than 0. teaching patients importance of anticoagulation therapy 10. usually. a. bundle branches and Purkinje fibers…. Explain the nurse's role in monitoring patients who are receiving anticoagulants. cause unknown but associated with smoking What happens in an ECG wave? Disturbances in the conductivity of the heart – too rapid de/repolarization/too slow de/repolarization/ pathway blocked /impulse travels an abnormal pathway P-Wave = originate in the SA node of R-atrium (Atrial depolarization) (Depolarization is when the normally (-) charged cells in heart muscle develop a (+) charge) Make sure: 1. Buerger’s: claudication in feet and lower extremities. 5. Abnormalities here: Elevated or depressed >1mm in 2 or more leads (the electrodes placed on the body) ST elevation can indicate MI. Causes ischemia and fibrosis of vessels in extremities with increased sensitivity to cold. 1. ventricular hypertrophy NSTEMI T wave = (Ventricular repolarization) Note shape and height of T-Wave. 3. Are QRS intervals less than or greater than 0. 2. (IV unfractionated heparin followed by PO warfarin.10 second) ST Segment = (Early ventricular repolarization). P waves are present.just before ventricular depolarization. 1. worse at night.20 second? 2. happens mainly in women. Thrombectomy. hyperkalemia.04 – 0. Causes red/white/blue skin color on exposure to cold temperatures or stress. Patient teaching i. Is there ONE P-wave for each QRS complex. Are PR interval less than 0. a.The T waves were wide in ischemic heart disease and thin and peaked in uremia. Each pt treatment is different and varies on pt response) b. hypokalemia. Make sure they are occurring regularly. Are QRS complexes similar in appearance across the ECG strip? (Normal = 0.12 second? 3. Foods to eat/avoid (Vitamin K) 11. Are PR intervals consistent across the ECG strip? QRS interval = Ventricular depolarization.

The blood then flows from the heart into the lungs where it becomes OXYGENATED. BASIC HEART PHYSIOLOGY So. we have the heart right? It has two atria and two ventricles. It is then dumped into the LEFT atrium and flows into the LEFT ventricle (Preload… aka FILLING UP with blood). the blood is pushed out the aorta and into the circulatory system. It then flows to the RIGHT ventricle. From there.QT interval = (time required for ventricular depolarization and repolarization to occur) Normal QT should be equal to or less than ½ the distance of the R to R interval. Systole: Diastole: . As the heart contracts. The superior and inferior vena cava as well as the coronary sinus all empty deoxygenated blood into the RIGHT atrium (Preload aka FILLING UP WITH BLOOD). the force from the contraction pushes the deoxygenated blood up from the ventricle into the Pulmonic valve (Afterload aka EJECTION of blood). When the heart contracts. this OXYGENATED blood enters the heart from the pulmonary veins (Dont let this trick you! Veins return blood to the heart!).